National Ambient Air Quality Standards for Ozone, 37818-37919 [E7-12416]

Agencies

• ENVIRONMENTAL PROTECTION AGENCY

[Federal Register Volume 72, Number 132 (Wednesday, July 11, 2007)]
[Proposed Rules]
[Pages 37818-37919]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E7-12416]



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Part II





Environmental Protection Agency





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40 CFR Part 50



National Ambient Air Quality Standards for Ozone; Proposed Rule

Federal Register / Vol. 72, No. 132 / Wednesday, July 11, 2007 / 
Proposed Rules

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 50

[EPA-HQ-OAR-2005-0172; FRL-8331-5]
RIN 2060-AN24


National Ambient Air Quality Standards for Ozone

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed rule.

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SUMMARY: Based on its review of the air quality criteria for ozone 
(O3) and related photochemical oxidants and national ambient 
air quality standards (NAAQS) for O3, EPA proposes to make 
revisions to the primary and secondary NAAQS for O3 to 
provide requisite protection of public health and welfare, 
respectively, and to make corresponding revisions in data handling 
conventions for O3.
    With regard to the primary standard for O3, EPA proposes 
to revise the level of the 8-hour standard to a level within the range 
of 0.070 to 0.075 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 nonaccidental and 
cardiopulmonary mortality. The EPA also proposes to specify the level 
of the primary standard to the nearest thousandth ppm. The EPA solicits 
comment on alternative levels down to 0.060 ppm and up to and including 
retaining the current 8-hour standard of 0.08 ppm (effectively 0.084 
ppm using current data rounding conventions).
    With regard to the secondary standard for O3, EPA 
proposes to revise the current 8-hour standard with one of two options 
to provide increased protection against O3-related adverse 
impacts on vegetation and forested ecosystems. One option is to replace 
the current standard with a cumulative, seasonal standard expressed as 
an index of the annual sum of weighted hourly concentrations, cumulated 
over 12 hours per day (8 a.m. to 8:00 p.m.) 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 21 ppm-hours. The other 
option is to make the secondary standard identical to the proposed 
primary 8-hour standard. The EPA solicits comment on specifying a 
cumulative, seasonal standard in terms of a 3-year average of the 
annual sums of weighted hourly concentrations; on the range of 
alternative 8-hour standard levels for which comment is being solicited 
for the primary standard, including retaining the current secondary 
standard, which is identical to the current primary standard; and on an 
alternative approach to setting a cumulative, seasonal secondary 
standard(s).

DATES: Written comments on this proposed rule must be received by 
October 9, 2007.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-HQ-
OAR-2005-0172, by one of the following methods:
     www.regulations.gov: Follow the on-line instructions for 
submitting comments.
     E-mail: a-and-r-Docket@epa.gov.
     Fax: 202-566-1741.
     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.
    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. For additional information about EPA's public docket, visit 
the EPA Docket Center homepage at https://www.epa.gov/epahome/
dockets.htm.
    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.
    Public Hearings: The EPA intends to hold public hearings around the 
end of August to early September in several cities across the country, 
and will announce in a separate Federal Register notice the dates, 
times, and addresses of the public hearings on this proposed rule.

FOR FURTHER INFORMATION CONTACT: Dr. David J. McKee, 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: 919-541-5288; fax: 919-
541-0237; e-mail: mckee.dave@epa.gov.

SUPPLEMENTARY INFORMATION:

General Information

What Should I Consider as I Prepare My Comments for EPA?

    1. Submitting CBI. Do not submit this information to EPA through 
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

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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.
     If you estimate potential costs or burdens, explain how 
you arrived at your estimate in sufficient detail to allow for it to be 
reproduced.
     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 (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.'' The 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 Staff Paper is available at https://www.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. EPA 
will be making available corrected versions of the final Staff Paper 
and human exposure and health risk assessment technical support 
documents on these same EPA Web sites on or around July 16, 2007. These 
and other related documents are also available for inspection and 
copying in the EPA docket identified above.

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
II. Rationale for Proposed Decision on the Primary Standard
    A. Health Effects Information
    1. Mechanisms
    2. Nature of Effects
    3. Interpretation and Integration of the Health Evidence
    4. O3-Related Impacts on Public Health
    B. Human Exposure and Health Risk Assessments
    1. Exposure Analyses
    2. Quantitative Health Risk Assessment
    C. Conclusions on the Adequacy of the Current Primary Standard
    1. Background
    2. Evidence- and Exposure/Risk-Based Considerations
    3. CASAC Views
    4. Administrator's Proposed Conclusions Concerning Adequacy of 
Current Standard
    D. Conclusions on the Elements of the Primary Standard
    1. Indicator
    2. Averaging Time
    3. Form
    4. Level
    E. Proposed Decision on the Primary Standard
III. Communication of Public Health Information
IV. Rationale for Proposed Decision on the Secondary Standard
    A. Vegetation Effects Information
    1. Mechanisms Governing Plant Response to Ozone
    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. Conclusions on the Adequacy of the Current Standard
    1. Background
    2. Evidence- and Exposure/Risk-Based Considerations
    3. CASAC Views
    4. Administrator's Proposed Conclusions Concerning Adequacy of 
Current Standard
    E. Conclusions on the Elements of the Secondary Standard
    1. Indicator
    2. Cumulative, Seasonal Standard
    3. 8-Hour Average Standard
    F. Proposed Decision on the Secondary Standard
V. Creation of Appendix P--Interpretation of the NAAQS for Ozone
    A. Data Completeness
    B. Data Handling and Rounding O3 Conventions
VI. Ambient Monitoring Related to Proposed Revised Standards
VII. Statutory and Executive Order Reviews
References

I. Background

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 his 
judgment, may reasonably be anticipated to endanger public health and 
welfare'' and 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 identifiable effects on public 
health or welfare which may be expected from the presence of [a] 
pollutant in ambient air * * *.''
    Section 109 (42 U.S.C. 7409) directs the Administrator to propose 
and promulgate ``primary'' and ``secondary'' NAAQS for pollutants 
listed under section 108. 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 [the] pollutant in the ambient 
air.'' \2\
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    \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.''

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    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 (D.C. 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 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) (Breyer, J., concurring 
in part and concurring in judgment).
    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. American 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. As discussed by Justice Breyer in Whitman v. 
American Trucking Associations, however, ``this interpretation of Sec.  
109 does not require the EPA to eliminate every health risk, however 
slight, at any economic cost, however great, to the point of 
``hurtling'' industry over ``the brink of ruin,'' or even forcing 
``deindustrialization.'' Id. at 494 (Breyer J., concurring in part and 
concurring in judgment) (citations omitted). Rather, as Justice Breyer 
explained:

    The statute, by its express terms, does not compel the 
elimination of all risk; and it grants the Administrator sufficient 
flexibility to avoid setting ambient air quality standards ruinous 
to industry.
    Section 109(b)(1) directs the Administrator to set standards 
that are ``requisite to protect the public health'' with ``an 
adequate margin of safety.'' But these words do not describe a world 
that is free of all risk--an impossible and undesirable objective. 
(citation omitted). Nor are the words ``requisite'' and ``public 
health'' to be understood independent of context. We consider 
football equipment ``safe'' even if its use entails a level of risk 
that would make drinking water ``unsafe'' for consumption. And what 
counts as ``requisite'' to protecting the public health will 
similarly vary with background circumstances, such as the public's 
ordinary tolerance of the particular health risk in the particular 
context at issue. The Administrator can consider such background 
circumstances when ``deciding what risks are acceptable in the world 
in which we live.'' (citation omitted).
    The statute also permits the Administrator to take account of 
comparative health risks. That is to say, she may consider whether a 
proposed rule promotes safety overall. A rule likely to cause more 
harm to health than it prevents is not a rule that is ``requisite to 
protect the public health.'' For example, as the Court of Appeals 
held and the parties do not contest, the Administrator has the 
authority to determine to what extent possible health risks stemming 
from reductions in tropospheric ozone (which, it is claimed, helps 
prevent cataracts and skin cancer) should be taken into account in 
setting the ambient air quality standard for ozone. (citation 
omitted).
    The statute ultimately specifies that the standard set must be 
``requisite to protect the public health'' ``in the judgment of the 
Administrator,'' Sec.  109(b)(1), 84 Stat. 1680 (emphasis added), a 
phrase that grants the Administrator considerable discretionary 
standard-setting authority.
    The statute's words, then, authorize the Administrator to 
consider the severity of a pollutant's potential adverse health 
effects, the number of those likely to be affected, the distribution 
of the adverse effects, and the uncertainties surrounding each 
estimate. (citation omitted). They permit the Administrator to take 
account of comparative health consequences. They allow her to take 
account of context when determining the acceptability of small risks 
to health. And they give her considerable discretion when she does 
so.
    This discretion would seem sufficient to avoid the extreme 
results that some of the industry parties fear. After all, the EPA, 
in setting standards that ``protect the public health'' with ``an 
adequate margin of safety,'' retains discretionary authority to 
avoid regulating risks that it reasonably concludes are trivial in 
context. Nor need regulation lead to deindustrialization. 
Preindustrial society was not a very healthy society; hence a 
standard demanding the return of the Stone Age would not prove 
``requisite to protect the public health.''
    Although I rely more heavily than does the Court upon 
legislative history and alternative sources of statutory 
flexibility, I reach the same ultimate conclusion. Section 109 does 
not delegate to the EPA authority to base the national ambient air 
quality standards, in whole or in part, upon the economic costs of 
compliance.

Id. at 494-496.
    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 NOX and 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.
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    \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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    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 current national 
standards. Under the Federal Motor Vehicle Control Program (FMVCP, see 
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. Recently 
EPA proposed new standards for locomotive and marine diesel engines. 
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. The EPA is currently working to 
finalize new federal rules, or amendments to existing rules, that will 
establish new nationwide VOC content limits for several categories of 
consumer and commercial products, including aerosol coatings, 
architectural and industrial maintenance coatings, and household and 
institutional commercial products. These rules will take effect in 
2009, and will yield significant new reductions in nationwide VOC 
emissions--about 200,000 tons per year. Additionally, in O3 
nonattainment areas, we anticipate reductions of an additional 25,000 
tons per year following completion of control technique recommendations 
for 3 additional consumer and commercial product categories. 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 and some large industrial boilers and 
turbines. The EPA's landmark Clean Air Interstate Rule (CAIR), issued 
on March 10, 2005, permanently caps power industry emissions of 
NOX in the eastern United States. The first phase of the cap 
begins in 2009, and a lower second phase cap begins in 2015. By 2015, 
EPA projects that the CAIR and other programs in the Eastern U.S. will 
reduce power industry O3 season NOX emissions in 
that region by about 50 percent and annual NOX emissions by 
about 60 percent from 2003 levels.
    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

    Tropospheric (ground-level) O3 is formed from biogenic 
and anthropogenic precursor emissions. Naturally occurring 
O3 in the troposphere can result from biogenic organic 
precursors reacting with naturally occurring nitrogen oxides 
(NOX) and by stratospheric O3 intrusion into the 
troposphere. Anthropogenic precursors of O3, specifically 
NOX and volatile organic compounds (VOC), originate from a 
wide variety of stationary and mobile sources. Ambient O3 
concentrations produced by these emissions are directly affected by 
temperature, solar radiation, wind speed and other meteorological 
factors.
    The last review of the O3 NAAQS was completed on July 
18, 1997, based on the 1996 O3 CD (U.S. EPA, 1996a) and 1996 
O3 Staff Paper (U.S. EPA, 1996b). EPA revised the primary 
and secondary O3 standards on the basis of the then latest 
scientific evidence linking exposures to ambient O3 to 
adverse health and welfare effects at levels allowed by the 1-hour 
average standards (62 FR 38856). The O3 standards were 
revised by replacing the existing primary 1-hour average standard with 
an 8-hour average O3 standard set at a level of 0.08 ppm, 
which is equivalent to 0.084 ppm using the standard rounding 
conventions. The form of the primary standard was changed to the annual 
fourth-highest daily maximum 8-hour average concentration, averaged 
over three years. The secondary O3 standard was changed by 
making it identical in all respects to the revised primary standard.
    Following promulgation of the revised O3 NAAQS, 
petitions for review were

[[Page 37822]]

filed addressing a broad range of issues. In May 1999, in response to 
those challenges, the U.S. Court of Appeals for the District of 
Columbia Circuit held that EPA's approach to establishing the level of 
the standards in 1997, both for the O3 and for the 
particulate matter (PM) NAAQS promulgated on the same day, effected 
``an unconstitutional delegation of legislative authority.'' American 
Trucking Associations v. EPA, 175 F.3d 1027 (DC Cir., 1999). Although 
the D.C. Circuit stated that ``factors EPA uses in determining the 
degree of public health concern associated with different levels of 
O3 and PM are reasonable,'' it remanded the rule to EPA, 
stating that when EPA considers these factors for potential non-
threshold pollutants ``what EPA lacks is any determinate criterion for 
drawing lines'' to determine where the standards should be set. Id. at 
1034. Consistent with EPA's long-standing interpretation and DC Circuit 
precedent, the court also reaffirmed prior rulings holding that in 
setting the NAAQS, it is ``not permitted to consider the cost of 
implementing those standards.'' Id. at 1040-41. The DC Circuit further 
directed EPA to consider on remand the potential indirect beneficial 
health effects of O3 pollution in shielding the public from 
the effects of solar ultraviolet (UV) radiation, as well as the direct 
adverse health effects of O3 pollution.
    Both sides filed cross appeals on the constitutional and cost 
issues to the United States Supreme Court, and the Court granted 
certiorari. On February 27, 2001, the U.S. Supreme Court issued a 
unanimous decision upholding the EPA's position on both the 
constitutional and the cost issues. Whitman v. American Trucking 
Associations, 531 U.S. at 464, 475-76. On the constitutional issue, the 
Court held that the statutory requirement that NAAQS be ``requisite'' 
to protect public health with an adequate margin of safety sufficiently 
guided EPA's discretion, affirming EPA's approach of setting standards 
that are neither more nor less stringent than necessary. The Supreme 
Court remanded the case to the D.C. Circuit for resolution of any 
remaining issues that had not been addressed by that Court's earlier 
decisions. Id. at 475-76. On March 26, 2002, the D.C. Circuit Court 
rejected all remaining challenges to the NAAQS, holding under 
traditional standard of review that EPA ``engaged in reasoned decision-
making'' in setting the 1997 O3 NAAQS. Whitman v. American 
Trucking Associations, 283 F.3d 355 (DC Cir. 2002).
    In response to the DC Circuit Court's remand to consider the 
potential indirect beneficial health effects of O3 in 
shielding the public from the effects of solar (UV) radiation, on 
November 14, 2001, EPA proposed to leave the 1997 8-hour NAAQS 
unchanged (66 FR 57267). After considering public comment on the 
proposed decision, EPA reaffirmed the 8-hour O3 NAAQS set in 
1997 (68 FR 614). Finally, on April 30, 2004, EPA issued an 8-hour 
implementation rule that, among other things, provided that the 1-hour 
O3 NAAQS would no longer apply to areas one year after the 
effective date of the designation of those areas for the 8-hour NAAQS 
(69 FR 23966).\4\ For most areas, the date that the 1-hour NAAQS no 
longer applied was June 15, 2005. (See 40 CFR 50.9 for details.)
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    \4\ On December 22, 2006, the D.C. Circuit vacated the April 30, 
2004 implementation rule. South Coast Air Quality Management 
District v. EPA, 472 F.3d 882. In March 2007, EPA requested the 
Court to reconsider its decision.
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    The EPA initiated this current review in September 2000 with a call 
for information (65 FR 57810) for the development of a revised Air 
Quality Criteria Document for O3 and Other Photochemical 
Oxidants (henceforth the ``Criteria Document''). A project work plan 
(U.S. EPA, 2002) for the preparation of the Criteria Document was 
released in November 2002 for CASAC and public review. 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, the CASAC offered 
final comments on all chapters of the Criteria Document (Henderson, 
2006a), and the final Criteria Document (EPA, 2006a) was released on 
March 21, 2006. In a June 8, 2006 letter (Henderson, 2006b) to the 
Administrator, the CASAC offered additional advice to the Agency 
concerning chapter 8 of the final 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 and 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 Staff Paper (EPA, 2007) was released on 
January 31, 2007. Around the time of the release of the final Staff 
Paper in January 2007, EPA discovered a small error in the exposure 
model that when corrected resulted in slight increases in the human 
exposure estimates. 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.\5\ 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.
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    \5\ EPA plans to make available corrected versions of the final 
Staff Paper and the human exposure and health risk assessment 
technical support documents on or around July 16, 2007 on the EPA 
web site listed in the Availability of Related Information section 
of this notice.
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    The schedule for completion of this review is governed by a consent 
decree resolving a lawsuit filed in March 2003 by a group of plaintiffs 
representing national environmental and public health organizations, 
alleging that EPA had failed to complete the current review within the 
period provided by statute.\6\ The modified consent decree that governs 
this review, entered by the court on December 16, 2004, provides 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. This 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.
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    \6\ American Lung Association v. Whitman (No. 1:03CV00778, 
D.D.C. 2003).
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    This action presents the Administrator's proposed decisions on the 
review of the current primary and secondary O3 standards. 
Throughout this preamble a number of conclusions, findings, and 
determinations proposed by the Administrator are noted. While

[[Page 37823]]

they identify the reasoning that supports this proposal, they are not 
intended to be final or conclusive in nature. The EPA invites general, 
specific, and/or technical comments on all issues involved with this 
proposal, including all such proposed judgments, conclusions, findings, 
and determinations.

II. Rationale for Proposed Decision on the Primary Standard

    This section presents the rationale for the Administrator's 
proposed decision to revise the existing 8-hour O3 primary 
standard by lowering the level of the standard to within a range from 
0.070 to 0.075 ppm, and to specify the standard to the nearest 
thousandth ppm (i.e., to the nearest parts per billion). As discussed 
more fully below, this rationale is based on a thorough review, in the 
Criteria Document, of the latest scientific information on human health 
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 policy-relevant information in the 
Criteria Document and staff analyses of air quality, human exposure, 
and health risks, presented in the Staff Paper, upon which staff 
recommendations for revisions to the primary O3 standard are 
based; (2) CASAC advice and recommendations, as reflected in 
discussions of drafts of the Criteria Document and Staff Paper at 
public meetings, in separate written comments, and in CASAC's letters 
to the Administrator; and (3) public comments received during the 
development of these documents, either in connection with CASAC 
meetings or separately.
    In developing this rationale, EPA has drawn upon an integrative 
synthesis of the entire body of evidence, published 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.\7\ In considering 
this evidence, EPA focuses on those health endpoints that have been 
demonstrated to be caused by exposure to O3, or for which 
the 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. Evidence- and exposure/
risk-based considerations that form the basis for the Administrator's 
proposed decisions on the adequacy of the current standard and on the 
elements of the range of proposed alternative standards are discussed 
below in sections II.C and II.D, respectively.
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    \7\ 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 Criteria Document and 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 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 
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 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

[[Page 37824]]

under varying air quality scenarios (e.g., just meeting the current or 
alternative standards), as well as characterizations of the kind and 
degree of uncertainties inherent in such estimates.
    In this review, 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.\8\ EPA emphasizes 
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. 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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    \8\ Exposures of concern were also considered in the last 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)
---------------------------------------------------------------------------

    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 human clinical 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. 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 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 
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 this review 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 
current and various alternative O3 standards in a number of 
example urban areas. There were two parts to this risk assessment: one 
part was based on combining information from controlled human exposure 
studies with modeled population exposure, and the other part was based 
on combining information from community epidemiological studies with 
either monitored or adjusted ambient concentrations levels. This 
assessment not only provided 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 provided 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 has been 
conducted since the last review of the O3 NAAQS, with 
important new information coming from epidemiologic studies as well as 
from controlled human exposure, toxicological, and dosimetric studies. 
The newly available research studies evaluated in the Criteria Document 
and the exposure and risk assessments presented in the Staff Paper have 
undergone intensive scrutiny through multiple layers of peer review and 
many opportunities for public review and comment. While important 
uncertainties remain in the qualitative and quantitative 
characterizations of health effects attributable to exposure to ambient 
O3, the review of this information has been extensive and 
deliberate. In the judgment of the Administrator, this intensive 
evaluation of the scientific evidence has provided an adequate basis 
for regulatory decision making. This review also provides important 
input to EPA's research plan for improving our future understanding of 
the effects of ambient O3 at lower levels, especially in at-
risk population groups.

A. Health Effects Information

    This section outlines key information contained in the Criteria 
Document (chapters 4-8) and in the 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'' 
subpopulations.
    The decision in the last review focused primarily on evidence from 
short-term (e.g., 1 to 3 hours) and prolonged ( 6 to 8 hours) 
controlled-exposure studies reporting lung function decrements, 
respiratory symptoms, and respiratory inflammation in humans, as well 
as epidemiology studies reporting excess

[[Page 37825]]

hospital admissions and emergency department (ED) visits for 
respiratory causes. The Criteria Document prepared for this review 
emphasizes a 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 emphasizes important new information from 
toxicology, dosimetry, and controlled human exposure studies. 
Highlights of the evidence include:
    (1) Two new controlled human-exposure studies are now available 
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 last review.
    (2) Numerous controlled human-exposure studies have examined 
indicators of O3-induced inflammatory response in both the 
upper respiratory tract (URT) and lower respiratory tract (LRT), while 
other studies have examined changes in host defense capability 
following O3 exposure of healthy young adults and increased 
airway responsiveness to allergens in subjects with allergic asthma and 
allergic rhinitis exposed to O3.
    (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 asthmatic subjects, as well as evidence on 
new health endpoints, such as the relationships between ambient 
O3 concentrations 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 respiratory diseases and 
on respiratory-related 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 last 
review, as well as recent meta-analyses that have evaluated potential 
sources of heterogeneity in O3-mortality associations.
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 Criteria Document.\9\ Evidence from dosimetry, 
toxicology, and 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 long-term 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 last review an emerging body of 
animal toxicology and human clinical 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.
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    \9\ 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.
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    With regard to the mechanisms related to short-term respiratory 
effects, scientific evidence discussed in the 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 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 can become 
apparent 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 individual susceptibility to 
O3, as discussed below. At the same O3 dose, 
individuals who are more susceptible to O3 will have a 
larger 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 x ventilation rate x 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 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 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

[[Page 37826