National Ambient Air Quality Standards for Ozone, 2938-3052 [2010-340]
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Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules
40 CFR Parts 50 and 58
[EPA–HQ–OAR–2005–0172; FRL–9102–1]
RIN 2060–AP98
National Ambient Air Quality
Standards for Ozone
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AGENCY: Environmental Protection
Agency (EPA).
ACTION: Proposed rule.
SUMMARY: Based on its reconsideration
of the primary and secondary national
ambient air quality standards (NAAQS)
for ozone (O3) set in March 2008, EPA
proposes to set different primary and
secondary standards than those set in
2008 to provide requisite protection of
public health and welfare, respectively.
With regard to the primary standard for
O3, EPA proposes that the level of the
8-hour primary standard, which was set
at 0.075 ppm in the 2008 final rule,
should instead be set at a lower level
within the range of 0.060 to 0.070 parts
per million (ppm), to provide increased
protection for children and other ‘‘at
risk’’ populations against an array of O3related adverse health effects that range
from decreased lung function and
increased respiratory symptoms to
serious indicators of respiratory
morbidity including emergency
department visits and hospital
admissions for respiratory causes, and
possibly cardiovascular-related
morbidity as well as total nonaccidental and cardiopulmonary
mortality. With regard to the secondary
standard for O3, EPA proposes that the
secondary O3 standard, which was set
identical to the revised primary
standard in the 2008 final rule, should
instead be a new cumulative, seasonal
standard expressed as an annual index
of the sum of weighted hourly
concentrations, cumulated over 12
hours per day (8 am to 8 pm) during the
consecutive 3-month period within the
O3 season with the maximum index
value, set at a level within the range of
7 to 15 ppm-hours, to provide increased
protection against O3-related adverse
impacts on vegetation and forested
ecosystems.
DATES: Written comments on this
proposed rule must be received by
March 22, 2010.
Public Hearings: Three public
hearings are scheduled for this proposed
rule. Two of the public hearings will be
held on February 2, 2010 in Arlington,
Virginia, and Houston, Texas. The third
public hearing will be held on February
4, 2010 in Sacramento, California.
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Submit your comments,
identified by Docket ID No. EPA–HQ–
OAR–2005–0172, by one of the
following methods:
• https://www.regulations.gov: Follow
the on-line instructions for submitting
comments.
• E-mail: a-and-r-Docket@epa.gov.
• Fax: 202–566–9744.
• Mail: Docket No. EPA–HQ–OAR–
2005–0172, Environmental Protection
Agency, Mail code 6102T, 1200
Pennsylvania Ave., NW., Washington,
DC 20460. Please include a total of two
copies.
• Hand Delivery: Docket No. EPA–
HQ–OAR–2005–0172, Environmental
Protection Agency, EPA West, Room
3334, 1301 Constitution Ave., NW.,
Washington, DC. Such deliveries are
only accepted during the Docket’s
normal hours of operation, and special
arrangements should be made for
deliveries of boxed information.
Public Hearings: Three public
hearings are scheduled for this proposed
rule. Two of the public hearings will be
held on February 2, 2010 in Arlington,
Virginia and Houston, Texas. The third
public hearing will be held on February
4, 2010 in Sacramento, California. The
hearings will be held at the following
locations:
ADDRESSES:
ENVIRONMENTAL PROTECTION
AGENCY
Arlington, Virginia—February 2, 2010
Hyatt Regency Crystal City @ Reagan
National Airport, Washington Room
(located on the Ballroom Level), 2799
Jefferson Davis Highway, Arlington,
Virginia 22202, Telephone: 703–418–
1234.
Houston, Texas—February 2, 2010
Hilton Houston Hobby Airport, Moody
Ballroom (located on the ground
floor), 8181 Airport Boulevard,
Houston, Texas 77061, Telephone:
713–645–3000.
Sacramento, California—February 4,
2010
Four Points by Sheraton Sacramento
International Airport, Natomas
Ballroom, 4900 Duckhorn Drive,
Sacramento, California 95834,
Telephone: 916–263–9000.
See the SUPPLEMENTARY INFORMATION
under ‘‘Public Hearings’’ for further
information.
Instructions: Direct your comments to
Docket ID No. EPA–HQ–OAR–2005–
0172. The EPA’s policy is that all
comments received will be included in
the public docket without change and
may be made available online at
www.regulations.gov, including any
personal information provided, unless
the comment includes information
claimed to be Confidential Business
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Information (CBI) or other information
whose disclosure is restricted by statute.
Do not submit information that you
consider to be CBI or otherwise
protected through www.regulations.gov
or e-mail. The www.regulations.gov Web
site is an ‘‘anonymous access’’ system,
which means EPA will not know your
identity or contact information unless
you provide it in the body of your
comment. If you send an e-mail
comment directly to EPA without going
through www.regulations.gov, your email address will be automatically
captured and included as part of the
comment that is placed in the public
docket and made available on the
Internet. If you submit an electronic
comment, EPA recommends that you
include your name and other contact
information in the body of your
comment and with any disk or CD–ROM
you submit. If EPA cannot read your
comment due to technical difficulties
and cannot contact you for clarification,
EPA may not be able to consider your
comment. Electronic files should avoid
the use of special characters, any form
of encryption, and be free of any defects
or viruses.
Docket: All documents in the docket
are listed in the www.regulations.gov
index. Although listed in the index,
some information is not publicly
available, e.g., CBI or other information
whose disclosure is restricted by statute.
Certain other material, such as
copyrighted material, will be publicly
available only in hard copy. Publicly
available docket materials are available
either electronically in
www.regulations.gov or in hard copy at
the Air and Radiation Docket and
Information Center, EPA/DC, EPA West,
Room 3334, 1301 Constitution Ave.,
NW., Washington, DC. The Public
Reading Room is open from 8:30 a.m. to
4:30 p.m., Monday through Friday,
excluding legal holidays. The telephone
number for the Public Reading Room is
(202) 566–1744 and the telephone
number for the Air and Radiation
Docket and Information Center is (202)
566–1742.
FOR FURTHER INFORMATION CONTACT: Ms.
Susan Lyon Stone, Health and
Environmental Impacts Division, Office
of Air Quality Planning and Standards,
U.S. Environmental Protection Agency,
Mail Code C504–06, Research Triangle
Park, NC 27711; telephone: 919–541–
1146; fax: 919–541–0237; e-mail:
stone.susan@epa.gov.
SUPPLEMENTARY INFORMATION:
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General Information
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What Should I Consider as I Prepare My
Comments for EPA?
1. Submitting CBI. Do not submit this
information to EPA through https://
www.regulations.gov or e-mail. Clearly
mark the part or all of the information
that you claim to be CBI. For CBI
information in a disk or CD–ROM that
you mail to EPA, mark the outside of the
disk or CD–ROM as CBI and then
identify electronically within the disk or
CD–ROM the specific information that
is claimed as CBI. In addition to one
complete version of the comment that
includes information claimed as CBI, a
copy of the comment that does not
contain the information claimed as CBI
must be submitted for inclusion in the
public docket. Information so marked
will not be disclosed except in
accordance with procedures set forth in
40 CFR part 2.
2. Tips for Preparing Your Comments.
When submitting comments, remember
to:
• Identify the rulemaking by docket
number and other identifying
information (subject heading, Federal
Register date and page number).
• Follow directions—The Agency
may ask you to respond to specific
questions or organize comments by
referencing a Code of Federal
Regulations (CFR) part or section
number.
• Explain why you agree or disagree,
suggest alternatives, and substitute
language for your requested changes.
• Describe any assumptions and
provide any technical information and/
or data that you used.
• Provide specific examples to
illustrate your concerns, and suggest
alternatives.
• Explain your views as clearly as
possible, avoiding the use of profanity
or personal threats.
• Make sure to submit your
comments by the comment period
deadline identified.
Availability of Related Information
A number of documents relevant to
this rulemaking are available on EPA
web sites. The Air Quality Criteria for
Ozone and Related Photochemical
Oxidants (2006 Criteria Document) (two
volumes, EPA/and EPA/, date) is
available on EPA’s National Center for
Environmental Assessment Web site. To
obtain this document, go to https://
www.epa.gov/ncea, and click on Ozone
in the Quick Finder section. This will
open a page with a link to the March
2006 Air Quality Criteria Document.
The 2007 Staff Paper, human exposure
and health risk assessments, vegetation
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exposure and impact assessment, and
other related technical documents are
available on EPA’s Office of Air Quality
Planning and Standards (OAQPS)
Technology Transfer Network (TTN)
web site. The updated final 2007 Staff
Paper is available at: https://epa.gov/ttn/
naaqs/standards/ozone/s_o3_cr_sp.html
and the exposure and risk assessments
and other related technical documents
are available at https://www.epa.gov/ttn/
naaqs/standards/ozone/
s_o3_cr_td.html. The Response to
Significant Comments Document is
available at: https://www.epa.gov/ttn/
naaqs/standards/ozone/
s_o3_cr_rc.html. These and other related
documents are also available for
inspection and copying in the EPA
docket identified above.
Public Hearings
The public hearings on February 2,
2010 and February 4, 2010 will provide
interested parties the opportunity to
present data, views, or arguments
concerning the proposed rule. The EPA
may ask clarifying questions during the
oral presentations, but will not respond
to the presentations at that time. Written
statements and supporting information
submitted during the comment period
will be considered with the same weight
as any oral comments and supporting
information presented at the public
hearing. Written comments must be
received by the last day of the comment
period, as specified in this proposed
rulemaking.
The public hearings will begin at 9:30
a.m. and continue until 7:30 p.m. (local
time) or later, if necessary, depending
on the number of speakers wishing to
participate. The EPA will make every
effort to accommodate all speakers that
arrive and register before 7:30 p.m. A
lunch break is scheduled from 12:30
p.m. until 2 p.m.
If you would like to present oral
testimony at the hearings, please notify
Ms. Tricia Crabtree (C504–02), U.S.
EPA, Research Triangle Park, NC 27711.
The preferred method for registering is
by e-mail (crabtree.tricia@epa.gov). Ms.
Crabtree may be reached by telephone at
(919) 541–5688. She will arrange a
general time slot for you to speak. The
EPA will make every effort to follow the
schedule as closely as possible on the
day of the hearing.
Oral testimony will be limited to five
(5) minutes for each commenter to
address the proposal. We will not be
providing equipment for commenters to
show overhead slides or make
computerized slide presentations unless
we receive special requests in advance.
Commenters should notify Ms. Crabtree
if they will need specific audiovisual
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(AV) equipment. Commenters should
also notify Ms. Crabtree if they need
specific translation services for nonEnglish speaking commenters. The EPA
encourages commenters to provide
written versions of their oral testimonies
either electronically on computer disk,
CD–ROM, or in paper copy.
The hearing schedules, including lists
of speakers, will be posted on EPA’s
Web site for the proposal at https://
www.epa.gov/ttn/naaqs/standards/
ozone/s_o3_cr_fr.html prior to the
hearing. Verbatim transcripts of the
hearings and written statements will be
included in the rulemaking docket.
Children’s Environmental Health
Consideration of children’s
environmental health plays a central
role in the reconsideration of the 2008
final decision on the O3 NAAQS and
EPA’s decision to propose to set the
8-hour primary O3 standard at a level
within the range of 0.060 to 0.070 ppm.
Technical information that pertains to
children, including the evaluation of
scientific evidence, policy
considerations, and exposure and risk
assessments, is discussed in all of the
documents listed above in the section
on the availability of related
information. These documents include:
the Air Quality Criteria for Ozone and
Other Related Photochemical Oxidants;
the 2007 Staff Paper; exposure and risk
assessments and other related
documents; and the Response to
Significant Comments. All of these
documents are available on the Web, as
described above, and are in the public
docket for this rulemaking. The public
is invited to submit comments or
identify peer-reviewed studies and data
that assess effects of early life exposure
to O3.
Table of Contents
The following topics are discussed in
this preamble:
I. Background
A. Legislative Requirements
B. Related Control Requirements
C. Review of Air Quality Criteria and
Standards for O3
D. Reconsideration of the 2008 O3 NAAQS
Final Rule
1. Decision to Initiate a Rulemaking to
Reconsider
2. Ongoing Litigation
II. Rationale for Proposed Decision on the
Level of the Primary Standard
A. Health Effects Information
1. Overview of Mechanisms
2. Nature of Effects
3. Interpretation and Integration of Health
Evidence
4. O3-Related Impacts on Public Health
B. Human Exposure and Health Risk
Assessments
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1. Exposure Analyses
2. Quantitative Health Risk Assessment
C. Reconsideration of the Level of the
Primary Standard
1. Evidence and Exposure/Risk-Based
Considerations
2. CASAC Views Prior to 2008 Decision
3. Basis for 2008 Decision on the Primary
Standard
4. CASAC Advice Following 2008 Decision
5. Administrator’s Proposed Conclusions
D. Proposed Decision on the Level of the
Primary Standard
III. Communication of Public Health
Information
IV. Rationale for Proposed Decision on the
Secondary Standard
A. Vegetation Effects Information
1. Mechanisms
2. Nature of Effects
3. Adversity of Effects
B. Biologically Relevant Exposure Indices
C. Vegetation Exposure and Impact
Assessment
1. Exposure Characterization
2. Assessment of Risks to Vegetation
D. Reconsideration of Secondary Standard
1. Considerations Regarding 2007 Proposed
Cumulative Seasonal Standard
2. Considerations Regarding 2007 Proposed
8-Hour Standard
3. Basis for 2008 Decision on the
Secondary Standard
4. CASAC Views Following 2008 Decision
5. Administrator’s Proposed Conclusions
E. Proposed Decision on the Secondary O3
Standard
V. Revision of Appendix P—Interpretation of
the NAAQS for O3 and Proposed
Revisions to the Exceptional Events Rule
A. Background
B. Interpretation of the Secondary O3
Standard
C. Clarifications Related to the Primary
Standard
D. Revisions to Exceptions From Standard
Data Completeness Requirements for the
Primary Standard
E. Elimination of the Requirement for 90
Percent Completeness of Daily Data
Across Three Years
F. Administrator Discretion To Use
Incomplete Data
G. Truncation Versus Rounding
H. Data Selection
I. Exceptional Events Information
Submission Schedule
VI. Ambient Monitoring Related to Proposed
O3 Standards
A. Background
B. Urban Monitoring Requirements
C. Non-Urban Monitoring Requirements
D. Revisions to the Length of the Required
O3 Monitoring Season
VII. Implementation of Proposed O3
Standards
A. Designations
B. State Implementation Plans
C. Trans-boundary Emissions
VIII. Statutory and Executive Order Reviews
A. Executive Order 12866: Regulatory
Planning and Review
B. Paperwork Reduction Act
C. Regulatory Flexibility Act
D. Unfunded Mandates Reform Act
E. Executive Order 13132: Federalism
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F. Executive Order 13175: Consultation
and Coordination With Indian Tribal
Governments
G. Executive Order 13045: Protection of
Children From Environmental Health
and Safety Risks
H. Executive Order 13211: Actions That
Significantly Affect Energy Supply,
Distribution or Use
I. National Technology Transfer and
Advancement Act
J. Executive Order 12898: Federal Actions
To Address Environmental Justice in
Minority Populations and Low-Income
Populations
References
I. Background
The proposed decisions presented in
this notice are based on a
reconsideration of the 2008 O3 NAAQS
final rule (73 FR 16436, March 27,
2008), which revised the level of the 8hour primary O3 standard to 0.075 ppm
and revised the secondary O3 standard
by making it identical to the revised
primary standard. This reconsideration
is based on the scientific and technical
information and analyses on which the
March 2008 O3 NAAQS rulemaking was
based. Therefore, much of the
information included in this notice is
drawn directly from information
included in the 2007 proposed rule (72
FR 37818, July 11, 2007) and the 2008
final rule (73 FR 16436).
A. Legislative Requirements
Two sections of the Clean Air Act
(CAA) govern the establishment and
revision of the NAAQS. Section 108 (42
U.S.C. 7408) directs the Administrator
to identify and list ‘‘air pollutants’’ that
in her ‘‘judgment, cause or contribute to
air pollution which may reasonably be
anticipated to endanger public health or
welfare’’ and satisfy two other criteria,
including ‘‘whose presence * * * in the
ambient air results from numerous or
diverse mobile or stationary sources’’
and to issue air quality criteria for those
that are listed. Air quality criteria are
intended to ‘‘accurately reflect the latest
scientific knowledge useful in
indicating the kind and extent of all
identifiable effects on public health or
welfare which may be expected from the
presence of [a] pollutant in the ambient
air. * * *’’
Section 109 (42 U.S.C. 7409) directs
the Administrator to propose and
promulgate ‘‘primary’’ and ‘‘secondary’’
NAAQS for pollutants for which air
quality criteria are issued. Section
109(b)(1) defines a primary standard as
one ‘‘the attainment and maintenance of
which in the judgment of the
Administrator, based on such criteria
and allowing an adequate margin of
safety, are requisite to protect the public
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health.’’ 1 A secondary standard, as
defined in section 109(b)(2), must
‘‘specify a level of air quality the
attainment and maintenance of which,
in the judgment of the Administrator,
based on such criteria, is requisite to
protect the public welfare from any
known or anticipated adverse effects
associated with the presence of such air
pollutant in the ambient air.’’ 2
The requirement that primary
standards include an adequate margin of
safety was intended to address
uncertainties associated with
inconclusive scientific and technical
information available at the time of
standard setting. It was also intended to
provide a reasonable degree of
protection against hazards that research
has not yet identified. Lead Industries
Association v. EPA, 647 F.2d 1130, 1154
(DC Cir 1980), cert. denied, 449 U.S.
1042 (1980); American Petroleum
Institute v. Costle, 665 F.2d 1176, 1186
(DC Cir. 1981), cert. denied, 455 U.S.
1034 (1982). Both kinds of uncertainties
are components of the risk associated
with pollution at levels below those at
which human health effects can be said
to occur with reasonable scientific
certainty. Thus, in selecting primary
standards that include an adequate
margin of safety, the Administrator is
seeking not only to prevent pollution
levels that have been demonstrated to be
harmful but also to prevent lower
pollutant levels that may pose an
unacceptable risk of harm, even if the
risk is not precisely identified as to
nature or degree. The CAA does not
require the Administrator to establish a
primary NAAQS at a zero-risk level or
at background concentration levels, see
Lead Industries Association v. EPA, 647
F.2d at 1156 n. 51, but rather at a level
that reduces risk sufficiently so as to
protect public health with an adequate
margin of safety.
In addressing the requirement for an
adequate margin of safety, EPA
considers such factors as the nature and
severity of the health effects involved,
the size of the population(s) at risk, and
the kind and degree of the uncertainties
1 The legislative history of section 109 indicates
that a primary standard is to be set at ‘‘the
maximum permissible ambient air level * * *
which will protect the health of any [sensitive]
group of the population,’’ and that for this purpose
‘‘reference should be made to a representative
sample of persons comprising the sensitive group
rather than to a single person in such a group’’ [S.
Rep. No. 91–1196, 91st Cong., 2d Sess. 10 (1970)].
2 Welfare effects as defined in section 302(h) (42
U.S.C. 7602(h)) include, but are not limited to,
‘‘effects on soils, water, crops, vegetation, man-made
materials, animals, wildlife, weather, visibility, and
climate, damage to and deterioration of property,
and hazards to transportation, as well as effects on
economic values and on personal comfort and wellbeing.’’
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that must be addressed. The selection of
any particular approach to providing an
adequate margin of safety is a policy
choice left specifically to the
Administrator’s judgment. Lead
Industries Association v. EPA, 647 F.2d
at 1161–62; Whitman v. American
Trucking Associations, 531 U.S. 457,
495 (2001).
In setting standards that are
‘‘requisite’’ to protect public health and
welfare, as provided in section 109(b),
EPA’s task is to establish standards that
are neither more nor less stringent than
necessary for these purposes. Whitman
v. America Trucking Associations, 531
U.S. 457, 473. In establishing ‘‘requisite’’
primary and secondary standards, EPA
may not consider the costs of
implementing the standards. Id. at 471.
Section 109(d)(1) of the CAA requires
that ‘‘not later than December 31, 1980,
and at 5-year intervals thereafter, the
Administrator shall complete a
thorough review of the criteria
published under section 108 and the
national ambient air quality standards
* * * and shall make such revisions in
such criteria and standards and
promulgate such new standards as may
be appropriate. * * *’’ Section 109(d)(2)
requires that an independent scientific
review committee ‘‘shall complete a
review of the criteria * * * and the
national primary and secondary ambient
air quality standards * * * and shall
recommend to the Administrator any
new * * * standards and revisions of
existing criteria and standards as may be
appropriate. * * *’’ This independent
review function is performed by the
Clean Air Scientific Advisory
Committee (CASAC) of EPA’s Science
Advisory Board.
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B. Related Control Requirements
States have primary responsibility for
ensuring attainment and maintenance of
ambient air quality standards once EPA
has established them. Under section 110
of the Act (42 U.S.C. 7410) and related
provisions, States are to submit, for EPA
approval, State implementation plans
(SIPs) that provide for the attainment
and maintenance of such standards
through control programs directed to
emission sources.
The majority of man-made nitrogen
oxides (NOX) and volatile organic
compounds (VOC) emissions that
contribute to O3 formation in the United
States come from three types of sources:
Mobile sources, industrial processes
(which include consumer and
commercial products), and the electric
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power industry.3 Mobile sources and
the electric power industry were
responsible for 78 percent of annual
NOX emissions in 2004. That same year,
99 percent of man-made VOC emissions
came from industrial processes
(including solvents) and mobile sources.
Emissions from natural sources, such as
trees, may also comprise a significant
portion of total VOC emissions in
certain regions of the country, especially
during the O3 season, which are
considered natural background
emissions.
The EPA has developed new
emissions standards for many types of
stationary sources and for nearly every
class of mobile sources in the last
decade to reduce O3 by decreasing
emissions of NOX and VOC. These
programs complement State and local
efforts to improve O3 air quality and
meet the 0.084 ppm 8-hour national
standards. Under title II of the CAA, 42
U.S.C. 7521–7574), EPA has established
new emissions standards for nearly
every type of automobile, truck, bus,
motorcycle, earth mover, and aircraft
engine, and for the fuels used to power
these engines. EPA also established new
standards for the smaller engines used
in small watercraft, lawn and garden
equipment. In March 2008, EPA
promulgated new standards for
locomotive and marine diesel engines
and in August 2009, proposed to control
emissions from ocean-going vessels.
Benefits from engine standards
increase modestly each year as older,
more-polluting vehicles and engines are
replaced with newer, cleaner models. In
time, these programs will yield
substantial emission reductions.
Benefits from fuel programs generally
begin as soon as a new fuel is available.
The reduction of VOC emissions from
industrial processes has been achieved
either directly or indirectly through
implementation of control technology
standards, including maximum
achievable control technology,
reasonably available control technology,
and best available control technology
standards; or are anticipated due to
proposed or upcoming proposals based
on generally available control
technology or best available controls
under provisions related to consumer
and commercial products. These
standards have resulted in VOC
emission reductions of almost a million
tons per year accumulated starting in
1997 from a variety of sources including
combustion sources, coating categories,
and chemical manufacturing. EPA has
3 See EPA report, Evaluating Ozone Control
Programs in the Eastern United States: Focus on the
NOX Budget Trading Program, 2004.
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also finalized emission standards and
fuel requirements for new stationary
engines. In the area of consumer and
commercial products, EPA has finalized
new national VOC emission standards
for aerosol coatings and is working
toward amending existing rules to
establish new nationwide VOC content
limits for household and institutional
consumer products and architectural
and industrial maintenance coatings.
The aerosol coatings rule took effect in
July 2009; the compliance date for both
the amended consumer product rule
and architectural coatings rule is
anticipated to be January 2011. These
actions are expected to yield significant
new VOC reductions—about 200,000
tons per year. Additionally, in ozone
nonattainment areas, we anticipate
reductions of an additional 25,000 tons
per year as States adopt rules this year
implementing control techniques
recommendations issued in 2008 for 4
additional categories of consumer and
commercial products, typically surface
coatings and adhesives used in
industrial manufacturing operations.
These emission reductions primarily
result from solvent controls and
typically occur where and when the
solvent is used, such as during
manufacturing processes.
The power industry is one of the
largest emitters of NOX in the United
States. Power industry emission sources
include large electric generating units
(EGU) and some large industrial boilers
and turbines. The EPA’s landmark Clean
Air Interstate Rule (CAIR), issued on
March 10, 2005, was designed to
permanently cap power industry
emissions of NOX in the eastern United
States. The first phase of the cap was to
begin in 2009, and a lower second phase
cap was to begin in 2015. The EPA had
projected that by 2015, the CAIR and
other programs would reduce NOX
emissions during the O3 season by about
50 percent and annual NOX emissions
by about 60 percent from 2003 levels in
the Eastern U.S. However, on July 11,
2008 and December 23, 2008, the U.S.
Court of Appeals for the DC Circuit
issued decisions on petitions for review
of the CAIR. In its July 11 opinion, the
court found CAIR unlawful and decided
to vacate CAIR and its associated
Federal implementation plans (FIPs) in
their entirety. On December 23, the
court granted EPA’s petition for
rehearing to the extent that it remanded
without vacatur for EPA to conduct
further proceedings consistent with the
Court’s prior opinion. Under this
decision, CAIR will remain in place
only until replaced by EPA with a rule
that is consistent with the Court’s July
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11 opinion. The EPA recognizes the
need in our CAIR replacement effort to
address the reconsidered ozone
standard, and we are currently assessing
our options for the best way to
accomplish this. It should also be noted
that new electric generating units
(EGUs) are also subject to NOX limits
under New Source Performance
Standards (NSPS) under CAA section
111, as well as either nonattainment
new source review or prevention of
significant deterioration requirements.
With respect to agricultural sources,
the U.S. Department of Agriculture
(USDA) has approved conservation
systems and activities that reduce
agricultural emissions of NOX and VOC.
Current practices that may reduce
emissions of NOX and VOC include
engine replacement programs, diesel
retrofit programs, manipulation of
pesticide applications including timing
of applications, and animal feeding
operations waste management
techniques. The EPA recognizes that
USDA has been working with the
agricultural community to develop
conservation systems and activities to
control emissions of O3 precursors.
These conservation activities are
voluntarily adopted through the use of
incentives provided to the agricultural
producer. In cases where the States need
these measures to attain the standard,
the measures could be adopted. The
EPA will continue to work with USDA
on these activities with efforts to
identify and/or improve the control
efficiencies, prioritize the adoption of
these conservation systems and
activities, and ensure that appropriate
criteria are used for identifying the most
effective application of conservation
systems and activities.
The EPA will work together with
USDA and with States to identify
appropriate measures to meet the
primary and secondary standards,
including site-specific conservation
systems and activities. Based on prior
experience identifying conservation
measures and practices to meet the PM
NAAQS requirements, the EPA will use
a similar process to identify measures
that could meet the O3 requirements.
The EPA anticipates that certain USDAapproved conservation systems and
activities that reduce agricultural
emissions of NOX and VOC may be able
to satisfy the requirements for
applicable sources to implement
reasonably available control measures
for purposes of attaining the primary
and secondary O3 NAAQS.
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C. Review of Air Quality Criteria and
Standards for O3
In 1971, EPA first established primary
and secondary NAAQS for
photochemical oxidants (36 FR 8186).
Both primary and secondary standards
were set at a level of 0.08 parts per
million (ppm), 1-hr average, total
photochemical oxidants, not to be
exceeded more than one hr per year. In
1977, EPA announced the first periodic
review of the air quality criteria in
accordance with section 109(d)(1) of the
Act. The EPA published a final decision
in 1979 (44 FR 8202). Both primary and
secondary standard levels were revised
from 0.08 to 0.12 ppm. The indicator
was revised from photochemical
oxidants to O3, and the form of the
standards was revised from a
deterministic to a statistical form, which
defined attainment of the standards as
occurring when the expected number of
days per calendar year with maximum
hourly average concentration greater
than 0.12 ppm is equal to or less than
one. In 1983, EPA announced that the
second periodic review of the primary
and secondary standards for O3 had
been initiated. Following review and
publication of air quality criteria and a
supplement, EPA published a proposed
decision (57 FR 35542) in August 1992
that announced EPA’s intention to
proceed as rapidly as possible with the
next review of the air quality criteria
and standards for O3 in light of
emerging evidence of health effects
related to 6- to 8-hr O3 exposures. In
March 1993, EPA concluded the review
by deciding that revisions to the
standards were not warranted at that
time (58 FR 13008).
In August 1992 (57 FR 35542), EPA
announced plans to initiate the third
periodic review of the air quality criteria
and O3 NAAQS. On the basis of the
scientific evidence contained in the
1996 CD (U.S. EPA 1996a) and the 1996
Staff Paper (U.S. EPA, 1996b), and
related technical support documents,
linking exposures to ambient O3 to
adverse health and welfare effects at
levels allowed by the then existing
standards, EPA proposed to revise the
primary and secondary O3 standards in
December 1996 (61 FR 65716). The EPA
proposed to replace the then existing
1-hour primary and secondary standards
with 8-hour average O3 standards set at
a level of 0.08 ppm (equivalent to 0.084
ppm using standard rounding
conventions). The EPA also proposed,
in the alternative, to establish a new
distinct secondary standard using a
biologically based cumulative seasonal
form. The EPA completed the review in
July 1997 (62 FR 38856) by setting the
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primary standard at a level of 0.08 ppm,
based on the annual fourth-highest daily
maximum 8-hr average concentration,
averaged over three years, and setting
the secondary standard identical to the
revised primary standard.
The EPA initiated the most recent
periodic review of the air quality criteria
and standards for O3 in September 2000
with a call for information (65 FR
57810; September 26, 2000) for the
development of a revised Air Quality
Criteria Document for O3 and Other
Photochemical Oxidants (henceforth the
‘‘2006 Criteria Document’’). A project
work plan (EPA, 2002) for the
preparation of the Criteria Document
was released in November 2002 for
CASAC and public review. The EPA
held a series of workshops in mid-2003
on several draft chapters of the Criteria
Document to obtain broad input from
the relevant scientific communities.
These workshops helped to inform the
preparation of the first draft Criteria
Document (EPA, 2005a), which was
released for CASAC and public review
on January 31, 2005; a CASAC meeting
was held on May 4–5, 2005 to review
the first draft Criteria Document. A
second draft Criteria Document (EPA,
2005b) was released for CASAC and
public review on August 31, 2005, and
was discussed along with a first draft
Staff Paper (EPA, 2005c) at a CASAC
meeting held on December 6–8, 2005. In
a February 16, 2006 letter to the
Administrator, CASAC provided
comments on the second draft Criteria
Document (Henderson, 2006a), and the
final 2006 Criteria Document (EPA,
2006a) was released on March 21, 2006.
In a June 8, 2006 letter to the
Administrator (Henderson, 2006b),
CASAC provided additional advice to
the Agency concerning chapter 8 of the
final 2006 Criteria Document
(Integrative Synthesis) to help inform
the second draft Staff Paper.
A second draft Staff Paper (EPA,
2006b) was released on July 17, 2006
and reviewed by CASAC on August 24–
25, 2006. In an October 24, 2006 letter
to the Administrator, CASAC provided
advice and recommendations to the
Agency concerning the second draft
Staff Paper (Henderson, 2006c). A final
2007 Staff Paper (EPA, 2007a) was
released on January 31, 2007. In a March
26, 2007 letter (Henderson, 2007),
CASAC offered additional advice to the
Administrator with regard to
recommendations and revisions to the
primary and secondary O3 NAAQS.
The schedule for completion of the
2008 rulemaking was governed by a
consent decree resolving a lawsuit filed
in March 2003 by a group of plaintiffs
representing national environmental
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and public health organizations,
alleging that EPA had failed to complete
the review within the period provided
by statute.4 The modified consent
decree that governed the 2008
rulemaking, entered by the court on
December 16, 2004, provided that EPA
sign for publication notices of proposed
and final rulemaking concerning its
review of the O3 NAAQS no later than
March 28, 2007 and December 19, 2007,
respectively. That consent decree was
further modified in October 2006 to
change these proposed and final
rulemaking dates to no later than May
30, 2007 and February 20, 2008,
respectively. These dates for signing the
publication notices of proposed and
final rulemaking were further extended
to no later than June 20, 2007 and
March 12, 2008, respectively. The
proposed decision was signed on June
20, 2007 and published in the Federal
Register on July 11, 2007 (72 FR 37818).
Public hearings on the proposed
decision were held on Thursday, August
30, 2007 in Philadelphia, PA and Los
Angeles, CA. On Wednesday, September
5, 2007, hearings were held in Atlanta,
GA, Chicago, IL, and Houston, TX. A
large number of comments were
received from various commenters on
the 2007 proposed revisions to the O3
NAAQS. A comprehensive summary of
all significant comments, along with
EPA’s responses (henceforth ‘‘Response
to Comments’’), can be found in the
docket for the 2008 rulemaking, which
is also the docket for this
reconsideration rulemaking.
The EPA’s final decision on the O3
NAAAQS was published in the Federal
Register on March 27, 2008 (73 FR
16436). In the 2008 rulemaking, EPA
revised the level of the 8-hour primary
standard for O3 to 0.075 parts per
million (ppm), expressed to three
decimal places. With regard to the
secondary standard for O3, EPA revised
the 8-hour standard by making it
identical to the revised primary
standard. The EPA also made
conforming changes to the Air Quality
Index (AQI) for O3, setting an AQI value
of 100 equal to 0.075 ppm, 8-hour
average, and making proportional
changes to the AQI values of 50, 150
and 200.
D. Reconsideration of the 2008 O3
NAAQS Final Rule
Consistent with a directive of the new
Administration regarding the review of
new and pending regulations (Emanuel
memorandum, 74 FR 4435; January 26,
2009), the Administrator reviewed a
4 American
Lung Association v. Whitman (No.
1:03CV00778, D.DC 2003).
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number of actions that were taken in the
last year by the previous
Administration. The 2008 final rule was
included in this review in recognition of
the central role that the NAAQS play in
enabling EPA to fulfill its mission to
protect the nation’s public health and
welfare. In her review, the
Administrator was mindful of the need
for judgments concerning the NAAQS to
be based on a strong scientific
foundation which is developed through
a transparent and credible NAAQS
review process, consistent with the core
values highlighted in President Obama’s
memorandum on scientific integrity
(March 9, 2009).
1. Decision To Initiate a Rulemaking To
Reconsider
In her review of the 2008 final rule,
several aspects of the final rule related
to the primary and secondary standards
stood out to the Administrator. As an
initial matter, the Administrator noted
that the 2008 final rule concluded that
the 1997 primary and secondary O3
standards were not adequate to protect
public health and public welfare, and
that revisions were necessary to provide
increased protection. With respect to
revision of the primary standard, the
Administrator noted that the revised
level established in the 2008 final rule
was above the range that had been
unanimously recommended by
CASAC.5 She also noted that EPA
received comments from a large number
of commenters from the medical and
public health communities, including
EPA’s Children’s Health Protection
Advisory Committee, all of which
endorsed levels within CASAC’s
recommended range.
With respect to revision of the
secondary O3 standard, the
Administrator noted that the 2008 final
rule differed substantially from
CASAC’s recommendations that EPA
adopt a new secondary O3 standard
based on a cumulative, seasonal
measure of exposure. The 2008 final
rule revised the secondary standard to
be identical to the revised primary
standard, which is based on an 8-hour
daily maximum measure of exposure.
She also noted that EPA received
comments from a number of
commenters representing environmental
interests, all of which endorsed
CASAC;s recommendation for a new
cumulative, seasonal secondary
standard.6
5 The level of the 8-hour primary ozone standard
was set at 0.075 ppm, while CASAC unanimously
recommended a range between 0.060 and 0.070
ppm.
6 The Administrator also noted the exchange that
had occurred between EPA and the Office of
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Subsequent to issuance of the 2008
final rule, in April 2008, CASAC took
the unusual step of sending EPA a letter
expressing strong, unanimous
disagreement with EPA’s decisions on
both the primary and secondary
standards (Henderson, 2008). The
CASAC explained that it did not
endorse the revised primary O3 standard
as being sufficiently protective of public
health because it failed to satisfy the
explicit stipulation of the Act to provide
an adequate margin of safety. The
CASAC also expressed the view that
failing to revise the secondary standard
to a cumulative, seasonal form was not
supported by the available science. In
addition to CASAC’s letter, the
Administrator noted a recent adverse
ruling issued by the U.S. Court of
Appeals for the District of Columbia
Circuit on another NAAQS decision. In
February 2009, the DC Circuit remanded
the Agency’s decisions on the primary
annual and secondary standards for fine
particles (PM2.5). In so doing, the Court
found that EPA had not adequately
explained the basis for its decisions,
including why CASAC’s
recommendations for a more healthprotective primary annual standard and
for secondary standards different from
the primary standards were not
accepted. American Farm Bureau v.
EPA, 559 F.3d. 512 (DC Cir. 2009).
Based on her review of the
information described above, the
Administrator is initiating a rulemaking
to reconsider parts of the 2008 final
rule. Specifically, the Administrator is
reconsidering the level of the primary
standard to ensure that it is sufficiently
protective of public health, as discussed
in section II below, and is reconsidering
all aspects of the secondary standard to
ensure that it appropriately reflects the
available science and is sufficiently
protective of public welfare, as
discussed in section IV below. Based on
her review, the Administrator has
serious cause for concern regarding
whether the revisions to the primary
and secondary O3 standards adopted in
the 2008 final rule satisfy the
requirements of the CAA, in light of the
body of scientific evidence before the
Agency. In addition, the importance of
the O3 NAAQS to public health and
welfare weigh heavily in favor of
reconsidering parts of the 2008 final
rule as soon as possible, based on the
scientific and technical information
upon which the 2008 final rule was
based.
Management and Budget (OMB) with regard to the
final decision on the secondary standard, as
discussed in the 2008 final rule (73 FR 16497).
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Also, EPA conducted a provisional
assessment of ‘‘new’’ scientific papers
(EPA, 2009) of scientific literature
evaluating health and ecological effects
of O3 exposure published since the close
of the 2006 Criteria Document upon
which the 2008 O3 NAAQS were based.
The Administrator notes that the
provisional assessment of ‘‘new’’ science
found that such studies did not
materially change the conclusions in the
2006 Criteria Document. This
provisional assessment is supportive of
the Administrator’s decision to
reconsider parts of the 2008 final rule at
this time, based on the scientific and
technical information available for the
2008 final rule, as compared to
foregoing such reconsideration and
taking appropriate action in the future
as part of the next periodic review of the
air quality criteria and NAAQS, which
will include such scientific and
technical information.
The reconsideration of parts of the
2008 final rule discussed in this notice
is based on the scientific and technical
record from the 2008 rulemaking,
including public comments and CASAC
advice and recommendations. The
information that was assessed during
the 2008 rulemaking includes
information in the 2006 Criteria
Document (EPA, 2006a), the 2007 Policy
Assessment of Scientific and Technical
Information, referred to as the 2007 Staff
Paper (EPA, 2007b), and related
technical support documents including
the 2007 REAs (U.S. EPA, 2007c; Abt
Associates, 2007a,b). Scientific and
technical information developed since
the 2006 Criteria Document will be
considered in the next periodic review,
instead of this reconsideration
rulemaking, allowing the new
information to receive careful and
comprehensive review by CASAC and
the public before it is used as a basis in
a rulemaking that determines whether to
revise the NAAQS.
2. Ongoing Litigation
In May 2008, following publication of
the 2008 final rule, numerous groups,
including state, public health,
environmental, and industry petitioners,
challenged EPA’s decisions in federal
court. The challenges were consolidated
as State of Mississippi, et al. v. EPA (No.
08–1200, DC Cir. 2008). On March 10,
2009, EPA filed an unopposed motion
requesting that the Court vacate the
briefing schedule and hold the
consolidated cases in abeyance. The
Agency stated its desire to allow time
for appropriate officials from the new
Administration to review the O3
standards to determine whether they
should be maintained, modified or
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otherwise reconsidered. The EPA
further requested that it be directed to
notify the Court and all the parties of
any actions it has taken or intends to
take, if any, within 180 days of the
Court vacating the briefing schedule. On
March 19, 2009, the Court granted EPA’s
motion. Pursuant to the Court’s order,
on September 16, 2009 EPA notified the
Court and the parties of its decision to
initiate a rulemaking to reconsider the
primary and secondary O3 standards set
in March 2008 to ensure they satisfy the
requirements of the CAA.7 In its notice
to the Court, EPA stated that this notice
of proposed rulemaking would be
signed by December 21, 2009, and that
the final rule will be signed by August
31, 2010.
II. Rationale for Proposed Decision on
the Level of the Primary Standard
As an initial matter, the Administrator
notes that the 2008 final rule concluded
that the 1997 primary O3 standard was
‘‘not sufficient and thus not requisite to
protect public health with an adequate
margin of safety, and that revision is
needed to provide increased public
health protection’’ (73 FR 16472). The
Administrator is not reconsidering this
aspect of the 2008 decision, which is
based on the reasons discussed in
section II.B of the 2008 final rule (73 FR
16443–16472). The Administrator also
notes that the 2008 final rule concluded
that it was appropriate to retain the O3
indicator, the 8-hour averaging time,
and form of the primary O3 standard
(specified as the annual fourth-highest
daily maximum 8-hour concentration,
averaged over 3 years), while
concluding that revision of the standard
level was appropriate.8 The
Administrator is not reconsidering these
aspects of the 2008 decision, which are
based on the reasons discussed in
sections II.C.1–3 of the 2008 final rule,
which address the indicator, averaging
time, and form, respectively, of the
primary O3 standard (73 FR 16472–
16475). For these reasons, the
Administrator is not reopening the 2008
7 The EPA also separately announced that it will
move quickly to implement any new standards that
might result from this reconsideration. To reduce
the workload for states during the interim period of
reconsideration, the Agency intends to propose to
defer compliance with the CAA requirement to
designate areas as attainment or nonattainment.
EPA will work with states, local governments and
tribes to ensure that air quality is protected during
that time.
8 The use of O as the indicator for photochemical
3
oxidants was adopted in the 1979 final rule and
retained in subsequent rulemaking. An 8-hour
averaging time and a form based on the annual
fourth-highest daily maximum 8-hour
concentration, averaged over 3 years, were adopted
in the 1997 final rule and retained in the 2008
rulemaking.
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decision with regard to the need to
revise the 1997 primary O3 standard nor
with regard to the indicator, averaging
time, and form of the 2008 primary O3
standard. Thus, the information that
follows in this section specifically
focuses on a reconsideration of level of
the primary O3 standard.
This section presents the rationale for
the Administrator’s proposed decision
that the O3 primary standard, which was
set at a level of 0.075 ppm in the 2008
final rule, should instead be set at a
lower level within the range from 0.060
to 0.070 ppm. As discussed more fully
below, the rationale for the proposed
range of standard levels is based on a
thorough review of the latest scientific
information on human health effects
associated with the presence of O3 in
the ambient air presented in the 2006
Criteria Document. This rationale also
takes into account: (1) Staff assessments
of the most policy-relevant information
in the 2006 Criteria Document and staff
analyses of air quality, human exposure,
and health risks, presented in the 2007
Staff Paper, upon which staff
recommendations for revisions to the
primary O3 standard in the 2008
rulemaking were based; (2) CASAC
advice and recommendations, as
reflected in discussions of drafts of the
2006 Criteria Document and 2007 Staff
Paper at public meetings, in separate
written comments, and in CASAC’s
letters to the Administrator both before
and after the 2008 rulemaking; and (3)
public comments received during the
development of these documents, either
in connection with CASAC meetings or
separately, and on the 2007 proposed
rule.
In developing this rationale, the
Administrator recognizes that the CAA
requires her to reach a public health
policy judgment as to what standard
would be requisite to protect public
health with an adequate margin of
safety, based on scientific evidence and
technical assessments that have
inherent uncertainties and limitations.
This judgment requires making
reasoned decisions as to what weight to
place on various types of evidence and
assessments, and on the related
uncertainties and limitations. Thus, in
selecting standard levels to propose, and
subsequently in selecting a final level,
the Administrator is seeking not only to
prevent O3 levels that have been
demonstrated to be harmful but also to
prevent lower O3 levels that may pose
an unacceptable risk of harm, even if the
risk is not precisely identified as to
nature or degree.
In this proposed rule, EPA has drawn
upon an integrative synthesis of the
entire body of evidence, published
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through early 2006, on human health
effects associated with the presence of
O3 in the ambient air. As discussed
below in section II.A, this body of
evidence addresses a broad range of
health endpoints associated with
exposure to ambient levels of O3 (EPA,
2006a, chapter 8), and includes over one
hundred epidemiologic studies
conducted in the U.S., Canada, and
many countries around the world.9 In
reconsidering this evidence, EPA
focuses on those health endpoints that
have been demonstrated to be caused by
exposure to O3, or for which the 2006
Criteria Document judges associations
with O3 to be causal, likely causal, or for
which the evidence is highly suggestive
that O3 contributes to the reported
effects. This rationale also draws upon
the results of quantitative exposure and
risk assessments, discussed below in
section II.B. Section II.C focuses on the
considerations upon which the
Administrator’s proposed conclusions
on the level of the primary standard are
based. Policy-relevant evidence-based
and exposure/risk-based considerations
are discussed, and the rationale for the
2008 final rulemaking on the primary
standard and CASAC advice, given both
prior to the development of the 2007
proposed rule and following the 2008
final rule, are summarized. Finally, the
Administrator’s proposed conclusions
on the level of the primary standard are
presented. Section II.D summarizes the
proposed decision on the level of the
primary O3 standard and the solicitation
of public comments.
Judgments made in the 2006 Criteria
Document and 2007 Staff Paper about
the extent to which relationships
between various health endpoints and
short-term exposures to ambient O3 are
likely causal have been informed by
several factors. As discussed below in
section II.A, these factors include the
nature of the evidence (i.e., controlled
human exposure, epidemiological, and/
or toxicological studies) and the weight
of evidence, which takes into account
such considerations as biological
plausibility, coherence of evidence,
strength of association, and consistency
of evidence.
In assessing the health effects data
base for O3, it is clear that human
studies provide the most directly
applicable information for determining
causality because they are not limited
9 In its assessment of the epidemiological
evidence judged to be most relevant to making
decisions on the level of the O3 primary standard,
EPA has placed greater weight on U.S. and
Canadian epidemiologic studies, since studies
conducted in other countries may well reflect
different demographic and air pollution
characteristics.
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by the uncertainties of dosimetry
differences and species sensitivity
differences, which would need to be
addressed in extrapolating animal
toxicology data to human health effects.
Controlled human exposure studies
provide data with the highest level of
confidence since they provide human
health effects data under closely
monitored conditions and can provide
exposure-response relationships.
Epidemiological data provide evidence
of associations between ambient O3
levels and more serious acute and
chronic health effects (e.g., hospital
admissions and mortality) that cannot
be assessed in controlled human
exposure studies. For these studies the
degree of uncertainty introduced by
potentially confounding variables (e.g.,
other pollutants, temperature) and other
factors affects the level of confidence
that the health effects being investigated
are attributable to O3 exposures, alone
and in combination with other
copollutants.
In using a weight of evidence
approach to inform judgments about the
degree of confidence that various health
effects are likely to be caused by
exposure to O3, confidence increases as
the number of studies consistently
reporting a particular health endpoint
grows and as other factors, such as
biological plausibility and strength,
consistency, and coherence of evidence,
increase. Conclusions regarding
biological plausibility, consistency, and
coherence of evidence of O3-related
health effects are drawn from the
integration of epidemiological studies
with mechanistic information from
controlled human exposure studies and
animal toxicological studies. As
discussed below, this type of
mechanistic linkage has been firmly
established for several respiratory
endpoints (e.g., lung function
decrements, lung inflammation) but
remains far more equivocal for
cardiovascular endpoints (e.g.,
cardiovascular-related hospital
admissions). For epidemiological
studies, strength of association refers to
the magnitude of the association and its
statistical strength, which includes
assessment of both effects estimate size
and precision. In general, when
associations yield large relative risk
estimates, it is less likely that the
association could be completely
accounted for by a potential confounder
or some other bias. Consistency refers to
the persistent finding of an association
between exposure and outcome in
multiple studies of adequate power in
different persons, places, circumstances
and times. For example, the magnitude
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of effect estimates is relatively
consistent across recent studies showing
association between short-term, but not
long-term, O3 exposure and mortality.
Based on the information discussed
below in sections II.A.1–II.A.3,
judgments concerning the extent to
which relationships between various
health endpoints and ambient O3
exposures are likely causal are
summarized below in section II.A.3.c.
These judgments reflect the nature of
the evidence and the overall weight of
the evidence, and are taken into
consideration in the quantitative
exposure and risk assessments,
discussed below in section II.B.
To put judgments about health effects
that have been demonstrated to be
caused by exposure to O3, or for which
the 2006 Criteria Document judges
associations with O3 to be causal, likely
causal, or for which the evidence is
highly suggestive that O3 contributes to
the reported effects into a broader
public health context, EPA has drawn
upon the results of the quantitative
exposure and risk assessments. These
assessments provide estimates of the
likelihood that individuals in particular
population groups that are at risk for
various O3-related physiological health
effects would experience ‘‘exposures of
concern’’ and specific health endpoints
under varying air quality scenarios (i.e.,
just meeting various standards 10), as
well as characterizations of the kind and
degree of uncertainties inherent in such
estimates.
In the 2008 final rulemaking and in
this reconsideration, the term
‘‘exposures of concern’’ is defined as
personal exposures while at moderate or
greater exertion to 8-hour average
ambient O3 levels at and above specific
benchmark levels which represent
exposure levels at which O3-related
health effects are known or can
reasonably be inferred to occur in some
individuals, as discussed below in
section II.B.1.11 The EPA emphasizes
10 The exposure assessment done as part of the
2008 final rulemaking considered several air quality
scenarios, including just meeting what was then the
current standard set at a level of 0.084 ppm, as well
as just meeting alternative standards at levels of
0.080, 0.074, 0.070, and 0.064 ppm.
11 Exposures of concern were also considered in
the 1997 review of the O3 NAAQS, and were judged
by EPA to be an important indicator of the public
health impacts of those O3-related effects for which
information was too limited to develop quantitative
estimates of risk but which had been observed in
humans at and above the benchmark level of 0.08
ppm for 6- to 8-hour exposures * * * including
increased nonspecific bronchial responsiveness (for
example, aggravation of asthma), decreased
pulmonary defense mechanisms (suggestive of
increased susceptibility to respiratory infection),
and indicators of pulmonary inflammation (related
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that although the analysis of ‘‘exposures
of concern’’ was conducted using three
discrete benchmark levels (i.e., 0.080,
0.070, and 0.060 ppm), the concept is
more appropriately viewed as a
continuum with greater confidence and
less uncertainty about the existence of
health effects at the upper end and less
confidence and greater uncertainty as
one considers increasingly lower O3
exposure levels. The EPA recognizes
that there is no sharp breakpoint within
the continuum ranging from at and
above 0.080 ppm down to 0.060 ppm. In
considering the concept of exposures of
concern, it is important to balance
concerns about the potential for health
effects and their severity with the
increasing uncertainty associated with
our understanding of the likelihood of
such effects at lower O3 levels.
Within the context of this continuum,
estimates of exposures of concern at
discrete benchmark levels provide some
perspective on the public health
impacts of O3-related health effects that
have been demonstrated in controlled
human exposure and toxicological
studies but cannot be evaluated in
quantitative risk assessments, such as
lung inflammation, increased airway
responsiveness, and changes in host
defenses. They also help in
understanding the extent to which such
impacts have the potential to be reduced
by meeting various standards. These O3related physiological effects are
plausibly linked to the increased
morbidity seen in epidemiological
studies (e.g., as indicated by increased
medication use in asthmatics, school
absences in all children, and emergency
department visits and hospital
admissions in people with lung
disease). Estimates of the number of
people likely to experience exposures of
concern cannot be directly translated
into quantitative estimates of the
number of people likely to experience
specific health effects, since sufficient
information to draw such comparisons
is not available—if such information
were available, these health outcomes
would have been included in the
quantitative risk assessment. Due to
individual variability in responsiveness,
only a subset of individuals who have
exposures at and above a specific
benchmark level can be expected to
experience such adverse health effects,
and susceptible subpopulations such as
those with asthma are expected to be
affected more by such exposures than
healthy individuals. The amount of
weight to place on the estimates of
exposures of concern at any of these
to potential aggravation of chronic bronchitis or
long-term damage to the lungs). (62 FR 38868)
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benchmark levels depends in part on
the weight of the scientific evidence
concerning health effects associated
with O3 exposures at and above that
benchmark level. It also depends on
judgments about the importance from a
public health perspective of the health
effects that are known or can reasonably
be inferred to occur as a result of
exposures at and above the benchmark
level. Such public health policy
judgments are embodied in the NAAQS
standard setting criteria (i.e., standards
that, in the judgment of the
Administrator, are requisite to protect
public health with an adequate margin
of safety).
As discussed below in section II.B.2,
the quantitative health risk assessment
conducted as part of the 2008 final
rulemaking includes estimates of risks
of lung function decrements in
asthmatic and all school age children,
respiratory symptoms in asthmatic
children, respiratory-related hospital
admissions, and non-accidental and
cardiorespiratory-related mortality
associated with recent ambient O3
levels, as well as risk reductions and
remaining risks associated with just
meeting the then current 0.084 ppm
standard and various alternative O3
standards in a number of example urban
areas. There are two parts to this risk
assessment: one part is based on
combining information from controlled
human exposure studies with modeled
population exposure, and the other part
is based on combining information from
community epidemiological studies
with either monitored or adjusted
ambient concentrations levels. This
assessment provides estimates of the
potential magnitude of O3-related health
effects, as well as a characterization of
the uncertainties and variability
inherent in such estimates. This
assessment also provides insights into
the distribution of risks and patterns of
risk reductions associated with meeting
alternative O3 standards.
As discussed below, a substantial
amount of new research conducted
since the 1997 review of the O3 NAAQS
was available to inform the 2008 final
rulemaking, with important new
information coming from epidemiologic
studies as well as from controlled
human exposure, toxicological, and
dosimetric studies. The research studies
newly available in the 2008 final
rulemaking that were evaluated in the
2006 Criteria Document and the
exposure and risk assessments
presented in the 2007 Staff Paper have
undergone intensive scrutiny through
multiple layers of peer review and many
opportunities for public review and
comment. While important
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uncertainties remain in the qualitative
and quantitative characterizations of
health effects attributable to exposure to
ambient O3, and while different
interpretations of these uncertainties
can result in different public health
policy judgments, the review of this
information has been extensive and
deliberate. In the judgment of the
Administrator, this intensive evaluation
of the scientific evidence provides an
adequate basis for this reconsideration
of the 2008 final rulemaking.
A. Health Effects Information
This section outlines key information
contained in the 2006 Criteria
Document (chapters 4–8) and in the
2007 Staff Paper (chapter 3) on known
or potential effects on public health
which may be expected from the
presence of O3 in ambient air. The
information highlighted here
summarizes: (1) New information
available on potential mechanisms for
health effects associated with exposure
to O3; (2) the nature of effects that have
been associated directly with exposure
to O3 and indirectly with the presence
of O3 in ambient air; (3) an integrative
interpretation of the evidence, focusing
on the biological plausibility and
coherence of the evidence; and (4)
considerations in characterizing the
public health impact of O3, including
the identification of ‘‘at risk’’
populations.
The decision in the 1997 review
focused primarily on evidence from
short-term (e.g., 1 to 3 hours) and
prolonged (6 to 8 hours) controlledexposure studies reporting lung
function decrements, respiratory
symptoms, and respiratory
inflammation in humans, as well as
epidemiology studies reporting excess
hospital admissions and emergency
department (ED) visits for respiratory
causes. The 2006 Criteria Document
prepared for the 2008 rulemaking
emphasized the large number of
epidemiological studies published since
the last review with these and
additional health endpoints, including
the effects of acute (short-term and
prolonged) and chronic exposures to O3
on lung function decrements and
enhanced respiratory symptoms in
asthmatic individuals, school absences,
and premature mortality. It also
emphasized important new information
from toxicology, dosimetry, and
controlled human exposure studies.
Highlights of the evidence include:
(1) Two new controlled humanexposure studies are now available that
examine respiratory effects associated
with prolonged O3 exposures at levels
below 0.080 ppm, which was the lowest
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exposure level that had been examined
in the 1997 review.
(2) Numerous controlled humanexposure studies have examined
indicators of O3-induced inflammatory
response in both the upper respiratory
tract (URT) and lower respiratory tract
(LRT), and increased airway
responsiveness to allergens in subjects
with allergic asthma and allergic rhinitis
exposed to O3, while other studies have
examined changes in host defense
capability following O3 exposure of
healthy young adults.
(3) Animal toxicology studies provide
new information regarding mechanisms
of action, increased susceptibility to
respiratory infection, and the biological
plausibility of acute effects and chronic,
irreversible respiratory damage.
(4) Numerous acute exposure
epidemiological studies published
during the past decade offer added
evidence of ambient O3-related lung
function decrements and respiratory
symptoms in physically active healthy
subjects and greater responses in
asthmatic subjects, as well as evidence
on new health endpoints, such as the
relationships between ambient O3
concentrations and asthma medication
use and school absenteeism, and
between ambient O3 and cardiac-related
physiological endpoints.
(5) Several additional studies have
been published over the last decade
examining the temporal associations
between O3 exposures and emergency
department visits for asthma and other
respiratory diseases and respiratoryrelated hospital admissions.
(6) A large number of newly available
epidemiological studies have examined
the effects of acute exposure to PM and
O3 on mortality, notably including large
multicity studies that provide much
more robust and credible information
than was available in the 1997 review,
as well as recent meta-analyses that
have evaluated potential sources of
heterogeneity in O3-mortality
associations.
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1. Overview of Mechanisms
Evidence on possible mechanisms by
which exposure to O3 may result in
acute and chronic health effects is
discussed in chapters 5 and 6 of the
2006 Criteria Document.12 Evidence
from dosimetry, toxicological, and
12 While most of the available evidence addresses
mechanisms for O3, O3 clearly serves as an indicator
for the total photochemical oxidant mixture found
in the ambient air. Some effects may be caused by
one or more components in the overall pollutant
mix, either separately or in combination with O3.
However, O3 clearly dominates these other oxidants
with their concentrations only being a few percent
of the O3 concentration.
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human exposure studies has contributed
to an understanding of the mechanisms
that help to explain the biological
plausibility and coherence of evidence
for O3-induced respiratory health effects
reported in epidemiological studies.
More detailed information about the
physiological mechanisms related to the
respiratory effects of short- and longterm exposure to O3 can be found in
section II.A.3.b.i and II.A.3.b.iii,
respectively. In the past, however, little
information was available to help
explain potential biological mechanisms
which linked O3 exposure to premature
mortality or cardiovascular effects. As
discussed more fully in section
II.A.3.b.ii below, since the 1997 review
an emerging body of animal toxicology
and controlled human exposure
evidence is beginning to suggest
mechanisms that may mediate acute O3
cardiovascular effects. While much is
known about mechanisms that play a
role in O3-related respiratory effects,
additional research is needed to more
clearly understand the role that O3 may
have in contributing to cardiovascular
effects.
With regard to the mechanisms
related to short-term respiratory effects,
scientific evidence discussed in the
2006 Criteria Document (section 5.2)
indicates that reactions of O3 with lipids
and antioxidants in the epithelial lining
fluid and the epithelial cell membranes
of the lung can be the initial step in
mediating deleterious health effects of
O3. This initial step activates a cascade
of events that lead to oxidative stress,
injury, inflammation, airway epithelial
damage and increased alveolar
permeability to vascular fluids.
Inflammation can be accompanied by
increased airway responsiveness, which
is an increased bronchoconstrictive
response to airway irritants and
allergens. Continued respiratory
inflammation also can alter the ability of
the body to respond to infectious agents,
allergens and toxins. Acute
inflammatory responses to O3 in some
healthy people are well documented,
and precursors to lung injury are
observed within 3 hours after exposure
in humans. Repeated respiratory
inflammation can lead to a chronic
inflammatory state with altered lung
structure and lung function and may
lead to chronic respiratory diseases such
as fibrosis and emphysema (EPA, 2006a,
section 8.6.2). The severity of symptoms
and magnitude of response to acute
exposures depend on inhaled dose, as
well as on individual susceptibility to
O3, as discussed below. At the same O3
dose, individuals who are more
susceptible to O3 will have a larger
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2947
response than those who are less
susceptible; among individuals with
similar susceptibility, those who receive
a larger dose will have a larger response
to O3.
The inhaled dose is the product of O3
concentration (C), minute ventilation or
ventilation rate, and duration of
exposure (T), or (C × ventilation rate ×
T). A large body of data regarding the
interdependent effect of these
components of inhaled dose on
pulmonary responses was assessed in
the 1986 and 1996 O3 Criteria
Documents. In an attempt to describe O3
dose-response characteristics, acute
responses were modeled as a function of
total inhaled O3 dose, which was
generally found to be a better predictor
of response than O3 concentration,
ventilation rate, or duration of exposure,
alone, or as a combination of any two
of these factors (EPA 2006a, section 6.2).
Predicted O3-induced decrements in
lung function have been shown to be a
function of exposure concentration,
duration and exercise level for healthy,
young adults (McDonnell et al., 1997). A
meta-analysis of 21 studies (Mudway
and Kelly, 2004) showed that markers of
inflammation and increased cellular
permeability in healthy subjects are
associated with total O3 dose.
The 2006 Criteria Document
summarizes information on potentially
susceptible and vulnerable groups in
section 8.7. As described there, the term
susceptibility refers to innate (e.g.,
genetic or developmental) or acquired
(e.g., personal risk factors, age) factors
that make individuals more likely to
experience effects with exposure to
pollutants. A number of population
groups and lifestages have been
identified as potentially susceptible to
health effects as a result of O3 exposure,
including people with existing lung
diseases, including asthma, children
and older adults, and people who have
larger than normal lung function
responses that may be due to genetic
susceptibility. In addition, some
population groups and lifestages have
been identified as having increased
vulnerability to O3-related effects due to
increased likelihood of exposure while
at elevated ventilation rates, including
healthy children and adults who are
active outdoors, for example, outdoor
workers, and joggers. Taken together,
the susceptible and vulnerable groups
are more commonly referred to as ‘‘atrisk’’ groups,13 as discussed more fully
below in section II.A.4.b.
13 In previous Staff Papers and Federal Register
notices announcing proposed and final decisions on
the O3 and other NAAQS, EPA has used the phrase
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Based on a substantial body of new
evidence from animal, controlled
human exposure and epidemiological
studies, the 2006 Criteria Document
concludes that people with asthma and
other preexisting pulmonary diseases
are likely to be among those at increased
risk from O3 exposure. Altered
physiological, morphological and
biochemical states typical of respiratory
diseases like asthma, COPD and chronic
bronchitis may render people sensitive
to additional oxidative burden induced
by O3 exposure (EPA 2006a, section
8.7). Children and adults with asthma
are the group that has been studied most
extensively. Evidence from controlled
human exposure studies indicates that
asthmatics may exhibit larger lung
function decrements in response to O3
exposure than healthy controls. As
discussed more fully in section
II.A.4.b.ii below, asthmatics present a
differential response profile for cellular,
molecular, and biochemical parameters
(EPA, 2006a, section 8.7.1) that are
altered in response to acute O3
exposure. They can have larger
inflammatory responses, as manifested
by larger increases in markers of
inflammation such as white bloods cells
(e.g., PMNs) or inflammatory cytokines.
Asthmatics, and people with allergic
rhinitis, are more likely to mount an
allergic-type response upon exposure to
O3, as manifested by increases in white
blood cells associated with allergy (i.e.,
eosinophils) and related molecules,
which increase inflammation in the
airways. The increased inflammatory
and allergic responses also may be
associated with the larger late-phase
responses that asthmatics can
experience, which can include
increased bronchoconstrictor responses
to irritant substances or allergens and
additional inflammation. In addition to
the experimental evidence of lung
function decrements, respiratory
symptoms, and other respiratory effects
in asthmatic populations, two large U.S.
epidemiological studies as well as
several smaller U.S. and international
studies, have reported fairly robust
associations between ambient O3
concentrations and measures of lung
function and daily symptoms (e.g., chest
tightness, wheeze, shortness of breath)
in children with moderate to severe
asthma and between O3 and increased
asthma medication use (EPA, 2007a,
chapter 6). These responses in
‘‘sensitive population groups’’ to include both
population groups that are at increased risk because
they are more intrinsically susceptible and
population groups that are more vulnerable due to
an increased potential for exposure. In this notice,
we use the phrase, ‘‘at risk’’ populations to include
both types of population groups.
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asthmatics and others with lung disease
provide biological plausibility for the
more serious respiratory morbidity
effects observed in epidemiological
studies, such as emergency department
visits and hospital admissions.
Children with and without asthma
were found to be particularly
susceptible to O3 effects on lung
function and generally have greater lung
function responses than older people.
The American Academy of Pediatrics
(2004) notes that children and infants
are among the population groups most
susceptible to many air pollutants,
including O3. This is in part because
their lungs are still developing. For
example, eighty percent of alveoli are
formed after birth, and changes in lung
development continue through
adolescence (Dietert et al., 2000).
Moreover, children have high minute
ventilation rates and relatively high
levels of physical activity which also
increases their O3 dose (Plunkett et al.,
1992). Thus, children are at-risk due to
both their susceptibility and
vulnerability.
Looking more broadly at age-related
differences in susceptibility, several
mortality studies have investigated agerelated differences in O3 effects (EPA,
2006a, section 7.6.7.2), primarily in the
older adult population. Among the
studies that observed positive
associations between O3 and mortality,
a comparison of all age or younger age
(65 years of age) O3-mortality effect
estimates to that of the elderly
population (>65 years) indicates that, in
general, the elderly population is more
susceptible to O3 mortality effects.
There is supporting evidence of agerelated differences in susceptibility to
O3 lung function effects. The 2006
Criteria Document (section 7.6.7.2)
concludes that the elderly population
(>65 years of age) appear to be at greater
risk of O3-related mortality and
hospitalizations compared to all ages or
younger populations, and children (<18
years of age) experience other
potentially adverse respiratory health
outcomes with increased O3 exposure.
Controlled human exposure studies
have also indicated a high degree of
interindividual variability in some of
the pulmonary physiological
parameters, such as lung function
decrements. The variable effects in
individuals have been found to be
reproducible, in other words, a person
who has a large lung function response
after exposure to O3 will likely have
about the same response if exposed
again to the same dose of O3 (EPA
2006a, section 6.1). In controlled human
exposure studies, group mean responses
are not representative of this segment of
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the population that has much larger
than average responses to O3. Recent
studies, discussed in section II.A.4.b.iv
below, reported a role for genetic
polymorphism (i.e., the occurrence
together in the same population of more
than one allele or genetic marker at the
same locus with the least frequent allele
or marker occurring more frequently
than can be accounted for by mutation
alone) in observed differences in
antioxidant enzymes and genes
involved in inflammation to modulate
pulmonary function and inflammatory
responses to O3 exposure. These
observations suggest a potential role for
these markers in the innate
susceptibility to O3, however, the
validity of these markers and their
relevance in the context of prediction to
population studies needs additional
experimentation.
Controlled human exposure studies
that provide information about
mechanisms of the initial response to O3
(e.g., lung function decrements,
inflammation, and injury to the lung)
also inform the selection of appropriate
lag times to analyze in epidemiological
studies through elucidation of the time
course of these responses (EPA 2006a,
section 8.4.3). Based on the results of
these studies, it would be reasonable to
expect that lung function decrements
could be detected epidemiologically
within lags of 0 (same day) or 1 to 2
days following O3 exposure, given the
rapid onset of lung function changes
and their persistence for 24 to 48 hours
among more responsive human subjects
in controlled human exposure studies.
Other responses take longer to develop
and can persist for longer periods of
time. For example, although asthmatic
individuals may begin to experience
symptoms soon after O3 exposure, it
may take anywhere from 1 to 3 days
after exposure for these subjects to seek
medical attention as a result of
increased airway responsiveness or
inflammation that may persist for 2 to
3 days. This may be reflected by
epidemiologic observations of
significantly increased risk for asthmarelated emergency department visits or
hospital admissions with 1- to 3-day
lags, or, perhaps, enhanced distributed
lag risks (combined across 3 days) for
such morbidity indicators. Analogously,
one might project increased mortality
within 0- to 3-day lags as a possible
consequence of O3-induced increases in
clotting agents arising from the cascade
of events, starting with cell injury
described above, occurring within 12 to
24 hours of O3 exposure. The time
course for many of these initial
responses to O3 is highly variable.
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Moreover these observations pertain
only to the initial response to O3.
Consequent responses can follow. For
¨
example, Jorres et al., (1996) found that
in subjects with asthma and allergic
rhinitis, a maximum percent fall in
FEV1 of 27.9% and 7.8%, respectively,
occurred 3 days after O3 exposure when
they were challenged with of the highest
common dose of allergen.
2. Nature of Effects
The 2006 Criteria Document provides
new evidence that notably enhances our
understanding of short-term and
prolonged exposure effects, including
effects on lung function, symptoms, and
inflammatory effects reported in
controlled exposure studies. These
studies support and extend the findings
of the previous Criteria Document.
There is also a significant body of new
epidemiological evidence of
associations between short-term and
prolonged exposure to O3 and effects
such as premature mortality, hospital
admissions and emergency department
visits for respiratory (e.g., asthma)
causes. Key epidemiological and
controlled human exposure studies are
summarized below and discussed in
chapter 3 of the 2007 Staff Paper, which
is based on scientific evidence critically
reviewed in chapters 5, 6, and 7 of the
2006 Criteria Document, as well as the
Criteria Document’s integration of
scientific evidence contained in chapter
8.14 Conclusions drawn about O3-related
health effects are based upon the full
body of evidence from controlled
human exposure, epidemiological and
toxicological data contained in the 2006
Criteria Document.
srobinson on DSKHWCL6B1PROD with PROPOSALS2
a. Morbidity
This section summarizes scientific
information on the effects of inhalation
of O3, including public health effects of
short-term, prolonged, and long-term
exposures on respiratory morbidity and
cardiovascular system effects, as
discussed in chapters 6, 7 and 8 of the
2006 Criteria Document and chapter 3 of
the 2007 Staff Paper. This section also
summarizes the uncertainty about the
potential indirect effects on public
health associated with changes due to
increases in UV–B radiation exposure,
such as UV–B radiation-related skin
cancers, that may be associated with
reductions in ambient levels of groundlevel O3, as discussed in chapter 10 of
the 2006 Criteria Document and chapter
3 of the 2007 Staff Paper.
14 Health effects discussions are also drawn from
the more detailed information and tables presented
in the Criteria Document’s annexes.
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i. Effects on the Respiratory System
From Short-term and Prolonged O3
Exposures
Controlled human exposure studies
have shown that O3 induces a variety of
health effects, including: Lung function
decrements, respiratory symptoms,
increased airway responsiveness,
respiratory inflammation and
permeability, increased susceptibility to
respiratory infection, and acute
morphological effects. Epidemiology
studies have reported associations
between O3 exposures (i.e., 1-hour, 8hour and 24-hour) and a wide range of
respiratory-related health effects
including: pulmonary function
decrements; respiratory symptoms;
increased asthma medication use;
increased school absences; increased
emergency department visits and
hospital admissions.
(a) Pulmonary Function Decrements,
Respiratory Symptoms, and Asthma
Medication Use
(i) Results From Controlled Human
Exposure Studies
A large number of studies published
prior to 1996 that investigated shortterm O3 exposure health effects on the
respiratory system from short-term O3
exposures were reviewed in the 1986
and 1996 Criteria Documents (EPA,
1986, 1996a). In the 1997 review, 0.50
ppm was the lowest O3 concentration at
which statistically significant
reductions in forced vital capacity (FVC)
and forced expiratory volume in 1
second (FEV1) were reported in
sedentary subjects. During exercise,
spirometric (lung function) and
symptomatic responses were observed
at much lower O3 exposures. When
minute ventilation was considerably
increased by continuous exercise (CE)
during O3 exposures lasting 2 hour or
less at ≥ 0.12 ppm, healthy subjects
generally experienced decreases in
FEV1, FVC, and other measures of lung
function; increases in specific airway
resistance (sRaw), breathing frequency,
and airway responsiveness; and
symptoms such as cough, pain on deep
inspiration, shortness of breath, throat
irritation, and wheezing. When
exposures were increased to 4- to 8hours in duration, statistically
significant lung function and symptom
responses were reported at O3
concentrations as low as 0.08 ppm and
at lower minute ventilation (i.e.,
moderate rather than high level
exercise) than the shorter duration
studies.
The most important observations
drawn from studies reviewed in the
1996 Criteria Document were that: (1)
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2949
Young healthy adults exposed to O3
concentrations ≥ 0.080 ppm develop
significant, reversible, transient
decrements in pulmonary function if
minute ventilation or duration of
exposure is increased sufficiently; (2)
children experience similar lung
function responses but report lesser
symptoms from O3 exposure relative to
young adults; (3) O3-induced lung
function responses are decreased in the
elderly relative to young adults; (4)
there is a large degree of intersubject
variability in physiological and
symptomatic responses to O3 but
responses tend to be reproducible
within a given individual over a period
of several months; (5) subjects exposed
repeatedly to O3 for several days show
an attenuation of response upon
successive exposures, but this
attenuation is lost after about a week
without exposure; and (6) acute O3
exposure initiates an inflammatory
response which may persist for at least
18 to 24 hours post exposure.
The development of these respiratory
effects is time-dependent during both
exposure and recovery periods, with
great overlap for development and
disappearance of the effects. In healthy
human subjects exposed to typical
ambient O3 levels near 0.120 ppm, lung
function responses largely resolve
within 4 to 6 hours postexposure, but
cellular effects persist for about 24
hours. In these healthy subjects, small
residual lung function effects are almost
completely gone within 24 hours, while
in hyperresponsive subjects, recovery
can take as much as 48 hour to return
to baseline. The majority of these
responses are attenuated after repeated
consecutive exposures, but such
attenuation to O3 is lost one week
postexposure.
Since 1996, there have been a number
of studies published investigating lung
function and symptomatic responses
that generally support the observations
previously drawn. Recent studies for
acute exposures of 1 to 2 hours and 6
to 8 hours in duration are compiled in
the 2007 Staff Paper (Appendix 3C). As
summarized in more detail in the 2007
Staff Paper (section 3.3.1.1), among the
more important of the recent studies
that examined changes in FEV1 in large
numbers of subjects over a range of
1–2 hours at exposure levels of 0.080 to
0.40 ppm were studies by McDonnell et
al. (1997) and Ultman et al. (2004).
These studies observed considerable
intersubject variability in FEV1
decrements, which was consistent with
findings in the 1996 Criteria Document.
For prolonged exposures (4 to 8
hours) in the range of 0.080 to 0.160
ppm O3 using moderate intermittent
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exercise and typically using squarewave exposure patterns (i.e., a constant
exposure level during time of exposure),
several pre- and post-1996 studies
(Folinsbee et al., 1988,1994; Horstman
et al., 1990; Adams, 2002, 2003a, 2006)
have reported statistically significant
lung function responses and increased
symptoms in healthy adults with
increasing duration of exposure, O3
concentration, and minute ventilation.
Studies that employed triangular
exposure patterns (i.e., integrated
exposures that begin at a low level, rise
to a peak, and return to a low level
during the exposure) (Hazucha et al.,
1992; Adams 2003a, 2006) suggest that
the triangular exposure pattern can
potentially lead to greater FEV1
decrements and respiratory symptoms
than square-wave exposures (when the
overall O3 doses are equal). These
results suggest that peak exposures,
reflective of the pattern of ambient O3
concentrations in some locations, are
important in terms of O3 health effects.
McDonnell (1996) used data from a
series of studies to investigate the
frequency distributions of FEV1
decrements following 6.6 hour
exposures and found statistically
significant, but relatively small, group
mean decreases in average FEV1
responses (between 5 and 10 percent) at
0.080 ppm O3.15 Notably, about 26
percent of the 60 exposed subjects had
lung function decrements > 10 percent,
including about 8 percent of the subjects
that experienced large decrements (> 20
percent) (EPA, 2007b, Figure 3–1A).
These results (which were not corrected
for exercise in filtered air responses)
demonstrate that while average
responses may be relatively small at the
0.080 ppm exposure level, some
individuals experience more severe
effects that may be clinically significant.
Similar results at the 0.080 ppm
exposure level (for 6.6 hours during
intermittent exercise) were seen in more
recent studies of 30 healthy young
adults by Adams (2002, 2006).16 In
Adams (2006), relatively small but
statistically significant lung function
decrements and respiratory symptom
responses were found (for both squarewave and triangular exposure patterns),
with 17 percent of the subjects (5 of 30)
experiencing ≥ 10 percent FEV1
15 This study and other studies (Folinsbee et al.,
1988; Horstman et al., 1990; and McDonnell et al.,
1991), conducted in EPA’s human studies research
facility in Chapel Hill, NC, measured ozone
concentrations to within +/¥ 5 percent or +/¥
0.004 ppm at the 0.080 ppm exposure level.
16 These studies, conducted at a facility at the
University of California, in Davis, CA, reported O3
concentrations to be accurate within +/¥ 0.003
ppm over the range of concentrations included in
these studies.
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decrements (comparing pre- and postexposures) when the results were not
corrected for the effects of exercise
alone in filtered air (EPA, 2007b, Figure
3–1B) and with 23 percent of subjects (7
of 30) experiencing such effects when
the results were corrected (EPA, 2007b,
p. 3–6).17
These studies by Adams (2002, 2006)
were notable in that they were the only
controlled exposure human studies
available at the time of the 2008
rulemaking that examined respiratory
effects associated with prolonged O3
exposures at levels below 0.080 ppm,
which was the lowest exposure level
that had been examined in the 1997
review. The Adams (2006) study
investigated a range of exposure levels
(0.000, 0.040, 0.060, and 0.080 ppm O3)
using square-wave and triangular
exposure patterns. The study was
designed to examine hour-by-hour
changes in pulmonary function (FEV1)
and respiratory symptom responses
(total subjective symptoms (TSS) and
pain on deep inspiration (PDI)) between
these various exposure protocols at six
different time points within the
exposure periods to investigate the
effects of different patterns of exposure.
At the 0.060 ppm exposure level, the
author reported no statistically
significant differences for FEV1
decrements nor for most respiratory
symptoms responses. Statistically
significant responses were reported only
for TSS for the triangular exposure
pattern toward the end of the exposure
period, with the PDI responses being
noted as following a closely similar
pattern (Adams, 2006, p. 131–132).
EPA’s reanalysis of the data from the
Adams (2006) study addressed the more
fundamental question of whether there
were statistically significant differences
in responses before and after the 6.6
hour exposure period (Brown, 2007),
and used a standard statistical method
appropriate for a simple before-and-after
comparison. The statistical method used
by EPA had been used previously by
other researchers to address this same
question. EPA’s reanalysis of the data
from the Adams (2006) study,
comparing FEV1 responses pre- and
post-exposure at the 0.060 ppm
exposure level, found small group mean
differences from responses to filtered air
that were statistically significant
(Brown, 2007).18
17 These
distributional results presented in the
Criteria Document and Staff Paper for the Adams
(2006) study are based on data for squate-wave
exposures to 0.080 ppm that were not included in
the publication but were obtained from the author.
18 Dr. Adams submitted comments on EPA’s
reanalysis in which he concluded that the FEV1
response in healthy young adults at the 0.060 ppm
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Further examination of the postexposure FEV1 data and mean data at
other time points and concentrations
also suggest a pattern of response at 0.06
ppm that is consistent with a doseresponse relationship rather than
random variability. For example, the
response at 5.6 hours was similar to that
of the post-exposure 6.6 hour response
and appeared to also differ from the FA
response. At the 0.08 ppm level, the
subjects in this study did not appear to
be more responsive to O3 than subjects
in previous studies, as the observed
response was similar to that of previous
studies (Adams, 2003a,b; Horstman et
al., 1990; McDonnell et al., 1991).
Although of much smaller magnitude,
the temporal pattern of the 0.06 ppm
response was generally consistent with
the temporal patterns of response to
higher concentrations of O3 in this and
other studies. These findings are not
unexpected because the previously
observed group mean FEV1 responses to
0.08 ppm were in the range of 6–9%
suggesting that exposure to lower
concentrations of O3 would result in
smaller, but real group mean FEV1
decrements, i.e., the responses to 0.060
ppm O3 are consistent with the presence
of a smooth exposure-response curve
with responses that do not end abruptly
below 0.080 ppm.
Moreover, the Adams studies (2002,
2006) also report a small percentage of
subjects experiencing moderate lung
function decrements (≥ 10 percent) at
the 0.060 ppm exposure level. Based on
study data (Adams, 2006) provided by
the author, 7 percent of the subjects (2
of 30 subjects) experienced notable
FEV1 decrements (≥ 10 percent) with the
square wave exposure pattern at the
0.060 ppm exposure level (comparing
pre- and post-exposures) when the
results were corrected for the effects of
exercise alone in filtered air (EPA,
2007b, p. 3–6). Furthermore, in a prior
publication (Adams, 2002), the author
stated that, ‘‘some sensitive subjects
experience notable effects at 0.06 ppm,’’
based on the observation that 20% of
subjects exposed to 0.06 ppm O3 (in a
face mask exposure study) had greater
than a 10% decrement in FEV1 even
though the group mean response was
not statistically different from the
filtered air response. The effects
described by Adams (2002), along with
exposure level in his study (Adams, 2006a) does not
demonstrate a significant mean effect by ordinarily
acceptable statistical analysis, but is rather in
somewhat of a gray area, both in terms of a
biologically meaningful response and a statistically
significant response (Adams, 2007). The EPA
responded to these comments in the 2008 final rule
(73 FR 16455) and in the Response to Comments
(EPA, 2008, pp. 26–28).
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the reanalysis of the Adams (2006) data
as described above, demonstrate
considerable inter-individual variability
in responses of healthy adults at the
0.060 ppm level with some individuals
experiencing greater than 10%
decrements in FEV1. The observation of
statistically significant small group
mean lung function decrements in
healthy adults at 0.060 ppm O3 lowers
the lowest-observed-effects level found
in controlled human exposure studies
for lung function decrements and
respiratory symptoms.
Of potentially greater concern is the
magnitude of the lung function
decrements in the small group of
healthy subjects who had the largest
responses (i.e., FEV1 decrements ≥
10%). This is a concern because for
active healthy people, moderate levels
of functional responses (e.g., FEV1
decrements of ≥ 10% but < 20%) and/
or moderate symptomatic responses
would likely interfere with normal
activity for relatively few responsive
individuals. However, for people with
lung disease, even moderate functional
or symptomatic responses would likely
interfere with normal activity for many
individuals, and would likely result in
more frequent use of medication (see
section II.A.4 below).
(ii) Results of Epidemiological and Field
Studies
A relatively large number of field
studies investigating the effects of
ambient O3 concentrations, in
combination with other air pollutants,
on lung function decrements and
respiratory symptoms has been
published over the last decade that
support the major findings of the 1996
Criteria Document that lung function
changes, as measured by decrements in
FEV1 or peak expiratory flow (PEF), and
respiratory symptoms in healthy adults
and asthmatic children are closely
correlated to ambient O3 concentrations.
Pre-1996 field studies focused primarily
on children attending summer camps
and found O3-related impacts on
measures of lung function, but not
respiratory symptoms, in healthy
children. The newer studies have
expanded to evaluate O3-related effects
on outdoor workers, athletes, the
elderly, hikers, school children, and
asthmatics. Collectively, these studies
confirm and extend clinical
observations that prolonged (i.e., 6–8
hour) exposure periods, combined with
elevated levels of exertion or exercise,
increase the dose of O3 to the lungs at
a given ambient exposure level and
result in larger lung function effects.
The results of one large study of hikers
(Korrick et al., 1998), which reported
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outcome measures stratified by several
factors (e.g., gender, age, smoking status,
presence of asthma) within a population
capable of more than normal exertion,
provide useful insight. In this study,
lung function was measured before and
after hiking, and individual O3
exposures were estimated by averaging
hourly O3 concentrations from ambient
monitors located at the base and
summit. The mean 8-hour average O3
concentration was 0.040 ppm (8-hour
average concentration range of 0.021
ppm to 0.074 ppm O3). Decreased lung
function was associated with O3
exposure, with the greatest effect
estimates reported for the subgroup that
reported having asthma or wheezing,
and for those who hiked for longer
periods of time.
Asthma panel studies conducted both
in the U.S. and in other countries have
reported that decrements in PEF are
associated with routine O3 exposures
among asthmatic and healthy people.
One large U.S. multicity study, the
National Cooperative Inner City Asthma
Study or NCICAS, (Mortimer et al.,
2002) examined O3-related changes in
PEF in 846 asthmatic children from 8
urban areas and reported that the
incidence of ≥ 10 percent decrements in
morning PEF are associated with
increases in 8-hour average O3 for a 5day cumulative lag, suggesting that O3
exposure may be associated with
clinically significant changes in PEF in
asthmatic children; however, no
associations were reported with evening
PEF. The mean 8-hour average O3 was
0.048 ppm across the 8 cities. Excluding
days when 8-hour average O3 was
greater than 0.080 ppm (less than 5
percent of days), the associations with
morning PEF remained statistically
significant. Mortimer et al. (2002)
discussed potential biological
mechanisms for delayed effects on
pulmonary function in asthma, which
included increased nonspecific airway
responsiveness secondary to airway
inflammation due to O3 exposure. Two
other panel studies (Romieu et al., 1996,
1997) carried out simultaneously in
northern and southwestern Mexico City
with mildly asthmatic school children
reported statistically significant O3related reductions in PEF, with
variations in effect depending on lag
time and time of day. Mean 1-hour
maximum O3 concentrations in these
locations ranged from 0.190 ppm in
northern Mexico City to 0.196 ppm in
southwestern Mexico City. While
several studies report statistically
significant associations between O3
exposure and reduced PEF in
asthmatics, other studies did not,
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2951
possibly due to low levels of O3
exposure. EPA concludes that these
studies collectively indicate that O3 may
be associated with short-term declines
in lung function in asthmatic
individuals and that the Mortimer et al.
(2002) study showed statistically
significant effects at concentrations in
the range below 0.080 ppm O3.
Most of the panel studies which have
investigated associations between O3
exposure and respiratory symptoms or
increased use of asthma medication are
focused on asthmatic children. Two
large U.S. studies (Mortimer et al., 2002;
Gent et al., 2003) have reported
associations between ambient O3
concentrations and daily symptoms/
asthma medication use, even after
adjustment for copollutants. Results
were more mixed, meaning that a
greater proportion of studies were not
both positive and statistically
significant, across smaller U.S. and
international studies that focused on
these health endpoints.
The NCICAS reported morning
symptoms in 846 asthmatic children
from 8 U.S. urban areas to be most
strongly associated with a cumulative
1- to 4-day lag of O3 concentrations
(Mortimer et al., 2002). The NCICAS
used standard protocols that included
instructing caretakers of the subjects to
record symptoms (including cough,
chest tightness, and wheeze) in the daily
diary by observing or asking the child.
While these associations were not
statistically significant in several cities,
when the individual data are pooled
from all eight cities, statistically
significant effects were observed for the
incidence of symptoms. The authors
also reported that the odds ratios
remained essentially the same and
statistically significant for the incidence
of morning symptoms when days with
8-hour O3 concentrations above 0.080
ppm were excluded. These days
represented less than 5 percent of days
in the study.
Gent and colleagues (2003) followed
271 asthmatic children under age 12
and living in southern New England for
6 months (April through September)
using a daily symptom diary. They
found that mean 1-hour max O3 and 8hour max O3 concentrations were
0.0586 ppm and 0.0513 ppm,
respectively. The data were analyzed for
two separate groups of subjects, those
who used maintenance asthma
medications during the follow-up
period and those who did not. The need
for regular medication was considered
to be a proxy for more severe asthma.
Not taking any medication on a regular
basis and not needing to use a
bronchodilator would suggest the
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presence of very mild asthma.
Statistically significant effects of 1-day
lag O3 were observed on a variety of
respiratory symptoms only in the
medication user group. Both daily
1-hour max and 8-hour max O3
concentrations were similarly related to
symptoms such as chest tightness and
shortness of breath. Effects of O3, but
not PM2.5, remained significant and
even increased in magnitude in twopollutant models. Some of the
associations were noted at 1-hour max
O3 levels below 0.060 ppm. In contrast,
no effects were observed among
asthmatics not using maintenance
medication. In terms of person-days of
follow-up, this is one of the larger
studies currently available that address
symptom outcomes in relation to O3 and
provides supportive evidence for effects
of O3 independent of PM2.5. Study
limitations include the post-hoc nature
of the population stratification by
medication use. Also, the study did not
account for all of the important
meteorological factors that might
influence these results, such as relative
humidity or dew point.
The multicity study by Mortimer et al.
(2002), which examined an asthmatic
population representative of the United
States, and several single-city studies
indicate a robust association of O3
concentrations with respiratory
symptoms and increased medication use
in asthmatics. While there are a number
of well-conducted, albeit relatively
smaller, U.S. studies which showed
only limited or a lack of evidence for
symptom increases associated with O3
exposure, these studies had less
statistical power and/or were conducted
in areas with relatively low 1-hour
maximum average O3 levels, in the
range of 0.03 to 0.09 ppm. The 2006
Criteria Document concludes that the
asthma panel studies, as a group, and
the NCICAS in particular, indicate a
positive association between ambient
concentrations and respiratory
symptoms and increased medication use
in asthmatics. The evidence has
continued to expand since 1996 and
now is considered to be much stronger
than in the 1997 review of the O3
primary standard.
School absenteeism is another
potential surrogate for the health
implications of O3 exposure in children.
The association between school
absenteeism and ambient O3
concentrations was assessed in two
relatively large field studies. The first
study, Chen et al. (2000), examined total
daily school absenteeism in about
28,000 elementary school students in
Nevada over a 2-year period (after
adjusting for PM10 and CO
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concentrations) and found that ambient
O3 concentrations with a distributed lag
of 14 days were statistically
significantly associated with an
increased rate of school absences. The
second study, Gilliland et al. (2001),
studied O3-related absences among
about 2,000 4th grade students in 12
southern California communities and
found statistically significant
associations between 8-hour average O3
concentrations (with a distributed lag
out to 30 days) and all absence
categories, and particularly for
respiratory causes. Neither PM10 nor
NO2 were associated with any
respiratory or nonrespiratory illnessrelated absences in single pollutant
models. The 2006 Criteria Document
concludes that these studies of school
absences suggest that ambient O3
concentrations, accumulated over two to
four weeks, may be associated with
school absenteeism, and particularly
illness-related absences, but further
replication is needed before firm
conclusions can be reached regarding
the effect of O3 on school absences. In
addition, more research is needed to
help shed light on the implications of
variation in the duration of the lag
structures (i.e., 1 day, 5 days, 14 days,
and 30 days) found both across studies
and within data sets by health endpoint
and exposure metric.
(b) Increased Airway Responsiveness
As discussed in more detail in the
2006 Criteria Document (section 6.8)
and the 2007 Staff Paper (section
3.3.1.1.2), increased airway
responsiveness, also known as airway
hyperresponsiveness (AHR) or bronchial
hyperreactivity, refers to a condition in
which the propensity for the airways to
bronchoconstrict due to a variety of
stimuli (e.g., exposure to cold air,
allergens, or exercise) becomes
augmented. This condition is typically
quantified by measuring the decrement
in pulmonary function after inhalation
exposure to specific (e.g., antigen,
allergen) or nonspecific (e.g.,
methacholine, histamine)
bronchoconstrictor stimuli. Exposure to
O3 causes an increase in airway
responsiveness as indicated by a
reduction in the concentration of
stimuli required to produce a given
reduction in FEV1 or increase in airway
obstruction. Increased airway
responsiveness is an important
consequence of exposure to O3 because
its presence means that the airways are
predisposed to narrowing on exposure
to various stimuli, such as specific
allergens, cold air or SO2. Statistically
significant and clinically relevant
decreases in pulmonary function have
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been observed in early phase allergen
response in subjects with allergic
rhinitis after consecutive (4-day) 3-hour
exposures to 0.125 ppm O3 (Holz et al.,
2002). Similar increased airway
responsiveness in asthmatics to house
dust mite antigen 16 to 18 hours after
exposure to a single dose of O3 (0.160
ppm for 7.6 hours) was observed. These
observations, based on O3 exposures to
levels much higher than the 0.084 ppm
standard level suggest that O3 exposure
may be a clinically important factor that
can exacerbate the response to ambient
bronchoconstrictor substances in
individuals with preexisting allergic
asthma or rhinitis. Further, O3 may have
an immediate impact on the lung
function of asthmatics as well as
contribute to effects that persist for
longer periods.
Kreit et al. (1989) found that O3 can
induce increased airway responsiveness
in asthmatic subjects to O3, who
typically have increased airway
responsiveness at baseline. A
¨
subsequent study (Jorres et al., 1996)
suggested an increase in specific (i.e.,
allergen-induced) airway reactivity in
subjects with allergic asthma, and to a
lesser extent in subjects with allergic
rhinitis after short-term exposure to
higher O3 levels; other studies reported
similar results. According to one study
(Folinsbee and Hazucha, 2000), changes
in airway responsiveness after O3
exposure resolve more slowly than
changes in FEV1 or respiratory
symptoms. Other studies of repeated
exposure to O3 suggest that changes in
airway responsiveness tend to be
somewhat less affected by attenuation
with consecutive exposures than
changes in FEV1 (EPA, 2006a, section
6.8).
The 2006 Criteria Document (section
6.8) concludes that O3 exposure is
linked with increased airway
responsiveness. Both human and animal
studies indicate that increased airway
responsiveness is not mechanistically
associated with inflammation, and does
not appear to be strongly associated
with initial decrements in lung function
or increases in symptoms. As a result of
increased airway responsiveness
induced by O3 exposure, human airways
may be more susceptible to a variety of
stimuli, including antigens, chemicals,
and particles. Because asthmatic
subjects typically have increased airway
responsiveness at baseline, enhanced
bronchial response to antigens in
asthmatics raises potential public health
concerns as they could lead to increased
morbidity (e.g., medication usage,
school absences, emergency room visits,
hospital admissions) or to more
persistent alterations in airway
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responsiveness (EPA 2006a, p. 8–21). As
such, increased airway responsiveness
after O3 exposure represents a plausible
link between O3 exposure and increased
hospital admissions.
(c) Respiratory Inflammation and
Increased Permeability
Based on evidence from the 1997
review, acute inflammatory responses in
the lung have been observed subsequent
to 6.6 hour O3 exposures to the lowest
tested level—0.080 ppm—in healthy
adults engaged in moderately high
exercise (section 6.9 of the 2006 Criteria
Document and section 3.3.1.3 of the
2007 Staff Paper). Some of these prior
studies suggest that inflammatory
responses may be detected in some
individuals following O3 exposures in
the absence of O3-induced pulmonary
decrements in those subjects. These
studies also demonstrate that short-term
exposures to O3 also can cause
increased permeability in the lungs of
humans and experimental animals.
Inflammatory responses and epithelial
permeability have been seen to be
independent of spirometric responses.
Not only are the newer lung
inflammation and increased cellular
permeability findings discussed in the
2006 Criteria Document (section 8.4.2)
consistent with the 1997 review, but
they provide better characterization of
the physiological mechanisms by which
O3 causes these effects.
Lung inflammation and increased
permeability, which are distinct events
controlled by different mechanisms, are
two commonly observed effects of O3
exposure observed in all of the species
studied. Increased cellular permeability
is a disruption of the lung barrier that
leads to leakage of serum proteins,
influx of polymorphonuclear leukocytes
(neutrophils or PMNs), release of
bioactive mediators, and movement of
compounds from the airspaces into the
blood.
A number of controlled human
exposure studies have analyzed
bronchoalveolar lavage (BAL) and nasal
lavage (NL) 19 fluids and cells for
markers of inflammation and lung
damage (EPA, 2006a, Annex AX6).
Increased lung inflammation is
demonstrated by the presence of
neutrophils found in BAL fluid in the
lungs, which has long been accepted as
a hallmark of inflammation. It is
apparent, however, that inflammation
19 Graham and Koren (1990) compared
inflammatory mediators present in NL and BAL
fluids of humans exposed to 0.4 ppm O3 for 2 hours
and found similar increases in PMNs in both fluids,
suggesting a qualitative correlation between
inflammatory changes in the lower airways (BAL)
and upper respiratory tract (NL).
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within airway tissues may persist
beyond the point that inflammatory
cells are found in the BAL fluid. Soluble
mediators of inflammation, such as
cytokines and arachidonic acid
metabolites have been measured in the
BAL fluid of humans exposed to O3. In
addition to their role in inflammation,
many of these compounds have
bronchoconstrictive properties and may
be involved in increased airway
responsiveness following O3 exposure.
An in vitro study of epithelial cells from
nonatopic and atopic asthmatics
exposed to 0.010 to 0.100 ppm O3
showed significantly increased
permeability compared to cells from
normal persons. This indicates a
potentially inherent susceptibility of
cells from asthmatic individuals for O3induced permeability.
In the 1996 Criteria Document,
assessment of controlled human
exposure studies indicated that a single,
acute (1 to 4 hours) O3 exposure (≥ 0.080
to 0.100 ppm) of subjects engaged in
moderate to heavy exercise could
induce a number of cellular and
biochemical changes suggestive of
pulmonary inflammation and lung
permeability (EPA, 2006a, p. 8–22).
These changes persisted for at least 18
hours. Markers from BAL fluid
following both 2-hour and 4-hour O3
exposures repeated up to 5 days
indicate that there is ongoing cellular
damage irrespective of attenuation of
some cellular inflammatory responses of
the airways, pulmonary function, and
symptom scores (EPA, 2006a, p. 8–22).
Acute airway inflammation was shown
in Devlin et al. (1990) to occur among
adults exposed to 0.080 ppm O3 for 6.6
hours with exercise. McBride et al.
(1994) reported that asthmatic subjects
were more sensitive than nonasthmatics to upper airway
inflammation for O3 exposures that did
not affect pulmonary function (EPA,
2006a, p. 6–33). However, the public
health significance of these changes is
not entirely clear.
The studies reporting inflammatory
responses and markers of lung injury
have clearly demonstrated that there is
significant variation in response of
subjects exposed, especially to 6.6 hours
O3 exposures at 0.080 and 0.100 ppm.
To provide some perspective on the
public health impact for these effects,
the 2007 Staff Paper (section 3.3.1.1.3)
notes that one study (Devlin et al., 1991)
showed that roughly 10 to 50 percent of
the 18 young healthy adult subjects
experienced notable increases (i.e., ≥ 2
fold increase) in most of the
inflammatory and cellular injury
indicators analyzed, associated with 6.6hour exposures at 0.080 ppm. Similar,
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2953
although in some cases higher, fractions
of the population of 10 healthy adults
tested saw > 2 fold increases associated
with 6.6-hour exposures to 0.100 ppm.
The authors of this study expressed the
view that ‘‘susceptible subpopulations
such as the very young, elderly, and
people with pulmonary impairment or
disease may be even more affected’’
(Devlin et al., 1991).
Since 1996, a substantial number of
human exposure studies have been
published which have provided
important new information on lung
inflammation and epithelial
permeability. Mudway and Kelly (2004)
examined O3-induced inflammatory
responses and epithelial permeability
with a meta-analysis of 21 controlled
human exposure studies and showed
that an influx in neutrophils and protein
in healthy subjects is associated with
total O3 dose (product of O3
concentration, exposure duration, and
minute ventilation) (EPA, 2006a, p. 6–
34). Results of the analysis suggest that
the time course for inflammatory
responses (including recruitment of
neutrophils and other soluble
mediators) is not clearly established, but
there is evidence that attenuation
profiles for many of these parameters
are different (EPA, 2006a, p. 8–22).
The 2006 Criteria Document (chapter
8) concludes that interaction of O3 with
lipid constituents of epithelial lining
fluid (ELF) and cell membranes and the
induction of oxidative stress is
implicated in injury and inflammation.
Alterations in the expression of
cytokines, chemokines, and adhesion
molecules, indicative of an ongoing
oxidative stress response, as well as
injury repair and regeneration
processes, have been reported in animal
toxicology and human in vitro studies
evaluating biochemical mediators
implicated in injury and inflammation.
While antioxidants in ELF confer some
protection, O3 reactivity is not
eliminated at environmentally relevant
exposures (2006 Criteria Document, p.
8–24). Further, antioxidant reactivity
with O3 is both species-specific and
dose-dependent.
(d) Increased Susceptibility to
Respiratory Infection
As discussed in more detail in the
2006 Criteria Document (sections 5.2.2,
6.9.6, and 8.4.2), short-term exposures
to O3 have been shown to impair
physiological defense capabilities in
experimental animals by depressing
alveolar macrophage (AM) functions
and by altering the mucociliary
clearance of inhaled particles and
microbes resulting in increased
susceptibility to respiratory infection.
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Short-term O3 exposures also interfere
with the clearance process by
accelerating clearance for low doses and
slowing clearance for high doses.
Animal toxicological studies have
reported that acute O3 exposures
suppress alveolar phagocytosis and
immune system functions. Impairment
of host defenses and subsequent
increased susceptibility to bacterial lung
infection in laboratory animals has been
induced by short-term exposures to O3
levels as low as 0.080 ppm.
A single controlled human exposure
study reviewed in the 1996 Criteria
Document (p. 8–26) reported that
exposure to 0.080 to 0.100 ppm O3 for
6.6 hours (with moderate exercise)
induced decrements in the ability of
AMs to phagocytose microorganisms.
Integrating the recent animal study
results with human exposure evidence
available in the 1996 Criteria Document,
the 2006 Criteria Document concludes
that available evidence indicates that
short-term O3 exposures have the
potential to impair host defenses in
humans, primarily by interfering with
AM function. Any impairment in AM
function may lead to decreased
clearance of microorganisms or
nonviable particles. Compromised AM
functions in asthmatics may increase
their susceptibility to other O3 effects,
the effects of particles, and respiratory
infections (EPA, 2006a, p. 8–26).
(e) Morphological Effects
The 1996 Criteria Document found
that short-term O3 exposures cause
similar alterations in lung morphology
in all laboratory animal species studied,
including primates. As discussed in the
2007 Staff Paper (section 3.3.1.1.5), cells
in the centriacinar region (CAR) of the
lung (the segment between the last
conducting airway and the gas exchange
region) have been recognized as a
primary target of O3-induced damage
(epithelial cell necrosis and remodeling
of respiratory bronchioles), possibly
because epithelium in this region
receives the greatest dose of O3
delivered to the lower respiratory tract.
Following chronic O3 exposure,
structural changes have been observed
in the CAR, the region typically affected
in most chronic airway diseases of the
human lung (EPA, 2006a, p. 8–24).
Ciliated cells in the nasal cavity and
airways, as well as Type I cells in the
gas-exchange region, are also identified
as targets. While short-term O3
exposures can cause epithelial cell
profileration and fibrolitic changes in
the CAR, these changes appear to be
transient with recovery occurring after
exposure, depending on species and O3
dose. The potential impacts of repeated
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short-term and chronic morphological
effects of O3 exposure are discussed
below in the section on effects from
long-term exposures. Long-term or
prolonged exposure has been found to
cause chronic lesions similar to early
lesions found in individuals with
respiratory bronchiolitis, which have
the potential to progress to fibrotic lung
disease (2006 Criteria Document, p.
8–25).
Recent studies continue to show that
short-term and sub-chronic exposures to
O3 cause similar alterations in lung
structure in a variety of experimental
animal species. For example, a series of
new studies that used infant rhesus
monkeys and simulated seasonal
ambient exposure (0.5 ppm 8 hours/day
for 5 days, every 14 days for 11
episodes) reported remodeling in the
distal airways; abnormalities in tracheal
basement membrane; eosinophil
accumulation in conducting airways;
and decrements in airway innervation
(2006 Criteria Document, p. 8–25).
Based on evidence from animal
toxicological studies, short-term and
sub-chronic exposures to O3 can cause
morphological changes in the
respiratory systems, particularly in the
CAR, of a number of laboratory animal
species (EPA, 2006a, section 5.2.4).
(f) Emergency Department Visits/
Hospital Admissions for Respiratory
Causes
Increased summertime emergency
department visits and hospital
admissions for respiratory causes have
been associated with ambient exposures
to O3. As discussed in section 3.3.1.1.6
of the 2007 Staff Paper, numerous
studies conducted in various locations
in the U.S. and Canada consistently
have shown a relationship between
ambient O3 levels and increased
incidence of emergency department
visits and hospital admissions for
respiratory causes, even after controlling
for modifying factors, such as weather
and copollutants. Such associations
between elevated ambient O3 during
summer months and increased hospital
admissions have a plausible biological
basis in the human and animal evidence
of functional, symptomatic, and
physiologic effects discussed above and
in the increased susceptibility to
respiratory infections observed in
laboratory animals.
In the 1997 review of the O3 NAAQS,
the Criteria Document evaluated
emergency department visits and
hospital admissions as possible
outcomes following exposure to O3
(EPA, 2006a, section 7.3). The evidence
was limited for emergency department
visits, but results of several studies
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generally indicated that short-term
exposures to O3 were associated with
respiratory emergency department
visits. The strongest and most consistent
evidence, at both lower levels (i.e.,
below 0.120 ppm 1-hour max O3) and at
higher levels (above 0.120 ppm 1-hour
max O3), was found in the group of
studies which investigated
summertime 20 daily hospital
admissions for respiratory causes in
different eastern North American cities.
These studies consistently demonstrated
that ambient O3 levels were associated
with increased hospital admissions and
accounted for about one to three excess
respiratory hospital admissions per
million persons with each 0.100 ppm
increase in 1-hour max O3, after
adjustment for possible confounding
effects of temperature and copollutants.
Overall, the 1996 Criteria Document
concluded that there was strong
evidence that ambient O3 exposures can
cause significant exacerbations of
preexisting respiratory disease in the
general public. Excess respiratoryrelated hospital admissions associated
with O3 exposures for the New York
City area (based on Thurston et al.,
1992) were included in the quantitative
risk assessment in the 1997 review and
are included in the current assessment
along with estimates for respiratoryrelated hospital admissions in
Cleveland, Detroit, and Los Angeles
based on more recent studies (2007 Staff
Paper, chapter 5). Significant
uncertainties and the difficulty of
obtaining reliable baseline incidence
numbers resulted in emergency
department visits not being used in the
quantitative risk assessment in either
the 1997 or the 2008 O3 NAAQS review.
In the past decade, a number of
studies have examined the temporal
pattern associations between O3
exposures and emergency department
visits for respiratory causes (EPA,
2006a, section 7.3.2). These studies are
summarized in the 2006 Criteria
Document (chapter 7 Annex) and some
are shown in Figure 1 (in section II.A.3).
Respiratory causes for emergency
department visits include asthma,
bronchitis, emphysema, pneumonia,
and other upper and lower respiratory
infections, such as influenza, but
asthma visits typically dominate the
daily incidence counts. Most studies
report positive associations with O3.
Among studies with adequate controls
for seasonal patterns, many reported at
least one significant positive association
involving O3.
20 Discussion of the reasons for focusing on warm
season studies is found in the section 2.A.3.a below.
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In reviewing evidence for associations
between emergency department visits
for asthma and short-term O3 exposures,
the 2006 Criteria Document (Figure 7–
8, p. 7–68) notes that in general, O3
effect estimates from summer only
analyses tended to be positive and larger
compared to results from cool season or
all year analyses. Several of the studies
reported significant associations
between O3 concentrations and
emergency department visits for
respiratory causes, in particular asthma.
However, inconsistencies were observed
which were at least partially attributable
to differences in model specifications
and analysis approach among various
studies. For example, ambient O3
concentrations, length of the study
period, and statistical methods used to
control confounding by seasonal
patterns and copollutants appear to
affect the observed O3 effect on
emergency department visits.
Hospital admissions studies focus
specifically on unscheduled admissions
because unscheduled hospital
admissions occur in response to
unanticipated disease exacerbations and
are more likely than scheduled
admissions to be affected by variations
in environmental factors, such as daily
O3 levels. Results of a fairly large
number of these studies published
during the past decade are summarized
in 2006 Criteria Document (chapter 7
Annex), and results of U.S. and
Canadian studies are shown in Figure 1
below (in section II.A.3). As a group,
these hospital admissions studies tend
to be larger geographically and
temporally than the emergency
department visit studies and provide
results that are generally more
consistent. The strongest associations of
respiratory hospital admissions with O3
concentrations were observed using
short lag periods, in particular for a 0day lag (same day exposure) and a 1-day
lag (previous day exposure). Most
studies in the United States and Canada
indicated positive, statistically
significant associations between
ambient O3 concentrations and
respiratory hospital admissions in the
warm season. However, not all studies
found a statistically significant
relationship with O3, possibly because
of very low ambient O3 levels. Analyses
for confounding using multipollutant
regression models suggest that
copollutants generally do not confound
the association between O3 and
respiratory hospitalizations. Ozone
effect estimates were robust to PM
adjustment in all-year and warm-season
only data.
Overall, the 2006 Criteria Document
concludes that positive and robust
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associations were found between
ambient O3 concentrations and various
respiratory disease hospitalization
outcomes, when focusing particularly
on results of warm-season analyses.
Recent studies also generally indicate a
positive association between O3
concentrations and emergency
department visits for asthma during the
warm season (EPA, 2006a, p. 7–175).
These positive and robust associations
are supported by the controlled human
exposure, animal toxicological, and
epidemiological evidence for lung
function decrements, increased
respiratory symptoms, airway
inflammation, and increased airway
responsiveness. Taken together, the
overall evidence supports a causal
relationship between acute ambient O3
exposures and increased respiratory
morbidity outcomes resulting in
increased emergency department visits
and hospitalizations during the warm
season (EPA, 2006a, p. 8–77).
ii. Effects on the Respiratory System of
Long-Term O3 Exposures
The 1996 Criteria Document
concluded that there was insufficient
evidence from the limited number of
studies to determine whether long-term
O3 exposures resulted in chronic health
effects at ambient levels observed in the
U.S. However, the aggregate evidence
suggested that O3 exposure, along with
other environmental factors, could be
responsible for health effects in exposed
populations. Animal toxicological
studies carried out in the 1980’s and
1990’s demonstrated that long-term
exposures can result in a variety of
morphological effects, including
permanent changes in the small airways
of the lungs, including remodeling of
the distal airways and CAR and
deposition of collagen, possibly
representing fibrotic changes. These
changes result from the damage and
repair processes that occur with
repeated exposure. Fibrotic changes
were also found to persist after months
of exposure providing a potential
pathophysiologic basis for changes in
airway function observed in children in
some recent epidemiological studies. It
appears that variable seasonal ambient
patterns of exposure may be of greater
concern than continuous daily
exposures.
Several studies published since 1996
have investigated lung function changes
over seasonal time periods (EPA, 2006a,
section 7.5.3). The 2006 Criteria
Document (p. 7–114) summarizes these
studies which collectively indicate that
seasonal O3 exposure is associated with
smaller growth-related increases in lung
function in children than they would
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have experienced living in areas with
lower O3 levels. There is some limited
evidence that seasonal O3 also may
affect lung function growth in young
adults, although the uncertainty about
the role of copollutants makes it
difficult to attribute the effects to O3
alone.
Lung capacity grows during
childhood and adolescence as body size
increases, reaches a maximum during
the twenties, and then begins to decline
steadily and progressively with age.
Long-term exposure to air pollution has
long been thought to contribute to
slower growth in lung capacity,
diminished maximally attained
capacity, and/or more rapid decline in
lung capacity with age (EPA, 2006a,
section 7.5.4). Toxicological findings
evaluated in the 1996 Criteria Document
demonstrated that repeated daily
exposure of rats to an episodic profile of
O3 caused small, but significant,
decrements in growth-related lung
function that were consistent with early
indicators of focal fibrogenesis in the
proximal alveolar region, without overt
fibrosis. Because O3 at sufficient
concentrations is a strong respiratory
irritant and has been shown to cause
inflammation and restructuring of the
respiratory airways, it is plausible that
long-term O3 exposures might have a
negative impact on baseline lung
function, particularly during childhood
when these exposures might be
associated with long-term risks.
Several epidemiological studies
published since 1996 have examined
the relationship between lung function
development and long-term O3
exposure. The most extensive and
robust study of respiratory effects in
relation to long-term air pollution
exposures among children in the U.S. is
the Children’s Health Study carried out
in 12 communities of southern
California starting in 1993. One analysis
(Peters et al., 1999a) examined the
relationship between long-term O3
exposures and self-reports of respiratory
symptoms and asthma in a cross
sectional analysis and found a limited
relationship between outcomes of
current asthma, bronchitis, cough and
wheeze and a 0.040 ppm increase in 1hour max O3 (EPA, 2006a, p. 7–115).
Another analysis (Peters et al., 1999b)
examined the relationship between lung
function at baseline and levels of air
pollution in the community. They
reported evidence that annual mean O3
levels were associated with decreases in
FVC, FEV1, PEF and forced expiratory
flow (FEF25¥75) (the latter two being
statistically significant) among females
but not males. In a separate analysis
(Gauderman et al., 2000) of 4th, 7th, and
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10th grade students, a longitudinal
analysis of lung function development
over four years found no association
with O3 exposure. The Children’s
Health Study enrolled a second cohort
of more than 1500 fourth graders in
1996 (Gauderman et al., 2002). While
the strongest associations with negative
lung function growth were observed
with acid vapors in this cohort, children
from communities with higher 4-year
average O3 levels also experienced
smaller increases in various lung
function parameters. The strongest
relationship with O3 was with PEF.
Specifically, children from the leastpolluted community had a small but
statistically significant increase in PEF
as compared to those from the mostpolluted communities. In two-pollutant
models, only 8-hour average O3 and NO2
were significant joint predictors of FEV1
and maximal midexpiratory flow
(MMEF). Although results from the
second cohort of children are supportive
of a weak association, the definitive 8year follow-up analysis of the first
cohort (Gauderman et al., 2004a)
provides little evidence that long-term
exposure to ambient O3 at current levels
is associated with significant deficits in
the growth rate of lung function in
children. Avol et al. (2001) examined
children who had moved away from
participating communities in southern
California to other states with improved
air quality. They found that a negative,
but not statistically significant,
association was observed between O3
and lung function parameters.
Collectively, the results of these reports
from the children’s health cohorts
provide little evidence to support an
impact of long-term O3 exposures on
lung function development.
Evidence for a significant relationship
between long-term O3 exposures and
decrements in maximally attained lung
function was reported in a nationwide
study of first year Yale students (Kinney
et al., 1998; Galizia and Kinney, 1999)
(EPA, 2006a, p. 7–120). Males had much
larger effect estimates than females,
which might reflect higher outdoor
activity levels and correspondingly
higher O3 exposures during childhood.
A similar study of college freshmen at
University of California at Berkeley also
reported significant effects of long-term
¨
O3 exposures on lung function (Kunzli
et al., 1997; Tager et al., 1998). In a
comparison of students whose city of
origin was either Los Angeles or San
Francisco, long-term O3 exposures were
associated with significant changes in
mid- and end-expiratory flow measures,
which could be considered early
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indicators for pathologic changes that
might progress to COPD.
There have been a few studies that
investigated associations between longterm O3 exposures and the onset of new
cases of asthma (EPA, 2006a, section
7.5.6). The Adventist Health and Smog
(AHSMOG) study cohort of about 4,000
was drawn from nonsmoking, nonHispanic white adult Seventh Day
Adventists living in California (Greer et
al., 1993; McDonnell et al., 1999).
During the ten-year follow-up in 1987,
a statistically significant increased
relative risk of asthma development was
observed in males, compared to a
nonsignificant relative risk in females
(Greer et al., 1993). In the 15-year
follow-up in 1992, it was reported that
for males, there was a statistically
significant increased relative risk of
developing asthma associated with 8hour average O3 exposures, but there
was no evidence of an association in
females. Consistency of results in the
two studies with different follow-up
times provides supportive evidence of
the potential for an association between
long-term O3 exposure and asthma
incidence in adult males; however,
representativeness of this cohort to the
general U.S. population may be limited
(EPA, 2006a, p. 7–125).
In a similar study (McConnell et al.,
2002) of incident asthma among
children (ages 9 to 16 at enrollment),
annual surveys of 3,535 children
initially without asthma were used to
identify new-onset asthma cases as part
of the Children’s Health Study. Six
high-O3 and six low-O3 communities
were identified where the children
resided. There were 265 children who
reported new-onset asthma during the
follow-up period. Although asthma risk
was no higher for all residents of the six
high-O3 communities versus the six
low-O3 communities, asthma risk was
3.3 times greater for children who
played three or more sports as compared
with children who played no sports
within the high-O3 communities. This
association was absent in the
communities with lower O3
concentrations. No other pollutants
were found to be associated with newonset asthma (EPA, 2006a, p. 7–125).
Playing sports may result in extended
outdoor activity and exposure occurring
during periods when O3 levels are
higher. It should be noted, however, that
the results of the Children’s Health
Study were based on a small number of
new-onset asthma cases among children
who played three or more sports. Future
replication of these findings in other
cohorts would help determine whether
a causal interpretation is appropriate.
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In animal toxicology studies, the
progression of morphological effects
reported during and after a chronic
exposure in the range of 0.50 to 1.00
ppm O3 (well above current ambient
levels) is complex, with inflammation
peaking over the first few days of
exposure, then dropping, then
plateauing, and finally, largely
disappearing (EPA, 2006a, section
5.2.4.4). By contrast, fibrotic changes in
the tissue increase very slowly over
months of exposure, and, after exposure
ceases, the changes sometimes persist or
increase. Epithelial hyperplasia peaks
soon after the inflammatory response
but is usually maintained in both the
nose and lungs with continuous
exposure; it also does not return to preexposure levels after the end of
exposure. Patterns of exposure in this
same concentration range determine
effects, with 18 months of daily
exposure, causing less morphologic
damage than exposures on alternating
months. This is important as
environmental O3 exposure is typically
seasonal. Long-term studies by Plopper
and colleagues (Evans et al., 2003;
Schelegle et al., 2003; Chen et al., 2003;
Plopper and Fanucchi, 2000)
investigated infant rhesus monkeys
exposed to simulated, seasonal O3 and
demonstrated: (1) Remodeling in the
distal airways, (2) abnormalities in
tracheal basement membrane; (3)
eosinophil accumulation in conducting
airways; and (4) decrements in airway
innervation (EPA, 2006a, p. 5–45).
These findings provide additional
information regarding possible injuryrepair processes occurring with longterm O3 exposures suggesting that these
processes are only partially reversible
and may progress following cessation of
O3 exposure. Further, these processes
may lead to nonreversible structural
damage to lung tissue; however, there is
still too much uncertainty to
characterize the significance of these
findings to human exposure profiles and
effect levels (EPA, 2006a, p. 8–25).
In summary, in the past decade,
important new longitudinal studies
have examined the effect of chronic O3
exposure on respiratory health
outcomes. Limited evidence from recent
long-term morbidity studies have
suggested in some cases that chronic
exposure to O3 may be associated with
seasonal declines in lung function or
reduced lung function development,
increases in inflammation, and
development of asthma in children and
adults. Seasonal decrements or smaller
increases in lung function measures
have been reported in several studies;
however, the extent to which these
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changes are transient remains uncertain.
While there is supportive evidence from
animal studies involving effects from
chronic exposures, large uncertainties
still remain as to whether current
ambient levels and exposure patterns
might cause these same effects in
human populations. The 2006 Criteria
Document concludes that
epidemiological studies of new asthma
development and longer-term lung
function declines remain inconclusive
at present (EPA, 2006a, p. 7–134).
iii. Effects on the Cardiovascular System
of O3 Exposure
At the time of the 1997 review, the
possibility of O3-induced cardiovascular
effects was largely unrecognized. Since
then, a very limited body of evidence
from animal, controlled human
exposure, and epidemiologic studies has
emerged that provides evidence for
some potential plausible mechanisms
for how O3 exposures might exert
cardiovascular system effects, however
further research is needed to
substantiate these potential
mechanisms. Possible mechanisms may
involve O3-induced secretions of
vasoconstrictive substances and/or
effects on neuronal reflexes that may
result in increased arterial blood
pressure and/or altered
electrophysiologic control of heart rate
or rhythm. Some animal toxicology
studies have shown O3-induced
decreases in heart rate, mean arterial
pressure, and core temperature. One
controlled human exposure study that
evaluated effects of O3 exposure on
cardiovascular health outcomes found
no significant O3-induced differences in
ECG or blood pressure in healthy or
hypertensive subjects but did observe a
significant O3-induced increase the
alveolar-to-arterial PO2 gradient and
heart rate in both groups resulting in an
overall increase in myocardial work and
impairment in pulmonary gas exchange
(Gong et al., 1998). In another controlled
human exposure study, inhalation of a
mixture of PM2.5 and O3 by healthy
subjects increased brachial artery
vasoconstriction and reactivity (Brook et
al., 2002).
The evidence from a few animal
studies also includes potential direct
effects such as O3-induced release from
lung epithelial cells of platelet
activating factor (PAF) that may
contribute to blood clot formation that
would have the potential to increase the
risk of serious cardiovascular outcomes
(e.g., heart attack, stroke, mortality).
Also, interactions of O3 with surfactant
components in epithelial lining fluid of
the lung may result in production of
oxysterols and reactive oxygen species
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that may exhibit PAF-like activity
contributing to clotting and also may
exert cytotoxic effects on lung and heart
muscle cells.
Epidemiological panel and field
studies that examined associations
between O3 and various cardiac
physiologic endpoints have yielded
limited evidence suggestive of a
potential association between acute O3
exposure and altered heart rate
variability (HRV), ventricular
arrhythmias, and incidence of heart
attacks (myocardial infarction or MI). A
number of epidemiological studies have
also reported associations between
short-term exposures and
hospitalization for cardiovascular
diseases. As shown in Figure 7–13 of
the 2006 Criteria Document, many of the
studies reported negative or inconsistent
associations. Some other studies,
especially those that examined the
relationship when O3 exposures were
higher, have found robust positive
associations between O3 and
cardiovascular hospital admissions
(EPA, 2006a, p. 7–82). For example, one
study reported a positive association
between O3 and cardiovascular hospital
admissions in Toronto, Canada in a
summer-only analysis (Burnett et al.,
1997b). The results were robust to
adjustment for various PM indices,
whereas the PM effects diminished
when adjusted for gaseous pollutants.
Other studies stratified their analysis by
temperature (i.e., by warms days versus
cool days). Several analyses using warm
season days consistently produced
positive associations.
The epidemiologic evidence for
cardiovascular morbidity is much
weaker than for respiratory morbidity,
with only one of several U.S. and
Canadian studies showing statistically
significant positive associations of
cardiovascular hospitalizations with
warm-season O3 concentrations. Most of
the available European and Australian
studies, all of which conducted all-year
O3 analyses, did not find an association
between short-term O3 concentrations
and cardiovascular hospitalizations.
Overall, the currently available evidence
is inconclusive regarding an association
between cardiovascular hospital
admissions and ambient O3 exposure
(EPA, 2006a, p. 7–83).
In summary, based on the evidence
from animal toxicology, controlled
human exposure, and epidemiological
studies, from the 2006 Criteria
Document (p. 8–77) concludes that this
generally limited body of evidence is
suggestive that O3 can directly and/or
indirectly contribute to cardiovascularrelated morbidity, but that much needs
to be done to more fully integrate links
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between ambient O3 exposures and
adverse cardiovascular outcomes.
b. Mortality
i. Mortality and Short-term O3 Exposure
The 1996 Criteria Document
concluded that an association between
daily mortality and O3 concentration for
areas with high O3 levels (e.g., Los
Angeles) was suggested. However, due
to a very limited number of studies
available at that time, there was
insufficient evidence to conclude that
the observed association was likely
causal.
The 2006 Criteria Document included
results from numerous epidemiological
analyses of the relationship between O3
and mortality. Additional single city
analyses have also been conducted since
1996, however, the most pivotal studies
in EPA’s (and CASAC’s) finding of
increased support for the relationship
between premature mortality and O3 is
in part related to differences in study
design—limiting analyses to warm
seasons, better control for copollutants,
particularly PM, and use of multicity
designs (both time series and metaanalytic designs). Key findings are
available from multicity time-series
studies that report associations between
O3 and mortality. These studies include
analyses using data from 90 U.S. cities
in the National Mortality, Morbidity and
Air Pollution (NMMAPS) study
(Dominici et al., 2003) and from 95 U.S.
communities in an extension to the
NMMAPS analyses (Bell et al., 2004).
The original 90-city NMMAPS
analysis, with data from 1987 to 1994,
was primarily focused on investigating
effects of PM10 on mortality. A
significant association was reported
between mortality and 24-hour average
O3 concentrations in analyses using all
available data as well as in the warm
season only analyses (Dominici et al.,
2003). The estimate using all available
data was about half that for the summeronly data at a lag of 1-day. The extended
NMMAPS analysis included data from
95 U.S. cities and included an
additional 6 years of data, from 1987–
2000 (Bell et al., 2004). Significant
associations were reported between O3
and mortality in analyses using all
available data. The effect estimate for
increased mortality was approximately
0.5 percent per 0.020 ppm change in 24hour average O3 measured on the same
day, and approximately 1.04 percent per
0.020 ppm change in 24-hour average O3
in a 7-day distributed lag model (EPA,
2006a, p. 7–88). In analyses using only
data from the warm season, the results
were not significantly different from the
full-year results. The authors also report
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that O3-mortality associations were
robust to adjustment for PM (EPA,
2006a, p. 7–100). Using a subset of the
NMMAPS data set, Huang et al. (2005)
focused on associations between
cardiopulmonary mortality and O3
exposure (24-hour average) during the
summer season only. The authors report
an approximate 1.47 percent increase
per 0.020 ppm change in O3
concentration measured on the same
day and an approximate 2.52 percent
increase per 0.020 ppm change in O3
concentration using a 7-day distributed
lag model. These findings suggest that
the effect of O3 on mortality is
immediate but also persists for several
days.
As discussed below in section
II.A.3.a, confounding by weather,
especially temperature, is complicated
by the fact that higher temperatures are
associated with the increased
photochemical activities that are
important for O3 formation. Using a
case-crossover study design, Schwartz
(2005) assessed associations between
daily maximum concentrations and
mortality, matching case and control
periods by temperature, and using data
only from the warm season. The
reported effect estimate of
approximately 0.92 percent change in
mortality per 0.040 ppm O3 (1-hour
maximum) was similar to time-series
analysis results with adjustment for
temperature (approximately 0.76
percent per 0.040 ppm O3), suggesting
that associations between O3 and
mortality were robust to the different
adjustment methods for temperature.
An initial publication from APHEA, a
European multicity study, reported
statistically significant associations
between daily maximum O3
concentrations and mortality in four
cities in a full year analysis (Toulomi et
al., 1997). An extended analysis was
done using data from 23 cities
throughout Europe (Gryparis et al.,
2004). In this report, a positive but not
statistically significant association was
found between mortality and 1-hour
daily maximum O3 in a full year
analysis. Gryparis et al. (2004) noted
that there was a considerable seasonal
difference in the O3 effect on mortality;
thus, the small effect for the all-year
data might be attributable to inadequate
adjustment for confounding by
seasonality. Focusing on analyses using
summer measurements, the authors
report statistically significant
associations with total mortality,
cardiovascular mortality and respiratory
mortality (EPA, 2006a, p. 7–93, 7–99).
Numerous single-city analyses have
also reported associations between
mortality and short-term O3 exposure,
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especially for those analyses using
warm season data. As shown in Figure
7–21 of the 2006 Criteria Document, the
results of recent publications show a
pattern of positive, often statistically
significant associations between shortterm O3 exposure and mortality during
the warm season. In considering results
from year-round analyses, there remains
a pattern of positive results but the
findings are less consistent. In most
single-city analyses, effect estimates
were not substantially changed with
adjustment for PM (EPA, 2006a, Figure
7–22).
In addition, several meta-analyses
have been conducted on the
relationship between O3 and mortality.
As described in section 7.4.4 of the 2006
Criteria Document, these analyses
reported fairly consistent and positive
combined effect estimates ranging from
approximately 1.5 to 2.5 percent
increase in mortality for a standardized
change in O3 (EPA, 2006a, Figure 7–20).
Three recent meta-analyses evaluated
potential sources of heterogeneity in O3mortality associations (Bell et al., 2005;
Ito et al., 2005; Levy et al., 2005). The
2006 Criteria Document (p. 7–96)
observes common findings across all
three analyses, in that all reported that
effect estimates were larger in warm
season analyses, reanalysis of results
using default convergence criteria in
generalized additive models (GAM) did
not change the effect estimates, and
there was no strong evidence of
confounding by PM. Bell et al. (2005)
and Ito et al. (2005) both provided
suggestive evidence of publication bias,
but O3-mortality associations remained
after accounting for that potential bias.
The 2006 Criteria Document concludes
that the ‘‘positive O3 effects estimates,
along with the sensitivity analyses in
these three meta-analyses, provide
evidence of a robust association
between ambient O3 and mortality’’
(EPA, 2006a, p. 7–97).
Most of the single-pollutant model
estimates from single-city studies range
from 0.5 to 5 percent excess deaths per
standardized increments. Corresponding
summary estimates in large U.S.
multicity studies ranged between 0.5 to
1 percent with some studies noting
heterogeneity across cities and studies
(EPA, 2006a, p. 7–110).
Finally, from those studies that
included assessment of associations
with specific causes of death, it appears
that effect estimates for associations
with cardiovascular mortality are larger
than those for total mortality. The metaanalysis by Bell et al. (2005) observed a
slightly larger effect estimate for
cardiovascular mortality compared to
mortality from all causes. The effect
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estimate for respiratory mortality was
approximately one-half that of
cardiovascular mortality in the metaanalysis. However, other studies have
observed larger effect estimates for
respiratory mortality compared to
cardiovascular mortality. The apparent
inconsistency regarding the effect size of
O3-related respiratory mortality may be
due to reduced statistical power in this
subcategory of mortality (EPA, 2006a, p.
7–108).
In summary, many single- and multicity studies observed positive
associations of ambient O3
concentrations with total nonaccidental
and cardiopulmonary mortality. The
2006 Criteria Document finds that the
results from U.S. multicity time-series
studies provide the strongest evidence
to date for O3 effects on acute mortality.
Recent meta-analyses also indicate
positive risk estimates that are unlikely
to be confounded by PM; however,
future work is needed to better
understand the influence of model
specifications on the risk coefficient
(EPA, 2006a, p. 7–175). A meta-analysis
that examined specific causes of
mortality found that the cardiovascular
mortality risk estimates were higher
than those for total mortality. For
cardiovascular mortality, the 2006
Criteria Document (Figure 7–25, p. 7–
106) suggests that effect estimates are
consistently positive and more likely to
be larger and statistically significant in
warm season analyses. The findings
regarding the effect size for respiratory
mortality have been less consistent,
possibly because of lower statistical
power in this subcategory of mortality.
The 2006 Criteria Document (p. 8–78)
concludes that these findings are highly
suggestive that short-term O3 exposure
directly or indirectly contribute to nonaccidental and cardiopulmonary-related
mortality, but additional research is
needed to more fully establish
underlying mechanisms by which such
effects occur.21
21 In commenting on the Criteria Document, the
CASAC Ozone Panel raised questions about the
implications of these time-series results in a policy
context, emphasizing that ‘‘* * * while the timeseries study design is a powerful tool to detect very
small effects that could not be detected using other
designs, it is also a blunt tool’’ (Henderson, 2006b).
They note that ‘‘* * * not only is the interpretation
of these associations complicated by the fact that
the day-to-day variation in concentrations of these
pollutants is, to a varying degree, determined by
meteorology, the pollutants are often part of a large
and highly correlated mix of pollutants, only a very
few of which are measured’’ (Henderson, 2006b).
Even with these uncertainties, the CASAC Ozone
Panel, in its review of the Staff Paper, found ‘‘* * *
premature total non-accidental and
cardiorespiratory mortality for inclusion in the
quantitative risk assessment to be appropriate.’’
(Henderson, 2006b)
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ii. Mortality and Long-Term O3
Exposure
Little evidence was available in the
1997 review on the potential for
associations between mortality and
long-term exposure to O3. In the
Harvard Six City prospective cohort
analysis, the authors report that
mortality was not associated with longterm exposure to O3 (Dockery et al.,
1993). The authors note that the range
of O3 concentrations across the six cities
was small, which may have limited the
power of the study to detect associations
between mortality and O3 levels (EPA,
2006a, p. 7–127).
As discussed in section 7.5.8 of the
2006 Criteria Document, in this review
there are results available from three
prospective cohort studies: the
American Cancer Society (ACS) study
(Pope et al., 2002), the Adventist Health
and Smog (AHSMOG) study (Beeson et
al., 1998; Abbey et al., 1999), and the
U.S. Veterans Cohort study (Lipfert et
al., 2000, 2003). In addition, a major
reanalysis report includes evaluation of
data from the Harvard Six City cohort
study (Krewski et al., 2000).22 This
reanalysis also includes additional
evaluation of data from the initial ACS
cohort study report that had only
reported results of associations between
mortality and long-term exposure to fine
particles and sulfates (Pope et al., 1995).
This reanalysis was discussed in the
2007 Staff Paper (section 3.3.2.2) but not
in the 2006 Criteria Document.
In this reanalysis of data from the
previous Harvard Six City prospective
cohort study, the investigators
replicated and validated the findings of
the original studies, and the report
included additional quantitative results
beyond those available in the original
report (Krewski et al., 2000). In the
reanalysis of data from the Harvard Six
Cities study, the effect estimate for the
association between long-term O3
concentrations and mortality was
negative and nearly statistically
significant (relative risk = 0.87, 95
percent CI: 0.76, 1.00).
The ACS study is based on health
data from a large prospective cohort of
approximately 500,000 adults and air
quality data from about 150 U.S. cities.
The initial report (Pope et al., 1995)
focused on associations with fine
particles and sulfates, for which
significant associations had been
reported in the earlier Harvard Six
Cities study (Dockery et al., 1993). As
part of the major reanalysis of these
22 This reanalysis report and the original
prospective cohort study findings are discussed in
more detail in section 8.2.3 of the Air Quality
Criteria for Particulate Matter (EPA, 2004).
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data, results for associations with other
air pollutants were also reported, and
the authors report that no significant
associations were found between O3 and
all-cause mortality. However, a
significant association was reported for
cardiopulmonary mortality in the warm
season (Krewski et al., 2000). The ACS
II study (Pope et al., 2002) reported
results of associations with an extended
data base; the mortality records for the
cohort had been updated to include 16
years of follow-up (compared with 8
years in the first report) and more recent
air quality data were included in the
analyses. Similar to the earlier
reanalysis, a marginally significant
association was observed between longterm exposure to O3 and
cardiopulmonary mortality in the warm
season. No other associations with
mortality were observed in both the fullyear and warm season analyses.
The Adventist Health and Smog
(AHSMOG) cohort includes about 6,000
adults living in California. In two
studies from this cohort, a significant
association has been reported between
long-term O3 exposure and increased
risk of lung cancer mortality among
males only (Beeson et al., 1998; Abbey
et al., 1999). No significant associations
were reported between long-term O3
exposure and mortality from all causes
or cardiopulmonary causes. Due to the
small numbers of lung cancer deaths (12
for males, 18 for females) and the
precision of the effect estimate (i.e., the
wide confidence intervals), the 2006
Criteria Document (p. 7–130) discussed
concerns about the plausibility of the
reported association with lung cancer.
The U.S. Veterans Cohort study
(Lipfert et al., 2000, 2003) of
approximately 50,000 middle-aged
males diagnosed with hypertension,
reported some positive associations
between mortality and peak O3
exposures (95th percentile level for
several years of data). The study
included numerous analyses using
subsets of exposure and mortality
follow-up periods which spanned the
years 1960 to 1996. In the results of
analyses using deaths and O3 exposure
estimates concurrently across the study
period, there were positive, statistically
significant associations between peak O3
and mortality (EPA, 2006a, p. 7–129).
Overall, the 2006 Criteria Document
(p. 7–130) concludes that consistent
associations have not been reported
between long-term O3 exposure and allcause, cardiopulmonary or lung cancer
mortality.
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c. Role of Ground-Level O3 in Solar
Radiation-Related Human Health Effects
Beyond the direct health effects
attributable to inhalation exposure to O3
in the ambient air discussed above, the
2006 Criteria Document also assesses
potential indirect effects related to the
presence of O3 in the ambient air by
considering the role of ground-level O3
in mediating human health effects that
may be directly attributable to exposure
to solar ultraviolet radiation (UV–B).
The 2006 Criteria Document (chapter
10) focuses this assessment on three key
factors, including those factors that
govern (1) UV–B radiation flux at the
earth’s surface, (2) human exposure to
UV–B radiation, and (3) human health
effects due to UV–B radiation. In so
doing, the 2006 Criteria Document
provides a thorough analysis of the
current understanding of the
relationship between reducing groundlevel O3 concentrations and the
potential impact these reductions might
have on increasing UV–B surface fluxes
and indirectly contributing to UV–B
related health effects.
There are many factors that influence
UV–B radiation penetration to the
earth’s surface, including latitude,
altitude, cloud cover, surface albedo,
PM concentration and composition, and
gas phase pollution. Of these, only
latitude and altitude can be defined
with small uncertainty in any effort to
assess the changes in UV–B flux that
may be attributable to any changes in
tropospheric O3 as a result of any
revision to the O3 NAAQS. Such an
assessment of UV–B related health
effects would also need to take into
account human habits, such as outdoor
activities (including age- and
occupation-related exposure patterns),
dress and skin care to adequately
estimate UV–B exposure levels.
However, little is known about the
impact of these factors on individual
exposure to UV–B.
Moreover, detailed information does
not exist regarding other factors that are
relevant to assessing changes in disease
incidence, including: Type (e.g., peak or
cumulative) and time period (e.g.,
childhood, lifetime, current) of
exposures related to various adverse
health outcomes (e.g., damage to the
skin, including skin cancer; damage to
the eye, such as cataracts; and immune
system suppression); wavelength
dependency of biological responses; and
interindividual variability in UV–B
resistance to such health outcomes.
Beyond these well recognized adverse
health effects associated with various
wavelengths of UV radiation, the 2006
Criteria Document (section 10.2.3.6) also
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discusses protective effects of UV–B
radiation. Recent reports indicate the
necessity of UV–B in producing vitamin
D. Vitamin D deficiency can cause
metabolic bone disease among children
and adults, and may also increase the
risk of many common chronic diseases
(e.g., type I diabetes and rheumatoid
arthritis) as well as the risk of various
types of cancers. Thus, the 2006 Criteria
Document concludes that any
assessment that attempts to quantify the
consequences of increased UV–B
exposure on humans due to reduced
ground-level O3 must include
consideration of both negative and
positive effects. However, as with other
impacts of UV–B on human health, this
beneficial effect of UV–B radiation has
not been studied in sufficient detail to
allow for a credible health benefits or
risk assessment. In conclusion, the
effect of changes in surface-level O3
concentrations on UV–B-induced health
outcomes cannot yet be critically
assessed within reasonable uncertainty
(2006 Criteria Document, p. 10–36).
The Agency last considered indirect
effects of O3 in the ambient air in its
2003 final response to a remand of the
Agency’s 1997 decision to revise the O3
NAAQS. In so doing, based on the
available information in the 1997
review, EPA determined that the
information linking (a) changes in
patterns of ground-level O3
concentrations likely to occur as a result
of programs implemented to attain the
1997 O3 NAAQS to (b) changes in
relevant exposures to UV–B radiation of
concern to public health was too
uncertain at that time to warrant any
relaxation in the level of public health
protection previously determined to be
requisite to protect against the
demonstrated direct adverse respiratory
effects of exposure to O3 in the ambient
air (68 FR 614). At that time, the more
recent information on protective effects
of UV–B radiation was not available,
such that only adverse UV–B-related
effects could be considered. Taking into
consideration the more recent
information available for the 2008
review, the 2006 Criteria Document and
2007 Staff Paper conclude that the effect
of changes in ground-level O3
concentrations, likely to occur as a
result of revising the O3 NAAQS, on
UV–B-induced health outcomes,
including whether these changes would
ultimately result in increased or
decreased incidence of UV–B-related
diseases, cannot yet be critically
assessed.
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3. Interpretation and Integration of
Health Evidence
As discussed below, in assessing the
health evidence, the 2006 Criteria
Document integrates findings from
experimental (e.g., toxicological,
dosimetric and controlled human
exposure) and epidemiological studies,
to make judgments about the extent to
which causal inferences can be made
about observed associations between
health endpoints and exposure to O3. In
evaluating the evidence from
epidemiological studies, the EPA
focuses on well-recognized criteria,
including: The strength of reported
associations, including the magnitude
and precision of reported effect
estimates and their statistical
significance; the robustness of reported
associations, or stability in the effect
estimates after considering factors such
as alternative models and model
specification, potential confounding by
co-pollutants, and issues related to the
consequences of exposure measurement
error; potential aggregation bias in
pooling data; and the consistency of the
effects associations as observed by
looking across results of multiple- and
single-city studies conducted by
different investigators in different places
and times. Consideration is also given to
evaluating concentration-response
relationships observed in
epidemiological studies to inform
judgments about the potential for
threshold levels for O3-related effects.
Integrating more broadly across
epidemiological and experimental
evidence, the 2006 Criteria Document
also focuses on the coherence and
plausibility of observed O3-related
health effects to reach judgments about
the extent to which causal inferences
can be made about observed
associations between health endpoints
and exposure to O3 in the ambient air.
a. Assessment of Evidence From
Epidemiological Studies
Key elements of the evaluation of
epidemiological studies are briefly
summarized below.
(1) The strength of associations most
directly refers to the magnitude of the
reported relative risk estimates. Taking
a broader view, the 2006 Criteria
Document draws upon the criteria
summarized in a recent report from the
U.S. Surgeon General, which define
strength of an association as ‘‘the
magnitude of the association and its
statistical strength’’ which includes
assessment of both effect estimate size
and precision, which is related to the
statistical power of the study (CDC,
2004). In general, when associations are
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strong in terms of yielding large relative
risk estimates, it is less likely that the
association could be completely
accounted for by a potential confounder
or some other source of bias, whereas
with associations that yield small
relative risk estimates it is especially
important to consider potential
confounding and other factors in
assessing causality. Effect estimates
between O3 and some of the health
outcomes are generally small in size and
could thus be characterized as weak. For
example, effect estimates for
associations with mortality generally
range from 0.5 to 5 percent increases per
0.040 ppm increase in 1-hour maximum
O3 or equivalent, whereas associations
for hospitalization range up to 50
percent increases per standardized O3
increment. However, the 2006 Criteria
Document notes that there are large
multicity studies that find small
associations between short-term O3
exposure and mortality or morbidity
and have done so with great precision
due to the statistical power of the
studies (p. 8–40). That is, the power of
the studies allows the authors to reliably
distinguish even weak relationships
from the null hypothesis with statistical
confidence.
(2) In evaluating the robustness of
associations, the 2006 Criteria
Document (sections 7.1.3 and 8.4.4.3)
and 2007 Staff Paper (section 3.4.2) have
primarily considered the impact of
exposure error, potential confounding
by copollutants, and alternative models
and model specifications.
In time-series and panel studies, the
temporal (e.g., daily or hourly) changes
in ambient O3 concentrations measured
at centrally-located ambient monitoring
stations are generally used to represent
a community’s exposure to ambient O3.
In prospective cohort or cross-sectional
studies, air quality data averaged over a
period of months to years are used as
indicators of a community’s long-term
exposure to ambient O3 and other
pollutants. In both types of analyses,
exposure error is an important
consideration, as actual exposures to
individuals in the population will vary
across the community.
Ozone concentrations measured at
central ambient monitoring sites may
explain, at least partially, the variance
in individual exposures to ambient O3;
however, this relationship is influenced
by various factors related to building
ventilation practices and personal
behaviors. Further, the pattern of
exposure misclassification error and the
influence of confounders may differ
across the outcomes of interest as well
as in susceptible populations. As
discussed in the 2006 Criteria Document
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(section 3.9), only a limited number of
studies have examined the relationship
between ambient O3 concentrations and
personal exposures to ambient O3. One
of the strongest predictors of the
relationship between ambient
concentrations and personal exposures
appears to be time spent outdoors. The
strongest relationships were observed in
outdoor workers (Brauer and Brook,
1995, 1997; O’Neill et al., 2004).
Statistically significant correlations
between ambient concentrations and
personal exposures were also observed
for children, who likely spend more
time outdoors in the warm season (Linn
et al., 1996; Xu et al., 2005). There is
some concern about the extent to which
ambient concentrations are
representative of personal O3 exposures
of another particularly susceptible
group of individuals, the debilitated
elderly, since those who suffer from
chronic cardiovascular or respiratory
conditions may tend to protect
themselves more than healthy
individuals from environmental threats
by reducing their exposure to both O3
and its confounders, such as high
temperature and PM. Studies by Sarnat
et al. (2001, 2005) that included this
susceptible group reported mixed
results for associations between ambient
O3 concentrations and personal
exposures to O3. Collectively, these
studies observed that the daily averaged
personal O3 exposures tend to be well
correlated with ambient O3
concentrations despite the substantial
variability that existed among the
personal measurements. These studies
provide supportive evidence that
ambient O3 concentrations from central
monitors may serve as valid surrogate
measures for mean personal exposures
experienced by the population, which is
of most relevance for time-series
studies. A better understanding of the
relationship between ambient
concentrations and personal exposures,
as well as of the other factors that affect
relationship will improve the
interpretation of concentrationpopulation health response associations
observed.
The 2006 Criteria Document (section
7.1.3.1) also discusses the potential
influence of exposure error on
epidemiologic study results. Zeger et al.
(2000) outlined the components to
exposure measurement error, finding
that ambient exposure can be assumed
to be the product of the ambient
concentration and an attenuation factor
(i.e., building filter) and that panel
studies and time-series studies that use
ambient concentrations instead of
personal exposure measurements will
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estimate a health risk that is attenuated
by that factor. Navidi et al. (1999) used
data from a children’s cohort study to
compare effect estimates from a
simulated ‘‘true’’ exposure level to
results of analyses from O3 exposures
determined by several methods, finding
that O3 exposures based on the use of
ambient monitoring data overestimate
the individual’s O3 exposure and thus
generally result in O3 effect estimates
that are biased downward (EPA, 2006a,
p. 7–8). Similarly, in a reanalysis of a
study by Burnett et al. (1994) on the
acute respiratory effects of ambient air
pollution, Zidek et al. (1998) reported
that accounting for measurement error,
as well as making a few additional
changes to the analysis, resulted in
qualitatively similar conclusions, but
the effects estimates were considerably
larger in magnitude (EPA, 2006a, p. 7–
8). A simulation study by Sheppard et
al. (2005) also considered attenuation of
the risk based on personal behavior,
their microenvironment, and the
qualities of the pollutant in time-series
studies. Of particular interest is their
finding that risk estimates were not
further attenuated in time-series studies
even when the correlations between
personal exposures and ambient
concentrations were weak. In addition
to overestimation of exposure and the
resulting underestimation of effects, the
use of ambient O3 concentrations may
obscure the presence of thresholds in
epidemiologic studies (EPA, 2006a, p.
7–9).
As discussed in the 2006 Criteria
Document (section 3.9), using ambient
concentrations to determine exposure
generally overestimates true personal O3
exposures by approximately 2- to 4-fold
in available studies, resulting in
attenuated risk estimates. The
implication is that the effects being
estimated occur at fairly low exposures
and the potency of O3 is greater than
these effects estimates indicate. As very
few studies evaluating O3 health effects
with personal O3 exposure
measurements exist in the literature,
effect estimates determined from
ambient O3 concentrations must be
evaluated and used with caution to
assess the health risks of O3. In the
absence of available data on personal O3
exposure, the use of routinely
monitored ambient O3 concentrations as
a surrogate for personal exposures is not
generally expected to change the
principal conclusions from O3
epidemiologic studies. Therefore,
population health risk estimates derived
using ambient O3 levels from currently
available observational studies, with
appropriate caveats about personal
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exposure considerations, remain useful.
The 2006 Criteria Document
recommends caution in the quantitative
use of effect estimates calculated using
ambient O3 concentrations as they may
lead to underestimation of the potency
of O3. However, the 2007 Staff Paper
observes that the use of these risk
estimates for comparing relative risk
reductions between alternative ambient
O3 standards considered in the risk
assessment (discussed below in section
II.B.2) is less likely to suffer from this
concern.
Confounding occurs when a health
effect that is caused by one risk factor
is attributed to another variable that is
correlated with the causal risk factor;
epidemiological analyses attempt to
adjust or control for potential
confounders. Copollutants (e.g., PM,
CO, SO2 and NO2) can meet the criteria
for potential confounding in O3-health
associations if they are potential risk
factors for the health effect under study
and are correlated with O3. Effect
modifiers include variables that may
influence the health response to the
pollutant exposure (e.g., co-pollutants,
individual susceptibility, smoking or
age). Both are important considerations
for evaluating effects in a mixture of
pollutants, but for confounding, the
emphasis is on controlling or adjusting
for potential confounders in estimating
the effects of one pollutant, while the
emphasis for effect modification is on
identifying and assessing the effects for
different modifiers.
The 2006 Criteria Document (p.
7–148) observes that O3 is generally not
highly correlated with other criteria
pollutants (e.g., PM10, CO, SO2 and
NO2), but may be more highly correlated
with secondary fine particles, especially
during the summer months, and that the
degree of correlation between O3 and
other pollutants may vary across
seasons. For example, positive
associations are observed between O3
and pollutants such as fine particles
during the warmer months, but negative
correlations may be observed during the
cooler months (EPA, 2006a, p. 7–17).
Thus, the 2006 Criteria Document
(section 7.6.4) pays particular attention
to the results of season-specific analyses
and studies that assess effects of PM in
potential confounding of O3-health
relationships. The 2006 Criteria
Document also discussed the limitations
of commonly used multipollutant
models that include the difficulty in
interpreting results where the
copollutants are highly colinear, or
where correlations between pollutants
change by season (EPA, 2006a, p.
7–150). This is particularly the situation
where O3 and a copollutant, such as
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sulfates, are formed under the same
atmospheric condition; in such cases
multipollutant models would produce
unstable and possibly misleading results
(EPA, 2006a, p. 7–152).
For mortality, the results from
numerous multicity and single-city
studies indicate that O3-mortality
associations do not appear to be
substantially changed in multipollutant
models including PM10 or PM2.5 (EPA,
2006a, p. 7–101; Figure 7–22). Focusing
on results of warm season analyses,
effect estimates for O3-mortality
associations are fairly robust to
adjustment for PM in multipollutant
models (EPA, 2006a, p. 7–102; Figure
7–23). The 2006 Criteria Document
concludes that in the few multipollutant
analyses conducted for these endpoints,
copollutants generally do not confound
the relationship between O3 and
respiratory hospitalization (EPA, 2006a,
p. 7–79 to 7–80; Figure 7–12).
Multipollutant models were not used as
commonly in studies of relationships
between respiratory symptoms or lung
function with O3, but the 2006 Criteria
Document reports that results of
available analyses indicate that such
associations generally were robust to
adjustment for PM2.5 (p. 7–154). For
example, in a large multicity study of
asthmatic children (Mortimer et al.,
2002), the O3 effect was attenuated, but
there was still a positive association; in
Gent et al. (2003), effects of O3, but not
PM2.5, remained statistically significant
and even increased in magnitude in
two-pollutant models (EPA, 2006a, p.
7–53). Considering this body of studies,
the 2006 Criteria Document (p. 7–154)
concludes: ‘‘Multipollultant regression
analyses indicated that O3 risk
estimates, in general, were not sensitive
to the inclusion of copollutants,
including PM2.5 and sulfate. These
results suggest that the effects of O3 on
respiratory health outcomes appear to
be robust and independent of the effects
of other copollutants.’’
The 2006 Criteria Document (p. 7–14)
observes that another challenge of timeseries epidemiological analysis is
assessing the relationship between O3
and health outcomes while avoiding
bias due to confounding by other timevarying factors, particularly seasonal
trends and weather variables. These
variables are of particular interest
because O3 concentrations have a wellcharacterized seasonal pattern and are
also highly correlated with changes in
temperature, such that it can be difficult
to distinguish whether effects are
associated with O3 or with seasonal or
weather variables in statistical analyses.
The 2006 Criteria Document (section
7.1.3.4) discusses statistical modeling
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approaches that have been used to
adjust for time-varying factors,
highlighting a series of analyses that
were done in a Health Effects Institutefunded reanalysis of numerous timeseries studies. While the focus of these
reanalyses was on associations with PM,
a number of investigators also examined
the sensitivity of O3 coefficients to the
extent of adjustment for temporal trends
and weather factors. In addition, several
recent studies, including U.S. multicity
studies (Bell et al., 2005; Huang et al.,
2005; Schwartz et al., 2005) and a metaanalysis study (Ito et al., 2005),
evaluated the effect of model
specification on O3-mortality
associations. As discussed in the 2006
Criteria Document (section 7.6.3.1),
these studies generally report that
associations reported with O3 are not
substantially changed with alternative
modeling strategies for adjusting for
temporal trends and meteorologic
effects. In the meta-analysis by Ito et al.
(2005), a separate multicity analysis was
presented that found that alternative
adjustments for weather resulted in up
to 2-fold difference in the O3 effect
estimate. Significant confounding can
occur when strong seasonal cycles are
present, suggesting that season-specific
results are more generally robust than
year-round results in such cases. A
number of epidemiological studies have
conducted season-specific analyses, and
have generally reported stronger and
more precise effect estimates for O3
associations in the warm season than in
analyses conducted in the cool seasons
or over the full year.
(3) Consistency refers to the persistent
finding of an association between
exposure and outcome in multiple
studies of adequate power in different
persons, places, circumstances and
times (CDC, 2004). In considering
results from multicity studies and
single-city studies in different areas, the
2006 Criteria Document (p. 8–41)
observes general consistency in effects
of short-term O3 exposure on mortality,
respiratory hospitalization and other
respiratory health outcomes. The
variations in effects that are observed
may be attributable to differences in
relative personal exposure to O3, as well
as varying concentrations and
composition of copollutants present in
different regions. Thus, the 2006 Criteria
Document (p. 8–41) concludes that
‘‘consideration of consistency or
heterogeneity of effects is appropriately
understood as an evaluation of the
similarity or general concordance of
results, rather than an expectation of
finding quantitative results with a very
narrow range.’’
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(4) The 2007 Staff Paper recognizes
that it is likely that there are biological
thresholds for different health effects in
individuals or groups of individuals
with similar innate characteristics and
health status. For O3 exposure,
individual thresholds would
presumably vary substantially from
person to person due to individual
differences in genetic susceptibility,
pre-existing disease conditions and
possibly individual risk factors such as
diet or exercise levels (and could even
vary from one time to another for a
given person). Thus, it would be
difficult to detect a distinct threshold at
the population level below which no
individual would experience a given
effect, especially if some members of a
population are unusually sensitive even
down to very low concentrations (EPA,
2004, p. 9–43, 9–44).
Some studies have tested associations
between O3 and health outcomes after
removal of days with higher O3 levels
from the data set; such analyses do not
necessarily indicate the presence or
absence of a threshold, but provide
some information on whether the
relationship is found using only lowerconcentration data. For example, using
data from 95 U.S. cities, Bell et al.
(2004) found that the effect estimate for
an association between short-term O3
exposure and mortality was little
changed when days exceeding 0.060
ppm (24-hour average) were excluded in
the analysis. Using data from 8 U.S.
cities, Mortimer and colleagues (2002)
also reported that associations between
O3 and both lung function and
respiratory symptoms remained
statistically significant and of the same
or greater magnitude in effect size when
concentrations greater than 0.080 ppm
(8-hour average) were excluded (EPA,
2006a, p. 7–46). Several single-city
studies also report similar findings of
associations that remain or are increased
in magnitude and statistical significance
when data at the upper end of the
concentration range are removed (EPA,
2006a, section 7.6.5).
Other time-series epidemiological
studies have used statistical modeling
approaches to evaluate whether
thresholds exist in associations between
short-term O3 exposure and mortality.
As discussed in section 7.6.5 of the 2006
Criteria Document, one European
multicity study included evaluation of
the shape of the concentration-response
curve, and observed no deviation from
a linear function across the range of O3
measurements from the study (Gryparis
et al., 2004; EPA, 2006a p. 7–154).
Several single-city studies also observed
a monotonic increase in associations
between O3 and morbidity that suggest
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that no population threshold exists
(EPA, 2006a, p. 7–159).
On the other hand, a study in Korea
used several different modeling
approaches and reported that a
threshold model provided the best fit for
the data. The results suggested a
potential threshold level of about 0.045
ppm (1-hour maximum concentration;
< 0.035 ppm, 8-hour average) for an
association between mortality and shortterm O3 exposure during the summer
months (Kim et al., 2004; EPA, 2006a,
p. 8–43). The authors reported larger
effect estimates for the association for
data above the potential threshold level,
suggesting that an O3-mortality
association might be underestimated in
the non-threshold model. A threshold
analysis recently reported by Bell et al.
(2006) for 98 U.S. communities,
including the same 95 communities in
Bell et al. (2004), indicated that if a
population threshold existed for
mortality, it would likely fall below a
24-hour average O3 concentration of
0.015 ppm (< 0.025 ppm, 8-hour
average). In addition, Burnett and
colleagues (1997a,b) plotted the
relationships between air pollutant
concentrations and both respiratory and
cardiovascular hospitalization, and it
appears in these results that the
associations with O3 are found in the
concentration range above about 0.030
ppm (1-hour maximum; < 0.025 ppm, 8hour average). Vedal and colleagues
(2003) reported a significant association
between O3 and mortality in British
Columbia where O3 concentrations were
quite low (mean 1-hour maximum
concentration of 0.0273 ppm). The
authors did not specifically test for
threshold levels, but the fact that the
association was found in an area with
such low O3 concentrations suggests
that any potential threshold level would
be quite low in this data set.
In summary, the 2006 Criteria
Document finds that, taken together, the
available evidence from controlled
human exposure and epidemiological
studies suggests that no clear conclusion
can now be reached with regard to
possible threshold levels for O3-related
effects (EPA, 2006a, p. 8–44). Thus, the
available epidemiological evidence
neither supports nor refutes the
existence of thresholds at the
population level for effects such as
increased hospital admissions and
premature mortality. There are
limitations in epidemiological studies
that make discerning thresholds in
populations difficult, including low
data density in the lower concentration
ranges, the possible influence of
exposure measurement error, and
interindividual differences in
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susceptibility to O3-related effects in
populations. There is the possibility that
thresholds for individuals may exist in
reported associations at fairly low levels
within the range of air quality observed
in the studies but not be detectable as
population thresholds in
epidemiological analyses.
b. Biological Plausibility and Coherence
of Evidence
The body of epidemiological studies
discussed in the 2007 Staff Paper
emphasizes the role of O3 in association
with a variety of adverse respiratory and
cardiovascular effects. While
recognizing a variety of plausible
mechanisms, there exists a general
consensus suggesting that O3, could
either directly or through initiation,
interfere with basic cellular oxidation
processes responsible for inflammation,
reduced antioxidant capacity,
atherosclerosis and other effects.
Reasoning that O3 influences cellular
chemistry through basic oxidative
properties (as opposed to a unique
chemical interaction), other reactive
oxidizing species (ROS) in the
atmosphere acting either independently
or in combination with O3 may also
contribute to a number of adverse
respiratory and cardiovascular health
effects. Consequently, the role of O3
should be considered more broadly as
O3 behaves as a generator of numerous
oxidative species in the atmosphere.
In considering the biological
plausibility of reported O3-related
effects, the 2007 Staff Paper (section
3.4.6) considers this broader question of
health effects of pollutant mixtures
containing O3. The potential for O3related enhancements of PM formation,
particle uptake, and exacerbation of PMinduced cardiovascular effects
underscores the importance of
considering contributions of O3
interactions with other often cooccurring air pollutants to health effects
due to O3-containing pollutant mixes.
The 2007 Staff Paper summarizes some
examples of important pollutant
mixture effects from studies that
evaluate interactions of O3 with other
co-occurring pollutants, as discussed in
chapters 4, 5, and 6 of the 2006 Criteria
Document.
All of the types of interactive effects
of O3 with other co-occurring gaseous
and nongaseous viable and nonviable
PM components of ambient air mixes
noted above argue that O3 acts not only
alone but that O3 also is a surrogate
indicator for air pollution mixes which
may enhance the risk of adverse effects
due to O3 acting in combination with
other pollutants. Viewed from this
perspective, those epidemiologic
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findings of morbidity and mortality
associations, with ambient O3
concentrations extending to quite low
levels in many cases, become more
understandable and plausible.
The 2006 Criteria Document
integrates epidemiological studies with
mechanistic information from
controlled human exposure studies and
animal toxicological studies to draw
conclusions regarding the coherence of
evidence and biological plausibility of
O3-related health effects to reach
judgments about the causal nature of
observed associations. As summarized
below, coherence and biological
plausibility is discussed for each of the
following types of O3-related effects:
Short-term effects on the respiratory
system, effects on the cardiovascular
system, effects related to long-term O3
exposure, and short-term mortalityrelated health endpoints.
i. Coherence and Plausibility of ShortTerm Effects on the Respiratory System
Acute respiratory morbidity effects
that have been associated with shortterm exposure to O3 include such health
endpoints as decrements in lung
function, increased respiratory
symptoms, increased airway
responsiveness, airway inflammation,
increased permeability related to
epithelial injury, immune system
effects, emergency department visits for
respiratory diseases, and hospitalization
due to respiratory illness.
Recent epidemiological studies have
supported evidence available in the
previous O3 NAAQS review on
associations between ambient O3
exposure and decline in lung function
for children. The 2006 Criteria
Document (p. 8–34) concludes that
exposure to ambient O3 has a significant
effect on lung function and is associated
with increased respiratory symptoms
and medication use, particularly in
asthmatics. Short-term exposure to O3
has also been associated with more
severe morbidity endpoints, such as
emergency department visits and
hospital admissions for respiratory
cases, including specific respiratory
illness (e.g., asthma) (EPA, 2006a,
sections 7.3.2 and 7.3.3). In addition, a
few epidemiological studies have
reported positive associations between
short-term O3 exposure and respiratory
mortality, though the associations are
not generally statistically significant
(EPA, 2006a, p. 7–108).
Considering the evidence from
epidemiological studies, the results
described above provide evidence for
coherence in O3-related effects on the
respiratory system. Effect estimates from
U.S. and Canadian studies are shown in
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Figure 1, where it can be seen that
mostly positive associations have been
reported with respiratory effects ranging
from respiratory symptoms, such as
cough or wheeze, to hospitalization for
various respiratory diseases, and there is
suggestive evidence for associations
with respiratory mortality. Many of the
reported associations are statistically
significant, particularly in the warm
season. In Figure 1, the central effect
estimate is indicated by a square for
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each result, with the vertical bar
representing the 95 percent confidence
interval around the estimate. In the
discussions that follow, an individual
study result is considered to be
statistically significant if the 95 percent
confidence interval does not include
zero.23 Positive effect estimates indicate
23 Results for studies of respiratory symptoms are
presented as odds ratios; an odds ratio of 1.0 is
equivalent to no effect, and thus is presented as
equivalent to the zero effect estimate line.
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increases in the health outcome with O3
exposure. In considering these results as
a whole, it is important to consider not
only whether statistical significance at
the 95 percent confidence level is
reported in individual studies but also
the general pattern of results, focusing
in particular on studies with greater
statistical power that report relatively
more precise results.
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Considering also evidence from
toxicological, controlled human
exposure, and field studies, the 2006
Criteria Document (section 8.6)
discusses biological plausibility and
coherence of evidence for acute O3induced respiratory health effects.
Inhalation of O3 for several hours while
subjects are physically active can elicit
both acute adverse pathophysiological
changes and subjective respiratory tract
symptoms (EPA, 2006a, section 8.4.2).
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Acute pulmonary responses observed in
healthy humans exposed to O3 at
ambient concentrations include:
decreased inspiratory capacity; mild
bronchoconstriction; rapid, shallow
breathing during exercise; subjective
symptoms of tracheobronchial airway
irritation, including cough and pain on
deep inspiration; decreases in measures
of lung function; and increased airway
resistance. The severity of symptoms
and magnitude of response depends on
inhaled dose, individual O3 sensitivity,
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2965
and the degree of attenuation or
enhancement of response resulting from
previous O3 exposures. Lung function
studies of several animal species acutely
exposed to relatively low O3 levels from
a toxicological perspective (i.e., 0.25 to
0.4 ppm) show responses similar to
those observed in humans, including
increased breathing frequency,
decreased tidal volume, increased
resistance, and decreased FVC.
Alterations in breathing pattern return
to normal within hours of exposure, and
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attenuation in functional responses
following repeated O3 exposures is
similar to those observed in humans.
Physiological and biochemical
alterations investigated in controlled
human exposure and animal toxicology
studies tend to support certain
hypotheses of underlying pathological
mechanisms which lead to the
development of respiratory-related
effects reported in epidemiology studies
(e.g., increased hospitalization and
medication use). Some of these are: (a)
Decrements in lung function, (b)
bronchoconstriction, (c) increased
airway responsiveness, (d) airway
inflammation, (e) epithelial injury, (f)
immune system activation, (g) host
defense impairment, and (h) sensitivity
of individuals, which depends on at
least a person’s age, disease status,
genetic susceptibility, and the degree of
attenuation present due to prior
exposures. The time sequence,
magnitude, and overlap of these
complex events, both in terms of
development and recovery, illustrate the
inherent difficulty of interpreting the
biological plausibility of O3-induced
cardiopulmonary health effects (EPA,
2006a, p. 8–48).
The interaction of O3 with airway
epithelial cell membranes and ELF to
form lipid ozonation products and ROS
is supported by numerous human,
animal and in vitro studies. Ozonation
products and ROS initiate a cascade of
events that lead to oxidative stress,
injury, inflammation, airway epithelial
damage and increased epithelial damage
and increased alveolar permeability to
vascular fluids. Repeated respiratory
inflammation can lead to a chronic
inflammatory state with altered lung
structure and lung function and may
lead to chronic respiratory diseases such
as fibrosis and emphysema (EPA, 2006a,
section 8.6.2). Continued respiratory
inflammation also can alter the ability to
respond to infectious agents, allergens
and toxins. Acute inflammatory
responses to O3 are well documented,
and lung injury appears within 3 hours
after exposure in humans.
Taken together, the 2006 Criteria
Document concludes that the evidence
from experimental human and animal
toxicology studies indicates that acute
O3 exposure is causally associated with
respiratory system effects. These effects
include O3-induced pulmonary function
decrements; respiratory symptoms; lung
inflammation and increased lung
permeability; airway
hyperresponsiveness; increased uptake
of nonviable and viable particles; and
consequent increased susceptibility to
PM-related toxic effects and respiratory
infections (EPA, 2006a, p. 8–48).
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ii. Coherence and Plausibility of Effects
on the Cardiovascular System
There is very limited experimental
evidence of animals and humans that
has evaluated possible mechanisms or
physiological pathways by which acute
O3 exposures may induce
cardiovascular system effects. Ozone
induces lung injury, inflammation, and
impaired mucociliary clearance, with a
host of associated biochemical changes
all leading to increased lung epithelial
permeability. As noted above in section
II.A.2.a, the generation of lipid
ozonation products and ROS in lung
tissues can influence pulmonary
hemodynamics, and ultimately the
cardiovascular system. Other potential
mechanisms by which O3 exposure may
be associated with cardiovascular
disease outcomes have been described.
Laboratory animals exposed to relatively
high O3 concentrations (≥ 0.5 ppm)
demonstrate tissue edema in the heart
and lungs. Ozone-induced changes in
heart rate, edema of heart tissue, and
increased tissue and serum levels of
ANF found with 8-hour 0.5 ppm O3
exposure in animal toxicology studies
(Vesely et al., 1994a,b,c) also raise the
possibility of potential cardiovascular
effects of acute ambient O3 exposures.
Animal toxicology studies have found
both transient and persistent ventilatory
responses with and without progressive
decreases in heart rate (Arito et al.,
1997). Observations of O3-induced
vasoconstriction in a controlled human
exposure study by Brook et al. (2002)
suggests another possible mechanism
for O3-related exacerbations of
preexisting cardiovascular disease. One
controlled human study (Gong et al.,
1998) evaluated potential cardiovascular
health effects of O3 exposure. The
overall results did not indicate acute
cardiovascular effects of O3 in either the
hypertensive or control subjects. The
authors observed an increase in ratepressure product and heart rate, a
decrement for FEV1, and a > 10 mm Hg
increase in the alveolar/arterial pressure
difference for O2 following O3 exposure.
Foster et al. (1993) demonstrated that
even in relatively young healthy adults,
O3 exposure can cause ventilation to
shift away from the well-perfused basal
lung. This effect of O3 on ventilation
distribution may persist beyond 24hours post-exposure (Foster et al.,
1997). These findings suggest that O3
may exert cardiovascular effects
indirectly by impairing alveolar-arterial
O2 transfer and potentially reducing O2
supply to the myocardium. Ozone
exposure may increase myocardial work
and impair pulmonary gas exchange to
a degree that could perhaps be clinically
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important in persons with significant
preexisting cardiovascular impairment.
As noted above in section II.A.2.a, a
limited number of new epidemiological
studies have reported associations
between short-term O3 exposure and
effects on the cardiovascular system.
Among these studies, three were
population-based and involved
relatively large cohorts; two of these
studies evaluated associations between
O3 and HRV and the other study
evaluated the association between O3
levels and the relative risk of MI or heart
attack. Such studies may offer more
informative results based on their large
subject-pool and design. Results from
these three studies were suggestive of an
association between O3 exposure and
the cardiovascular endpoints studied. In
other recent studies on the incidence of
heart attacks and some more subtle
cardiovascular health endpoints, such
as changes in HRV or cardiac
arrhythmia, some but not all studies
reported associations with short-term
exposure to O3 (EPA, 2006a, section
7.2.7.1). From these studies, the 2006
Criteria Document concludes that the
‘‘current evidence is rather limited but
suggestive of a potential effect on HRV,
ventricular arrhythmias, and MI
incidence’’ (EPA, 2006a, p. 7–65).
An increasing number of studies have
evaluated the association between O3
exposure and cardiovascular hospital
admissions. As discussed in section
7.3.4 of the 2006 Criteria Document,
many reported negative or inconsistent
associations, whereas other studies,
especially those that examined the
relationship when O3 exposures were
higher, have found positive and robust
associations between O3 and
cardiovascular hospital admissions. The
2006 Criteria Document (p. 7–83) finds
that the overall evidence from these
studies remains inconclusive regarding
the effect of O3 on cardiovascular
hospitalizations. The 2006 Criteria
Document notes that the suggestive
positive epidemiologic findings of O3
exposure on cardiac autonomic control,
including effects on HRV, ventricular
arrhythmias and heart attacks, and
reported associations between O3
exposure and cardiovascular
hospitalizations generally in the warm
season gain credibility and scientific
support from the results of experimental
animal toxicology and controlled
human exposure studies, which are
indicative of plausible pathways by
which O3 may exert cardiovascular
effects (EPA, 2006a, section 8.6.1).
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iii. Coherence and Plausibility of Effects
Related to Long-Term O3 Exposure
Controlled human exposure studies
cannot evaluate effects of long-term
exposures to O3; there is some evidence
available from toxicological studies.
While early animal toxicology studies of
long-term O3 exposures were conducted
using continuous exposures, more
recent studies have focused on
exposures which mimic diurnal and
seasonal patterns and more realistic O3
exposure levels (EPA, 2006a, p. 8–50).
Studies of monkeys that compared these
two exposure scenarios found increased
airway pathology only with the latter
design. Persistent and irreversible
effects reported in chronic animal
toxicology studies suggest that
additional complementary human data
are needed from epidemiologic studies
(EPA, 2006a, p. 8–50).
There is limited evidence from human
studies for long-term O3-induced effects
on lung function. As discussed in
section 8.6.2 of the 2006 Criteria
Document, previous epidemiological
studies have provided only inconclusive
evidence for either mortality or
morbidity effects of long-term O3
exposure. The 2006 Criteria Document
(p. 8–50) observes that the inconsistency
in findings may be due to a lack of
precise exposure information, the
possibility of selection bias, and the
difficulty of controlling for confounders.
Several new longitudinal epidemiology
studies have evaluated associations
between long-term O3 exposures and
morbidity and mortality and suggest
that these long-term exposures may be
related to changes in lung function in
children; however, little evidence is
available to support a relationship
between chronic O3 exposure and
mortality or lung cancer incidence
(EPA, 2006a, p. 8–50).
The 2006 Criteria Document (p. 8–51)
concludes that evidence from animal
toxicology studies strongly suggests that
chronic O3 exposure is capable of
damaging the distal airways and
proximal alveoli, resulting in lung tissue
remodeling leading to apparent
irreversible changes. Such structural
changes and compromised lung
function caused by persistent
inflammation may exacerbate the
progression and development of chronic
lung disease. Together with the limited
evidence available from epidemiological
studies, these findings offer some
insight into potential biological
mechanisms for suggested associations
between long-term or seasonal
exposures to O3 and reduced lung
function development in children
which have been observed in
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epidemiologic studies (EPA, 2006a, p.
8–51).
iv. Coherence and Plausibility of ShortTerm Mortality-Related Health
Endpoints
An extensive epidemiological
literature on air pollution related
mortality risk estimates from the U.S.,
Canada, and Europe is discussed in the
2006 Criteria Document (sections 7.4
and 8.6.3). These single- and multicity
mortality studies coupled with results
from meta-analyses generally indicate
associations between acute O3 exposure
and elevated risk for all-cause mortality,
even after adjustment for the influence
of season and PM exposure. Several
single-city studies that specifically
evaluated the relationship between O3
exposure and cardiopulmonary
mortality also reported results
suggestive of a positive association
(EPA, 2006a, p. 8–51). These mortality
studies suggest a pattern of effects for
causality that have biologically
plausible explanations, but our
knowledge regarding potential
underlying mechanisms is very limited
at this time and requires further
research. Most of the physiological and
biochemical parameters investigated in
human and animal studies suggest that
O3-induced biochemical effects are
relatively transient and attenuate over
time. The 2006 Criteria Document (p.
8–52) hypothesizes a generic pathway of
O3-induced lung damage, potentially
involving oxidative lung damage with
subsequent inflammation and/or decline
in lung function leading to respiratory
distress in some sensitive population
groups (e.g., asthmatics), or other
plausible pathways noted below that
may lead to O3-related contributions to
cardiovascular effects that ultimately
increase risk of mortality.
The third National Health and
Nutrition Examination Survey follow-up
data analysis indicates that about 20
percent of the adult population has
reduced FEV1 values, suggesting
impaired lung function in a significant
portion of the population. Most of these
individuals have COPD, asthma or
fibrotic lung disease (Manino et al.,
2003), which are associated with
persistent low-grade inflammation.
Furthermore, patients with COPD are at
increased risk for cardiovascular
disease. Also, lung disease with
underlying inflammation may be linked
to low-grade systemic inflammation
associated with atherosclerosis,
independent of cigarette smoking (EPA,
2006a, p. 8–52). Lung function
decrements in persons with
cardiopulmonary disease have been
associated with inflammatory markers,
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such as C-reactive protein (CRP) in the
blood. At a population level it has been
found that individuals with the lowest
FEV1 values have the highest levels of
CRP, and those with the highest FEV1
values have the lowest CRP levels
(Manino et al., 2003; Sin and Man,
2003). This complex series of
physiological and biochemical reactions
following O3 exposure may tilt the
biological homeostasis mechanisms
which could lead to adverse health
effects in people with compromised
cardiopulmonary systems.
Several other types of newly available
data also support reasonable hypotheses
that may help to explain the findings of
O3-related increases in cardiovascular
mortality observed in some
epidemiological studies. These include
the direct effect of O3 on increasing PAF
in lung tissue that can then enter the
general circulation and possibly
contribute to increased risk of blood clot
formation and the consequent increased
risk of heart attacks, cerebrovascular
events (stroke), or associated
cardiovascular-related mortality. Ozone
reactions with cholesterol in lung
surfactant to form epoxides and
oxysterols that are cytotoxic to lung and
heart muscles and that contribute to
atherosclerotic plaque formation in
arterial walls represent another
potential pathway. Stimulation of
airway irritant receptors may lead to
increases in tissue and serum levels of
ANF, changes in heart rate, and edema
of heart tissue. A few new field and
panel studies of human adults have
reported associations between ambient
O3 concentrations and changes in
cardiac autonomic control (e.g., HRV,
ventricular arrhythmias, and MI). These
represent plausible pathways that may
lead to O3-related contributions to
cardiovascular effects that ultimately
increase the risk of mortality.
In addition, O3-induced increases in
lung permeability allow more ready
entry for inhaled PM into the blood
stream, and thus O3 exposure may
increase the risk of PM-related
cardiovascular effects. Furthermore,
increased ambient O3 levels contribute
to ultrafine PM formation in the ambient
air and indoor environments. Thus, the
contributions of elevated ambient O3
concentrations to ultrafine PM
formation and human exposure, along
with the enhanced uptake of inhaled
fine particles, consequently may
contribute to exacerbation of PMinduced cardiovascular effects in
addition to those more directly induced
by O3 (EPA, 2006a, p. 8–53).
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c. Summary
Judgments concerning the extent to
which relationships between various
health endpoints and ambient O3
exposures are likely to be causal are
informed by the conclusions and
discussion in the 2006 Criteria
Document as discussed above and
summarized in section 3.7.5 of the 2007
Staff Paper. These judgments reflect the
nature of the evidence and the overall
weight of the evidence, and are taken
into consideration in the quantitative
risk assessment discussed below in
section II.B.2.
For example, there is a very high level
of confidence that O3 induces lung
function decrements in healthy adults
and children due in part to the dozens
of controlled human exposure and
epidemiological studies consistently
showing such effects. The 2006 Criteria
Document (p. 8–74) states that these
studies provide clear evidence of
causality for associations between shortterm O3 exposures and statistically
significant declines in lung function in
children, asthmatics and adults who
exercise outdoors. An increase in
respiratory symptoms (e.g., cough,
shortness of breath) has been observed
in controlled human exposure studies of
short-term O3 exposures, and significant
associations between ambient O3
exposures and a wide variety of
respiratory symptoms have been
reported in epidemiology studies (EPA,
2006a, p. 8–75). Population time-series
studies showing robust associations
between O3 exposures and respiratory
hospital admissions and emergency
department visits are strongly supported
by controlled human exposure, animal
toxicological, and epidemiological
evidence for O3-related lung function
decrements, respiratory symptoms,
airway inflammation, and airway
hyperreactivity. The 2006 Criteria
Document (p. 8–77) concludes that,
taken together, the overall evidence
supports the inference of a causal
relationship between acute ambient O3
exposures and increased respiratory
morbidity outcomes resulting in
increased emergency department visits
and hospitalizations during the warm
season. Further, recent epidemiologic
evidence has been characterized in the
2006 Criteria Document (p. 8–78) as
highly suggestive that O3 directly or
indirectly contributes to non-accidental
and cardiopulmonary-related mortality.
4. O3-Related Impacts on Public Health
The following discussion draws from
chapters 6 and 7 and section 8.7 of the
2006 Criteria Document and section 3.6
of the 2007 Staff Paper to characterize
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factors which modify responsiveness to
O3, populations potentially at risk for
O3-related health effects, the adversity
of O3-related effects, and the size of the
at-risk populations in the U.S. These
considerations are all important
elements in characterizing the potential
public health impacts associated with
exposure to ambient O3.
a. Factors That Modify Responsiveness
to Ozone
There are numerous factors that can
modify individual responsiveness to O3.
These include: influence of physical
activity; age; gender and hormonal
influences; racial, ethnic and
socioeconomic status (SES) factors;
environmental factors; and oxidantantioxidant balance. These factors are
discussed in more detail in section 6.5
of the 2006 Criteria Document.
It is well established that physical
activity increases an individual’s
minute ventilation and will thus
increase the dose of O3 inhaled (EPA,
2006a, section 6.5.4). Increased physical
activity results in deeper penetration of
O3 into more distal regions of the lungs,
which are more sensitive to acute O3
response and injury. This will result in
greater lung function decrements for
acute exposures of individuals during
increased physical activity. Research
has shown that respiratory effects are
observed at lower O3 concentrations if
the level of exertion is increased and/or
duration of exposure and exertion are
extended. Predicted O3-induced
decrements in lung function have been
shown to be a function of exposure
concentration, duration and exercise
level for healthy, young adults
(McDonnell et al., 1997).
Most of the studies investigating the
influence of age have used lung function
decrements and symptoms as measures
of response. For healthy adults, lung
function and symptom responses to O3
decline as age increases. The rate of
decline in O3 responsiveness appears
greater in those 18 to 35 years old
compared to those 35 to 55 years old,
while there is very little change after age
55. In one study (Seal et al., 1996)
analyzing a large data set, a 5.4%
decrement in FEV1 on average was
estimated for 20-year-old individuals
exposed to 0.12 ppm O3 for 2.3 hours,
whereas similar exposure of 35-year-old
individuals resulted in a 2.6%
decrement on average. While healthy
children tend not to report respiratory
symptoms when exposed to low levels
of O3, for subjects 18 to 36 years old
symptom responses induced by O3 are
observed but tend to decrease with
increasing age within this range
(McDonnell et al., 1999).
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Limited evidence of gender
differences in response to O3 exposure
has suggested that females may be
predisposed to a greater susceptibility to
O3. Lower plasma and NL fluid levels of
the most prevalent antioxidant, uric
acid, in females relative to males may be
a contributing factor. Consequently,
reduced removal of O3 in the upper
airways may promote deeper
penetration. However, most of the
evidence on gender differences appears
to be equivocal, with one study
(Hazucha et al., 2003) suggesting that
physiological responses of young
healthy males and females may be
comparable (EPA, 2006a, section 6.5.2).
A few studies have suggested that
ethnic minorities might be more
responsive to O3 than Caucasian
population groups (EPA, 2006a, section
6.5.3). This may be more the result of a
lack of adequate health care and
socioeconomic status (SES) than any
differences in sensitivity to O3. The
limited data available, which have
investigated the influence of race, ethnic
or other related factors on
responsiveness to O3, prevent drawing
any clear conclusions at this time.
Few human studies have examined
the potential influence of environmental
factors such as the sensitivity of
individuals who voluntarily smoke
tobacco (i.e., smokers) and the effect of
high temperatures on O3
responsiveness. New controlled human
exposure studies have confirmed that
smokers are less responsive to O3 than
nonsmokers; however, time course of
development and recovery of these
effects, as well as reproducibility, was
not different from nonsmokers (EPA,
2006a, section 6.5.5). Influence of
ambient temperature on pulmonary
effects induced by O3 has been studied
very little, but additive effects of heat
and O3 exposure have been reported.
Antioxidants, which scavenge free
radicals and limit lipid peroxidation in
the ELF, are the first line of defense
against oxidative stress. Ozone exposure
leads to absorption of O3 in the ELF
with subsequent depletion of
antioxidant in the nasal ELF, but
concentration and antioxidant enzyme
activity in ELF or plasma do not appear
related to O3 responsiveness (EPA
2006a, section 6.5.6). Controlled studies
of dietary antioxidant supplements have
shown some protective effects on lung
function decrements but not on
symptoms and airway inflammatory
responses. Dietary antioxidant
supplements have provided some
protection to asthmatics by attenuating
post-exposure airway
hyperresponsiveness. Animal studies
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b. At-Risk Subgroups for O3-Related
Effects
Several characteristics may increase
the extent to which a population group
shows increased susceptibility or
vulnerability. Information on potentially
susceptible and vulnerable groups is
summarized in section 8.7 of the 2006
Criteria Document. As described there,
the term susceptibility refers to innate
(e.g., genetic or developmental) or
acquired (e.g., personal risk factors, age)
factors that make individuals more
likely to experience effects with
exposure to pollutants. A number of
population groups have been identified
as potentially susceptible to health
effects as a result of O3 exposure,
including people with existing lung
diseases, including asthma, children
and older adults, and people who have
larger than normal lung function
responses that may be due to genetic
susceptibility. In addition, some
population groups have been identified
as having increased vulnerability to O3related effects due to increased
likelihood of exposure while at elevated
ventilation rates, including healthy
children and adults who are active
outdoors, for example, outdoor workers
and joggers. Taken together, the
susceptible and vulnerable groups make
up ‘‘at-risk’’ groups.24
i. Active People
A large group of individuals at risk
from O3 exposure consists of outdoor
workers and children, adolescents, and
adults who engage in outdoor activities
involving exertion or exercise during
summer daylight hours when ambient
O3 concentrations tend to be higher.
This conclusion is based on a large
number of controlled-human exposure
studies and several epidemiologic field/
panel studies which have been
conducted with healthy children and
adults and those with preexisting
respiratory diseases (EPA 2006a,
sections 6.2, 6.3, 7.2, and 8.4.4). The
controlled human exposure studies
show a clear O3 exposure-response
relationship with increasing spirometric
and symptomatic response as exercise
level increases. Furthermore, O3induced response increases as time of
exposure increases. Studies of outdoor
workers and others who participate in
outdoor activities indicate that extended
exposures to O3 at elevated exertion
24 In the Staff Paper and documents from previous
O3 NAAQS reviews, ‘‘at-risk’’ groups have also been
called ‘‘sensitive’’ groups, to mean both groups with
greater inherent susceptibility and those more likely
to be exposed.
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levels can produce marked effects on
lung function, as discussed above in
¨
section IIA.2 (Brauer et al., 1996; Hoppe
et al., 1995; Korrick et al., 1998;
McConnell et al., 2002).
These field studies with subjects at
elevated exertion levels support the
extensive evidence derived from
controlled human exposure studies. The
majority of controlled human exposure
studies has examined the effects of O3
exposure in subjects performing
continuous or intermittent exercise for
variable periods of time and has
reported significant O3-induced
respiratory responses. The
epidemiologic studies discussed above
also indicate that prolonged exposure
periods, combined with elevated levels
of exertion or exercise, may magnify O3
effects on lung function. Thus, outdoor
workers and others who participate in
higher exertion activities outdoors
during the time of day when high peak
O3 concentrations occur appear to be
particularly vulnerable to O3 effects on
respiratory health. Although these
studies show a wide variability of
response and sensitivity among subjects
and the factors contributing to this
variability continue to be incompletely
understood, the effect of increased
exertion is consistent. It should be noted
that this wide variability of response
and sensitivity among subjects may be
in part due to the wide range of other
highly reactive photochemical oxidants
coexisting with O3 in the ambient air.
ii. People With Lung Disease
People with preexisting pulmonary
disease are among those at increased
risk from O3 exposure. Altered
physiological, morphological, and
biochemical states typical of respiratory
diseases like asthma, COPD, and
chronic bronchitis may render people
sensitive to additional oxidative burden
induced by O3 exposure. At the time of
the 1997 review, it was concluded that
these groups were at greater risk because
the impact of O3-induced responses on
already-compromised respiratory
systems would noticeably impair an
individual’s ability to engage in normal
activity or would be more likely to
result in increased self-medication or
medical treatment. At that time there
was little evidence that people with preexisting disease were more responsive
than healthy individuals in terms of the
magnitude of lung function decrements
or symptomatic responses. The new
results from controlled exposure and
epidemiologic studies continue to
indicate that individuals with
preexisting pulmonary disease are a
sensitive population for O3-related
health effects.
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Several controlled human exposure
studies reviewed in the 1996 Criteria
Document on atopic and asthmatic
subjects have suggested but not clearly
demonstrated enhanced responsiveness
to acute O3 exposure compared to
healthy subjects. The majority of the
newer studies reviewed in Chapter 6 of
the 2006 Criteria Document indicate
that asthmatics are more sensitive than
normal subjects in manifesting O3induced lung function decrements. In
one key study (Horstman et al., 1995),
the FEV1 decrement observed in the
asthmatics was significantly larger than
in the healthy subjects (19% versus
10%, respectively). There was also a
notable tendency for a greater group
mean O3-induced decrease in FEF25–75
in asthmatics relative to the healthy
subjects (24% versus 15%,
respectively). A significant positive
correlation in asthmatics was also
reported between the magnitude of O3induced spirometric responses and
baseline lung function, i.e., responses
increased with severity of disease.
Asthmatics present a differential
response profile for cellular, molecular,
and biochemical parameters (2006
Criteria Document, Figure 8–1) that are
altered in response to acute O3
exposure. Ozone-induced increases in
neutrophils, IL–8 and protein were
found to be significantly higher in the
BAL fluid from asthmatics compared to
healthy subjects, suggesting
mechanisms for the increased
sensitivity of asthmatics (Basha et al.,
1994; McBride et al., 1994; Scannell et
al., 1996; Hiltermann et al., 1999; Holz
et al., 1999; Bosson et al., 2003).
Neutrophils, or PMNs, are the white
blood cells most associated with
inflammation. IL–8 is an inflammatory
cytokine with a number of biological
effects, primarily on neutrophils. The
major role of this cytokine is to attract
and activate neutrophils. Protein in the
airways is leaked from the circulatory
system, and is a marker for increased
cellular permeability.
Bronchial constriction following
provocation with O3 and/or allergens
presents a two-phase response. The
early response is mediated by release of
histamine and leukotrienes that leads to
contraction of smooth muscle cells in
the bronchi, narrowing the lumen and
decreasing the airflow. In people with
allergic airway disease, including
people with rhinitis and asthma, these
mediators also cause accumulation of
eosinophils in the airways (Bascom et
al., 1990; Jorres et al., 1996; Peden et al.,
1995 and 1997; Frampton et al., 1997;
Michelson et al., 1999; Hiltermann et
al., 1999; Holz et al., 2002; Vagaggini et
al., 2002). In asthma, the eosinophil,
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which increases inflammation and
allergic responses, is the cell most
frequently associated with exacerbations
of the disease. A study by Bosson et al.
(2003) evaluated the difference in O3induced bronchial epithelial cytokine
expression between healthy and
asthmatic subjects. After O3 exposure
the epithelial expression of IL–5 and
GM–CSF increased significantly in
asthmatics, compared to healthy
subjects. Asthma is associated with Th2related airway response (allergic
response), and IL–5 is an important
Th2-related cytokine. The O3-induced
increase in IL–5, and also in GM–CSF,
which affects the growth, activation and
survival of eosinophils, may indicate an
effect on the Th2-related airway
response and on airway eosinophils.
The authors reported that the O3induced Th2-related cytokine responses
that were found within the asthmatic
group may indicate a worsening of their
asthmatic airway inflammation and thus
suggest a plausible link to
epidemiological data indicating O3associated increases in bronchial
reactivity and hospital admissions.
The accumulation of eosinophils in
the airways of asthmatics is followed by
production of mucus and a late-phase
bronchial constriction and reduced
airflow. In a study of 16 intermittent
asthmatics, Hiltermann et al. (1999)
found that there was a significant
inverse correlation between the O3induced change in the percentage of
eosinophils in induced sputum and the
change in PC20, the concentration of
methacholine causing a 20% decrease in
FEV1. Characteristic O3-induced
inflammatory airway neutrophilia at one
time was considered a leading
mechanism of airway
hyperresponsiveness. However,
Hiltermann et al. (1999) determined that
the O3-induced change in percentage
neutrophils in sputum was not
significantly related to the change in
PC20. These results are consistent with
the results of Zhang et al. (1995), which
found neutrophilia in a murine model to
be only coincidentally associated with
airway hyperresponsiveness, i.e., there
was no cause and effect relationship.
(2006 Criteria Document, AX 6–26).
Hiltermann et al. (1999) concluded that
the results point to the role of
eosinophils in O3-induced airway
hyperresponsiveness. Increases in O3induced nonspecific airway
responsiveness incidence and duration
could have important clinical
implications for asthmatics.
¨
Two studies (Jorres et al., 1996; Holz
et al., 2002) observed increased airway
responsiveness to O3 exposure with
bronchial allergen challenge in subjects
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with preexisting allergic airway disease.
¨
Jorres et al. (1996) found that O3 causes
an increased response to bronchial
allergen challenge in subjects with
allergic rhinitis and mild allergic
asthma. The subjects were exposed to
0.25 ppm O3 for 3 hours with IE. Airway
responsiveness to methacholine was
determined 1 hour before and after
exposure; responsiveness to allergen
was determined 3 hours after exposure.
Statistically significant decreases in
FEV1 occurred in subjects with allergic
rhinitis (13.8%) and allergic asthma
(10.6%), and in healthy controls (7.3%).
Methacholine responsiveness was
statistically increased in asthmatics, but
not in subjects with allergic rhinitis or
healthy controls. Airway responsiveness
to an individual’s historical allergen
(either grass and birch pollen, house
dust mite, or animal dander) was
significantly increased after O3 exposure
when compared to FA exposure. In
subjects with asthma and allergic
rhinitis, a maximum percent fall in
FEV1 of 27.9% and 7.8%, respectively,
occurred 3 days after O3 exposure when
they were challenged with of the highest
common dose of allergen. The authors
concluded that subjects with asthma or
allergic rhinitis, without asthma, could
be at risk if a high O3 exposure is
followed by a high dose of allergen.
Holz et al. (2002) reported an early
phase lung function response in subjects
with rhinitis after a consecutive 4-day
exposure to 0.125 ppm O3 that resulted
in a clinically relevant (>20%) decrease
in FEV1. Ozone-induced exacerbation of
airway responsiveness persists longer
and attenuates more slowly than O3induced lung function decrements and
respiratory symptom responses and can
have important clinical implications for
asthmatics.
A small number of in vitro studies
corroborate the differences in the
responses of asthmatic and healthy
subject generally found in controlled
human exposure studies. In vitro
studies (Schierhorn et al., 1999) of nasal
mucosal biopsies from atopic and
nonatopic subjects exposed to 0.1 ppm
O3 found significant differences in
release of IL–4, IL–6, IL–8, and TNF-a.
Another study by Schierhorn et al.
(2002) found significant differences in
the O3-induced release of the
neuropeptides neurokinin A and
substance P for allergic patients in
comparison to nonallergic controls,
suggesting increased activation of
sensory nerves by O3 in the allergic
tissues. Another study by Bayram et al.
(2002) using in vitro culture of
bronchial epithelial cells recovered from
atopic and nonatopic asthmatics also
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found significant increases in epithelial
permeability in response to O3
exposure.
The new data on airway
responsiveness, inflammation, and
various molecular markers of
inflammation and bronchoconstriction
indicate that people with asthma and
allergic rhinitis (with or without
asthma) comprise susceptible groups for
O3-induced adverse effects. This body of
evidence indicates that controlled
human exposure and epidemiological
panel studies of lung function
decrements and respiratory symptoms
that evaluate only healthy, nonasthmatic subjects likely underestimate
the effects of O3 exposure on asthmatics
and other susceptible populations. The
effects of O3 on lung function,
inflammation, and increased airway
responsiveness demonstrated in subjects
with asthma and other allergic airway
diseases, provide plausible mechanisms
underlying the more serious respiratory
morbidity effects, such as emergency
department visits and hospital
admissions, and respiratory mortality
effects.
A number of epidemiological studies
have been conducted using asthmatic
study populations. The majority of
epidemiological panel studies that
evaluated respiratory symptoms and
medication use related to O3 exposures
focused on children. These studies
suggest that O3 exposure is associated
with increased respiratory symptoms
and medication use in children with
asthma. Other reported effects include
respiratory symptoms, lung function
decrements, and emergency department
visits, as discussed in the 2006 Criteria
Document (section 7.6.7.1). Strong
evidence from a large multicity study
(Mortimer et al., 2002), along with
support from several single-city studies
indicate that O3 exposure is associated
with increased respiratory symptoms
and medication use in children with
asthma. With regard to ambient O3
levels and increased hospital
admissions and emergency department
visits for asthma and other respiratory
causes, strong and consistent evidence
establishes a correlation between O3
exposure and increased exacerbations of
preexisting respiratory disease for 1hour maximum O3 concentrations <0.12
ppm. As discussed above and in the
2006 Criteria Document, section 7.3,
several hospital admission and
emergency department visit studies in
the U.S., Canada, and Europe have
reported positive associations between
increase in O3 and increased risk of
emergency department visits and
hospital admissions for asthma other
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respiratory diseases, especially during
the warm season.
In summary, based on a substantial
new body of evidence from animal,
controlled human exposure and
epidemiological studies the 2006
Criteria Document (section x.x)
concludes that people with asthma and
other preexisting pulmonary diseases
are among those at increased risk from
O3 exposure. Evidence from controlled
human exposure studies indicates that
asthmatics may exhibit larger lung
function decrements and can have larger
inflammatory responses in response to
O3 exposure than healthy controls.
Asthmatics present a different response
profile for cellular, molecular, and
biochemical parameters that are altered
in response to acute O3 exposure.
Asthmatics, and people with allergic
rhinitis, are more likely to mount an
allergic-type response upon exposure to
O3, as manifested by increases in white
blood cells associated with allergy and
related molecules, which increase
inflammation in the airways. The
increased inflammatory and allergic
responses also may be associated with
the larger late-phase responses that
asthmatics can experience, which can
include increased bronchoconstrictor
responses to irritant substances or
allergens and additional inflammation.
Epidemiological studies have reported
fairly robust associations between
ambient O3 concentrations and
measures of lung function and daily
respiratory symptoms (e.g., chest
tightness, wheeze, shortness of breath)
in children with moderate to severe
asthma and between O3 and increased
asthma medication use. These more
serious responses in asthmatics and
others with lung disease provide
biological plausibility for the respiratory
morbidity effects observed in
epidemiological studies, such as
emergency department visits and
hospital admissions. The body of
evidence from controlled human
exposure and epidemiological studies,
which includes asthmatic as well as
non-asthmatic subjects, indicates that
controlled human exposure studies of
lung function decrements and
respiratory symptoms that evaluate only
healthy, non-asthmatic subjects likely
underestimate the effects of O3 exposure
on asthmatics and other susceptible
populations.
Newly available reports from
controlled human exposure studies (see
chapter 6 in the 2006 Criteria
Document) utilized subjects with
preexisting cardiopulmonary diseases
such as COPD, asthma, allergic rhinitis,
and hypertension. The data generated
from these studies that evaluated
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changes in spirometry did not find clear
differences between filtered air and O3
exposure in COPD subjects. However,
the new data on airway responsiveness,
inflammation, and various molecular
markers of inflammation and
bronchoconstriction indicate that
people with atopic asthma and allergic
rhinitis comprise susceptible groups for
O3-induced adverse health effects.
Although controlled human exposure
studies have not found evidence of
larger spirometric responses to O3 in
people with COPD relative to healthy
subjects, this may be due to the fact that
most people with COPD are older adults
who would not be expected to be as
responsive based on their age. However,
in section 8.7.1, the 2006 Criteria
Document notes that new
epidemiological evidence indicates that
people with COPD may be more likely
to experience other effects, including
emergency room visits, hospital
admissions, or premature mortality. For
example, results from an analysis of five
European cities indicated strong and
consistent O3 effects on unscheduled
respiratory hospital admissions,
including COPD (Anderson et al., 1997).
Also, an analysis of a 9-year data set for
the whole population of the Netherlands
provided risk estimates for more
specific causes of mortality, including
COPD (Hoek et al., 2000, 2001;
reanalysis Hoek, 2003); a positive, but
nonsignificant, excess risk of COPDrelated mortality was found to be
associated with short-term O3
concentrations. Moreover, as indicated
by Gong et al. (1998), the effects of O3
exposure on alveolar-arterial oxygen
gradients may be more pronounced in
patients with preexisting obstructive
lung diseases. Relative to healthy
elderly subjects, COPD patients have
reduced gas exchange and low SaO2.
Any inflammatory or edematous
responses due to O3 delivered to the
well-ventilated regions of the lung in
COPD subjects could further inhibit gas
exchange and reduce oxygen saturation.
In addition, O3-induced
vasoconstriction could also acutely
induce pulmonary hypertension.
Inducing pulmonary vasoconstriction
and hypertension in these patients
would perhaps worsen their condition,
especially if their right ventricular
function was already compromised
(EPA, 2006a, section 6.10). These
controlled human exposure and
epidemiological studies indicate that
people with pre-existing lung diseases
other than asthma are also at greater risk
from O3 exposure than people without
lung disease.
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iii. Children and Older Adults
Supporting evidence exists for
heterogeneity in the effects of O3 by age.
As discussed in section 6.5.1 of the 2006
Criteria Document, children,
adolescents, and young adults (<18 yrs
of age) appear, on average, to have
nearly equivalent spirometric responses
to O3, but have greater responses than
middle-aged and older adults when
exposed to comparable O3 doses.
Symptomatic responses to O3 exposure,
however, do not appear to occur in
healthy children, but are observed in
asthmatic children, particularly those
who use maintenance medications. For
adults (>17 yrs of age) symptoms
gradually decrease with increasing age.
In contrast to young adults, the
diminished symptomatic responses in
children and the diminished
symptomatic and spirometric responses
in older adults increases the likelihood
that these groups continue outdoor
activities leading to greater O3 exposure
and dose.
As described in the section 7.6.7.2 of
the 2006 Criteria Document, many
epidemiological field studies focused on
the effect of O3 on the respiratory health
of school children. In general, children
experienced decrements in lung
function parameters, including PEF,
FEV1, and FVC. Increases in respiratory
symptoms and asthma medication use
were also observed in asthmatic
children. In one German study, children
with and without asthma were found to
be particularly susceptible to O3 effects
on lung function. Approximately 20
percent of the children, both with and
without asthma, experienced a greater
than 10 percent change in FEV1,
compared to only 5 percent of the
¨
elderly population and athletes (Hoppe
et al., 2003).
The American Academy of Pediatrics
(2004) notes that children and infants
are among the population groups most
susceptible to many air pollutants,
including O3. This is in part because
their lungs are still developing. For
example, eighty percent of alveoli are
formed after birth, and changes in lung
development continue through
adolescence (Dietert et al., 2000).
Children are also likely to spend more
time outdoors than adults, which results
in increased exposure to air pollutants
(Wiley et al., 1991a,b). Moreover,
children have high minute ventilation
rates and high levels of physical activity
which also increases their dose
(Plunkett et al., 1992).
Several mortality studies have
investigated age-related differences in
O3 effects (EPA, 2006a, section 7.6.7.2).
Older adults are also often classified as
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being particularly susceptible to air
pollution. The 2006 Criteria Document
(p. 8–60) concludes that the basis for
increased O3 sensitivity among the
elderly is not known, but one
hypothesis is that it may be related to
changes in the respiratory tract lining
fluid antioxidant defense network (Kelly
et al., 2003). Older adults have lower
baseline lung function than younger
people, and are also more likely to have
preexisting lung and heart disease.
Increased susceptibility of older adults
to O3 health effects is most clearly
indicated in the newer mortality
studies. Among the studies that
observed positive associations between
O3 and mortality, a comparison of all
age or younger age (≤ 65 years of age) O3mortality effect estimates to that of the
elderly population (> 65 years) indicates
that, in general, the elderly population
is more susceptible to O3 mortality
effects. The meta-analysis by Bell et al.
(2005) found a larger mortality effect
estimate for the elderly than for all ages.
In the large U.S. 95 communities study
(Bell et al., 2004), mortality effect
estimates were slightly higher for those
aged 65 to 74 years, compared to
individuals less than 65 years and 75
years or greater. The absolute effect of
O3 on premature mortality may be
substantially greater in the elderly
population because of higher rates of
preexisting respiratory and cardiac
diseases. The 2006 Criteria Document
(p. 7–177) concludes that the elderly
population (>65 years of age) appear to
be at greater risk of O3-related mortality
and hospitalizations compared to all
ages or younger populations.
The 2006 Criteria Document notes
that, collectively, there is supporting
evidence of age-related differences in
susceptibility to O3 lung function
effects. The elderly population (> 65
years of age) appear to be at increased
risk of O3-related mortality and
hospitalizations, and children (< 18
years of age) experience other
potentially adverse respiratory health
outcomes with increased O3 exposure
(EPA, 2006a, section 7.6.7.2).
iv. People With Increased
Responsiveness to Ozone
New animal toxicology studies using
various strains of mice and rats have
identified O3-sensitive and resistant
strains and illustrated the importance of
genetic background in determining O3
susceptibility (EPA, 2006a, section
8.7.4). Controlled human exposure
studies have also indicated a high
degree of variability in some of the
pulmonary physiological parameters.
The variable effects in individuals have
been found to be reproducible, in other
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words, a person who has a large lung
function response after exposure to O3
will likely have about the same response
if exposed again to the same dose of O3.
In controlled human exposure studies,
group mean responses are not
representative of this segment of the
population that has much larger than
average responses to O3. Recent studies
of asthmatics by David et al. (2003) and
Romieu et al. (2004) reported a role for
genetic polymorphism in observed
differences in antioxidant enzymes and
genes involved in inflammation to
modulate lung function and
inflammatory responses to O3
exposure.25
Biochemical and molecular
parameters extensively evaluated in
these experiments were used to identify
specific loci on chromosomes and, in
some cases, to relate the differential
expression of specific genes to
biochemical and physiological
differences observed among these
species. Utilizing O3-sensitive and O3resistant species, it has been possible to
identify the involvement of increased
airway reactivity and inflammation
processes in O3 susceptibility. However,
most of these studies were carried out
using relatively high doses of O3,
making the relevance of these studies
questionable in human health effects
assessment. The genes and genetic loci
identified in these studies may serve as
useful biomarkers in the future.
cardiovascular effects evidence from
some field studies is rather limited but
supportive of a potential effect of shortterm O3 exposure and HRV, cardiac
arrhythmia, and heart attack incidence.
In the 2006 Criteria Document’s
evaluation of studies of hospital
admissions for cardiovascular disease
(EPA 2006a, section 7.3.4), it is
concluded that evidence from this
growing group of studies is generally
inconclusive regarding an association
with O3 in studies conducted during the
warm season (EPA 2006a, p. 7–83). This
body of evidence suggests that people
with heart disease may be at increased
risk from short-term exposures to O3´
however, more evidence is needed to
conclude that people with heart disease
are a susceptible population.
Other groups that might have
enhanced sensitivity to O3, but for
which there is currently very little
evidence, include groups based on race,
gender and SES, and those with
nutritional deficiencies, which presents
factors which modify responsiveness to
O3.
v. Other Population Groups
There is limited, new evidence
supporting associations between shortterm O3 exposures and a range of effects
on the cardiovascular system. Some but
not all, epidemiological studies have
reported associations between shortterm O3 exposures and the incidence of
heart attacks and more subtle
cardiovascular health endpoints, such
as changes in HRV and cardiac
arrhythmia. Others have reported
associations with hospitalization or
emergency department visits for
cardiovascular diseases, although the
results across the studies are not
consistent. Studies also report
associations between short-term O3
exposure and mortality from
cardiovascular or cardiopulmonary
causes. The 2006 Criteria Document (p.
7–65) concludes that current
c. Adversity of Effects
In the 2008 rulemaking, in making
judgments as to when various O3-related
effects become regarded as adverse to
the health of individuals, EPA looked to
guidelines published by the American
Thoracic Society (ATS) and the advice
of CASAC. While recognizing that
perceptions of ‘‘medical significance’’
and ‘‘normal activity’’ may differ among
physicians, lung physiologists and
experimental subjects, the ATS (1985) 26
defined adverse respiratory health
effects as ‘‘medically significant
physiologic changes generally
evidenced by one or more of the
following: (1) Interference with the
normal activity of the affected person or
persons, (2) episodic respiratory illness,
(3) incapacitating illness, (4) permanent
respiratory injury, and/or (5) progressive
respiratory dysfunction.’’ During the
1997 review, it was concluded that there
was evidence of causal associations
from controlled human exposure studies
for effects in the first of these five ATSdefined categories, evidence of
statistically significant associations from
epidemiological studies for effects in the
second and third categories, and
evidence from animal toxicology
25 Similar to animal toxicology studies referred
above, a polymorphism in a specific
proinflammatory cytokine gene has been implicated
in O3-induced lung function changes in healthy,
mild asthmatics and individuals with rhinitis.
These observations suggest a potential role for these
markers in the innate susceptibility to O3, however,
the validity of these markers and their relevance in
the context of prediction to population studies
requires additional research.
26 In 2000, the American Thoracic Society (ATS)
published an official statement on ‘‘What
Constitutes an Adverse Health Effect of Air
Pollution?’’ (ATS, 2000), which updated its earlier
guidance (ATS, 1985). Overall, the new guidance
does not fundamentally change the approach
previously taken to define adversity, nor does it
suggest a need at this time to change the structure
or content of the tables describing gradation of
severity and adversity of effects described below.
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studies, which could be extrapolated to
humans only with a significant degree
of uncertainty, for the last two
categories.
For ethical reasons, clear causal
evidence from controlled human
exposure studies still covers only effects
in the first category. However, for this
review there are results from
epidemiological studies, upon which to
base judgments about adversity, for
effects in all of the categories.
Statistically significant and robust
associations have been reported in
epidemiology studies falling into the
second and third categories. These more
serious effects include respiratory
events (e.g., triggering asthma attacks)
that may require medication (e.g.,
asthma), but not necessarily
hospitalization, as well as respiratory
hospital admissions and emergency
department visits for respiratory causes.
Less conclusive, but still positive
associations have been reported for
school absences and cardiovascular
hospital admissions. Human health
effects for which associations have been
suggested through evidence from
epidemiological and animal toxicology
studies, but have not been conclusively
demonstrated still fall primarily into the
last two categories. In the 1997 review
of the O3 standard, evidence for these
more serious effects came from studies
of effects in laboratory animals.
Evidence from animal studies evaluated
in the 2006 Criteria Document strongly
suggests that O3 is capable of damaging
the distal airways and proximal alveoli,
resulting in lung tissue remodeling
leading to apparently irreversible
changes. Recent advancements of
dosimetry modeling also provide a
better basis for extrapolation from
animals to humans. Information from
epidemiological studies provides
supporting, but limited evidence of
irreversible respiratory effects in
humans than was available in the prior
review. Moreover, the findings from
single-city and multicity time-series
epidemiology studies and meta-analyses
of these epidemiological studies are
highly suggestive of an association
between short-term O3 exposure and
mortality particularly in the warm
season.
While O3 has been associated with
effects that are clearly adverse,
application of these guidelines, in
particular to the least serious category of
effects related to ambient O3 exposures,
involves judgments about which
medical experts on the CASAC panel
and public commenters have expressed
diverse views in the past. To help frame
such judgments, EPA staff have defined
specific ranges of functional responses
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(e.g., decrements in FEV1 and airway
responsiveness) and symptomatic
responses (e.g., cough, chest pain,
wheeze), together with judgments as to
the potential impact on individuals
experiencing varying degrees of severity
of these responses, that have been used
in previous NAAQS reviews. These
ranges of pulmonary responses and their
associated potential impacts are
summarized in Tables 3–2 and 3–3 of
the 2007 Staff Paper.
For active healthy people, moderate
levels of functional responses (e.g., FEV1
decrements of ≥ 10 percent but < 20
percent, lasting up to 24 hours) and/or
moderate symptomatic responses (e.g.,
frequent spontaneous cough, marked
discomfort on exercise or deep breath,
lasting up to 24 hours) would likely
interfere with normal activity for
relatively few responsive individuals.
On the other hand, EPA staff
determined that large functional
responses (e.g., FEV1 decrements ≥ 20
percent, lasting longer than 24 hours)
and/or severe symptomatic responses
(e.g., persistent uncontrollable cough,
severe discomfort on exercise or deep
breath, lasting longer than 24 hours)
would likely interfere with normal
activities for many responsive
individuals. EPA staff determined that
these would be considered adverse
under ATS guidelines. In the context of
standard setting, CASAC indicated that
a focus on the mid to upper end of the
range of moderate levels of functional
responses (e.g., FEV1 decrements ≥ 15
percent but < 20 percent) is appropriate
for estimating potentially adverse lung
function decrements in active healthy
people. However, for people with lung
disease, even moderate functional (e.g.,
FEV1 decrements ≥ 10 percent but < 20
percent, lasting up to 24 hours) or
symptomatic responses (e.g., frequent
spontaneous cough, marked discomfort
on exercise or with deep breath, wheeze
accompanied by shortness of breath,
lasting up to 24 hours) would likely
interfere with normal activity for many
individuals, and would likely result in
more frequent use of medication. For
people with lung disease, large
functional responses (e.g., FEV1
decrements ≥ 20 percent, lasting longer
than 24 hours) and/or severe
symptomatic responses (e.g., persistent
uncontrollable cough, severe discomfort
on exercise or deep breath, persistent
wheeze accompanied by shortness of
breath, lasting longer than 24 hours)
would likely interfere with normal
activity for most individuals and would
increase the likelihood that these
individuals would seek medical
treatment. In the context of standard
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setting, the CASAC indicated
(Henderson, 2006c) that a focus on the
lower end of the range of moderate
levels of functional responses (e.g., FEV1
decrements ≥ 10 percent) is most
appropriate for estimating potentially
adverse lung function decrements in
people with lung disease.
In judging the extent to which these
impacts represent effects that should be
regarded as adverse to the health status
of individuals, an additional factor that
has been considered in previous
NAAQS reviews is whether such effects
are experienced repeatedly during the
course of a year or only on a single
occasion. While some experts would
judge single occurrences of moderate
responses to be a ‘‘nuisance,’’ especially
for healthy individuals, a more general
consensus view of the adversity of such
moderate responses emerges as the
frequency of occurrence increases.
The new guidance builds upon and
expands the 1985 definition of adversity
in several ways. There is an increased
focus on quality of life measures as
indicators of adversity. There is also a
more specific consideration of
population risk. Exposure to air
pollution that increases the risk of an
adverse effect to the entire population is
adverse, even though it may not
increase the risk of any individual to an
unacceptable level. For example, a
population of asthmatics could have a
distribution of lung function such that
no individual has a level associated
with significant impairment. Exposure
to air pollution could shift the
distribution to lower levels that still do
not bring any individual to a level that
is associated with clinically relevant
effects. However, this would be
considered to be adverse because
individuals within the population
would have diminished reserve
function, and therefore would be at
increased risk if affected by another
agent.
Of the various effects of O3 exposure
that have been studied, many would
meet the ATS definition of adversity.
Such effects include, for example, any
detectible level of permanent lung
function loss attributable to air
pollution, including both reductions in
lung growth or acceleration of the agerelated decline of lung function;
exacerbations of disease in individuals
with chronic cardiopulmonary diseases;
reversible loss of lung function in
combination with the presence of
symptoms; as well as more serious
effects such as those requiring medical
care including hospitalization and,
obviously, mortality.
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d. Size of At-Risk Populations
Although O3-related health risk
estimates may appear to be small, their
significance from an overall public
health perspective is determined by the
large numbers of individuals in the
population groups potentially at risk for
O3-related health effects discussed
above. For example, a population of
concern includes people with
respiratory disease, which includes
approximately 11 percent of U.S. adults
and 13 percent of children who have
been diagnosed with asthma and 6
percent of adults with chronic
obstructive pulmonary disease (chronic
bronchitis and/or emphysema) in 2002
and 2003 (Table 8–4 in the 2006 Criteria
Document, section 8.7.5.2). More
broadly, individuals with preexisting
cardiopulmonary disease may constitute
an additional population of concern,
with potentially tens of millions of
people included in each disease
category. In addition, populations based
on age group also comprise substantial
segments of the population that may be
potentially at risk for O3-related health
impacts. Based on U.S. census data from
2003, about 26 percent of the U.S.
population are under 18 years of age
and 12 percent are 65 years of age or
older. Hence, large proportions of the
U.S. population are included in life
stages that are most likely to have
increased susceptibility to the health
effects of O3 and/or those with the
highest ambient O3 exposures.
The 2006 Criteria Document (section
8.7.5.2) notes that the health statistics
data illustrate what is known as the
‘‘pyramid’’ of effects. At the top of the
pyramid, there are approximately 2.5
millions deaths from all causes per year
in the U.S. population, with about
100,000 deaths from chronic lower
respiratory diseases. For respiratory
health diseases, there are nearly 4
million hospital discharges per year, 14
million emergency department visits,
112 million ambulatory care visits, and
an estimated 700 million restricted
activity days per year due to respiratory
conditions from all causes per year.
Applying small risk estimates for the
O3-related contribution to such health
effects with relatively large baseline
levels of health outcomes can result in
quite large public health impacts related
to ambient O3 exposure. Thus, even a
small percentage reduction in O3 health
impacts on cardiopulmonary diseases
would reflect a large number of avoided
cases. In considering this information
together with the concentrationresponse relationships that have been
observed between exposure to O3 and
various health endpoints, the 2006
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Criteria Document (section 8.7.5.2)
concludes that exposure to ambient O3
likely has a significant impact on public
health in the U.S.
B. Human Exposure and Health Risk
Assessments
To put judgments about health effects
that are adverse for individuals into a
broader public health context, EPA has
developed and applied models to
estimate human exposures and health
risks. This broader context includes
consideration of the size of particular
population groups at risk for various
effects, the likelihood that exposures of
concern will occur for individuals in
such groups under varying air quality
scenarios, estimates of the number of
people likely to experience O3-related
effects, the variability in estimated
exposures and risks, and the kind and
degree of uncertainties inherent in
assessing the exposures and risks
involved.
As discussed below there are a
number of important uncertainties that
affect the exposure and health risk
estimates. It is also important to note
that there have been significant
improvements in both the exposure and
health risk model. CASAC expressed the
view that the exposure analysis
represents a state-of-the-art modeling
approach and that the health risk
assessment was ‘‘well done, balanced
and reasonably communicated
(Henderson, 2006c). While recognizing
and considering the kind and degree of
uncertainties in both the exposure and
health risk estimates, the 2007 Staff
Paper (pp. 6–20 to 6–21) judged that the
quality of the estimates is such that they
are suitable to be used as an input to the
Administrator’s decisions on the O3
primary standard.
In modeling exposures and health
risks associated with just meeting the
current and alternative O3 standards,
EPA has simulated air quality to
represent conditions just meeting these
standards based on O3 air quality
patterns in several recent years and on
how the shape of the O3 air quality
distribution have changed over time
based on historical trends in monitored
O3 air quality data. As described in the
2007 Staff Paper (EPA, 2007b, section
4.5.8) and discussed below, recent O3
air quality distributions have been
statistically adjusted to simulate just
meeting the current and selected
alternative standards. These simulations
do not reflect any consideration of
specific control programs or strategies
designed to achieve the reductions in
emissions required to meet the specified
standards. Further, these simulations do
not represent predictions of when,
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whether, or how areas might meet the
specified standards.27
As noted in section I.C above, around
the time of the release of the final 2007
Staff Paper in January 2007, EPA
discovered a small error in the exposure
model that when corrected resulted in
slight increases in the simulated
exposures. Since the exposure estimates
are an input to the lung function portion
of the health risk assessment, this
correction also resulted in slight
increases in the lung function risk
estimates as well. The exposure and risk
estimates discussed in this notice reflect
the corrected estimates, and thus are
slightly different than the exposure and
risk estimates cited in the January 31,
2007 Staff Paper.28
1. Exposure Analyses
a. Overview
As part of the 2008 rulemaking, the
EPA conducted exposure analyses using
a simulation model to estimate O3
exposures for the general population,
school age children (ages 5–18), and
school age children with asthma living
in 12 U.S. metropolitan areas
representing different regions of the
country where the then current 8-hour
O3 standard is not met. The emphasis on
children reflects the finding of the 1997
O3 NAAQS review that children are an
important at-risk group. The 12 modeled
areas combined represent a significant
fraction of the U.S. urban population, 89
million people, including 18 million
school age children of whom
approximately 2.6 million have asthma.
The selection of urban areas to include
in the exposure analysis took into
consideration the location of O3
epidemiological studies, the availability
of ambient O3 data, and the desire to
represent a range of geographic areas,
population demographics, and O3
climatology. These selection criteria are
discussed further in chapter 5 of the
2007 Staff Paper (EPA, 2007b). The
geographic extent of each modeled area
consists of the census tracts in the
combined statistical area (CSA) as
defined by OMB (OMB, 2005).29
27 Modeling that projects whether and how areas
might attain alternative standards in a future year
is presented in the Regulatory Impact Analysis
being prepared in connection with this rulemaking.
28 EPA made available corrected versions of the
final 2007 Staff Paper, and human exposure and
health risk assessment technical support documents
in July 2007 on the EPA Web site listed in the
Availability of Related Information section of this
notice.
29 The 12 CSAs modeled are: Atlanta-Sandy
Springs-Gainesville, GA–AL; Boston-WorcesterManchester, MA–NH; Chicago-Naperville-Michigan
City, IL–IN–WI; Cleveland-Akron-Elyria, OH;
Detroit-Warren-Flint, MI; Houston-BaytownHuntsville, TX; Los Angeles-Long Beach-Riverside,
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Exposure estimates were developed
using a probabilistic exposure model
that is designed to explicitly model the
numerous sources of variability that
affect people’s exposures. As discussed
below, the model estimates population
exposures by simulating human activity
patterns, air conditioning prevalence,
air exchange rates, and other factors.
The modeled exposure estimates were
developed for three recent years of
ambient O3 concentrations (2002, 2003,
and 2004), as well as for O3
concentrations adjusted to simulate
conditions associated with just meeting
the then current NAAQS and various
alternative 8-hour standards based on
the three year period 2002–2004.30 This
exposure assessment is more fully
described and presented in the 2007
Staff Paper and in a technical support
document, Ozone Population Exposure
Analysis for Selected Urban Areas (EPA,
2007c; hereafter Exposure Analysis
TSD). The scope and methodology for
this exposure assessment were
developed over the last few years with
considerable input from the CASAC
Ozone Panel and the public.31
The goals of the O3 exposure
assessment were: (1) To provide
estimates of the size of at-risk
populations exposed to various levels
associated with recent O3
concentrations, and with just meeting
the current O3 NAAQS and alternative
O3 standards, in specific urban areas; (2)
to provide distributions of exposure
estimates over the entire range of
ambient O3 concentrations as an
important input to the lung function
risk assessment summarized below in
section II.B.2; (3) to develop a better
understanding of the influence of
various inputs and assumptions on the
exposure estimates; and (4) to gain
insight into the distribution of
exposures and patterns of exposure
CA; New York-Newark-Bridgeport, NY–NJ–CT–PA;
Philadelphia-Camden-Vineland, PA–NJ–DE–MD;
Sacramento—Arden-Arcade—Truckee, CA–NV; St.
Louis-St. Charles-Farmington, MO–IL; WashingtonBaltimore-N. Virginia, DC–MD–VA–WV.
30 All 12 of the CSAs modeled did not meet the
0.084 ppm O3 NAAQS for the three year period
examined.
31 The general approach used in the human
exposure assessment was described in the draft
Health Assessment Plan (EPA, 2005d) that was
released to the CASAC and general public in April
2005 and was the subject of a consultation with the
CASAC O3 Panel on May 5, 2005. In October 2005,
OAQPS released the first draft of the Staff Paper
containing a chapter discussing the exposure
analyses and first draft of the Exposure Analyses
TSD for CASAC consultation and public review on
December 8, 2005. In July 2006, OAQPS released
the second draft of the Staff Paper and second draft
of the Exposure Analyses TSD for CASAC review
and public comment which was held by the CASAC
O3 Panel on August 24–25, 2006.
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reductions associated with meeting
alternative O3 standards.
The EPA recognizes that there are
many sources of variability and
uncertainty inherent in the inputs to
this assessment and that there is
uncertainty in the resulting O3 exposure
estimates. With respect to variability,
the exposure modeling approach
accounts for variability in ambient O3
levels, demographic characteristics,
physiological attributes, activity
patterns, and factors affecting
microenvironmental (e.g., indoor)
concentrations. In EPA’s judgment, the
most important uncertainties affecting
the exposure estimates are related to the
modeling of human activity patterns
over an O3 season, the modeling of
variations in ambient concentrations
near roadways, and the modeling of air
exchange rates that affect the amount of
O3 that penetrates indoors. Another
important uncertainty that affects the
estimation of how many exposures are
associated with moderate or greater
exertion is the characterization of
energy expenditure for children engaged
in various activities. As discussed in
more detail in the 2007 Staff Paper
(EPA, 2007b, section 4.3.4.7), the
uncertainty in energy expenditure
values carries over to the uncertainty of
the modeled breathing rates, which are
important since they are used to classify
exposures occurring at moderate or
greater exertion which are the relevant
exposures since O3-related effects
observed in controlled human exposure
studies only are observed when
individuals are engaged in some form of
exercise. The uncertainties in the
exposure model inputs and the
estimated exposures have been assessed
using quantitative uncertainty and
sensitivity analyses. Details are
discussed in the 2007 Staff Paper
(section 4.6) and in a technical
memorandum describing the exposure
modeling uncertainty analysis
(Langstaff, 2007).
b. Scope and Key Components
Population exposures to O3 are
primarily driven by ambient outdoor
concentrations, which vary by time of
day, location, and peoples’ activities.
Outdoor O3 concentration estimates
used in the exposure assessment are
provided by measurements and
statistical adjustments to the measured
concentrations. The current exposure
analysis allows comparisons of
population exposures to O3 within each
urban area, associated with current O3
levels and with O3 levels just meeting
several potential alternative air quality
standards or scenarios. Human
exposure, regardless of the pollutant,
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2975
depends on where individuals are
located and what they are doing.
Inhalation exposure models are useful
in realistically estimating personal
exposures to O3 based on activityspecific breathing rates, particularly
when recognizing that large scale
population exposure measurement
studies have not been conducted that
are representative of the overall
population or at risk subpopulations.
The model EPA used to simulate O3
population exposure is the Air
Pollutants Exposure Model (APEX), the
human inhalation exposure model
within the Total Risk Integrated
Methodology (TRIM) framework (EPA,
2006c,d). APEX is conceptually based
on the probabilistic NAAQS exposure
model for O3 (pNEM/O3) used in the last
O3 NAAQS review. Since that time the
model has been restructured, improved,
and expanded to reflect conceptual
advances in the science of exposure
modeling and newer input data
available for the model. Key
improvements to algorithms include
replacement of the cohort approach
with a probabilistic sampling approach
focused on individuals, accounting for
fatigue and oxygen debt after exercise in
the calculation of breathing rates, and a
new approach for construction of
longitudinal activity patterns for
simulated persons. Major improvements
to data input to the model include
updated air exchange rates, more recent
census and commuting data, and a
greatly expanded daily time-activities
database.
APEX is a probabilistic model
designed to explicitly model the
numerous sources of variability that
affect people’s exposures. APEX
simulates the movement of individuals
through time and space and estimates
their exposures to O3 in indoor, outdoor,
and in-vehicle microenvironments. The
exposure model takes into account the
most significant factors contributing to
total human O3 exposure, including the
temporal and spatial distribution of
people and O3 concentrations
throughout an urban area, the variation
of O3 levels within each
microenvironment, and the effects of
exertion on breathing rate in exposed
individuals. A more detailed
description of APEX and its application
is presented in chapter 4 of the 2007
Staff Paper and associated technical
documents (EPA, 2006b,c,d).
Several methods have been used to
evaluate the APEX model and to
characterize the uncertainty of the
model estimates. These include
conducting model evaluation,
sensitivity analyses, and a detailed
uncertainty analysis for one urban area.
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These are discussed fully in the 2007
Staff Paper (section 4.6) and in Langstaff
(2007). The uncertainty of model
structure was judged to be of lesser
importance than the uncertainties of the
model inputs and parameters. Model
structure refers to the algorithms in
APEX designed to simulate the
processes that result in people’s
exposures, for example, the way that
APEX models exposures to individuals
when they are near roads. The
uncertainties in the model input data
(e.g., measurement error, ambient
concentrations, air exchange rates, and
activity pattern data) have been assessed
individually, and their impact on the
uncertainty in the modeled exposure
estimates was assessed in a unified
quantitative analysis with results
expressed in the form of estimated
confidence ranges around the estimated
measures of exposure. This uncertainty
analysis was conducted for one urban
area (Boston) using the observed 2002
O3 concentrations and 2002
concentrations adjusted to simulate just
meeting the current standard, with the
expectation that the results would be
similar for other cities and years. One
significant source of uncertainty, due to
limitations in the database used to
model peoples’ daily activities, was not
included in the unified analysis, and
was assessed through separate
sensitivity analyses. This analysis
indicates that the uncertainty of the
exposure results is relatively small. For
example, 95 percent uncertainty
intervals were calculated for the APEX
estimates of the percent of children or
asthmatic children with exposures
above 0.060, 0.070, or 0.080 ppm under
moderate exertion, for two air quality
scenarios (current 2002 and 2002
adjusted to simulate just meeting the
current standard) in Boston (Langstaff,
2007, Tables 26 and 27). The 95 percent
uncertainty intervals for this set of 12
exposure estimates indicate the
possibility of underpredictions of the
exposure estimates ranging from 3 to 25
percent of the modeled estimates, and
overpredictions ranging from 4 to 11
percent of the estimates. For example,
APEX estimates the percent of asthmatic
children with exposures above 0.070
ppm under moderate exertion to be 24
percent, for Boston 2002 O3
concentrations adjusted to simulate just
meeting the current standard. The 95
percent uncertainty interval for this
estimate is 23¥30 percent, or ¥4 to +25
percent of the estimate. These
uncertainty intervals do not include the
uncertainty engendered by limitations
of the activity database, which is in the
range of one to ten percent.
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The exposure periods modeled here
are the O3 seasons in 2002, 2003, and
2004. The O3 season in each area
includes the period of the year where
elevated O3 levels tend to be observed
and for which routine hourly O3
monitoring data are available. Typically
this period spans from March or April
through September or October, or in
some areas, spanning the entire year.
Three years were modeled to reflect the
substantial year-to-year variability that
occurs in O3 levels and related
meteorological conditions, and because
the standard is specified in terms of a
three-year period. The year-to-year
variability observed in O3 levels is due
to a combination of different weather
patterns and the variation in emissions
of O3 precursors. Nationally, 2002 was
a relatively high year with respect to the
4th highest daily maximum 8-hour O3
levels observed in urban areas across the
U.S. (EPA, 2007b, Figure 2–16), with the
mean of the distribution of O3 levels for
the urban monitors being in the upper
third among the years 1990 through
2006. In contrast, on a national basis,
2004 is the lowest year on record
through 2006 for this same air quality
statistic, and 8-hour daily maximum O3
levels observed in most, but not all of
the 12 urban areas included in the
exposure and risk analyses were
relatively low compared to other recent
years. The 4th highest daily maximum
8-hour O3 levels observed in 2003 in the
12 urban areas and nationally generally
were between those observed in 2002
and 2004.
Regulatory scenarios examined in the
2008 rulemaking include the then
current 0.08 ppm, average of the 4th
daily maximum 8-hour averages over a
three year period standard; standards
with the same form but with alternative
levels of 0.080, 0.074, 0.070, and 0.064
ppm; standards specified as the average
of the 3rd highest daily maximum 8hour averages over a three year period
with alternative levels of 0.084 and
0.074 ppm; and a standard specified as
the average of the 5th highest daily
maximum 8-hour averages over a three
year period with a level of 0.074 ppm.32
The then current standard used a
rounding convention that allows areas
to have an average of the 4th daily
maximum 8-hour averages as high as
32 The 8-hour O standard established in 1997
3
was 0.08 ppm, but the rounding convention
specified that the average of the 4th daily maximum
8-hour average concentrations over a three-year
period must be at 0.084 ppm or lower to be in
attainment of this standard. When EPA staff
selected alternative standards to analyze, it was
presumed that the same type of rounding
convention would be used, and thus alternative
standards of 0.084, 0.074, 0.064 ppm were chosen.
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0.084 ppm and still meet the standard.
All alternative standards analyzed were
intended to reflect improved precision
in the measurement of ambient
concentrations (in ppm), where the
precision would extend to three instead
of two decimal places.
The then current standard and all
alternative standards were modeled
using a quadratic rollback approach to
adjust the hourly concentrations
observed in 2002–2004 to yield a design
value 33 corresponding to the standard
being analyzed. The quadratic rollback
technique reduces higher concentrations
more than lower concentrations near
ambient background levels.34 This
procedure was considered in a
sensitivity analysis in the 1997 review
of the O3 standard and has been shown
to be more realistic than a linear,
proportional rollback method, where all
of the ambient concentrations are
reduced by the same factor.
c. Exposure Estimates and Key
Observations
The exposure assessment, which
provides estimates of the number of
people exposed to different levels of
ambient O3 while at specified exertion
levels,35 serve two purposes. First, the
entire range of modeled personal
exposures to ambient O3 is an essential
input to the portion of the health risk
assessment based on exposure-response
functions from controlled human
exposure studies, discussed in the next
section. Second, estimates of personal
exposures to ambient O3 concentrations
at and above specific benchmark levels
provide some perspective on the public
33 A design value is a statistic that describes the
air quality status of a given area relative to the level
of the NAAQS. Design values are often based on
multiple years of data, consistent with specification
of the NAAQS in Part 50 of the CFR. For the 8-hour
O3 NAAQS, the 3-year average of the annual 4thhighest daily maximum 8-hour average
concentrations, based on the monitor within (or
downwind of) an urban area yielding the highest
3-year average, is the design value.
34 The quadratic rollback approach and
evaluation of this approach are described by
Johnson (1997), Duff et al. (1998) and Rizzo (2005,
2006).
35 As discussed above in Section II.A, O health
3
responses observed in controlled human exposure
studies are associated with exposures while
engaged in moderate or greater exertion and,
therefore, these are the exposure measures of
interest. The level of exertion of individuals
engaged in particular activities is measured by an
equivalent ventilation rate (EVR), ventilation
normalized by body surface area (BSA, in m2),
which is calculated as VE/BSA, where VE is the
ventilation rate (liters/minute). Moderate and
greater exertion levels were defined as EVR > 13
liters/min-m2 (Whitfield et al., 1996) to correspond
to the exertion levels measured in most subjects
studied in the controlled human exposure studies
that reported health effects associated with 6.6 hour
O3 exposures.
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health impacts of health effects that
cannot currently be evaluated in
quantitative risk assessments that may
occur at current air quality levels, and
the extent to which such impacts might
be reduced by meeting the current and
alternative standards. This is especially
true when there are exposure levels at
which it is known or can reasonably be
inferred that specific O3-related health
effects are occurring. In this notice,
exposures at and above these
benchmark concentrations are referred
to as ‘‘exposures of concern.’’
It is important to note that although
the analysis of ‘‘exposures of concern’’
was conducted using three discrete
benchmark levels (i.e., 0.080, 0.070, and
0.060 ppm), the concept is more
appropriately viewed as a continuum
with greater confidence and less
uncertainty about the existence of
health effects at the upper end and less
confidence and greater uncertainty as
one considers increasingly lower O3
exposure levels. The EPA recognizes
that there is no sharp breakpoint within
the continuum ranging from at and
above 0.080 ppm down to 0.060 ppm. In
considering the concept of exposures of
concern, it is important to balance
concerns about the potential for health
effects and their severity with the
increasing uncertainty associated with
our understanding of the likelihood of
such effects at lower O3 levels.
Within the context of this continuum,
estimates of exposures of concern at
discrete benchmark levels provide some
perspective on the public health
impacts of O3-related health effects that
have been demonstrated in controlled
human exposure and toxicological
studies but cannot be evaluated in
quantitative risk assessments, such as
lung inflammation, increased airway
responsiveness, and changes in host
defenses. They also help in
understanding the extent to which such
impacts have the potential to be reduced
by meeting the current and alternative
standards. In the selection of specific
benchmark concentrations for this
analysis, staff first considered the
exposure level of 0.080 ppm, at which
there is a substantial amount of
controlled human exposure evidence
demonstrating a range of O3-related
health effects including lung
inflammation and airway
responsiveness in healthy individuals.
Thus, as in the 1997 review, this level
was selected as a benchmark level for
this assessment of exposures of concern.
Evidence newly available in this review
is the basis for identifying additional,
lower benchmark levels of 0.070 and
0.060 ppm for this assessment.
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More specifically, as discussed above
in section II.A.2, evidence available
from controlled human exposure and
epidemiological studies indicates that
people with asthma have larger and
more serious effects than healthy
individuals, including lung function,
respiratory symptoms, increased airway
responsiveness, and pulmonary
inflammation, which has been shown to
be a more sensitive marker than lung
function responses. Further, a
substantial new body of evidence from
epidemiological studies shows
associations with serious respiratory
morbidity and cardiopulmonary
mortality effects at O3 levels that extend
below 0.080 ppm. Additional, but very
limited new evidence from controlled
human exposure studies shows lung
function decrements and respiratory
symptoms in healthy subjects at an O3
exposure level of 0.060 ppm. The
selected benchmark level of 0.070 ppm
reflects the new information that
asthmatics have larger and more serious
effects than healthy people and
therefore controlled human exposure
studies done with healthy subjects may
underestimate effects in this group, as
well as the substantial body of
epidemiological evidence of
associations with O3 levels below 0.080
ppm. The selected benchmark level of
0.060 ppm additionally reflects the very
limited new evidence from controlled
human exposure studies that show lung
function decrements and respiratory
symptoms in some healthy subjects at
the 0.060 ppm exposure level,
recognizing that asthmatics are likely to
have more serious responses and that
lung function is not likely to be as
sensitive a marker for O3 effects as is
lung inflammation.
The estimates of exposures of concern
were reported in terms of both ‘‘people
exposed’’ (the number and percent of
people who experience a given level of
O3 concentrations, or higher, at least one
time during the O3 season in a given
year) and ‘‘occurrences of exposure’’ (the
number of times a given level of
pollution is experienced by the
population of interest, expressed in
terms of person-days of occurrences).
Estimating exposures of concern is
important because it provides some
indication of the potential public health
impacts of a range of O3-related health
outcomes, such as lung inflammation,
increased airway responsiveness, and
changes in host defenses. These
particular health effects have been
demonstrated in controlled human
exposure studies of healthy individuals
to occur at levels as low as 0.080 ppm
O3, but have not been evaluated at lower
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2977
levels in controlled human exposure
studies. The EPA did not include these
effects in the quantitative risk
assessment due to a lack of adequate
information on the exposure-response
relationships.
The 1997 O3 NAAQS review
estimated exposures associated with
1-hour heavy exertion, 1-hour moderate
exertion, and 8-hour moderate exertion
for children, outdoor workers, and the
general population. The EPA’s analysis
in the 1997 Staff Paper showed that
exposure estimates based on the 8-hour
moderate exertion scenario for children
yielded the largest number of children
experiencing exposures at or above
exposures of concern. Consequently,
EPA chose to focus on the 8-hour
moderate and greater exertion exposures
in all and asthmatic school age children
in the current exposure assessment.
While outdoor workers and other adults
who engage in moderate or greater
exertion for prolonged durations while
outdoors during the day in areas
experiencing elevated O3 concentrations
also are at risk for experiencing
exposures associated with O3-related
health effects, EPA did not focus on
quantitative estimates for these
populations due to the lack of
information about the number of
individuals who regularly work or
exercise outdoors. Thus, the exposure
estimates presented here and in the
2007 Staff Paper are most useful for
making relative comparisons across
alternative air quality scenarios and do
not represent the total exposures in all
children or other groups within the
general population associated with the
air quality scenarios.
Population exposures to O3 were
estimated in 12 urban areas for 2002,
2003, and 2004 air quality, and also
using O3 concentrations adjusted to just
meet the then current and several
alternative standards. The estimates of
8-hour exposures of concern at and
above benchmark levels of 0.080, 0.070,
and 0.060 ppm aggregated across all 12
areas are shown in Table 1 for air
quality scenarios just meeting the
current and four alternative 8-hour
average standards.36 Table 1 provides
estimates of the number and percent of
school age children and asthmatic
school age children exposed, with daily
8-hour maximum exposures at or above
each O3 benchmark level of exposures of
concern, while at intermittent moderate
or greater exertion and based on O3
concentrations observed in 2002 and
36 The full range of quantitative exposure
estimates associated with just meeting the 0.084
ppm and alternative O3 standards are presented in
chapter 4 and Appendix 4A of the 2007 Staff Paper.
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2004. Table 1 summarizes estimates for
2002 and 2004 because these years
reflect years that bracket relatively
higher and lower O3 levels, with year
2003 generally containing O3 levels in
between when considering the 12 urban
areas modeled. This table also reports
the percent change in the number of
persons exposed when a given
alternative standard is compared with
the then current standard.
Key observations important in
comparing exposure estimates
associated with just meeting the current
NAAQS and alternative standards under
consideration include:
(1) As shown in Table 6–1 of the 2007
Staff Paper, the patterns of exposure in
terms of percentages of the population
exceeding a given exposure level are
very similar for the general population
and for asthmatic and all school age
(5–18) children, although children are
about twice as likely to be exposed,
based on the percent of the population
exposed, at any given level.
(2) As shown in Table 1 below, the
number and percentage of asthmatic and
all school-age children aggregated across
the 12 urban areas estimated to
experience one or more exposures of
concern decline from simulations of just
meeting the then current 0.084 ppm
standard to simulations of alternative 8hour standards by varying amounts
depending on the benchmark level, the
population subgroup considered, and
the year chosen. For example, the
estimated percentage of school age
children experiencing one or more
exposures ≥ 0.070 ppm, while engaged
in moderate or greater exertion, during
an O3 season is about 18 percent of this
population when the 0.084 ppm
standard is met using the 2002
simulation; this is reduced to about 12,
4, 1, and 0.2 percent of children upon
meeting alternative standards of 0.080,
0.074, 0.070, and 0.064 ppm,
respectively (all specified in terms of
the 4th highest daily maximum 8-hour
average), using the 2002 simulation.
TABLE 1—NUMBER AND PERCENT OF ALL AND ASTHMATIC SCHOOL AGE CHILDREN IN 12 URBAN AREAS ESTIMATED TO
EXPERIENCE 8-HOUR OZONE EXPOSURES ABOVE 0.080, 0.070, AND 0.060 PPM WHILE AT MODERATE OR GREATER
EXERTION, ONE OR MORE TIMES PER SEASON, AND THE NUMBER OF OCCURRENCES ASSOCIATED WITH JUST MEETING ALTERNATIVE 8-HOUR STANDARDS BASED ON ADJUSTING 2002 AND 2004 AIR QUALITY DATA1 2
Benchmark levels
of exposures of
concern (ppm)
All children, ages 5–18
Aggregate for 12 urban areas
Number of children exposed (% of all)
[% reduction from 0.084 ppm standard]
8–Hour air
quality
standards 3
(ppm)
2002
Asthmatic children, ages 5–18
Aggregate for 12 urban areas
Number of children exposed (% of group)
[% reduction from 0.084 ppm standard]
2004
2002
2004
0.080 ....................
0.084
0.080
0.074
0.070
0.064
700,000 (4%)
290,000 (2%) [70%]
60,000 (0%) [91%]
10,000 (0%) [98%]
0 (0%) [100%]
30,000 (0%)
10,000 (0%) [67%]
0 (0%) [100%]
0 (0%) [100%]
0 (0%) [100%]
110,000 (4%)
50,000 (2%) [54%]
10,000 (0%) [91%]
0 (0%) [100%]
0 (0%) [100%]
0
0
0
0
0
(0%)
(0%)
(0%)
(0%)
(0%)
0.070 ....................
0.084
0.080
0.074
0.070
0.064
3,340,000 (18%)
2,160,000 (12%) [35%]
770,000 (4%) [77%]
270,000 (1%) [92%]
30,000 (0.2%) [99%]
260,000 (1%)
100,000 (1%) [62%]
20,000 (0%) [92%]
0 (0%) [100%]
0 (0%) [100%]
520,000 (20%)
330,000 (13%) [36%]
120,000 (5%) [77% ]
50,000 (2%) [90%]
10,000 (0.2%) [98% ]
40,000 (1%)
10,000 (0%) [75%]
0 (0%) [100%]
0 (0%) [100%]
0 (0%) [100%]
0.060 ....................
0.084
0.080
0.074
0.070
0.064
7,970,000 (44%)
6,730,000 (37%) [16%]
4,550,000 (25%) [43%]
3,000,000 (16%) [62%]
950,000 (5%) [88%]
1,800,000 (10%)
1,050,000 (6%) [42%]
350,000 (2%) [80%]
110,000 (1%) [94%]
10,000 (0%) [99%]
1,210,000 (47%)
1,020,000 (40%) [16%]
700,000 (27%) [42%]
460,000 (18%) [62%]
150,000 (6%) [88%]
270,000 (11%)
150,000 (6%) [44%]
50,000 (2%) [81%]
10,000 (1%) [96%]
0 (0%) [100%]
Moderate or greater exertion is defined as having an 8-hour average equivalent ventilation rate ≥ 13 l-min/m2.
Estimates are the aggregate results based on 12 combined statistical areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington, DC). Estimates are for the ozone season which is all year in Houston,
Los Angeles and Sacramento and March or April to September or October for the remaining urban areas.
3 All standards summarized here have the same form as the 8-hour standard established in 1997 which is specified as the 3-year average of
the annual 4th highest daily maximum 8-hour average concentrations must be at or below the concentration level specified. As described in the
2007 Staff Paper (EPA, 2007b, section 4.5.8), recent O3 air quality distributions have been statistically adjusted to simulate just meeting the
0.084 ppm standard and selected alternative standards. These simulations do not represent predictions of when, whether, or how areas might
meet the specified standards.
1
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2
(3) Substantial year-to-year variability
in exposure estimates is observed over
the three-year modeling period. For
example, the estimated number of
school age children experiencing one or
more exposures ≥ 0.070 ppm during an
O3 season when a 0.084 ppm standard
is met in the 12 urban areas included in
the analysis is 3.3, 1.0, or 0.3 million for
the 2002, 2003, and 2004 simulations,
respectively.
(4) There is substantial variability
observed across the 12 urban areas in
the percent of the population subgroups
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estimated to experience exposures of
concern. For example, when 2002 O3
concentrations are simulated to just
meet a 0.084 ppm standard, the
aggregate 12 urban area estimate is 18
percent of all school age children are
estimated to experience O3 exposures
≥ 0.070 ppm (Table 1 below), while the
range of exposure estimates in the 12
urban areas considered separately for all
children range from 1 to 38 percent
(EPA, 2007b, p. 4–48, Exhibit 2). There
was also variability in exposure
estimates among the modeled areas
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when using the 2004 air quality
simulation for the same scenario;
however it was reduced and ranged
from 0 to 7 percent in the 12 urban areas
(EPA, 2007b, p. 4–60, Exhibit 8).
(5) Of particular note, as discussed
above in section II.A of this notice, high
inter-individual variability in
responsiveness means that only a subset
of individuals in these groups who are
exposed at and above a given
benchmark level would actually be
expected to experience such adverse
health effects.
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(6) In considering these observations,
it is important to take into account the
variability, uncertainties, and
limitations associated with this
assessment, including the degree of
uncertainty associated with a number of
model inputs and uncertainty in the
model itself, as discussed above.
2. Quantitative Health Risk Assessment
This section discusses the approach
used to develop quantitative health risk
estimates associated with exposures to
O3 building upon a more limited risk
assessment that was conducted during
the last review.37 As part of the 1997
review, EPA conducted a health risk
assessment that produced risk estimates
for the number and percent of children
and outdoor workers experiencing lung
function and respiratory symptoms
associated with O3 exposures for 9
urban areas.38 The risk assessment for
the 1997 review also included risk
estimates for excess respiratory-related
hospital admissions related to O3
concentrations for New York City. In the
last review, the risk estimates played a
significant role in both the staff
recommendations and in the proposed
and final decisions to revise the O3
standards. The health risk assessment
conducted for the current review builds
upon the methodology and lessons
learned from the prior review.
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a. Overview
The updated health risk assessment
conducted as part of the 2008
rulemaking includes estimates of (1)
risks of lung function decrements in all
and asthmatic school age children,
respiratory symptoms in asthmatic
children, respiratory-related hospital
admissions, and non-accidental and
cardiorespiratory-related mortality
associated with recent ambient O3
levels; (2) risk reductions and remaining
risks associated with just meeting the
then current 0.084 ppm 8-hour O3
NAAQS; and (3) risk reductions and
remaining risks associated with just
meeting various alternative 8-hour O3
NAAQS in a number of example urban
areas. This risk assessment is more fully
described and presented in chapter 5 of
the 2007 Staff Paper and in a technical
support document (TSD), Ozone Health
Risk Assessment for Selected Urban
37 The methodology, scope, and results from the
risk assessment conducted in the last review are
described in Chapter 6 of the 1996 Staff Paper (EPA,
1996) and in several technical reports (Whitfield et
al., 1996; Whitfield, 1997) and publication
(Whitfield et al., 1998).
38 The 9 urban study areas included in the
exposure and risk analyses conducted during the
last review were: Chicago, Denver, Houston, Los
Angeles, Miami, New York City, Philadelphia, St.
Louis, and Washington, DC.
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Areas (Abt Associates, 2007a, hereafter
referred to as ‘‘Risk Assessment TSD’’).
The scope and methodology for this risk
assessment were developed over the last
few years with considerable input from
the CASAC O3 Panel and the public.39
The information contained in these
documents included specific criteria for
the selection of health endpoints,
studies, and locations to include in the
assessment. In a peer review letter sent
by CASAC to the Administrator
documenting its advice in October 2006
(Henderson, 2006c), the CASAC O3
Panel concluded that the risk
assessment was ‘‘well done, balanced,
and reasonably communicated’’ and that
the selection of health endpoints for
inclusion in the quantitative risk
assessment was appropriate.
The goals of the risk assessment are:
(1) To provide estimates of the potential
magnitude of several morbidity effects
and mortality associated with current O3
levels, and with meeting the then
current 0.084 ppm standard and
alternative 8-hour O3 standards in
specific urban areas; (2) to develop a
better understanding of the influence of
various inputs and assumptions on the
risk estimates; and (3) to gain insights
into the distribution of risks and
patterns of risk reductions associated
with meeting alternative O3 standards.
The health risk assessment is intended
to be dependent on and reflect the
overall weight and nature of the health
effects evidence discussed above in
section II.A and in more detail in the
2006 Criteria Document and 2007 Staff
Paper. While not independent of the
overall evaluation of the health effects
evidence, the quantitative health risk
assessment provides additional insights
regarding the relative public health
implications associated with just
meeting a 0.084 ppm standard and
several alternative 8-hour standards.
The risk assessment covers a variety
of health effects for which there is
adequate information to develop
quantitative risk estimates. However, as
noted by CASAC (Henderson, 2007) and
in the 2007 Staff Paper, there are a
number of health endpoints (e.g.,
increased lung inflammation, increased
39 The general approach used in the health risk
assessment was described in the draft Health
Assessment Plan (EPA, 2005d) that was released to
the CASAC and general public in April 2005 and
was the subject of a consultation with the CASAC
O3 Panel on May 5, 2005. In October 2005, OAQPS
released the first draft of the Staff Paper containing
a chapter discussing the risk assessment and first
draft of the Risk Assessment TSD for CASAC
consultation and public review on December 8,
2005. In July 2006, OAQPS released the second
draft of the Staff Paper and second draft of the Risk
Assessment TSD for CASAC review and public
comment which was held by the CASAC O3 Panel
on August 24–25, 2006.
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airway responsiveness, impaired host
defenses, increased medication usage
for asthmatics, increased emergency
department visits for respiratory causes,
and increased school absences) for
which there currently is insufficient
information to develop quantitative risk
estimates, but which are important to
consider in assessing the overall public
health impacts associated with
exposures to O3. These additional health
endpoints are discussed above in
section II.A.2 and are also taken into
account in considering the level of
exposures of concern in populations
particularly at risk, discussed above in
this notice.
There are two parts to the health risk
assessment: One based on combining
information from controlled human
exposure studies with modeled
population exposure and the other
based on combining information from
community epidemiological studies
with either monitored or adjusted
ambient concentrations levels. Both
parts of the risk assessment were
implemented within a new probabilistic
version of TRIM.Risk, the component of
EPA’s Total Risk Integrated
Methodology (TRIM) model framework
that estimates human health risks.
The EPA recognizes that there are
many sources of uncertainty and
variability in the inputs to this
assessment and that there is significant
variability and uncertainty in the
resulting O3 risk estimates. As discussed
in chapters 2, 5, and 6 of the 2007 Staff
Paper, there is significant year-to-year
and city-to-city variability related to the
air quality data that affects both the
controlled human exposure studiesbased and epidemiological studiesbased parts of the risk assessment. There
are also uncertainties associated with
the air quality adjustment procedure
used to simulate just meeting various
alternative standards. In the prior
review, different statistical approaches
using alternative functional forms (i.e.,
quadratic, proportional, Weibull) were
used to reflect how O3 air quality
concentrations have historically
changed. Based on sensitivity analyses
conducted in the prior review, the
choice of alternative air quality
adjustment procedures had only a
modest impact on the risk estimates
(EPA, 2007b, p. 6–20). With respect to
uncertainties about estimated
background concentrations, as
discussed below and in the 2007 Staff
Paper (section 5.4.3), alternative
assumptions about background levels
have a variable impact depending on the
location, standard, and health endpoint
analyzed.
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With respect to the lung function part
of the health risk assessment, key
uncertainties include uncertainties in
the exposure estimates, discussed
above, and uncertainties associated with
the shape of the exposure-response
relationship, especially at levels below
0.08 ppm, 8-hour average, where only
very limited data are available down to
0.04 ppm and there is an absence of data
below 0.04 ppm (EPA, 2007b, pp. 6–20
to 6–21). Concerning the part of the risk
assessment based on effects reported in
epidemiological studies, important
uncertainties include uncertainties (1)
surrounding estimates of the O3
coefficients for concentration-response
relationships used in the assessment, (2)
involving the shape of the
concentration-response relationship and
whether or not a population threshold
or non-linear relationship exists within
the range of concentrations examined in
the studies, (3) related to the extent to
which concentration-response
relationships derived from studies in a
given location and time when O3 levels
were higher or behavior and/or housing
conditions were different provide
accurate representations of the
relationships for the same locations
with lower air quality distributions and/
or different behavior and/or housing
conditions, and (4) concerning the
possible role of co-pollutants which also
may have varied between the time of the
studies and the current assessment
period. An important additional
uncertainty for the mortality risk
estimates is the extent to which the
associations reported between O3 and
non-accidental and cardiorespiratory
mortality actually reflect causal
relationships.
As discussed below, some of these
uncertainties have been addressed
quantitatively in the form of estimated
confidence ranges around central risk
estimates; others are addressed through
separate sensitivity analyses (e.g., the
influence of alternative estimates for
policy-relevant background levels) or
are characterized qualitatively. For both
parts of the health risk assessment,
statistical uncertainty due to sampling
error has been characterized and is
expressed in terms of 95 percent
credible intervals. The EPA recognizes
that these credible intervals do not
reflect all of the uncertainties noted
above.
ppm standard and alternative 8-hour O3
NAAQS and with several individual
recent years of air quality (i.e., 2002,
2003, and 2004). The risk assessment
considers the same alternative air
quality scenarios that were examined in
the human exposure analyses described
above. Risk estimates were developed
for up to 12 urban areas selected to
illustrate the public health impacts
associated with these air quality
scenarios.40 As discussed above in
section II.B.1, the selection of urban
areas was largely determined by
identifying areas in the U.S. which
represented a range of geographic areas,
population demographics, and
climatology; with an emphasis on areas
that did not meet the then current 0.084
ppm 8-hour O3 NAAQS and which
included the largest areas with O3
nonattainment problems. The selection
criteria also included whether or not
there were acceptable epidemiological
studies available that reported
concentration-response relationships for
the health endpoints selected for
inclusion in the assessment.
The short-term exposure related
health endpoints selected for inclusion
in the quantitative risk assessment
include those for which the 2006
Criteria Document or the 2007 Staff
Paper concluded that the evidence as a
whole supports the general conclusion
that O3, acting alone and/or in
combination with other components in
the ambient air pollution mix, is either
clearly causal or is judged to be likely
causal. Some health effects met this
criterion of likely causality, but were
not included in the risk assessment for
other reasons, such as insufficient
exposure-response data or lack of
baseline incidence data.
As discussed in the section above
describing the exposure analysis, in
order to estimate the health risks
associated with just meeting various
alternative 8-hour O3 NAAQS, it is
necessary to estimate the distribution of
hourly O3 concentrations that would
occur under any given standard. Since
compliance is based on a 3-year average,
the amount of control has been applied
to each year of data (i.e., 2002 to 2004)
to estimate risks for a single O3 season
or single warm O3 season, depending on
the health effect, based on a simulation
that adjusted each of these individual
b. Scope and Key Components
The health risk assessment is based
on the information evaluated in the
2006 Criteria Document. The risk
assessment includes several categories
of health effects and estimates risks
associated with just meeting a 0.084
40 The 12 urban areas are the same urban areas
evaluated in the exposure analysis discussed in the
prior section. However, for most of the health
endpoints based on findings from epidemiological
studies, the geographic areas and populations
examined in the health risk assessment were
limited to those counties included in the original
epidemiological studies that served as the basis for
the concentration-response relationships.
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years so that the three year period
would just meet the specified standard.
Consistent with the risk assessment
approach used in the last review, the
risk estimates developed for both recent
air quality levels and just meeting the
then current 0.084 ppm standard and
selected alternative 8-hour standards
represent risks associated with O3 levels
attributable to anthropogenic sources
and activities (i.e., risk associated with
concentrations above ‘‘policy-relevant
background’’). Policy-relevant
background O3 concentrations used in
the O3 risk assessment were defined in
chapter 2 of the 2007 Staff Paper (pp.
2–48—2–55) as the O3 concentrations
that would be observed in the U.S. in
the absence of anthropogenic emissions
of precursors (e.g., VOC, NOX, and CO)
in the U.S., Canada, and Mexico. The
results of a global tropospheric O3
model (GEOS–CHEM) have been used to
estimate monthly background daily
diurnal profiles for each of the 12 urban
areas for each month of the O3 season
using meteorology for the year 2001.
Based on the results of the GEOS–CHEM
model, the Criteria Document indicates
that background O3 concentrations are
generally predicted to be in the range of
0.015 to 0.035 ppm in the afternoon,
and they are generally lower under
conditions conducive to man-made O3
episodes.41
This approach of estimating risks in
excess of background is judged to be
more relevant to policy decisions
regarding ambient air quality standards
than risk estimates that include effects
potentially attributable to
uncontrollable background O3
concentrations. Sensitivity analyses
examining the impact of alternative
estimates for background on lung
function and mortality risk estimates
have been developed and are included
in the 2007 Staff Paper and Risk
Assessment TSD and key observations
are discussed below. Further, CASAC
noted the difficulties and complexities
associated with available approaches to
estimating policy-relevant background
concentrations (Henderson, 2007).
In the first part of the risk assessment,
lung function decrement, as measured
by FEV1, is the only health response that
is based on data from controlled human
exposure studies. As discussed above,
there is clear evidence of a causal
relationship between lung function
decrements and O3 exposures for school
age children engaged in moderate
41 EPA notes that the estimated level of policyrelevant background O3 used in the prior risk
assessment was a single concentration of 0.04 ppm,
which was the midpoint of the range of levels for
policy-relevant background that was provided in
the 1996 Criteria Document.
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exertion based on numerous controlled
human exposure and summer camp
field studies conducted by various
investigators. Risk estimates have been
developed for O3-related lung function
decrements (measured as changes in
FEV1) for all school age children (ages
5 to 18) and a subset of this group,
asthmatic school age children (ages 5 to
18), whose average exertion over an
8-hour period was moderate or greater.
The exposure period and exertion level
were chosen to generally match the
exposure period and exertion level used
in the controlled human exposure
studies that were the basis for the
exposure-response relationships. A
combined data set including individual
level data from the Folinsbee et al.
(1988), Horstman et al. (1990), and
McDonnell et al. (1991) studies, used in
the previous risk assessment, and more
recent data from Adams (2002, 2003a,
2006) have been used to estimate
probabilistic exposure-response
relationships for 8-hour exposures
under different definitions of lung
function response (i.e., ≥ 10, 15, and 20
percent decrements in FEV1). As
discussed in the 2007 Staff Paper (p.
5–27), while these specific controlled
human exposure studies only included
healthy adults aged 18–35, findings
from other controlled human exposure
studies and summer camp field studies
involving school age children in at least
six different locations in the
northeastern United States, Canada, and
Southern California indicated changes
in lung function in healthy children
similar to those observed in healthy
adults exposed to O3 under controlled
chamber conditions.
Consistent with advice from CASAC
(Henderson, 2006c), EPA has considered
both linear and logistic functional forms
in estimating the probabilistic exposureresponse relationships for lung function
responses. A Bayesian Markov Chain
Monte Carlo approach, described in
more detail in the Risk Assessment TSD,
has been used that incorporates both
model uncertainty and uncertainty due
to sample size in the combined data set
that served as the basis for the
assessment. The EPA has chosen a
model reflecting a 90 percent weighting
on a logistic form and a 10 percent
weighting on a linear form as the base
case for the risk assessment. The basis
for this choice is that the logistic form
provides a very good fit to the combined
data set, but a linear model cannot be
entirely ruled out since there are only
very limited data (i.e., 30 subjects) at the
two lowest exposure levels (i.e., 0.040
and 0.060 ppm). The EPA has
conducted a sensitivity analysis which
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examines the impact on the lung
function risk estimates of two
alternative choices, an 80 percent
logistic/20 percent linear split and a 50
percent logistic/50 percent linear split.
As noted above, risk estimates have
been developed for three measures of
lung function response (i.e., ≥ 10, 15,
and 20 percent decrements in FEV1).
However, the 2007 Staff Paper and risk
estimates summarized below focus on
FEV1 decrements ≥ 15 percent for all
school age children and ≥ 10 percent for
asthmatic school age children,
consistent with the advice from CASAC
(Henderson, 2006c) that these levels of
response represent indicators of adverse
health effects in these populations. The
Risk Assessment TSD and 2007 Staff
Paper present the broader range of risk
estimates including all three measures
of lung function response.
Developing risk estimates for lung
function decrements involved
combining probabilistic exposureresponse relationships based on the
combined data set from several
controlled human exposure studies with
population exposure distributions for all
and asthmatic school age children
associated with recent air quality and
air quality simulated to just meet the
then current 0.084 ppm standard and
alternative 8-hour O3 NAAQS based on
the results from the exposure analysis
described in the previous section. The
risk estimates have been developed for
12 large urban areas for the O3 season.42
These 12 urban areas include
approximately 18.3 million school age
children, of which 2.6 million are
asthmatic school age children.43
In addition to uncertainties arising
from sample size considerations, which
are quantitatively characterized and
presented as 95 percentile credible
intervals, there are additional
uncertainties and caveats associated
with the lung function risk estimates.
These include uncertainties about the
shape of the exposure-response
relationship, particularly at levels below
0.080 ppm, and about policy-relevant
background levels, for which sensitivity
analyses have been conducted.
Additional important caveats and
uncertainties concerning the lung
function portion of the health risk
assessment include: (1) The
42 As discussed above in section II.B.1, the urban
areas were defined using the consolidated statistical
areas definition and the total population residing in
the 12 urban areas was approximately 88.5 million
people.
43 For 9 of the 12 urban areas, the O season is
3
defined as a period running from March or April
to September or October. In 3 of the urban areas
(Houston, Los Angeles, and Sacramento), the O3
season is defined as the entire year.
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2981
uncertainties and limitations associated
with the exposure estimates discussed
above and (2) the inability to account for
some factors which are known to affect
the exposure-response relationships
(e.g., assigning healthy and asthmatic
children the same responses as observed
in healthy adult subjects and not
adjusting response rates to reflect the
increase and attenuation of responses
that have been observed in studies of
lung function responses upon repeated
exposures). A more complete discussion
of assumptions and uncertainties is
contained in chapter 5 of the 2007 Staff
Paper and in the Risk Assessment TSD.
The second part of the risk assessment
is based on health effects observed in
epidemiological studies. Based on a
review of the evidence evaluated in the
2006 Criteria Document and 2007 Staff
Paper, as well as the criteria discussed
in chapter 5 of the 2007 Staff Paper, the
following categories of health endpoints
associated with short-term exposures to
ambient O3 concentrations were
included in the risk assessment:
respiratory symptoms in moderate to
severe asthmatic children, hospital
admissions for respiratory causes, and
non-accidental and cardiorespiratory
mortality. As discussed above, there is
strong evidence of a causal relationship
for the respiratory morbidity endpoints
included in the risk assessment. With
respect to nonaccidental and
cardiorespiratory mortality, the 2006
Criteria Document concludes that there
is strong evidence which is highly
suggestive of a causal relationship
between nonaccidental and
cardiorespiratory-related mortality and
O3 exposures during the warm O3
season. As discussed in the 2007 Staff
Paper (chapter 5), EPA also recognizes
that for some of the effects observed in
epidemiological studies, such as
increased respiratory-related hospital
admissions and nonaccidental and
cardiorespiratory mortality, O3 may be
serving as an indicator for reactive
oxidant species in the overall
photochemical oxidant mix and that
these other constituents may be
responsible in whole or part for the
observed effects.
Risk estimates for each health
endpoint category were only developed
for areas that were the same or close to
the location where at least one
concentration-response function for the
health endpoint had been estimated.44
44 The geographic boundaries for the urban areas
included in this portion of the risk assessment were
generally matched to the geographic boundaries
used in the epidemiological studies that served as
the basis for the concentration-response functions.
In most cases, the urban areas were defined as
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Thus, for respiratory symptoms in
moderate to severe asthmatic children
only the Boston urban area was
included and four urban areas were
included for respiratory-related hospital
admissions. Nonaccidental mortality
risk estimates were developed for 12
urban areas and 8 urban areas were
included for cardiorespiratory mortality.
The concentration-response
relationships used in the assessment are
based on findings from human
epidemiological studies that have relied
on fixed-site ambient monitors as a
surrogate for actual ambient O3
exposures. In order to estimate the
incidence of a particular health effect
associated with recent air quality in a
specific county or set of counties
attributable to ambient O3 exposures in
excess of background, as well as the
change in incidence corresponding to a
given change in O3 levels resulting from
just meeting various 8-hour O3
standards, three elements are required
for this part of the risk assessment.
These elements are: (1) Air quality
information (including recent air quality
data for O3 from ambient monitors for
the selected location, estimates of
background O3 concentrations
appropriate for that location, and a
method for adjusting the recent data to
reflect patterns of air quality estimated
to occur when the area just meets a
given O3 standard); (2) relative riskbased concentration-response functions
that provide an estimate of the
relationship between the health
endpoints of interest and ambient O3
concentration; and (3) annual or
seasonal baseline health effects
incidence rates and population data,
which are needed to provide an estimate
of the seasonal baseline incidence of
health effects in an area before any
changes in O3 air quality.
A key component in the portion of the
risk assessment based on
epidemiological studies is the set of
concentration-response functions which
provide estimates of the relationships
between each health endpoint of
interest and changes in ambient O3
concentrations. Studies often report
more than one estimated concentrationresponse function for the same location
and health endpoint. Sometimes models
include different sets of co-pollutants
and/or different lag periods between the
ambient concentrations and reported
health responses. For some health
endpoints, there are studies that
estimated multicity and single-city O3
concentration-response functions. While
the Risk Assessment TSD and chapter 5
either a single county or a few counties for this
portion of the risk assessment.
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of the 2007 Staff Paper present a more
comprehensive set of risk estimates,
EPA has focused on estimates based on
multicity studies where available. As
discussed in chapter 5 of the 2007 Staff
Paper, the advantages of relying more
heavily on concentration-response
functions based on multicity studies
include: (1) More precise effect
estimates due to larger data sets,
reducing the uncertainty around the
estimated coefficient; (2) greater
consistency in data handling and model
specification that can eliminate city-tocity variation due to study design; and
(3) less likelihood of publication bias or
exclusion of reporting of negative or
nonsignificant findings. Where studies
reported different effect estimates for
varying lag periods, consistent with the
2006 Criteria Document, single day lag
periods of 0 to 1 days were used for
associations with respiratory hospital
admissions and mortality. For mortality
associated with exposure to O3 which
may result over a several day period
after exposure, distributed lag models,
which take into account the
contribution to mortality effects over
several days, were used where available
One of the most important elements
affecting uncertainties in the
epidemiological-based portion of the
risk assessment is the concentrationresponse relationships used in the
assessment. The uncertainty resulting
from the statistical uncertainty
associated with the estimate of the O3
coefficient in the concentrationresponse function was characterized
either by confidence intervals or by
Bayesian credible intervals around the
corresponding point estimates of risk.
Confidence and credible intervals
express the range within which the true
risk is likely to fall if the only
uncertainty surrounding the O3
coefficient involved sampling error.
Other uncertainties, such as differences
in study location, time period (i.e., the
years in which the study was
conducted), and model uncertainties are
not represented by the confidence or
credible intervals presented, but were
addressed by presenting estimates for
different urban areas, by including risk
estimates based on studies using
different time periods and models,
where available, and/or are discussed
throughout section 5.3 of the 2007 Staff
Paper. Because O3 effects observed in
the epidemiological studies have been
more clearly and consistently shown for
warm season analyses, all analyses for
this portion of the risk assessment were
carried out for the same time period,
April through September.
The 2006 Criteria Document (p. 8–44)
finds that no definitive conclusion can
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be reached with regard to the existence
of population thresholds in
epidemiological studies. The EPA
recognizes, however, the possibility that
thresholds for individuals may exist for
reported associations at fairly low levels
within the range of air quality observed
in the studies, but not be detectable as
population thresholds in
epidemiological analyses. Based on the
2006 Criteria Document’s conclusions,
EPA judged and CASAC concurred, that
there is insufficient evidence to support
use of potential population threshold
levels in the quantitative risk
assessment. However, EPA recognizes
that there is increasing uncertainty
about the concentration-response
relationship at lower concentrations
which is not captured by the
characterization of the statistical
uncertainty due to sampling error.
Therefore, the risk estimates for
respiratory symptoms in moderate to
severe asthmatic children, respiratoryrelated hospital admissions, and
premature mortality associated with
exposure to O3 must be considered in
light of uncertainties about whether or
not these O3-related effects occur in
these populations at very low O3
concentrations.
With respect to variability within this
portion of the risk assessment, there is
variability among concentrationresponse functions describing the
relation between O3 and both
respiratory-related hospital admissions
and nonaccidental and cardiorespiratory
mortality across urban areas. This
variability is likely due to differences in
population (e.g., age distribution),
population activities that affect
exposure to O3 (e.g., use of air
conditioning), levels and composition of
co-pollutants, baseline incidence rates,
and/or other factors that vary across
urban areas. The risk assessment
incorporates some of the variability in
key inputs to the analysis by using
location-specific inputs (e.g., locationspecific concentration-response
functions, baseline incidence rates, and
air quality data). Although spatial
variability in these key inputs across all
U.S. locations has not been fully
characterized, variability across the
selected locations is imbedded in the
analysis by using, to the extent possible,
inputs specific to each urban area.
c. Risk Estimates and Key Observations
The 2007 Staff Paper (chapter 5) and
Risk Assessment TSD present risk
estimates associated with just meeting
the then current 0.084 ppm standard
and several alternative 8-hour
standards, as well as three recent years
of air quality as represented by 2002,
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2003, and 2004 monitoring data. As
discussed in the exposure analysis
section above, there is considerable cityto-city and year-to-year variability in the
O3 levels during this period, which
results in significant variability in both
portions of the health risk assessment.
In the 1997 risk assessment, risks for
lung function decrements associated
with 1-hour heavy exertion, 1-hour
moderate exertion, and 8-hour moderate
exertion exposures were estimated.
Since the 8-hour moderate exertion
exposure scenario for children clearly
resulted in the greatest health risks in
terms of lung function decrements, EPA
chose to include only the 8-hour
moderate exertion exposures in the risk
assessment for this health endpoint.
Thus, the risk estimates presented here
and in the 2007 Staff Paper are most
useful for making relative comparisons
across alternative air quality scenarios
and do not represent the total risks for
lung function decrements in children or
other groups within the general
population associated with any of the
air quality scenarios. Thus, some
outdoor workers and adults engaged in
moderate exertion over multi-hour
periods (e.g., 6–8 hour exposures) also
would be expected to experience similar
lung function decrements. However, the
percentage of each of these other
subpopulations expected to experience
these effects is expected to be smaller
than all school age children who tend to
spend more hours outdoors while active
based on the exposure analyses
conducted during the prior review.
Table 2 presents a summary of the
risk estimates for lung function
decrements for the 0.084 ppm standard
set in 1997 and several alternative 8hour standard levels with the same
form.
TABLE 2—NUMBER AND PERCENT OF ALL AND ASTHMATIC SCHOOL AGE CHILDREN IN SEVERAL URBAN AREAS ESTIMATED TO EXPERIENCE MODERATE OR GREATER LUNG FUNCTION RESPONSES ONE OR MORE TIMES PER SEASON
ASSOCIATED WITH 8-HOUR OZONE EXPOSURES ASSOCIATED WITH JUST MEETING ALTERNATIVE 8-HOUR STANDARDS
BASED ON ADJUSTING 2002 AND 2004 AIR QUALITY DATA 1 2
All children, ages 5–18 FEV1 ≥ 15 percent
Aggregate for 12 urban areas
Number of children affected (% of all)
[% reduction from 0.084 ppm standard]
8-Hour air quality
standards 3
Asthmatic Children, ages 5–18 FEV1 ≥ 10 percent
Aggregate for 5 urban areas
Number of children affected (% of group)
[% reduction from 0.084 ppm standard]
2002
0.084 ppm (Standard set in
1997).
0.080 ppm .........................
0.074 ppm .........................
0.070 ppm .........................
0.064 ppm .........................
2004
2002
610,000 (3.3%)
230,000 (1.2%)
130,000 (7.8%)
70,000 (4.2%)
180,000 (1.0%) [22% reduction]
130,000 (0.7%) [43% reduction]
100,000 (0.5%) [57% reduction]
70,000 (0.4%) [70% reduction]
NA 4
NA
90,000 (5.0%) [31% reduction]
NA
40,000 (2.7%) [43% reduction]
NA
50,000 (3.0%) [62% reduction]
20,000 (1.5%) [71% reduction]
490,000 (2.7%)
duction]
340,000 (1.9%)
duction]
260,000 (1.5%)
duction]
180,000 (1.0%)
duction]
[20% re[44% re[57% re[70% re-
2004
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1 Associated with exposures while engaged in moderate or greater exertion, which is defined as having an 8-hour average equivalent ventilation rate ≥ 13 l-min/m 2.
2 Estimates are the aggregate central tendency results based on either 12 urban areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston,
Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington, DC) or 5 urban areas (Atlanta, Chicago, Houston, Los Angeles,
New York). Estimates are for the O3 season which is all year in Houston, Los Angeles and Sacramento and March or April to September or October for the remaining urban areas.
3 All standards summarized here have the same form as the 8-hour standard set in 1997, which is specified as the 3-year average of the annual 4th highest daily maximum 8-hour average concentrations. As described in the 2007 Staff Paper (section 4.5.8), recent O3 air quality distributions have been statistically adjusted to simulate just meeting the 0.084 ppm standard set in 1997 and selected alternative standards. These
simulations do not represent predictions of when, whether, or how areas might meet the specified standards
4 NA (not available) indicates that EPA did not develop risk estimates for these scenarios for the asthmatic school age children population.
The estimates are for the aggregate
number and percent of all school age
children across 12 urban areas and the
aggregate number and percent of
asthmatic school age children across 5
urban areas 45 who are estimated to have
at least 1 moderate or greater lung
function response (defined as FEV1 ≥ 15
percent in all children and ≥ 10 percent
in asthmatic children) associated with
8-hour exposures to O3 while engaged in
moderate or greater exertion on average
over the 8-hour period. The lung
function risk estimates summarized in
45 Due to time constraints, lung function risk
estimates for asthmatic school age children were
developed for only 5 of the 12 urban areas, and the
areas were selected to represent different
geographic regions. The 5 areas were: Atlanta,
Chicago, Houston, Los Angeles, and New York City.
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Table 2 illustrate the year-to-year
variability in both remaining risk
associated with a relatively high year
(i.e., based on adjusting 2002 O3 air
quality data) and relatively low year
(based on adjusting 2004 O3 air quality
data) as well as the year-to-year
variability in the risk reduction
estimated to occur associated with
various alternative standards relative to
just meeting the then current 0.084 ppm
standard. For example, it is estimated
that about 610,000 school age children
(3.2 percent of school age children)
would experience 1 or more moderate
lung function decrements for the 12
urban areas associated with O3 levels
just meeting a 0.084 ppm standard
based on 2002 air quality data compared
to 230,000 (1.2 percent of children)
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associated with just meeting a 0.084
ppm standard based on 2004 air quality
data.
As discussed in the 2007 Staff Paper,
a child may experience multiple
occurrences of a lung function response
during the O3 season. For example,
upon meeting a 0.084 ppm 8-hour
standard, the median estimates are that
about 610,000 children would
experience a moderate or greater lung
function response 1 or more times for
the aggregate of the 12 urban areas over
a single O3 season (based on the 2002
simulation), and that there would be
almost 3.2 million total occurrences.
Thus, on average it is estimated that
there would be about 5 occurrences per
O3 season per responding child for air
quality just meeting a 0.084 ppm 8-hour
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standard across the 12 urban areas.
While the estimated number of
occurrences per O3 season is lower
when based on the 2004 simulation than
for the 2002 simulation, the estimated
number of occurrences per responding
child is similar. The EPA recognizes
that some children in the population
might have only 1 or 2 occurrences
while others may have 6 or more
occurrences per O3 season. Risk
estimates based on adjusting 2003 air
quality to simulate just meeting the a
0.084 ppm standard and alternative
8-hour standards are intermediate to the
estimates presented in Table 2 above in
this notice and are presented in the
2007 Staff Paper (chapter 5) and Risk
Assessment TSD.
For just meeting a 0.084 ppm 8-hour
standard, Table 5–8 in the 2007 Staff
Paper shows that median estimates
across the 12 urban areas for all school
age children experiencing 1 or more
moderate lung function decrements
ranges from 0.9 to 5.4 percent based on
the 2002 simulation and from 0.8 to 2.2
percent based on the 2004 simulation.
Risk estimates for each urban area
included in the assessment, for each of
the three years analyzed, and for
additional alternative standards are
presented in chapter 5 of the 2007 Staff
Paper and in the Risk Assessment TSD.
For just meeting a 0.084 ppm 8-hour
standard, the median estimates across
the 5 urban areas for asthmatic school
age children range from 3.4 to 10.9
percent based on the 2002 simulation
and from 3.2 to 6.9 percent based on the
2004 simulation.
Key observations important in
comparing estimated lung function risks
associated with just meeting the 0.084
ppm NAAQS and alternative standards
under consideration include:
(1) As discussed above, there is
significant year to year variability in the
range of median estimates of the number
of school age children (ages 5–18)
estimated to experience at least one
FEV1 decrement ≥ 15 percent due to
8-hour O3 exposures across the 12 urban
areas analyzed, and similarly across the
5 urban areas analyzed for asthmatic
school age children (ages 5–18)
estimated to experience at least one
FEV1 decrement ≥ 10 percent, when
various 8-hour standards are just met.
(2) For asthmatic school age children,
the median estimates of occurrences of
FEV1 decrements ≥ 10% range from
52,000 to nearly 510,000 responses
associated with just meeting a 0.084
ppm standard (based on the 2002
simulation) and range from 61,000 to
about 240,000 occurrences (based on the
2004 simulation). These risk estimates
would be reduced to a range of 14,000
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to about 275,000 occurrences (2002
simulation) and to about 18,000 to
nearly 125,000 occurrences (2004
simulation) upon just meeting the most
stringent alternative 8-hour standard
(0.064 ppm, 4th highest). The average
number of occurrences per asthmatic
child in an O3 season ranged from about
6 to 11 associated with just meeting a
0.084 ppm standard (2002 simulation).
The average number of occurrences per
asthmatic child ranged from 4 to 12
upon meeting the most stringent
alternative examined (0.064 ppm, 4thhighest) based on the 2002 simulation.
The number of occurrences per
asthmatic child is similar for the
scenarios based on the 2004 simulation.
As discussed above, several
epidemiological studies have reported
increased respiratory morbidity
outcomes (e.g., respiratory symptoms in
moderate to severe asthmatic children,
respiratory-related hospital admissions)
and increased nonaccidental and
cardiorespiratory mortality associated
with exposure to ambient O3
concentrations. The results and key
observations from this portion of the
risk assessment are presented below:
(1) Estimates for increased respiratory
symptoms (i.e., chest tightness,
shortness of breath, and wheeze) in
moderate/severe asthmatic children
(ages 0–12) were developed for the
Boston urban area only. The median
estimated number of days involving
chest tightness (using the concentrationresponse relationship with only O3 in
the model) is about 6,100 (based on the
2002 simulation) and about 4,500 (based
on the 2004 simulation) upon meeting a
0.084 ppm 8-hour standard and this is
reduced to about 4,600 days (2002
simulation) and 3,100 days (2004
simulation) upon meeting the most
stringent alternative examined (0.064
ppm, 4th-highest daily maximum 8hour average). This corresponds to 11
percent (2002 simulation) and 8 percent
(2004 simulation) of total incidence of
chest tightness upon meeting a 0.084
ppm 8-hour standard and to about 8
percent (2002 simulation) and 5.5
percent (2004 simulation) of total
incidence of chest tightness upon
meeting a 0.064 ppm, 4th-highest daily
maximum 8-hour average standard.
Similar patterns of effects and
reductions in effects are observed for
each of the respiratory symptoms
examined.
(2) The 2007 Staff Paper and Risk
Assessment TSD present unscheduled
hospital admission risk estimates for
respiratory illness and asthma in New
York City associated with short-term
exposures to O3 concentrations in
excess of background levels from April
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through September for several recent
years (2002, 2003, and 2004) and upon
just meeting a 0.084 ppm standard and
alternative 8-hour standards based on
simulating O3 levels using 2002–2004
O3 air quality data. For total respiratory
illness, EPA estimates about 6.4 cases
per 100,000 relevant population (2002
simulation) and about 4.6 cases per
100,000 relevant population (2004
simulation), which represents 1.5
percent (2002 simulation) and 1.0
percent (2004 simulation) of total
incidence or about 510 cases (2002
simulation) and about 370 cases (2004
simulation) upon just meeting a 0.084
ppm 8-hour standard. For asthmarelated hospital admissions, which are a
subset of total respiratory illness
admissions, the estimates are about 5.5
cases per 100,000 relevant population
(2002 simulation) and about 3.9 cases
per 100,000 relevant population (2004
simulation), which represents about 3.3
percent (2002 simulation) and 2.4
percent (2004 simulation) of total
incidence or about 440 cases (2002) and
about 310 cases (2004) for this same air
quality scenario.
For increasingly more stringent
alternative 8-hour standards, there is a
gradual reduction in respiratory illness
cases per 100,000 relevant population
from 6.4 cases per 100,000 upon just
meeting a 0.084 ppm 8-hour standard to
4.6 cases per 100,000 under the most
stringent 8-hour standard (i.e., 0.064
ppm, average 4th-highest daily
maximum) analyzed based on the 2002
simulation. Similarly, based on the 2004
simulation there is a gradual reduction
from 4.6 cases per 100,000 relevant
population upon just meeting a 0.084
ppm 8-hour standard to 3.0 cases per
100,000 under a 0.064 ppm, average 4thhighest daily maximum standard.
Additional respiratory-related
hospital admission estimates for three
other locations are provided in the Risk
Assessment TSD. The EPA notes that
the concentration-response functions for
each of these locations examined
different outcomes in different age
groups (e.g., > age 30 in Los Angeles,
> age 64 in Cleveland and Detroit, vs. all
ages in New York City), making
comparison of the risk estimates across
the areas very difficult.
(3) Based on the median estimates for
incidence for nonaccidental mortality
(based on the Bell et al. (2004) 95 cities
concentration-response function),
meeting the most stringent standard
(0.064 ppm) is estimated to reduce
mortality by 40 percent of what it would
be associated with just meeting a 0.084
ppm standard (based on the 2002
simulation). The patterns for
cardiorespiratory mortality are similar.
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The aggregate O3-related
cardiorespiratory mortality upon just
meeting the most stringent standard
shown is estimated to be about 42
percent of what it would be upon just
meeting a 0.084 ppm standard, using
simulated O3 concentrations that just
meet a 0.084 ppm standard and
alternative 8-hour standards based on
the 2002 simulation. Using the 2004
simulation, the corresponding
reductions show a similar pattern but
are somewhat greater.
(4) Much of the contribution to the
risk estimates for non-accidental and
cardiorespiratory mortality upon just
meeting a 0.084 ppm 8-hour standard is
associated with 24-hour O3
concentrations between background and
0.040 ppm. Based on examining
relationships between 24-hour
concentrations averaged across the
monitors within an urban area and
8-hour daily maximum concentrations,
8-hour daily maximum levels at the
highest monitor in an urban area
associated with these averaged 24-hour
levels are generally about twice as high
as the 24-hour levels. Thus, most O3related nonaccidental mortality is
estimated to occur when O3
concentrations are between background
and when the highest monitor in the
urban area is at or below 0.080 ppm,
8-hour average concentration.
The discussion below highlights
additional observations and insights
from the O3 risk assessment, together
with important uncertainties and
limitations.
(1) As discussed in the 2007 Staff
Paper (section 5.4.5), EPA has greater
confidence in relative comparisons in
risk estimates between alternative
standards than in the absolute
magnitude of risk estimates associated
with any particular standard.
(2) Significant year-to-year variability
in O3 concentrations combined with the
use of a 3-year design value to
determine the amount of air quality
adjustment to be applied to each year
analyzed, results in significant year-toyear variability in the annual health risk
estimates upon just meeting various 8hour standards.
(3) There is noticeable city-to-city
variability in estimated O3-related
incidence of morbidity and mortality
across the 12 urban areas analyzed for
both recent years of air quality and for
air quality adjusted to simulate just
meeting a 0.084 ppm standard and
selected potential alternative standards.
This variability is likely due to
differences in air quality distributions,
differences in exposure related to many
factors including varying activity
patterns and air exchange rates,
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differences in baseline incidence rates,
and differences in susceptible
populations and age distributions across
the 12 urban areas.
(4) With respect to the uncertainties
about estimated policy-relevant
background concentrations, as
discussed in the 2007 Staff Paper
(section 5.4.3), alternative assumptions
about background levels had a variable
impact depending on the health effect
considered and the location and
standard analyzed in terms of the
absolute magnitude and relative changes
in the risk estimates. There was
relatively little impact on either
absolute magnitude or relative changes
in lung function risk estimates due to
alternative assumptions about
background levels. With respect to O3related non-accidental mortality, while
notable differences (i.e., greater than 50
percent) 46 were observed for
nonaccidental mortality in some areas,
particularly for more stringent
standards, the overall pattern of
estimated reductions, expressed in
terms of percentage reduction relative to
the 0.084 ppm standard, was
significantly less impacted.
C. Reconsideration of the Level of the
Primary Standard
1. Evidence and Exposure/Risk-Based
Considerations
The approach used in the 2007 Staff
Paper as a basis for staff
recommendations on standard levels
builds upon and broadens the general
approach used by EPA in the 1997
review. This approach reflects the more
extensive and stronger body of evidence
available for the 2008 rulemaking on a
broader range of health effects
associated with exposure to O3,
including: (1) Additional respiratoryrelated endpoints; (2) new information
about the mechanisms underlying
respiratory morbidity effects supporting
a judgment that the link between O3
exposure and these effects is causal; (3)
newly identified cardiovascular-related
health endpoints from animal
toxicology and controlled human
exposures studies that are highly
suggestive that O3 can directly or
indirectly contribute to cardiovascular
morbidity, and (4) new U.S. multicity
time series studies, single city studies,
and several meta-analyses of these
46 For example, assuming lower background
levels resulted in increased estimates of nonaccidental mortality incidence per 100,000 that
were often 50 to 100 percent greater than the base
case estimates; assuming higher background levels
resulted in decreased estimates of non-accidental
mortality incidence per 100,000 that were less than
the base case estimates by 50 percent or more in
many of the areas.
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studies that provide relatively strong
evidence for associations between shortterm O3 exposures and all-cause
(nonaccidental) mortality, at levels
below the current primary standard: As
well as (5) a substantial body of new
evidence of increased susceptibility in
people with asthma and other lung
diseases. In evaluating evidence-based
and exposure/risk-based considerations,
the 2007 Staff Paper considered: (1) The
ranges of levels of alternative standards
that are supported by the evidence, and
the uncertainties and limitations in that
evidence and (2) the extent to which
specific levels of alternative standards
reduce the estimated exposures of
concern and risks attributable to O3 and
other photochemical oxidants, and the
uncertainties associated with the
estimated exposure and risk reductions.
a. Evidence-Based Considerations
In taking into account evidence-based
considerations, the 2007 Staff Paper
evaluated available evidence from
controlled human exposure studies and
epidemiological studies, as well as the
uncertainties and limitations in that
evidence. In particular, it focused on the
extent to which controlled human
exposure studies provide evidence of
lowest-observed-effects levels and the
extent to which epidemiological studies
provide evidence of associations that
extend down to the lower levels of O3
concentrations observed in the studies
or some indication of potential effect
thresholds in terms of 8-hour average O3
concentrations.
The most certain evidence of adverse
health effects from exposure to O3
comes from the controlled human
exposure studies, as discussed above in
section II.A.2, and the large bulk of this
evidence derives from studies of
exposures at levels of 0.080 ppm and
above. At those levels, there is
consistent evidence of lung function
decrements and respiratory symptoms
in healthy young adults, as well as
evidence of inflammation and other
medically significant airway responses.
Two studies by Adams (2002, 2006),
newly available for consideration in the
2008 rulemaking, are the only available
controlled human exposure studies that
examine respiratory effects associated
with prolonged O3 exposures at levels
below 0.080 ppm, which was the lowest
exposure level that had been examined
in the 1997 review. As discussed above
in section II.A.2.a.i.(a)(i), the Adams
(2006) study investigated a range of
exposure levels, including 0.060 and
0.080 ppm O3, and analyzed hour-byhour changes in responses, including
lung function (measured in term of
decrements in FEV1) and respiratory
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symptoms, to investigate the effects of
different patterns of exposure. At the
0.060 ppm exposure level, the author
reported no statistically significant
differences for lung function
decrements; statistically significant
responses were reported for total
subjective respiratory symptoms toward
the end of the exposure period for one
exposure pattern. The EPA’s reanalysis
(Brown, 2007) of the data from the
Adams (2006) study addressed the more
fundamental question of whether there
were statistically significant changes in
lung function from a 6.6-hour exposure
to 0.060 ppm O3 versus filtered air and
used a standard statistical method
appropriate for a simple paired
comparison. This reanalysis found small
group mean lung function decrements
in healthy adults at the 0.060 ppm
exposure level to be statistically
significantly different from responses
associated with filtered air exposure.
Moreover, the Adams’ studies also
report a small percentage of subjects (7
to 20 percent) experienced lung
function decrements (> 10 percent) at
the 0.060 ppm exposure level. This is a
concern because, for active healthy
people, moderate levels of functional
responses (e.g., FEV1 decrements of
> 10% but < 20%) and/or moderate
respiratory symptom responses would
likely interfere with normal activity for
relatively few responsive individuals.
However, for people with lung disease,
even moderate functional or
symptomatic responses would likely
interfere with normal activity for many
individuals, and would likely result in
more frequent use of medication. In the
context of standard setting, the CASAC
indicated (Henderson, 2006c) that a
focus on the lower end of the range of
moderate levels of functional responses
(e.g., FEV1 decrements ≥ 10%) is most
appropriate for estimating potentially
adverse lung function decrements in
people with lung disease. Therefore, the
results of the Adams studies which
indicate that a small percentage of
healthy, non-asthmatic subjects are
likely to experience FEV1 decrements
≥ 10% when exposed to 0.060 ppm O3
have implications for setting a standard
that protects public health, including
the health of sensitive populations such
as asthmatics, with an adequate margin
of safety.
In considering these most recent
controlled human exposure studies, the
2007 Staff Paper concluded that these
studies provide evidence of a lowestobserved-effects level of 0.060 ppm for
potentially adverse lung function
decrements and respiratory symptoms
in some healthy adults while at
prolonged moderate exertion. It further
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concluded that since people with
asthma, particularly children, have been
found to be more sensitive and to
experience larger decrements in lung
function in response to O3 exposures
than would healthy adults, the 0.060
ppm exposure level also can be
interpreted as representing a level likely
to cause adverse lung function
decrements and respiratory symptoms
in children with asthma and more
generally in people with respiratory
disease.
In considering controlled human
exposure studies of pulmonary
inflammation, airway responsiveness,
and impaired host defense capabilities,
discussed above in section II.A.2.a.i, the
2007 Staff Paper noted that these studies
provide evidence of a lowest-observedeffects level for such effects in healthy
adults at prolonged moderate exertion of
0.080 ppm, the lowest level tested.
Moreover there is no evidence that the
0.080 ppm level is a threshold for these
effects. Studies reporting inflammatory
responses and markers of lung injury
have clearly demonstrated that there is
significant variation in response of
subjects exposed, even to O3 exposures
at 0.080 ppm. One study showed
notable interindividual variability in
young healthy adult subjects in most of
the inflammatory and cellular injury
indicators analyzed at 0.080 ppm. This
inter-individual variability suggests that
some portion of the population would
likely experience such effects at
exposure levels extending well below
0.080 ppm.
As discussed above, these
physiological effects have been linked to
aggravation of asthma and increased
susceptibility to respiratory infection,
potentially leading to increased
medication use, increased school and
work absences, increased visits to
doctors’ offices and emergency
departments, and increased hospital
admissions. Further, pulmonary
inflammation is related to increased
cellular permeability in the lung, which
may be a mechanism by which O3
exposure can lead to cardiovascular
system effects, and to potential chronic
effects such as chronic bronchitis or
long-term damage to the lungs that can
lead to reduced quality of life. These are
all indicators of adverse O3-related
morbidity effects, which are consistent
with and lend plausibility to the adverse
morbidity effects and mortality effects
observed in epidemiological studies.
Significant associations between
ambient O3 exposures and a wide
variety of respiratory symptoms and
other morbidity outcomes (e.g., asthma
medication use, school absences,
emergency department visits, and
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hospital admissions) have been reported
in epidemiological studies, as discussed
above in section II.A.2.a.i. Overall, the
2006 Criteria Document concludes that
positive and robust associations were
found between ambient O3
concentrations and various respiratory
disease hospitalization outcomes, when
focusing particularly on results of
warm-season analyses. Recent studies
also generally indicate a positive
association between O3 concentrations
and emergency department visits for
asthma during the warm season. These
positive and robust associations are
supported by the controlled human
exposure, animal toxicological, and
epidemiological evidence for lung
function decrements, increased
respiratory symptoms, airway
inflammation, and increased airway
responsiveness. Taken together, the
overall evidence supports a causal
relationship between acute ambient O3
exposures and increased respiratory
morbidity outcomes resulting in
increased emergency department visits
and hospitalizations during the warm
season (EPA, 2006a, p. 8–77).
Moreover, many single- and multicity
epidemiological studies observed
positive associations of ambient O3
concentrations with total nonaccidental
and cardiopulmonary mortality. As
discussed above in section II.A.2.b.i, the
2006 Criteria Document finds that the
results from U.S. multicity time-series
studies provide the strongest evidence
to date for O3 effects on acute mortality.
Recent meta-analyses also indicate
positive risk estimates that are unlikely
to be confounded by PM; however,
future work is needed to better
understand the influence of model
specifications on the magnitude of risk.
The 2006 Criteria Document concludes
that the ‘‘positive O3 effects estimates,
along with the sensitivity analyses in
these three meta-analyses, provide
evidence of a robust association
between ambient O3 and mortality’’
(EPA, 2006a, p. 7–97). In summary, the
2006 Criteria Document (p. 8–78)
concludes that these findings are highly
suggestive that short-term O3 exposure
directly or indirectly contribute to nonaccidental and cardiopulmonary-related
mortality, but additional research is
needed to more fully establish
underlying mechanisms by which such
effects occur.
The 2007 Staff Paper considered the
epidemiological studies to evaluate
evidence related to potential effects
thresholds at the population level for
morbidity and mortality effects. As
discussed above in section II.A.3.a (and
more fully in the 2007 Staff Paper in
chapter 3 and the 2006 Criteria
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Document in chapter 7), a number of
time-series studies have used statistical
modeling approaches to evaluate
potential thresholds at the population
level. A few such studies reported some
suggestive evidence of possible
thresholds for morbidity and mortality
outcomes in terms of 24-hour, 8-hour,
and 1-hour averaging times. These
results, taken together, provide some
indication of possible 8-hour average
threshold levels from below about 0.025
to 0.035 ppm (within the range of
background concentrations) up to
approximately 0.050 ppm. Other
studies, however, observe linear
concentration-response functions
suggesting no effect threshold. The 2007
Staff Paper (p.6–60) concluded that the
statistically significant associations
between ambient O3 concentrations and
lung function decrements, respiratory
symptoms, indicators of respiratory
morbidity including increase emergency
department visits and hospital
admissions, and possibly mortality
reported in a large number of studies
likely extend down to ambient O3
concentrations that are well below the
level of the then current standard (0.084
ppm). These associations also extend
well below the level of the standard set
in 2008 (0.075 ppm) in that the highest
level at which there is any indication of
a threshold is approximately 0.050 ppm.
Toward the lower end of the range of O3
concentrations observed in such studies,
ranging down to background levels (i.e.,
0.035 to 0.015 ppm), however, the 2007
Staff Paper stated that there is
increasing uncertainty as to whether the
observed associations remain plausibly
related to exposures to ambient O3,
rather than to the broader mix of air
pollutants present in the ambient
atmosphere.
The 2007 Staff Paper also considered
studies that did subset analyses, which
included only days with ambient O3
concentrations below the level of the
then current standard, or below even
lower O3 concentrations, and continue
to report statistically significant
associations. Notably, as discussed
above, Bell et al. (2006) conducted a
subset analysis that continued to show
statistically significant mortality
associations even when only days with
a maximum 8-hour average O3
concentration below a value of
approximately 0.061 ppm were
included.47 Also of note is the large
multicity NCICAS (Mortimer et al.,
47 Bell et al. (2006) referred to this level as being
approximately equivalent to 120 μg/m3, daily 8hour maximum, the World Health Organization
guideline and European Commission target value
for O3.
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2002) that reported statistically
significant associations between
ambient O3 concentrations and lung
function decrements even when days
with 8-hour average O3 levels greater
than 0.080 ppm were excluded (which
consisted of less than 5 percent of the
days in the eight urban areas in the
study).
Further, as discussed above in section
II.A.3.a, there are limitations in
epidemiological studies that make
discerning thresholds in populations
difficult, including low data density in
the lower concentration ranges, the
possible influence of exposure
measurement error, and interindividual
differences in susceptibility to O3related effects in populations. There is
the possibility that thresholds for
individuals may exist in reported
associations at fairly low levels within
the range of air quality observed in the
studies but not be detectable as
population thresholds in
epidemiological analyses.
Based on the above considerations,
the 2007 Staff Paper recognized that the
available evidence neither supports nor
refutes the existence of effect thresholds
at the population level for morbidity
and mortality effects, and that if a
population threshold level does exist, it
would likely be well below the level of
the then current standard and possibly
within the range of background levels.
Taken together, these considerations
also support the conclusion that if a
population threshold level does exist, it
would likely be well below the level of
the 0.075 ppm, 8-hour average, standard
set in 2008.
In looking more broadly at evidence
from animal toxicological, controlled
human exposure, and epidemiological
studies, the 2006 Criteria Document
found substantial evidence, newly
available in the 2008 rulemaking, that
people with asthma and other
preexisting pulmonary diseases are
among those at increased risk from O3
exposure. Altered physiological,
morphological, and biochemical states
typical of respiratory diseases like
asthma, COPD, and chronic bronchitis
may render people sensitive to
additional oxidative burden induced by
O3 exposure (EPA, 2006a, section 8.7).
Children and adults with asthma are the
groups that have been studied most
extensively. Evidence from controlled
human exposure studies indicates that
asthmatics may exhibit larger lung
function decrements in response to O3
exposure than healthy controls. As
discussed more fully in section II.A.4
above, asthmatics present a different
response profile for cellular, molecular,
and biochemical parameters (EPA,
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2987
2006a, Figure 8–1) that are altered in
response to acute O3 exposure. They can
have larger inflammatory responses, as
manifested by larger increases in
markers of inflammation such as white
bloods cells (e.g., PMNs) or
inflammatory cytokines. Asthmatics,
and people with allergic rhinitis, are
more likely to have an allergic-type
response upon exposure to O3, as
manifested by increases in white blood
cells associated with allergy (i.e.,
eosinophils) and related molecules,
which increase inflammation in the
airways. The increased inflammatory
and allergic responses also may be
associated with the larger late-phase
responses that asthmatics can
experience, which can include
increased bronchoconstrictor responses
to irritant substances or allergens and
additional inflammation.
In addition to the experimental
evidence of lung function decrements,
respiratory symptoms, and other
respiratory effects in asthmatic
populations, two large U.S.
epidemiological studies as well as
several smaller U.S. and international
studies, have reported fairly robust
associations between ambient O3
concentrations and measures of lung
function and daily respiratory
symptoms (e.g., chest tightness, wheeze,
shortness of breath) in children with
moderate to severe asthma and between
O3 and increased asthma medication use
(EPA, 2007a, chapter 6). These more
serious responses in asthmatics and
others with lung disease provide
biological plausibility for the respiratory
morbidity effects observed in
epidemiological studies, such as
emergency department visits and
hospital admissions.
The body of evidence from controlled
human exposure and epidemiological
studies, which includes asthmatic as
well as non-asthmatic subjects,
indicates that controlled human
exposure studies of lung function
decrements and respiratory symptoms
that evaluate only healthy, nonasthmatic subjects likely underestimate
the effects of O3 exposure on asthmatics
and other susceptible populations.
Therefore, relative to the healthy, nonasthmatic subjects used in most
controlled human exposure studies,
including the Adams (2002, 2006)
studies, a greater proportion of people
with asthma may be affected, and those
who are affected may have as large or
larger lung function and symptomatic
responses at ambient exposures to 0.060
ppm O3. This indicates that the lowestobserved-effects levels demonstrated in
controlled human exposure studies that
use only healthy subjects may not
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reflect the lowest levels at which people
with asthma or other lung diseases may
respond.
Being mindful of the uncertainties
and limitations inherent in interpreting
the available evidence, the 2007 Staff
Paper stated the view that the range of
alternative O3 standards for
consideration should take into account
information on lowest-observed-effects
levels in controlled human exposure
studies as well as indications of possible
effects thresholds reported in some
epidemiological studies and questions
of biological plausibility in attributing
associations observed down to
background levels to O3 exposures
alone. Based on the evidence and these
considerations, it concluded that the
upper end of the range of consideration
should be somewhat below 0.080 ppm,
the lowest-observed-effects level for
effects such as pulmonary
inflammation, increased airway
responsiveness and impaired hostdefense capabilities in healthy adults
while at prolonged moderate exertion.
The 2007 Staff Paper also concluded
that the lower end of the range of
alternative O3 standards appropriate for
consideration should be the lowestobserved-effects level for potentially
adverse lung function decrements and
respiratory symptoms in some healthy
adults, 0.060 ppm.
srobinson on DSKHWCL6B1PROD with PROPOSALS2
b. Exposure and Risk-Based
Considerations
In addition to the evidence-based
considerations informing staff
recommendations on alternative levels,
as discussed above in section II.B, the
2007 Staff Paper also evaluated
quantitative exposures and health risks
estimated to occur upon meeting the
then current 0.084 ppm standard and
alternative standards.48 In so doing, it
presented the important uncertainties
and limitations associated with these
exposure and risk assessments
(discussed above in section II.B and
more fully in chapters 4 and 5 of the
2007 Staff Paper).
The 2007 Staff Paper (and the
CASAC) also recognized that the
exposure and risk analyses could not
provide a full picture of the O3
exposures and O3-related health risks
48 As described in the 2007 Staff Paper (section
4.5.8) and discussed above in section II.B, recent O3
air quality distributions have been statistically
adjusted to simulate just meeting the then current
0.084 ppm standard and selected alternative
standards. These simulations do not represent
predictions of when, whether, or how areas might
meet the specified standards. Modeling that projects
whether and how areas might attain alternative
standards in a future year is presented in the
Regulatory Impact Analysis being prepared in
connection with this rulemaking.
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posed nationally. The EPA did not have
sufficient information to evaluate all
relevant at-risk groups (e.g., outdoor
workers) or all O3-related health
outcomes (e.g., increased medication
use, school absences, and emergency
department visits that are part of the
broader pyramid of effects discussed
above in section II.A.4.d), and the scope
of the 2007 Staff Paper analyses was
generally limited to estimating
exposures and risks in 12 urban areas
across the U.S., and to only five or just
one area for some health effects
included in the risk assessment. Thus,
national-scale public health impacts of
ambient O3 exposures are clearly much
larger than the quantitative estimates of
O3-related incidences of adverse health
effects and the numbers of children
likely to experience exposures of
concern associated with meeting the
0.084 ppm standard or alternative
standards. On the other hand, interindividual variability in responsiveness
means that only a subset of individuals
in each group estimated to experience
exposures exceeding a given benchmark
exposure of concern level would
actually be expected to experience such
adverse health effects.
The 2007 Staff Paper focused on
alternative standards with the same
form as the then current 0.084 ppm O3
standard (i.e. the 0.074/4, 0.070/4 and
0.064/4 scenarios).49 Having concluded
in the 2007 Staff Paper that it was
appropriate to consider a range of
standard levels from somewhat below
0.080 ppm down to as low as 0.060
ppm, the 2007 Staff Paper looked to
results of the analyses of exposure and
risk for the 0.074/4 scenario to represent
the public health impacts of selecting a
standard in the upper part of the range,
the results of analyses of the 0.070/4
scenario to represent the impacts in the
middle part of the range, and the results
of the analyses of the 0.064/4 scenario
to represent the lower part of the range.
As discussed in section II.B.1 of this
notice, the exposure estimates presented
in the 2007 Staff Paper are for the
number and percent of all children and
asthmatic children exposed, and the
number of person-days (occurrences) of
exposures, with daily 8-hour maximum
exposures at or above several
benchmark levels while at intermittent
moderate or greater exertion. Exposures
above selected benchmark levels
provide some perspective on the public
49 The abbreviated notation used to identify the
then current 0.084 ppm standard and alternative
standards in this section and in the risk assessment
section of the Staff Paper is in terms of ppm and
the nth highest daily maximum 8-hour average. For
example, the 8-hour standard established in 1997 is
identified as ‘‘0.084/4.’’
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health impacts of health effects that
cannot currently be evaluated in
quantitative risk assessments but that
may occur at existing air quality levels,
and the extent to which such impacts
might be reduced by meeting alternative
standard levels. As described in section
II.B.1.c above, the 2007 Staff Paper
refers to exposures at and above these
benchmark levels as ‘‘exposures of
concern.’’ The 2007 Staff Paper notes
that exposures of concern, and the
health outcomes they represent, likely
occur across a range of O3 exposure
levels, such that there is no one
exposure level that addresses all public
health concerns. As noted above in
section II.B., EPA also has
acknowledged that the concept is more
appropriately viewed as a continuum
with greater confidence and less
uncertainty about the existence of
health effects at the upper end and less
confidence and greater uncertainty as
one considers increasingly lower O3
exposure levels.
Consistent with advice from CASAC,
the 2007 Staff Paper estimates exposures
of concern not only at 0.080 ppm O3, a
level at which there are clearly
demonstrated effects, but also at 0.070
and 0.060 ppm O3 levels where there is
some evidence that health effects are
likely to occur in some individuals. The
2007 Staff Paper recognizes that there
will be varying degrees of concern about
exposures at each of these levels, based
in part on the population groups
experiencing them. Given that there is
clear evidence of inflammation,
increased airway responsiveness, and
changes in host defenses in healthy
people exposed to 0.080 ppm and
reason to infer that such effects will
continue at lower exposure levels, but
with increasing uncertainty about the
extent to which such effects occur at
lower O3 concentrations, the 2007 Staff
Paper and discussion below, focus on
exposures of concern at or above
benchmark levels of 0.070 and 0.060
ppm O3 for purposes of evaluating
alternative standards. The focus on
these two benchmark levels reflects the
following evidence-based
considerations, discussed above in
section II.C.1, that raise concerns about
adverse health effects likely occurring at
levels below 0.080 ppm: (1) That there
is limited, but important, new evidence
from controlled human exposure studies
showing lung function decrements and
respiratory symptoms in some healthy
subjects at 0.060 ppm; (2) that
asthmatics are likely to have more
serious responses than healthy
individuals; (3) that lung function is not
likely to be as sensitive a marker for O3
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effects as lung inflammation; and (4)
that there is epidemiological evidence
which reports associations with O3
levels that extend well below 0.080
ppm.
Table 3 below summarizes the
exposure estimates for all children and
asthmatic children for the 0.060 and
0.070 ppm health effect benchmark
levels associated with O3 levels adjusted
to just meet 0.074/4, 0.070/4, and 0.064/
4 alternative 8-hour standards based on
a generally poorer year of air quality
(2002) and based on a generally better
year of air quality (2004). This table
includes exposure estimates reflecting
the aggregate estimate for the 12 urban
areas as well as the range across these
same 12 areas. As shown in Table 3
below, the percent of population
exposed over the selected benchmark
levels is very similar for all and
asthmatic school age children. Thus, the
following discussion focuses primarily
on the exposure estimates for asthmatic
children, recognizing that the pattern of
exposure estimates is similar for all
children when expressed in terms of
percentage of the population.
As noted in section II.B.2 and shown
in Tables 1 and 3 of this notice,
substantial year-to-year variability is
observed, ranging to over an order of
magnitude at the higher alternative
standard levels, in estimates of the
number of children and the number of
occurrences of exposures of concern at
both the 0.060 and 0.070 ppm
benchmark levels. As shown in Table 3,
and discussed more fully below,
aggregate estimates of exposures of
concern for the 12 urban areas included
in the assessment are considerably
larger for the benchmark level of ≥ 0.060
ppm O3, compared to the 0.070 ppm
benchmark, while the pattern of year-toyear variability is fairly similar.
As shown in Table 3, aggregate
estimates of exposures of concern for a
0.060 ppm benchmark level vary
considerably among the three
alternative standards included in this
table, particularly for the 2002
simulations (a year with generally
poorer air quality in most, but not all
areas). For air quality just meeting a
0.074/4 standard approximately 27% of
asthmatic children, based on the 2002
simulation, and approximately 2% of
asthmatic children based on the 2004
simulation (a year with better air quality
in most but not all areas), are estimated
to experience one or more exposures of
concern at the benchmark level of ≥
0.060 ppm O3. Considering a 0.070/4
standard using the same benchmark
level (0.060 ppm), about 18% of
asthmatic children are estimated to
experience one or more exposures of
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concern, in a year with poorer air
quality (2002), and only about 1% in a
year with better air quality (2004). For
the most stringent standard examined (a
0.064/4 standard), about 6% of
asthmatic children are estimated to
experience one or more exposures of
concern in the simulation based on the
year with poorer air quality (2002), and
exposures of concern at the 0.060 ppm
benchmark level are essentially
eliminated based on a year with better
air quality (2004).
Table 3 also provides aggregate
exposure estimates for the 12 urban
areas where a benchmark level of
≥ 0.070 ppm is used. Based on the year
with poorer air quality (2002), the
estimate of the percent of asthmatic
children exposed one or more times is
about 5% when a 0.074/4 standard is
just met; based on a year with better air
quality (2004), exposures of concern are
essentially eliminated. For this same
benchmark (0.070 ppm), when a 0.070/
4 standard is just met, estimates range
from about 2% of asthmatic children
exposed one or more times over this
benchmark based on a year with poorer
air quality (2002), and exposures of
concern are essentially eliminated based
on a year with better air quality (2004).
At the 0.070 ppm benchmark, just
meeting a 0.064/4 standard essentially
eliminates exposures of concern
regardless of the year that is used as the
basis for the analysis.
The 2007 Staff Paper also notes that
there is substantial city-to-city
variability in these estimates, and notes
that it is appropriate to consider not just
the aggregate estimates across all cities,
but also to consider the public health
impacts in cities that receive relatively
less protection from the alternative
standards. As shown in Table 3, in
considering the benchmark level of
≥ 0.060 ppm, while the aggregate
percentage of asthmatic children
estimated to experience one or more
exposures of concern across all 12 cities
for a 0.074/4 standard is about 27%
based on the year with poorer air quality
(2002), it ranges up to approximately
51% for asthmatic children in the city
with the least degree of protection from
that alternative standard. Similarly, for
air quality just meeting a 0.070/4
standard, the aggregate percentage of
asthmatic children estimated to
experience one or more exposures of
concern across all 12 cities is 18% based
on the year with poorer air quality, but
it ranges up to about 41% in the city
with the least degree of protection
associated with just meeting that
alternative standard. For just meeting a
0.064/4 standard, the aggregate estimate
of asthmatic children experiencing
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2989
exposures of concern for the 0.060 ppm
benchmark is about 6% based on the
year with poorer air quality and ranges
up to 16% in the city with the least
degree of protection.
This pattern of city-to-city variability
also occurs at the benchmark level of
≥ 0.070 ppm associated with air quality
just meeting these same three alternative
standards (i.e., 0.074/4, 0.070/4, and
0.064/4). While the aggregate percentage
of asthmatic children estimated to
experience such exposures of concern
across all 12 cities is about 5% based on
the year with poorer air quality for just
meeting the 0.074/4 standard, it ranges
up to 14% in the city with the least
degree of protection associated with that
alternative standard. For just meeting a
0.070/4 standard the aggregate estimate
is 2% of asthmatic children
experiencing exposures of concern for
the 0.070 ppm benchmark based on the
year with poorer air quality and ranges
up to 6% in the city with the least
degree of protection. The aggregate
estimate for exposures of concern is
further reduced to 0.2% of asthmatic
children for this same benchmark level
for air quality just meeting a 0.064/4
standard based on the year with poorer
air quality and ranges up to 1% in the
city with the least degree of protection.
In addition to observing the fraction
of the population estimated to
experience exposures of concern
associated with just meeting alternative
standards, EPA also took into
consideration in the 2007 Staff Paper
the percent reduction in exposures of
concern and health risks associated with
alternative standards relative to just
meeting the then current 0.084/4
standards. For the current decision it is
also informative to consider the
incremental reductions in exposures of
concern associated with more stringent
alternative standards relative to the
0.075 ppm standard. As shown in Table
1 above, at the ≥ 0.060 ppm benchmark
level based on a year with poorer air
quality, the reduction in exposures of
concern for asthmatic children in going
from the 0.074/4 standard (which
approximates the 0.075 ppm standard
adopted in 2008) down to a 0.064/4
standard is observed to be very similar
to the reduction estimated to occur in
going from then current 0.084/4
standard down to a 0.074/4 standard.
More specifically, the estimates for
asthmatic children are reduced from
47% (about 1.2 million children)
associated with meeting a 0.084/4
standard down to 27% (about 700,000
children) for just meeting a 0.074/4
standard and the estimates are reduced
further to about 6% (about 150,000
children) associated with just meeting a
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0.064/4 standard in the 12 urban areas
included in the assessment. In a year
with better air quality (2004), exposures
estimated to exceed the 0.060 ppm
benchmark in asthmatic children one or
more times in a year are reduced from
11% associated with just meeting a
0.084/4 standard down to about 2% for
a 0.074/4 standard and are essentially
eliminated when a 0.064/4 standard is
just met.
Turning to consideration of the risk
assessment estimates, Table 2 above
summarizes the risk estimates for
moderate lung function decrements in
both all school age children and
asthmatic school age children associated
with just meeting several alternative
standards based on simulations
involving a year with relatively poorer
air quality (2002) and a year with
relatively better air quality (2004). As
shown in Table 2, for the 2002
simulation the reduction in the number
of asthmatic children estimated to
experience one or more moderate lung
function decrements going from a 0.074/
4 standard down to a 0.064/4 standard
is roughly equivalent to the additional
health protection afforded associated
with just meeting a 0.074/4 standard
relative to then current 0.084/4
standard. More specifically, for just 5
urban areas, it is estimated that nearly
8% of asthmatic children (130,000
children) would experience one or more
occurrences of moderate lung function
decrements per year at a 0.084/4
standard and this would be reduced to
about 5% (90,000 children) at a 0.074/
4 standard and further reduced down to
about 3% (50,000 children) at a 0.064/
4 standard. Based on the 2002
simulations, the percent reduction
associated with just meeting a 0.064/4
standard relative to then current 0.084/
4 standard is about 62% which is about
twice the reduction in risk compared to
the estimated 31% reduction associated
with just meeting a 0.074/4 standard. As
shown in Table 2 above, similar patterns
were observed in reductions in lung
function risk for all school age children
in 12 urban areas associated with these
alternative standards.
Figures 6–5 and 6–6 in the 2007 Staff
Paper (EPA, 2007b) show the percent
reduction in non-accidental mortality
risk estimates associated with just
meeting the same alternative standards
discussed above relative to just meeting
the then current 0.084/4 standard for 12
urban areas, based on adjusting 2002
and 2004 air quality data. These figures
also provide perspective on the extent to
which the risks in these years (i.e., 2002
and 2004) are greater than those
estimated to occur upon meeting the
then current 0.084/4 standard (in terms
of a negative percent reduction relative
to a 0.084/4 standard). Based on the
2002 simulations (EPA, 2007b, Figure
6–5), the estimated reduction in nonaccidental mortality is about 30 to 70%
across the 12 urban areas for just
meeting a 0.064/4 standard relative to
the then current 0.084/4 standard. This
reduction is roughly twice the 15 to
30% estimated reduction across the 12
urban areas associated with just meeting
a 0.074/4 standard relative to a 0.084/4
standard. While the estimated incidence
is lower based on the 2004 simulations
(EPA, 2007b, Figure 6–6), the pattern of
risk reductions among alternative
standards is roughly similar to that
observed for the 2002 simulations.
In addition to the risk estimates for
lung function decrements in all school
age children and non-accidental
mortality that were estimated for 12
urban areas and lung function
decrements in asthmatic children for 5
urban areas, a similar pattern of
incremental reductions in health risks
was shown for two health outcomes
where risks were estimated in one city
only for each of these outcomes. These
included reductions in respiratory
symptoms in asthmatic children (EPA,
2007b; Boston, Table 6–9) and
respiratory-related hospital admissions
(EPA, 2007a; New York City, Table
6–10) associated with just meeting
alternative 8-hour standards set at 0.074
ppm, 0.070 ppm, and 0.064 ppm
relative to just meeting the then current
0.084 ppm standard. Using the 2002
simulation, a standard set at 0.074/4 is
estimated to reduce the incidence of
symptom days in children with
moderate to severe asthma in the Boston
area by about 15 percent relative to a
0.084/4 standard. With this reduction, it
is estimated that about 1 respiratory
symptom day in 8 during the O3 season
would be attributable to O3 exposure. A
standard set at 0.064/4 is estimated,
based on the 2002 simulation, to reduce
the incidence of symptom days in
children with moderate to severe
asthma in the Boston area by about a 25
to 30 percent reduction relative to a
0.084 ppm standard, which is roughly
twice the reduction compared to that
provided by a 0.074/4 standard. But
even with this reduction, it is estimated
that 1 respiratory symptom day in 10
during the O3 season is attributable to
O3 exposure.
As shown in Table 6–10 (EPA, 2007b)
estimated incidence of respiratoryrelated hospital admissions in one
urban area (New York City) was reduced
by 14 to 17 percent by a standard set at
0.074/4 relative to then current 0.084/4
standard, in the year with relatively
high and relatively low O3 air quality
levels, respectively. Similar to the
pattern observed for the other health
outcomes discussed above, the
reduction in incidence of respiratoryrelated hospital admissions for a 0.064/
4 standard relative to a 0.084/4 standard
is about twice that associated with a
0.074/4 standard relative to a 0.084/4
standard.
srobinson on DSKHWCL6B1PROD with PROPOSALS2
TABLE 3—NUMBER AND PERCENT OF ALL AND ASTHMATIC SCHOOL AGE CHILDREN IN 12 URBAN AREAS ESTIMATED TO
EXPERIENCE 8-HOUR OZONE EXPOSURES ABOVE 0.060 AND 0.070 PPM WHILE AT MODERATE OR GREATER EXERTION, ONE OR MORE TIMES PER SEASON ASSOCIATED WITH JUST MEETING ALTERNATIVE 8-HOUR STANDARDS
BASED ON ADJUSTING 2002 AND 2004 AIR QUALITY DATA1 2
Benchmark levels of exposures of
concern
(ppm)
8-Hour air quality
standards 3
(ppm)
All children, ages 5–18
Aggregate for 12 urban areas
Number of children exposed
(% of all children)
[Range across 12 cities, % of all children]
2002
0.070 ............................................
0.074
0.070
0.064
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2004
770,000 (4%)
[0–13%]
270,000 (1%)
[0–5%]
30,000 (0.2%)
[0–1%]
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20,000 (0%)
[0–1%]
0 (0%)
[0%]
0 (0%)
[0%]
E:\FR\FM\19JAP2.SGM
Asthmatic children, ages 5–18
Aggregate for 12 urban areas
Number of children exposed
(% of group)
[Range across 12 cities, % of group]
2002
120,000 (5%)
[0–14%]
50,000 (2%)
[0–6%]
10,000 (0.2%)
[0–1% ]
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0 (0%)
[0–1%]
0 (0%)
[0%]
0 (0%)
[0%]
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TABLE 3—NUMBER AND PERCENT OF ALL AND ASTHMATIC SCHOOL AGE CHILDREN IN 12 URBAN AREAS ESTIMATED TO
EXPERIENCE 8-HOUR OZONE EXPOSURES ABOVE 0.060 AND 0.070 PPM WHILE AT MODERATE OR GREATER EXERTION, ONE OR MORE TIMES PER SEASON ASSOCIATED WITH JUST MEETING ALTERNATIVE 8-HOUR STANDARDS
BASED ON ADJUSTING 2002 AND 2004 AIR QUALITY DATA1 2—Continued
Benchmark levels of exposures of
concern
(ppm)
8-Hour air quality
standards 3
(ppm)
All children, ages 5–18
Aggregate for 12 urban areas
Number of children exposed
(% of all children)
[Range across 12 cities, % of all children]
2002
0.060 ............................................
0.074
0.070
0.064
2004
4,550,000 (25%)
[1–48%]
3,000,000 (16%)
[1–36%]
950,000 (5%)
[0–17%]
Asthmatic children, ages 5–18
Aggregate for 12 urban areas
Number of children exposed
(% of group)
[Range across 12 cities, % of group]
2002
350,000 (2%)
[0–9%]
110,000 (1%)
[0–4%]
10,000 (0%)
[0–1%]
700,000 (27%)
[1–51%]
460,000 (18%)
[0–41%]
150,000 (6%)
[0–16%]
2004
50,000 (2%)
[0–9%]
10,000 (1%)
[0–3%]
0 (0%)
[0–1%]
or greater exertion is defined as having an 8-hour average equivalent ventilation rate ≥ 13 1-min/m2.
are the aggregate results based on 12 combined statistical areas (Atlanta, Boston, Chicago, Cleveland, Detroit, Houston, Los Angeles, New York, Philadelphia, Sacramento, St. Louis, and Washington, DC). Estimates are for the ozone season which is all year in Houston,
Los Angeles and Sacramento and March or April to September or October for the remaining urban areas.
3 All standards summarized here have the same form as the 8-hour standard established in 1997 which is specified as the 3-year average of
the annual 4th highest daily maximum 8-hour average concentrations must be at or below the concentration level specified. As described in the
2007 Staff Paper (EPA, 2007b, section 4.5.8), recent O3 air quality distributions have been statistically adjusted to simulate just meeting the
0.084 ppm standard and selected alternative standards. These simulations do not represent predictions of when, whether, or how areas might
meet the specified standards.
1 Moderate
srobinson on DSKHWCL6B1PROD with PROPOSALS2
2 Estimates
2. CASAC Views Prior to 2008 Decision
In comments on the second draft Staff
Paper, CASAC stated in its letter to the
Administrator, ‘‘the CASAC
unanimously recommends that the
current primary ozone NAAQS be
revised and that the level that should be
considered for the revised standard be
from 0.060 to 0.070 ppm’’ (Henderson,
2006c, p. 5). This recommendation
followed from its more general
recommendation that the 0.084 ppm
standard needed to be substantially
reduced to be protective of human
health, particularly in at-risk
subpopulations.
The CASAC Panel noted that
beneficial reductions in some adverse
health effects were estimated to occur
upon meeting the lowest standard level
(0.064 ppm) considered in the risk
assessment (Henderson, 2006c, p. 4).
The lower end of this range reflects
CASAC’s views that ‘‘[w]hile data exist
that adverse health effects may occur at
levels lower than 0.060 ppm, these data
are less certain and achievable gains in
protecting human health can be
accomplished through lowering the
ozone NAAQS to a level between 0.060
and 0.070 ppm.’’ (id.).
In a subsequent letter sent specifically
to offer advice to aid the Administrator
and Agency staff in developing the O3
proposal, the CASAC reiterated that the
Panel members ‘‘were unanimous in
recommending that the level of the
current primary ozone standard should
be lowered from 0.08 ppm to no greater
than 0.070 ppm’’ (Henderson, 2007, p.
2). Further, the CASAC Panel expressed
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the view that the 2006 Criteria
Document and 2007 Staff Paper,
together with the information in its
earlier letter, provide ‘‘overwhelming
scientific evidence for this
recommendation,’’ and emphasized the
Clean Air Act requirement that the
primary standard must be set to protect
the public health with an adequate
margin of safety (id.).
3. Basis for 2008 Decision on the
Primary Standard
This section presents the rationale for
the 2008 final decision on the primary
O3 standard as presented in the 2008
final rule (73 FR 16475). The EPA’s
conclusions on the level of the standard
began by noting that, having carefully
considered the public comments on the
appropriate level of the O3 standard,
EPA concluded that the fundamental
scientific conclusions on the effects of
O3 reached in the 2006 Criteria
Document and 2007 Staff Paper
remained valid. In considering the level
at which the primary O3 standard
should be set, EPA placed primary
consideration on the body of scientific
evidence available in the 2008 final
rulemaking on the health effects
associated with O3 exposure, while
viewing the results of exposure and risk
assessments as providing information in
support of the decision. In considering
the available scientific evidence, EPA
concluded that a focus on the proposed
range of 0.070 to 0.075 ppm was
appropriate in light of the large body of
controlled human exposure and
epidemiological and other scientific
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evidence. The notice stated that this
body of evidence did not support
retaining the then current 0.084 ppm
8-hour O3 standard, as suggested by
some commenters, nor did it support
setting a level just below 0.080 ppm,
because, based on the entire body of
evidence, such a level would not
provide a significant increase in
protection compared to the 0.084 ppm
standard. Further, such a level would
not be appreciably below the level in
controlled human exposure studies at
which adverse effects have been
demonstrated (i.e., 0.080 ppm). The
notice also stated that the body of
evidence did not support setting a level
of 0.060 ppm or below, as suggested by
other commenters. In evaluating the
information from the exposure
assessment and the risk assessment,
EPA judged that this information did
not provide a clear enough basis for
choosing a specific level within the
range of 0.075 to 0.070 ppm.
In making a final judgment about the
level of the primary O3 standard, EPA
noted that the level of 0.075 ppm is
above the range recommended by the
CASAC (i.e., 0.070 to 0.060 ppm). The
notice stated that in placing great weight
on the views of CASAC, careful
consideration had been given to
CASAC’s stated views and the scientific
basis and policy views for the range it
recommended. In so doing, EPA fully
agreed that the scientific evidence
supports the conclusion that the current
standard was not adequate and must be
revised.
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With respect to CASAC’s
recommended range of standard levels,
EPA observed that the basis for
CASAC’s recommendation appeared to
be a mixture of scientific and policy
considerations. While in general
agreement with CASAC’s views
concerning the interpretation of the
scientific evidence, EPA noted that
there was no bright line clearly directing
the choice of level, and the choice of
what was appropriate was clearly a
public health policy judgment entrusted
to the EPA Administrator. This
judgment must include consideration of
the strengths and limitations of the
evidence and the appropriate inferences
to be drawn from the evidence and the
exposure and risk assessments. In
reviewing the basis for the CASAC
Panel’s recommendation for the range of
the O3 standard, EPA observed that it
reached a different policy judgment
than the CASAC Panel based on
apparently placing different weight in
two areas: The role of the evidence from
the Adams studies and the relative
weight placed on the results from the
exposure and risk assessments. While
EPA found the evidence reporting
effects at the 0.060 ppm level from the
Adams studies to be too limited to
support a primary focus at this level,
EPA observed that the CASAC Panel
appeared to place greater weight on this
evidence, as indicated by its
recommendation of a range down to
0.060 ppm. It was noted that while the
CASAC Panel supported a level of 0.060
ppm, they also supported a level above
0.060, which indicated that they did not
believe that the results of Adams studies
meant that the level of the standard had
to be set at 0.060 ppm. The EPA also
observed that the CASAC Panel
appeared to place greater weight on the
results of the risk assessment as a basis
for its recommended range. In referring
to the risk assessment results for lung
function, respiratory symptoms,
hospital admissions and mortality, the
CASAC Panel concluded that:
‘‘beneficial effects in terms of reduction
of adverse health effects were calculated
to occur at the lowest concentration
considered (i.e., 0.064 ppm)’’
(Henderson, 2006c, p. 4). However, EPA
more heavily weighed the implications
of the uncertainties associated with the
Agency’s quantitative human exposure
and health risk assessments. Given these
uncertainties, EPA did not agree that
these assessment results appropriately
served as a primary basis for concluding
that levels at or below 0.070 ppm were
required for the 8-hour O3 standard.
The notice stated that after carefully
taking the above comments and
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considerations into account, and fully
considering the scientific and policy
views of the CASAC, EPA decided to
revise the level of the primary 8-hour O3
standard to 0.075 ppm. The EPA judged,
based on the available evidence, that a
standard set at this level would be
requisite to protect public health with
an adequate margin of safety, including
the health of sensitive subpopulations,
from serious health effects including
respiratory morbidity, that were judged
to be causally associated with shortterm and prolonged exposures to O3,
and premature mortality. The EPA also
judged that a standard set at this level
provides a significant increase in
protection compared to the 0.084 ppm
standard, and is appreciably below
0.080 ppm, the level in controlled
human exposure studies at which
adverse effects have been demonstrated.
At a level of 0.075 ppm, exposures at
and above the benchmark of 0.080 ppm
are essentially eliminated, and
exposures at and above the benchmark
of 0.070 are substantially reduced or
eliminated for the vast majority of
people in at-risk groups. A standard set
at a level lower than 0.075 would only
result in significant further public
health protection if, in fact, there is a
continuum of health risks in areas with
8-hour average O3 concentrations that
are well below the concentrations
observed in the key controlled human
exposure studies and if the reported
associations observed in
epidemiological studies are, in fact,
causally related to O3 at those lower
levels. Based on the available evidence,
EPA was not prepared to make these
assumptions. Taking into account the
uncertainties that remained in
interpreting the evidence from available
controlled human exposure and
epidemiological studies at very low
levels, EPA noted that the likelihood of
obtaining benefits to public health
decreased with a standard set below
0.075 ppm O3, while the likelihood of
requiring reductions in ambient
concentrations that go beyond those that
are needed to protect public health
increased. The EPA judged that the
appropriate balance to be drawn, based
on the entire body of evidence and
information available in the 2008 final
rulemaking, was to set the 8-hour
primary standard at 0.075 ppm. The
EPA expressed the belief that a standard
set at 0.075 ppm would be sufficient to
protect public health with an adequate
margin of safety, and did not believe
that a lower standard was needed to
provide this degree of protection. The
EPA further asserted that this judgment
appropriately considered the
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requirement for a standard that was
neither more nor less stringent than
necessary for this purpose and
recognized that the CAA does not
require that primary standards be set at
a zero-risk level, but rather at a level
that reduces risk sufficiently so as to
protect public health with an adequate
margin of safety.
4. CASAC Advice Following 2008
Decision
Following the 2008 decision on the O3
standard, serious questions were raised
as to whether the standard met the
requirements of the CAA. In April 2008,
the members of the CASAC Ozone
Review Panel sent a letter to EPA stating
‘‘In our most-recent letters to you on this
subject—dated October 2006 and March
2007—the CASAC unanimously
recommended selection of an 8-hour
average Ozone NAAQS within the range
of 0.060 to 0.070 parts per million for
the primary (human health-based)
Ozone NAAQS’’ (Henderson, 2008). The
letter continued: ‘‘The CASAC now
wishes to convey, by means of this
letter, its additional, unsolicited advice
with regard to the primary and
secondary Ozone NAAQS. In doing so,
the participating members of the
CASAC Ozone Review Panel are
unanimous in strongly urging you or
your successor as EPA Administrator to
ensure that these recommendations be
considered during the next review cycle
for the Ozone NAAQS that will begin
next year’’ (id.). Moreover, the CASAC
Panel noted that ‘‘numerous medical
organizations and public health groups
have also expressed their support of
these CASAC recommendations.’’ (id.)
The letter further stated the following
strong, unanimous view:
[the CASAC did] ‘‘not endorse the
new primary ozone standard as being
sufficient protective of public health.
The CASAC—as the Agency’s
statutorily-established science advisory
committee for advising you on the
national ambient air quality standards—
unanimously recommended decreasing
the primary standard to within the range
of 0.060–0.070 ppm. It is the
Committee’s consensus scientific
opinion that your decision to set the
primary ozone standard above this range
fails to satisfy the explicit stipulations
of the Clean Air Act that you ensure an
adequate margin of safety for all
individuals, including sensitive
populations’’ (Henderson, 2008).
5. Administrator’s Proposed
Conclusions
For the reasons discussed below, the
Administrator proposes to set a new
level for the 8-hour primary O3 within
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the range from 0.060 to 0.070 ppm.50 In
reaching this proposed decision, the
Administrator has considered: the
evidence-based considerations from the
2006 Criteria Document and the 2007
Staff Paper; the results of the exposure
and risk assessments discussed above
and in the 2007 Staff Paper; CASAC
advice and recommendations provided
in CASAC’s letters to the Administrator
both during and following the 2008
rulemaking; EPA staff
recommendations; and public
comments received in conjunction with
review of drafts of these documents and
on the 2007 proposed rule. In
considering what level of an 8-hour O3
standard is requisite to protect public
health with an adequate margin of
safety, the Administrator is mindful that
this choice requires judgments based on
an interpretation of the evidence and
other information that neither overstates
nor understates the strength and
limitations of the evidence and
information.
The Administrator notes that the most
certain evidence of adverse health
effects from exposure to O3 comes from
the controlled human exposure studies,
and that the large bulk of this evidence
derives from studies of exposures at
levels of 0.080 ppm and above. At those
levels, there is consistent evidence of
lung function decrements and
respiratory symptoms in healthy young
adults, as well as evidence of O3induced pulmonary inflammation,
airway responsiveness, impaired host
defense capabilities, and other
medically significant airway responses.
Moreover, there is no evidence that the
0.080 ppm exposure level is a threshold
for any of these types of respiratory
effects. Rather, there is now controlled
human exposure evidence, including
studies of lung function decrements and
respiratory symptoms at the 0.060 ppm
exposure level, that strengthens our
previous understanding that this array
of respiratory responses are likely to
occur in some healthy adults at such
lower levels.
In particular, the Administrator notes
two studies by Adams (2002, 2006),
newly available in the 2008 rulemaking,
that examined lung function and
respiratory symptom effects associated
with prolonged O3 exposures at levels
below 0.080 ppm, as well as EPA’s
50 As discussed above at the beginning of section
II, the Administrator has focused her
reconsideration of the primary O3 standard set in
the 2008 final rule on the level of the standard,
having decided not to reopen the 2008 final rule
with regard to the need to revise the 1997 primary
O3 standard to provide increased public health
protection nor with regard to the indicator,
averaging period, and form of the 2008 standard.
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reanalysis of the data from the Adams
(2006) study at a 0.060 ppm exposure
level. As discussed above, while the
author’s analysis focused on hour-byhour comparisons of effects, for the
purpose of exploring responses
associated with different patterns of
exposure, EPA’s reanalysis focused on
addressing the more fundamental
question of whether the pre- to postexposure change in lung function
differed between a 6.6-hour exposure to
0.060 ppm O3 versus a 6.6 hour
exposure to clean filtered air. The
Administrator notes that this reanalysis
found small, but statistically significant
group mean differences in lung function
decrements in healthy adults at the
0.060 ppm exposure level, which is now
the lowest-observed-effects level for
these effects. Moreover, these studies
also report a small percentage of
subjects (7 to 20 percent) experienced
moderate lung function decrements
(≥ 10 percent) at the 0.060 ppm exposure
level. While for active healthy people,
moderate levels of functional responses
(e.g., FEV1 decrements of ≥ 10% but
< 20%) and/or moderate respiratory
symptom responses would likely
interfere with normal activity for
relatively few responsive individuals,
the Administrator notes that for people
with lung disease, even moderate
functional or symptomatic responses
would likely interfere with normal
activity for many individuals, and
would likely result in more frequent use
of medication. Further, she notes that
CASAC indicated that a focus on the
lower end of the range of moderate
levels of functional responses (e.g., FEV1
decrements ≥ 10%) is most appropriate
for estimating potentially adverse lung
function decrements in people with
lung disease (Henderson, 2006c).
The Administrator also notes that
many public commenters on the 2007
proposed rule raised a number of
questions about the weight that should
be placed on the Adams studies and
EPA’s reanalysis of data from the Adams
(2006) study. Some commenters
expressed the view that the results of
these studies and EPA’s reanalysis
provided support for setting a standard
level below the proposed range, while
others raised questions about EPA’s
reanalysis and generally expressed the
view that the study results were not
robust enough to reach conclusions
about respiratory effects at the 0.060
ppm exposure level.51
Based on all the above considerations,
the Administrator concludes that the
Adams studies provide limited but
51 The EPA responded to these comments in the
2008 final rule (73 FR 16454–5).
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important evidence which adds to the
overall body of evidence that informs
her proposed decision on the range of
levels within which a standard could be
set that would be requisite to protect
public health with an adequate margin
of safety, including the health of at-risk
populations such as people with lung
disease.
In considering controlled human
exposure studies reporting O3-induced
pulmonary inflammation, airway
responsiveness, and impaired host
defense capabilities at exposure levels
down to 0.080 ppm, the lowest level at
which these effects have been tested, the
Administrator notes that these
physiological effects have been linked to
aggravation of asthma and increased
susceptibility to respiratory infection,
potentially leading to increased
medication use, increased school and
work absences, increased visits to
doctors’ offices and emergency
departments, and increased hospital
admissions, especially in people with
lung disease. These physiological effects
are all indicators of potential adverse
O3-related morbidity effects, which are
consistent with and lend plausibility to
the associations observed between O3
and adverse morbidity effects and
mortality effects in epidemiological
studies.
With regard to epidemiological
studies, the Administrator observes that
statistically significant associations
between ambient O3 levels and a wide
array of respiratory symptoms and other
morbidity outcomes including school
absences, emergency department visits,
and hospital admissions have been
reported in a large number of studies.
More specifically, positive and robust
associations were found between
ambient O3 concentrations and
respiratory hospital admissions and
emergency department visits, when
focusing particularly on the results of
warm season analyses. Taken together,
the overall body of evidence from
controlled human exposure,
toxicological, and epidemiological
studies supports the inference of a
causal relationship between acute
ambient O3 exposures and increased
respiratory morbidity outcomes
resulting in increased emergency
department visits and hospitalizations
during the warm season. Further, the
Administrator notes that recent
epidemiological evidence is highly
suggestive that O3 directly or indirectly
contributes to non-accidental and
cardiopulmonary-related mortality.
The Administrator also considered
the epidemiological evidence with
regard to considering potential effects
thresholds at the population level for
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morbidity and mortality effects. As
discussed above, while some studies
provide some indication of possible 8hour average threshold levels from
below about 0.025 to 0.035 ppm (within
the range of background concentrations)
up to approximately 0.050 ppm, other
studies observe linear concentrationresponse functions suggesting that there
may be no effects thresholds at the
population level above background
concentrations. In addition, other
studies conducted subset analyses that
included only days with ambient O3
concentrations below the level of the
then current standard, or below even
lower O3 concentrations, including a
level as low as 0.061 ppm, and continue
to report statistically significant
associations. The Administrator notes
that the relationships between ambient
O3 concentrations and lung function
decrements, respiratory symptoms,
indicators of respiratory morbidity
including increased respiratory-related
emergency department visits and
hospital admissions, and possibly
mortality reported in a large number of
studies likely extend down to ambient
O3 concentrations well below the level
of the standard set in 2008 (0.075 ppm),
in that the highest level at which there
is any indication of a threshold is
approximately 0.050 ppm. The
Administrator notes as well that toward
the lower end of the range of O3
concentrations observed in such studies,
ranging down to background levels (i.e.,
0.035 to 0.015 ppm), there is increasing
uncertainty as to whether the observed
associations remain plausibly related to
exposures to ambient O3, rather than to
the broader mix of air pollutants present
in the ambient atmosphere. She also
notes that there are limitations in
epidemiological studies that make
discerning population thresholds
difficult, as discussed above, such that
there is the possibility that thresholds
for individuals may exist in reported
associations at fairly low levels within
the range of air quality observed in the
studies but not be detectable as
population thresholds in
epidemiological analyses.
In looking more broadly at evidence
from animal toxicological, controlled
human exposure, and epidemiological
studies, the Administrator finds
substantial evidence, newly available
for consideration in the 2008
rulemaking, that people with asthma
and other preexisting pulmonary
diseases are among those at increased
risk from O3 exposure. As discussed
above, altered physiological,
morphological, and biochemical states
typical of respiratory diseases like
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asthma, COPD, and chronic bronchitis
may render people sensitive to
additional oxidative burden induced by
O3 exposure. Children and adults with
asthma are the group that has been
studied most extensively. Evidence from
controlled human exposure studies
indicates that asthmatics and people
with allergic rhinitis may exhibit larger
lung function decrements in response to
O3 exposure than healthy subjects and
that they can have larger inflammatory
responses. The Administrator also notes
that two large U.S. epidemiological
studies, as well as several smaller U.S.
and international studies, have reported
fairly robust associations between
ambient O3 concentrations and
measures of lung function and daily
symptoms (e.g., chest tightness, wheeze,
shortness of breath) in children with
moderate to severe asthma and between
O3 and increased asthma medication
use. These more serious responses in
asthmatics and others with lung disease
provide biological plausibility for the
respiratory morbidity effects observed in
epidemiological studies, such as
respiratory-related emergency
department visits and hospital
admissions.
The Administrator also observes that
a substantial body of evidence from
controlled human exposure and
epidemiological studies indicates that
relative to the healthy, non-asthmatic
subjects used in most controlled human
exposure studies, a greater proportion of
people with asthma may be affected,
and those who are affected may have as
large or larger lung function and
symptomatic responses to O3 exposures.
Thus, the Administrator concludes that
controlled human exposure studies of
lung function decrements and
respiratory symptoms that evaluate only
healthy, non-asthmatic subjects likely
underestimate the effects of O3 exposure
on asthmatics and other susceptible
populations.
In addition to the evidence-based
considerations discussed above, the
Administrator also considered
quantitative exposures and health risks
estimated to occur associated with air
quality simulated to just meet various
standard levels to help inform
judgments about a range of standard
levels for consideration that could
provide an appropriate degree of public
health protection. In so doing, she is
mindful of the important uncertainties
and limitations that are associated with
the exposure and risk assessments, as
discussed in more detail in the 2007
Staff Paper, and above in sections II.B
and II.C.1.b. Beyond these uncertainties,
the Administrator also recognized
important limitations related to the
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exposure and risk analyses. For
example, EPA did not have sufficient
information to evaluate all relevant atrisk groups (e.g., outdoor workers) or all
O3-related health outcomes (e.g.,
increased medication use, school
absences, emergency department visits),
and the scope of the analyses was
generally limited to estimating
exposures and risks in 12 urban areas
across the U.S., and to only five or just
one area for some health effects. Thus,
it is clear that national-scale public
health impacts of ambient O3 exposures
are much larger than the quantitative
estimates of O3-related incidences of
adverse health effects and the numbers
of children likely to experience
exposures of concern associated with
meeting the then current standard or
alternative standards. Taking these
limitations into account, the CASAC
advised EPA not to rely solely on the
results of the exposure and risk
assessments in considering alternative
standards, but also to place significant
weight on the body of evidence of O3related health effects in drawing
conclusions about an appropriate range
of levels for consideration. The
Administrator agrees with this advice.
Turning first to the results of the
exposure assessment, the Administrator
focused on the extent to which
alternative standard levels,
approximately at and below the 0.075
ppm O3 standard set in the 2008 final
rule, are estimated to reduce exposures
over the 0.060 and 0.070 ppm health
effects benchmark levels, for all and
asthmatic school age children in the 12
urban areas included in the
assessment.52 The Administrator also
took note that the lowest standard level
included in the exposure and health risk
assessments was 0.064 ppm and that
additional reductions in exposures over
the selected health benchmark levels
would be anticipated for just meeting a
0.060 ppm standard.
As an initial matter, the Administrator
recognized that the concept of
‘‘exposures of concern’’ is more
appropriately viewed as a continuum,
with greater confidence and less
uncertainty about the existence of
health effects at the upper end and less
confidence and greater uncertainty as
one considers increasingly lower O3
exposure levels. In considering the
concept of exposures of concern, the
Administrator also noted that it is
important to balance concerns about the
potential for health effects and their
52 As noted in section II.C.1.b.above, the
Administrator focused on alternative standards
with different levels but the same form and
averaging time as the primary standard set in 2008.
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severity with the increasing uncertainty
associated with our understanding of
the likelihood of such effects at lower
O3 levels. Within the context of this
continuum, estimates of exposures of
concern at discrete benchmark levels
provide some perspective on the public
health impacts of O3-related
physiological effects that have been
demonstrated in controlled human
exposure and toxicological studies but
cannot be evaluated in quantitative risk
assessments, such as lung inflammation,
increased airway responsiveness, and
changes in host defenses. They also help
in understanding the extent to which
such impacts have the potential to be
reduced by meeting alternative
standards. As discussed in II.C.1.a
above, these O3-related physiological
effects are plausibly linked to the
increased morbidity seen in
epidemiological studies (e.g., as
indicated by increased medication use
in asthmatics, school absences in all
children, and emergency department
visits and hospital admissions in people
with lung disease).
Estimates of the number of people
likely to experience exposures of
concern cannot be directly translated
into quantitative estimates of the
number of people likely to experience
specific health effects, since sufficient
information to draw such comparisons
is not available—if such information
were available, these health outcomes
would have been included in the
quantitative risk assessment. Due to
individual variability in responsiveness,
only a subset of individuals who have
exposures at and above a specific
benchmark level are expected to
experience such adverse health effects,
and susceptible population groups such
as those with asthma are expected to be
affected more by such exposures than
healthy individuals.
For the reasons discussed in section
II.C.1.b above, the Administrator has
concluded that it is appropriate to focus
on both the 0.060 and 0.070 ppm health
effect benchmarks for her decision on
the primary standard. In summary, the
focus on these two benchmark levels
reflects the following evidence-based
considerations, discussed above in
section II.C.1.a, that raise concerns
about adverse health effects likely
occurring at levels below 0.080 ppm: (1)
That there is limited, but important,
new evidence from controlled human
exposure studies showing lung function
decrements and respiratory symptoms
in some healthy subjects at 0.060 ppm;
(2) that asthmatics are likely to have
more serious responses than healthy
individuals; (3) that lung function is not
likely to be as sensitive a marker for O3
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effects as lung inflammation; and (4)
that there is epidemiological evidence
which reports associations between
ambient O3 concentrations and
respiratory symptoms, ED visits,
hospital admissions, and premature
mortality in areas with O3 levels that
extend well below 0.080 ppm.
Based on the exposure and risk
considerations discussed in detail in the
2007 Staff Paper and presented in
sections II.B and II.C.1.b above, the
Administrator notes the following
important observations from these
assessments: (1) There is a similar
pattern for all children and asthmatic
school age children in terms of
exposures of concern over selected
benchmark levels when estimates are
expressed in terms of percentage of the
population; (2) the aggregate estimates
of exposures of concern reflecting
estimates for the 12 urban areas
included in the assessment are
considerably larger for the benchmark
level of 0.060 ppm compared to the
0.070 ppm benchmark; (3) there is
notable year-to-year variability in
exposure and risk estimates with higher
exposure and risk estimates occurring in
simulations involving a year with
generally poorer air quality in most
areas (2002) compared to a year with
generally better air quality (2004); and
(4) there is significant city-to-city
variability in exposure and risk
estimates, with some cities receiving
considerably less protection associated
with air quality just meeting the same
standard. As discussed above, the
Administrator believes that it is
appropriate to consider not just the
aggregate estimates across all cities, but
also to consider the public health
impacts in cities that receive relatively
less protection from alternative
standards under consideration.
Similarly, the Administrator believes
that year-to-year variability should also
be considered in making judgments
about which standards will protect
public health with an adequate margin
of safety.
In addition, significant reductions in
exposures of concern and risk have been
estimated to occur across standard
levels analyzed. The magnitudes of
exposure and risk reductions estimated
to occur in going from a 0.074 ppm
standard to a 0.064 ppm standard are as
large as those estimated to occur in
going from the then current 0.084 ppm
standard to a 0.074 ppm standard.
Consequently, the reduction in risk that
can be achieved by going from a
standard of 0.074 ppm to a standard of
0.064 ppm is comparable to the risk
reduction that can be achieved by
moving from the 1997 O3 standard,
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effectively a 0.084 ppm standard, to a
standard very close to the 2008 standard
of 0.075 ppm.
The Administrator also observes that
estimates of exposures of concern
associated with air quality just meeting
the alternative standards below 0.080
ppm (i.e., 0.074, 0.070, and 0.064 ppm,
the levels included in the assessment)
are notably lower than estimates for
alternative standards set at and above
0.080 ppm. As shown in Table 6–8 in
the 2007 Staff Paper, just meeting a
0.080 ppm standard is associated with
an aggregate estimate of exposures of
concern of about 13% of asthmatic
children at the 0.070 ppm benchmark
level, ranging up to 31% in the city with
the least degree of protection in a year
with generally poorer air quality, and an
aggregate estimate of exposures of
concern of about 40% of asthmatic
children, ranging up to 63% in the city
with the least degree of protection at the
0.060 ppm benchmark level. Based on
the exposure estimates presented in
Table 3 in this notice, she observes that
standards included in the assessment
below 0.080 ppm (i.e., 0.074, 0.070, and
0.064 ppm), are estimated to have
substantially lower estimates of
exposures of concern at the 0.070 ppm
benchmark level. Similarly, she notes
that exposures of concern at the 0.060
ppm benchmark associated with
alternative standards below 0.080 ppm
are appreciably lower than exposures
associated with standards at or above
0.080 ppm, especially for standards set
at 0.064 and 0.070 ppm.
As noted previously, the
Administrator also recognizes that the
risk estimates for health outcomes
included in the risk assessment are
limited and that the overall health
effects evidence is indicative of a much
broader array of O3-related health effects
that are part of a ‘‘pyramid of effects’’
that include various indicators of
morbidity that could not be included in
the risk assessment (e.g., school
absences, increased medication use,
doctor’s visits, and emergency
department visits), some of which have
a greater impact on at-risk groups.
Consideration of such unquantified
risks for this array of health effects,
taken together with the estimates of
exposures of concern and the quantified
health risks discussed above, supports
the Administrator’s evidence-based
conclusion that revising the standard
level to a level well below 0.080 ppm
will provide important increased public
health protection, especially for at-risk
groups such as people with asthma or
other lung disease, as well as children
and older adults, particularly those
active outdoors, and outdoor workers.
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Based on the evidence- and exposure/
risk-based considerations discussed
above, the Administrator concludes that
it is appropriate to set the level of the
primary O3 standard to a level well
below 0.080 ppm, a level at which the
evidence provides a high degree of
certainty about the adverse effects of O3
exposure in healthy people, to provide
an adequate margin of safety for at-risk
groups. In selecting a proposed range of
levels, the Administrator believes it is
appropriate to consider the following
information: (1) The strong body of
evidence from controlled human
exposure studies evaluating healthy
people at exposure levels of 0.080 ppm
and above that demonstrated lung
function decrements, respiratory
symptoms, pulmonary inflammation,
and other medically significant airway
responses, as well as limited but
important evidence of lung function
decrements and respiratory symptoms
in healthy people down to O3 exposure
levels of 0.060 ppm; (2) the substantial
body of evidence from controlled
human exposure and epidemiological
studies indicating that people with
asthma are likely to experience larger
and more serious effects than healthy
people; (3) the body of epidemiological
evidence indicating associations are
observed for a wide range of serious
health effects, including respiratoryrelated emergency department visits and
hospital admissions and premature
mortality, across distributions of
ambient O3 concentrations that extend
below the current standard level of
0.075 ppm, as well as questions of
biological plausibility in attributing the
observed effects to O3 alone at the lower
end of the concentration ranges
extending down to background levels;
and (4) the estimates of exposures of
concern and risks for a range of health
effects that indicate that important
improvements in public health are very
likely associated with O3 levels just
meeting alternative standards,
especially for standards set at 0.070 and
0.064 ppm (the lowest levels included
in the assessment), relative to standards
set at and above 0.080 ppm.
The Administrator next considered
what standard level well below 0.080
ppm would be requisite to protect
public health, including the health of atrisk groups, with an adequate margin of
safety that is sufficient but not more
than necessary to achieve that result.
The assessment of a standard level calls
for consideration of both the degree of
risk to public health at alternative levels
of the standard as well as the certainty
that such risk will occur at any specific
level. Based on the information
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available in the 2008 rulemaking, there
is no evidence-based bright line that
indicates a single appropriate level.
Instead there is a combination of
scientific evidence and other
information that needs to be considered
as a whole in making this public health
policy judgment, and selecting a
standard level from a range of
potentially reasonable values.
As an initial matter, the Administrator
considered whether the standard level
of 0.075 ppm set in the 2008 final rule
is sufficiently below 0.080 ppm to be
requisite to protect public health with
an adequate margin of safety. In
considering this standard level, the
Administrator looked to the rationale for
selecting this level presented in the
2008 final rule, as summarized above in
section II.C.3. In that rationale, EPA
observed that a level of 0.075 ppm is
above the range of 0.060 to 0.070 ppm
recommended by CASAC, and that the
CASAC Panel appeared to place greater
weight on the evidence from the Adams
studies and on the results of the
exposure and risk assessments, whereas
EPA placed greater weight on the
limitations and uncertainties associated
with that evidence and the quantitative
exposure and risk assessments.
Additionally, EPA’s rationale did not
discuss and thus placed no weight on
exposures of concern relative to the
0.060 ppm benchmark. Further, EPA
concluded that ‘‘[a] standard set at a
lower level than 0.075 ppm would only
result in significant further public
health protection if, in fact, there is a
continuum of health risks in areas with
8-hour average O3 concentrations that
are well below the concentrations
observed in the key controlled human
exposure studies and if the reported
associations observed in
epidemiological studies are, in fact,
causally related to O3 at those lower
levels. Based on the available evidence,
[EPA] is not prepared to make these
assumptions’’ (73 FR 16483).
In reconsidering the entire body of
evidence available in the 2008
rulemaking, including the Agency’s own
assessment of the epidemiological
evidence in the 2006 Criteria Document,
and placing significant weight on the
views of CASAC, the Administrator now
concludes that important and significant
risks to public health are likely to occur
at a standard level of 0.075 ppm. She
judges that a standard level of 0.075
ppm is not sufficient to provide
protection with an adequate margin of
safety. In support of this conclusion, the
Administrator finds that setting a
standard that would protect public
health, including the health of at-risk
populations, with an adequate margin of
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safety should reasonably depend upon
giving some weight to the results of the
Adams studies and EPA’s reanalysis of
the Adams’s data, and to how effectively
alternative standard levels would serve
to limit exposures of concern relative to
the 0.060 ppm benchmark level as well
as to the 0.070 ppm benchmark level.
The Administrator notes that EPA’s risk
assessment estimates comparable risk
reductions in going from a 0.074 ppm
standard to a 0.064 ppm standard as
were estimated in going from the then
current 0.084 ppm standard down to a
0.074 ppm standard for an array of
health effects analyzed. These estimates
include reductions in risk for lung
function decrements in all and
asthmatic school age children,
respiratory symptoms in asthmatic
children, respiratory-related hospital
admissions, and non-accidental
mortality.
Further, based on the exposure
assessment estimates discussed above,
the Administrator notes that for air
quality just meeting a 0.074 ppm
standard, approximately 27% of
asthmatic school age children and 25%
of all school age children are estimated
to experience one or more exposures of
concern over the 0.060 ppm benchmark
level based on simulations for a year
with generally poorer air quality; this
estimate increases to about 50% of
asthmatic and all children in the city
with the least degree of protection. The
Administrator judges that these
estimates are large and strongly suggest
significant public health impacts would
likely remain in many areas with air
quality just meeting a 0.075 ppm O3
standard.
In light of these estimates and the
available evidence, the Administrator
agrees with CASAC’s conclusion that
important public health protections can
be achieved by a standard set below
0.075 ppm, within the range of 0.060 to
0.070 ppm. In addition, based on both
the evidence- and exposure/risk-based
considerations summarized above, the
Administrator concludes that a standard
set as high as 0.075 would not be
considered requisite to protect public
health with an adequate margin of
safety, and that consideration of lower
levels is warranted. In considering such
lower levels, the Administrator
recognizes that the CAA requires her to
reach a public health policy judgment as
to what standard would be requisite to
protect public health with an adequate
margin of safety, based on scientific
evidence and technical assessments that
have inherent uncertainties and
limitations. This judgment requires
making reasoned decisions as to what
weight to place on various types of
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evidence and assessments and on the
related uncertainties and limitations.
In selecting a level below 0.075 ppm
that would serve as an appropriate
upper end for a range of levels to
propose, the Administrator has
considered a more cautious approach to
interpreting the available evidence and
exposure/risk-based information—that
is, an approach that places significant
weight on uncertainties and limitations
in the information so as to avoid
potentially overestimating public health
risks and protection likely to be
associated with just meeting a particular
standard level. In so doing, she notes
that the most certain evidence of
adverse health effects from exposure to
O3 comes from the controlled human
exposure studies, and that the large bulk
of this evidence derives from studies of
exposures at levels of 0.080 ppm and
above. At those levels, there is
consistent evidence of lung function
decrements and respiratory symptoms
in healthy young adults, as well as
evidence of inflammation and other
medically significant airway responses.
Further, she takes note of the limited
but important evidence from controlled
human exposure studies indicating that
lung function decrements and
symptoms can occur in healthy people
at levels as low as 0.060 ppm, while also
recognizing the limitations in that
evidence, as discussed above in sections
II.A.1 and II.C.1.a. She also notes that
some people with asthma are likely to
experience larger and more serious
effects than the healthy subjects
evaluated in the controlled exposure
studies, while recognizing that there is
uncertainty about the magnitude of such
differences. In considering the available
epidemiological studies, she recognizes
that they provide evidence of serious
respiratory morbidity effects, including
respiratory-related emergency
department visits and hospital
admissions, and non-accidental
mortality at levels well below 0.080
ppm, while also recognizing that there
is increasing uncertainty associated
with the likelihood that such effects
occur at decreasing O3 levels down to
background levels. Considering the
exposure/risk information, as shown in
Table 3, the Administrator observes that
a standard set at 0.070 ppm would
likely substantially limit exposures of
concern relative to the 0.070 ppm
benchmark level, while affording far
less protection against exposures of
concern relative to the 0.060 ppm
benchmark level. To the extent that
more weight is placed on protection
relative to the higher benchmark level,
and more weight is placed on the
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uncertainties associated with the
epidemiological evidence, a standard set
at 0.070 ppm might be considered to be
adequately protective. Taken together,
this type of cautious approach to
interpreting the evidence and the
exposure/risk information serves as the
basis for the Administrator’s conclusion
that the upper end of the proposed
range should be set at 0.070 ppm O3.
In selecting a level that would serve
as an appropriate lower end for a range
of levels to propose, the Administrator
has considered a more precautionary
approach to interpreting the available
evidence and exposure/risk-based
information—that is, an approach that
places less weight on uncertainties and
limitations in the information so as to
avoid potentially underestimating
public health improvements likely to be
associated with just meeting a particular
standard level. In so doing, the
Administrator notes the limited, but
important evidence of a lowestobserved-effects level at 0.060 ppm O3
from controlled human exposure studies
reporting lung function decrements and
respiratory symptoms in healthy
subjects. Notably, these studies also
report that a small percentage of
subjects (7 to 20 percent) experienced
moderate lung function decrements
(≥ 10 percent) at the 0.060 ppm
exposure level, recognizing that for
people with lung disease, such
moderate functional or symptomatic
responses would likely interfere with
normal activity for many individuals,
and would likely result in more frequent
use of medication. In addition, a
substantial body of evidence indicates
that people with asthma are likely to
experience larger and more serious
effects than healthy people and
therefore controlled human exposure
studies done with healthy subjects
likely underestimate effects in this atrisk population.
Moreover, epidemiological studies
provide evidence of serious respiratory
morbidity effects, including respiratoryrelated emergency department visits and
hospital admissions, and non-accidental
mortality at O3 levels that may plausibly
extend down to at least 0.060 ppm even
when considering the uncertainties
inherent in such studies. The
Administrator notes that the controlled
human exposure studies conducted at
0.060 ppm provide some biological
plausibility for associations between
respiratory morbidity and mortality
effects found in epidemiological studies
and O3 exposures down to 0.060 ppm.
Considering the exposure information,
as shown in Table 3, the Administrator
observes that a standard set at 0.064
ppm would likely essentially eliminate
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exposures of concern relative to the
0.070 ppm benchmark level, while
appreciably limiting exposures of
concern relative to the 0.060 ppm
benchmark level to approximately 6
percent of asthmatic children in the
aggregate across 12 cities and up to 16
percent in the city that would receive
the least protection. While not
addressed in the exposure assessment
done as part of the 2008 rulemaking, a
standard set at 0.060 ppm would be
expected to provide somewhat greater
protection from such exposures, which
is important to the extent that more
weight is placed on providing
protection relative to the lower
benchmark level. Taken together, the
Administrator concludes that this
precautionary approach to interpreting
the evidence and the exposure/risk
information supports a level of 0.060
ppm as the lower end of the proposed
range.
The Administrator has also concluded
that the lower end of the proposed range
should not extend below 0.060 ppm O3.
In reaching this conclusion, she gives
significant weight to the
recommendation of the CASAC panel
that 0.060 ppm should be the lower end
of the range for consideration
(Henderson, 2006c). In the
Administrator’s view, the evidence from
controlled human exposure studies at
the 0.060 ppm exposure level, the
lowest level tested, is not robust enough
to support consideration of a lower
level. While some epidemiological
studies provide evidence of serious
respiratory morbidity effects and nonaccidental mortality with no evidence of
a threshold, the Administrator notes
that other studies provide evidence of a
potential threshold somewhat below
0.060 ppm. Moreover, there are
limitations in epidemiological studies
that make discerning population
thresholds difficult, including fewer
observations in the range of lower
concentrations, concerns related to
exposure measurement error, the
possible role of copollutants and effects
modifiers, and interindividual
differences in susceptibility to O3related effects. In the Administrator’s
judgment, these limitations in
epidemiological studies, including the
limitations in judging the causality of
observed associations at lower O3 levels,
and the lack of robust controlled human
exposure data at 0.060 ppm make it
difficult to interpret this evidence as a
basis for a standard level set below
0.060 ppm. Thus, in selecting 0.060
ppm as the lower end of the range for
the proposed level of the O3 standard,
the Administrator has taken into
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account information on the lowestobserved-effects levels in controlled
human exposure studies, indications of
possible thresholds reported in some
epidemiological studies, the increasing
uncertainty in the epidemiological
evidence at even lower levels, as well as
evidence about increased susceptibility
of people with asthma and also other
lung diseases. In so doing, she
concludes that a primary O3 standard
set below 0.060 ppm would be more
than is necessary to protect public
health with an adequate margin of safety
for at-risk groups.
In reaching her proposed decision, the
Administrator has also considered the
public comments that were received on
the 2007 proposed rule (72 FR 37818).
The Administrator notes that there were
sharply divergent views expressed by
two general sets of commenters with
regard to considering the health effects
evidence, results of exposure and risk
assessments, and the advice of the
CASAC panel. On one hand, medical
groups, health effects researchers,
public health organizations,
environmental groups, and some state,
tribal and local air pollution control
agencies strongly supported a standard
set within the range recommended by
the CASAC. These commenters
generally placed significant weight on
the more recent evidence from
controlled human exposure studies,
down to the 0.060 ppm exposure level,
as well as on the epidemiological
studies and the results of the exposure
and risk assessment conducted for the
2008 rulemaking. Many of these
commenters took a more precautionary
view and supported a standard set at
0.060 ppm O3, the lower end of the
CASAC recommended range. The
Administrator notes that these views are
generally consistent with her proposed
conclusions. On the other hand, another
group of commenters primarily
representing industry associations and
businesses and some state
environmental agencies, primarily
expressed the view that the more recent
evidence from controlled human
exposure, the epidemiological studies,
and the results of exposure and human
health risk assessments were so
uncertain that they did not provide a
basis for making any changes to the then
current 0.084 ppm O3 standard set in
1997. This group of commenters
generally argued that the health effects
evidence newly available in the 2008
rulemaking, the results of the exposure
and health risk assessments, and the
advice of the CASAC were flawed. For
the reasons discussed above, the
Administrator does not agree with the
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later group of commenters that
essentially no weight should be placed
on any of the new evidence or
assessments that were available for
consideration in the 2008 rulemaking.
Based on consideration of the entire
body of evidence and information
available in the 2008 rulemaking,
including exposure and risk estimates,
as well as the recommendations of
CASAC, the Administrator proposes to
set the level of the primary 8-hour O3
standard to a level within the range of
0.060 to 0.070 ppm. A standard level
within this range would reduce the risk
of a variety of health effects associated
with exposure to O3, including the
respiratory symptoms and lung function
effects demonstrated in the controlled
human exposure studies, and the
respiratory-related emergency
department visits, hospital admissions
and mortality effects observed in the
epidemiological studies. All of these
effects are indicative of a much broader
array of O3-related health endpoints,
such as school absences and increased
medication use, that are plausibly
linked to these observed effects.
Depending on the weight placed on the
evidence and information available in
the 2008 rulemaking, as well as the
uncertainties and limitations in the
evidence and information, a standard
could be set within this range at a level
that would be requisite to protect public
health with an adequate margin of
safety.
In reaching this proposed decision, as
discussed above, the Administrator has
focused on the nature of the increased
public health protection that would be
afforded by a standard set within the
proposed range of levels relative to the
protection afforded by the standard set
in 2008. Having considered the public
comments received on the 2007
proposed rule in reaching this proposed
decision that reconsiders the 2008 final
rule, the Administrator is interested in
again receiving public comment on the
benefits to public health associated with
a standard set at specific levels within
the proposed range relative to the
benefits associated with the standard set
in 2008.
D. Proposed Decision on the Level of the
Primary Standard
For the reasons discussed above, and
taking into account information and
assessments presented in the 2006
Criteria Document and 2007 Staff Paper,
the advice and recommendations of
CASAC, and public comments received
during the 2008 rulemaking, the
Administrator proposes to set a new
level for the 8-hour primary O3
standard. Specifically, the
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Administrator proposes to set the level
of the 8-hour primary O3 standard to
within a range of 0.060 to 0.070 ppm.
The proposed 8-hour primary standard
would be met at an ambient air
monitoring site when the 3-year average
of the annual fourth-highest daily
maximum 8-hour average O3
concentration is less than or equal to the
level of the standard that is
promulgated. Thus, the Administrator
proposes to set a standard with a level
within this range. She solicits comment
on this range and on the appropriate
weight to place on the various types of
available evidence, the exposure and
risk assessment results, and the
uncertainties and limitations related to
this information, as well as on the
benefits to public health associated with
a standard set within this range relative
to the benefits associated with the
standard set in 2008.
III. Communication of Public Health
Information
Information on the public health
implications of ambient concentrations
of criteria pollutants is currently made
available primarily through EPA’s Air
Quality Index (AQI) program. The
current Air Quality Index has been in
use since its inception in 1999 (64 FR
42530). It provides accurate, timely, and
easily understandable information about
daily levels of pollution (40 CFR 58.50).
The AQI establishes a nationally
uniform system of indexing pollution
levels for O3, carbon monoxide, nitrogen
dioxide, particulate matter and sulfur
dioxide. The AQI converts pollutant
concentrations in a community’s air to
a number on a scale from 0 to 500.
Reported AQI values enable the public
to know whether air pollution levels in
a particular location are characterized as
good (0–50), moderate (51–100),
unhealthy for sensitive groups (101–
150), unhealthy (151–200), very
unhealthy (201–300), or hazardous
(300–500). The AQI index value of 100
typically corresponds to the level of the
short-term NAAQS for each pollutant.
An AQI value greater than 100 means
that a pollutant is in one of the
unhealthy categories (i.e., unhealthy for
sensitive groups, unhealthy, very
unhealthy, or hazardous) on a given
day; whereas an AQI value at or below
100 means that a pollutant
concentration is in one of the
satisfactory categories (i.e., moderate or
good). Decisions about the pollutant
concentrations at which to set the
various AQI breakpoints, that delineate
the various AQI categories, draw
directly from the underlying health
information that supports the NAAQS
review.
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daily W 126 =
EPA proposes to require that the AQI be
reported in all metropolitan and
micropolitan statistical areas where O3
monitoring is required, as discussed
below in section VI. The Agency solicits
comments on our proposed approach to
AQI reporting requirements. We are also
revising 40 CFR Part 58, § 58.50(c) to
require the reporting requirements to be
based on the latest available census
figures, rather than the most recent
decennial U.S. census. This change is
consistent with our current practice of
using the latest population figures to
make monitoring requirements more
responsive to changes in population.
IV. Rationale for Proposed Decision on
the Secondary Standard
As an initial matter, the Administrator
notes that the 2008 final rule concluded
that (1) the protection afforded by the
1997 secondary O3 standard was ‘‘not
sufficient and that the standard needs to
be revised to provide additional
protection from known and anticipated
adverse effects on sensitive natural
vegetation and sensitive ecosystems,
and that such a revised standard could
also be expected to provide additional
protection to sensitive ornamental
vegetation’’ and (2) ‘‘that there is not
adequate information to establish a
separate secondary standard based on
other effects of O3 on public welfare’’ (73
FR 16497). The Administrator is not
reconsidering these aspects of the 2008
decision, which are based on the
reasons discussed in section IV.B of the
2008 final rule (73 FR 16489–16497).
The Administrator also notes that the
2008 final rule concluded that it was
appropriate to retain the O3 indicator for
i <8 pm
∑
wci Ci , where Ci = hourly O3 at hour i, and wc =
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The daily index values are then
summed over each month within the O3
season, and the annual highest
consecutive three month sum is
determined. The proposed standard
consists of the three-year average of this
highest three-month statistic, set at a
level within the range of 7 to 15 ppmhours.
As discussed more fully below, the
rationale for this proposed new standard
is based on a thorough review, in the
2006 Criteria Document, of the latest
scientific information on vegetation,
ecological and other public welfare
effects associated with the presence of
O3 in the ambient air. This rationale also
takes into account and is consistent
with: (1) Staff assessments of the most
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the secondary O3 standard. The
Administrator is not reconsidering this
aspect of the 2008 decision, which was
based on the reasons discussed in
sections IV.B and IV.C of the 2008 final
rule (73 FR 16489–16497). For these
reasons, the Administrator is not
reopening the 2008 decision with regard
to the need to revise the 1997 secondary
O3 standard to provide additional
protection from known and anticipated
adverse effects on sensitive natural
vegetation and sensitive ecosystems, nor
with regard to the appropriate indicator
for the secondary standard. Thus, the
information that follows in this section
specifically focuses on a reconsideration
of the 8-hour secondary O3 standard set
in the 2008 final rule for the purpose of
determining whether and, if so, how to
revise the form, averaging time, and
level of the standard to provide
appropriate protection from known and
anticipated adverse effects on sensitive
natural vegetation and sensitive
ecosystems.
This section presents the rationale for
the Administrator’s proposed decision
that the secondary O3 standard, which
was set identical to the revised primary
standard in the 2008 final rule, should
instead be a new cumulative, seasonal
standard. This standard is expressed in
terms of a concentration-weighted form
commonly called W126, which uses a
sigmoidal weighting function to assign a
weight to each hourly O3 concentration
within the 12-hour daylight period (8
am to 8 pm). This daily ozone index is
defined as follows:
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policy-relevant information in the 2006
Criteria Document and staff analyses of
air quality, vegetation effects evidence,
exposure, and risks, presented in the
2007 Staff Paper, upon which staff
recommendations for revisions to the
secondary O3 standard are based; (2)
CASAC advice and recommendations as
reflected in discussions of drafts of the
2006 Criteria Document and 2007 Staff
Paper at public meetings, in separate
written comments, and in CASAC’s
letters to the Administrator, both before
and after the 2008 rulemaking, and (3)
public comments received during
development of these documents, either
in conjunction with CASAC meetings or
separately; and on the 2007 proposed
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1
1 + 4403e−126C
⋅
rule, and (4) consideration of the degree
of protection to vegetation potentially
afforded by the 2008 8-hour standard.
In developing this rationale, the
Administrator has again focused on
direct O3 effects on vegetation,
specifically drawing upon an integrative
synthesis of the entire body of evidence
(EPA, 2006a, chapter 9), published
through early 2006, on the broad array
of vegetation effects associated with the
presence of O3 in the ambient air. In
addition, because O3 can also indirectly
affect other ecosystem components such
as soils, water, and wildlife, and their
associated ecosystem goods and
services, through its effects on
vegetation, a qualitative discussion of
these other indirect impacts is also
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In the 2008 rulemaking, the AQI for
O3 was revised by setting an AQI value
of 100 equal to 0.075 ppm, 8-hour
average, the level of the revised primary
O3 standard. The other AQI breakpoints
were also revised as follows: An AQI
value of 50 is set at 0.059 ppm; an AQI
value of 150 was set at 0.095 ppm; and
an AQI value of 200 was set at 0.115
ppm. All these levels are averaged over
8 hours. These levels were developed by
making proportional adjustments to the
other AQI breakpoints (i.e., AQI values
of 50, 150 and 200).
The Agency recognizes the
importance of revising the AQI in a
timely manner to be consistent with any
revisions to the NAAQS. Therefore,
having proposed to set a new level for
the 2008 primary 8-hour O3 standard in
this action, EPA also proposes to
finalize conforming changes to the AQI
in connection with the Agency’s final
decision on the level of the primary O3
standard. These conforming changes
would include setting the 100 level of
the AQI at the same level as that set for
the primary O3 standard resulting from
this rulemaking, and also making
proportional adjustments to AQI
breakpoints at the lower end of the
range (i.e., AQI values of 50, 150 and
200). EPA does not propose to change
breakpoints at the higher end of the
range (from 300 to 500), which would
apply to state contingency plans or the
Significant Harm Level (40 CFR 51.16),
because the information from this
reconsideration of the 2008 final rule
does not inform decisions about
breakpoints at those higher levels.
With respect to reporting
requirements (40 CFR Part 58, § 58.50),
2999
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included, though these effects were not
quantifiable at the time of the 2008
rulemaking. As discussed below in
section IV.A, the peer-reviewed
literature includes studies conducted in
the U.S., Canada, Europe, and many
other countries around the world.53 In
reconsidering this evidence, as was
concluded in the 2008 rulemaking, and
based on the body of scientific literature
assessed in the 2006 Criteria Document,
the Administrator continues to believe
that it is reasonable to conclude that a
secondary standard protecting the
public welfare from known or
anticipated adverse effects to trees and
native vegetation would also afford
increased protection from adverse
effects to other environmental
components relevant to the public
welfare, including ecosystem services
and function. Section IV.B focuses on
considerations related to biologically
relevant exposure indices. This
rationale also draws upon the results of
quantitative exposure and risk
assessments, discussed below in section
IV.C. Section IV.D focuses on the
considerations upon which the
Administrator’s proposed conclusions
are based. Considerations regarding a
cumulative seasonal standard as well as
an 8-hour standard are discussed, and
the rationale for the 2008 decision on
the secondary standard and CASAC
advice, given both prior to the
development of the 2007 proposed rule
and following the 2008 final rule, are
summarized. Finally, the
Administrator’s proposed conclusions
on the secondary standard are
presented. Section IV.E summarizes the
proposed decision on the secondary O3
standard and the solicitation of public
comments.
As with virtually any policy-relevant
vegetation effects research, there is
uncertainty in the characterization of
vegetation effects attributable to
exposure to ambient O3. As discussed
below, however, research conducted
since the 1997 review provides
important information coming from
field-based exposure studies, including
free air, gradient, and biomonitoring
surveys, in addition to the more
traditional open top chamber (OTC)
studies. Moreover, the newly available
studies evaluated in the 2006 Criteria
Document have undergone intensive
scrutiny through multiple layers of peer
review and many opportunities for
public review and comment. While
53 In its assessment of the evidence judged to be
most relevant to making decisions on the level of
the O3 secondary standard, however, EPA has
placed greater weight on U.S. studies, due to the
often species-, site- and climate-specific nature of
O3-related vegetation response.
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important uncertainties remain, the
review of the vegetation effects
information has been extensive and
deliberate. In the judgment of the
Administrator, the intensive evaluation
of the scientific evidence that has
occurred provides an adequate basis for
this reconsideration of the 2008
rulemaking.
A. Vegetation Effects Information
This section outlines key information
contained in the 2006 Criteria
Document (chapter 9) and in the 2007
Staff Paper (chapter 7) on known or
anticipated effects on public welfare
associated with the presence of O3 in
ambient air. The information
highlighted here summarizes: (1) New
information available in the 2008
rulemaking on potential mechanisms for
vegetation effects associated with
exposure to O3; (2) the nature of effects
on vegetation that have been associated
with exposure to O3 and consequent
potential impacts on ecosystems; and (3)
considerations in characterizing what
constitutes an adverse welfare impact of
O3.
Exposures to O3 have been associated
quantitatively and qualitatively with a
wide range of vegetation effects. The
decision in the 1997 review to set a
more protective secondary standard
primarily reflected consideration of the
quantitative information on vegetation
effects available at that time,
particularly growth impairment (e.g.,
biomass loss) in sensitive forest tree
species during the seedling growth stage
and yield loss in important commercial
crops. This information, derived mainly
using the open top chamber (OTC)
exposure method, found cumulative,
seasonal O3 exposures were most
strongly associated with observed
vegetation response. The 2006 Criteria
Document discusses a number of
additional studies that support and
strengthen key conclusions regarding O3
effects on vegetation and ecosystems
found in the previous Criteria Document
(EPA, 1996a, 2006a), including further
clarification of the underlying
mechanistic and physiological processes
at the sub-cellular, cellular, and whole
system levels within the plant. More
importantly, however, in the context of
this review, new quantitative
information is now available across a
broader array of vegetation effects (e.g.,
growth impairment during seedlings,
saplings and mature tree growth stages,
visible foliar injury, and yield loss in
annual crops) and across a more diverse
set of exposure methods, including
chamber, free air, gradient, model, and
field-based observation. The nonchambered, field-based study results
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begin to address one of the key data
gaps cited by EPA in the 1997 review.
The following discussion of the
policy-relevant science regarding
vegetation effects associated with
cumulative, seasonal exposures to
ambient levels of O3 integrates
information from the 2006 Criteria
Document (chapter 9) and the 2007 Staff
Paper (chapter 7).
1. Mechanisms
Scientific understanding regarding O3
impacts at the genetic, physiological,
and mechanistic levels helps to explain
the biological plausibility and
coherence of the evidence for O3induced vegetation effects and informs
the interpretation of predictions of risk
associated with vegetation response at
ambient O3 exposure levels. In most
cases, the mechanisms of response are
similar regardless of the degree of
sensitivity of the species. The evidence
assessed in the 2006 Criteria Document
(EPA, 2006a) regarding the O3-induced
changes in physiology continues to
support the information discussed in
the 1997 review (EPA, 1996a, 2006a). In
addition, during the last decade
understanding of the cellular processes
within plants has been further clarified
and enhanced. This section reviews the
key scientific conclusions identified in
1996 Criteria Document (EPA, 1996a),
and incorporates recent information
from the Criteria Document (EPA,
2006a). This section describes: (1) Plant
uptake of O3, (2) O3-induced cellular to
systemic response, (3) plant
compensation and detoxification
mechanisms, (4) O3-induced changes to
plant metabolism, and (5) plant
response to chronic O3 exposures.
a. Plant Uptake of Ozone
To cause injury, O3 must first enter
the plant through openings in the leaves
called stomata. Leaves exist in a three
dimensional environment called the
plant canopy, where each leaf has a
unique orientation and receives a
different exposure to ambient air,
microclimatological conditions, and
sunlight. In addition, a plant may be
located within a stand of other plants
which further modifies ambient air
exchange with individual leaves. Not all
O3 entering a plant canopy is absorbed
into the leaf stomata, but may be
adsorbed to other surfaces e.g., leaf
cuticles, stems, and soil (termed nonstomatal deposition) or scavenged by
reactions with intra-canopy biogenic
VOCs and naturally occurring NOx
emissions from soils. Because O3 does
not typically penetrate the leaf’s cuticle,
it must reach the stomatal openings in
the leaf for absorption to occur. The
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movement of O3 and other gases such as
CO2 into and out of leaves is controlled
by stomatal guard cells that regulate the
size of the stomatal apertures. These
guard cells respond to a variety of
internal species-specific factors as well
as external site specific environmental
factors such as light, temperature,
humidity, CO2 concentration, soil
fertility, water status, and in some cases,
the presence of air pollutants, including
O3. These modifying factors produce
stomatal conductances that vary
between leaves of the same plant,
individuals and genotypes within a
species as well as diurnally and
seasonally.
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b. Cellular to Systemic Response
Once inside the leaf, O3 can react with
a variety of biochemical compounds
that are exposed to the air spaces within
the leaf or it can be dissolved into the
water lining the cell wall of the air
spaces. Once in the aqueous phase, O3
can be rapidly altered to form oxidative
products that can diffuse more readily
into and through the cell and react with
many biochemical compounds. Early
steps in a series of O3-induced events
that can lead to leaf injury seems to
involve alteration in cell membrane
function, including membrane transport
properties (EPA, 2006a) and/or reactions
with organic molecules that in certain
circumstances result in the generation of
signaling compounds. The generation of
such signaling compounds can lead to a
cascade of events. One such signaling
molecule is hydrogen peroxide (H2O2).
The presence of higher-than-normal
levels of H2O2 within the leaf is a
potential trigger for a set of metabolic
reactions that include those typical of
the well documented ‘‘wounding’’
response or pathogen defense pathway
generated by cutting of the leaf or by
pathogen/insect attack. Ethylene is
another compound produced when
plants are subjected to biotic or abiotic
stressors. Increased ethylene production
by plants exposed to O3 stress was
identified as a consistent marker for O3
exposure in studies conducted decades
ago (Tingey et al., 1976).
c. Compensation and Detoxification
Ozone injury will not occur if (1) the
rate and amount of O3 uptake is small
enough for the plant to detoxify or
metabolize O3 or its metabolites or (2)
the plant is able to repair or compensate
for the O3 impacts (Tingey and Taylor,
1982; U.S. EPA, 1996a). With regard to
the first, a few studies have documented
direct stomatal closure or restriction in
the presence of O3 in some species,
which limits O3 uptake and potential
subsequent injury. This response may
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be initiated ranging from within
minutes to hours or days of exposure
(Moldau et al., 1990; Dann and Pell,
1989; Weber et al., 1993). However,
exclusion of O3 simultaneously restricts
the uptake of CO2, which also limits
photosynthesis and growth. In addition,
antioxidants present in plants can
effectively protect tissue against damage
from low levels of oxidants by
dissipating excess oxidizing power.
Since 1996, the role of detoxification in
providing a level of resistance to O3 has
been further investigated. A number of
antioxidants have been found in plants.
However, the pattern of changes in the
amounts of these antioxidants varies
greatly among different species and
conditions. Most recent reports indicate
that ascorbate within the cell wall
provides the first significant
opportunity for detoxification to occur.
In spite of the new research, however,
it is still not clear as to what extent
detoxification protects against O3 injury.
Specifically, data are needed on
potential rates of antioxidant
production, sub-cellular location(s) of
antioxidants, and whether generation of
these antioxidants in response to O3induced stress potentially diverts
resources and energy away from other
vital uses. Thus, the 2006 Criteria
Document concludes that scientific
understanding of the detoxification
mechanisms is not yet complete and
requires further investigation (EPA,
2006a).
Regarding the second, once O3 injury
has occurred in leaf tissue, some plants
are able to repair or compensate for the
impacts. In general, plants have a
variety of compensatory mechanisms for
low levels of stress including
reallocation of resources, changes in
root/shoot ratio, production of new
tissue, and/or biochemical shifts, such
as increased photosynthetic capacity in
new foliage and changes in respiration
rates, indicating possible repair or
replacement of damaged membranes or
enzymes. Since these mechanisms are
genetically determined, not all plants
have the same complement of
compensatory mechanisms or degree of
tolerance, and these may vary over the
life of the plant as not all stages of a
plant’s development are equally
sensitive to O3. At higher levels or over
longer periods of O3 stress, some of
these compensatory mechanisms, such
as a reallocation of resources away from
storage in the roots in favor of leaves or
shoots, could occur at a cost to the
overall health of the plant. However, it
is not yet clear to what degree or how
the use of plant resources for repair or
compensatory processes affects the
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overall carbohydrate budget or
subsequent plant response to O3 or other
stresses (EPA, 1996a, EPA, 2006a).
d. Changes to Plant Metabolism
Ozone inhibits photosynthesis, the
process by which plants produce energy
rich compounds (e.g., carbohydrates) in
the leaves. This impairment can result
from direct impact to chloroplast
function and/or O3-induced stomatal
closure resulting in reduced uptake of
CO2. A large body of literature
published since 1996 has further
elucidated the mechanism of effect of O3
within the chloroplast. Pell et al. (1997)
showed that O3 exposure results in a
loss of the central carboxylating enzyme
that plays an important role in the
production of carbohydrates. Due to its
central importance, any decrease in this
enzyme may have severe consequences
for the plant’s productivity. Several
recent studies have found that O3 has a
greater effect as leaves age, with the
greatest impact of O3 occurring on the
oldest leaves (Fiscus et al., 1997; Reid
and Fiscus, 1998; Noormets et al., 2001;
Morgan et al., 2004). The loss of this key
enzyme as a function of increasing O3
exposure is also linked to an early
senescence or a speeding up of normal
development leading to senescence. If
total plant photosynthesis is sufficiently
reduced, the plant will respond by
reallocating the remaining carbohydrate
at the level of the whole organism (EPA,
1996a, 2006a). This reallocation of
carbohydrate away from the roots into
above ground vegetative components
can have serious implications for
perennial species, as discussed below.
e. Plant Response to Chronic Ozone
Exposures
Though many changes that occur with
O3 exposure can be observed within
hours, or perhaps days, of the exposure,
including those connected with
wounding, other effects take longer to
occur and tend to become most obvious
after chronic seasonal exposures to low
O3 concentrations. These lower chronic
exposures have been linked to
senescence or some other physiological
response very closely linked to
senescence. In perennial plant species,
a reduction in carbohydrate storage in
one year may result in the limitation of
growth the following year (Andersen et
al., 1997). Such ‘‘carry-over’’ effects have
been documented in the growth of tree
seedlings (Hogsett et al., 1989; Sasek et
al., 1991; Temple et al., 1993; EPA,
1996a) and in roots (Andersen et al.,
1991; EPA, 1996a). Though it is not
fully understood how chronic seasonal
O3 exposure affects long-term growth
and resistance to other biotic and abiotic
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insults in long-lived trees, accumulation
of these carry-over effects over time
could affect survival and reproduction.
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2. Nature of Effects
Ozone injury at the cellular level can
accumulate sufficiently to induce effects
at the level of a whole leaf or plant.
These larger scale effects can include:
Reduced carbohydrate production and/
or reallocation; reduced growth and/or
reproduction; visible foliar injury and/
or premature senescence; and reduced
plant vigor. Much of what is now
known about these O3-related effects, as
summarized below, is based on research
that was available in the 1997 review.
Studies available in the 2008
rulemaking continue to support and
expand this knowledge (EPA, 2006a).
a. Carbohydrate Production and
Allocation
When total plant photosynthesis is
sufficiently reduced, the plant will
respond by reallocating the remaining
carbohydrate at the level of the whole
organism. Many studies have
demonstrated that root growth is more
sensitive to O3 exposure than stem or
leaf growth (EPA, 2006a). When fewer
carbohydrates are present in the roots,
less energy is available for root-related
functions such as acquisition of water
and nutrients. In addition, by inhibiting
photosynthesis and the amount of
carbohydrates available for transfer to
the roots, O3 can disrupt the association
between soil fungi and host plants.
Fungi in the soil form a symbiotic
relationship with many terrestrial
plants. For host plants, these fungi
improve the uptake of nutrients, protect
the roots against pathogens, produce
plant growth hormones, and may
transport carbohydrates from one plant
to another (EPA, 1996a). These below
ground effects have recently been
documented in the field (Grulke et al.,
1998; Grulke and Balduman, 1999). Data
from a long-studied pollution gradient
in the San Bernardino Mountains of
southern California suggest that O3
substantially reduces root growth in
natural stands of Ponderosa pine (Pinus
ponderosa). Root growth in mature trees
was decreased at least 87 percent in a
high-pollution site as compared to a
low-pollution site (Grulke et al., 1998),
and a similar pattern was found in a
separate study with whole-tree harvest
along this gradient (Grulke and
Balduman, 1999). Though effects on
other ecosystem components were not
examined, a reduction of root growth of
this magnitude could have significant
implications for the below-ground
communities at those sites. Because
effects on leaf and needle carbohydrate
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content under O3 stress can range from
a reduction (Barnes et al., 1990; Miller
et al., 1989), to no effect (Alscher et al.,
1989), to an increase (Luethy-Krause
and Landolt, 1990), studies that
examine only above-ground vegetative
components may miss important O3induced changes below ground. These
below-ground changes could signal a
shift in nutrient cycling with
significance at the ecosystem level
(Young and Sanzone, 2002).
b. Growth Effects on Trees
Studies comparing the O3-related
growth response of different vegetation
types (coniferous and deciduous) and
growth stages (e.g., seedling and mature)
have established that on average,
individual coniferous trees are less
sensitive than deciduous trees, and
deciduous trees are generally less
sensitive to O3 than most annual plants,
with the exception of a few fast growing
deciduous tree species (e.g., quaking
aspen, black cherry, and cottonwood),
which are highly sensitive and, in some
cases, as much or more sensitive to O3
than sensitive annual plants. In
addition, studies have shown that the
relationship between O3 sensitivity in
seedling and mature growth stages of
trees can vary widely, with seedling
growth being more sensitive to O3
exposures in some species, while in
others, the mature growth stage is the
more O3 sensitive. In general, mature
deciduous trees are likely to be more
sensitive to O3 than deciduous
seedlings, and mature evergreen trees
are likely to be less sensitive to O3 than
their seedling counterparts. Based on
these results, stomatal conductance, O3
uptake, and O3 effects cannot be
assumed to be equivalent in seedlings
and mature trees.
In the 1997 review (EPA, 1996b),
analyses of the effects of O3 on trees
were limited to 11 tree species for
which concentration-response (C–R)
functions for the seedling growth stage
had been developed from OTC studies
conducted by the National Health and
Environmental Effects Research Lab,
Western Ecology Division (NHEERL–
WED). A number of replicate studies
were conducted on these species,
leading to a total of 49 experimental
cases. The 2007 Staff Paper presented a
graph of the composite regression
equation that combines the results of the
C–R functions developed for each of the
49 cases. The NHEERL–WED study
predicted relative biomass loss at
various exposure levels in terms of a 12hour W126. For example, 50 percent of
the tree seedling cases would be
protected from greater than 10 percent
biomass loss at a 3-month, 12-hour
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W126 of approximately 24 ppm-hour,
while 75 percent of cases would be
protected from 10 percent biomass loss
at a 3-month, 12-hour W126 level of
approximately 16 ppm-hour.
Since the 1997 review, only a few
studies have developed C–R functions
for additional tree seedling species
(EPA, 2006a). One such study is of
particular importance because it
documented growth effects in the field
of a similar magnitude as those
previously seen in OTC studies but
without the use of chambers or other
fumigation methods (Gregg et al., 2003).
This study placed eastern cottonwood
(Populus deltoides) saplings at sites
along a continuum of ambient O3
exposures that gradually increased from
urban to rural areas in the New York
City area (Gregg et al., 2003). Eastern
cottonwood is a fast growing O3
sensitive tree species that is important
ecologically along streams and
commercially for pulpwood, furniture
manufacturing, and as a possible new
source for energy biomass (Burns and
Hankola, 1990). Gregg et al. (2003)
found that the cottonwood saplings
grown in urban New York City grew
faster than saplings grown in downwind
rural areas. Because these saplings were
grown in pots with carefully controlled
soil nutrient and moisture levels, the
authors were able to control for most of
the differences between sites. After
carefully considering these and other
factors, the authors concluded the
primary explanation for the difference
in growth was the gradient of
cumulative O3 exposures that increased
as one moved downwind from urban to
less urban and more rural sites. It was
determined that the lower O3 exposure
within the city center was due to NOX
titration reactions which removed O3
from the ambient air. The authors were
able to reproduce the growth responses
observed in the field in a companion
OTC experiment, confirming O3 as the
stressor inducing the growth loss
response (Gregg et al., 2003).
Another recent set of studies
employed a modified Free Air CO2
Enrichment (FACE) methodology to
expose vegetation to elevated O3
without the use of chambers. This
exposure method was originally
developed to expose vegetation to
elevated levels of CO2, but was later
modified to include O3 exposure in
Illinois (SoyFACE) and Wisconsin
(AspenFACE) for soybean and
deciduous trees, respectively (Dickson
et al., 2000; Morgan et al., 2004). The
FACE method releases gas (e.g., CO2, O3)
from a series of orifices placed along the
length of the vertical pipes surrounding
a circular field plot and uses the
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prevailing wind to distribute it. This
exposure method has many
characteristics that differ from those
associated with the OTC. Most
significantly, this exposure method
more closely replicates conditions in the
field than do OTCs. This is because,
except for O3 levels which are varied
across co-located plots, plants are
exposed to the same ambient growing
conditions that occur naturally in the
field (e.g., location-specific pollutant
mixtures; climate conditions such as
light, temperature and precipitation;
insect pests, pathogens). By using one of
several co-located plots as a control
(e.g., receives no additional O3), and by
exposing the other rings to differing
levels of elevated O3, the growth
response signal that is due solely to the
change in O3 exposure can be clearly
determined. Furthermore, the FACE
system can expand vertically with the
growth of trees, allowing for exposure
experiments to span numerous years, an
especially useful capability in forest
research.
On the other hand, the FACE
methodology also has the undesirable
characteristic of potentially creating
hotspots near O3 gas release orifices or
gradients of exposure in the outer ring
of trees within the plots, such that
averaging results across the entire ring
potentially overestimates the response.
In recognition of this possibility,
researchers at the AspenFACE
experimental site only measured trees in
the center core of each ring, (e.g., at least
5–6 meters away from the emission sites
of O3) (Dickson et al., 2000, Karnosky et
al., 2005). By taking this precaution, it
is unlikely that their measurements
were influenced by any potential
hotspots or gradients of exposure within
the FACE rings. Taking all of the above
into account, results from the Wisconsin
FACE site on quaking aspen appear to
demonstrate that the detrimental effects
of O3 exposure seen on tree growth and
symptom expression in OTCs can be
observed in the field using this exposure
method (Karnosky et al., 1999; 2005).
The 2007 Staff Paper thus concluded
that the combined evidence from the
AspenFACE and Gregg et al. (2003) field
studies provide compelling and
important support for the
appropriateness of continued use of the
C–R functions derived using OTC from
the NHEERL–WED studies to estimate
risk to these tree seedlings under
ambient field exposure conditions.
These studies make a significant
contribution to the coherence of the
weight of evidence available in this
review and provide additional evidence
that O3-induced effects observed in
chambers also occur in the field.
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Trees and other perennials, in
addition to cumulating the effects of O3
exposures over the annual growing
season, can also cumulate effects across
multiple years. It has been reported that
effects can ‘‘carry over’’ from one year to
another (EPA, 2006a). Growth affected
by a reduction in carbohydrate storage
in one year may result in the limitation
of growth in the following year
(Andersen et al., 1997). Carry-over
effects have been documented in the
growth of some tree seedlings (Hogsett
et al., 1989; Simini et al., 1992; Temple
et al., 1993) and in roots (Andersen et
al., 1991; EPA, 1996a). On the basis of
past and recent OTC and field study
data, ambient O3 exposures that occur
during the growing season in the United
States are sufficient to potentially affect
the annual growth of a number of
sensitive seedling tree species.
However, because most studies do not
take into account the possibility of carry
over effects on growth in subsequent
years, the true implication of these
annual biomass losses may be missed. It
is likely that under ambient exposure
conditions, some sensitive trees and
perennial plants could experience
compounded impacts that result from
multiple year exposures.
c. Visible Foliar Injury
Cellular injury to leaves due to
exposure to O3 can and often does
become visible. Acute injury usually
appears within 24 hours after exposure
to O3 and, depending on species, can
occur under a range of exposures and
durations from 0.040 ppm for a period
of 4 hours to 0.410 ppm for 0.5 hours
for crops and 0.060 ppm for 4 hours to
0.510 ppm for 1 hour for trees and
shrubs (Jacobson, 1977). Chronic injury
may be mild to severe. In some cases,
cell death or premature leaf senescence
may occur. The significance of O3 injury
at the leaf and whole plant levels
depends on how much of the total leaf
area of the plant has been affected, as
well as the plant’s age, size,
developmental stage, and degree of
functional redundancy among the
existing leaf area. As a result, it is not
presently possible to determine, with
consistency across species and
environments, what degree of injury at
the leaf level has significance to the
vigor of the whole plant.
The presence of visible symptoms due
to O3 exposures can, however, by itself,
represent an adverse impact to the
public welfare. Specifically, it can
reduce the market value of certain leafy
crops (such as spinach, lettuce), impact
the aesthetic value of ornamentals (such
as petunia, geranium, and poinsettia) in
urban landscapes, and affect the
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aesthetic value of scenic vistas in
protected natural areas such as national
parks and wilderness areas. Many
businesses rely on healthy looking
vegetation for their livelihoods (e.g.,
horticulturalists, landscapers, Christmas
tree growers, farmers of leafy crops) and
a variety of ornamental species have
been listed as sensitive to O3 (Abt
Associates Inc., 1995). Though not
quantified, there is likely some level of
economic impact to businesses and
homeowners from O3-related injury on
sensitive ornamental species due to the
cost associated with more frequent
replacement and/or increased
maintenance (fertilizer or pesticide
application). In addition, because O3 not
only results in discoloration of leaves
but can lead to more rapid senescence
(early shedding of leaves) there
potentially could be some lost tourist
dollars at sites where fall foliage is less
available or attractive.
The use of sensitive plants as
biological indicators to detect
phytotoxic levels of O3 is a longstanding
and effective methodology (Chappelka
and Samuelson, 1998; Manning and
Krupa, 1992). Each bioindicator exhibits
typical O3 injury symptoms when
exposed under appropriate conditions.
These symptoms are considered
diagnostic as they have been verified in
exposure-response studies under
experimental conditions. In recent
years, field surveys of visible foliar
injury symptoms have become more
common, with greater attention to the
standardization of methods and the use
of reliable indicator species (Campbell
et al., 2000; Smith et al., 2003).
Specifically, the United States Forest
Service (USFS) through the Forest
Health Monitoring Program (FHM)
(1990–2001) and currently the Forest
Inventory and Analysis (FIA) Program
collects data regarding the incidence
and severity of visible foliar injury on a
variety of O3 sensitive plant species
throughout the U.S. (Coulston et al.,
2003, 2004; Smith et al., 2003).
Since the conclusion of the 1997
review, the FIA monitoring program
network and database has continued to
expand. This network continues to
document foliar injury symptoms in the
field under ambient exposure
conditions. Recent survey results show
that O3-induced foliar injury incidence
is widespread across the country. The
visible foliar injury indicator has been
identified as a means to track O3
exposure stress trends in the nation’s
natural plant communities as
highlighted in EPA’s most recent Report
on the Environment (EPA, 2003a; https://
www.epa.gov/indicators/roe).
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Previous Criteria Documents have
noted the difficulty in relating visible
foliar injury symptoms to other
vegetation effects such as individual
tree growth, stand growth, or ecosystem
characteristics (EPA, 1996a) and this
difficulty remains to the present day
(EPA, 2006a). It is important to note that
direct links between O3 induced visible
foliar injury symptoms and other
adverse effects are not always found.
Therefore, visible foliar injury cannot
serve as a reliable surrogate measure for
other O3-related vegetation effects
because other effects (e.g., biomass loss)
have been reported with and without
visible injury. In some cases, visible
foliar symptoms have been correlated
with decreased vegetative growth
(Karnosky et al., 1996; Peterson et al.,
1987; Somers et al., 1998) and with
impaired reproductive function (Black
et al., 2000; Chappelka, 2002).
Therefore, the lack of visible injury
should not be construed to indicate a
lack of phytotoxic concentrations of O3
nor absence of other non-visible O3
effects.
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d. Reduced Plant Vigor
Though O3 levels over most of the
U.S. are not high enough to kill
vegetation directly, current levels have
been shown to reduce the ability of
many sensitive species and genotypes
within species to adapt to or withstand
other environmental stresses. These O3
effects may include increased
susceptibility to freezing temperatures,
increased vulnerability to pest
infestations and/or root disease, and
compromised ability to compete for
available resources. As an example of
the latter, when species with differing
O3-sensitivities occur together, O3sensitive species may experience a
greater reduction in growth than more
O3-tolerant species, which then can
better compete for available resources.
The result of such above effects can
produce a loss in plant vigor in O3sensitive species that over time may
lead to premature plant death.
e. Ecosystems
Ecosystems are comprised of complex
assemblages of organisms and the
physical environment with which they
interact. Each level of organization
within an ecosystem has functional and
structural characteristics. At the
ecosystem level, functional
characteristics include, but are not
limited to, energy flow; nutrient,
hydrologic, and biogeochemical cycling;
and maintenance of food chains. The
sum of the functions carried out by
ecosystem components provides many
benefits to humankind, as in the case of
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forest ecosystems (Smith, 1992). Some
of these benefits, also termed
‘‘ecosystem goods and services’’, include
food, fiber production, aesthetics,
genetic diversity, maintenance of water
quality, air quality, and climate, and
energy exchange. A conceptual
framework for discussing the effects of
stressors, including air pollutants such
as O3, on ecosystems was developed by
the EPA Science Advisory Board (Young
and Sanzone, 2002). In this report, the
authors identify six essential ecological
attributes (EEAs) of ecosystems
including landscape condition, biotic
condition, chemical/physical condition,
ecological processes, hydrology/
geomorphology, and natural disturbance
regime. Each EEA is depicted as one of
six triangles that together build a
hexagon. On the outside of each triangle
is a list of stressors that can act on the
EEA. Tropospheric O3 is listed as a
stressor of both biotic condition and the
chemical/physical condition of
ecosystems. As each EEA is linked to all
the others, it is clearly envisioned in
this framework that O3 could either
directly or indirectly impact all of the
EEAs associated with an ecosystem that
is being stressed by O3.
Vegetation often plays an influential
role in defining the structure and
function of an ecosystem, as evidenced
by the use of dominant vegetation forms
to classify many types of natural
ecosystems, e.g., tundra, wetland,
deciduous forest, and conifer forest.
Plants simultaneously inhabit both
above-and below-ground environments,
integrating and influencing key
ecosystem cycles of energy, water, and
nutrients. When a sufficient number of
individual plants within a community
have been affected, O3-related effects
can be propagated up to ecosystem-level
effects. Thus, through its impact on
vegetation, O3 can be an important
ecosystem stressor.
i. Potential Ozone Alteration of
Ecosystem Structure and Function
The 2006 Criteria Document outlines
seven case studies where O3 effects on
ecosystems have either been
documented or are suspected. The
oldest and clearest example involves the
San Bernardino Mountain forest
ecosystem in California. This system
experienced chronic high O3 exposures
over a period of 50 or more years. The
O3-sensitive and co-dominant species of
ponderosa and Jeffrey pine
demonstrated severe levels of foliar
injury, premature senescence, and
needle fall that decreased the
photosynthetic capacity of stressed
pines and reduced the production of
carbohydrates resulting in a decrease in
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radial growth and in the height of
stressed trees. It was also observed that
ponderosa and Jeffrey pines with slight
to severe crown injury lost basal area in
relation to competing species that are
more tolerant to O3. Due to a loss of
vigor, these trees eventually succumbed
to the bark beetle, leading to elevated
levels of tree death. Increased mortality
of susceptible trees shifted the
community composition towards white
fir and incense cedar, effectively
reversing the development of the normal
fire climax mixture dominated by
ponderosa and Jeffrey pines, and
leading to increased fire susceptibility.
At the same time, numerous other
organisms and processes were also
affected either directly or indirectly,
including successional patterns of
fungal microflora and their relationship
to the decomposer community. Nutrient
availability was influenced by the heavy
litter and thick needle layer under
stands with the most severe needle
injury and defoliation. In this example,
O3 appeared to be a predisposing factor
that led to increased drought stress,
windthrow, root diseases, and insect
infestation (Takemoto et al., 2001).
Thus, through its effects on tree water
balance, cold hardiness, tolerance to
wind, and susceptibility to insect and
disease pests, O3 potentially impacted
the ecosystem-related EEA of natural
disturbance regime (e.g., fire, erosion).
Although the role of O3 was extremely
difficult to separate from other
confounding factors, such as high
nitrogen deposition, there is evidence
that this shift in species composition
has altered the structure and dynamics
of associated food webs (Pronos et al.,
1999) and carbon (C) and nitrogen (N)
cycling (Arbaugh et al., 2003). Ongoing
and new research in this important
ecosystem is needed to reveal the extent
to which ecosystem services have been
affected and to what extent strong
causal linkages between historic and/or
current ambient O3 exposures and
observed ecosystem-level effects can be
made.
Ozone has also been reported to be a
selective pressure among sensitive tree
species (e.g., eastern white pine) in the
east. The nature of community
dynamics in eastern forests is different,
however, than in the west, consisting of
a wider diversity of species and uneven
aged stands, and the O3 levels are less
severe. Therefore, lower level chronic
O3 stress in the east is more likely to
produce subtle long-term forest
responses such as shifts in species
composition, rather than wide-spread
community degradation.
Some of the best-documented studies
of population and community response
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to O3 effects are the long-term studies of
common plantain (Plantago major) in
native plant communities in the United
Kingdom (Davison and Reiling, 1995;
Lyons et al., 1997; Reiling and Davison,
1992c). Elevated O3 significantly
decreased the growth of sensitive
populations of common plantain
(Pearson et al., 1996; Reiling and
Davison, 1992a, b; Whitfield et al.,
1997) and reduced its fitness as
determined by decreased reproductive
success (Pearson et al., 1996; Reiling
and Davison, 1992a). While spatial
comparisons of population responses to
O3 are complicated by other
environmental factors, rapid changes in
O3 resistance were imposed by ambient
levels and variations in O3 exposure
(Davison and Reiling, 1995).
Specifically, in this case study, it
appeared that O3-sensitive individuals
are being removed by O3 stress and the
genetic variation represented in the
population could be declining. If genetic
diversity and variation is lost in
ecosystems, there may be increased
vulnerability of the system to other
biotic and abiotic stressors, and
ultimately a change in the EEAs and
associated services provided by those
ecosystems.
Recent free-air exposure experiments
have also provided new insight into
how O3 may be altering ecosystem
structure and function (Karnosky et al.,
2005). For example, a field O3 exposure
experiment at the AspenFACE site in
Wisconsin (described in section
IV.A.2.b. above) was designed to
examine the effects of both elevated CO2
and O3 on mixed stands of aspen
(Populus tremuloides), birch (Betula
papyrifera), and sugar maple (Acer
saccharum) that are characteristic of
Great Lakes aspen-dominated forests
(Karnosky et al., 2003; Karnosky et al.,
1999). They found evidence that the
effects on above- and below-ground
growth and physiological processes
have cascaded through the ecosystem,
even affecting microbial communities
(Larson et al., 2002; Phillips et al.,
2002). This study also confirmed earlier
observations of O3-induced changes in
trophic interactions involving keystone
tree species, as well as important insect
pests and their natural enemies
(Awmack et al., 2004; Holton et al.,
2003; Percy et al., 2002).
Collectively these examples suggest
that O3 is an important stressor in
natural ecosystems, but it is difficult to
quantify the contribution of O3 due to
the combination of other stresses
present in ecosystems. In most cases,
because only a few components in each
of these ecosystems have been examined
and characterized for O3 effects, the full
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extent of ecosystem changes in these
example ecosystems is not fully
understood. Clearly, there is a need for
highly integrated ecosystem studies that
specifically investigate the effect of O3
on ecosystem structure and function in
order to fully determine the extent to
which O3 is altering ecosystem services.
Continued research, employing new
approaches, will be necessary to fully
understand the extent to which O3 is
affecting ecosystem services.
ii. Effects on Ecosystem Services and
Carbon Sequestration
Since it has been established that O3
affects photosynthesis and growth of
plants, O3 is most likely affecting the
productivity of forest ecosystems.
Therefore, it is desirable to link effects
on growth and productivity to essential
ecosystem services. However, it is very
difficult to quantify ecosystem-level
productivity losses because of the
amount of complexity in scaling from
the leaf-level or individual plant to the
ecosystem level, and because not all
organisms in an ecosystem are equally
affected by O3.
Terrestrial ecosystems are important
in the Earth’s carbon (C) balance and
could help offset emissions of CO2 by
humans if anthropogenic C is
sequestered in vegetation and soils. The
annual increase in atmospheric CO2 is
less than the total inputs from fossil fuel
burning and land use changes (Prentice
et al., 2001), and much of this
discrepancy is thought to be attributable
to CO2 uptake by plant photosynthesis
(Tans & White, 1998). Temperate forests
of the northern hemisphere have been
estimated to be a net sink of about 0.6
to 0.7 petagrams (Pg) C per year
(Goodale et al. 2002). Ozone interferes
with photosynthesis, causes some plants
to senesce leaves prematurely, and in
some cases, reduces allocation to stem
and root tissue. Thus, O3 decreases the
potential for C sequestration. For the
purposes of this discussion, C
sequestration is defined as the net
exchange of carbon by the terrestrial
biosphere. However, long-term storage
in the soil organic matter is considered
to be the most stable form of C storage
in ecosystems.
In a study including all ecosystem
types, Felzer et al. (2004), estimated that
U.S. net primary production (net flux of
C into an ecosystem) was decreased by
2.6–6.8 percent due to O3 pollution in
the late 1980s to early 1990s. Ozone not
only reduces C sequestration in existing
forests, it can also affect reforestation
projects (Beedlow et al. 2004). This
effect, in turn, has been found to
ultimately inhibit C sequestration in
forest soils which act as long-term C
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storage (Loya et al., 2003; Beedlow et al.
2004). The interaction of rising O3
pollution and rising CO2 concentrations
in the coming decades complicates
predictions of future sequestration
potential. Models generally predict that,
in the future, C sequestration will
increase with increasing CO2, but often
do not account for the decrease in
productivity due to the local effects of
current or potentially increasing levels
of tropospheric O3. In the presence of
high O3 levels, the stimulatory effect of
rising CO2 concentrations on forest
productivity has been estimated to be
reduced by more that 20 percent (Tingey
et al., 2001; Ollinger et al. 2002;
Karnosky et al., 2003).
In summary, it would be anticipated
that meeting lower O3 standards would
increase the amount of CO2 uptake by
many ecosystems in the U.S. However,
the amount of this improvement would
be heavily dependent on the species
composition of those ecosystems. Many
ecosystems in the U.S. do have O3
sensitive plants. For example, forest
ecosystems with dominant species such
as aspen or ponderosa pine would be
expected to increase CO2 uptake more
with lower O3 than forests with more O3
tolerant species.
A recent critique of the secondary
NAAQS review process published in the
report by the National Academy of
Sciences on Air Quality Management in
the United States (NRC, 2004) stated
that ‘‘EPA’s current practice for setting
secondary standards for most criteria
pollutants does not appear to be
sufficiently protective of sensitive crops
and ecosystems * * *’’ This report
made several specific recommendations
for improving the secondary NAAQS
process and concluded that ‘‘There is
growing evidence that tighter standards
to protect sensitive ecosystems in the
United States are needed. * * *’’ An
effort has been recently initiated within
the Agency to identify indicators of
ecological condition whose responses
can be clearly linked to changes in air
quality that are attributable to Agency
environmental programs. Using a single
indicator to represent the complex
linkages and dynamic cycles that define
ecosystem condition will always have
limitations. With respect to O3-related
impacts on ecosystem condition, only
two candidate indicators, foliar injury
(as described above) and radial growth
in trees, have been suggested. Thus,
while at the present time, most O3related effects on ecosystems must be
inferred from observed or predicted O3related effects on individual plants,
additional research at the ecosystem
level could identify new indicators and/
or establish stronger causal linkages
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between O3-induced plant effects and
ecosystem condition.
f. Yield Reductions in Crops
Ozone can interfere with carbon gain
(photosynthesis) and allocation of
carbon with or without the presence of
visible foliar injury. As a result of
decreased carbohydrate availability,
fewer carbohydrates are available for
plant growth, reproduction, and/or
yield. Recent studies have further
confirmed and demonstrated O3 effects
on different stages of plant
reproduction, including pollen
germination, pollen tube growth,
fertilization, and abortion of
reproductive structures, as reviewed by
Black et al. (2000). For seed-bearing
plants, these reproductive effects will
culminate in reduced seed production
or yield.
As described in the 1997 review and
again in the 2006 Criteria Document and
2007 Staff Paper, the National Crop Loss
Assessment Network (NCLAN) studies
undertaken in the early to mid-1980s
provide the largest, most uniform
database on the effects of O3 on
agricultural crop yields. The NCLAN
protocol was designed to produce crop
exposure-response data representative
of the areas in the U.S. where the crops
were typically grown. In total, 15
species (e.g., corn, soybean, winter
wheat, tobacco, sorghum, cotton, barley,
peanuts, dry beans, potato, lettuce,
turnip, and hay [alfalfa, clover, and
fescue]), accounting for greater than 85
percent of U.S. agricultural acreage
planted at that time, were studied. Of
these 15 species, 13 species including
38 different cultivars were combined in
54 cases representing unique
combinations of cultivars, sites, water
regimes, and exposure conditions. Crops
were grown under typical farm
conditions and exposed in open-top
chambers to ambient O3, sub-ambient
O3, and above ambient O3. Robust C–R
functions were developed for each of
these crop species. These results
showed that 50 percent of the studied
cases would be protected from greater
than 10 percent yield loss at a W126
level of 21 ppm-hour, while a W126 of
13 ppm-hour would provide protection
for 75 percent of the cases studied from
greater than 10 percent yield loss.
Recent studies continue to find yield
loss levels in crop species studied
previously under NCLAN that reflect
the earlier findings. In other words,
there has been no evidence that crops
are becoming more tolerant of O3 (EPA,
2006a). For cotton, some newer varieties
have been found to have higher yield
loss due to O3 compared to older
varieties (Olszyk et al., 1993, Grantz and
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McCool, 1992). In a meta-analysis of 53
studies, Morgan et al. (2003) found
consistent deleterious effects of O3
exposures on soybean from studies
published between 1973 and 2001.
Further, early results from the fieldbased exposure experiment SoyFACE in
Illinois indicate a lack of any apparent
difference in the O3 tolerance of old and
recent cultivars of soybean in a study of
22 soybean varieties (Long et al., 2002).
Thus, the 2007 Staff Paper concluded
that the recent scientific literature
continues to support the conclusions of
the 1996 Criteria Document that
ambient O3 concentrations are reducing
the yield of major crops in the U.S.
In addition to the effects described on
annual crop species, several studies
published since the 1997 review have
focused on perennial forage crops (EPA,
2006a). These recent results confirm
that O3 is also impacting yields and
quality of multiple-year forage crops at
sufficient magnitude to have nutritional
and possibly economic implications to
their use as ruminant animal feed at O3
exposures that occur in some years over
large areas of the U.S.
3. Adversity of Effects
The 2007 Staff Paper recognized that
the statute requires that a secondary
standard be protective against ‘‘adverse’’
O3 effects, not all identifiable O3induced effects. In considering what
constitutes a vegetation effect that is
adverse to the public welfare, the 2007
Staff Paper recognizes that O3 can cause
a variety of vegetation effects, beginning
at the level of the individual cell and
accumulating up to the level of whole
leaves, plants, plant populations,
communities and whole ecosystems, not
all of which have been classified in past
reviews as ‘‘adverse’’ to public welfare.
Previous reviews have classified O3
vegetation effects as either ‘‘injury’’ or
‘‘damage’’ to help in determining
adversity. Specifically, ‘‘injury’’ is
defined as encompassing all plant
reactions, including reversible changes
or changes in plant metabolism (e.g.,
altered photosynthetic rate), altered
plant quality, or reduced growth, that
does not impair the intended use or
value of the plant (Guderian, 1977). In
contrast, ‘‘damage’’ has been defined to
include those injury effects that reach
sufficient magnitude as to also reduce or
impair the intended use or value of the
plant. Examples of effects that are
classified as damage include reductions
in aesthetic values (e.g., foliar injury in
ornamental species) as well as losses in
terms of weight, number, or size of the
plant part that is harvested (reduced
yield or biomass production). Yield loss
also may include changes in crop
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quality, i.e., physical appearance,
chemical composition, or the ability to
withstand storage, while biomass loss
includes slower growth in species
harvested for timber or other fiber uses.
While this construct has proved useful
in the past, it appears to be most useful
in the context of evaluating effects on
single plants or species grown in
monocultures such as agricultural crops
or managed forests. It is less clear how
it might apply to potential effects on
natural forests or entire ecosystems
when O3-induced species level impacts
lead to shifts in species composition
and/or associated ecosystem services
such as nutrient cycling or hydrologic
cycles, where the intended use or value
of the system has not been specifically
identified.
A more recent construct for assessing
risks to forests described in Hogsett et
al. (1997) suggests that ‘‘adverse effects
could be classified into one or more of
the following categories: (1) Economic
production, (2) ecological structure, (3)
genetic resources, and (4) cultural
values.’’ This approach expands the
context for evaluating the adversity of
O3-related effects beyond the species
level. Another recent publication, A
Framework for Assessing and Reporting
on Ecological Condition: An SAB report
(Young and Sanzone, 2002), provides
additional support for expanding the
consideration of adversity beyond the
species level by making explicit the
linkages between stress-related effects
(e.g., O3 exposure) at the species level
and at higher levels within an
ecosystem hierarchy. Taking this recent
literature into account, the 2007 Staff
Paper concludes that a determination of
what constitutes an ‘‘adverse’’ welfare
effect in the context of the secondary
NAAQS review can appropriately occur
within this broader paradigm.
B. Biologically Relevant Exposure
Indices
The 2006 Criteria Document
concluded that O3 exposure indices that
cumulate differentially weighted hourly
concentrations are the best candidates
for relating exposure to plant growth
responses. This conclusion follows from
the extensive evaluation of the relevant
studies in the 1996 Criteria Document
(EPA, 1996a) and the recent evaluation
of studies that have been published
since that time. The following
selections, taken from the 1996 Criteria
Document (EPA, 1996a, section 5.5),
further elucidate the depth and strength
of these conclusions. Specifically, with
respect to the importance of taking into
account exposure duration, the 1996
Criteria Document stated, ‘‘when O3
effects are the primary cause of variation
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in plant response, plants from replicate
studies of varying duration showed
greater reductions in yield or growth
when exposed for the longer duration’’
and ‘‘the mean exposure index of
unspecified duration could not account
for the year-to-year variation in
response’’ (EPA, 1996a, pg. 5–96).
Further, ‘‘because the mean exposure
index treats all concentrations equally
and does not specifically include an
exposure duration component, the use
of a mean exposure index for
characterizing plant exposures appears
inappropriate for relating exposure with
vegetation effects’’ (EPA, 1996a, pg. 5–
88). Regarding the relative importance
of higher concentrations than lower in
determining plant response, the 1996
Criteria Document concluded that ‘‘the
ultimate impact of long-term exposures
to O3 on crops and seedling biomass
response depends on the integration of
repeated peak concentrations during the
growth of the plant’’ (EPA, 1996a, pg. 5–
104). Further, ‘‘at this time, exposure
indices that weight the hourly O3
concentrations differentially appear to
be the best candidates for relating
exposure with predicted plant response’’
(EPA, 1996a, pgs. 5–136).
At the conclusion of the 1997 review,
the biological basis for a cumulative,
seasonal form was not in dispute. There
was general agreement between EPA
and CASAC, based on their review of
the air quality criteria, that a
cumulative, seasonal form was more
biologically based than the then current
1-hour and newly proposed 8-hour
average form. However, in selecting a
specific form appropriate for a
secondary standard, there was less
agreement. An evaluation of the
performance of several cumulative
seasonal forms in predicting plant
response data taken from OTC
experiments had found that all
performed about equally well and was
unable to distinguish between them
(EPA, 1996a). In selecting between two
of these cumulative forms, the SUM06 54
and W126, in the absence of biological
evidence to distinguish between them,
EPA based its decision on both science
and policy considerations. Specifically,
these were: (1) All cumulative, peakweighted exposure indices considered,
including W126 and SUM06, were
about equally good as exposure
measures to predict exposure-response
relationships reported in the NCLAN
crop studies; and (2) the SUM06 form
would not be influenced by PRB O3
concentrations (defined at the time as
54 The SUM06 index is defined as the sum of all
hourly O3 concentrations greater or equal to 0.06
ppm over a specified time.
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0.03 to 0.05 ppm) under many typical
air quality distributions. On the basis of
these considerations, EPA chose the
SUM06 as the most appropriate
cumulative, seasonal form to consider
when proposing an alternative
secondary standard form (61 FR 65716).
Though the scientific justification for
a cumulative, seasonal form was
generally accepted in the 1997 review,
an analysis undertaken by EPA at that
time had shown that there was
considerable overlap between areas that
would be expected not to meet the range
of alternative 8-hour standards being
considered for the primary NAAQS and
those expected not to meet the range of
values (expressed in terms of the
seasonal SUM06 index) of concern for
vegetation. This result suggested that
improvements in national air quality
expected to result from attaining an 8hour primary standard within the
recommended range of levels would
also be expected to significantly reduce
levels of concern for vegetation in those
same areas. Thus, in the 1996 proposed
rule, EPA proposed two alternatives for
consideration: one alternative was to
make the secondary standard equal in
every way to the proposed 8-hour, 0.08
ppm primary standard; and the second
was to establish a cumulative, seasonal
secondary standard in terms of a SUM06
form as also appropriate to protect
public welfare from known or
anticipated adverse effects given the
available scientific knowledge and that
such a seasonal standard ‘‘* * * is more
biologically relevant * * *’’ (61 FR
65716).
In the 1997 final rule, EPA decided to
make the secondary standard identical
to the primary standard. The EPA
acknowledged, however, that ‘‘it
remained uncertain as to the extent to
which air quality improvements
designed to reduce 8-hr average O3
concentrations averaged over a 3-year
period would reduce O3 exposures
measured by a seasonal SUM06 index.’’
(62 FR 38876) In other words, it was
uncertain as to whether the 8-hour
average form would, in practice, provide
sufficient protection for vegetation from
the cumulative, seasonal and
concentration-weighted exposures
described in the scientific literature as
of concern.
On the basis of that history, the 2007
Staff Paper (chapter 7) revisited the
issue of whether the SUM06 was still
the most appropriate choice of
cumulative, seasonal form for a
secondary standard to protect the public
welfare from known and anticipated
adverse vegetation effects in light of the
new information available in this
review. Specifically, the 2007 Staff
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3007
Paper considered: (1) The continued
lack of evidence within the vegetation
effects literature of a biological
threshold for vegetation exposures of
concern; and (2) new estimates of PRB
that were lower than in the 1997 review.
The W126 form, also evaluated in the
1997 review, was again selected for
comparison with the SUM06 form.
Regarding the first consideration, the
2007 Staff Paper noted that the W126
form, by its incorporation of a
continuous sigmoidal weighting
scheme, does not create an artificially
imposed concentration threshold, yet
also gives proportionally more weight to
the higher and typically more
biologically potent concentrations, as
supported by the scientific evidence.
Second, the index value is not
significantly influenced by O3
concentrations within the range of
estimated PRB, as the weights assigned
by the sigmoidal weighting scheme to
concentrations in this range are near
zero. Thus, it would also provide a more
appropriate target for air quality
management programs designed to
reduce emissions from anthropogenic
sources contributing to O3 formation.
On the basis of these considerations, the
2007 Staff Paper concluded that the
W126 form was the most biologicallyrelevant cumulative, seasonal form
appropriate to consider in the context of
the 2008 rulemaking.
C. Vegetation Exposure and Impact
Assessment
The vegetation exposure and impact
assessment conducted for the 2008
rulemaking and described in the 2007
Staff paper, consisted of exposure, risk
and benefits analyses and improved and
built upon similar analyses performed
in the 1997 review (EPA 1996b). The
vegetation exposure assessment was
performed using interpolation and
included information from ambient
monitoring networks and results from
air quality modeling. The vegetation risk
assessment included both tree and crop
analyses. The tree risk analysis includes
three distinct lines of evidence: (1)
Observations of visible foliar injury in
the field linked to monitored O3 air
quality for the years 2001–2004; (2)
estimates of seedling growth loss under
then current and alternative O3
exposure conditions; and (3) simulated
mature tree growth reductions using the
TREGRO model to simulate the effect of
meeting alternative air quality standards
on the predicted annual growth of a
single western species (ponderosa pine)
and two eastern species (red maple and
tulip poplar). The crop analysis
includes estimates of the risks to crop
yields from then current and alternative
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O3 exposure conditions and the
associated change in economic benefits
expected to accrue in the agriculture
sector upon meeting the levels of
various alternative standards. Each
element of the assessment is described
below, including discussions of known
sources and ranges of uncertainties
associated with the elements of this
assessment.
1. Exposure Characterization
Though numerous effects of O3 on
vegetation have been documented as
discussed above, it is important in
considering risk to examine O3 air
quality patterns in the U.S. relative to
the location of O3 sensitive species that
have a known concentration-response in
order to predict whether adverse effects
are occurring at current levels of air
quality, and whether they are likely to
occur under alternative standard forms
and levels.
The most important information about
exposure to vegetation comes from the
O3 monitoring data that are available
from two national networks: (1) Air
Quality System (AQS; https://
www.epa.gov/ttn/airs/airsaqs) and (2)
Clean Air Status and Trends Network
(CASTNET; https://www.epa.gov/
castnet/). The AQS monitoring network
currently has over 1100 active O3
monitors which are generally sited near
population centers. However, this
network also includes approximately 36
monitors located in national parks.
CASTNET is the nation’s primary
source for data on dry acidic deposition
and rural, ground-level O3. It consists of
over 80 sites across the eastern and
western U.S. and is cooperatively
operated and funded with the National
Park Service. In the 1997 O3 NAAQS
final rule, it was acknowledged that
because the national air quality
surveillance network for O3 was
designed principally to monitor O3
exposure in populated areas, there was
limited measured data available to
characterize O3 air quality in rural and
remote sites. Since the 1997 review,
there has been a small increase in the
number of CASTNET sites (from
approximately 52 sites in 1992 to 84
sites in 2004), however these monitors
are not used for attainment
designations.
National parks represent areas of
nationally recognized ecological and
public welfare significance, which have
been afforded a high level of protection
by Congress. Two recent reports
presented some discussion of O3 trends
in a subset of national parks: The Ozone
Report: Measuring Progress Through
2003 (EPA, 2004), and 2005 Annual
Performance and Progress Report: Air
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Quality in National Parks (NPS, 2005).
Unfortunately, much of this information
is presented only in terms of the current
8-hr average form. The 2007 Staff Paper
analyzed available air quality data in
terms of the cumulative 12-hour W126
form from 2001 to 2005 for a subset of
national parks and other significant
natural areas representing 4 general
regions of the U.S. Many of these
national parks and natural areas have
monitored O3 levels above
concentrations that have been shown to
decrease plant growth and above the
12-hour W126 levels analyzed in this
review. For example, the Great Smokey
Mountain, Rocky Mountain, Grand
Canyon, Yosemite and Sequoia National
Parks all had more than one year within
the 2001–2005 period with a 12-hour
W126 above 21 ppm-hour. This level of
exposure has been associated with
approximately no more than 10 percent
biomass loss in 50 percent of the 49 tree
seedling cases studied in the NHEERL–
WED experiments (Lee and Hogsett,
1996). Black cherry (Prunus serotina),
an important O3-sensitive tree species in
the eastern U.S., occurs in the Great
Smoky Mountain National Park and is
estimated to have O3-related seedling
biomass loss of approximately 40
percent when exposed to a 3 month,
12-hour W126 O3 level greater than 21
ppm-hour. Ponderosa pine (Pinus
ponderosa) which occurs in the Grand
Canyon, Yosemite and Sequoia National
Parks has been reported to have
approximately 10 percent biomass
losses at 3 month, 12 hour W126 O3
levels as low as 17 ppm-hour (Lee and
Hogsett, 1996). Impacts on seedlings
may potentially affect long-term tree
growth and survival, ultimately
affecting the competitiveness of O3sensitive tree species and genotypes
within forest stands.
In order to characterize exposures to
vegetation at the national scale,
however, the 2007 Staff Paper
concluded that it could not rely solely
on limited site-specific monitoring data,
and that it was necessary to select an
interpolation method that could be used
to characterize O3 air quality over broad
geographic areas. The 2007 Staff Paper
therefore investigated the
appropriateness of using the O3 outputs
from the EPA/NOAA Community Multiscale Air Quality (CMAQ) 55 model
55 The CMAQ model is a multi-pollutant,
multiscale air quality model that contains state-ofthe-science techniques for simulating atmospheric
and land processes that affect the transport,
transformation, and deposition of atmospheric
pollutants and/or their precursors on both regional
and urban scales. It is designed as a science-based
modeling tool for handling many major pollutants
(including photochemical oxidants/O3, particulate
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system (https://www.epa.gov/asmdnerl/
CMAQ, Byun and Ching, 1999; Arnold
et al. 2003, Eder and Yu, 2005) to
improve spatial interpolations based
solely on existing monitoring networks.
Due to the significant resources required
to run CMAQ, model outputs were only
available for a limited number of years.
For the 2008 rulemaking, the most
recent outputs available at the time from
CMAQ version 4.5 were for the year
2001.
Based on the significant difference in
monitor network density between the
eastern and western U.S., the 2007 Staff
Paper concluded that it was appropriate
to use separate interpolation techniques
in these two regions. Only AQS and
CASTNET monitoring data were used
for the eastern interpolation, since it
was determined that enhancing the
interpolation with CMAQ data did not
add much information to the eastern
U.S. interpolation. In the western U.S.,
however, where rural monitoring is
more sparse, O3 values generated by the
CMAQ model were used to develop
scaling factors to augment the
interpolation.
In order to characterize uncertainties
associated with the interpolation
method, monitored O3 concentrations
were systematically compared to
interpolated O3 concentrations in areas
where monitors were located. In
general, the interpolation method used
in the current review performed well in
many areas in the U.S., although it
under-predicted higher 12-hour W126
exposures in rural areas. Due to the
important influence of higher exposures
in determining risks to plants, this
feature of the interpolated surface could
result in an under-estimation of risks to
vegetation in some areas. Taking these
uncertainties into account, and given
the absence of more complete rural
monitoring data, this approach was used
in developing national vegetation
exposure and risk assessments that
estimate relative changes in risk for the
various alternative standards analyzed.
To evaluate changing vegetation
exposures and risks under selected air
quality scenarios, the 2007 Staff Paper
utilized 2001 base year O3 air quality
distributions that had been adjusted
with a rollback method (Horst and Duff,
1995; Rizzo, 2005, 2006) to reflect
meeting the then current and alternative
secondary standard options. This
technique combines both linear and
quadratic elements to reduce higher O3
matter, and nutrient deposition) holistically. The
CMAQ model can generate estimates of hourly O3
concentrations for the contiguous U.S., making it
possible to express model outputs in terms of a
variety of exposure indices (e.g., W126, 8-hour
average).
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concentrations more than lower ones. In
this regard, the rollback method
attempts to account for reductions in
emissions without greatly affecting
lower concentrations. The following O3
air quality scenarios were analyzed: (1)
4th-highest daily maximum 8-hour
average: 0.084 ppm (the effective level
of the then current standard) and 0.070
ppm levels; (2) 3-month, 12-hour.
SUM06: 25 ppm-hour (proposed in the
1997 review) and 15 ppm-hour levels;
and (3) 3-month, 12-hour W126: 21
ppm-hour and 13 ppm-hour levels.
The two 8-hour average levels were
chosen as possible alternatives of the
then current form for comparison with
the cumulative, seasonal alternative
forms. The SUM06 scenarios were very
similar to the W126 scenarios. Since the
W126 was judged to be the more
biologically-relevant cumulative,
seasonal form, only the results for the
W126 scenarios are summarized below.
For the W126 form, the two levels were
selected on the basis of the associated
levels of tree seedling biomass loss and
crop yield loss protection identified in
the NHEERL–WED and NCLAN studies,
respectively. Specifically, the upper
level of W126 (21 ppm-hour) was
associated with a level of tree and crop
protection of approximately no more
than 10 percent growth or yield loss in
50 percent of cases studied.
Alternatively, the lower level of W126
(13 ppm-hour) was associated with a
level of tree seedling and crop
protection of approximately no more
than 10 percent growth or yield loss in
75 percent of studied cases.
The following discussion highlights
key observations drawn from comparing
predicted changes in interpolated air
quality under each alternative standard
form and level scenario for the base
year, 2001:
(1) Under the base year (2001) ‘‘as is’’
air quality, a large portion of California
had 12-hr W126 O3 levels above 31
ppm-hour, which has been associated
with approximately no more than 14
percent biomass loss in 50 percent of
tree seedling cases studies. Broader
multi-state regions in the east (NC, TN,
KY, IN, OH, PA, NJ, NY, DE, MD, VA)
and west (CA, NV, AZ, OK, TX) are
predicted to have levels of air quality
above the W126 level of 21 ppm-hour,
which is approximately equal to the
secondary standard proposed in 1996
and is associated with approximately no
more than 10 percent biomass loss in 50
percent of tree seedling cases studied.
Much of the east and Arizona and
California have 12-hour W126 O3 levels
above 13 ppm-hour, which has been
associated with approximately no more
than 10 percent biomass loss in 75
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percent of tree seedling cases studied.
The results of the exposure assessment
indicate that current air quality levels
could result in significant impacts to
vegetation in some areas.
(2) When 2001 air quality was rolled
back to meet the then current 8-hour,
0.084 ppm secondary standard, the
overall 3-month 12-hour W126 O3 levels
were somewhat improved, but not
substantially. Under this scenario, there
were still many areas in California with
12-hour W126 O3 levels above 31 ppmhour. A broad multi-state region in the
east (NC, TN, KY, IN, OH, PA, MD) and
west (CA, NV, AZ, OK, TX) were still
predicted to have O3 levels above the
W126 level of 21 ppm-hour.
(3) Exposures generated for just
meeting a 0.070 ppm, 4th-highest
maximum 8-hour average alternative
standard showed substantially
improved O3 air quality when compared
to just meeting the then current 8-hour
standard. Most areas were predicted to
have O3 levels below the W126 level of
21 ppm-hour, although some areas in
the east (KY, TN, MI, AR, MO, IL) and
west (CA, NV, AZ, UT, NM, CO, OK,
TX) were still predicted to have O3
levels above the W126 level of 13 ppmhour.
These results suggest that meeting a
0.070 ppm, 8-hour secondary standard
would provide substantially improved
protection in some areas for vegetation
from seasonal O3 exposures of concern.
The 2007 Staff Paper recognizes,
however, that some areas meeting a
0.070 ppm 8-hour standard could
continue to have elevated seasonal
exposures, including forested park lands
and other natural areas, and Class I
areas which are federally mandated to
preserve certain air quality related
values. This is especially important in
the high elevation forests in the Western
U.S. where there are few O3 monitors.
This is because the air quality patterns
in remote areas can result in relatively
low 8-hour averages while still
experiencing relatively high cumulative
exposures.
To further characterize O3 air quality
in terms of various secondary standard
forms, an analysis was performed in the
2007 Staff Paper to evaluate the extent
to which county-level O3 air quality
measured in terms of various levels of
the current 8-hour average form
overlapped with that measured in terms
of various levels of the 12-hour W126
cumulative, seasonal form. The 2007
Staff Paper presented this analysis using
2002–2004 56 county-level O3 air quality
56 This analysis was updated using 2003–2005 air
quality as it became available, finding similar
results.
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3009
data from AQS sites and the subset of
CASTNET sites having the highest O3
levels for the counties in which they are
located. Since the current 8-hour
average secondary form is a 3-year
average, the analysis initially compared
the 3-year averages of both the 8-hour
and W126 forms. In addition,
recognizing that some vegetation effects
(e.g. crop yield loss and foliar injury) are
driven solely by annual O3 exposures
and are typically evaluated with respect
to exposures within the annual growing
season, the 2007 Staff Paper also
presented a comparison of the current
3-year average 8-hour form to the annual
W126 form for the individual years,
2002 and 2004.
Results of the 3-year average
comparisons showed that of the
counties with air quality meeting the 3year average form of a 0.084 ppm,
8-hour average standard, 7 counties
showed 3-year average W126 values
above the 21 ppm-hour level. At the
lower W126 level of 13 ppm-hour, 135
counties with air quality meeting the
3-year average form of a 0.084 ppm,
8-hour average standard, would be
above this W126 level. In addition,
when the 3-year average of an 8-hour
form was compared to annual W126
values, further variability in the degree
of overlap between the 8-hour form and
W126 form became apparent. For
example, the relatively high 2002 O3 air
quality year showed a greater degree of
overlap between those areas that would
meet the levels analyzed for the current
8-hour and alternative levels of the
W126 form than did the relatively low
O3 2004 air quality year. This lack of a
consistent degree of overlap between the
two forms in different air quality years
demonstrates that annual vegetation
would be expected to receive widely
differing degrees of protection from
cumulative seasonal exposures in some
areas from year to year, even when the
3-year average of the 8-hour form was
consistently met.
It is clear that this analysis is limited
by the lack of monitoring in rural areas
where important vegetation and
ecosystems are located, especially at
higher elevation sites. This is because
O3 air quality distributions at high
elevation sites often do not reflect the
typical urban and near-urban pattern of
low morning and evening O3
concentrations with a high mid-day
peak, but instead maintain relatively flat
patterns with many concentrations in
the mid-range (e.g., 0.05–0.09 ppm) for
extended periods. These conditions can
lead to relatively low daily maximum
8-hour averages concurrently with high
cumulative values so that there is
potentially less overlap between an 8-
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hour average and a cumulative, seasonal
form at these sites. The 2007 Staff Paper
concluded that it is reasonable to
anticipate that additional unmonitored
rural high elevation areas important for
vegetation may not be adequately
protected even with a lower level of the
8-hour form.
The 2006 Criteria Document discusses
policy relevant background (PRB) levels
for high elevation sites and makes the
following observations: (1) PRB
concentrations of 0.04 to 0.05 ppm
occur occasionally at high-elevation
sites (e.g., > 1.5 km) in the spring due to
the free-tropospheric influence,
including some limited contribution
from hemispheric pollution (O3
produced from anthropogenic emissions
outside North America); and (2) while
stratospheric intrusions might
occasionally elevate O3 at high-altitude
sites, these events are rare at surface
sites. Therefore, the 2007 Staff Paper
concluded that springtime PRB levels in
the range identified above and rare
stratospheric intrusions of O3 are
unlikely to be a major influence on
3-month cumulative seasonal W126
values.
It further remains uncertain as to the
extent to which air quality
improvements designed to reduce
8-hour O3 average concentrations would
reduce O3 exposures measured by a
seasonal, cumulative W126 index. The
2007 Staff Paper indicated this to be an
important consideration because: (1)
The biological database stresses the
importance of cumulative, seasonal
exposures in determining plant
response; (2) plants have not been
specifically tested for the importance of
daily maximum 8-hour O3
concentrations in relation to plant
response; and (3) the effects of
attainment of a 8-hour standard in
upwind urban areas on rural air quality
distributions cannot be characterized
with confidence due to the lack of
monitoring data in rural and remote
areas. These factors are important
considerations in determining whether
the current 8-hour form can
appropriately provide requisite
protection for vegetation.
2. Assessment of Risks to Vegetation
The 2007 Staff Paper presents results
from quantitative and qualitative risk
assessments of O3 risks to vegetation
(EPA, 2007). In the 1997 review, crop
yield and seedling biomass loss OTC
data provided the basis for staff
analyses, conclusions, and
recommendations (EPA, 1996b). Since
then, several additional lines of
evidence have progressed sufficiently to
provide staff with a more complete and
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coherent picture of the scope of O3related vegetation risks, especially those
faced by seedling, sapling and mature
tree species growing in field settings,
and indirectly, forested ecosystems.
Specifically, research published after
the 1997 review reflects an increased
emphasis on field-based exposure
methods (e.g., free air exposure and
ambient gradient), improved field
survey biomonitoring techniques, and
mechanistic tree process models.
Findings from each of these research
areas are discussed separately below. In
conducting these assessments, the Staff
Paper analyses relied on both measured
and modeled air quality information.
For some effects, like visible foliar
injury and modeled mature tree growth
response, only monitored air quality
information was used. For other effects
categories (e.g., crop yield and tree
seedling growth), staff relied on
interpolated O3 exposures.
a. Visible Foliar Injury
As discussed above (section IV.A.2.c),
systematic injury surveys have
documented visible foliar injury
symptoms diagnostic of phytotoxic O3
exposures on sensitive bioindicator
plants. These surveys have produced
more expansive evidence than that
available at the time of the 1997 review
that visible foliar injury is occurring in
many areas of the U.S. under current
ambient conditions. The 2007 Staff
Paper presents an assessment combining
recent U.S. Forest Service Forest
Inventory and Analysis (FIA)
biomonitoring site data with the county
level air quality data for those counties
containing the FIA biomonitoring sites.
This assessment showed that incidence
of visible foliar injury ranged from 21 to
39 percent during the four-year period
(2001–2004) across all counties with air
quality levels at or below that of a 0.084
ppm, 8-hour standard. Of the counties
that met an 8-hour level of 0.070 ppm
in those years, 11 to 30 percent still had
incidence of visible foliar injury. The
magnitude of these percentages suggests
that phytotoxic exposures sufficient to
induce visible foliar injury would still
occur in many areas after meeting the
level of a 0.084 ppm secondary standard
or alternative 0.070 ppm 8-hour
standard. Additionally, the data showed
that visible foliar injury occurrence was
geographically widespread and
occurring on a variety of plant species
in forested and other natural systems.
Linking visible foliar injury to other
plant effects is still problematic.
However, its presence indicates that
other O3-related vegetation effects could
also be present.
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b. Seedling and Mature Tree Biomass
Loss
In the 1997 review, analyses of the
effects of O3 on trees were limited to 11
tree species for which C–R functions for
the seedling growth stage had been
developed from OTC studies conducted
by the NHEERL–WED. Important tree
species such as quaking aspen,
ponderosa pine, black cherry, and tulip
poplar were found to be sensitive to
cumulative seasonal O3 exposures.
Work done since the 1997 review at the
AspenFACE site in Wisconsin on
quaking aspen (Karnosky et al., 2005)
and a gradient study performed in the
New York City area (Gregg et al. 2003)
has confirmed the detrimental effects of
O3 exposure on tree growth in field
studies without chambers and beyond
the seedling stage (King et al. 2005).
These field studies are discussed above
in section IV.A.
To update the seedling biomass loss
risk analysis, C–R functions for biomass
loss for available seedling tree species
taken from the 2006 Criteria Document
and information on tree growing regions
derived from the U.S. Department of
Agriculture’s Atlas of United States
Trees were combined with projections
of O3 air quality based on 2001
interpolated exposures, to produce
estimated biomass loss for each of the
seedling tree species individually. Maps
of these biomass loss projections are
presented in the 2007 Staff Paper. For
example, quaking aspen had a wide
range of O3 exposures across its growing
range and therefore, showed significant
variability in percentages of projected
seedling biomass loss across its range.
Quaking aspen seedling biomass loss
was projected to be greater than 4
percent over much of its geographic
range, though it can reach above 10
percent in areas of Ohio, Pennsylvania,
New York, New Jersey and California.
Biomass loss for black cherry was
projected to be greater than 20 percent
in approximately half its range. Greater
than 30 percent biomass loss for black
cherry was projected in North Carolina,
Tennessee, Indiana, Ohio, Pennsylvania,
Arizona, Michigan, New York, New
Jersey, Maryland and Delaware. For
ponderosa pine, an important tree
species in the western U.S., biomass
loss was projected to be above 10
percent in much of its range in
California. Biomass loss still occurred in
many tree species when O3 air quality
was adjusted to meet the then current 8hour standard of 0.084 ppm. For
instance, black cherry, ponderosa pine,
eastern white pine, and aspen had
estimated median seedling biomass
losses over portions of their growing
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range as high as 24, 11, 6, and 6 percent,
respectively, when O3 air quality was
rolled back to just meet a 0.084 ppm,
8-hour standard. The 2007 Staff Paper
noted that these results are for tree
seedlings and that mature trees of the
same species may have more or less of
a response to O3 exposure. Due to the
potential for compounding effects over
multiple years, experts at a consensus
workshop on O3 vegetation effects and
secondary standards, hereinafter
referred to as the 1996 Consensus
Workshop, reported in a subsequent
1997 Workshop Report, that a biomass
loss greater than 2 percent annually can
be significant (Heck and Cowling, 1997).
Decreased seedling root growth and
survivability could affect overall stand
health and composition in the long
term.
In addition to the estimation of O3
effects on seedling growth, recent work
available in the 2008 rulemaking has
enhanced our understanding of risks
beyond the seedling stage. In order to
better characterize the potential O3
effects on mature tree growth, a tree
growth model (TREGRO) was used as a
tool to evaluate the effect of changing O3
air quality under just meet scenarios for
selected alternative O3 standards on the
growth of mature trees. TREGRO is a
process-based, individual tree growth
simulation model (Weinstein et al,
1991). This model has been used to
evaluate the effects of a variety of O3
exposure scenarios on several species of
trees by incorporating concurrent
climate data in different regions of the
U.S. to account for O3 and climate/
meteorology interactions (Tingey et al.,
2001; Weinstein et al., 1991; Retzlaff et
al., 2000; Laurence et al., 1993;
Laurence et al., 2001; Weinstein et al.,
2005). The model provides an analytical
framework that accounts for the
nonlinear relationship between O3
exposure and response. The interactions
between O3 exposure, precipitation and
temperature are integrated as they affect
vegetation, thus providing an internal
consistency for comparing effects in
trees under different exposure scenarios
and climatic conditions. An earlier
assessment of the effectiveness of
national ambient air quality standards
in place since the early 1970s took
advantage of 40 years of air quality and
climate data for the Crestline site in the
San Bernardino Mountains of California
to simulate ponderosa pine growth over
time with the improving air quality
using TREGRO (Tingey et al., 2004).
The TREGRO model was used to
assess growth of Ponderosa pine in the
San Bernardino Mountains of California
(Crestline) and the growth of yellow
poplar and red maple in the
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Appalachian mountains of Virginia and
North Carolina, Shenandoah National
Park (Big Meadows) and Linville Gorge
Wilderness Area (Cranberry),
respectively. Total tree growth
associated with ‘‘as is’’ air quality, and
air quality adjusted to just meet
alternative O3 standards was assessed.
Ponderosa pine is one of the most
widely distributed pines in western
North America, a major source of
timber, important as wildlife habitat,
and valued for aesthetics (Burns and
Honkala, 1990). Red maple is one of the
most abundant species in the eastern
U.S. and is important for its brilliant fall
foliage and highly desirable wildlife
browse food (Burns and Honkala, 1990).
Yellow poplar is an abundant species in
the southern Appalachian forest. It is 10
percent of the cove hardwood stands in
southern Appalachians which are
widely viewed as some of the country’s
most treasured forests because the
protected, rich, moist set of conditions
permit trees to grow the largest in the
eastern U.S. The wood has high
commercial value because of its
versatility and as a substitute for
increasingly scarce softwoods in
furniture and framing construction.
Yellow poplar is also valued as a honey
tree, a source of wildlife food, and a
shade tree for large areas (Burns and
Honkala, 1990).
The 2007 Staff Paper analyses found
that just meeting a 0.084 ppm standard
would likely continue to allow O3related reductions in annual net
biomass gain in these species. This is
based on model outputs that estimate
that as O3 levels are reduced below
those of a 0.084 ppm standard,
significant improvements in growth
would occur. For instance, estimated
growth in red maple increased by 4 and
3 percent at Big Meadows and Cranberry
sites, respectively, when air quality was
rolled back to just met a W126 value of
13 ppm-hour. Yellow poplar was
projected to have a growth increase
between 0.6 and 8 percent under the
same scenario at the two eastern sites.
Though there is uncertainty
associated with the above analyses, this
information should be given careful
consideration in light of several other
pieces of evidence. Specifically, new
evidence from experimental studies that
go beyond the seedling growth stage
continues to show decreased growth
under elevated O3 (King et al. 2005).
Some mature trees such as red oak have
shown an even greater sensitivity of
photosynthesis to O3 than seedlings of
the same species (Hanson et al., 1994).
As indicated above, smaller growth loss
increments may be significant for
perennial species. The potential for
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cumulative ‘‘carry over’’ effects as well
as compounding also must be
considered. The accumulation of such
‘‘carry-over’’ effects over time may affect
long-term survival and reproduction of
individuals and ultimately the
abundance of sensitive tree species in
forest stands.
c. Crops
As discussed in the 2007 Staff Paper,
risk of O3 exposure and associated
monetized benefits were estimated for
commodity crops, fruits and vegetables.
Similar to the tree seedling analysis, this
analysis combined C–R information on
crops, crop growing regions and
interpolated exposures during each crop
growing season. NCLAN crop functions
were used for commodity crops.
According to USDA National
Agricultural Statistical Survey (NASS)
data, the 9 commodity crop species (e.g.,
cotton, field corn, grain sorghum,
peanut, soybean, winter wheat, lettuce,
kidney bean, potato) included in the
2007 Staff Paper analysis accounted for
69 percent of 2004 principal crop
acreage planted in the U.S. in 2004.57
The C–R functions for six fruit and
vegetable species (tomatoes-processing,
grapes, onions, rice, cantaloupes,
Valencia oranges) were identified from
the California fruit and vegetable
analysis from the 1997 review (Abt
Associates Inc, 1995). The 2007 Staff
Paper noted that fruit and vegetable
studies were not part of the NCLAN
program and C–R functions were
available only in terms of seasonal 7hour or 12-hour mean index. This index
form is considered less effective in
predicting plant response for a given
change in air quality than the
cumulative form used with other crops.
Therefore, the fruit and vegetable C–R
functions were considered more
uncertain than those for commodity
crops.
Analyses in the 2007 Staff Paper
showed that some of the most important
commodity crops such as soybean,
winter wheat and cotton had some
projected losses under the 2001 base
year air quality. Soybean yield losses
were projected to be 2–4 percent in
parts of Pennsylvania, New Jersey,
Maryland and Texas. Winter wheat was
projected to have yield losses of 2–6
percent in parts of California.
57 Principal crops as defined by the USDA
include corn, sorghum, oats, barley, winter wheat,
rye, Durum wheat, other spring wheat, rice,
soybeans, peanuts, sunflower, cotton, dry edible
beans, potatoes, sugar beets, canola, proso millet,
hay, tobacco, and sugarcane. Acreage data for the
principal crops were taken from the USDA NASS
2005 Acreage Report (https://
usda.mannlib.cornell.edu/reports/nassr/field/pcpbba/acrg0605.pdf).
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Additionally, cotton was projected to
have yield losses of above 6 percent in
parts of California, Texas and North
Carolina in 2001. The risk assessment
estimated that just meeting the then
current 0.084 ppm, 8-hour standard
would still allow O3=related yield loss
to occur in some commodity crop
species and fruit and vegetable species
currently grown in the U.S. For
example, based on median C–R function
response, in counties with the highest
O3 levels, potatoes and cotton had
estimated yield losses of 9–15 percent
and 5–10 percent, respectively, when O3
air quality just met the level of a 0.084
ppm, 8-hour standard. Estimated yield
improved in these counties when the
alternative W126 standard levels were
met. The very important soybean crop
had generally small yield losses
throughout the country under just
meeting the then current standard (0–4
percent).
The 2007 Staff Paper also presented
estimates of monetized benefits for
crops associated with a 0.084 ppm, 8hour and alternative standards. The
Agriculture Simulation Model (AGSIM)
(Taylor, 1994; Taylor, 1993) was used to
calculate annual average changes in
total undiscounted economic surplus for
commodity crops and fruits and
vegetables when the then current and
alternative standard levels were met.
Meeting the various alternative
standards did show some significant
benefits beyond a 0.084 ppm, 8-hour
standard. However, the 2007 Staff Paper
recognized that the AGSIM economic
benefits estimates also incorporate
several sources of uncertainty,
including: (1) Estimates of economic
benefits derived from use of the more
uncertain C–R relationships for fruits
and vegetables; (2) uncertain
assumptions about the treatment and
effect of government farm payment
programs; and (3) uncertain
assumptions about near-term changes in
the agriculture sector due to the
increased use of crops as biofuels.
Although the AGSIM model results
provided a relative comparison of
agricultural benefits between alternative
standards, these uncertainties limited
the utility of the absolute numbers.
D. Reconsideration of Secondary
Standard
As discussed above at the beginning
of section IV, this reconsideration of the
secondary O3 standard set in the 2008
rulemaking focuses on reconsidering
certain elements of the standard, the
form, averaging times, and level. The
general approach for setting a secondary
O3 standard used in the 2008
rulemaking, and in the previous 1997
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rulemaking, was to consider two basic
policy options: Setting a distinct
secondary standard with a biologically
relevant form and averaging times, or
setting a secondary standard identical to
the primary standard. In the 2007
proposed rule, both such options were
evaluated, commented on by CASAC
and the public, and proposed, as
discussed below in sections IV.D.1 and
IV.D.2, respectively. In the 2008 final
rule, EPA decided to set the secondary
standard identical to the revised 8-hour
primary standard, as discussed below in
section IV.D.3. Section IV.D.4
summarizes comments received from
CASAC following the 2008 decision.
The Administrator’s proposed
conclusions based on this
reconsideration are presented in section
IV.D.5.
1. Considerations Regarding the 2007
Proposed Cumulative Seasonal Standard
a. Form
The 2006 Criteria Document and 2007
Staff Paper concluded that the recent
vegetation effects literature evaluated in
the 2008 rulemaking strengthened and
reaffirmed conclusions made in the
1997 review that the use of a cumulative
exposure index that differentially
weights ambient concentrations is best
able to relate ambient exposures to
vegetation response at this time (EPA,
2006a, b; see also discussion in IV.B
above). The 1997 review focused in
particular on two of these cumulative
forms, the SUM06 and W126. In the
2008 rulemaking, the 2007 Staff Paper
again evaluated these two forms in light
of two key pieces of then recent
information: Estimates of PRB that were
lower than in the 1997 review, and
continued lack of evidence within the
vegetation effects literature of a
biological threshold for vegetation
exposures of concern. On the basis of
those policy and science-related
considerations, the 2007 Staff Paper
concluded that the W126 form was more
appropriate in the context of the 2008
rulemaking. Specifically, the W126
form, by its incorporation of a sigmoidal
weighting scheme, does not create an
artificially imposed concentration
threshold, gives proportionally more
weight to the higher and typically more
biologically potent concentrations, and
is not significantly influenced by O3
concentrations within the range of
estimated PRB. The Staff Paper further
concluded that ‘‘it is not appropriate to
continue to use an 8-hour averaging
time for the secondary standard’’ and
that ‘‘the 8-hour average form should be
replaced with a cumulative, seasonal,
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concentration weighted form’’ (EPA,
2007b; pg. 8–25).
The CASAC, based on its assessment
of the same vegetation effects science,
agreed with the 2006 Criteria Document
and 2007 Staff Paper and unanimously
concluded that it is not appropriate to
try to protect vegetation from the known
or anticipated adverse effects of ambient
O3 by continuing to promulgate
identical primary and secondary
standards for O3. Moreover, the
members of the CASAC and a
substantial majority of the CASAC O3
Panel agreed with 2007 Staff Paper
conclusions and encouraged EPA to
establish an alternative cumulative
secondary standard for O3 and related
photochemical oxidants that is
distinctly different in averaging time,
form and level from the current or
potentially revised 8-hour primary
standard. The CASAC also stated that
‘‘the recommended metric for the
secondary ozone standard is the
(sigmoidally-weighted) W126 index’’
(Henderson, 2007).
The EPA agreed with the conclusions
drawn in the 2006 Criteria Document,
2007 Staff Paper and by CASAC that the
scientific evidence available in the 2008
rulemaking continued to demonstrate
the cumulative nature of O3-induced
plant effects and the need to give greater
weight to higher concentrations. Thus,
EPA concluded that a cumulative
exposure index that differentially
weights O3 concentrations represents a
reasonable policy choice for a seasonal
secondary standard to protect against
the effects of O3 on vegetation. The EPA
further agreed with both the 2007 Staff
Paper and CASAC that the most
appropriate cumulative, concentrationweighted form to consider in the 2008
rulemaking was the sigmoidally
weighted W126 form, due to EPA’s
recognition that there is no evidence in
the literature for an exposure threshold
that would be appropriate across all O3sensitive vegetation and that this form is
unlikely to be significantly influenced
by O3 air quality within the range of
PRB levels identified in this rulemaking.
Thus, in 2007 EPA proposed as one
option to replace the then current 0.084
ppm, 8-hour average secondary standard
with a standard defined in terms of the
cumulative, seasonal W126 form. The
EPA also proposed the option of making
the secondary identical to the proposed
revised primary standard.
b. Averaging Times 58
The 2007 Staff Paper, in addition to
form, also considered what exposure
58 While the term ‘‘averaging time’’ is used, for the
cumulative, seasonal standard the seasonal and
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periods or durations are most relevant
for vegetation, which, unlike people, is
exposed to ambient air continuously
throughout its lifespan. For annual
species, this lifespan encompasses a
period of only one year or less; while for
perennials, lifespans can range from a
few years to decades or centuries.
However, because O3 levels are not
continuously elevated and plants are
not equally sensitive to O3 over the
course of a day, season or lifetime, it
becomes necessary to identify periods of
exposure that have the most relevance
for plant response. The 2007 Staff Paper
discussed exposure periods relevant for
vegetation in terms of a seasonal
window and a diurnal window, and it
also discussed defining the standard in
terms of an annual index value versus
a 3-year average of annual index values.
The numbered paragraphs below
present the 2007 Staff Paper discussions
on these exposure periods, and the
annual versus 3-year average index
value, followed by a discussion of
CASAC views and EPA proposed
conclusions.
(1) In considering an appropriate
seasonal window, the 2007 Staff Paper
recognized that, in general, many
annual crops are grown for periods of a
few months before being harvested. In
contrast, other annual and perennial
species may be photosynthetically
active longer, and for some species and
locations, throughout the entire year. In
general, the period of maximum
physiological activity and thus,
maximum potential O3 uptake for
annual crops, herbaceous species, and
deciduous trees and shrubs coincides
with some or all of the intra-annual
period defined as the O3 season, which
varies on a state-by-state basis. This is
because the high temperature and high
light conditions that promote the
formation of tropospheric O3 also
promote physiological activity in
vegetation.
The 2007 Staff Paper noted that the
selection of any single seasonal
exposure period for a national standard
would represent a compromise, given
the significant variability in growth
patterns and lengths of growing seasons
among the wide range of vegetation
species occurring within the U.S. that
may experience adverse effects
associated with O3 exposures. However,
the 2007 Staff Paper further concluded
that the consecutive 3-month period
within the O3 season with the highest
W126 index value (e.g., maximum
3-month period) would, in most cases,
diurnal time periods at issue are those over which
exposures during a specified period of time are
cumulated, not averaged.
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likely coincide with the period of
greatest plant sensitivity on an annual
basis. Therefore, the 2007 Staff Paper
again concluded, as it did in the 1997
review, that the annual maximum
consecutive 3-month period is a
reasonable seasonal time period, when
combined with a cumulative,
concentration weighted form, for
protection of sensitive vegetation.
(2) In considering an appropriate
diurnal window, the Staff Paper
recognized that over the course of the
24-hour diurnal period, plant stomatal
conductance varies in response to
changes in light level, soil moisture and
other environmentally and genetically
controlled factors. In general, stomata
are most open during daylight hours in
order to allow sufficient CO2 uptake for
use in carbohydrate production through
the light-driven process of
photosynthesis. At most locations, O3
concentrations are also highest during
the daytime, and thus, most likely to
coincide with maximum stomatal
uptake. It is also known however, that
in some species, stomata may remain
open sufficiently at night to allow for
some nocturnal uptake to occur. In
addition, at some rural, high elevation
sites, the O3 concentrations remain
relatively flat over the course of the day,
often at levels above estimated PRB. At
these sites, nighttime W126 values can
be of similar magnitude as daytime
values, though the significance of these
exposures is much less certain. This is
because O3 uptake during daylight
hours is known to impair the lightdriven process of photosynthesis, which
can then lead to impacts on
carbohydrate production, plant growth,
reproduction (yield) and root function.
It is less clear at this time to what extent
and by what mechanisms O3 uptake at
night adversely impacts plant function.
In addition, many species have not been
shown to take up O3 at night and/or do
not occur in areas with elevated
nighttime O3 concentrations.
In reviewing the information on this
topic that became available after the
1997 review, the 2007 Staff Paper
considered the information compiled in
a summary report by Musselman and
Minnick (2000). This work reported that
some species take up O3 at night, but
that the degree of nocturnal stomatal
conductance varies widely between
species and its relevance to overall O3induced vegetation effects remain
unclear. In considering this information,
the 2007 Staff Paper concluded that for
the vast majority of studied species,
daytime exposures represent the
majority of diurnal plant O3 uptake and
are responsible for inducing the plant
response of most significance to the
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health and productivity of the plant
(e.g., reduced carbohydrate production).
Until additional information is available
about the extent to which co-occurrence
of sensitive species and elevated
nocturnal O3 exposures exists, and what
levels of nighttime uptake are adverse to
affected species, the 2007 Staff Paper
concluded that this information
continues to be preliminary, and does
not provide a basis for reaching a
different conclusion regarding the
diurnal window at this time. The 2007
Staff Paper further noted that additional
research is needed to address the degree
to which a 12-hour diurnal window may
be under-protective in areas where
elevated nighttime levels of O3 co-occur
with sensitive species with a high
degree of nocturnal stomatal
conductance. Thus, as in the 1997
review, the 2007 Staff Paper again
concluded that based on the available
science, the daytime 12-hour window (8
a.m. to 8 p.m.) is the most appropriate
period over which to cumulate diurnal
O3 exposures, specifically those most
relevant to plant growth and yield
responses.
(3) In considering whether the
standard should be defined in terms of
an annual index value or a 3-year
average of annual index values, the 2007
Staff Paper recognized that though most
cumulative seasonal exposure levels of
concern for vegetation have been
expressed in terms of the annual
timeframe, it may be appropriate to
consider a 3-year average for purposes
of standard stability. However, the 2007
Staff Paper noted that for certain welfare
effects of concern (e.g., foliar injury,
yield loss for annual crops, growth
effects on other annual vegetation and
potentially tree seedlings), an annual
time frame may be a more appropriate
period in which to assess what level
would provide the requisite degree of
protection, while for other welfare
effects (e.g., mature tree biomass loss), a
3-year average may also be appropriate.
Thus, the 2007 Staff Paper concluded
that it is appropriate to consider both an
annual and a 3-year average. Further,
the 2007 Staff Paper concluded that
should a 3-year average of the 12-hour
W126 form be selected, a lower standard
level should be considered to reduce the
potential of adverse impacts to annual
species from a single high O3 year that
could still occur while attaining a
standard on average over 3 years.
The CASAC, in considering what
seasonal, diurnal, and annual or
multiyear time periods are most
appropriate when combined with a
cumulative, seasonal form to protect
vegetation from exposures of concern,
agreed that the 2007 Staff Paper
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conclusion regarding the 3-month
seasonal period and 12-hour daylight
window was appropriate, with the
distinction that both of these time
periods likely represents the minimum
time periods of importance. In
particular, one O3 Panel member
commented that for some species,
additional O3 exposures of importance
were occurring outside the 3-month
seasonal and 12-hour diurnal windows.
Further, the CASAC concluded that
multi-year averaging to promote a
‘‘stable’’ secondary standard is less
appropriate for a cumulative, seasonal
secondary standard than for a primary
standard based on daily maximum 8hour concentrations. The CASAC
further concluded that if multi-year
averaging is employed to afford greater
stability of the secondary standard, the
level of the standard should be revised
downward to assure that the desired
degree of protection is not exceeded in
individual years.
The EPA, in determining which
seasonal and diurnal time periods are
most appropriate to propose, took into
account the 2007 Staff Paper and
CASAC views. In being careful to
consider what is needed to provide the
requisite degree of protection, no more
and no less, in 2007 EPA proposed that
the 3-month seasonal period and 12hour daylight period are appropriate.
Based on the 2007 Staff Paper
conclusions discussed above, EPA was
mindful that there is the potential for
under-protection with a 12-hour diurnal
window in areas with sufficiently
elevated nighttime levels of O3 where
sensitive species with a high degree of
nocturnal stomatal conductance occur.
On the other hand, EPA also recognized
that a longer diurnal window (e.g., 24hour) has the possibility of overprotecting vegetation in areas where
nighttime O3 levels remain relatively
high but where no species having
significant nocturnal uptake exist. In
weighing these considerations, EPA
agreed with the 2007 Staff Paper
conclusion that until additional
information is available about the extent
to which this co-occurrence of sensitive
species and elevated nocturnal O3
exposures exists, and what levels of
nighttime uptake are adverse to affected
species, this information does not
provide a basis for reaching a different
conclusion at this time. The EPA also
considered to what extent the 3-month
period within the O3 season was
appropriate, recognizing that many
species of vegetation have longer
growing seasons. The EPA further
proposed that the maximum 3-month
period is sufficient and appropriate to
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characterize O3 exposure levels
associated with known levels of plant
response. Therefore, EPA proposed that
the most appropriate exposure periods
for a cumulative, seasonal form is the
daytime 12-hour window (8 a.m. to 8
p.m.) during the consecutive 3-month
period within the O3 monitoring season
with the maximum W126 index value.
The EPA also proposed an annual
rather than a multi-year cumulative,
seasonal standard. In proposing this
option, EPA also believed that it was
appropriate to consider the benefits to
the public welfare that would accrue
from establishing a 3-year average
secondary standard, and solicited
comment on this alternative. In so
doing, EPA also agreed with 2007 Staff
Paper and CASAC conclusions that
should a 3-year standard be finalized,
the level of the standard should be set
so as to provide the requisite degree of
protection for those vegetation effects
judged to be adverse to the public
welfare within a single annual period.
c. Level
The 2007 Staff Paper, in identifying a
range of levels for a 3-month, 12-hour
W126 annual form appropriate to
protect the public welfare from adverse
impacts to vegetation from O3
exposures, considered what information
from the array of vegetation effects
evidence and exposure and risk
assessment results was most useful.
Regarding the vegetation effects
evidence, the 2007 Staff Paper found
stronger support than what was
available at the time of the 1997 review
for an increased level of protection for
trees and ecosystems. Specifically, this
expanded body of support includes: (1)
Additional field based data from free
air, gradient and biomonitoring surveys
demonstrating adverse levels of O3induced above and/or below-ground
growth reductions on trees at the
seedling, sapling and mature growth
stages and incidence of visible foliar
injury occurring at biomonitoring sites
in the field at ambient levels of
exposure; (2) qualitative support from
free air (e.g., AspenFACE) and gradient
studies on a limited number of tree
species for the continued
appropriateness of using OTC-derived
C–R functions to predict tree seedling
response in the field; (3) studies that
continue to document below-ground
effects on root growth and ‘‘carry-over’’
effects occurring in subsequent years
from O3 exposures; and (4) increased
recognition and understanding of the
structure and function of ecosystems
and the complex linkages through
which O3, and other stressors, acting at
the organism and species level can
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influence higher levels within the
ecosystem hierarchy and disrupt
essential ecological attributes critical to
the maintenance of ecosystem goods
and services important to the public
welfare.
Based on the above observations and
on the vegetation effects and the results
of the exposure and impact assessment
summarized above, the 2007 Staff Paper
concluded that just meeting the then
current standard would still allow
adverse levels of tree seedling biomass
loss in sensitive commercially and
ecologically important tree species in
many regions of the country. Seedling
risk assessment results showed that
some tree seedling species are extremely
sensitive (e.g., cottonwood, black cherry
and aspen), with annual biomass losses
occurring in the field of the same or
greater magnitude that that of annual
crops. Such information from the tree
seedling risk assessment suggests that
O3 levels would need to be substantially
reduced to protect sensitive tree
seedlings like black cherry from growth
and foliar injury effects.
In addition to the currently
quantifiable risks to trees from ambient
exposures, the 2007 Staff Paper also
considered the more subtle impacts of
O3 acting in synergy with other natural
and man-made stressors to adversely
affect individual plants, populations
and whole systems. By disrupting the
photosynthetic process, decreasing
carbon storage in the roots, increasing
early senescence of leaves and affecting
water use efficiency in trees, O3
exposures could potentially disrupt or
change the nutrient and water flow of an
entire system. Weakened trees can
become more susceptible to other
environmental stresses such as pest and
pathogen outbreaks or harsh weather
conditions. Though it is not possible to
quantify all the ecological and societal
benefits associated with varying levels
of alternative secondary standards, the
2007 Staff Paper concluded that this
information should be weighed in
considering the extent to which a
secondary standard should be set so as
to provide potential protection against
effects that are anticipated to occur.
In addition, the 2007 Staff Paper also
recognized that in the 1997 review, EPA
took into account the results of a 1996
Consensus Workshop. At this workshop,
a group of independent scientists
expressed their judgments on what
standard form(s) and level(s) would
provide vegetation with adequate
protection from O3-related adverse
effects. Consensus was reached with
respect to selecting appropriate ranges
of levels in terms of a cumulative,
seasonal 3-month, 12-hr SUM06
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standard for a number of vegetation
effects endpoints. These ranges are
identified below, with the estimated
approximate equivalent W126 standard
values shown in parentheses. For
growth effects to tree seedlings in
natural forest stands, a consensus was
reached that a SUM06 range of 10 to 15
(W126 range of 7 to 13) ppm-hour
would be protective. For growth effects
to tree seedlings and saplings in
plantations, the consensus SUM06 range
was 12 to 16 (W126 range of 9 to 14)
ppm-hour. For visible foliar injury to
natural ecosystems, the consensus
SUM06 range was 8 to 12 (W126 range
of 5 to 9) ppm-hour.
Taking these consensus statements
into account, EPA stated in the 1997
final rule (62 FR 38856) that ‘‘the report
lends important support to the view that
the current secondary standard is not
adequately protective of vegetation
* * * [and] * * * foreshadows the
direction of future scientific research in
this area, the results of which could be
important in future reviews of the O3
secondary standard’’ (62 FR 38856).
Given the importance EPA put on the
consensus report in the 1997 review, the
2007 Staff Paper considered to what
extent research published after 1997
provided empirical support for the
ranges of levels identified by the experts
as protective of different types of O3induced effects. With regard to O3induced biomass loss in sensitive tree
seedlings/saplings growing in natural
forest stands, the information discussed
in the 2007 Staff Paper, including the
evidence from free air and gradient
studies, provides additional direct
support for the conclusion that the 1996
Consensus Workshop approximate
W126 range of 7–13 ppm-hour was an
appropriate range to consider in
selecting a protective level. With regard
to visible foliar injury, the available
evidence, including the 2007 Staff Paper
analysis of incidence in counties with
FIA monitoring sites and air quality
data, showed significant levels of
county-level visible foliar injury
incidence at the W126 level of 13 ppmhour. However, because this analysis
did not address risks of this effect at
lower levels of O3 air quality, and
because there is a significant
uncertainty in predicting the degree of
visible foliar injury symptoms expected
for lower levels of O3 air quality, the
evidence provides less certain but
qualitative directional support for the
1996 Consensus Workshop range of 5 to
9 ppm-hour to protect against this effect.
With regard to O3-induced effects on
plantation trees, there is far less direct
information available. Though some
forest plantation trees are O3-sensitive,
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the monoculture nature of these stands
makes uncertain the degree to which
competition for resources might play a
role and to what degree the variety of
management practices applied would be
expected to mitigate the O3-induced
effects. Thus, it is difficult to
distinguish a protective range of levels
for plantation trees from a range of
levels that would be protective of O3sensitive tree seedlings and saplings in
natural forest stands. Therefore, on the
basis of the strength of the evidence
available, the 2007 Staff Paper
concluded that it was appropriate to
consider a range for a 3-month, 12-hour,
W126 standard that included the 1996
consensus recommendations for growth
effects in tree seedlings in natural forest
stands (i.e., 7–13 ppm-hour in terms of
a W126 form).
In considering the available
information on O3-related effects on
crops in the 2008 rulemaking, the 2007
Staff Paper observed the following
regarding the strength of the underlying
crop science: (1) Nothing in the recent
literature points to a change in the
relationship between O3 exposure and
crop response across the range of
species and/or cultivars of commodity
crops currently grown in the U.S. that
could be construed to make less
appropriate the use of commodity crop
C–R functions developed in the NCLAN
program; (2) new field-based studies
(e.g., SoyFACE) provide qualitative
support in a few limited cases for the
appropriateness of using OTC-derived
C–R functions to predict crop response
in the field; and (3) refinements in the
exposure, risk and benefits assessments
in this review reduce some of the
uncertainties present in the 1997
review. On the basis of these
observations, the 2007 Staff Paper
concluded that nothing in the newly
assessed information called into
question the strength of the underlying
science upon which EPA based its
proposed decision in the 1997 review to
select a level of a cumulative, seasonal
form associated with protecting 50
percent of crop cases from no more than
10 percent yield loss as providing the
requisite degree of protection for
commodity crops.
The 2007 Staff Paper then considered
whether any additional information is
available to inform judgments as to the
adversity of various O3-induced levels
of crop yield loss to the public welfare.
As noted above, the 2007 Staff Paper
observed that agricultural systems are
heavily managed, and that in addition to
stress from O3, the annual productivity
of agricultural systems is vulnerable to
disruption from many other stressors
(e.g., weather, insects, disease), whose
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impact in any given year can greatly
outweigh the direct reduction in annual
productivity resulting from elevated O3
exposures. On the other hand, O3 can
also more subtly impact crop and forage
nutritive quality and indirectly
exacerbate the severity of the impact
from other stressors. Though these latter
effects currently cannot be quantified,
they should be considered in judging to
what extent a level of protection
selected to protect commodity crops
should be precautionary.
Based on the above considerations,
the 2007 Staff Paper concluded that the
level of protection (no more than 10%
yield or biomass loss in 50% of studied
cases) judged requisite in the 1997
review to protect the public welfare
from adverse levels of O3-induced
reductions in crop yields and tree
seedling biomass loss, as provided by a
W126 level of 21 ppm-hour, remains
appropriate for consideration as an
upper bound of a range of appropriate
levels.
Thus, the 2007 Staff Paper concluded,
based on all the above considerations,
that an appropriate range of 3-month,
12-hour W126 levels was 7 to 21 ppmhour, recognizing that the level selected
is largely a policy judgment as to the
requisite level of protection needed. In
determining the requisite level of
protection for crops and trees, and
indirectly, ecosystems, the 2007 Staff
Paper recognized that it is appropriate
to weigh the importance of the
predicted risks of these effects in the
overall context of public welfare
protection, along with a determination
as to the appropriate weight to place on
the associated uncertainties and
limitations of this information.
The CASAC, in its final letter to the
Administrator (Henderson, 2007),
agreed with the 2007 Staff Paper
recommendations that the lower bound
of the range within which a seasonal
W126 welfare-based (secondary) O3
standard should be considered is
approximately 7 ppm-hour; however, it
did not agree with staff’s
recommendation that the upper bound
of the range for consideration should be
as high as 21 ppm-hour. Rather, CASAC
recommended that the upper bound of
the range considered should be no
higher than 15 ppm-hour, which is just
above the upper ends of the ranges
identified in the 1996 Consensus
Workshop as being protective of tree
seedlings and saplings grown in natural
forest stands and in plantations. The
lower end of this range (7 ppm-hour) is
the same as the lower end of the range
identified in the 1996 Consensus
Workshop as protective of tree seedlings
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in natural forest stands from growth
effects.
In the 2007 proposed rule, taking
2007 Staff Paper and CASAC views into
account, EPA proposed a range of levels
for a cumulative, seasonal secondary
standard as expressed in terms of the
maximum 3 month, 12-hour W126 form,
in the range of 7 to 21 ppm-hour. This
range encompasses the range of levels
recommended by CASAC, and also
includes a higher level as recommended
for consideration in the 2007 Staff
Paper. Given the uncertainty in
determining the risk attributable to
various levels of exposure to O3, EPA
believed, as a public welfare policy
judgment, that this was a reasonable
range to propose.
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2. Considerations Regarding the 2007
Proposed 8-Hour Standard
In the 1997 review, the 1996 Staff
Paper included an analysis to compare
the degree of overlap between areas that
would be expected not to meet the range
of alternative 8-hour standards being
considered for the primary NAAQS and
those expected not to meet the range of
values (expressed in terms of the
seasonal SUM06 index) of concern for
vegetation. This result suggested that
improvements in national air quality
expected to result from attaining an 8hour primary standard within the
recommended range of levels would
also be expected to reduce levels of
concern for vegetation in those same
areas. In the 1997 final rule, the
decision was made, on the basis of both
science and policy considerations, to
make the secondary identical to the
primary standard. It acknowledged,
however, that uncertainties remained
‘‘as to the extent to which air quality
improvements designed to reduce 8hour average O3 concentrations
averaged over a 3-year period would
reduce O3 exposures measured by a
seasonal SUM06 index’’ (62 FR 38876).
On the basis of that history, the 2007
Staff Paper analyzed the degree of
overlap expected between alternative 8hour and cumulative seasonal
secondary standards (as discussed above
in section IV.C.1) using then recent air
quality. Based on the results, the 2007
Staff Paper concluded that the degree to
which the then current 8-hour standard
form and level would overlap with areas
of concern for vegetation expressed in
terms of the 12-hour W126 standard is
inconsistent from year to year and
would depend greatly on the level of the
12-hour W126 and 8-hour standards
selected and the distribution of hourly
O3 concentrations within the annual
and/or 3-year average period.
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Thus, though the 2007 Staff Paper
recognized again that meeting the
current or alternative levels of the 8hour average standard could result in air
quality improvements that would
potentially benefit vegetation in some
areas, it urged caution be used in
evaluating the likely vegetation impacts
associated with a given level of air
quality expressed in terms of the 8-hour
average form in the absence of parallel
W126 information. This caution was
due to the concern that the analysis in
the 2007 Staff Paper may not be an
accurate reflection of the true situation
in non-monitored, rural counties due to
the lack of more complete monitor
coverage in many rural areas. Further, of
the counties that did not show overlap
between the two standard forms, most
were located in rural/remote high
elevation areas which have O3 air
quality patterns that are typically
different from those associated with
urban and near urban sites at lower
elevations. Because the majority of such
areas are currently not monitored, it is
believed there are likely to be additional
areas that have similar air quality
distributions that would lead to the
same disconnect between forms. Thus,
the 2007 Staff Paper concluded that it
remained problematic to determine the
appropriate level of protection for
vegetation using an 8-hour average form.
The CASAC recognized that an
important difference between the effects
of acute exposures to O3 on human
health and the effects of O3 exposures
on welfare is that vegetation effects are
more dependent on the cumulative
exposure to, and uptake of, O3 over the
course of the entire growing season
(Henderson, 2006c). The CASAC O3
Panel members were unanimous in
concluding the protection of natural
terrestrial ecosystems and managed
agricultural crops requires a secondary
O3 standard that is substantially
different from the primary O3 standard
in averaging time, level, and form
(Henderson, 2007).
In considering the appropriateness of
proposing a revised secondary standard
that would be identical to the proposed
primary standard, EPA took into
account the approach used by the
Agency in the 1997 review, the
conclusions of the 2007 Staff Paper,
CASAC advice, and the views of public
commenters. The EPA first considered
the 2007 Staff Paper analysis of the
projected degree of overlap between
counties with air quality expected to
meet various alternative levels of an 8hour standard and alternative levels of
a W126 standard based on monitored air
quality data. This analysis showed
significant overlap within the proposed
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range of the primary 8-hour form and
selected levels of the W126 standard
form being considered, with the degree
of overlap between these two forms
depending greatly on the levels selected
and the distribution of hourly O3
concentrations within the annual and/or
3-year average period. On this basis,
EPA concluded that a secondary
standard set identical to the proposed
primary standard would provide a
significant degree of additional
protection for vegetation as compared to
that provided by the current secondary
standard. The EPA also recognized that
lack of rural monitoring data made
uncertain the degree to which the
proposed 8-hour or W126 alternatives
would be protective, and that there
would be the potential for not providing
the appropriate degree of protection for
vegetation in areas with air quality
distributions that result in a high
cumulative, seasonal exposure but do
not result in high 8-hour average
exposures. While this potential for
under-protection using an 8-hour
standard was clear, the number and size
of areas at issue and the degree of risk
was hard to determine. On the other
hand, EPA also considered at that time
that there was a potential risk of overprotection with a cumulative, seasonal
standard given the inherent
uncertainties associated with moving to
a new form for the secondary standard,
in particular those associated with
predicting exposure and risk patterns
based on a limited rural monitoring
network.
The EPA also considered the views
and recommendations of CASAC, and
agreed that a cumulative, seasonal
standard is the most biologically
relevant way to relate exposure to plant
growth response. However, as reflected
in the public comments, EPA also
recognized that there remained
significant uncertainties in determining
or quantifying the degree of risk
attributable to varying levels of O3
exposure, the degree of protection that
any specific cumulative, seasonal
standard would produce, and the
associated potential for error in
determining the standard that will
provide a requisite degree of
protection—i.e., sufficient but not more
than what is necessary. Given this
uncertainty, EPA also believed it was
appropriate to consider the degree of
protection that would be afforded by a
secondary standard that was identical to
the then proposed primary standard.
Based on its consideration of the full
range of views as described above, and
in the 2007 proposed rule, EPA
proposed as a second option to revise
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the secondary standard to be identical
in every way to the then proposed
primary standard.
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3. Basis for 2008 Decision on the
Secondary Standard
In the 2008 final rule, EPA noted that
deciding on the appropriate secondary
standard involved making a choice
between two possible alternatives, each
with their strengths and weaknesses.
The 2008 final rule reported that within
the Administration at that time there
had been a robust discussion of the
same strengths and weaknesses
associated with each option that were
identified earlier. The process by which
EPA reached its final conclusion is
described in the final rule (73 FR
16497). The rationale for the 2008
decision presented in the final rule (73
FR 16499–16500) is described below.
In considering the appropriateness of
establishing a new standard defined in
terms of a cumulative, seasonal form, or
revising the then current secondary
standard by making it identical to the
revised primary standard, EPA took into
account the approach used by the
Agency in the 1997 review, the
conclusions of the 2007 Staff Paper,
CASAC advice, and the views of public
commenters. In giving consideration to
the approach taken in the 1997 review,
EPA first considered the 2007 Staff
Paper analysis of the projected degree of
overlap between counties with air
quality expected to meet the revised 8hour primary standard, set at a level of
0.075 ppm, and alternative levels of a
W126 standard based on currently
monitored air quality data. This analysis
showed significant overlap between the
revised 8-hour primary standard and
selected levels of the W126 standard
form being considered, with the degree
of overlap between these alternative
standards depending greatly on the
W126 level selected and the distribution
of hourly O3 concentrations within the
annual and/or 3-year average period.59
On this basis, as an initial matter, EPA
concluded that a secondary standard set
identical to the proposed primary
standard would provide a significant
degree of additional protection for
vegetation as compared to that provided
by the then current 0.084 ppm
secondary standard. In further
considering the significant uncertainties
that remain in the available body of
evidence of O3-related vegetation effects
and in the exposure and risk analyses
conducted for the 2008 rulemaking, and
59 Prior to publication of the 2008 final rule, EPA
did further analysis of the degree of overlap to
extend the 2007 Staff Paper analyses, and that
analysis was available in the docket.
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the difficulty in determining at what
point various types of vegetation effects
become adverse for sensitive vegetation
and ecosystems, EPA focused its
consideration on a level for an
alternative W126 standard at the upper
end of the proposed range (i.e., 21 ppmhour). The 2007 Staff Paper analysis
showed that at that W126 standard
level, there would be essentially no
counties with air quality that would be
expected both to exceed such an
alternative W126 standard and to meet
the revised 8-hour primary standard—
that is, based on this analysis of
currently monitored counties, a W126
standard would be unlikely to provide
additional protection in any monitored
areas beyond that likely to be provided
by the revised primary standard.
The EPA also recognized that the
general lack of rural monitoring data
made uncertain the degree to which the
revised 8-hour standard or an
alternative W126 standard would be
protective in those areas, and that there
would be the potential for not providing
the appropriate degree of protection for
vegetation in areas with air quality
distributions that result in a high
cumulative, seasonal exposure but do
not result in high 8-hour average
exposures. While this potential for
under-protection using an 8-hour
standard was clear, the number and size
of areas at issue and the degree of risk
was hard to determine. However, EPA
concluded at that time that an 8-hour
standard would also tend to avoid the
potential for providing more protection
than is necessary, a risk that EPA
concluded would arise from moving to
a new form for the secondary standard
despite significant uncertainty in
determining the degree of risk for any
exposure level and the appropriate level
of protection, as well as uncertainty in
predicting exposure and risk patterns.
The EPA also considered the views
and recommendations of CASAC, and
agreed that a cumulative, seasonal
standard was the most biologically
relevant way to relate exposure to plant
growth response. However, as reflected
in some public comments, EPA also
judged that there remained significant
uncertainties in determining or
quantifying the degree of risk
attributable to varying levels of O3
exposure, the degree of protection that
any specific cumulative, seasonal
standard would produce, and the
associated potential for error in
determining the standard that will
provide a requisite degree of
protection—i.e., sufficient but not more
than what is necessary. Given these
significant uncertainties, EPA
concluded at that time that establishing
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a new secondary standard with a
cumulative, seasonal form would result
in uncertain benefits beyond those
afforded by the revised primary
standard and therefore may be more
than necessary to provide the requisite
degree of protection.
Based on its consideration of the
views discussed above, EPA judged in
the 2008 rulemaking that the
appropriate balance to be drawn was to
revise the secondary standard to be
identical in every way to the revised
primary standard. The EPA believed
that such a standard would be sufficient
to protect public welfare from known or
anticipated adverse effects, and did not
believe that an alternative cumulative,
seasonal standard was needed to
provide this degree of protection. The
EPA believed that this judgment
appropriately considered the
requirement for a standard that is
neither more nor less stringent than
necessary for this purpose.
For the reasons discussed above, and
taking into account information and
assessments presented in the 2006
Criteria Document and 2007 Staff Paper,
the advice and recommendations of the
CASAC Panel, and the public comments
to date, EPA decided to revise the
existing 8-hour secondary standard.
Specifically, EPA revised the then
current 8-hour average 0.084 ppm
secondary standard by making it
identical to the revised 8-hour primary
standard set at a level of 0.075 ppm.
4. CASAC Views Following 2008
Decision
Following the 2008 decision on the O3
standards, serious questions were raised
as to whether the standards met the
requirements of the CAA. In April 2008,
the members of the CASAC Ozone
Review Panel sent a letter to EPA stating
‘‘In our most-recent letters to you on this
subject—dated October 2006 and March
2007—* * * the Committee
recommended an alternative secondary
standard of cumulative form that is
substantially different from the primary
Ozone NAAQS in averaging time, level
and form—specifically, the W126 index
within the range of 7 to 15 ppm-hour,
accumulated over at least the 12
‘‘daylight’’ hours and the three
maximum ozone months of the summer
growing season’’ (Henderson, 2008). The
letter continued: ‘‘The CASAC now
wishes to convey, by means of this
letter, its additional, unsolicited advice
with regard to the primary and
secondary Ozone NAAQS. In doing so,
the participating members of the
CASAC Ozone Review Panel are
unanimous in strongly urging you or
your successor as EPA Administrator to
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ensure that these recommendations be
considered during the next review cycle
for the Ozone NAAQS that will begin
next year’’ (id.). The letter further stated
the following views:
The CASAC was * * * greatly
disappointed that you failed to change the
form of the secondary standard to make it
different from the primary standard. As
stated in the preamble to the Final Rule, even
in the previous 1996 ozone review, ‘‘there
was general agreement between the EPA staff,
CASAC, and the Administrator, * * * that a
cumulative, seasonal form was more
biologically relevant than the previous
1-hour and new 8-hour average forms (61 FR
65716)’’ for the secondary standard.
Therefore, in both the previous review and in
this review, the Agency staff and its advisors
agreed that a change in the form of the
secondary standard was scientifically welljustified.
*
*
*
*
*
srobinson on DSKHWCL6B1PROD with PROPOSALS2
Unfortunately, this scientifically-sound
approach of using a cumulative exposure
index for welfare effects was not adopted,
and the default position of using the primary
standard for the secondary standard was once
again instituted. Keeping the same form for
the secondary Ozone NAAQS as for the
primary standard is not supported by current
scientific knowledge indicating that different
indicator variables are needed to protect
vegetation compared to public health. The
CASAC was further disappointed that a
secondary standard of the W126 form was
not considered from within the Committee’s
previously-recommended range of 7 to 15
ppm-hour. The CASAC sincerely hopes that,
in the next round of Ozone NAAQS review,
the Agency will be able to support and
establish a reasonable and scientificallydefensible cumulative form for the secondary
standard. (Henderson, 2008)
5. Administrator’s Proposed
Conclusions
For the reasons discussed below, the
Administrator proposes to set a
cumulative seasonal standard expressed
as an annual index of the sum of
weighted hourly concentrations (i.e., the
W126 form), cumulated over 12 hours
per day (8 am to 8 pm) during the
consecutive 3-month period within the
O3 season with the maximum index
value, set at a level within the range of
7 to 15 ppm-hour. This proposed
decision takes into account the
information and assessments presented
in the 2006 Criteria Document and the
2007 Staff Paper and related technical
support documents, the advice and
recommendations of CASAC both
during and following the 2008
rulemaking, and public comments
received in conjunction with review of
drafts of these documents and on the
2007 proposed rule.
a. Form
As discussed above in section IV.B,
the 2006 Criteria Document and 2007
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Staff Paper concluded that the recent
vegetation effects literature evaluated in
the 2008 rulemaking strengthens and
reaffirms conclusions made in the 1997
review that the use of a cumulative
exposure index that differentially
weights ambient concentrations is best
able to relate ambient exposures to
vegetation response. The 1997 review
focused in particular on two of these
cumulative forms, the SUM06 and
W126 (EPA, 1996). Given that the data
available at that time were unable to
distinguish between these forms, the
EPA, based on the policy consideration
of not including O3 concentrations
considered to be within the PRB,
estimated at that time to be between
0.03 and 0.05 ppm, concluded that the
SUM06 form would be the more
appropriate choice for a cumulative,
exposure index for a secondary
standard.
In the 2008 rulemaking, the 2007 Staff
Paper evaluated the continued
appropriateness of the SUM06 form in
light of new estimates of PRB that were
lower than in the 1997 review, and the
continued lack of evidence within the
vegetation effects literature of a
biological threshold for vegetation
exposures of concern. On the basis of
these policy and science-related
considerations, the 2007 Staff Paper
concluded that the W126 form was the
more appropriate cumulative,
concentration-weighted form.
Specifically, the W126, by its
incorporation of a sigmoidal weighting
scheme, does not create an artificially
imposed concentration threshold, gives
proportionally more weight to the
higher and typically more biologically
potent concentrations, and is not
significantly influenced by O3
concentrations within the range of
estimated PRB.
As discussed above, the CASAC,
based on its assessment of the same
vegetation effects science, agreed with
the 2006 Criteria Document and 2007
Staff Paper and unanimously concluded
that protection of vegetation from the
known or anticipated adverse effects of
ambient O3 ‘‘requires a secondary
standard that is substantially different
from the primary standard in averaging
time, level, and form,’’ i.e. not identical
to the primary standard for O3
(Henderson, 2007). Moreover, the
members of CASAC and a substantial
majority of the other CASAC Panel
members agreed with 2007 Staff Paper
conclusions and encouraged EPA to
establish an alternative cumulative
secondary standard for O3 and related
photochemical oxidants that is
distinctly different in averaging time,
form and level from the then current or
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potentially revised 8-hour primary
standard (Henderson, 2006c). The
CASAC Panel also stated that ‘‘the
recommended metric for the secondary
ozone standard is the (sigmoidally
weighted) W126 index’’ (Henderson,
2007).
In reconsidering the 2008 final rule,
the Administrator agrees with the
conclusions drawn in the 2006 Criteria
Document, 2007 Staff Paper and by
CASAC that the scientific evidence
available in the 2008 rulemaking
continues to demonstrate the
cumulative nature of O3-induced plant
effects and the need to give greater
weight to higher concentrations. Thus,
the Administrator concludes that a
cumulative exposure index that
differentially weights O3 concentrations
represents a reasonable policy choice for
a secondary standard to protect against
the effects of O3 on vegetation. The
Administrator further agrees with both
the 2007 Staff Paper and CASAC that
the most appropriate cumulative,
concentration-weighted form to
consider is the sigmoidally weighted
W126 form.
The Administrator notes that in the
2007 proposed rule, EPA proposed a
second option of revising the then
current 8-hour average secondary
standard by making it identical to the
proposed 8-hour primary standard. The
2007 Staff Paper analyzed the degree of
overlap expected between alternative
8-hour and cumulative seasonal
secondary standards using recent air
quality monitoring data. Based on the
results, the 2007 Staff Paper concluded
that the degree to which the current
8-hour standard form and level would
overlap with areas of concern for
vegetation expressed in terms of the
12-hour W126 standard is inconsistent
from year to year and would depend
greatly on the level of the 12-hour W126
and 8-hour standards selected and the
distribution of hourly O3 concentrations
within the annual and/or 3-year average
period. The 2007 Staff Paper also
recognized that meeting the then current
or alternative levels of the 8-hour
average standard could result in air
quality improvements that would
potentially benefit vegetation in some
areas, but urged caution be used in
evaluating the likely vegetation impacts
associated with a given level of air
quality expressed in terms of the 8-hour
average form in the absence of parallel
W126 information. This caution was
due to the concern that the analysis in
the 2007 Staff Paper may not be an
accurate reflection of the true situation
in non-monitored, rural counties due to
the lack of more complete monitor
coverage in many rural areas. Further, of
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the counties that did not show overlap
between the two standard forms, most
were located in rural/remote high
elevation areas which have O3 air
quality patterns that are typically
different from those associated with
urban and near urban sites at lower
elevations. Because the majority of such
areas are currently not monitored, there
are likely to be additional areas that
have similar air quality distributions
that would lead to the same disconnect
between forms. Thus, the 2007 Staff
Paper concluded that it remains
problematic to determine the
appropriate level of protection for
vegetation using an 8-hour average form.
The Administrator also notes that
CASAC recognized that an important
difference between the effects of acute
exposures to O3 on human health and
the effects of O3 exposures on welfare is
that vegetation effects are more
dependent on the cumulative exposure
to, and uptake of, O3 over the course of
the entire growing season (Henderson,
2006c). The CASAC O3 Panel members
were unanimous in concluding the
protection of natural terrestrial
ecosystems and managed agricultural
crops requires a secondary O3 standard
that is substantially different from the
primary O3 standard in form, averaging
time, and level (Henderson, 2007).
In reaching her proposed decision in
this reconsideration of the 2008 final
rule, the Administrator has considered
the comments received on the 2007
proposed rule regarding revising the
secondary standard either to reflect a
new, cumulative form or by remaining
equal to a revised primary standard. The
commenters generally fell into two
groups.
One group of commenters, including
environmental organizations, strongly
supported the proposed option of
moving to a cumulative, seasonal
standard, generally based on the
reasoning explained in the 2007
proposal. Commenters in this group also
expressed serious concerns with the
other proposed option of setting a
secondary O3 standard in terms of the
same form and averaging time (i.e., daily
maximum 8-hour average O3
concentration) as the primary standard.
These commenters expressed the view
that such a standard would fail to
protect public welfare because the
maximum daily 8-hour average O3
concentration failed to adequately
characterize harmful O3 exposures to
vegetation. This view was generally
based on the observation that there is no
consistent relationship in areas across
the U.S. between 8-hour peak O3
concentrations and the longer-term
cumulative exposures aggregated over a
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growing season that are biologically
relevant in characterizing O3-related
effects on sensitive vegetation. Thus, as
EPA noted in the 2007 proposed rule,
there is a lack of a rational connection
between the level of an 8-hour standard
and the requisite degree of protection
required for a secondary O3 NAAQS.
Another group of commenters,
including industry organizations, agreed
that a cumulative form of the standard
may better match the underlying data,
but expressed the view that remaining
uncertainties associated with the
vegetation effects evidence and/or EPA’s
exposure, risk and benefits assessments
were so great that the available
information did not provide an adequate
basis to adopt a standard with a level
based on a cumulative, seasonal form.
These commenters asserted that because
of the substantial uncertainties
remaining at the time of the 2008
rulemaking, the benefits of changing to
a W126 form were too uncertain to
warrant revising the form of the
standard at that time.
The Administrator notes that in both
the 1997 and the 2008 decisions, EPA
recognized that the risk to vegetation
from O3 exposures comes from
cumulative exposures over a season or
seasons. The CASAC has fully endorsed
this view based on the available
scientific evidence and assessments,
and there is no significant disagreement
on this issue by commenters. Thus, it is
clear that the purpose of the secondary
O3 NAAQS should be to provide an
appropriate degree of protection against
cumulative, seasonal exposures to O3
that are known or anticipated to harm
sensitive vegetation or ecosystems. In
reconsidering the 2008 final rule, the
Administrator recognizes that the issue
before the Agency is what form of the
standard is most appropriate to perform
that function.
Within this framework, the
Administrator recognizes that it is clear
that a cumulative, seasonal form has a
distinct advantage in protecting against
cumulative, seasonal exposures. Such a
form is specifically designed to measure
directly the kind of O3 exposures that
can cause harm to vegetation. In
contrast, an 8-hour standard does not
measure cumulative, seasonal exposures
directly, and can only indirectly afford
some degree of protection against such
exposures. To the extent that clear
relationships exist between 8-hour daily
peak O3 concentrations and cumulative,
seasonal exposures, the 8-hour form and
averaging time would have the potential
to be effective as an indirect surrogate.
However, as discussed in the 2007
proposed rule and the 2008 final rule,
the evidence shows that there are
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known types of O3 air quality patterns
that can lead to high levels of
cumulative, seasonal O3 exposures
without the occurrence of high daily 8hour peak O3 concentrations. An 8-hour
form and averaging time is an indirect
way to measure biologically relevant
exposure patterns, is poorly correlated
with such exposure patterns, and
therefore is less likely to identify and
protect against the kind of cumulative,
seasonal exposure patterns that have
been determined to be harmful.
Past arguments or reasons for not
moving to a cumulative, seasonal form,
with appropriate exposure periods, have
not been based on disagreement over the
biological relevance of the cumulative,
seasonal form, or the recognized
disadvantages of an 8-hour standard in
measuring and identifying a specified
cumulative, seasonal exposure pattern.
The reasons for not moving to such a
form have been based on concerns over
whether EPA has an adequate basis to
identify the nature and magnitude of
cumulative, seasonal exposure patterns
that the standard should be designed to
protect against, given the various
uncertainties in the evidence and the
lack of rural O3 monitoring data. This
most directly translates into a concern
over whether EPA has an adequate basis
to determine an appropriate level for a
cumulative, seasonal secondary
standard.
The Administrator has also
considered issues associated with
selection of the W126 cumulative form,
as reflected in the following assertions
made by some commenters on the 2007
proposed rule: (1) The W126 form lacks
a biological basis, since it is merely a
mathematical expression of exposure
that has been fit to specific responses in
OTC studies, such that its relevance for
real world biological responses is
unclear; (2) a flux-based model would
be a better choice than a cumulative
metric because it is an improvement
over the many limitations and
simplifications associated with the
cumulative form; however, there is
insufficient data to apply such a model
at present; (3) the European experience
with cumulative O3 metrics has been
disappointing and now Europeans are
working on their second level approach,
which will be flux-based; and (4) a
second index that reflects the
accumulation of peaks at or above 0.10
ppm (called N100) should be added to
a W126 index to achieve appropriate
protection.
With regard to whether the W126
index lacks a biological basis, the
Administrator finds no basis for
reaching such a conclusion. As
discussed above in section IV.B, the
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vegetation effects science is clear that
exposures of concern to plants are not
based on one discrete 8-hour period but
on the repeated occurrence of elevated
O3 levels throughout the plant’s growing
season. The cumulative nature of the
W126 is supported by the basic
biological understanding that plants in
the U.S. are generally most biologically
active during the warm season and are
exposed to ambient O3 throughout this
biologically active period. In addition, it
has been shown in the scientific
literature that all else being equal,
plants respond more to higher O3
concentrations, with no evidence of an
exposure threshold for vegetation
effects. The W126 sigmoidal weighting
function reflects both of these
understandings, by not including a
threshold below which concentrations
are not included, and by differentially
weighting concentrations to give greater
weight to higher concentrations and less
weight to lower ones.
With regard to whether a flux-based
model would be a better choice, the
2007 Staff Paper acknowledged that flux
models may produce a more accurate
calculation of dose to a specific plant
species in a specific area. However,
dose-response relationships have not
been developed for these flux
calculations for plants growing in the
U.S. Further, flux calculations require
large amounts of data for the physiology
of each plant species and the local
conditions for the growing range of each
plant species. These exercises may be
useful for limited small-scale risk
assessments, but do not provide an
appropriate basis for a national standard
at this time.
With regard to dissatisfaction with the
performance of a particular cumulative
index in use in Europe,60 and growing
interest in development of flux-based
models, the 2007 Staff Paper (Appendix
7A) noted that ‘‘because of a lack of fluxresponse data, a cumulative, cutoff
concentration based (e.g., AOT40)
exposure index will remain in use in
Europe for the near future for most
crops and for forests and semi-natural
herbaceous vegetation (Ashmore et al.,
2004a).’’ Further, like the SUM06 index,
the AOT40 index incorporates a
threshold below which concentrations
are not considered. Though the AOT40
threshold is lower than the threshold
value in SUM06, the 2007 Staff Paper
concluded that the vegetation effects
60 The AOT40 index used in Europe is a
cumulative index that incorporates a threshold at
0.04 ppm (40 ppb). This index is calculated as the
area over the threshold (AOT) by subtracting 40 ppb
from the value of each hourly concentration above
that threshold and then cumulating each hourly
difference over a specified window.
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information does not provide evidence
of an effects threshold that applies to all
species. Thus, the Administrator
concludes neither of these forms is as
biologically relevant as the W126 form.
With regard to consideration of
coupling a W126 form with a separate
N100 index, there was very little
research on the N100 index or a coupled
approach to be evaluated in the 2008
rulemaking. The CASAC, after
reviewing all the information in the
2006 Criteria Document and the 2007
Staff Paper, did not recommend an
additional N100 index for
consideration. Therefore, there is no
basis at this time to judge the extent to
which such a coupled W126–N100 form
would be a better choice than the
proposed W126 form. Further, the W126
form incorporates a weighting scheme
that places greater weight on increasing
concentrations and gives every
concentration of 0.10 ppm and above an
equal weight of 1, which is the highest
weight in this sigmoidal weighting
function.
In summary, having considered the
scientific information and assessment
results available in the 2008 rulemaking
as discussed above in this proposal
notice, as well as the recommendations
of the staff and CASAC, and having
taken into consideration issues raised in
public comments received as part of the
2008 rulemaking, and recognizing the
determinations made below in section
IV.D.5.c on level, the Administrator
concludes that it is appropriate to set
the secondary standard using a
cumulative, seasonal form. The
Administrator also concludes that the
W126 form is best suited to reflect the
biological impacts of O3 exposure on
vegetation, and that there is adequate
certainty in the information available in
the 2008 rulemaking to support such a
change in form. Thus, the Administrator
proposes to set the secondary standard
using a cumulative, seasonal W126
form.
b. Averaging Times 61
The Administrator, in addition to
reconsidering what form of a secondary
standard is most appropriate for
protecting vegetation, is also
reconsidering what exposure periods
(e.g., seasonal window, diurnal
window), and what standard index, in
terms of an annual index value versus
a 3-year average of annual index values,
are most appropriate when used in
conjunction with the W126 cumulative
61 While the term ‘‘averaging time’’ is used, for the
cumulative, seasonal standard the seasonal and
diurnal time periods at issue are those over which
exposures during a specified period of time are
cumulated, not averaged.
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seasonal form. Based on the information
set forth in the 2007 Staff Paper, as well
as CASAC views, as discussed above in
section IV.D.1.b, the Administrator has
reached conclusions regarding exposure
periods, and the annual versus 3-year
average index, that have the most
biological relevance for plant response,
as discussed below.
In considering an appropriate
seasonal window, the Administrator
notes that the 2007 Staff Paper
concluded that the consecutive 3-month
period within the O3 season with the
highest W126 index value (e.g.,
maximum 3-month period) was a
reasonable seasonal time period to
consider. The Administrator further
notes that the 2007 Staff Paper
acknowledged that the selection of any
single seasonal exposure period for a
national standard would necessarily
represent a compromise, given the
significant variability in growth patterns
and lengths of growing seasons among
the wide range of sensitive vegetation
species occurring within the U.S.
However, the Administrator also
considered the Staff Paper conclusion
that the period of maximum potential
plant uptake of O3 would also likely
coincide with the period of highest O3
occurring within the intra-annual period
defined as the O3 season, since the high
temperature and light conditions
conducive to O3 formation are also
conducive for plant activity. The
Administrator also observes that the
CASAC panel was supportive of the
Staff Paper views, while recognizing
that 3 months likely represented the
minimum timeframe appropriate to
consider. Therefore, the Administrator
concludes, on these bases, that the
consecutive 3-month period within the
O3 season with the highest W126 index
value (e.g., maximum 3-month period)
remains an appropriate seasonal
window to propose for the protection of
sensitive vegetation.
With regard to consideration of an
appropriate diurnal window, the
Administrator has taken into account
the 2007 Staff Paper conclusion that for
the vast majority of studied species,
daytime exposures represent the
majority of diurnal plant O3 uptake and
are responsible for inducing the plant
response of most significance to the
health and productivity of the plant
(e.g., reduced carbohydrate production).
The Administrator is also aware, based
on discussions in the 2007 Staff Paper
that there are some number of species
that show non-negligible amounts of O3
uptake at night due to incomplete
stomatal closure. In reaching her
conclusion that the 2007 Staff Paper
recommendation of a 12-hour daytime
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window (8 a.m. to 8 p.m.) remains the
most appropriate period over which to
cumulate diurnal O3 exposures,
specifically those most relevant to plant
growth and yield responses, the
Administrator places weight on the fact
that the CASAC comments were also
supportive of this diurnal window,
recognizing again that it likely
represents a minimum period over
which plants can be vulnerable to O3
uptake. Therefore, the Administrator is
again proposing the 12-hour daytime
window (8 a.m. to 8 p.m.) as an
appropriate diurnal window to protect
against O3-induced plant effects.
Lastly, in considering whether an
annual or a 3-year average index is more
appropriate, the Administrator notes
that in addition to the available
scientific evidence regarding plant
effects that can be brought to bear, there
are also other public welfare
considerations that may be appropriate
to consider. In taking this view, the
Administrator notes that the 2007 Staff
Paper recognized that though most
cumulative seasonal exposure levels of
concern for vegetation have been
expressed in terms of the annual
timeframe, it may be appropriate to
consider a 3-year average for purposes
of standard stability. The Administrator
has considered that while the 2007 Staff
Paper notes that for certain welfare
effects of concern (e.g., foliar injury,
yield loss for annual crops, growth
effects on other annual vegetation and
potentially tree seedlings), an annual
time frame may be a more appropriate
period in which to assess what level
would provide the requisite degree of
protection, for other welfare effects (e.g.,
mature tree biomass loss), it also points
out that a 3-year average may also be
appropriate. The Administrator further
observes that in concluding that it was
appropriate to consider both an annual
and a 3-year average, the 2007 Staff
Paper also concluded that should a 3year average of the 3-month, 12-hour
W126 form be selected, a potentially
lower level should be considered to
reduce the potential of adverse impacts
to annual species from a single high O3
year that could still occur while
attaining a standard on average over
3-years. The Administrator also took
note that the CASAC Panel, in
addressing this issue of annual versus 3year average concluded that multi-year
averaging to promote a ‘‘stable’’
secondary standard is less appropriate
for a cumulative, seasonal secondary
standard than for a primary standard
based on maximum 8-hour
concentrations, and further concluded
that if multi-year averaging is employed
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to increase the stability of the secondary
standard, the level of the standard
should be revised downward to assure
that the desired degree of protection is
not exceeded in individual years. The
Administrator, in considering the merits
of both the annual and 3-year average,
and taking into account both the 2007
Staff Paper and CASAC views,
concludes that it is important to place
more weight on the public welfare
benefit in having a stable standard, and
that appropriate protection for
vegetation can be achieved using a
3-year average form. The Administrator
is thus proposing a 3-year average.
However, given the uncertain nature of
the evidence and potential concerns
with using a 3-year average form, the
Administrator is proposing to take
comment on the appropriateness of the
specific seasonal and diurnal exposure
periods proposed, as well as the use of
a 3-year average, and, as discussed
below, the impact that selection of these
proposed seasonal and diurnal exposure
periods would have, in conjunction
with a 3-year average form, on the
appropriateness of the proposed range
of levels.
c. Level
i. Considerations Regarding 2007
Proposed Range of Levels
The 2007 Staff Paper, in identifying a
range of levels for a 3-month, 12-hour
(daytime) W126 standard appropriate
for the Administrator to consider in
protecting the public welfare from
known or anticipated adverse effects to
vegetation from O3 exposures,
considered what information from the
array of vegetation effects evidence and
exposure and risk assessment results
was most useful. With respect to the
vegetation effects evidence, the 2007
Staff Paper found stronger support than
what was available at the time of the
1997 review for an increased level of
protection for trees and forested
ecosystems. Specifically, the expanded
body of evidence included: (1)
Additional field based data from free
air, gradient and biomonitoring surveys
demonstrating adverse levels of O3induced growth reductions on trees at
the seedling, sapling and mature growth
stages and incidence of visible foliar
injury occurring at biomonitoring sites
in the field at ambient levels of
exposure; (2) qualitative support from
free air (e.g., AspenFACE) and gradient
studies on a limited number of tree
species for the continued
appropriateness of using OTC-derived
C–R functions to predict tree seedling
response in the field; (3) studies that
continued to document below-ground
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effects on root growth and ‘‘carry-over’’
effects occurring in subsequent years
from O3 exposures; and (4) increased
recognition and understanding of the
structure and function of ecosystems
and the complex linkages through
which O3, and other stressors, acting at
the organism and species level can
influence higher levels within the
ecosystem hierarchy and disrupt
essential ecological attributes critical to
the maintenance of ecosystem goods
and services important to the public
welfare.
Based on the above sources of
vegetation effects information and the
results of the exposure and risk
assessments summarized above, the
2007 Staff Paper concluded that just
meeting the then current 0.084 ppm,
8-hour average standard would continue
to allow adverse levels of O3-induced
effects to occur in sensitive
commercially and ecologically
important tree species in many regions
of the country. The 2007 Staff Paper
further concluded that air quality levels
would need to be substantially reduced
to protect sensitive tree seedlings, such
as black cherry, aspen, and cottonwood,
from these growth and foliar injury
effects.
In addition to the currently
quantifiable risks to trees from ambient
exposures, the 2007 Staff Paper also
considered the more subtle impacts of
O3 acting in synergy with other natural
and man-made stressors to adversely
affect individual plants, populations
and whole systems. By disrupting the
photosynthetic process, decreasing
carbon storage in the roots, increasing
early senescence of leaves and affecting
water use efficiency in trees, O3
exposures could potentially disrupt or
change the nutrient and water flow of an
entire system. Weakened trees can
become more susceptible to other
environmental stresses such as pest and
pathogen outbreaks or harsh weather
conditions. Though it is not possible to
quantify all the ecological and societal
benefits associated with varying levels
of alternative secondary standards, the
2007 Staff Paper concluded that this
information should be weighed in
considering the extent to which a
secondary standard should be set so as
to provide potential protection against
effects that are anticipated to occur.
The 2007 Staff Paper also recognized
that in the 1997 review, EPA took into
account the results of a 1996 Consensus
Workshop. At this workshop, a group of
independent scientists expressed their
judgments on what standard form(s) and
level(s) would provide vegetation with
adequate protection from O3-related
adverse effects. Consensus was reached
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on protective ranges of levels in terms
of a cumulative, seasonal 3-month, 12hr SUM06 standard for a number of
vegetation effects endpoints. These
ranges are identified below, with the
estimated approximate equivalent W126
standard levels shown in parentheses.
For growth effects to tree seedlings in
natural forest stands, a consensus was
reached that a SUM06 range of 10 to 15
(W126 range of 7 to 13) ppm-hour
would be protective. For growth effects
to tree seedlings and saplings in
plantations, the consensus SUM06 range
was 12 to 16 (W126 range of 9 to 14)
ppm-hour. For visible foliar injury to
natural ecosystems, the consensus
SUM06 range was 8 to 12 (W126 range
of 5 to 9) ppm-hour.
The 2007 Staff Paper then considered
to what extent recent research provided
empirical support for the ranges of
levels identified by the experts as
protective of different types of O3induced effects. As discussed above in
section IV.D.1.c, the 2007 Staff Paper
concluded on the basis of the available
evidence that it was appropriate to
consider a range for a 3-month, 12-hour,
W126 standard level that included the
1996 Consensus Workshop
recommendations regarding a range of
levels protective against O3-induced
growth effects in tree seedlings in
natural forest stands (i.e., 7–13 ppmhour in terms of a W126 form).
In considering the newly available
information on O3-related effects on
crops in this review, the 2007 Staff
Paper observed the following regarding
the strength of the underlying crop
science: (1) Nothing in the recent
literature points to a change in the
relationship between O3 exposure and
crop response across the range of
species and/or cultivars of commodity
crops currently grown in the U.S. that
could be construed to make less
appropriate the use of commodity crop
C–R functions developed in the NCLAN
program; (2) new field-based studies
(e.g., SoyFACE) provide qualitative
support in a few limited cases for the
appropriateness of using OTC-derived
C–R functions to predict crop response
in the field; and (3) refinements in the
exposure, risk and benefits assessments
in this review reduce some of the
uncertainties present in 1996. On the
basis of these observations, the 2007
Staff Paper concluded that nothing in
the newly assessed information calls
into question the strength of the
underlying science upon which EPA
based its proposed decision in the last
review to select a level of a cumulative,
seasonal form associated with protecting
50 percent of crop cases from no more
than 10 percent yield loss as providing
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the requisite degree of protection for
commodity crops.
The 2007 Staff Paper then considered
whether any additional information was
available to inform judgments as to the
adversity of various O3-induced levels
of crop yield loss to the public welfare.
As noted above, the 2007 Staff Paper
observed that agricultural systems are
heavily managed, and that in addition to
stress from O3, the annual productivity
of agricultural systems is vulnerable to
disruption from many other stressors
(e.g., weather, insects, disease), whose
impact in any given year can greatly
outweigh the direct reduction in annual
productivity resulting from elevated O3
exposures. On the other hand, O3 can
also more subtly impact crop and forage
nutritive quality and indirectly
exacerbate the severity of the impact
from other stressors. Since these latter
effects could not be quantified at that
time, they could only be considered
qualitatively in reaching judgments
about an appropriate degree of
protection for commodity crops from
O3-related effects.
Based on the above considerations,
the 2007 Staff Paper concluded that the
level of protection judged requisite in
the 1997 review to protect the public
welfare from adverse levels of O3induced reductions in crop yields and
tree seedling biomass loss, as
approximately provided by a W126
level of 21 ppm-hour, remained
appropriate for consideration as an
upper bound of a range of appropriate
levels. The 2007 Staff Paper also
recognized that a standard set at this
level would not protect the most
sensitive species or individuals within a
species from all potential effects related
to O3 exposures and further, that this
level derives from the extensive and
quantitative historic and recent crop
effects database, as well as current staff
exposure and risk analyses (EPA, 2007,
pg. 8–22).
In identifying a lower bound for the
range of alternative standard levels
appropriate for consideration, staff
concluded that several lines of evidence
pointed to the need for greater
protection for tree seedlings, mature
trees, and associated forested
ecosystems. Staff believed that tree
growth was an important endpoint to
consider because it is related to other
aspects of societal welfare such as
sustainable production of timber and
related goods, recreation, and carbon
(CO2) sequestration. Impacts on tree
growth can also affect ecosystems
through shifts in species composition
and the loss of genetic diversity due to
the loss of O3 sensitive individuals or
species. In selecting an appropriate level
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of protection for trees, staff considered
the results of the 1996 Consensus
Workshop which identified the SUM06
range of 10 to 15 (W126 of 7 to 13) ppmhour for growth effects to tree seedlings
in natural forest stands.
Because staff believed that O3-related
effects on forest tree species are
important public welfare effects of
concern, it therefore concluded, based
on the above, that it was appropriate to
include 7 ppm-hour as the lower bound
of the recommended range, the lower
end of the approximate range
recommended by CASAC (Henderson,
2006c) and identified by the 1996
Consensus Workshop participants as
protective of forest trees. At this lower
end of the range, staff anticipated, based
on its analyses of risks of tree seedling
biomass loss and mature tree growth
reductions and on the basis of the
scientific effects literature, that adverse
effects of O3 on forested ecosystems
would be substantially reduced.
Further, staff anticipated that the lower
end of this range would provide
increased protection from the more
subtle impacts of O3 acting in synergy
with other natural and man-made
stressors to adversely affect individual
plants, populations and whole systems.
Staff also noted that by disrupting the
photosynthetic process, decreasing
carbon storage in the roots, increasing
early senescence of leaves and affecting
water use efficiency in trees, O3
exposure could potentially disrupt or
change the nutrient and water flow of an
entire system. Such weakened trees can
become more susceptible to other
environmental stresses such as pest and
pathogen outbreaks or harsh weather
conditions. While recognizing that it is
not possible to quantify all the
ecological and societal benefits
associated with varying levels of
alternative secondary standards, staff
believed that this information should be
weighed in considering the extent to
which a secondary standard should be
precautionary in nature in protecting
against effects that have not yet been
adequately studied and evaluated.
Thus, the 2007 Staff Paper concluded,
based on all the above considerations,
that an appropriate range of levels, for
an annual standard using a 3-month,
12-hour W126 form, for the
Administrator to consider was 7 to 21
ppm-hour, recognizing that the level
selected is largely a policy judgment as
to the requisite level of protection
needed. In determining the requisite
level of protection for crops and trees,
the 2007 Staff Paper recognized that it
was appropriate to weigh the
importance of the predicted risks of
these effects in the overall context of
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public welfare protection, along with a
determination as to the appropriate
weight to place on the associated
uncertainties and limitations of this
information.
ii. CASAC and Public Comments Prior
to 2008 Decision
In considering the evidence described
in both the 2006 Criteria Document and
2006 draft Staff Paper, CASAC, in its
October 24, 2006 letter to the
Administrator, expressed its view
regarding the appropriate form and
range of levels for the Administrator to
consider. The CASAC preferred a
seasonal 3-month W126 standard in a
range that is the approximate equivalent
of the SUM06 at 10 to 20 ppm-hour.
Following the 2007 proposal, EPA
received additional CASAC and public
comments regarding an appropriate
range of levels of a W126 form for the
Administrator to consider in finalizing a
revised secondary NAAQS for O3. The
CASAC, in its final letter to the
Administrator (Henderson, 2007),
agreed with the 2007 Staff Paper
recommendations that the lower bound
of the range within which a seasonal
W126 secondary O3 standard should be
considered is approximately 7 ppmhour; however, it did not agree with
staff’s recommendation that the upper
bound of the range should be as high as
21 ppm-hour. Rather, as discussed
above in section IV.D.1.c, the CASAC
Panel recommended that the upper
bound of the range considered should
be no higher than a W126 of 15 ppmhour for an annual standard.
The comments received from the
public fell into two groups. One group
of commenters supported the CASAC
recommended range of 7–15 ppm-hour
for a W126 standard. Many of these
same commenters further emphasized
the lower end of the proposed range as
necessary to provide adequate
protection for sensitive species. These
commenters based their
recommendation primarily on four
sources of information: (1) Field-based
evidence of foliar injury occurring on
sensitive species at air quality levels
well below that of the current standard;
(2) the 1996 Consensus Workshop
recommendations for protective levels
in terms of cumulative exposures for
different vegetation types; (3) CASAC
advice and recommendations; and (4)
studies published after the close of the
2006 Criteria Document that potentially
strengthen the link between species
level impacts and ecosystem response.
The other group of commenters did
not support revising the current
secondary standard. These commenters
primarily focused on uncertainties
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regarding the sources of information
relied upon by the first group of
commenters as support for a level
within the range of levels recommended
by CASAC. These uncertainties
included: (1) potential confounders,
such as soil moisture, on visible foliar
injury and the lack of a clear
relationship between visible foliar
injury symptoms and other vegetation
effects; (2) lack of documentation of the
basis for the recommendations from the
1996 Consensus Workshop in selecting
a range of levels, indicating that these
recommendations should be used with
great caution; (3) failure of CASAC and
EPA to take into account the monitor
height measurement gradient when
making their recommendations
concerning the level of the secondary
standard; and (4) inability to
quantitatively estimate ecosystem
effects of O3 or to extrapolate
meaningfully from effects on individual
plants to ecosystem effects due to
inadequate data.
iii. Conclusions on Level
The Administrator is proposing to set
a cumulative, seasonal standard
expressed in terms of the maximum
3-month, 12-hour W126 form, in the
range of 7 to 15 ppm-hour. In reaching
this proposed decision about an
appropriate range of levels for the
secondary standard, the Administrator
has considered the following: the
evidence described in the 2006 Criteria
Document and the 2007 Staff Paper; the
results of the vegetation exposure and
risk assessments discussed above and in
the 2007 Staff Paper, giving weight to
the assessments as judged appropriate;
the CASAC Panel’s advice and
recommendations in the CASAC’s
letters to the Administrator; EPA staff
recommendations; and public
comments received during the
development of these documents, either
in connection with CASAC meetings or
separately. In considering what range of
levels of a cumulative 3-month standard
to propose, the Administrator notes that
this choice requires judgment as to what
standard will protect the public welfare
from any known or anticipated adverse
effects. This choice must be based on an
interpretation of the evidence and other
information, such as the exposure and
risk assessments, that neither overstates
nor understates the strength and
limitations of the evidence and
information nor the appropriate
inferences to be drawn. In taking all of
the above into consideration, the
Administrator also notes that there is no
bright line clearly directing the choice
of level for any of the effects of concern,
and the choice of what is appropriate is
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clearly a public welfare policy judgment
entrusted to the Administrator.
In particular, the Administrator has
given careful consideration to the
following: (1) The nature and degree of
effects of O3 to the public welfare,
including what constitutes an adverse
effect; (2) the strengths and limitations
of the evidence that is available
regarding known or anticipated adverse
effects from cumulative, seasonal
exposures, and its usefulness in
informing selection of a proposed range;
and (3) CASAC’s views regarding the
strength of the evidence and its
adequacy to inform a range of levels.
Each of these topics is discussed in turn
below.
In determining the nature and degree
of effects of O3 on the public welfare,
the Administrator recognizes that the
significance to the public welfare of O3induced effects on sensitive vegetation
growing within the U.S. can vary,
depending on the nature of the effect,
the intended use of the sensitive plants
or ecosystems, and the types of
environments in which the sensitive
vegetation and ecosystems are located.
Any given O3-related effect on
vegetation and ecosystems (e.g., biomass
loss, foliar injury), therefore, may be
judged to have a different degree of
impact on the public depending, for
example, on whether that effect occurs
in a Class I area, a city park, or
commercial cropland. In her judgment,
it is appropriate that this variation in
the significance of O3-related vegetation
effects should be taken into
consideration in judging the level of
ambient O3 that is requisite to protect
the public welfare from any known or
anticipated adverse effects. In this
regard, the Administrator agrees with
the definition of adversity as described
above in section IV.A.3 and in the 2008
rulemaking. As a result, the
Administrator concludes that of those
known and anticipated O3-related
vegetation and ecosystem effects
identified and discussed in this
reconsideration, the highest priority and
significance should be given to those
that occur on sensitive species that are
known to or are likely to occur in
federally protected areas such as Class
I areas 62 or on lands set aside by States,
Tribes and public interest groups to
provide similar benefits to the public
62 For example, the level of protection granted by
Congress under the Wilderness Act of 1964 for
designated ‘‘wilderness areas’’ requires that these
areas ‘‘shall be administered for the use and
enjoyment of the American people in such manner
as will leave them unimpaired for future use as
wilderness, and so as to provide for the protection
of these areas, the preservation of their wilderness
character’’ (The Wilderness Act, 1964).
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welfare, for residents on those lands, as
well as visitors to those areas.
Likewise, the Administrator also
notes that the same known or
anticipated O3-induced effects,
occurring in other areas may call for less
protection. For example, the
maintenance of adequate agricultural
crop yields is extremely important to
the public welfare and is currently
achieved through the application of
intensive management practices,
including in some cases, genetic
engineering. These management
practices, in conjunction with market
forces and government programs, assure
an appropriate balance is reached
between costs of production and market
availability. Thus, while research on
agricultural crop species remains useful
in illuminating mechanisms of action
and physiological processes,
information from this sector on O3induced effects is considered less useful
in informing judgments on what level(s)
would be sufficient but not more than
necessary to protect the public welfare.
With respect to commercial production
of commodities, the Administrator notes
that judgments about the extent to
which O3-related effects on
commercially managed vegetation are
adverse from a public welfare
perspective are particularly difficult to
reach, given that what is known about
the relationship between O3 exposures
and agricultural crop yield response
derives largely from data generated
almost 20 years ago. The Administrator
recognizes that there is substantial
uncertainty at this time as to whether
these data remain relevant to the
majority of species and cultivars of
crops being grown in the field today. In
addition, the extensive management of
such vegetation may to some degree
mitigate potential O3-related effects. The
management practices used on these
lands are highly variable and are
designed to achieve optimal yields,
taking into consideration various
environmental conditions. Thus, the
Administrator concludes there is no
need for such additional protection for
agricultural crops through the NAAQS.
The Administrator also recognizes
that O3-related effects on sensitive
vegetation can occur in other areas that
have not been afforded special Federal
protections, ranging from effects on
vegetation growing in residential or
commercial settings, such as
ornamentals used in urban/suburban
landscaping, to vegetation grown in
land use categories that are heavily
managed for commercial production of
commodities such as timber. For
vegetation used for residential or
commercial ornamental purposes, such
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as urban/suburban landscaping, the
Administrator believes that there is not
adequate information at this time to
establish a secondary standard based
specifically on impairment of urban/
suburban landscaping and other uses of
ornamental vegetation, but notes that a
secondary standard revised to provide
protection for sensitive natural
vegetation and ecosystems would likely
also provide some degree of protection
for such ornamental vegetation.
Based on the above, the Administrator
finds that the types of information most
useful in informing the selection of an
appropriate range of protective levels is
appropriately focused on information
regarding exposures and responses of
sensitive trees and other native species
known or anticipated to occur in
protected areas such as Class I areas or
on lands set aside by States, Tribes and
public interest groups to provide similar
benefits to the public welfare, for
residents on those lands, as well as
visitors to those areas.
With regard to the available evidence,
the Administrator finds the coherence
and strength of the weight of evidence
from the large body of available
literature compelling. This evidence
addresses a broad array of O3-induced
effects on a variety of tree species across
a range of growth stages (i.e., seedlings,
saplings and mature trees) using diverse
field-based (e.g. free air, gradient and
ambient) and OTC exposure methods. It
demonstrates that significant numbers
of forest tree species are potentially
experiencing O3-induced stress under
levels of ambient air quality, both at and
below the level of the 1997 standard.
In particular, the Administrator notes
the evidence from recent field-based
studies and a gradient study of eastern
cottonwood saplings (Gregg et al., 2003).
She observes that this study found that
cottonwood saplings grown in urban
New York City grew faster than saplings
grown in downwind rural areas where
cumulative O3 exposures were higher,
and the difference in biomass
production between the urban site with
the lowest cumulative exposure and the
rural site with the highest cumulative
exposure is dramatic (Figure 7–17 in the
2007 Staff Paper). The Administrator
further notes that cottonwood is one of
the most sensitive tree species studied
to date and it is also important both
from an ecological and public welfare
perspective, as discussed above in
section IV.A.2.b and in the 2007 Staff
Paper.
The Administrator also notes the
evidence related to the O3-induced
effect of visible foliar injury. The
Administrator observes that the visible
foliar injury database created from the
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ambient field-based monitoring network
managed by the Unites States Forest
Service (USFS) Forest Inventory and
Analysis (FIA) Program has continued
to expand since the conclusion of the
1997 review. In utilizing this dataset,
EPA staff collaborated with FIA staff to
compare the incidence of visible foliar
injury at different levels of air quality by
county throughout the U.S. in counties
with FIA monitoring sites. In
considering the results of this analysis,
depicted in Table 7–4 of the 2007 Staff
Paper, the Administrator notes that for
the 2001–2004 period, the percent of
counties with documented foliar injury
at a level approximately equivalent to
the W126 of 21 ppm-hour, was 26 to 49
percent, while at the lower level
approximately equivalent to a W126 of
13 ppm-hour, incidence values ranged
from 12 to 35 percent. The
Administrator believes it likely that
some sensitive species occurring in
specially protected areas would also
exhibit visible foliar injury symptoms to
a similar degree at these exposure
levels. She further notes that while
direct links between O3 induced visible
foliar injury symptoms and other
adverse effects (e.g., biomass loss) are
not always found, visible foliar injury in
itself is considered by the National Park
Service (NPS) to affect adversely air
quality related values (AQRV) in Class
I areas.
The Administrator places significant
weight on the judgments of CASAC. In
so doing, the Administrator has
carefully considered its stated views
and the basis for the range of levels the
CASAC O3 Panel recommended. In its
2007 letter to the Administrator, the
CASAC O3 Panel agreed with EPA staff
recommendations that the lower bound
of the range within which a seasonal
W126 O3 standard should be considered
is approximately 7 ppm-hour. However,
‘‘it does not agree with Staff’s
recommendations that the upper bound
of the range should be as high as 21
ppm-hour. Rather, the Panel
recommends that the upper bound of
the range considered should be no
higher than 15 ppm-hour, which the
Panel estimates is approximately
equivalent to a seasonal 12-hour SUM06
level of 20 ppm-hour’’ (Henderson,
2007). The Administrator notes that
CASAC views concerning an
appropriate range of levels for the
Administrator to consider were
presented after CASAC had considered
the entire body of evidence presented in
both the 2006 Criteria Document and
2007 Staff Paper, and are generally
consistent with the 1996 Consensus
Workshop recommendations.
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In considering the issues raised by
commenters on the 2007 proposed rule,
the Administrator noted that many
public commenters supported the range
of levels recommended by CASAC. The
Administrator also considered the views
expressed by the NPS as to what range
of levels it identified as useful in
helping it achieve its mandate to protect
AQRVs in national parks and
wilderness areas and to provide a level
of protection for its resources in keeping
with the Congressional mandate set
forth in The Wilderness Act of 1964. In
so doing, the Administrator notes that
the NPS supported the range
recommended by CASAC, while
emphasizing that the lower end of the
range was more appropriate. The NPS
notes that though some visible foliar
injury would still be expected to occur
above the lower end of the CASAC
recommended range (i.e. 7 ppm-hour),
the potential for growth impacts at that
level would be very low. It further notes
that most of these parks contain aspen,
black cherry, or ponderosa pine, all
sensitive species predicted to have
significant growth effects at current
W126 levels.
The Administrator also considered
those comments that highlighted
sources of uncertainty in the evidence
and risk assessments (summarized
above in section IV.D.5.c.ii) to inform
her judgments on how much weight to
place on these associated uncertainties,
as discussed below.
With regard to the issue of possible
confounders of foliar injury information,
the Administrator recognizes that
visible foliar injury, like other O3induced plant effects, is moderated by
environmental factors other than O3
exposure. However, the Administrator
also notes that the O3-related visible
foliar injury effect persisted across a
four year period (2001–2004), despite
year-to-year variability in meteorology
and other environmental factors (see
Table 7–4 in the 2007 Staff Paper). She
also notes that approximately 26 to 49
percent of counties had visible foliar
injury incidence at the approximate
W126 level of 21 ppm-hour, while at a
W126 level of 13 ppm-hour, this range
of percentages dropped to
approximately 12 to 23 percent. In an
area such as a national park, where
visitors come in part for the aesthetic
quality of the landscape, the
Administrator recognizes that visible
foliar injury incidence is an important
welfare effect which should be
considered in determining an
appropriately protective standard level.
With regard to the issues of what
weight to place on the recommendations
from the 1996 Consensus Workshop in
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selecting a range of levels, as the 1997
Workshop Report did not clearly
document the basis for its
recommendations, the Administrator
recognizes that the absence of such
documentation does call for care in
placing weight on such
recommendations. However, the
Administrator notes that the workshop
participants were asked to review both
the 1996 O3 Criteria Document and Staff
Paper, representing the most up to date
compilation of the state of the science
available at that time, in order to ensure
that their expert judgments made were
also informed by the latest science. She
also notes that another group of experts,
the CASAC O3 Panel, reached a similar
consensus based upon an expanded
body of scientific evidence. In addition,
the 2007 Staff Paper evaluated the same
recommendations in the context of
subsequent empirical evidence, and
reached similar views, with the
exception of the upper end of the
recommended range, which in the 2007
Staff Paper was based on effects on
commercial crops that had been
considered in the 1997 review. While it
would always be more useful to have
documentation of the reasoning and
basis for an expert’s advice, in this case
the Administrator judges that the 1996
Consensus Workshop recommendations
should be given substantial weight.
With regard to other issues raised by
some commenters related to
uncertainties in the technical evidence
and analyses, the Administrator notes
that such issues had been addressed in
the 2007 Staff Paper that reflected
CASAC’s advice on such issues. For
example, while the Administrator
recognizes that uncertainty remains as
to what level of annual tree seedling
biomass loss when compounded over
multiple years should be judged adverse
to the public welfare, she believes that
the potential for such anticipated effects
should be considered in judging to what
degree a standard should be
precautionary.
In considering all of the issues
discussed above, the Administrator has
decided to propose a range of 7–15
ppm-hour. In selecting as an upper
bound a level of 15 ppm-hour, the
Administrator notes that this level was
specifically supported by the CASAC O3
Panel and is just above the range
identified in the 1996 Consensus
Workshop report as needed to provide
adequate protection for trees growing in
natural areas. In addition, the NPS,
along with many public commenters,
were in support of the CASAC range,
including the upper bound of 15 ppmhour, and indicated that lower values
within this range would be more
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protective for sensitive trees in
protected areas from biomass loss and
visible foliar injury symptoms.
While the upper end of this range is
lower than the upper end of 21 ppmhour recommended in the 2007 Staff
Paper, this upper level of 21 ppm-hour
was originally put forward in the 1997
review in terms of a SUM06 of 25 ppmhour (W126 of 21 ppm-hour) and was
justified on the basis that it was
predicted to allow up to 10% biomass
loss annually in 50% of studied
commercial crops and tree seedling
species. Recognizing the significant
uncertainties that are associated with
evaluating effects on commercial crops
from a public welfare perspective, the
Administrator now concludes that
commercial crop data are no longer
useful for setting the upper level of the
range for proposal.
With regard to her selection of a
proposed range, the Administrator has
considered that the direction from
Congress to provide a high degree of
protection in Class I areas creates a
clearer target for gauging what types and
magnitudes of effects would be known
or anticipated to affect the intended use
of these and other similarly protected
areas, that would thus be considered
adverse to the public welfare. Such
similar areas include lands set aside by
States, Tribes and public interest groups
to provide similar benefits to the public
welfare, for residents on those lands, as
well as visitors to those areas. The
Administrator also believes that in order
to preserve wilderness areas in an
unimpaired state for future generations,
she must consider a level that affords
substantial protection from known
adverse O3-related effects of biomass
loss and foliar injury on sensitive tree
species, as well as a level that takes into
account potential ‘‘anticipated’’ adverse
O3-related effects, including effects that
result in continued impairment in the
year following O3 exposure (i.e., carryover effects), below ground impacts,
ecosystem level impacts, and reduced
CO2 sequestration
While the Administrator
acknowledges that growth effects and
visible foliar injury can still occur in
sensitive species at levels below the
upper bound of the proposed range, the
Administrator also recognizes that some
significant uncertainties remain
regarding the risk of these effects, as
discussed above. For example, the
Administrator concludes that remaining
uncertainties make it difficult to judge
the point at which visible foliar injury
becomes adverse to the public welfare
in various types of specially protected
areas. Uncertainties associated with
monitoring ambient exposures must be
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considered in evaluating the strength of
predictions regarding the degree of tree
seedling growth impairment estimated
to occur at varying ambient exposures.
These uncertainties add to the challenge
of judging which exposure levels are
expected to be associated with levels of
tree seedling growth effects considered
adverse to public welfare The
Administrator believes that it is
important to consider these
uncertainties, and the weight to place
on such uncertainties, in selecting a
range of standard levels to propose.
Establishing 15 ppm-hour as the upper
end of the proposed range reflects her
judgment regarding the appropriate
weight to place on these uncertainties in
determining the degree of protection
that is warranted for known and
anticipated adverse effects.
With regard to her selection of a lower
bound for the proposed range, the
Administrator believes that if weight is
placed on taking a more precautionary
approach, recognizing that the real
world impacts on trees and ecosystems
could, in some cases, be greater than
predicted, then the lower end of the
range of 7 ppm-hour could be
warranted. There is clear evidence that
higher cumulative exposures can occur
in rural areas downwind of urban areas
and potentially in Class I areas.
Unmonitored high elevation sites would
also likely have higher cumulative
exposures than lower elevation sites
that are currently monitored. All of
these considerations lead the
Administrator to propose 7 ppm-hour as
the low end of the proposed range.
As discussed above in section
IV.D.5.a, the main opposition to
changing to a secondary standard with
a cumulative, seasonal form has been
the view that EPA does not have an
adequate basis to identify the kinds and
types of cumulative, seasonal exposure
patterns that the standard should be
designed to protect against, given the
various uncertainties in the evidence,
and whether EPA has an adequate basis
to determine an appropriate level for a
cumulative, seasonal secondary
standard. While EPA agreed with this
position in the 1997 review, the
Administrator believes that the evidence
before her appropriately supports a
secondary standard that is distinctly
different in form and averaging time
from the 8-hour primary standard, and
that such a standard is necessary to
provide sufficient protection from
cumulative, seasonal exposures to O3.
While a different conclusion on this
issue was reached in the 1997 review,
the current conclusion that an exposure
index that is cumulative and seasonal in
nature, and therefore that setting a
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standard based on such a form is
necessary and appropriate, is based on
information newly available in the 2008
rulemaking, which strengthens the
information available in the 1997 review
and reduces remaining uncertainties.
Such newly available information
includes quantitative information for a
broader array of vegetation effects
(extending to sapling and mature tree
growth stages) obtained using a more
diverse set of field-based research study
designs and improved analytical
methods for assessing O3-related
exposures and risks as discussed above
in sections IV.A–C.
These newly available studies also
provide important support to the
quantitative estimates of impaired tree
growth based on earlier studies
available in the 1997 review and
address one of the key data gaps cited
in the 1997 review. Additional
qualitative information is also available
regarding improved understanding of
linkages between stress-related effects of
O3 exposures at the species level and
those at higher levels within
ecosystems. Finally, this information
includes the use of new analytical
methods, including a new multipollutant, multi-scale air quality model
used to characterize exposures of O3sensitive tree and crop species further
address uncertainties in the assessments
done in the 1997 review. In total, this
newly available information increases
the Administrator’s confidence in
important aspects of this rulemaking
The decision in 2008 to set the
secondary O3 standard identical to the
8-hour primary standard largely
mirrored the decision in 1997, but failed
to account for this significant increase
in the body of knowledge available to
support the 2008 rulemaking. This body
of knowledge, while continuing to
reflect significant uncertainties,
provides an appropriate basis for
determining a level of a cumulative,
seasonal standard that, in the judgment
of the Administrator, provides sufficient
but not more than necessary protection
from cumulative, seasonal exposures to
O3. This is clearly so when compared to
a standard that uses an indirect form
that is not biologically relevant, an 8hour average standard aimed at peak
daily exposures. This judgment is fully
consistent with the advice provided by
CASAC.
After carefully taking the above
considerations into account, and giving
significant weight to the views of
CASAC, the Administrator has decided
to propose a range of levels of 7–15
ppm-hour for a cumulative, seasonal
secondary O3 standard expressed as an
index of the annual sum of weighted
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hourly concentrations (i.e., the W126
form), cumulated over 12 hours per day
during the consecutive 3-month period
within the O3 season with the maximum
index value, averaged over three years.
In the Administrator’s judgment, based
on the information available in the 2008
rulemaking, a standard could be set
within this range that would be
requisite to protect public welfare from
known or anticipated adverse effects to
O3-sensitive vegetation and ecosystems.
In the Administrator’s judgment, a
standard set at a level below the lower
end of the range is not now supported
by the weight of evidence and would
not give sufficient weight to the
important uncertainties and limitations
inherent in the available scientific
evidence and in the quantitative
assessments conducted for the 2008
rulemaking. A standard set at a level
above the upper end of the range is also
not now supported by the weight of
evidence and would not give sufficient
weight to the credible inferences that
the Agency has drawn from the
scientific evidence nor to the
quantitative assessments conducted for
the 2008 rulemaking. The Administrator
judges that the appropriate balance to be
drawn, based on the entire body of
evidence and information available in
the 2008 rulemaking, is a range between
7 and 15 ppm-hour. On balance, the
Administrator believes that a standard
could be set within this range that
would be sufficient but not more than
necessary to protect public welfare from
known or anticipated adverse effects
due to O3.
In reaching this proposed decision, as
discussed above, the Administrator has
focused on the nature of the benefits
associated with setting a distinct
secondary standard with a cumulative,
seasonal form relative to a standard with
a peak daily 8-hour average form, as
well as on assessments that quantify the
degree of protection likely to be afforded
by such standards. In so doing, the
Administrator has acknowledged
limitations in quantifying the expected
benefits associated with the proposed
cumulative seasonal standard relative to
the secondary standard set in 2008.
Having considered the public comments
received on the 2007 proposed rule in
reaching this proposed decision, the
Administrator is interested in again
receiving public comment on the
benefits to public welfare associated
with the proposed cumulative seasonal
standard set at specific levels within the
proposed range relative to the standard
set in 2008.
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E. Proposed Decision on the Secondary
O3 Standard
For the reasons discussed above, and
taking into account information and
assessments presented in the 2006
Criteria Document and 2007 Staff Paper,
the advice and recommendations of
CASAC, and the public comments
received in conjunction with the 2008
rulemaking, the Administrator has
decided to propose to set a new
cumulative, seasonal secondary O3
standard with a form expressed as an
index of the annual sum of weighted
hourly concentrations (i.e., the W126
form), cumulated over 12 hours per day
(8 a.m. to 8 p.m.) during the consecutive
3-month period within the O3 season
with the maximum index value,
averaged over three years, set within a
range of 7 to 15 ppm-hour. The
Administrator solicits comment on the
weight that is appropriately placed on
the various types of evidence and
analyses upon which this proposed
standard is based, and on the
appropriate weight to be placed on the
uncertainties in this information, as
well as on the benefits to public welfare
associated with the proposed standard
relative to the benefits associated with
the standard set in 2008.
Data handling conventions for the
proposed new secondary O3 standard
are specified in the proposed addition of
a new section to 40 CFR 50 Appendix
P, as discussed in section V below.
Issues related to monitoring
requirements for the proposed new
secondary O3 standard are discussed
below in section VI.
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V. Interpretation of the NAAQS for O3
and Proposed Revisions to the
Exceptional Events Rule
Appendix P to 40 CFR part 50,
Interpretation of the Primary and
Secondary National Ambient Air
Quality Standards for Ozone, addresses
data completeness requirements, data
reporting, handling, and rounding
conventions, and example calculations.
The current Appendix P explains the
computations necessary for determining
when the current identical primary and
secondary standards are met. The EPA
is proposing to revise Appendix P to
reflect the proposed revisions to the
primary and secondary O3 NAAQS
discussed above and to make other
changes described below.
As discussed below, the proposed
revisions to Appendix P include the
following: The addition of data
interpretation procedures applicable to
the proposed cumulative, seasonal
secondary NAAQS (see section V.B);
clarification of certain language in the
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current provisions applicable to the
primary NAAQS to reduce potential
confusion (section V.C); revisions to the
provisions regarding the use of
incomplete data sets for purposes of the
primary NAAQS and the data
completeness requirements across three
years (sections V.D and V.E); the
addition of a provision providing the
Administrator discretion to use
incomplete data as if it were complete,
for the purpose of the primary NAAQS
(section V.F); a change from truncation
to rounding of multi-hour and multiyear average O3 concentrations for the
purposes of the primary standard
(section V.G); and the addition of
provisions addressing data to be used in
making comparisons to the NAAQS
(section V.H). The proposed revisions
also include changes in organization for
greater clarity and consistency with
other data interpretation appendices to
40 CFR part 50, which are not further
described in this preamble.
The EPA is also proposing changes to
the O3-specific deadlines, in 40 CFR
50.14, by which states must flag ambient
air data that they believe have been
affected by exceptional events and
submit initial descriptions of those
events, and the deadlines by which
states must submit detailed
justifications to support the exclusion of
that data from EPA determinations of
attainment or nonattainment with the
NAAQS. The O3-specific deadlines in
the current 40 CFR 50.14 would not be
appropriate given the anticipated
schedule for the designations of areas
under the proposed revised O3 NAAQS.
A. Background
The purpose of a data interpretation
appendix in general is to provide the
practical details on how to make a
comparison between multi-day and
possibly multi-monitor ambient air
concentration data and the level of the
NAAQS, so that determinations of
compliance and violation are as
objective as possible. Data interpretation
guidelines also provide criteria for
determining whether there are sufficient
data to make a NAAQS level
comparison at all. Appendix P was
promulgated in March 2008 along with
the most recent revisions to the primary
and secondary O3 NAAQS. It is very
similar to Appendix I, Interpretation of
the 8-Hour Primary and Secondary
National Ambient Air Quality Standards
for Ozone, which was adopted in 1997
when the O3 NAAQS were first revised
to have an 8-hour averaging period
rather than the earlier 1-hour averaging
period, along with other changes in
form and level. The only substantive
difference between Appendix I and the
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current version of Appendix P is that
Appendix P contains truncation
procedures consistent with the
additional decimal digit used to express
the level of the 2008 NAAQS in parts
per million (0.075 ppm) compared to
the 1997 NAAQS (0.08 ppm). In July
2007, EPA had also proposed to include
in Appendix P data interpretation
procedures for the proposed cumulative,
seasonal secondary O3 NAAQS, but
these procedures were not finalized
given that the final secondary NAAQS
was identical in all respects to the final
primary NAAQS.
An exceptional event is defined in 40
CFR 50.1 as an event that affects air
quality, is not reasonably controllable or
preventable, is an event caused by
human activity that is unlikely to recur
at a particular location or a natural
event, and is determined by the
Administrator in accordance with 40
CFR 50.14 to be an exceptional event.
Air quality data that are determined to
have been affected by an exceptional
event under the procedural steps and
substantive criteria specified in section
50.14 may be excluded from
consideration when EPA makes a
determination that an area is meeting or
violating the associated NAAQS. The
key procedural deadlines in section
50.14 are that a state must notify EPA
that data have been affected by an event,
i.e., ‘‘flag’’ the data in the Air Quality
Systems (AQS) database, and provide an
initial description of the event by July
1 of the year after the data are collected,
and that the State must submit the full
justification for exclusion within 3 years
after the quarter in which the data were
collected. However, if a regulatory
decision based on the data, for example
a designation action, is anticipated, the
schedule is shortened and all
information must be submitted to EPA
no later than a year before the decision
is to be made. This generic schedule
presents problems when a NAAQS has
been recently revised, as discussed in
section V.I below. On May 15, 2009,
EPA finalized a set of O3-specific
deadlines that corrected these problems
at the time with respect to the 2008
NAAQS revisions (74 FR 23307).
However, because of the anticipated
effect of the current reconsideration on
the schedule for O3 designations, the
schedule problems will resurface unless
the deadlines are adjusted again.
B. Interpretation of the Secondary O3
Standard
The EPA is proposing data
interpretation procedures for the
proposed secondary O3 NAAQS, which
is defined in terms of a specific
cumulative, seasonal form, commonly
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referred to as the W126 form, as
described above in section IV. The
proposed new section 4 of Appendix P
on data interpretation for the secondary
standard contains the following main
features.
The ‘‘design value’’ for the secondary
standard, the statistic for a monitoring
site which would be compared to the
level of the secondary standard to
determine if the site meets the standard,
would be the average of the annual
maximum values of the three-month
index value from three calendar years.
The new section would provide clear
directions and examples for the
calculation of the daily index value, the
monthly cumulative index value, the
annual maximum index value for a year,
and the design value itself.
Only the data from the required O3
monitoring season would be examined
to determine the annual maximum
index value; any additional period of
monitoring undertaken voluntarily by a
state would not be considered. The EPA
believes that because of the recently
proposed extension of the required
monitoring seasons in many states (74
FR 34525, July 16, 2009), as discussed
below in section VI, such a period of
voluntary monitoring would be unlikely
to have such high index values as to
affect the annual maximum index value.
Moreover, the proposed required
monitoring season may encompass the
most active growing season in many
areas. The EPA invites comment on
whether instead the entire actual O3
monitoring period should be
considered, to eliminate any possibility
that the highest cumulative index value
that can be determined with available
data might be missed.
For each month in a three-month
period, O3 data would have to be
available for at least 75 percent of
daylight hours (defined for this purpose
as 8 a.m.–7:59 p.m. LST). If data are
available for at least 75 percent but
fewer than 100 percent of these daylight
hours in a month, the cumulative index
value calculated from the available
daylight hours in the month would be
increased to compensate for the missing
hours, based on an assumption that the
missing hours would have the same
distribution of O3 concentrations as the
available hours. A substitution test is
also proposed, by which months in
which fewer than 75 percent of daylight
hours have O3 concentration data might
also be useable for calculating a valid
cumulative index value. Such months
would be used if the available O3
concentrations are so high that even
substituting low concentration values
for enough missing data to meet the 75
percent requirement would result in a
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design value greater than the level of the
standard. The low value that would be
substituted would be the lowest 1-hour
O3 concentration observed at the
monitoring site during daylight hours
during the required O3 monitoring
season, in that calendar year, or one-half
the method detection limit (MDL) of the
ozone instrument, whichever is
higher.63
The EPA notes that while this
proposed approach to identifying the
substitution value for the secondary
standard is technically appropriate, it
would necessitate data processing
efforts during implementation that
might be avoidable via some other
approach that is also technically
reasonable. We therefore invite
comment on such alternative
approaches, and we may adopt another
approach in the final rule. For example,
for simplicity the substituted 1-hour O3
concentration value could instead
simply always be zero or one-half the
MDL of the O3 instrument, noting that
because of the sigmoidal weighting
factor the exact magnitude of the low
substitution value may typically make
very little difference to the annual index
value. Also, using the previous calendar
year as the source of the substitution
value instead of the current calendar
year would have the advantage of
allowing all parties to know early in
each year what the substitution value
will be.
The EPA is proposing that all decimal
digits be retained in intermediate steps
of the calculation of the cumulative
index, with the result rounded to have
no decimal digits when expressed in
ppm-hours before comparison the level
of the secondary NAAQS.
EPA expects that the three months
over which the cumulative weighted
index value is highest will generally
occur in the middle of each year.
Therefore, the proposed new section 4
of Appendix P presumes this, and does
not address a situation in which the
three months of maximum cumulative
index spans two calendar years, for
example December to February. The
EPA invites comment on whether a
provision addressing such a remote
possibility is needed and what its terms
63 Because only enough missing 1-hour ozone
values would be substituted as needed to meet the
75 percent completeness requirement, to avoid
unreasonable underestimation of the true W126
index, tying the the selection of the substitution
value to the hour of the missing value, as is
proposed for data substitution for the purpose of the
primary standard (see section V.D), would
introduce considerable complexity by requiring an
algorithm for determining which specific missing
values would be substituted. Therfore, EPA is
proposing this simpler substitution approach for the
secondary standard.
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should be. For example, the process of
checking each three month period in a
calendar year to determine which gives
the highest index value could include
the combinations of December/January/
February and November/December/
January within one calendar year.
C. Clarifications Related to the Primary
Standard
The EPA is proposing two clarifying
changes to Appendix P to make
unambiguous two aspects of data
interpretation for the primary 8-hour
standard. The first change clarifies that
the standard data completeness
requirement that valid daily maximum
8-hour values exist for 75 percent of all
days refers to days within the required
O3 monitoring season only. The current
wording of Appendix P is somewhat
open to a reading that the requirement
applies to all days in the actual
monitoring record for the site in
question, which could be longer than
the required season if a state voluntarily
monitors on additional days, or shorter
than the required season if a monitor
has started or ceased operation
sometime during the required season.
The O3 data completeness requirement
is intended to avoid a determination
that an area has met the NAAQS when
in fact more than a reasonable number
of days with high O3 potential were not
successfully monitored. This purpose
can be served if the data within the
required O3 monitoring season only are
reasonably complete, because as
mentioned above EPA has proposed to
revise the required O3 seasons so that
they encompass all days with potential
for an exceedance of even the lowest
proposed level for the primary standard.
Unsuccessful monitoring outside the
required season should not be an
obstacle to a finding of attainment.
However, if an O3 monitor has missed
more than 25 percent of the required O3
monitoring season, for example because
it started or stopped operation midseason, this should prevent a finding of
attainment based on a three-year period
that includes that season. The proposed
clarifying language reflects EPA’s actual
intention and our past practice in
applying Appendix P for regulatory
purposes, and Appendix I as well.64
64 At present, EPA’s Air Quality System (AQS) for
storing and reporting air quality data provides a
completeness report that is based on yet a third
approach, in which the period for reporting data
completeness is the required monitoring season
plus any extension needed to encompass any
exceedances that may have occurred outside the
required season. However, EPA’s practice for
regulatory purposes has been to consider
completeness only over the required ozone
monitoring season.
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The second proposed clarifying
change would make it clear that when
determining the fourth-highest daily
maximum 8-hour O3 concentration for a
year, all days with monitoring data are
to be considered, not just days within
the required O3 monitoring season. This
proposed clarifying language also
reflects EPA’s actual intention and our
past practice in applying Appendix P,
and Appendix I as well. While EPA
believes it to be quite unlikely that an
exceedance will occur outside the
proposed revised required O3
monitoring seasons and have a high
enough concentration to affect the
selection of the fourth-highest
concentration for the year, when and if
such an occurrence does happen, the
data should not be ignored.
D. Revision to Exceptions From
Standard Data Completeness
Requirements for the Primary Standard
The EPA is proposing to revise
portions of Appendix P that describe
certain exceptions to the standard data
completeness requirements, under
which a monitoring site can in some
cases be determined to be meeting or
violating the primary NAAQS despite
not meeting the standard data
completeness requirements. These
changes would make Appendix P more
logical in certain types of cases with
incomplete data. While the particular
types of cases whose outcome would be
different with these changes have been
rare historically, there may be more
such affected cases in the future in
conjunction with a primary O3 standard
revised to a level within the range of
levels proposed in this action.
The standard data completeness
requirements in Appendix P for the
primary O3 NAAQS apply a 75 percent
requirement at each of three stages of
data completeness testing. As discussed
below, for each stage, there is an
existing exception to the 75 percent
requirement.
In the first stage, an 8-hour period can
be considered to have a valid 8-hour
average O3 concentration only if at least
75 percent of the hours, i.e., 6 or more
hours, have a valid hourly O3 value. The
provided exception is that if there are 5
or fewer hours but if substituting a very
low value (specifically, one-half the
MDL of the O3 instrument) for all the
missing hours results in a hypothetical
8-hour average that is above the level of
the primary standard, the 8-hour period
is considered valid and is assigned the
hypothetical level resulting from the
data substitution.65 For example, if the
65 Actually, it is an interpretation of the text of
Appendix P, section 2.1, that the average resulting
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O3 concentration was 0.125 ppm for 5
hours, substituting a typical MDL/2
value of 0.0025 ppm for three missing
hours would result in an 8-hour average
of 0.079 ppm, which is an exceedance
of the current primary standard, so the
valid 8-hour average for the period
would be taken to be 0.079 ppm. If this
value is higher than one or more of the
highest four daily maximum 8-hour
concentrations otherwise calculated for
the year, considering it to be valid
affects the value identified as the fourthhighest for the year and thus also affects
the final design value. The logical
problem with this approach is that it is
possible for a hypothetical
8-hour average with such substitution to
be below the level of the NAAQS, thus
not meeting the current condition for
the exception, but for it to still make a
critical difference in making the threeyear design value be above the level of
the NAAQS, because a three-year design
value can include (and be sensitive to
the exact value of) an annual fourthhighest daily maximum that is not
above the level of the NAAQS. This
could be the case if the hypothetical 8hour average with substitution is the
maximum concentration 8-hour period
for its day, and the day is one of the
highest four O3 days of the year.
Whether it actually is the case would
further depend on the value of the
8-hour average itself, the values of the
next highest daily maximum 8-hour
average concentration in the year, and
the values of the annual fourth-highest
daily maximum 8-hour concentration
from the other two years. If the
substituted 8-hour average would make
a critical difference, it should be treated
as valid and used in the calculation of
the three-year design value, even if it is
not itself above the level of the standard.
Another problem is that one-half of the
MDL, which typically is about 0.0025
ppm, is very likely to be considerably
lower than the actual O3 concentrations
that were not successfully measured.
Thus, while the one-half-MDLsubstituted value is prevented from
being an overestimate of the actual
8-hour average concentration, it is an
unreasonably low estimate of that
concentration which may have the effect
of allowing a site with actual O3 levels
above the standard to be found to meet
the standard. The condition in the
exception requiring a one-half-MDLsubstituted ‘‘8-hour’’ average to be above
the level of the NAAQS is therefore
inappropriate.
In the second stage of data
completeness testing, 75 percent of the
24 possible 8-hour time blocks, which is
18 or more, must have valid 8-hour
average concentrations values. The
intent of this requirement is to make
sure that most of the day was actually
monitored, such that the highest
concentration 8-hour period was likely
to be captured in the data. When this is
not the case, the day is not considered
in selecting the annual fourth-highest
daily maximum 8-hour concentration
and no credit for the day’s monitoring
is given towards the third stage of data
interpretation (see below). The provided
exception in the current Appendix P is
that a day is considered valid if at least
one 8-hour period has an average
concentration above the level of the
standard. However, as in the first stage,
it is possible for an 8-hour period with
an average concentration at or below the
level of the NAAQS to play a critical
role in whether the three-year design
value meets the standard. Invalidating
the day could have the effect of causing
a lower value to be selected as the
annual fourth-highest daily maximum
8-hour concentration, leading to a threeyear design value that does not exceed
the NAAQS while it would have
exceeded if the day and the 8-hour
average value had been treated as valid.
The condition in the exception
requiring at least one 8-hour average
during the day to be above the level of
the NAAQS is therefore inappropriate.
In the third stage of data completeness
testing, a completeness criterion is
applied for the number of days in the
required O3 season that have a valid
maximum 8-hour average, i.e., days that
have met the completeness conditions
in the first two stages or have met the
condition for an exception. Specifically,
for each of the three years being used in
the design value calculation, the
number of valid days within the
required O3 monitoring season (with no
credit for extra days outside the season)
must be at least 75 percent of the days
in the required O3 season, and the
number of valid days across all three
years must be 90 percent of the days in
the three seasons.66 The provided
exception to the 75/90 percent
requirement is that data from a year
with less than 75 percent of seasonal
days can nevertheless be used if during
the year at least one day’s maximum 8hour average O3 concentration was
from the data substitution is to be taken as the ‘‘8hour’’ average, rather than the average of the
available 5 or fewer hours of data, which would be
higher. The text is not entirely clear on this point.
66 EPA also is proposing eliminate this 90 percent
requirement, see section V.E. The point made in
this paragraph applies with or without the 90
percent requirement in place.
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above the level of the standard and if
the three-year design value is also above
the standard.67 The problem with this
exception, similar to the problems with
the exceptions in the first and second
stages of data completeness testing, is
that a daily maximum 8-hour
concentration that is at or below the
level of the NAAQS can nevertheless
make a critical difference in making the
three-year design value be above the
level of the NAAQS. When it does, an
incorrect final result will be reached if
the year of data is not granted an
exception to the 75/90 percent
requirement. Specifically, there would
be no valid three-year design value and
no conclusion would be reached as to
attainment or nonattainment, despite it
being clear that the actual situation is
nonattainment, in the sense that
successful collection of additional hours
and days of monitoring data could not
possibly have resulted in a passing
three-year design value. Moreover, since
the three-year design value is the
average of the fourth-highest daily
maximum 8-hour concentration from
each year, there is no logical connection
between the design value and the
existence of a single daily maximum
concentration greater than the level of
the standard, which is the current
condition for the exception for this stage
of testing for data incompleteness.
EPA proposes to remedy this situation
by replacing the three separate
statements of the exceptions to the three
standard completeness requirements
with a new data substitution step that
addresses the root cause of the data
incompleteness situation: missing
hourly concentrations which make it
doubtful whether actual maximum daily
8-hour concentrations were measured
on a reasonably large percentage of the
days during the required O3 monitoring
season of each year. In the event that
only 1, 2, 3, 4, or 5 hourly averages are
available for an 8-hour period, a
partially substituted 8-hour average
would be computed by substituting for
all the hours without hourly averages a
low hourly average value selected as
follows, and then using 8 as the
divisor.68 For days within the required
O3 monitoring season, the substitution
67 EPA notes that in the current versions of
Appendix I and P, it is not explicit that this
provided exception also applies in the case of three
years which each have 75 percent or more of days
with valid data but less than 90 percent across three
years. Because EPA is proposing to remove the 90
percent requirement (see section V.E) this
ambiguity does not need correction.
68 Appendix P now provides that in the event that
only 6 or 7 hourly averages are available, the valid
8-hour average shall be computed on the basis of
the hours available, using 6 or 7 as the divisor. We
are not proposing to change this provision.
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value would be the lowest hourly
average O3 concentration observed for
that hour of the day (local standard
time) on any day during the required O3
monitoring season of that year, or onehalf the MDL, whichever is higher.
Using this value makes it highly
unlikely that the resulting partially
substituted 8-hour average
concentration is higher than the actual
concentration. Therefore, using the
partially substituted 8-hour average in
the design value calculation procedure
is highly unlikely to result in an
incorrect finding that a site does not
meet the standard, but it may lead to a
correct finding that a site does not meet
the standard in some cases in which
there would be no finding possible or an
incorrect finding under the current
version of Appendix P. However, the
use of the higher of the lowest observed
same-hour concentration or one-half the
MDL could be problematic if a robust
set of hourly measurements is not
available for the year, for example if a
monitor began operation late in an
ozone season. In such a case, the lowest
observed same-hour concentration
might not be low enough to eliminate all
possibility that the value used for
substitution is higher than the missing
concentration value. To reduce this
likelihood to essentially zero, we are
proposing that if the number of samehour concentration values available for
the required O3 monitoring season for
the year is less than 50 percent of the
number of days during the required O3
monitoring season, one-half the MDL of
the O3 instrument would be used in the
substitution instead of the lowest
observed concentration. We invite
comment on whether another
percentage should be used for this
purpose instead of 50 percent.
The EPA notes that while this
proposed approach to identifying the
substitution value for the primary
standard is technically appropriate, it
would necessitate new data processing
efforts during implementation that
might be avoidable via some other
approach that is also technically
reasonable. There may also be
approaches which are more technically
appropriate. We therefore invite
comment on such alternative
approaches, and we may adopt another
approach in the final rule. Examples of
simpler approaches would be to identify
in the final rule a fixed substitution
value other than one-half the MDL, to
accept as valid 8-hour periods with only
five measured hourly concentrations, to
interpret between two hourly
concentrations to obtain a substitute for
a single missing hourly concentration,
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or to use the previous calendar year as
the source of the substitution value
instead of the current calendar year
(thereby allowing all parties to know
early in each year what the substitution
value will be). Examples of more
complex approaches that might be more
technically appropriate include
selecting a low percentile of the
available same-hour concentration data
rather than the lowest value to be the
substitution value, or selecting the
lowest same-hour value from the same
calendar quarter or month (of the
current year or the most recent year)
rather than from the entire required
ozone monitoring season. We also invite
comment on whether the proposed
approach to substitution should be used
at all and if not what other approach
should be used to address the potential
problem just described.
We propose that for simplicity and to
further reduce any risk of a false finding
that a site does not meet the standard,
for days outside the required O3
monitoring season, the substitution
value would always be one-half the
MDL of the O3 instrument. We similarly
invite comment on this aspect.
There would be no condition that a
partially substituted 8-hour average
exceed the level of the standard for it be
used in calculating the design value,
unlike is now the case. An 8-hour
period with no available hourly
averages at all would not have a valid
8-hour average, as is now the case.
In addition, to complete the solution
to the problems described above, we are
proposing that a design value that is
greater than the level of the primary
standard would be valid provided that
in each year there were at least four
days with at least one valid 8-hour
concentration.69 One or more of these
8-hour average concentrations could be
the partially substituted 8-hour average
concentration resulting from the above
described substitution procedure. In
such a case, there is essentially no
possibility that more complete
monitoring data would have shown the
site to be meeting the NAAQS. It is
appropriate to include all 8-hour
averages including those involving
substitution when testing for an
exceedance of the standard, because
those averages are extremely unlike to
69 The requirement that there be at least four days
with at least one hourly measurement is actually
redundant and is stated only for ease of
understanding, since there would be no annual
fourth-highest daily maximum 8-hour concentration
unless there are at least four days with monitoring
data, and a single hourly data point is necessary
and sufficient (with the proposed substitution step)
to generate a daily maximum 8-hour concentration.
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be overestimates of actual
concentrations.
Finally, a design value equal to or less
than the level of the standard would be
valid only if at least 75 percent of the
days in the required O3 monitoring
season of each year have daily
maximum 8-hour concentrations that
are based on at least 18 periods with at
least 6 hourly concentrations. This
ensures that a site will be found to meet
the standard only when a reasonably
high percentage of the days in the
required O3 monitoring season have
reasonably complete hourly data. In this
situation, it would be inappropriate to
count the 8-hour periods with five or
fewer actual hourly measurement values
towards the 75 percent requirement
when testing for whether a site meets
the standard, because those 8-hour
averages will be based on substitution of
low values and therefore will be
underestimates of actual concentrations.
The only way to be reasonably certain
that no 8-hour period had a high enough
concentration so as to contribute to a
design value over the level of the
standard is to have at least 18 periods
in which substitution for missing O3
values was not needed. This provision
has the same effect as several elements
of the current Appendix P considered
together, and thus is not a substantive
change.
E. Elimination of the Requirement for 90
Percent Completeness of Daily Data
Across Three Years
As stated above in section VI.D,
Appendix P currently requires that in
order for a design value equal to or less
than the standard to be valid, at least 75
percent of days in each of three years
must have a valid daily maximum
8-hour average concentration value, i.e.,
that many days must have at least 18
8-hour periods with at least 6 reported
hourly concentrations each. Appendix P
also requires that the average of the
percentages from three consecutive
years be at least 90 percent. The EPA is
proposing to eliminate this 90 percent
requirement for the average of three
years and to retain only the requirement
that each individual year have a
percentage of at least 75 percent.
The 90 percent requirement was
incorporated into Appendix I (the data
interpretation appendix for the 0.08
ppm O3 NAAQS) in 1997 with an
explanation that EPA had observed that
90 percent of O3 monitoring sites
routinely achieved 90 percent data
capture. The EPA now notes, however,
that while the majority of monitoring
sites do achieve 90 percent or better
data capture in any given year, there are
exceptions every year. The 90 percent
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requirement applied to the average
percentage over three years is quite
unforgiving if there has been one year
with relatively low data completeness.
For example, if one year just met the 75
percent requirement, the remaining two
years would have to achieve a 97.5
percent data capture rate in order for the
three years to meet the 90 percent
requirement. This would allow only 4
missed hours of measurements per
week, which would be challenging. The
consequences for states could be
important, under the current
requirement. One possible result could
be that an area actually in
nonattainment with the NAAQS might
have to be designated unclassifiable,
although the substitution procedure
proposed for cases of incomplete data,
as described above in section VI.D,
provides a path to an appropriate
nonattainment finding in at least some
cases. Another possible result is that a
nonattainment area which had actually
come into attainment could be unable to
receive an attainment determination
until three more years of sufficiently
complete data are collected. This might,
for example, result in an area which has
achieved needed emissions reductions
by its attainment deadline nevertheless
being bumped up to a higher
classification.
The 90 percent requirement over three
years has the potential to treat two areas
disparately, for no obvious logical
reason. Consider two areas with
identical air quality. Suppose the first
area has annual completeness
percentages of 75, 95, and 95 percent
(averaging to 85 percent and thus failing
the 90 percent requirement) and the
second area has annual completeness
percentages of 75, 98, and 98 percent
(averaging to 90 percent). Suppose that
the three-year design values in both
areas are below the level of the NAAQS.
Practically speaking, the most important
uncertainty about whether each area
actually meets the NAAQS is the low
data capture rate in the first year. There
is no obvious logic why the fact that the
second area achieves marginally better
data capture in the second and third
year should permit it to receive an
attainment finding despite this
uncertainty, while the first area may
not.
The EPA also notes that for the other
gaseous criteria pollutants—sulfur
dioxide, carbon monoxide and nitrogen
dioxide—the completeness requirement
is for 75 percent completeness of hourly
measurements in an individual year.70
70 EPA
has recently proposed to amend the
completeness requirements for sulfur dioxide and
nitrogen dioxide to add quarterly 75 percent
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3031
For these reasons, EPA proposes to
eliminate the 90 percent requirement
across three years of data but to retain
the 75 percent requirement for
individual years. The EPA notes that as
a practical matter, the current 90
percent requirement in effect requires a
minimum data capture rate somewhat
above 75 percent in each year, because
if data capture in any one year were as
low as 75 percent the required data
capture in the other years would be very
hard to achieve. The minimum annual
data capture rate is effectively
somewhere in the range of 80 percent
(implying a requirement to achieve 95
percent data capture in the two
remaining years in order to meet the 90
percent requirement across three years)
and 85 percent (implying a requirement
to achieve 92.5 percent data capture in
the two remaining years). The EPA
invites comment on whether instead of
retaining the 75 percent completeness
requirement in each individual year, the
requirement should be 80 percent or 85
percent.
F. Administrator Discretion To Use
Incomplete Data
The EPA is proposing that the
Administrator have general discretion to
use incomplete data to calculate design
values that would be treated as valid for
comparison to the NAAQS despite the
incompleteness, either at the request of
a state or at her own initiative. Similar
provisions exist already for the PM2.5
and lead NAAQS, and EPA has recently
proposed such provisions to accompany
the proposed 1-hour NO2 and SO2
primary NAAQS. The Administrator
would consider monitoring site
closures/moves, monitoring diligence,
and nearby concentrations in
determining whether to use such data.
G. Truncation Versus Rounding
Almost all State agencies now report
hourly O3 concentrations in parts per
million to three decimal places, since
the typical incremental sensitivity of
currently used O3 monitors is 0.001
ppm. In the current Appendix P
approach, in calculating 8-hour average
O3 concentrations from such hourly data
any calculated digits past the third
decimal place are truncated rather than
retained or rounded back to three
decimal places. Also, in calculating
3-year averages of the fourth-highest
daily maximum 8-hour average
concentrations, Appendix P currently
requires the result to be reported to the
completeness requirements in connection with
proposals to establish 1-hour primary NAAQS for
these pollutants, still with no requirement for 90
percent completeness across three years.
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third decimal place with digits to the
right of the third decimal place
truncated. In this regard, Appendix P
follows the precedent of Appendix I,
except that Appendix P is based on a
NAAQS level specified to three decimal
places (0.075 ppm) while Appendix I
addressed the case of a NAAQS level
specified to only two decimal places
(0.08 ppm). In the rulemaking that
concluded in 2008 by establishing the
0.075 ppm level, EPA noted that the
2007 Staff Paper demonstrated that
taking into account the precision and
bias in 1-hour O3 measurements, the
8-hour design value had an uncertainty
of approximately 0.001 ppm. Thus, EPA
considered any value less than 0.001
ppm to be highly uncertain and,
therefore, proposed and adopted
truncation to the third decimal place for
reporting 1-hour O3 concentrations and
for both the individual 8-hour averages
used to determine the annual fourth
maximum and the 3-year average of the
fourth maxima.
The effect of this repeated truncation
is that there is a consistent downward
bias in the calculation of the three-year
design value. The size of this bias can
be notable. For example, seven hours
with O3 concentrations of 0.076 ppm
plus one hour of 0.075 ppm results in
an 8-hour average of 0.075 ppm after
truncation, nearly a full 0.001 ppm
below the actual 8-hour average of
0.075875 ppm. Seven hours with O3
concentrations of 0.077 ppm plus one
hour of 0.076 ppm results in an 8-hour
average of 0.076 ppm after truncation.
One year with the first pattern plus two
years with the second pattern would
give a three-year design value of 0.075
ppm, meeting the NAAQS, even though
23 of the 24 individual 1-hour
concentrations involved in the
calculation of the design value were
above 0.075 ppm.
The EPA has decided to reconsider
this aspect of O3 data interpretation.
Specifically, we are proposing that (1)
1-hour concentrations continue to be
reported to only three decimal places,
the same as is now specified in
Appendix P, i.e., that the current
practice of truncation of the 1-hour data
to the nearest 0.001 ppm be retained; (2)
all digits resulting from the calculation
of 8-hour averages be retained; and (3)
the three-year average of annual fourthhighest daily maximum 8-hour
concentrations be rounded to three
decimal places before comparison to the
NAAQS. The EPA continues to believe
that given the uncertainty in individual
1-hour O3 concentration measurements
it is appropriate to truncate those
measurements at three decimal places
(many O3 instruments are programmed
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to only report three digits anyway).
However, the calculations of 8-hour
averages and three-year averages are
mathematical steps, not a measurement
process subject to uncertainties, and
EPA perceives no logic in having a
consistent downward bias by truncating
the results of these mathematical steps.
The EPA notes that the O3 NAAQS is
the only NAAQS for which multi-hour,
multi-day, or multi-year averages of
concentrations are truncated rather than
rounded. The proposed change will
make this aspect of O3 data
interpretation consistent with data
interpretation procedures for the other
criteria pollutants.
H. Data Selection
The current version of Appendix P
does not explicitly address the issue of
what ambient monitoring data for O3
can and must be compared to the O3
NAAQS. The EPA proposes to add to
Appendix P language addressing this
issue. This language is similar to
provisions recently proposed to be
included in new data interpretation
appendices for nitrogen dioxide and
sulfur dioxide. The new section of
Appendix P would clarify that all
quality assured data collected with
approved monitoring methods and
known to EPA shall be compared to the
NAAQS, even if not submitted to EPA’s
Air Quality System. The section also
addresses the question of what O3 data
should be used when two or more O3
monitors have been operating and have
reported data for the same period at one
monitoring site.
I. Exceptional Events Information
Submission Schedule
States are responsible for identifying
air quality data that they believe warrant
special consideration, including data
affected by exceptional events. States
identify such data by flagging (making a
notation in a designated field in the
electronic data record) specific values in
the Air Quality System (AQS) database.
States must flag the data and submit a
justification that the data are affected by
exceptional events if they wish EPA to
consider excluding the data in
determining whether or not an area is
attaining the new O3 NAAQS.
All states that include areas that could
exceed the O3 NAAQS and could
therefore be designated as
nonattainment for the O3 NAAQS have
the potential to be affected by this
rulemaking. Therefore, this action
applies to all states; to local air quality
agencies to which a state has delegated
relevant responsibilities for air quality
management including air quality
monitoring and data analysis; and to
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Tribal air quality agencies where
appropriate. The Exceptional Events
Rule preamble describes in greater
detail to whom the rule applies (72 FR
13562–13563, March 22, 2007).
The CAA Section 319(b)(2) authorizes
EPA to promulgate regulations that
govern the review and handling of air
quality monitoring data influenced by
exceptional events. Under this
authority, EPA promulgated the
Exceptional Events Rule (Treatment of
Data Influenced by Exceptional Events
(72 FR 13560, March 22, 2007) which
sets a schedule for states to flag
monitored data affected by exceptional
events in AQS and for them to submit
documentation to demonstrate that the
flagged data values were caused by an
exceptional event. Under this schedule,
a state must initially notify EPA that
data have been affected by an
exceptional event by July 1 of the year
after the data are collected; this is
accomplished by flagging the data in
AQS. The state must also include an
initial description of the event when
flagging the data. In addition, the state
is required to submit a full
demonstration to justify exclusion of
such data within three years after the
quarter in which the data were
collected, or if a regulatory decision
based on the data (such as a designation
action) is anticipated, the demonstration
must be submitted to EPA no later than
one year before the decision is to be
made.
The rule also authorizes EPA to revise
data flagging and documentation
schedules for data used in the initial
designation of areas under a new
NAAQS. The generic schedule, while
appropriate for the period after initial
designations have been made under a
NAAQS, may need adjustment when a
new NAAQS is promulgated because
until the level and form of the NAAQS
have been promulgated, a state would
not have complete knowledge of the
criteria for excluding data. In these
cases, the generic schedule may
preclude states from submitting timely
flags and associated documentation for
otherwise approvable exceptional
events. This could, if not modified,
result in some areas receiving a
nonattainment designation when the
NAAQS violations were legitimately
due to exceptional events.
As a result of the Administrator’s
decision to reconsider the 2008 O3
NAAQS, EPA is proposing to revise the
exceptional events flagging and
documentation schedule to correspond
to the designations schedules that EPA
is considering for the proposed
revisions to the primary and secondary
O3 NAAQS. The designation schedules
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under consideration are discussed in
greater detail below in section VII.A and
summarized here. The CAA requires
EPA to promulgate the initial
designations for all areas no later than
2 years from the promulgation of a new
NAAQS. Such period may be extended
for up to one year if EPA has
insufficient information. (See CAA
section 107(d).) For a new primary O3
standard, EPA intends to issue
designations on an accelerated
schedule. For a new seasonal secondary
O3 standard, EPA is considering two
alternative schedules for initial area
designations.
Primary Standard: If, as a result of the
reconsideration, EPA promulgates a new
primary O3 standard on August 31,
2010, EPA is proposing that state
Governors would need to submit their
initial designation recommendations to
EPA by January 7, 2011. EPA would
promulgate the final designations in
July 2011 to allow sufficient time for the
designations to be published and
effective by August 31, 2011. EPA
expects to base the final designations for
the primary O3 standard on three
consecutive years of certified air quality
monitoring data from the years 2007–
2009 or 2008–2010, if available. EPA is
proposing that for exceptional event
claims made for data years 2007–2009,
states must flag and provide an initial
description and detailed documentation
by November 1, 2010. For data collected
during data year 2010, EPA is proposing
that exceptional event data that states
want EPA to exclude from consideration
in the designations process must be
flagged with an initial description and
fully documented by March 1, 2011 or
60 days after the end of the quarter
when the event occurred, whichever
date is first. To meet this proposed 60day deadline, a state would also have to
submit the O3 concentration data to
AQS sooner than the normal deadline
for such submission, which is 90 days
after the end of the calendar quarter.
EPA believes this is a reasonable
expectation given that most states
currently submit O3 data earlier than the
90-day deadline.
Secondary Standard: If, as a result of
the reconsideration, EPA promulgates a
new seasonal secondary O3 standard by
August 31, 2010, EPA is taking
comment on two alternative
designations schedules. Under the first
alternative, EPA would designate areas
for the secondary standard on the same
accelerated schedule discussed above
for the primary standard. Under the
second alternative, EPA would
designate areas for the secondary
standard on the maximum 2-year
schedule provided under the CAA.
Accelerated Schedule: Under the
accelerated schedule for a seasonal
secondary O3 NAAQS, EPA is proposing
that for exceptional event claims made
for data years 2007–2009, states must
flag and provide an initial description
and detailed documentation by
November 1, 2010. For data collected
during data year 2010, EPA is proposing
that exceptional event data that states
want EPA to exclude from consideration
in the designations process must be
flagged with an initial description and
3033
fully documented by March 1, 2011 or
60 days after the end of the quarter
when the event occurred, whichever
date is first.
2-year Schedule: Under the 2-year
schedule, states would have 1 year, or
by August 2011, to submit their
designations recommendations and EPA
would finalize designations under the
new secondary standard by August
2012. EPA expects to base final
designations for a new seasonal
secondary standard on the most recent
three years of certified air quality
monitoring data, which would typically
be from the years 2009–2011 in this
case. Exceptional event data claims used
from years 2008–2010 must be flagged
with an initial description included in
AQS and submitted with complete
documentation supporting such claims
by July 1, 2011. Exceptional event data
claims from data year 2011 must be
flagged with an initial description and
submitted with complete
documentation supporting such claims
60 days after the end of the calendar
quarter when the event occurred or
March 1, 2012, whichever occurs first.
Therefore, using the authority
provided in CAA section 319(b)(2) and
in the Exceptional Events Rule at 40
CFR 50.14(c)(2)(vi), EPA is proposing to
modify the schedule for data flagging
and submission of demonstrations for
exceptional events data considered for
initial designations under the proposed
reconsidered O3 primary and secondary
NAAQS, as follows:
TABLE 1—SCHEDULE FOR EXCEPTIONAL EVENT FLAGGING AND DOCUMENTATION SUBMISSION FOR DATA TO BE USED IN
DESIGNATIONS DECISIONS FOR NEW NAAQS
NAAQS Pollutant/standard/(level)/
promulgation date
Air quality data
collected for
calendar year
Event flagging & initial description
deadline
Detailed documentation submission
deadline
2007–2009
November 1, 2010 b ................................
November 1, 2010.b
2010
Primary Ozone/8-Hr Standard (Level
TBD)/promulgated by August 31, 2010.
60 Days after the end of the calendar
quarter in which the event occurred or
March 1, 2011, whichever date occurs
first.b
July 1, 2011b ...........................................
60 Days after the end of the calendar
quarter in which the event occurred or
March 1, 2011, whichever date occurs
first.b
July 1, 2011.a
July 1, 2011b ...........................................
60 Days after the end of the calendar
quarter in which the event occurred or
March 1, 2012, whichever occurs
first.b
November 1, 2010 b ................................
July 1, 2011.b
60 Days after the end of the calendar
quarter in which the event occurred or
March 1, 2012, whichever occurs
first.b
November 1, 2010.b
60 Days after the end of the calendar
quarter in which the event occurred or
March 1, 2011, whichever date occurs
first.b
60 Days after the end of the calendar
quarter in which the event occurred or
March 1, 2011, whichever date occurs
first.b
Secondary Ozone/(Level TBD) Alternative 2-year Schedule—to be promulgated by August 31, 2010.
2008
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2009–2010
2011
Secondary Ozone/(Level TBD)—Alternative Accelerated Schedule—to be
promulgated by August 31, 2010.
2007–2009
2010
a These
dates are unchanged from those published in the original rulemaking.
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b Indicates
change from general schedule in 40 CFR 50.14.
Note: EPA notes that the table of revised deadlines only applies to data EPA will use to establish the final initial designations for new NAAQS.
The general schedule applies for all other purposes, most notably, for data used by EPA for redesignations to attainment.
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VI. Ambient Monitoring Related to
Proposed O3 Standards
Presently, States (including the
District of Columbia, Puerto Rico, and
the Virgin Islands, and including local
agencies when so delegated by the State)
are required to operate minimum
numbers of EPA-approved O3 monitors
based on the population of each of their
Metropolitan Statistical Areas (MSA)
and the most recently measured O3
levels in each area. Each State (or in
some cases portions of a State) also has
a required O3 monitoring season based
on historical experience on when O3
levels are high enough to be of
regulatory or public health concern.
These requirements are contained in 40
CFR part 58 Appendix D, Network
Design Criteria for Ambient Air Quality
Monitoring. See section 4.1, especially
Tables D–2 and D–3. These
requirements were last revised on
October 17, 2006 as part of a
comprehensive review of ambient
monitoring requirements for all criteria
pollutants (71 FR 61236).
A. Background
In the 2007 proposed rule for the O3
NAAQS (72 FR 37818), EPA did not
propose specific changes to monitoring
requirements to support the proposed
NAAQS revisions, but instead solicited
comment on several key matters that
were expected to be important issues
affecting the potential redesign of
monitoring networks if revisions to the
NAAQS were finalized. These matters
included O3 monitoring requirements in
urban areas, the potential need for
monitoring to support multiple
objectives important to characterization
in non-urban areas including the
support of the secondary O3 NAAQS,
and the length of the required O3
monitoring seasons. Comments on these
monitoring issues were received during
the ensuing public comment period, and
these comments were summarized in
the 2008 final rule for the O3 NAAQS
(73 FR 16501). As noted in that action,
EPA stated its intention to propose, in
a separate rulemaking, the specific
changes to O3 monitoring requirements
that were deemed necessary to support
the revised 2008 O3 NAAQS which set
the level of the primary 8-hour O3
standard to 0.075 ppm and set the
secondary standard identical in all
respects to the primary standard. EPA
published these proposed changes to O3
monitoring requirements in a proposal
dated July 16, 2009, Ambient Ozone
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Monitoring Regulations: Revisions to
Network Design Requirements (74 FR
34525). The EPA currently plans to
finalize these changes in a final O3
monitoring rule in 2010, either before or
in conjunction with the final rule on the
O3 NAAQS.
In the following sections, the specific
provisions of the 2009 O3 monitoring
proposal are briefly reviewed, and then
discussed in the context of the proposed
revisions of the 2008 O3 NAAQS that
have been discussed earlier in this
notice.
B. Urban Monitoring Requirements
As noted earlier, current O3
monitoring requirements for urban areas
are based on two factors: MSA
population and the most recent 3-year
design value concentrations within each
MSA. There are higher minimum
monitoring requirements for areas that
have most recent design values greater
than or equal to 85 percent of the
NAAQS (i.e., design value
concentrations that are greater than or
equal to 85 percent of the level of the
NAAQS), and lower requirements for
areas that have design values less than
85 percent of the NAAQS. These
minimum monitoring requirements for
O3 were revised during the 2006
monitoring rulemaking to ensure that
additional monitors would be required
in areas with higher design values and
to also ensure that these requirements
would remain applicable through future
NAAQS reviews and potential revisions
of the standards. Accordingly, these
requirements do not need to be updated
with the revisions of the O3 NAAQS
proposed in this action since the 85
percent threshold will be applied to the
standard levels that are finalized for the
primary and secondary standards.71 For
example, given the range of levels of the
primary standard being proposed, the
level of the 85 percent threshold that
requires greater minimum monitoring
requirements ranges from 0.051 ppm (85
percent of 0.060 ppm) to 0.060 ppm (85
percent of 0.070 ppm).
EPA did propose one change to urban
monitoring requirements in the 2009 O3
71 The requirements specified in Table D–2 of
Appendix D to part 58, as noted in the third
footnote of Table D–2, are applicable to the levels
of the O3 NAAQS as defined in 40 CFR part 50.
Accordingly, the 85 percent threshold for requiring
higher minimum monitoring requirements within
MSAs would apply to the proposed levels for the
cumulative, seasonal secondary standard as well as
to the proposed levels of the 8-hour primary
standard.
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monitoring proposal. Specifically, EPA
proposed to modify the minimum O3
monitoring requirements to require one
monitor to be placed in MSAs of
populations ranging from 50,000 to less
than 350,000 in situations where there
is no current monitor and no history of
O3 monitoring within the previous 5
years indicating a design value of less
than 85 percent of the revised
NAAQS.72 Since this proposed change
to minimum requirements is also
subject to the 85 percent threshold, EPA
believes that the proposed change
remains appropriate to support the
revisions to the primary and secondary
O3 NAAQS proposed in this action.
C. Non-Urban Monitoring Requirements
In the 2007 proposed rule for the O3
NAAQS, EPA solicited comment on the
status of monitoring requirements for
non-urban areas, specifically whether
non-urban areas with sensitive
vegetation that are only currently
sparsely monitored for O3 could
experience undetected violations of the
secondary NAAQS as a result of
transport from urban areas with high
precursor emissions and/or O3
concentrations or from formation of
additional O3 from precursors emitted
from sources outside urban areas.
Comments that were received in
response to the 2009 O3 NAAQS
monitoring proposal noted the
voluntary nature of most non-urban O3
monitoring and the resulting relative
lack of non-urban O3 monitors in some
areas. These commenters stated that
EPA should consider adding monitoring
requirements to support the secondary
NAAQS by requiring O3 monitors in
locations that contain O3-sensitive
plants or ecosystems. These commenters
also noted that the placement of current
O3 monitors may not be appropriate for
evaluating issues such as vegetation
exposure since many of these monitors
were likely located to meet other
objectives.
Based on these comments as well as
analyses of O3 concentrations from
discretionary non-urban monitors
located across the U.S, EPA included
new proposed non-urban O3 monitoring
requirements in the 2009 O3 monitoring
proposal. These proposed requirements
are intended to satisfy several important
objectives including: (1) Better
characterization of O3 concentrations to
which O3-sensitive vegetation and
72 These MSAs are not currently required to
monitor for O3.
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ecosystems are exposed in rural/remote
areas to ensure that potential secondary
NAAQS violations are measured; (2)
assessment of O3 concentrations in
smaller communities located outside of
the larger urban MSAs covered by urban
monitoring requirements; and (3) the
assessment of the location and severity
of maximum O3 concentrations that
occur in non-urban areas and may be
attributable to upwind urban sources.
For reasons noted below, EPA believes
that these proposed O3 monitoring
requirements are sufficient to support
the revisions to the O3 NAAQS
proposed in this action.
With regard to the first objective, we
note uncertainties will remain about the
O3 concentrations to which sensitive
natural vegetation and ecosystems are
exposed until additional monitors are
sited in National Parks, State and/or
tribal areas, wilderness areas, and other
similar locations with sensitive
ecosystems that are set aside to provide
similar public welfare benefits. These
monitors would support evaluation of
the secondary NAAQS with a more
robust data set than is now available. As
noted in the 2009 O3 monitoring
proposal, EPA proposed that States
operate at least one monitor to be
located in areas such as some Federal,
State, Tribal, or private lands, including
wilderness areas that have O3-sensitive
natural vegetation and/or ecosystems. If
EPA finalizes a cumulative, seasonal
secondary standard at the lower end of
the proposed range, then it is plausible
that additional O3 monitors, above the
number required by the monitoring
proposal, may be needed in such areas
to provide adequate coverage of
locations likely to experience violations
of the revised secondary NAAQS. These
additional monitors could be
established through discretionary State
initiatives to supplement minimum
monitoring requirements, negotiated
agreements between States and EPA
Regional Administrators, or through a
future rulemaking that addresses
potential increased O3 monitoring
requirements to specifically address the
need for additional monitoring to ensure
detection of secondary standard
violations.
With regard to the second objective of
characterizing elevated ambient O3
levels to which people are exposed in
smaller communities located outside of
the larger urban MSAs, the likelihood of
measuring concentrations that approach
or exceed the levels of the NAAQS due
to the transport of O3 from upwind areas
and/or the formation of O3 due to
precursor emissions from industrial
sources outside of urban areas is clearly
increased due to the revised NAAQS
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proposed in this action. Given that the
analyses described in the 2009 O3
monitoring proposal demonstrated that
50 percent of existing monitors located
in such Micropolitan Statistical Areas 73
exceeded the current NAAQS and
nearly all monitors recorded design
values greater than or equal to 85
percent of the current NAAQS, the
potential for violations in such areas can
only be increased with the NAAQS
revisions proposed in this action. As
noted for the first non-urban monitoring
objective, it is plausible that additional
O3 monitors, above the number required
by the 2009 monitoring proposal may be
needed in Micropolitan Statistical Areas
to provide adequate coverage of
locations likely to experience violations
of the proposed lower primary NAAQS
levels. These additional monitors could
be established through discretionary
State initiatives to supplement
minimum monitoring requirements,
negotiated requirements between States
and EPA Regional Administrators, or
through a future rulemaking that
addresses potential increased O3
monitoring requirements to specifically
address the need for additional
monitoring to ensure detection of
primary standard violations in smaller
communities.
The third proposed non-urban
monitoring objective, requiring O3
monitors to be located in the area of
expected maximum O3 concentration
outside of any MSA, potentially
including the far downwind transport
zones of currently well-monitored urban
areas, is not directly related to the level
of the O3 NAAQS. It is instead intended
to ensure that all parts of a State meet
the NAAQS and that all necessary
emission control strategies have been
included in State Implementation Plans.
Accordingly, this proposed monitoring
objective remains applicable
independent of revisions to the O3
NAAQS proposed in this action.
D. Revisions to the Length of the
Required O3 Monitoring Seasons
Ozone monitoring is only required
during the seasons of the year that are
conducive to O3 formation. These
seasons vary in length as the conditions
that determine the likely O3 formation
(i.e., seasonally-dependent factors such
as ambient temperature, strength of
solar insolation, and length of day)
differ by location. In some locations,
conditions conducive to O3 formation
are limited to a few summer months of
the year while in other locations these
73 Defined as areas having at least one urban
cluster of at least 10,000 but less than a population
of 50,000.
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conditions occur year-round. As a
result, the length of currently required
O3 monitoring seasons can vary from a
length of 4 months in colder climates to
a length of 12 months in warmer
climates.
The 2009 O3 monitoring proposal also
addressed the issue of whether in some
areas the required O3 monitoring season
should be made longer. The proposal
also addressed the status of any
currently effective Regional
Administrator-granted waiver approvals
to O3 monitoring seasons, and the
impact of proposed changes to
monitoring requirements on such
waiver approvals.
The EPA performed several analyses
in support of proposed changes to the
required O3 monitoring seasons. The
first analysis determined the number of
observed exceedances of the 0.075 ppm
level of the current 8-hour NAAQS in
the months falling outside the currently
required local O3 monitoring season
using monitors in areas that collected O3
data year-round in 2004–2006. The
second analysis examined observed
occurrences of daily maximum 8-hour
O3 averages of at least 0.060 ppm. This
threshold was chosen because it
represented 80 percent of the current
0.075 ppm NAAQS level and provides
an indicator of ambient conditions that
may be conducive to the formation of O3
concentrations that approach or exceed
the NAAQS. While proposals for
revising each State’s required
monitoring season were based on
observed data in and surrounding each
State, statistically predicted
exceedances were also used to validate
conclusions for each State.
The aforementioned analyses
provided several results. The analysis of
observed exceedances of the 0.075 ppm
level of the current O3 NAAQS
indicated occurrences in eight States
during months outside of the current
required monitoring season. The eight
States were Maine, Massachusetts, New
Hampshire, New Jersey, New York,
South Carolina, Vermont, and
Wyoming. With the exception of
Wyoming, these exceedances occurred
in a very limited manner and timeframe,
just before the beginning of these States’
required O3 monitoring season
(beginning in these States on April 1).
The frequency of observed occurrences
of maximum 8-hour average O3 levels of
at least 0.060 ppm was quite high across
the country in months outside of the
current required monitoring season. A
total of 32 States experienced such
occurrences; 22 States had such levels
only before the required monitoring
season; 9 States had such levels both
before and after the required monitoring
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season; and 1 State had such levels only
after the required monitoring season. In
a number of cases, the frequency of such
ambient concentrations was high, with
some States experiencing between 31 to
46 out-of-season days during 2004 to
2006 at a high percentage of all
operating year-round O3 monitors.
Based on these analyses, EPA
proposed a lengthening of the O3
monitoring season requirements in
many areas. The 2009 proposed changes
were based not only on the goal of
monitoring out-of-season O3 NAAQS
violations but also on the goal of
ensuring monitoring when ambient O3
levels reach 80 percent of the NAAQS
so that persons unusually sensitive to
O3 would be alerted to potential
NAAQS exceedances.
The EPA believes that the factors used
to support the 2009 proposed changes to
O3 monitoring seasons are appropriate
to support the revisions of the O3
NAAQS proposed in this action. With
regard to the primary standard, we note
that the lower end of the range being
proposed is an 8-hour level of 0.060
ppm, which is identical to the ambient
O3 level that was utilized in one of the
analyses discussed above. Although that
level was chosen to provide an indicator
of ambient levels that were below but
approaching the level of the NAAQS
and hence to serve as an alert to
potential exceedances, we note that
EPA’s traditional practice had been to
base the length of required O3
monitoring seasons on the likelihood of
measuring exceedances of the level of
the NAAQS. Therefore, if EPA finalizes
the level of the primary standard at the
lower end of the proposed range, the O3
monitoring seasons that have been
proposed as part of the 2009 O3
monitoring proposal would provide
sufficient monitoring coverage to ensure
the goal of measuring potential
violations of the primary standard.
One O3 monitoring season issue that
was not considered in the 2009 O3
monitoring proposal was the question of
whether analyses of ambient data based
on 8-hour average statistics would also
indicate whether the resulting proposed
monitoring seasons would capture the
cumulative maximum consecutive 3month O3 levels necessary to compute
design values based on the secondary
NAAQS proposed in this action, which
is defined in terms of a W126
cumulative peak-weighted index, as
discussed above in section IV. If areas
experienced high cumulative index
values during months outside of the
required O3 monitoring seasons (based
on 8-hour statistics), then further
revisions to the required monitoring
seasons might be necessary to ensure
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monitoring during all months important
to the calculation of design values for
the revised form proposed for the
secondary NAAQS. A related issue is
whether such high cumulative O3 values
also occurred during time periods that
are biologically relevant for O3-sensitive
vegetation.
The EPA is not proposing additional
revisions to O3 monitoring seasons at
this time. Additional analyses of the
distribution of elevated cumulative
W126 index values will be conducted,
and the biologically relevant seasonal
issue will be further reviewed. Based on
the results of these analyses, EPA may
consider proposing further revisions to
the O3 monitoring season as related to
the secondary O3 NAAQS.
VII. Implementation of Proposed O3
Standards
A. Designations
After EPA establishes or revises a
NAAQS, the CAA directs EPA and the
states to take steps to ensure that the
new or revised NAAQS are met. The
first step is to identify areas of the
country that do not meet the new or
revised NAAQS. This step is known as
the initial area designations.
The CAA provides that, ‘‘By such date
as the Administrator may reasonably
require, but not later than 1 year after
promulgation of a new or revised
national ambient air quality standard for
any pollutant under section 109, the
Governor of each state shall * * *
submit to the Administrator a list of all
areas (or portions thereof) in the state’’
that designates those areas as
nonattainment, attainment, or
unclassifiable. The CAA specifies that,
‘‘The Administrator may not require the
Governor to submit the required list
sooner than 120 days after promulgating
a new or revised national ambient air
quality standard.’’ The CAA defines an
area as nonattainment if it is violating
the NAAQS or if it is contributing to a
violation in a nearby area. (See CAA
section 107(d)(1).)
The CAA further provides, ‘‘Upon
promulgation or revision of a national
ambient air quality standard, the
Administrator shall promulgate the
designations of all areas (or portions
thereof) * * * as expeditiously as
practicable, but in no case later than 2
years from the date of promulgation of
the new or revised national ambient air
quality standard. Such period may be
extended for up to one year in the event
the Administrator has insufficient
information to promulgate the
designations.’’ EPA is required to notify
states of any intended modifications to
their recommendations that EPA may
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deem necessary no later than 120 days
prior to promulgating designations.
States then have an opportunity to
demonstrate why any such proposed
modification is inappropriate. Whether
or not a state provides a
recommendation, EPA must promulgate
the designation that the Agency deems
appropriate. (See CAA section
107(d)(1)(B).)
On September 16, 2009, when the
Administrator announced her decision
to reconsider the 2008 O3 NAAQS, she
also indicated that the Agency would
work with states to accelerate
implementation of the standards
adopted after reconsideration, including
the initial area designations process.
Acceleration of designations for the
primary standard would help limit any
delays in health protections associated
with the reconsideration of the
standards. If a secondary standard
different from the primary standard is
adopted, this would be the first time
different primary and secondary
standards would be in place for the O3
standards. While welfare protection is
also important, for the reasons provided
below, we are providing alternative
schedules for designating areas for the
secondary standard.
If, as a result of the reconsideration,
EPA determines that the record supports
a primary standard different from that
promulgated in 2008 and promulgates
such different primary O3 NAAQS in
2010, EPA intends to promulgate final
designations on an accelerated schedule
to allow the designations to be effective
in 1 year. In order to meet such a
schedule, EPA is proposing that the
deadline for states to submit their
designations recommendations for the
revised 2010 primary standard be 129
days after promulgation of that primary
standard. EPA recognizes that the
proposed deadline would be an
ambitious schedule. Therefore, EPA
intends to provide technical information
and guidance for states as early as
possible to facilitate the development of
their recommendations. Many of the
areas that would be violating the
proposed primary ozone standard are
also violating the 2008 ozone standards.
State Governors have provided
recommendations on these areas
pursuant to the 2008 standards and
recommendations may not need much
further evaluation.
Based on this proposed schedule, if
EPA promulgates a new primary
standard on August 31, 2010, state
Governors would need to submit their
initial designation recommendations to
EPA by January 7, 2011. If the
Administrator intends to modify any
state recommendation, EPA would
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notify the Governor no later than March
2011, 120 days prior to promulgating
the final designations. States would
then have an opportunity to comment
on EPA’s intended designations before
EPA promulgates the final designations.
EPA would promulgate the final
designations in July 2011 to allow
sufficient time for the designations to be
published and effective by August 31,
2011. EPA expects to base the final
designations for the primary O3
standard on three consecutive years of
certified air quality monitoring data
from the years 2007–2009 or from 2008–
2010, if available.
If, as a result of the reconsideration,
EPA promulgates a distinct secondary
standard that differs from that
promulgated in 2008 and also differs
from the 2010 primary standard, as
proposed above, EPA is proposing two
alternative deadlines for states to submit
their designations recommendations.
Under the first alternative, EPA would
designate areas for the secondary
standard on the same accelerated
schedule discussed above for the
primary standard. In order to meet that
schedule, EPA is proposing that states
submit their recommendations for the
revised 2010 secondary standard 129
days after promulgation of that
secondary standard. Accordingly, if EPA
promulgates the new secondary
standard on August 31, 2010, state
Governors would need to submit their
initial designation recommendations to
EPA by January 7, 2011.
Weighing in favor of designating areas
for the secondary standard at the same
time as designations for the primary
standard is that planning for both
standards would occur on the same
schedule. Our examination of current
air quality data from the existing
monitoring network indicates that for
levels of the primary and secondary
standards proposed in this action, it is
likely that the vast majority of areas
violating the secondary standard would
overlap with areas violating the primary
standard. In this case, implementing
requirements for the primary and
secondary standards on different
schedules could present resource
challenges to state and local agencies by
requiring duplication of effort and
hindering consideration of all factors
when deciding which control strategies
to adopt for each standard. For example,
if designations for the secondary
standard were delayed by a certain
period (e.g., a year) beyond the
designations for the primary standard,
then EPA would likely delay
submission of attainment SIPs for the
secondary standard for a similar period
beyond the proposed date for
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submission of the attainment SIPs for
the primary standard. In this case, the
initial transportation conformity
determination for the secondary
standard would be required later than
the initial determination for the primary
standard by the difference in time
between the effective dates of the two
designations.
Under the second alternative, EPA
would designate areas for the secondary
standard on the maximum 2-year
schedule provided under the CAA. To
meet that 2-year schedule, EPA is
proposing that states submit their
recommendations for the revised
secondary standard no later than 1 year
after promulgation of the 2010
secondary standard. Accordingly, if EPA
promulgates a secondary standard on
August 31, 2010, that differs from the
primary standard, as proposed, under
the alternative 2-year designations
schedule, state Governors would need to
submit their initial designation
recommendations to EPA by August 31,
2011. If the Administrator intends to
modify any state recommendation, EPA
would notify the Governor no later than
May 2012, 120 days prior to the 2-year
deadline for promulgating the final
designations. States would then have an
opportunity to comment on EPA’s
intended designations before EPA
promulgates the final designations. EPA
would promulgate the final designations
for the secondary standard by August
31, 2012. EPA expects to base the final
designations in August 2012 for a
different secondary standard on the
most recent three consecutive years of
certified air quality monitoring data,
which would be from the years 2009–
2011.
In the past, EPA has always set the
secondary O3 standard to be identical to
the primary O3 standard and the
standards have embodied relatively
short-term average concentrations (e.g.,
1-hour or 8-hour). In this action, EPA is
proposing a cumulative, seasonal
secondary standard that differs from the
proposed primary standard. EPA has not
previously set a seasonal secondary
standard for O3. Therefore, EPA and
states do not have experience in
implementing this type of secondary O3
standard or in determining what area
boundaries would be appropriate. As we
further explore implementation
considerations for the secondary
standard, we may encounter
unanticipated issues that may require
additional time to address. Thus, EPA is
considering whether an accelerated
schedule for a seasonal secondary
standard would provide adequate time
for resolving issues that we cannot now
anticipate. If EPA designates areas for
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the secondary standard on a 2-year
schedule, we note that we expect that
accelerated implementation of the
health-based primary standard would
also result in accelerated welfare
benefits. EPA requests comment on
factors affecting the efficient and
effective implementation of a secondary
standard that differs from the primary
standard in the context of establishing
designations schedules.
EPA notes, as discussed in greater
detail above in section VI, that it has
proposed a monitoring rule that would
increase the density of monitoring in
National Parks and other non-urban and
lesser populated areas (July 16, 2009; 74
FR 34525). The proposed requirements
are intended to satisfy several important
objectives, including better
characterization of O3 exposures to O3sensitive vegetation and ecosystems in
rural/remote areas to ensure that
potential secondary NAAQS violations
are measured. As proposed, the new
monitors would not be deployed until
2012 or 2013. Therefore, data from these
monitors would not be available for use
within the statutory timeframe for EPA
to complete designations for a 2010
secondary standard regardless of which
schedule EPA follows.
While CAA section 107 specifically
addresses states, EPA intends to follow
the same process for tribes to the extent
practicable, pursuant to section 301(d)
of the CAA regarding tribal authority,
and the Tribal Authority Rule (63 FR
7254; February 12, 1998).
In a separate notice elsewhere in
today’s Federal Register, EPA is
announcing that it is using its authority
under the CAA to extend by 1 year the
deadline for promulgating initial area
designations for the O3 NAAQS that
were promulgated in March 2008. The
new deadline is March 12, 2011. That
notice explains the basis for the
deadline extension. As mentioned
above, on September 16, 2009, EPA
notified the Court of its decision to
initiate a rulemaking to reconsider the
primary and secondary O3 NAAQS set
in March 2008 to ensure they satisfy the
requirements of the CAA. In its notice
to the Court, EPA stated that the final
rule would be signed by August 31,
2010. Extending the deadline for
promulgating designations for the 2008
O3 NAAQS until March 12, 2011 will
allow EPA to complete the
reconsideration rulemaking for the 2008
O3 NAAQS before determining whether
it is necessary to finalize designations
for those NAAQS or, instead, whether it
is necessary to begin the designation
process for different NAAQS
promulgated pursuant to the
reconsideration.
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B. State Implementation Plans
The CAA section 110 provides the
general requirements for SIPs. Within 3
years after the promulgation of new or
revised NAAQS (or such shorter period
as the Administrator may prescribe)
each State must adopt and submit
‘‘infrastructure’’ SIPs to EPA to address
the requirements of section 110(a)(1).
Thus, States should submit these SIPs
no later than August 21, 2013, three
years after promulgation of the
reconsidered ozone standard in 2010.
These ‘‘infrastructure SIPs’’ provide
assurances of State resources and
authorities, and establish the basic State
programs, to implement, maintain, and
enforce new or revised standards.
In addition to the infrastructure SIPs,
which apply to all States, CAA title I,
part D outlines the State requirements
for achieving clean air in designated
nonattainment areas. These
requirements include timelines for
when designated nonattainment areas
must attain the standards, deadlines for
developing SIPs that demonstrate how
the State will ensure attainment of the
standards, and specific emissions
control requirements. EPA plans to
address how these requirements, such
as attainment demonstrations and
attainment dates, reasonable further
progress, new source review,
conformity, and other implementation
requirements, apply to the O3 NAAQS
promulgated pursuant to the
reconsideration in a subsequent
rulemaking. Also in that rulemaking
EPA will establish deadlines for
submission of nonattainment area SIPs
but anticipates that the deadlines will
be no later than the end of December
2013, or 28 months after final
designations.
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C. Trans-Boundary Emissions
Cross border O3 contributions from
within North America (Canada and
Mexico) entering the U.S. are generally
thought to be small. Section 179B of the
Clean Air Act allows designated
nonattainment areas to petition EPA to
consider whether such a locality might
have met a clean air standard ‘‘but for’’
cross border contributions. To date, few
areas have petitioned EPA under this
authority. The impact of foreign
emissions on domestic air quality in the
United States is a challenging and
complex problem to assess. EPA is
engaged in a number of activities to
improve our understanding of
international transport. As work
progresses on these activities, EPA will
be able to better address the
uncertainties associated with trans-
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boundary flows of air pollution and
their impacts.
VIII. Statutory and Executive Order
Reviews
A. Executive Order 12866: Regulatory
Planning and Review
Under section 3(f)(1) of Executive
Order (EO) 12866 (58 FR 51735, October
4, 1993), the O3 NAAQS action is an
‘‘economically significant regulatory
action’’ because it is likely to have an
annual effect on the economy of $100
million or more. Accordingly, EPA
submitted this action to the Office of
Management and Budget (OMB) for
review under EO 12866 and any
changes made in response to OMB
recommendations have been
documented in the docket for this
action. In addition, EPA prepared this
regulatory impact analysis (RIA) of the
potential costs and benefits associated
with this action. This analysis is
contained in the Regulatory Impact
Analysis for the Ozone NAAQS
Reconsideration, October 2009
(henceforth, ‘‘RIA’’). A copy of the
analysis is available in the RIA docket
(EPA–HQ–OAR–2007–0225) and the
analysis is briefly summarized here. The
RIA estimates the costs and monetized
human health and welfare benefits of
attaining five alternative O3 NAAQS
nationwide. Specifically, the RIA
examines the alternatives of 0.079 ppm,
0.075 ppm, 0.070 ppm, 0.065 ppm, and
0.060 ppm. The RIA contains
illustrative analyses that consider a
limited number of emissions control
scenarios that States and Regional
Planning Organizations might
implement to achieve these alternative
O3 NAAQS. However, the Clean Air Act
(CAA) and judicial decisions make clear
that the economic and technical
feasibility of attaining ambient
standards are not to be considered in
setting or revising NAAQS, although
such factors may be considered in the
development of State plans to
implement the standards. Accordingly,
although an RIA has been prepared, the
results of the RIA have not been
considered in issuing this proposed
rule.
B. Paperwork Reduction Act
This action does not impose an
information collection burden under the
provisions of the Paperwork Reduction
Act, 44 U.S.C. 3501 et seq. There are no
information collection requirements
directly associated with the
establishment of a NAAQS under
section 109 of the CAA.
Burden means the total time, effort, or
financial resources expended by persons
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to generate, maintain, retain, or disclose
or provide information to or for a
Federal agency. This includes the time
needed to review instructions; develop,
acquire, install, and utilize technology
and systems for the purposes of
collecting, validating, and verifying
information, processing and
maintaining information, and disclosing
and providing information; adjust the
existing ways to comply with any
previously applicable instructions and
requirements; train personnel to be able
to respond to a collection of
information; search data sources;
complete and review the collection of
information; and transmit or otherwise
disclose the information.
An agency may not conduct or
sponsor, and a person is not required to
respond to a collection of information
unless it displays a currently valid OMB
control number. The OMB control
numbers for EPA’s regulations in 40
CFR are listed in 40 CFR part 9.
C. Regulatory Flexibility Act
The Regulatory Flexibility Act (RFA)
generally requires an agency to prepare
a regulatory flexibility analysis of any
rule subject to notice and comment
rulemaking requirements under the
Administrative Procedure Act or any
other statute unless the agency certifies
that the rule will not have a significant
economic impact on a substantial
number of small entities. Small entities
include small businesses, small
organizations, and small governmental
jurisdictions.
For purposes of assessing the impacts
of today’s proposed rule on small
entities, small entity is defined as: (1) A
small business that is a small industrial
entity as defined by the Small Business
Administration’s (SBA) regulations at 13
CFR 121.201; (2) a small governmental
jurisdiction that is a government of a
city, county, town, school district or
special district with a population of less
than 50,000; and (3) a small
organization that is any not-for-profit
enterprise which is independently
owned and operated and is not
dominant in its field.
After considering the economic
impacts of today’s proposed rule on
small entities, I certify that this action
will not have a significant economic
impact on a substantial number of small
entities. This proposed rule will not
impose any requirements on small
entities. Rather, this rule establishes
national standards for allowable
concentrations of O3 in ambient air as
required by section 109 of the CAA. See
also American Trucking Associations v.
EPA. 175 F. 3d at 1044–45 (NAAQS do
not have significant impacts upon small
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entities because NAAQS themselves
impose no regulations upon small
entities). We continue to be interested in
the potential impacts of the proposed
rule on small entities and welcome
comments on issues related to such
impacts
D. Unfunded Mandates Reform Act
Title II of the Unfunded Mandates
Reform Act of 1995 (UMRA), Public
Law 104–4, establishes requirements for
Federal agencies to assess the effects of
their regulatory actions on State, local,
and Tribal governments and the private
sector. Under section 202 of the UMRA,
EPA generally must prepare a written
statement, including a cost-benefit
analysis, for proposed and final rules
with ‘‘Federal mandates’’ that may result
in expenditures to State, local, and
Tribal governments, in the aggregate, or
to the private sector, of $100 million or
more in any 1 year. Before promulgating
an EPA rule for which a written
statement is needed, section 205 of the
UMRA generally requires EPA to
identify and consider a reasonable
number of regulatory alternatives and to
adopt the least costly, most costeffective or least burdensome alternative
that achieves the objectives of the rule.
The provisions of section 205 do not
apply when they are inconsistent with
applicable law. Moreover, section 205
allows EPA to adopt an alternative other
than the least costly, most cost-effective
or least burdensome alternative if the
Administrator publishes with the final
rule an explanation why that alternative
was not adopted. Before EPA establishes
any regulatory requirements that may
significantly or uniquely affect small
governments, including Tribal
governments, it must have developed
under section 203 of the UMRA a small
government agency plan. The plan must
provide for notifying potentially
affected small governments, enabling
officials of affected small governments
to have meaningful and timely input in
the development of EPA regulatory
proposals with significant Federal
intergovernmental mandates, and
informing, educating, and advising
small governments on compliance with
the regulatory requirements.
Today’s proposed rule contains no
Federal mandates (under the regulatory
provisions of Title II of the UMRA) for
State, local, or Tribal governments or
the private sector. The proposed rule
imposes no new expenditure or
enforceable duty on any State, local or
Tribal governments or the private sector,
and EPA has determined that this
proposed rule contains no regulatory
requirements that might significantly or
uniquely affect small governments.
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Furthermore, as indicated previously, in
setting a NAAQS EPA cannot consider
the economic or technological feasibility
of attaining ambient air quality
standards, although such factors may be
considered to a degree in the
development of State plans to
implement the standards. See also
American Trucking Associations v.
EPA, 175 F. 3d at 1043 (noting that
because EPA is precluded from
considering costs of implementation in
establishing NAAQS, preparation of a
Regulatory Impact Analysis pursuant to
the Unfunded Mandates Reform Act
would not furnish any information
which the court could consider in
reviewing the NAAQS). Accordingly,
EPA has determined that the provisions
of sections 202, 203, and 205 of the
UMRA do not apply to this proposed
decision. The EPA acknowledges,
however, that any corresponding
revisions to associated SIP requirements
and air quality surveillance
requirements, 40 CFR part 51 and 40
CFR part 58, respectively, might result
in such effects. Accordingly, EPA will
address, as appropriate, unfunded
mandates if and when it proposes any
revisions to 40 CFR parts 51 or 58.
E. Executive Order 13132: Federalism
Executive Order 13132, entitled
‘‘Federalism’’ (64 FR 43255, August 10,
1999), requires EPA to develop an
accountable process to ensure
‘‘meaningful and timely input by State
and local officials in the development of
regulatory policies that have federalism
implications.’’ ‘‘Policies that have
federalism implications’’ is defined in
the Executive Order to include
regulations that have ‘‘substantial direct
effects on the States, on the relationship
between the national government and
the States, or on the distribution of
power and responsibilities among the
various levels of government.’’
This proposed rule does not have
federalism implications. It will not have
substantial direct effects on the States,
on the relationship between the national
government and the States, or on the
distribution of power and
responsibilities among the various
levels of government, as specified in
Executive Order 13132. The rule does
not alter the relationship between the
Federal government and the States
regarding the establishment and
implementation of air quality
improvement programs as codified in
the CAA. Under section 109 of the CAA,
EPA is mandated to establish NAAQS;
however, CAA section 116 preserves the
rights of States to establish more
stringent requirements if deemed
necessary by a State. Furthermore, this
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proposed rule does not impact CAA
section 107 which establishes that the
States have primary responsibility for
implementation of the NAAQS. Finally,
as noted in section E (above) on UMRA,
this rule does not impose significant
costs on State, local, or Tribal
governments or the private sector. Thus,
Executive Order 13132 does not apply
to this rule.
However, as also noted in section D
(above) on UMRA, EPA recognizes that
States will have a substantial interest in
this rule and any corresponding
revisions to associated SIP requirements
and air quality surveillance
requirements, 40 CFR part 51 and 40
CFR part 58, respectively. Therefore, in
the spirit of Executive Order 13132, and
consistent with EPA policy to promote
communications between EPA and State
and local governments, EPA specifically
solicits comment on this proposed rule
from State and local officials.
F. Executive Order 13175: Consultation
and Coordination With Indian Tribal
Governments
Executive Order 13175, entitled
‘‘Consultation and Coordination with
Indian Tribal Governments’’ (65 FR
67249, November 9, 2000), requires EPA
to develop an accountable process to
ensure ‘‘meaningful and timely input by
tribal officials in the development of
regulatory policies that have tribal
implications.’’ This rule concerns the
establishment of O3 NAAQS. The Tribal
Authority Rule gives Tribes the
opportunity to develop and implement
CAA programs such as the O3 NAAQS,
but it leaves to the discretion of the
Tribe whether to develop these
programs and which programs, or
appropriate elements of a program, they
will adopt.
This proposed rule does not have
Tribal implications, as specified in
Executive Order 13175. It does not have
a substantial direct effect on one or
more Indian Tribes, since Tribes are not
obligated to adopt or implement any
NAAQS. Thus, Executive Order 13175
does not apply to this rule.
Although Executive Order 13175 does
not apply to this rule, EPA contacted
tribal environmental professionals
during the development of the March
2008 rule. The EPA staff participated in
the regularly scheduled Tribal Air call
sponsored by the National Tribal Air
Association during the spring of 2007 as
the proposal was under development.
EPA specifically solicits additional
comment on this proposed rule from
Tribal officials.
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srobinson on DSKHWCL6B1PROD with PROPOSALS2
G. Executive Order 13045: Protection of
Children From Environmental Health
and Safety Risks
H. Executive Order 13211: Actions That
Significantly Affect Energy Supply,
Distribution or Use
Executive Order 13045, ‘‘Protection of
Children from Environmental Health
Risks and Safety Risks’’ (62 FR 19885,
April 23, 1997) applies to any rule that:
(1) Is determined to be ‘‘economically
significant’’ as defined under Executive
Order 12866, and (2) concerns an
environmental health or safety risk that
EPA has reason to believe may have a
disproportionate effect on children. If
the regulatory action meets both criteria,
the Agency must evaluate the
environmental health or safety effects of
the planned rule on children, and
explain why the planned regulation is
preferable to other potentially effective
and reasonably feasible alternatives
considered by the Agency.
This proposed rule is subject to
Executive Order 13045 because it is an
economically significant regulatory
action as defined by Executive Order
12866, and we believe that the
environmental health risk addressed by
this action may have a disproportionate
effect on children. The proposed rule
will establish uniform national ambient
air quality standards for O3; these
standards are designed to protect public
health with an adequate margin of
safety, as required by CAA section 109.
However, the protection offered by these
standards may be especially important
for children because children, especially
children with asthma, along with other
sensitive population subgroups such as
all people with lung disease and people
active outdoors, are potentially
susceptible to health effects resulting
from O3 exposure. Because children are
considered a potentially susceptible
population, we have carefully evaluated
the environmental health effects of
exposure to O3 pollution among
children. Discussions of the results of
the evaluation of the scientific evidence,
policy considerations, and the exposure
and risk assessments pertaining to
children are contained in sections II.B
and II.C of this preamble. A listing of
the documents that contain the
evaluation of scientific evidence, policy
considerations, and exposure and risk
assessments that pertain to children is
found in the section on Children’s
Environmental Health in the
Supplementary Information section of
this preamble, and a copy of all
documents have been placed in the
public docket for this action. The public
is invited to submit comments or
identify peer-reviewed studies and data
that assess effects of early life exposure
to O3.
This proposed rule is not a
‘‘significant energy action’’ as defined in
Executive Order 13211, ‘‘Actions
Concerning Regulations That
Significantly Affect Energy Supply,
Distribution, or Use’’ (66 FR 28355 (May
22, 2001)) because in the Agency’s
judgment it is not likely to have a
significant adverse effect on the supply,
distribution, or use of energy. The
purpose of this rule is to establish
revised NAAQS for O3. The rule does
not prescribe specific pollution control
strategies by which these ambient
standards will be met. Such strategies
will be developed by States on a caseby-case basis, and EPA cannot predict
whether the control options selected by
States will include regulations on
energy suppliers, distributors, or users.
Thus, EPA concludes that this rule is
not likely to have any adverse energy
effects and does not constitute a
significant energy action as defined in
Executive Order 13211.
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I. National Technology Transfer and
Advancement Act
Section 12(d) of the National
Technology Transfer and Advancement
Act of 1995 (NTTAA), Public Law 104–
113, section 12(d) (15 U.S.C. 272 note)
directs EPA to use voluntary consensus
standards in its regulatory activities
unless to do so would be inconsistent
with applicable law or otherwise
impractical. Voluntary consensus
standards are technical standards (e.g.,
materials specifications, test methods,
sampling procedures, and business
practices) that are developed or adopted
by voluntary consensus standards
bodies. The NTTAA directs EPA to
provide Congress, through OMB,
explanations when the Agency decides
not to use available and applicable
voluntary consensus standards.
This proposed rulemaking does not
involve technical standards. Therefore,
EPA is not considering the use of any
voluntary consensus standards.
J. Executive Order 12898: Federal
Actions To Address Environmental
Justice in Minority Populations and
Low-Income Populations
Executive Order 12898 (59 FR 7629
(Feb. 16, 1994)) establishes federal
executive policy on environmental
justice. Its main provision directs
federal agencies, to the greatest extent
practicable and permitted by law, to
make environmental justice part of their
mission by identifying and addressing,
as appropriate, disproportionately high
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and adverse human health or
environmental effects of their programs,
policies, and activities on minority
populations and low-income
populations in the United States.
EPA has determined that this
proposed rule will not have
disproportionately high and adverse
human health or environmental effects
on minority or low-income populations
because it increases the level of
environmental protection for all affected
populations without having any
disproportionately high and adverse
human health or environmental effects
on any population, including any
minority or low-income population. The
proposed rule will establish uniform
national standards for O3 air pollution.
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Whitfield, R.; Biller, W.; Jusko, M.; and
Keisler, J. (1996) A Probabilistic
Assessment of Health Risks Associated
with Short- and Long-Term Exposure to
Tropospheric Ozone. Argonne National
Laboratory, Argonne, IL.
Whitfield, R. (1997) A Probabilistic
Assessment of Health Risks Associated
with Short-term Exposure to
Tropospheric Ozone: A Supplement.
Argonne National Laboratory, Argonne,
IL.
Whitfield, C. P.; Davison, A. W.; Ashenden,
T. W. (1997) Artificial selection and
heritability of ozone resistance in two
populations of Plantago major. New
Phytol. 137: 645–655.
Whitfield, R.G.; Richmond, H.M.; and
Johnson, T.R. (1998) ‘‘Overview of Ozone
Human Exposure and Health Risk
Analyses Used in the U.S. EPA’s Review
of the Ozone Air Quality Standard,’’
pp.483–516 in: T. Schneider, ed. Air
Pollution in the 21st Century: Priority
Issues and Policy Elsevier; Amsterdam.
Wolff, G.T. (1995) Letter from Chairman of
Clean Air Scientific Advisory Committee
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19JAP2
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Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules
to the EPA Administrator, dated
November 30, 1995. EPA–SAB–CASAC–
LTR–96–002.
Wolff, G.T. (1996) Letter from Chairman of
Clean Air Scientific Advisory Committee
to the EPA Administrator, dated April 4,
1996. EPA–SAB–CASAC–LTR–96–006.
Xu, X.; Ding, H.; Wang, X. (1995) Acute
effects of total suspended particles and
sulfur dioxides on preterm delivery: a
community-based cohort study. Arch.
Environ. Health 50: 407–415.
Young, T. F.; Sanzone, S., eds. (2002) A
framework for assessing and reporting on
ecological condition: an SAB report.
Washington, DC: U.S. Environmental
Protection Agency, Science Advisory
Board; report no. EPA–SAB–EPEC–02–
009. Available online at: https://yosemite.
epa.gov/sab/sabproduct.nsf/C3F89E598
D843B58852570CA0075717E/$File/epec
02009a.pdf.
Zeger, S. L.; Thomas, D.; Dominici, F.; Samet,
J. M.; Schwartz, J.; Dockery, D.; Cohen,
A. (2000) Exposure measurement error in
time-series studies of air pollution:
concepts and consequences. Environ.
Health Perspect. 108: 419–426.
Zhang, L.-Y.; Levitt, R. C.; Kleeberger, S. R.
(1995) Differential susceptibility to
ozone-induced airways hyperreactivity
in inbred strains of mice. Exp. Lung Res.
21: 503–518.
Zidek, J. V.; White, R.; Le, N. D.; Sun, W.;
Burnett, R. T. (1998) Imputing
unmeasured explanatory variables in
environmental epidemiology with
application to health impact analysis of
air pollution. Environ. Ecol. Stat. 5: 99–
115.
List of Subjects in 40 CFR Parts 50 and
58
Environmental protection, Air
pollution control, Carbon monoxide,
Lead, Nitrogen dioxide, Ozone,
Particulate matter, Sulfur oxides.
Dated: January 6, 2010.
Lisa P. Jackson,
Administrator.
For the reasons set forth in the
preamble, parts 50 and 58 of chapter 1
of title 40 of the code of Federal
regulations are proposed to be amended
as follows:
PART 50—NATIONAL PRIMARY AND
SECONDARY AMBIENT AIR QUALITY
STANDARDS
1. The authority citation for part 50
continues to read as follows:
Authority: 42 U.S.C. 7401 et seq.
2. Section 50.15 is revised to read as
follows:
§ 50.15 National primary and secondary
ambient air quality standards for ozone.
(a) The level of the national 8-hour
primary ambient air quality standard for
O3 is (0.060–0.070) parts per million
(ppm), daily maximum 8-hour average,
measured by a reference method based
on Appendix D to this part and
designated in accordance with part 53 of
this chapter or an equivalent method
designated in accordance with part 53 of
this chapter.
(b) The 8-hour primary O3 ambient air
quality standard is met at an ambient air
quality monitoring site when the
average of the annual fourth-highest
daily maximum 8-hour average O3
concentration is less than or equal to
(0.060–0.070) ppm, as determined in
accordance with appendix P to this part.
(c) The level of the national secondary
ambient air quality standard for O3 is a
cumulative index value of (7–15) ppmhours, measured by a reference method
based on Appendix D to this part and
designated in accordance with part 53 of
this chapter or an equivalent method
designated in accordance with part 53 of
this chapter.
(d) The secondary O3 ambient air
quality standard is a seasonal standard
expressed as a sum of weighted hourly
concentrations, cumulated over the 12
hour daylight period from 8 a.m. to 8
p.m. local standard time, during the
consecutive 3-month period within the
O3 monitoring season with the
maximum index value. The secondary
O3 standard is met at an ambient air
quality monitoring site when the annual
maximum consecutive 3-month
cumulative index value (W126) is less
than or equal to (7–15) ppm-hours, as
determined in accordance with
appendix P to this part.
3. Section 50.14 is amended by
adding entries for primary and
secondary ozone standards to the end of
Table 1 in paragraph (c)(2)(vi) to read as
follows:
§ 50.14 Treatment of air quality monitoring
data influenced by exceptional events.
*
*
*
(c) * * *
(2) * * *
(vi) * * *
*
*
TABLE 1—SCHEDULE FOR EXCEPTIONAL EVENT FLAGGING AND DOCUMENTATION SUBMISSION FOR DATA TO BE USED IN
DESIGNATIONS DECISIONS FOR NEW NAAQS
NAAQS pollutant/
standard/(level)/
promulgation date
Air quality data
collected for
calendar year
*
*
Primary Ozone/8-Hr .................................
Standard (Level TBD)/promulgated by
August 31, 2010.
*
2007–2009
2010
Secondary Ozone/(Level TBD) Alternative 2-year Schedule—to be Promulgated by August 31, 2010.
2008
srobinson on DSKHWCL6B1PROD with PROPOSALS2
2009–2010
2011
Secondary Ozone/(Level TBD)—Alternative Accelerated Schedule—to be
promulgated by August 31, 2010.
2007–2009
2010
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PO 00000
Event flagging & initial description
deadline
Detailed documentation submission
deadline
*
*
November 1, 2010 b ................................
60 Days after the end of the calendar
quarter in which the event occurred or
March 1, 2011, whichever date occurs
first.b
July 1, 2011 b ...........................................
*
*
November 1, 2010.b
60 Days after the end of the calendar
quarter in which the event occurred or
March 1, 2011, whichever date occurs
first.b
July 1, 2011.a
July 1, 2011 b ...........................................
60 Days after the end of the calendar
quarter in which the event occurred or
March 1, 2012, whichever occurs
first.b
November 1, 2010 b ................................
July 1, 2011.b
60 Days after the end of the calendar
quarter in which the event occurred or
March 1, 2012, whichever occurs
first.b
November 1, 2010.b
60 Days after the end of the calendar
quarter in which the event occurred or
March 1, 2011, whichever date occurs
first.b
60 Days after the end of the calendar
quarter in which the event occurred or
March 1, 2011, whichever date occurs
first.b
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TABLE 1—SCHEDULE FOR EXCEPTIONAL EVENT FLAGGING AND DOCUMENTATION SUBMISSION FOR DATA TO BE USED IN
DESIGNATIONS DECISIONS FOR NEW NAAQS—Continued
NAAQS pollutant/
standard/(level)/
promulgation date
*
Air quality data
collected for
calendar year
*
Event flagging & initial description
deadline
*
*
Detailed documentation submission
deadline
*
*
*
a These
dates are unchanged from those published in the original rulemaking.
change from general schedule in 40 CFR 50.14.
Note: EPA notes that the table of revised deadlines only applies to data EPA will use to establish the final initial designations for new NAAQS.
The general schedule applies for all other purposes, most notably, for data used by EPA for redesignations to attainment.
b Indicates
4. Appendix P to part 50 is revised to
read as follows:
srobinson on DSKHWCL6B1PROD with PROPOSALS2
Appendix P to Part 50—Interpretation
of the Primary and Secondary National
Ambient Air Quality Standards for
Ozone
1. General
(a) This appendix explains the data
handling conventions and computations
necessary for determining whether the 8-hour
primary and secondary national ambient air
quality standards for ozone specified in
§ 50.15 are met at an ambient ozone air
quality monitoring site. Ozone is measured in
the ambient air by a reference method based
on Appendix D of this part, as applicable,
and designated in accordance with part 53 of
this chapter, or by an equivalent method
designated in accordance with part 53 of this
chapter. Data reporting, data handling, and
computation procedures to be used in
making comparisons between reported ozone
concentrations and the levels of the ozone
standards are specified in the following
sections.
(b) Whether to exclude, retain, or make
adjustments to the data affected by
exceptional events, including stratospheric
ozone intrusion and other natural events, is
determined by the requirements under
§§ 50.1, 50.14 and 51.930.
(c) The terms used in this appendix are
defined as follows:
8-hour average is the rolling average of
eight hourly ozone concentrations as
explained in section 3 of this appendix.
Annual fourth-highest daily maximum
refers to the fourth-highest value measured at
a monitoring site during a particular year.
Annual Cumulative W126 Index is the
maximum sum over three consecutive
calendar months of the monthly W126 index
in a year, as explained in section 4 of this
appendix.
Daily maximum 8-hour average
concentration refers to the maximum
calculated 8-hour average for a particular day
as explained in section 3 of this appendix.
Daily W126 Index is the sum of the
sigmoidally weighted hourly ozone
concentrations during the 12-hour daylight
period, 8 a.m. to 7:59 p.m. local standard
time (LST).
Design values are the metrics (i.e.,
statistics) that are compared to the primary
and secondary NAAQS levels to determine
compliance, calculated as shown in sections
3 and 4 of this appendix.
Monthly W126 Index is the sum of the
daily W126 index over one calendar month
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during the required ozone monitoring season,
adjusted for incomplete data if appropriate,
as explained in section 4 of this appendix.
Required ozone monitoring season refers to
the span of time within a calendar year when
individual States are required to measure
ambient ozone concentrations as listed in
part 58 Appendix D to this chapter.
Year refers to calendar year.
2. Requirements for Data Used for
Comparisons With the Ozone NAAQS
(a) All valid FRM/FEM ozone data
submitted to EPA’s Air Quality System
(AQS), or otherwise available to EPA,
meeting the requirements of part 58 of this
chapter including appendices A, C, and E
shall be used in design value calculations.
(b) When two or more ozone monitors are
operated at a site, the state may in advance
designate one of them as the primary
monitor. If the state has not made this
designation, the Administrator will make the
designation, either in advance or
retrospectively. Design values will be
developed using only the data from the
primary monitor, if this results in a valid
design value. If data from the primary
monitor do not allow the development of a
valid design value, data solely from the other
monitor(s) will be used in turn to develop a
valid design value, if this results in a valid
design value. If there are three or more
monitors, the order for such comparison of
the other monitors will be determined by the
Administrator. The Administrator may
combine data from different monitors in
different years for the purpose of developing
a valid primary or secondary standard design
value, if a valid design value cannot be
developed solely with the data from a single
monitor. However, data from two or more
monitors in the same year at the same site
will not be combined in an attempt to meet
data completeness requirements, except if
one monitor has physically replaced another
instrument permanently, in which case the
two instruments will be considered to be the
same monitor, or if the state has switched the
designation of the primary monitor from one
instrument to another during the year.
(c) Hourly average concentrations shall be
reported in parts per million (ppm) to the
third decimal place, with additional digits to
the right of the third decimal place truncated.
The start of each hour shall be identified in
local standard time (LST).
PO 00000
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3. Comparison to the Primary Standard for
Ozone
(a) Computing 8-Hour Averages
Running 8-hour averages shall be
computed from the hourly ozone
concentration data for each hour of the year
and shall be stored in the first, or start, hour
of the 8-hour period. In the event that only
6 or 7 hourly averages are available, the valid
8-hour average shall be computed on the
basis of the hours available, using 6 or 7 as
the divisor. In the event that only 1, 2, 3, 4,
or 5 hourly averages are available, the 8-hour
average shall be computed on the basis of
substituting for all the hours without hourly
averages a low hourly average value selected
as follows, using 8 as the divisor. For days
within the required ozone monitoring season,
the substitution value shall be the lowest
hourly average ozone concentration observed
during the same hour (local standard time) of
any day in the required ozone monitoring
season of that year, or one-half of the method
detection limit of the ozone instrument,
whichever is higher. However, if the number
of same-hour concentration values available
for the required ozone monitoring season for
the year, from which the lowest observed
hourly concentration would be identified for
purposes of this substitution, is less than
50% of the number of days during the
required ozone monitoring season, one-half
the method detection limit of the ozone
instrument shall be used in the substitution.
For days outside the required ozone
monitoring season, the substitution value
shall be one-half the method detection limit
of the ozone instrument. An 8-hour period
with no available hourly averages does not
have a valid 8-hour average. The computed
8-hour average ozone concentrations are not
rounded or truncated.
(b) Daily Maximum 8-Hour Average
Concentrations
There are 24 8-hour periods in each
calendar day. Some of these may not have
valid 8-hour averages, under section 3(a). The
daily maximum 8-hour concentration for a
given calendar day is the highest of the valid
8-hour average concentrations computed for
that day. This process is repeated, yielding a
daily maximum 8-hour average ozone
concentration for each day with ambient
ozone monitoring data, including days
outside the required ozone monitoring season
if data are available. The daily maximum 8hour concentrations from two consecutive
days may have some hourly concentrations
in common. Generally, overlapping daily
maximum 8-hour averages are not likely,
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except in those non-urban monitoring
locations with less pronounced diurnal
variation in hourly concentrations. In these
cases, the maximum 8-hour average
concentration from each day is used, even if
the two averages have some hours in
common.
(c) Primary Standard Design Value
The primary standard design value is the
annual fourth-highest daily maximum 8-hour
ozone concentration considering all days
with monitoring data including any days
outside the required ozone monitoring
season, expressed in parts per million,
averaged over three years. The 3-year average
shall be computed using the three most
recent, consecutive years of monitoring data
that can yield a valid design value. For a
design value to be valid for comparison to the
standard, the monitoring data set on which
it is based must meet the data completeness
requirements described in section 3(d). The
computed 3-year average of the annual
fourth-highest daily maximum 8-hour
average ozone concentrations shall be
rounded to three decimal places. Values
equal to or greater than 0.xxx5 ppm shall
round up.
(d) Data Completeness Requirements for a
Valid Design Value
(i) A design value greater than the standard
is valid if in each of the three years there are
at least four days with a daily maximum 8hour average concentration. Under sections
3(a) and 3(b), there will be a daily maximum
8-hour average concentration on any day
with at least one hourly concentration. One
or more of these four days may be outside the
required ozone monitoring season.
(ii) A design value less than or equal to the
standard is valid if for at least 75% of the
days in the required ozone monitoring season
in each of the three years there are at least
18 8-hour averages in the day that are based
on at least 6 measured hourly average
concentrations.
(iii) When computing whether the
minimum data completeness requirement in
section 3(d)(ii) has been met for the purpose
of showing that a design value equal to or
less than the standard is valid,
meteorological or ambient data may be
sufficient to demonstrate that ozone levels on
days with missing data would not have
affected the design value. At the request of
the state, the Regional Administrator may
consider demonstrations that meteorological
conditions on one or more days in the
required ozone monitoring season which do
not have at least 18 8-hour averages in the
day that are based on at least 6 measured
hourly average concentrations could not have
caused a daily maximum 8-hour
concentration high enough to have been one
Percent valid
days (within
the required
monitoring
season)
Year
1st Highest
daily max
8-hour conc.
(ppm)
2nd Highest
daily max
8-hour conc.
(ppm)
of the four highest daily maximum 8-hour
concentrations for the year. At the request of
the state, days so demonstrated may be
counted towards the 75% requirement for the
purpose of validating the design value,
subject to the approval of the Regional
Administrator.
(vi) Years that do not meet the
completeness criteria stated in 3(d)(ii) may
nevertheless be used to calculate a design
value that will be deemed valid with the
approval of, or at the initiative of, the
Administrator, who may consider factors
such as monitoring site closures/moves,
monitoring diligence, the consistency and
levels of the valid concentration
measurements that are available, and nearby
concentrations in determining whether to use
such data.
(e) Comparison With the Primary Ozone
Standard
(i) The primary ozone ambient air quality
standard is met at an ambient air quality
monitoring site when the design value is less
than or equal to [0.075] ppm.
(ii) Comparison with the primary ozone
standard is demonstrated by examples 1 and
2 as follows:
Example 1. Ambient monitoring site
attaining the primary ozone standard.
3rd Highest
daily max
8-hour conc.
(ppm)
4th Highest
daily max
8-hour conc.
(ppm)
5th Highest
daily max
8-hour conc.
(ppm)
2006 .......................................................
2007 .......................................................
2008 .......................................................
80
96
98
0.092500
0.084750
0.080875
0.090375
0.083500
0.079750
0.085125
0.075375
0.077625
0.078375
0.071875
0.075500
0.078125
0.070625
0.060375
Average ...........................................
........................
........................
........................
........................
0.075250
........................
Rounded .........................................
........................
........................
........................
........................
0.075
........................
As shown in Example 1, this monitoring
site meets the primary ozone standard
because the 3-year average of the annual
fourth-highest daily maximum 8-hour
average ozone concentrations (i.e., 0.075256
ppm, rounded to 0.075 ppm) is less than or
equal to [0.075] ppm. The data completeness
requirement is also met because no single
year has less than 75% data completeness. In
Example 1, the individual 8-hour averages
and the 3-year average are shown with six
decimal digits. In actual calculations, all
Percent valid
days (within
the required
monitoring
season)
(percent)
Year
1st
Highest daily
max
8-hour conc.
(ppm)
2nd
Highest daily
max
8-hour conc.
(ppm)
digits supported by the calculator or
calculation software must be retained.
Example 2. Ambient monitoring site failing
to meet the primary ozone standard.
3rd
Highest daily
max
8-hour conc.
(ppm)
4th
Highest daily
max
8-hour conc.
(ppm)
5th
Highest daily
max
8-hour conc.
(ppm)
srobinson on DSKHWCL6B1PROD with PROPOSALS2
2006 .......................................................
2007 .......................................................
2008 .......................................................
96
74
98
0.105125
0.104250
0.103125
0.103500
0.103625
0.101875
0.101125
0.093000
0.101750
0.078625
0.080250
0.075375
0.072375
0.069500
0.074625
Average ...........................................
........................
........................
........................
........................
0.078083
........................
Rounded .........................................
........................
........................
........................
........................
0.078
........................
As shown in Example 2, the data capture
in 2007 is less than 75%. The primary ozone
standard is not met for this monitoring site
because the 3-year average of the fourth-
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highest daily maximum 8-hour average ozone
concentrations (i.e., 0.078083 ppm, rounded
to 0.078 ppm) is greater than [0.075] ppm and
is therefore valid despite this
PO 00000
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incompleteness. In Example 2, the individual
8-hour averages and the 3-year average are
shown with six decimal digits. In actual
calculations, all digits supported by the
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calculator or calculation software must be
retained.
4. Secondary Ambient Air Quality Standard
for Ozone
(a) Computing the daily W126 index value.
The secondary ozone ambient air quality
standard is a seasonal standard expressed as
a sum of weighted hourly concentrations,
cumulated over the 12 hour daylight period
from 8 a.m. to 8 p.m. local standard time,
during the consecutive 3-month period
within the ozone monitoring season with the
maximum index value. The first step in
determining whether the standard is met at
a monitoring site is to compute the daily
W126 index value for each day by applying
the sigmoidal weighting function in Equation
1 to each reported measurement of hourly
average concentration.
Equation 1
daily W 126 =
i <8 pm
∑
wci Ci
i=8am
Where:
Ci = hourly O3 at hour i, and
wc =
1
1 + 4403e−126C
⋅
The computed value of the sigmoidally
weighted hourly concentration is not
rounded or truncated. The daily W126 index
is formed by summing the twelve computed
hourly values, retaining all decimal places.
An illustration of computing a daily W126
index value is below:
Example 3. Daily W126 index value
calculation for an ambient ozone monitoring
site.
Concentration
(ppm)
Start of hour
Weighted
concentration
(ppm)
8:00 a.m. ......................................................................................................................................................
9:00 a.m. ......................................................................................................................................................
10:00 a.m. ....................................................................................................................................................
11:00 a.m. ....................................................................................................................................................
12:00 p.m. ....................................................................................................................................................
1:00 p.m. ......................................................................................................................................................
2:00 p.m. ......................................................................................................................................................
3:00 p.m. ......................................................................................................................................................
4:00 p.m. ......................................................................................................................................................
5:00 p.m. ......................................................................................................................................................
6:00 p.m. ......................................................................................................................................................
7:00 p.m. ......................................................................................................................................................
0.045
0.060
0.075
0.080
0.079
0.082
0.085
0.088
0.083
0.081
0.065
0.056
0.002781
0.018218
0.055701
0.067537
0.065327
0.071715
0.077394
0.082448
0.073683
0.069667
0.029260
0.011676
Sum=Daily W126 index value ..............................................................................................................
..............................
* 0.625406
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⎡ n
⎤
M.I. = ⎢ ∑ (D.I.)⎥ ∗ (n ∗ 12)/v
⎢ j=1
⎥
⎣
⎦
where
M.I. = the adjusted monthly W126 index,
D.I. = daily W126 index (i.e., the daily sum
of the sigmoidally weighted daylight
hourly concentrations),
n = the number of days in the calendar
month,
v = the number of daylight reporting hours
(8 a.m.–7:59 p.m. LST) in the month
with reported valid hourly ozone
concentrations.
The resulting adjusted value of the
monthly W126 index shall not be rounded or
truncated.
(c) Secondary Standard Design Value
The secondary standard design value is the
3-year average of the annual maximum
consecutive 3-month sum of adjusted
monthly W126 index values expressed in
ppm-hours. Specifically, the annual W126
index value is computed on a calendar year
basis using the three highest, consecutive
adjusted monthly W126 index values. The 3year average shall be computed using the
most recent, consecutive three calendar years
of monitoring data meeting the data
completeness requirements described in
section 4(c). The computed 3-year average of
the annual maximum consecutive 3-month
sum of adjusted monthly W126 index values
in ppm-hours shall be rounded to a whole
PO 00000
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Sfmt 4702
number with decimal values equal to or
greater than 0.500 rounding up.
(c) Data Completeness Requirement
(i) The annual W126 index is valid for
purposes of calculating a 3-year design value
if each full calendar month in the required
ozone monitoring season has at least 75%
data completeness for daylight hours.
(ii) If one or more months during the ozone
monitoring seasons of three successive years
has less than 75% data completeness, the
three years shall nevertheless be used in the
computation of a valid design value for the
site if substituting the lowest hourly ozone
concentration observed during daylight hours
in the required ozone monitoring season of
each year, or one-half of the method
detection limit of the ozone instrument,
whichever is higher, for enough of the
missing hourly concentrations within each
incomplete month to make the month 75%
complete, and then adjusting for the
remaining missing data using Equation 2,
above results in a design value greater than
the level of the standard.
(d) Comparisons With the Secondary Ozone
Standard
(i) The secondary ambient ozone air quality
standard is met at an ambient air quality
monitoring site when the design value is less
than or equal to [15] ppm-hours.
(ii) Comparison with the secondary ozone
standard is demonstrated by example 4 as
follows:
Example 4. Ambient Monitoring Site
Failing to Meet the Secondary Ozone
Standard
E:\FR\FM\19JAP2.SGM
19JAP2
EP19JA10.003
Equation 2
EP19JA10.002
In Example 3, the individual weighted
concentrations and their sum are shown with
six decimal digits. In actual calculations, all
digits supported by the calculator or
calculation software must be retained. There
are no data completeness requirements for
the daily index. If fewer than 12 hourly
values are available, only the available hours
are weighted and summed. However, there
are data completeness requirements for the
monthly W126 index values and a required
adjustment for incomplete data, as describe
in the next section.
(b) Computing the Monthly W126 Index
As described in section 4(a), the daily
index value is computed at each monitoring
site for each calendar day in each month
during the required ozone monitoring season
with no rounding or truncation. The monthly
W126 index is the sum of the daily index
values over one calendar month. At an
individual monitoring site, a monthly W126
index is valid if hourly average ozone
concentrations are available for at least 75%
of the possible daylight hours in the month.
For months with more than 75% but less
than 100% data completeness, the monthly
W126 value shall be adjusted for incomplete
data by multiplying the unadjusted monthly
W126 index value by the ratio of the number
of possible reporting hours to the number of
hours with reported ambient hourly
concentrations using Equation 2 in this
appendix:
EP19JA10.001
srobinson on DSKHWCL6B1PROD with PROPOSALS2
* ppm-hours.
3052
Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 / Proposed Rules
April
May
June
July
2006
Adjusted monthly W126 index .....................
3-Month sum ................................................
2006 Maximum ............................................
4.442
na
................
9.124
na
................
12.983
26.549
................
16.153
38.260
................
2007
Adjusted monthly W126 index .....................
3-Month sum ................................................
2007 Maximum ............................................
3.114
na
................
7.214
na
................
8.214
18.542
................
2008
Adjusted monthly W126 index .....................
3-Month sum ................................................
2008 Maximum ............................................
3-Year average W126 index ........................
4.574
na
................
................
5.978
na
................
................
Rounded ...............................................
................
................
As shown in example 4, the secondary
ozone standard is not met for this monitoring
site because the 3-year average of the annual
W126 index value for this site is greater than
[15] ppm-hours:
3-year average W126 index = (42.691 +
23.780 + 20.978)/3 = 29.149666, which
rounds to 29 ppm-hours.
In Example 4, the adjusted monthly W126
index values and the 3-month sums of the
adjusted monthly W126 index values are
shown with three decimal digits. In actual
calculations, all digits supported by the
calculator or calculation software must be
retained.
PART 58—AMBIENT AIR QUALITY
SURVEILLANCE
srobinson on DSKHWCL6B1PROD with PROPOSALS2
5. The authority citation for part 58
continues to read as follows:
VerDate Nov<24>2008
17:06 Jan 15, 2010
Jkt 220001
August
September
October
Overall
13.555
42.691
42.691
4.364
34.072
..................
1.302
19.221
................
..................
..................
42.691
8.111
23.539
................
7.455
23.780
23.780
7.331
22.897
..................
5.115
19.901
................
..................
..................
23.780
6.786
17.338
................
................
8.214
20.978
20.978
................
5.579
20.579
................
................
4.331
18.124
..................
..................
2.115
12.025
................
................
..................
..................
20.978
29.149666
................
................
................
..................
................
29
Authority: 42 U.S.C. 7410 7403, 7410,
7601(a), 7611, and 7619.
7. Appendix G of Part 58 is amended
by revising section 3. to read as follows:
6. Section 58.50 is amended by
revising paragraph (c) and adding
paragraph (d) to read as follows:
Appendix G to Part 58—Uniform Air
Quality Index (AQI) and Daily
Reporting
§ 58.50
*
Index reporting.
*
*
*
*
*
(c) The population of a metropolitan
statistical area for purposes of index
reporting is the latest available U.S.
census population.
(d) For O3, reporting is required in
metropolitan and micropolitan
statistical areas wherever monitoring is
required under Appendix D to Part 58—
SLAMS Minimum O3 Monitoring
Requirements.
PO 00000
Frm 00115
Fmt 4701
Sfmt 9990
*
*
*
*
3. Must I Report the AQI?
You must report the AQI daily if yours is
a metropolitan statistical area (MSA) with a
population over 350,000. For O3, reporting is
required in metropolitan and micropolitan
statistical areas wherever monitoring is
required under Appendix D to Part 58—
SLAMS Minimum O3 Monitoring
Requirements.
*
*
*
*
*
[FR Doc. 2010–340 Filed 1–15–10; 8:45 am]
BILLING CODE 6560–50–P
E:\FR\FM\19JAP2.SGM
19JAP2
Agencies
[Federal Register Volume 75, Number 11 (Tuesday, January 19, 2010)]
[Proposed Rules]
[Pages 2938-3052]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2010-340]
Federal Register / Vol. 75, No. 11 / Tuesday, January 19, 2010 /
Proposed Rules
[[Page 2938]]
-----------------------------------------------------------------------
ENVIRONMENTAL PROTECTION AGENCY
40 CFR Parts 50 and 58
[EPA-HQ-OAR-2005-0172; FRL-9102-1]
RIN 2060-AP98
National Ambient Air Quality Standards for Ozone
AGENCY: Environmental Protection Agency (EPA).
ACTION: Proposed rule.
-----------------------------------------------------------------------
SUMMARY: Based on its reconsideration of the primary and secondary
national ambient air quality standards (NAAQS) for ozone
(O3) set in March 2008, EPA proposes to set different
primary and secondary standards than those set in 2008 to provide
requisite protection of public health and welfare, respectively. With
regard to the primary standard for O3, EPA proposes that the
level of the 8-hour primary standard, which was set at 0.075 ppm in the
2008 final rule, should instead be set at a lower level within the
range of 0.060 to 0.070 parts per million (ppm), to provide increased
protection for children and other ``at risk'' populations against an
array of O3-related adverse health effects that range from
decreased lung function and increased respiratory symptoms to serious
indicators of respiratory morbidity including emergency department
visits and hospital admissions for respiratory causes, and possibly
cardiovascular-related morbidity as well as total non-accidental and
cardiopulmonary mortality. With regard to the secondary standard for
O3, EPA proposes that the secondary O3 standard,
which was set identical to the revised primary standard in the 2008
final rule, should instead be a new cumulative, seasonal standard
expressed as an annual index of the sum of weighted hourly
concentrations, cumulated over 12 hours per day (8 am to 8 pm) during
the consecutive 3-month period within the O3 season with the
maximum index value, set at a level within the range of 7 to 15 ppm-
hours, to provide increased protection against O3-related
adverse impacts on vegetation and forested ecosystems.
DATES: Written comments on this proposed rule must be received by March
22, 2010.
Public Hearings: Three public hearings are scheduled for this
proposed rule. Two of the public hearings will be held on February 2,
2010 in Arlington, Virginia, and Houston, Texas. The third public
hearing will be held on February 4, 2010 in Sacramento, California.
ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2005-0172, by one of the following methods:
https://www.regulations.gov: Follow the on-line
instructions for submitting comments.
E-mail: a-and-r-Docket@epa.gov.
Fax: 202-566-9744.
Mail: Docket No. EPA-HQ-OAR-2005-0172, Environmental
Protection Agency, Mail code 6102T, 1200 Pennsylvania Ave., NW.,
Washington, DC 20460. Please include a total of two copies.
Hand Delivery: Docket No. EPA-HQ-OAR-2005-0172,
Environmental Protection Agency, EPA West, Room 3334, 1301 Constitution
Ave., NW., Washington, DC. Such deliveries are only accepted during the
Docket's normal hours of operation, and special arrangements should be
made for deliveries of boxed information.
Public Hearings: Three public hearings are scheduled for this
proposed rule. Two of the public hearings will be held on February 2,
2010 in Arlington, Virginia and Houston, Texas. The third public
hearing will be held on February 4, 2010 in Sacramento, California. The
hearings will be held at the following locations:
Arlington, Virginia--February 2, 2010
Hyatt Regency Crystal City @ Reagan National Airport, Washington Room
(located on the Ballroom Level), 2799 Jefferson Davis Highway,
Arlington, Virginia 22202, Telephone: 703-418-1234.
Houston, Texas--February 2, 2010
Hilton Houston Hobby Airport, Moody Ballroom (located on the ground
floor), 8181 Airport Boulevard, Houston, Texas 77061, Telephone: 713-
645-3000.
Sacramento, California--February 4, 2010
Four Points by Sheraton Sacramento International Airport, Natomas
Ballroom, 4900 Duckhorn Drive, Sacramento, California 95834, Telephone:
916-263-9000.
See the SUPPLEMENTARY INFORMATION under ``Public Hearings'' for
further information.
Instructions: Direct your comments to Docket ID No. EPA-HQ-OAR-
2005-0172. The EPA's policy is that all comments received will be
included in the public docket without change and may be made available
online at www.regulations.gov, including any personal information
provided, unless the comment includes information claimed to be
Confidential Business Information (CBI) or other information whose
disclosure is restricted by statute. Do not submit information that you
consider to be CBI or otherwise protected through www.regulations.gov
or e-mail. The www.regulations.gov Web site is an ``anonymous access''
system, which means EPA will not know your identity or contact
information unless you provide it in the body of your comment. If you
send an e-mail comment directly to EPA without going through
www.regulations.gov, your e-mail address will be automatically captured
and included as part of the comment that is placed in the public docket
and made available on the Internet. If you submit an electronic
comment, EPA recommends that you include your name and other contact
information in the body of your comment and with any disk or CD-ROM you
submit. If EPA cannot read your comment due to technical difficulties
and cannot contact you for clarification, EPA may not be able to
consider your comment. Electronic files should avoid the use of special
characters, any form of encryption, and be free of any defects or
viruses.
Docket: All documents in the docket are listed in the
www.regulations.gov index. Although listed in the index, some
information is not publicly available, e.g., CBI or other information
whose disclosure is restricted by statute. Certain other material, such
as copyrighted material, will be publicly available only in hard copy.
Publicly available docket materials are available either electronically
in www.regulations.gov or in hard copy at the Air and Radiation Docket
and Information Center, EPA/DC, EPA West, Room 3334, 1301 Constitution
Ave., NW., Washington, DC. The Public Reading Room is open from 8:30
a.m. to 4:30 p.m., Monday through Friday, excluding legal holidays. The
telephone number for the Public Reading Room is (202) 566-1744 and the
telephone number for the Air and Radiation Docket and Information
Center is (202) 566-1742.
FOR FURTHER INFORMATION CONTACT: Ms. Susan Lyon Stone, Health and
Environmental Impacts Division, Office of Air Quality Planning and
Standards, U.S. Environmental Protection Agency, Mail Code C504-06,
Research Triangle Park, NC 27711; telephone: 919-541-1146; fax: 919-
541-0237; e-mail: stone.susan@epa.gov.
SUPPLEMENTARY INFORMATION:
[[Page 2939]]
General Information
What Should I Consider as I Prepare My Comments for EPA?
1. Submitting CBI. Do not submit this information to EPA through
https://www.regulations.gov or e-mail. Clearly mark the part or all of
the information that you claim to be CBI. For CBI information in a disk
or CD-ROM that you mail to EPA, mark the outside of the disk or CD-ROM
as CBI and then identify electronically within the disk or CD-ROM the
specific information that is claimed as CBI. In addition to one
complete version of the comment that includes information claimed as
CBI, a copy of the comment that does not contain the information
claimed as CBI must be submitted for inclusion in the public docket.
Information so marked will not be disclosed except in accordance with
procedures set forth in 40 CFR part 2.
2. Tips for Preparing Your Comments. When submitting comments,
remember to:
Identify the rulemaking by docket number and other
identifying information (subject heading, Federal Register date and
page number).
Follow directions--The Agency may ask you to respond to
specific questions or organize comments by referencing a Code of
Federal Regulations (CFR) part or section number.
Explain why you agree or disagree, suggest alternatives,
and substitute language for your requested changes.
Describe any assumptions and provide any technical
information and/or data that you used.
Provide specific examples to illustrate your concerns, and
suggest alternatives.
Explain your views as clearly as possible, avoiding the
use of profanity or personal threats.
Make sure to submit your comments by the comment period
deadline identified.
Availability of Related Information
A number of documents relevant to this rulemaking are available on
EPA web sites. The Air Quality Criteria for Ozone and Related
Photochemical Oxidants (2006 Criteria Document) (two volumes, EPA/and
EPA/, date) is available on EPA's National Center for Environmental
Assessment Web site. To obtain this document, go to https://www.epa.gov/ncea, and click on Ozone in the Quick Finder section. This will open a
page with a link to the March 2006 Air Quality Criteria Document. The
2007 Staff Paper, human exposure and health risk assessments,
vegetation exposure and impact assessment, and other related technical
documents are available on EPA's Office of Air Quality Planning and
Standards (OAQPS) Technology Transfer Network (TTN) web site. The
updated final 2007 Staff Paper is available at: https://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html and the exposure and risk
assessments and other related technical documents are available at
https://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_td.html. The
Response to Significant Comments Document is available at: https://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_rc.html. These and
other related documents are also available for inspection and copying
in the EPA docket identified above.
Public Hearings
The public hearings on February 2, 2010 and February 4, 2010 will
provide interested parties the opportunity to present data, views, or
arguments concerning the proposed rule. The EPA may ask clarifying
questions during the oral presentations, but will not respond to the
presentations at that time. Written statements and supporting
information submitted during the comment period will be considered with
the same weight as any oral comments and supporting information
presented at the public hearing. Written comments must be received by
the last day of the comment period, as specified in this proposed
rulemaking.
The public hearings will begin at 9:30 a.m. and continue until 7:30
p.m. (local time) or later, if necessary, depending on the number of
speakers wishing to participate. The EPA will make every effort to
accommodate all speakers that arrive and register before 7:30 p.m. A
lunch break is scheduled from 12:30 p.m. until 2 p.m.
If you would like to present oral testimony at the hearings, please
notify Ms. Tricia Crabtree (C504-02), U.S. EPA, Research Triangle Park,
NC 27711. The preferred method for registering is by e-mail
(crabtree.tricia@epa.gov). Ms. Crabtree may be reached by telephone at
(919) 541-5688. She will arrange a general time slot for you to speak.
The EPA will make every effort to follow the schedule as closely as
possible on the day of the hearing.
Oral testimony will be limited to five (5) minutes for each
commenter to address the proposal. We will not be providing equipment
for commenters to show overhead slides or make computerized slide
presentations unless we receive special requests in advance. Commenters
should notify Ms. Crabtree if they will need specific audiovisual (AV)
equipment. Commenters should also notify Ms. Crabtree if they need
specific translation services for non-English speaking commenters. The
EPA encourages commenters to provide written versions of their oral
testimonies either electronically on computer disk, CD-ROM, or in paper
copy.
The hearing schedules, including lists of speakers, will be posted
on EPA's Web site for the proposal at https://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_fr.html prior to the hearing. Verbatim
transcripts of the hearings and written statements will be included in
the rulemaking docket.
Children's Environmental Health
Consideration of children's environmental health plays a central
role in the reconsideration of the 2008 final decision on the
O3 NAAQS and EPA's decision to propose to set the 8-hour
primary O3 standard at a level within the range of 0.060 to
0.070 ppm. Technical information that pertains to children, including
the evaluation of scientific evidence, policy considerations, and
exposure and risk assessments, is discussed in all of the documents
listed above in the section on the availability of related information.
These documents include: the Air Quality Criteria for Ozone and Other
Related Photochemical Oxidants; the 2007 Staff Paper; exposure and risk
assessments and other related documents; and the Response to
Significant Comments. All of these documents are available on the Web,
as described above, and are in the public docket for this rulemaking.
The public is invited to submit comments or identify peer-reviewed
studies and data that assess effects of early life exposure to
O3.
Table of Contents
The following topics are discussed in this preamble:
I. Background
A. Legislative Requirements
B. Related Control Requirements
C. Review of Air Quality Criteria and Standards for
O3
D. Reconsideration of the 2008 O3 NAAQS Final Rule
1. Decision to Initiate a Rulemaking to Reconsider
2. Ongoing Litigation
II. Rationale for Proposed Decision on the Level of the Primary
Standard
A. Health Effects Information
1. Overview of Mechanisms
2. Nature of Effects
3. Interpretation and Integration of Health Evidence
4. O3-Related Impacts on Public Health
B. Human Exposure and Health Risk Assessments
[[Page 2940]]
1. Exposure Analyses
2. Quantitative Health Risk Assessment
C. Reconsideration of the Level of the Primary Standard
1. Evidence and Exposure/Risk-Based Considerations
2. CASAC Views Prior to 2008 Decision
3. Basis for 2008 Decision on the Primary Standard
4. CASAC Advice Following 2008 Decision
5. Administrator's Proposed Conclusions
D. Proposed Decision on the Level of the Primary Standard
III. Communication of Public Health Information
IV. Rationale for Proposed Decision on the Secondary Standard
A. Vegetation Effects Information
1. Mechanisms
2. Nature of Effects
3. Adversity of Effects
B. Biologically Relevant Exposure Indices
C. Vegetation Exposure and Impact Assessment
1. Exposure Characterization
2. Assessment of Risks to Vegetation
D. Reconsideration of Secondary Standard
1. Considerations Regarding 2007 Proposed Cumulative Seasonal
Standard
2. Considerations Regarding 2007 Proposed 8-Hour Standard
3. Basis for 2008 Decision on the Secondary Standard
4. CASAC Views Following 2008 Decision
5. Administrator's Proposed Conclusions
E. Proposed Decision on the Secondary O3 Standard
V. Revision of Appendix P--Interpretation of the NAAQS for
O3 and Proposed Revisions to the Exceptional Events Rule
A. Background
B. Interpretation of the Secondary O3 Standard
C. Clarifications Related to the Primary Standard
D. Revisions to Exceptions From Standard Data Completeness
Requirements for the Primary Standard
E. Elimination of the Requirement for 90 Percent Completeness of
Daily Data Across Three Years
F. Administrator Discretion To Use Incomplete Data
G. Truncation Versus Rounding
H. Data Selection
I. Exceptional Events Information Submission Schedule
VI. Ambient Monitoring Related to Proposed O3 Standards
A. Background
B. Urban Monitoring Requirements
C. Non-Urban Monitoring Requirements
D. Revisions to the Length of the Required O3
Monitoring Season
VII. Implementation of Proposed O3 Standards
A. Designations
B. State Implementation Plans
C. Trans-boundary Emissions
VIII. Statutory and Executive Order Reviews
A. Executive Order 12866: Regulatory Planning and Review
B. Paperwork Reduction Act
C. Regulatory Flexibility Act
D. Unfunded Mandates Reform Act
E. Executive Order 13132: Federalism
F. Executive Order 13175: Consultation and Coordination With
Indian Tribal Governments
G. Executive Order 13045: Protection of Children From
Environmental Health and Safety Risks
H. Executive Order 13211: Actions That Significantly Affect
Energy Supply, Distribution or Use
I. National Technology Transfer and Advancement Act
J. Executive Order 12898: Federal Actions To Address
Environmental Justice in Minority Populations and Low-Income
Populations
References
I. Background
The proposed decisions presented in this notice are based on a
reconsideration of the 2008 O3 NAAQS final rule (73 FR
16436, March 27, 2008), which revised the level of the 8-hour primary
O3 standard to 0.075 ppm and revised the secondary
O3 standard by making it identical to the revised primary
standard. This reconsideration is based on the scientific and technical
information and analyses on which the March 2008 O3 NAAQS
rulemaking was based. Therefore, much of the information included in
this notice is drawn directly from information included in the 2007
proposed rule (72 FR 37818, July 11, 2007) and the 2008 final rule (73
FR 16436).
A. Legislative Requirements
Two sections of the Clean Air Act (CAA) govern the establishment
and revision of the NAAQS. Section 108 (42 U.S.C. 7408) directs the
Administrator to identify and list ``air pollutants'' that in her
``judgment, cause or contribute to air pollution which may reasonably
be anticipated to endanger public health or welfare'' and satisfy two
other criteria, including ``whose presence * * * in the ambient air
results from numerous or diverse mobile or stationary sources'' and to
issue air quality criteria for those that are listed. Air quality
criteria are intended to ``accurately reflect the latest scientific
knowledge useful in indicating the kind and extent of all identifiable
effects on public health or welfare which may be expected from the
presence of [a] pollutant in the ambient air. * * *''
Section 109 (42 U.S.C. 7409) directs the Administrator to propose
and promulgate ``primary'' and ``secondary'' NAAQS for pollutants for
which air quality criteria are issued. Section 109(b)(1) defines a
primary standard as one ``the attainment and maintenance of which in
the judgment of the Administrator, based on such criteria and allowing
an adequate margin of safety, are requisite to protect the public
health.'' \1\ A secondary standard, as defined in section 109(b)(2),
must ``specify a level of air quality the attainment and maintenance of
which, in the judgment of the Administrator, based on such criteria, is
requisite to protect the public welfare from any known or anticipated
adverse effects associated with the presence of such air pollutant in
the ambient air.'' \2\
---------------------------------------------------------------------------
\1\ The legislative history of section 109 indicates that a
primary standard is to be set at ``the maximum permissible ambient
air level * * * which will protect the health of any [sensitive]
group of the population,'' and that for this purpose ``reference
should be made to a representative sample of persons comprising the
sensitive group rather than to a single person in such a group'' [S.
Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970)].
\2\ Welfare effects as defined in section 302(h) (42 U.S.C.
7602(h)) include, but are not limited to, ``effects on soils, water,
crops, vegetation, man-made materials, animals, wildlife, weather,
visibility, and climate, damage to and deterioration of property,
and hazards to transportation, as well as effects on economic values
and on personal comfort and well-being.''
---------------------------------------------------------------------------
The requirement that primary standards include an adequate margin
of safety was intended to address uncertainties associated with
inconclusive scientific and technical information available at the time
of standard setting. It was also intended to provide a reasonable
degree of protection against hazards that research has not yet
identified. Lead Industries Association v. EPA, 647 F.2d 1130, 1154 (DC
Cir 1980), cert. denied, 449 U.S. 1042 (1980); American Petroleum
Institute v. Costle, 665 F.2d 1176, 1186 (DC Cir. 1981), cert. denied,
455 U.S. 1034 (1982). Both kinds of uncertainties are components of the
risk associated with pollution at levels below those at which human
health effects can be said to occur with reasonable scientific
certainty. Thus, in selecting primary standards that include an
adequate margin of safety, the Administrator is seeking not only to
prevent pollution levels that have been demonstrated to be harmful but
also to prevent lower pollutant levels that may pose an unacceptable
risk of harm, even if the risk is not precisely identified as to nature
or degree. The CAA does not require the Administrator to establish a
primary NAAQS at a zero-risk level or at background concentration
levels, see Lead Industries Association v. EPA, 647 F.2d at 1156 n. 51,
but rather at a level that reduces risk sufficiently so as to protect
public health with an adequate margin of safety.
In addressing the requirement for an adequate margin of safety, EPA
considers such factors as the nature and severity of the health effects
involved, the size of the population(s) at risk, and the kind and
degree of the uncertainties
[[Page 2941]]
that must be addressed. The selection of any particular approach to
providing an adequate margin of safety is a policy choice left
specifically to the Administrator's judgment. Lead Industries
Association v. EPA, 647 F.2d at 1161-62; Whitman v. American Trucking
Associations, 531 U.S. 457, 495 (2001).
In setting standards that are ``requisite'' to protect public
health and welfare, as provided in section 109(b), EPA's task is to
establish standards that are neither more nor less stringent than
necessary for these purposes. Whitman v. America Trucking Associations,
531 U.S. 457, 473. In establishing ``requisite'' primary and secondary
standards, EPA may not consider the costs of implementing the
standards. Id. at 471.
Section 109(d)(1) of the CAA requires that ``not later than
December 31, 1980, and at 5-year intervals thereafter, the
Administrator shall complete a thorough review of the criteria
published under section 108 and the national ambient air quality
standards * * * and shall make such revisions in such criteria and
standards and promulgate such new standards as may be appropriate. * *
*'' Section 109(d)(2) requires that an independent scientific review
committee ``shall complete a review of the criteria * * * and the
national primary and secondary ambient air quality standards * * * and
shall recommend to the Administrator any new * * * standards and
revisions of existing criteria and standards as may be appropriate. * *
*'' This independent review function is performed by the Clean Air
Scientific Advisory Committee (CASAC) of EPA's Science Advisory Board.
B. Related Control Requirements
States have primary responsibility for ensuring attainment and
maintenance of ambient air quality standards once EPA has established
them. Under section 110 of the Act (42 U.S.C. 7410) and related
provisions, States are to submit, for EPA approval, State
implementation plans (SIPs) that provide for the attainment and
maintenance of such standards through control programs directed to
emission sources.
The majority of man-made nitrogen oxides (NOX) and
volatile organic compounds (VOC) emissions that contribute to
O3 formation in the United States come from three types of
sources: Mobile sources, industrial processes (which include consumer
and commercial products), and the electric power industry.\3\ Mobile
sources and the electric power industry were responsible for 78 percent
of annual NOX emissions in 2004. That same year, 99 percent
of man-made VOC emissions came from industrial processes (including
solvents) and mobile sources. Emissions from natural sources, such as
trees, may also comprise a significant portion of total VOC emissions
in certain regions of the country, especially during the O3
season, which are considered natural background emissions.
---------------------------------------------------------------------------
\3\ See EPA report, Evaluating Ozone Control Programs in the
Eastern United States: Focus on the NOX Budget Trading Program,
2004.
---------------------------------------------------------------------------
The EPA has developed new emissions standards for many types of
stationary sources and for nearly every class of mobile sources in the
last decade to reduce O3 by decreasing emissions of
NOX and VOC. These programs complement State and local
efforts to improve O3 air quality and meet the 0.084 ppm 8-
hour national standards. Under title II of the CAA, 42 U.S.C. 7521-
7574), EPA has established new emissions standards for nearly every
type of automobile, truck, bus, motorcycle, earth mover, and aircraft
engine, and for the fuels used to power these engines. EPA also
established new standards for the smaller engines used in small
watercraft, lawn and garden equipment. In March 2008, EPA promulgated
new standards for locomotive and marine diesel engines and in August
2009, proposed to control emissions from ocean-going vessels.
Benefits from engine standards increase modestly each year as
older, more-polluting vehicles and engines are replaced with newer,
cleaner models. In time, these programs will yield substantial emission
reductions. Benefits from fuel programs generally begin as soon as a
new fuel is available.
The reduction of VOC emissions from industrial processes has been
achieved either directly or indirectly through implementation of
control technology standards, including maximum achievable control
technology, reasonably available control technology, and best available
control technology standards; or are anticipated due to proposed or
upcoming proposals based on generally available control technology or
best available controls under provisions related to consumer and
commercial products. These standards have resulted in VOC emission
reductions of almost a million tons per year accumulated starting in
1997 from a variety of sources including combustion sources, coating
categories, and chemical manufacturing. EPA has also finalized emission
standards and fuel requirements for new stationary engines. In the area
of consumer and commercial products, EPA has finalized new national VOC
emission standards for aerosol coatings and is working toward amending
existing rules to establish new nationwide VOC content limits for
household and institutional consumer products and architectural and
industrial maintenance coatings. The aerosol coatings rule took effect
in July 2009; the compliance date for both the amended consumer product
rule and architectural coatings rule is anticipated to be January 2011.
These actions are expected to yield significant new VOC reductions--
about 200,000 tons per year. Additionally, in ozone nonattainment
areas, we anticipate reductions of an additional 25,000 tons per year
as States adopt rules this year implementing control techniques
recommendations issued in 2008 for 4 additional categories of consumer
and commercial products, typically surface coatings and adhesives used
in industrial manufacturing operations. These emission reductions
primarily result from solvent controls and typically occur where and
when the solvent is used, such as during manufacturing processes.
The power industry is one of the largest emitters of NOX
in the United States. Power industry emission sources include large
electric generating units (EGU) and some large industrial boilers and
turbines. The EPA's landmark Clean Air Interstate Rule (CAIR), issued
on March 10, 2005, was designed to permanently cap power industry
emissions of NOX in the eastern United States. The first
phase of the cap was to begin in 2009, and a lower second phase cap was
to begin in 2015. The EPA had projected that by 2015, the CAIR and
other programs would reduce NOX emissions during the
O3 season by about 50 percent and annual NOX
emissions by about 60 percent from 2003 levels in the Eastern U.S.
However, on July 11, 2008 and December 23, 2008, the U.S. Court of
Appeals for the DC Circuit issued decisions on petitions for review of
the CAIR. In its July 11 opinion, the court found CAIR unlawful and
decided to vacate CAIR and its associated Federal implementation plans
(FIPs) in their entirety. On December 23, the court granted EPA's
petition for rehearing to the extent that it remanded without vacatur
for EPA to conduct further proceedings consistent with the Court's
prior opinion. Under this decision, CAIR will remain in place only
until replaced by EPA with a rule that is consistent with the Court's
July
[[Page 2942]]
11 opinion. The EPA recognizes the need in our CAIR replacement effort
to address the reconsidered ozone standard, and we are currently
assessing our options for the best way to accomplish this. It should
also be noted that new electric generating units (EGUs) are also
subject to NOX limits under New Source Performance Standards
(NSPS) under CAA section 111, as well as either nonattainment new
source review or prevention of significant deterioration requirements.
With respect to agricultural sources, the U.S. Department of
Agriculture (USDA) has approved conservation systems and activities
that reduce agricultural emissions of NOX and VOC. Current
practices that may reduce emissions of NOX and VOC include
engine replacement programs, diesel retrofit programs, manipulation of
pesticide applications including timing of applications, and animal
feeding operations waste management techniques. The EPA recognizes that
USDA has been working with the agricultural community to develop
conservation systems and activities to control emissions of
O3 precursors.
These conservation activities are voluntarily adopted through the
use of incentives provided to the agricultural producer. In cases where
the States need these measures to attain the standard, the measures
could be adopted. The EPA will continue to work with USDA on these
activities with efforts to identify and/or improve the control
efficiencies, prioritize the adoption of these conservation systems and
activities, and ensure that appropriate criteria are used for
identifying the most effective application of conservation systems and
activities.
The EPA will work together with USDA and with States to identify
appropriate measures to meet the primary and secondary standards,
including site-specific conservation systems and activities. Based on
prior experience identifying conservation measures and practices to
meet the PM NAAQS requirements, the EPA will use a similar process to
identify measures that could meet the O3 requirements. The
EPA anticipates that certain USDA-approved conservation systems and
activities that reduce agricultural emissions of NOX and VOC
may be able to satisfy the requirements for applicable sources to
implement reasonably available control measures for purposes of
attaining the primary and secondary O3 NAAQS.
C. Review of Air Quality Criteria and Standards for O3
In 1971, EPA first established primary and secondary NAAQS for
photochemical oxidants (36 FR 8186). Both primary and secondary
standards were set at a level of 0.08 parts per million (ppm), 1-hr
average, total photochemical oxidants, not to be exceeded more than one
hr per year. In 1977, EPA announced the first periodic review of the
air quality criteria in accordance with section 109(d)(1) of the Act.
The EPA published a final decision in 1979 (44 FR 8202). Both primary
and secondary standard levels were revised from 0.08 to 0.12 ppm. The
indicator was revised from photochemical oxidants to O3, and
the form of the standards was revised from a deterministic to a
statistical form, which defined attainment of the standards as
occurring when the expected number of days per calendar year with
maximum hourly average concentration greater than 0.12 ppm is equal to
or less than one. In 1983, EPA announced that the second periodic
review of the primary and secondary standards for O3 had
been initiated. Following review and publication of air quality
criteria and a supplement, EPA published a proposed decision (57 FR
35542) in August 1992 that announced EPA's intention to proceed as
rapidly as possible with the next review of the air quality criteria
and standards for O3 in light of emerging evidence of health
effects related to 6- to 8-hr O3 exposures. In March 1993,
EPA concluded the review by deciding that revisions to the standards
were not warranted at that time (58 FR 13008).
In August 1992 (57 FR 35542), EPA announced plans to initiate the
third periodic review of the air quality criteria and O3
NAAQS. On the basis of the scientific evidence contained in the 1996 CD
(U.S. EPA 1996a) and the 1996 Staff Paper (U.S. EPA, 1996b), and
related technical support documents, linking exposures to ambient
O3 to adverse health and welfare effects at levels allowed
by the then existing standards, EPA proposed to revise the primary and
secondary O3 standards in December 1996 (61 FR 65716). The
EPA proposed to replace the then existing 1-hour primary and secondary
standards with 8-hour average O3 standards set at a level of
0.08 ppm (equivalent to 0.084 ppm using standard rounding conventions).
The EPA also proposed, in the alternative, to establish a new distinct
secondary standard using a biologically based cumulative seasonal form.
The EPA completed the review in July 1997 (62 FR 38856) by setting the
primary standard at a level of 0.08 ppm, based on the annual fourth-
highest daily maximum 8-hr average concentration, averaged over three
years, and setting the secondary standard identical to the revised
primary standard.
The EPA initiated the most recent periodic review of the air
quality criteria and standards for O3 in September 2000 with
a call for information (65 FR 57810; September 26, 2000) for the
development of a revised Air Quality Criteria Document for
O3 and Other Photochemical Oxidants (henceforth the ``2006
Criteria Document''). A project work plan (EPA, 2002) for the
preparation of the Criteria Document was released in November 2002 for
CASAC and public review. The EPA held a series of workshops in mid-2003
on several draft chapters of the Criteria Document to obtain broad
input from the relevant scientific communities. These workshops helped
to inform the preparation of the first draft Criteria Document (EPA,
2005a), which was released for CASAC and public review on January 31,
2005; a CASAC meeting was held on May 4-5, 2005 to review the first
draft Criteria Document. A second draft Criteria Document (EPA, 2005b)
was released for CASAC and public review on August 31, 2005, and was
discussed along with a first draft Staff Paper (EPA, 2005c) at a CASAC
meeting held on December 6-8, 2005. In a February 16, 2006 letter to
the Administrator, CASAC provided comments on the second draft Criteria
Document (Henderson, 2006a), and the final 2006 Criteria Document (EPA,
2006a) was released on March 21, 2006. In a June 8, 2006 letter to the
Administrator (Henderson, 2006b), CASAC provided additional advice to
the Agency concerning chapter 8 of the final 2006 Criteria Document
(Integrative Synthesis) to help inform the second draft Staff Paper.
A second draft Staff Paper (EPA, 2006b) was released on July 17,
2006 and reviewed by CASAC on August 24-25, 2006. In an October 24,
2006 letter to the Administrator, CASAC provided advice and
recommendations to the Agency concerning the second draft Staff Paper
(Henderson, 2006c). A final 2007 Staff Paper (EPA, 2007a) was released
on January 31, 2007. In a March 26, 2007 letter (Henderson, 2007),
CASAC offered additional advice to the Administrator with regard to
recommendations and revisions to the primary and secondary
O3 NAAQS.
The schedule for completion of the 2008 rulemaking was governed by
a consent decree resolving a lawsuit filed in March 2003 by a group of
plaintiffs representing national environmental
[[Page 2943]]
and public health organizations, alleging that EPA had failed to
complete the review within the period provided by statute.\4\ The
modified consent decree that governed the 2008 rulemaking, entered by
the court on December 16, 2004, provided that EPA sign for publication
notices of proposed and final rulemaking concerning its review of the
O3 NAAQS no later than March 28, 2007 and December 19, 2007,
respectively. That consent decree was further modified in October 2006
to change these proposed and final rulemaking dates to no later than
May 30, 2007 and February 20, 2008, respectively. These dates for
signing the publication notices of proposed and final rulemaking were
further extended to no later than June 20, 2007 and March 12, 2008,
respectively. The proposed decision was signed on June 20, 2007 and
published in the Federal Register on July 11, 2007 (72 FR 37818).
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\4\ American Lung Association v. Whitman (No. 1:03CV00778, D.DC
2003).
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Public hearings on the proposed decision were held on Thursday,
August 30, 2007 in Philadelphia, PA and Los Angeles, CA. On Wednesday,
September 5, 2007, hearings were held in Atlanta, GA, Chicago, IL, and
Houston, TX. A large number of comments were received from various
commenters on the 2007 proposed revisions to the O3 NAAQS. A
comprehensive summary of all significant comments, along with EPA's
responses (henceforth ``Response to Comments''), can be found in the
docket for the 2008 rulemaking, which is also the docket for this
reconsideration rulemaking.
The EPA's final decision on the O3 NAAAQS was published
in the Federal Register on March 27, 2008 (73 FR 16436). In the 2008
rulemaking, EPA revised the level of the 8-hour primary standard for
O3 to 0.075 parts per million (ppm), expressed to three
decimal places. With regard to the secondary standard for
O3, EPA revised the 8-hour standard by making it identical
to the revised primary standard. The EPA also made conforming changes
to the Air Quality Index (AQI) for O3, setting an AQI value
of 100 equal to 0.075 ppm, 8-hour average, and making proportional
changes to the AQI values of 50, 150 and 200.
D. Reconsideration of the 2008 O3 NAAQS Final Rule
Consistent with a directive of the new Administration regarding the
review of new and pending regulations (Emanuel memorandum, 74 FR 4435;
January 26, 2009), the Administrator reviewed a number of actions that
were taken in the last year by the previous Administration. The 2008
final rule was included in this review in recognition of the central
role that the NAAQS play in enabling EPA to fulfill its mission to
protect the nation's public health and welfare. In her review, the
Administrator was mindful of the need for judgments concerning the
NAAQS to be based on a strong scientific foundation which is developed
through a transparent and credible NAAQS review process, consistent
with the core values highlighted in President Obama's memorandum on
scientific integrity (March 9, 2009).
1. Decision To Initiate a Rulemaking To Reconsider
In her review of the 2008 final rule, several aspects of the final
rule related to the primary and secondary standards stood out to the
Administrator. As an initial matter, the Administrator noted that the
2008 final rule concluded that the 1997 primary and secondary
O3 standards were not adequate to protect public health and
public welfare, and that revisions were necessary to provide increased
protection. With respect to revision of the primary standard, the
Administrator noted that the revised level established in the 2008
final rule was above the range that had been unanimously recommended by
CASAC.\5\ She also noted that EPA received comments from a large number
of commenters from the medical and public health communities, including
EPA's Children's Health Protection Advisory Committee, all of which
endorsed levels within CASAC's recommended range.
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\5\ The level of the 8-hour primary ozone standard was set at
0.075 ppm, while CASAC unanimously recommended a range between 0.060
and 0.070 ppm.
---------------------------------------------------------------------------
With respect to revision of the secondary O3 standard,
the Administrator noted that the 2008 final rule differed substantially
from CASAC's recommendations that EPA adopt a new secondary
O3 standard based on a cumulative, seasonal measure of
exposure. The 2008 final rule revised the secondary standard to be
identical to the revised primary standard, which is based on an 8-hour
daily maximum measure of exposure. She also noted that EPA received
comments from a number of commenters representing environmental
interests, all of which endorsed CASAC;s recommendation for a new
cumulative, seasonal secondary standard.\6\
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\6\ The Administrator also noted the exchange that had occurred
between EPA and the Office of Management and Budget (OMB) with
regard to the final decision on the secondary standard, as discussed
in the 2008 final rule (73 FR 16497).
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Subsequent to issuance of the 2008 final rule, in April 2008, CASAC
took the unusual step of sending EPA a letter expressing strong,
unanimous disagreement with EPA's decisions on both the primary and
secondary standards (Henderson, 2008). The CASAC explained that it did
not endorse the revised primary O3 standard as being
sufficiently protective of public health because it failed to satisfy
the explicit stipulation of the Act to provide an adequate margin of
safety. The CASAC also expressed the view that failing to revise the
secondary standard to a cumulative, seasonal form was not supported by
the available science. In addition to CASAC's letter, the Administrator
noted a recent adverse ruling issued by the U.S. Court of Appeals for
the District of Columbia Circuit on another NAAQS decision. In February
2009, the DC Circuit remanded the Agency's decisions on the primary
annual and secondary standards for fine particles (PM2.5).
In so doing, the Court found that EPA had not adequately explained the
basis for its decisions, including why CASAC's recommendations for a
more health-protective primary annual standard and for secondary
standards different from the primary standards were not accepted.
American Farm Bureau v. EPA, 559 F.3d. 512 (DC Cir. 2009).
Based on her review of the information described above, the
Administrator is initiating a rulemaking to reconsider parts of the
2008 final rule. Specifically, the Administrator is reconsidering the
level of the primary standard to ensure that it is sufficiently
protective of public health, as discussed in section II below, and is
reconsidering all aspects of the secondary standard to ensure that it
appropriately reflects the available science and is sufficiently
protective of public welfare, as discussed in section IV below. Based
on her review, the Administrator has serious cause for concern
regarding whether the revisions to the primary and secondary
O3 standards adopted in the 2008 final rule satisfy the
requirements of the CAA, in light of the body of scientific evidence
before the Agency. In addition, the importance of the O3
NAAQS to public health and welfare weigh heavily in favor of
reconsidering parts of the 2008 final rule as soon as possible, based
on the scientific and technical information upon which the 2008 final
rule was based.
[[Page 2944]]
Also, EPA conducted a provisional assessment of ``new'' scientific
papers (EPA, 2009) of scientific literature evaluating health and
ecological effects of O3 exposure published since the close
of the 2006 Criteria Document upon which the 2008 O3 NAAQS
were based. The Administrator notes that the provisional assessment of
``new'' science found that such studies did not materially change the
conclusions in the 2006 Criteria Document. This provisional assessment
is supportive of the Administrator's decision to reconsider parts of
the 2008 final rule at this time, based on the scientific and technical
information available for the 2008 final rule, as compared to foregoing
such reconsideration and taking appropriate action in the future as
part of the next periodic review of the air quality criteria and NAAQS,
which will include such scientific and technical information.
The reconsideration of parts of the 2008 final rule discussed in
this notice is based on the scientific and technical record from the
2008 rulemaking, including public comments and CASAC advice and
recommendations. The information that was assessed during the 2008
rulemaking includes information in the 2006 Criteria Document (EPA,
2006a), the 2007 Policy Assessment of Scientific and Technical
Information, referred to as the 2007 Staff Paper (EPA, 2007b), and
related technical support documents including the 2007 REAs (U.S. EPA,
2007c; Abt Associates, 2007a,b). Scientific and technical information
developed since the 2006 Criteria Document will be considered in the
next periodic review, instead of this reconsideration rulemaking,
allowing the new information to receive careful and comprehensive
review by CASAC and the public before it is used as a basis in a
rulemaking that determines whether to revise the NAAQS.
2. Ongoing Litigation
In May 2008, following publication of the 2008 final rule, numerous
groups, including state, public health, environmental, and industry
petitioners, challenged EPA's decisions in federal court. The
challenges were consolidated as State of Mississippi, et al. v. EPA
(No. 08-1200, DC Cir. 2008). On March 10, 2009, EPA filed an unopposed
motion requesting that the Court vacate the briefing schedule and hold
the consolidated cases in abeyance. The Agency stated its desire to
allow time for appropriate officials from the new Administration to
review the O3 standards to determine whether they should be
maintained, modified or otherwise reconsidered. The EPA further
requested that it be directed to notify the Court and all the parties
of any actions it has taken or intends to take, if any, within 180 days
of the Court vacating the briefing schedule. On March 19, 2009, the
Court granted EPA's motion. Pursuant to the Court's order, on September
16, 2009 EPA notified the Court and the parties of its decision to
initiate a rulemaking to reconsider the primary and secondary
O3 standards set in March 2008 to ensure they satisfy the
requirements of the CAA.\7\ In its notice to the Court, EPA stated that
this notice of proposed rulemaking would be signed by December 21,
2009, and that the final rule will be signed by August 31, 2010.
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\7\ The EPA also separately announced that it will move quickly
to implement any new standards that might result from this
reconsideration. To reduce the workload for states during the
interim period of reconsideration, the Agency intends to propose to
defer compliance with the CAA requirement to designate areas as
attainment or nonattainment. EPA will work with states, local
governments and tribes to ensure that air quality is protected
during that time.
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II. Rationale for Proposed Decision on the Level of the Primary
Standard
As an initial matter, the Administrator notes that the 2008 final
rule concluded that the 1997 primary O3 standard was ``not
sufficient and thus not requisite to protect public health with an
adequate margin of safety, and that revision is needed to provide
increased public health protection'' (73 FR 16472). The Administrator
is not reconsidering this aspect of the 2008 decision, which is based
on the reasons discussed in section II.B of the 2008 final rule (73 FR
16443-16472). The Administrator also notes that the 2008 final rule
concluded that it was appropriate to retain the O3
indicator, the 8-hour averaging time, and form of the primary
O3 standard (specified as the annual fourth-highest daily
maximum 8-hour concentration, averaged over 3 years), while concluding
that revision of the standard level was appropriate.\8\ The
Administrator is not reconsidering these aspects of the 2008 decision,
which are based on the reasons discussed in sections II.C.1-3 of the
2008 final rule, which address the indicator, averaging time, and form,
respectively, of the primary O3 standard (73 FR 16472-
16475). For these reasons, the Administrator is not reopening the 2008
decision with regard to the need to revise the 1997 primary
O3 standard nor with regard to the indicator, averaging
time, and form of the 2008 primary O3 standard. Thus, the
information that follows in this section specifically focuses on a
reconsideration of level of the primary O3 standard.
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\8\ The use of O3 as the indicator for photochemical
oxidants was adopted in the 1979 final rule and retained in
subsequent rulemaking. An 8-hour averaging time and a form based on
the annual fourth-highest daily maximum 8-hour concentration,
averaged over 3 years, were adopted in the 1997 final rule and
retained in the 2008 rulemaking.
---------------------------------------------------------------------------
This section presents the rationale for the Administrator's
proposed decision that the O3 primary standard, which was
set at a level of 0.075 ppm in the 2008 final rule, should instead be
set at a lower level within the range from 0.060 to 0.070 ppm. As
discussed more fully below, the rationale for the proposed range of
standard levels is based on a thorough review of the latest scientific
information on human health effects associated with the presence of
O3 in the ambient air presented in the 2006 Criteria
Document. This rationale also takes into account: (1) Staff assessments
of the most policy-relevant information in the 2006 Criteria Document
and staff analyses of air quality, human exposure, and health risks,
presented in the 2007 Staff Paper, upon which staff recommendations for
revisions to the primary O3 standard in the 2008 rulemaking
were based; (2) CASAC advice and recommendations, as reflected in
discussions of drafts of the 2006 Criteria Document and 2007 Staff
Paper at public meetings, in separate written comments, and in CASAC's
letters to the Administrator both before and after the 2008 rulemaking;
and (3) public comments received during the development of these
documents, either in connection with CASAC meetings or separately, and
on the 2007 proposed rule.
In developing this rationale, the Administrator recognizes that the
CAA requires her to reach a public health policy judgment as to what
standard would be requisite to protect public health with an adequate
margin of safety, based on scientific evidence and technical
assessments that have inherent uncertainties and limitations. This
judgment requires making reasoned decisions as to what weight to place
on various types of evidence and assessments, and on the related
uncertainties and limitations. Thus, in selecting standard levels to
propose, and subsequently in selecting a final level, the Administrator
is seeking not only to prevent O3 levels that have been
demonstrated to be harmful but also to prevent lower O3
levels that may pose an unacceptable risk of harm, even if the risk is
not precisely identified as to nature or degree.
In this proposed rule, EPA has drawn upon an integrative synthesis
of the entire body of evidence, published
[[Page 2945]]
through early 2006, on human health effects associated with the
presence of O3 in the ambient air. As discussed below in
section II.A, this body of evidence addresses a broad range of health
endpoints associated with exposure to ambient levels of O3
(EPA, 2006a, chapter 8), and includes over one hundred epidemiologic
studies conducted in the U.S., Canada, and many countries around the
world.\9\ In reconsidering this evidence, EPA focuses on those health
endpoints that have been demonstrated to be caused by exposure to
O3, or for which the 2006 Criteria Document judges
associations with O3 to be causal, likely causal, or for
which the evidence is highly suggestive that O3 contributes
to the reported effects. This rationale also draws upon the results of
quantitative exposure and risk assessments, discussed below in section
II.B. Section II.C focuses on the considerations upon which the
Administrator's proposed conclusions on the level of the primary
standard are based. Policy-relevant evidence-based and exposure/risk-
based considerations are discussed, and the rationale for the 2008
final rulemaking on the primary standard and CASAC advice, given both
prior to the development of the 2007 proposed rule and following the
2008 final rule, are summarized. Finally, the Administrator's proposed
conclusions on the level of the primary standard are presented. Section
II.D summarizes the proposed decision on the level of the primary
O3 standard and the solicitation of public comments.
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\9\ In its assessment of the epidemiological evidence judged to
be most relevant to making decisions on the level of the
O3 primary standard, EPA has placed greater weight on
U.S. and Canadian epidemiologic studies, since studies conducted in
other countries may well reflect different demographic and air
pollution characteristics.
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Judgments made in the 2006 Criteria Document and 2007 Staff Paper
about the extent to which relationships between various health
endpoints and short-term exposures to ambient O3 are likely
causal have been informed by several factors. As discussed below in
section II.A, these factors include the nature of the evidence (i.e.,
controlled human exposure, epidemiological, and/or toxicological
studies) and the weight of evidence, which takes into account such
considerations as biological plausibility, coherence of evidence,
strength of association, and consistency of evidence.
In assessing the health effects data base for O3, it is
clear that human studies provide the most directly applicable
information for determining causality because they are not limited by
the uncertainties of dosimetry differences and species sensitivity
differences, which would need to be addressed in extrapolating animal
toxicology data to human health effects. Controlled human exposure
studies provide data with the highest level of confidence since they
provide human health effects data under closely monitored conditions
and can provide exposure-response relationships. Epidemiological data
provide evidence of associations between ambient O3 levels
and more serious acute and chronic health effects (e.g., hospital
admissions and mortality) that cannot be assessed in controlled human
exposure studies. For these studies the degree of uncertainty
introduced by potentially confounding variables (e.g., other
pollutants, temperature) and other factors affects the level of
confidence that the health effects being investigated are attributable
to O3 exposures, alone and in combination with other
copollutants.
In using a weight of evidence approach to inform judgments about
the degree of confidence that various health effects are likely to be
caused by exposure to O3, confidence increases as the number
of studies consistently reporting a particular health endpoint grows
and as other factors, such as biological plausibility and strength,
consistency, and coherence of evidence, increase. Conclusions regarding
biological plausibility, consistency, and coherence of evidence of
O3-related health effects are drawn from the integration of
epidemiological studies with mechanistic information from controlled
human exposure studies and animal toxicological studies. As discussed
below, this type of mechanistic linkage has been firmly established for
several respiratory endpoints (e.g., lung function decrements, lung
inflammation) but remains far more equivocal for cardiovascular
endpoints (e.g., cardiovascular-related hospital admissions). For
epidemiological studies, strength of association refers to the
magnitude of the association and its statistical strength, which
includes assessment of both effects estimate size and precision. In
general, when associations yield large relative risk estimates, it is
less likely that the association could be completely accounted for by a
potential confounder or some other bias. Consistency refers to the
persistent finding of an association between exposure and outcome in
multiple studies of adequate power in different persons, places,
circumstances and times. For example, the magnitude of effect estimates
is relatively consistent across recent studies showing association
between short-term, but not long-term, O3 exposure and
mortality.
Based on the information discussed below in sections II.A.1-II.A.3,
judgments concerning the extent to which relationships between various
health endpoints and ambient O3 exposures are likely causal
are summarized below in section II.A.3.c. These judgments reflect the
nature of the evidence and the overall weight of the evidence, and are
taken into consideration in the quantitative exposure and risk
assessments, discussed below in section II.B.
To put judgments about health effects that have been demonstrated
to be caused by exposure to O3, or for which the 2006
Criteria Document judges associations with O3 to be causal,
likely causal, or for which the evidence is highly suggestive that
O3 contributes to the reported effects into a broader public
health context, EPA has drawn upon the results of the quantitative
exposure and risk assessments. These assessments provide estimates of
the likelihood that individuals in particular population groups that
are at risk for various O3-related physiological health
effects would experience ``exposures of concern'' and specific health
endpoints under varying air quality scenarios (i.e., just meeting
various standards \10\), as well as characterizations of the kind and
degree of uncertainties inherent in such estimates.
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\10\ The exposure assessment done as part of the 2008 final
rulemaking considered several air quality scenarios, including just
meeting what was then the current standard set at a level of 0.084
ppm, as well as just meeting alternative standards at levels of
0.080, 0.074, 0.070, and 0.064 ppm.
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In the 2008 final rulemaking and in this reconsideration, the term
``exposures of concern'' is defined as personal exposures while at
moderate or greater exertion to 8-hour average ambient O3
levels at and above specific benchmark levels which represent exposure
levels at which O3-related health effects are known or can
reasonably be inferred to occur in some individuals, as discussed below
in section II.B.1.\11\ The EPA emphasizes
[[Page 2946]]
that although the analysis of ``exposures of concern'' was conducted
using three discrete benchmark levels (i.e., 0.080, 0.070, and 0.060
ppm), the concept is more appropriately viewed as a continuum with
greater confidence and less uncertainty about the existence of health
effects at the upper end and less confidence and greater uncertainty as
one considers increasingly lower O3 exposure levels. The EPA
recognizes that there is no sharp breakpoint within the continuum
ranging from at and above 0.080 ppm down to 0.060 ppm. In considering
the concept of exposures of concern, it is important to balance
concerns about the potential for health effects and their severity with
the increasing uncertainty associated with our understanding of the
likelihood of such effects at lower O3 levels.
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\11\ Exposures of concern were also considered in the 1997
review of the O3 NAAQS, and were judged by EPA to be an
important indicator of the public health impacts of those
O3-related effects for which information was too limited
to develop quantitative estimates of risk but which had been
observed in humans at and above the benchmark level of 0.08 ppm for
6- to 8-hour exposures * * * including increased nonspecific
bronchial responsiveness (for example, aggravation of asthma),
decreased pulmonary defense mechanisms (suggestive of increased
susceptibility to respiratory infection), and indicators of
pulmonary inflammation (related to potential aggravation of chronic
bronchitis or long-term damage to the lungs). (62 FR 38868)
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Within the context of this continuum, estimates of exposures of
concern at discrete benchmark levels provide some perspective on the
public health impacts of O3-related health effects that have
been demonstrated in controlled human exposure and toxicological
studies but cannot be evaluated in quantitative risk assessments, such
as lung inflammation, increased airway responsiveness, and changes in
host defenses. They also help in understanding the extent to which such
impacts have the potential to be reduced by meeting various standards.
These O3-relate