Review of National Ambient Air Quality Standards for Carbon Monoxide, 54294-54343 [2011-21359]

Agencies

• ENVIRONMENTAL PROTECTION AGENCY

[Federal Register Volume 76, Number 169 (Wednesday, August 31, 2011)]
[Rules and Regulations]
[Pages 54294-54343]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: 2011-21359]



[[Page 54293]]

Vol. 76

Wednesday,

No. 169

August 31, 2011

Part II





Environmental Protection Agency





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40 CFR Parts 50, 53 and 58





Review of National Ambient Air Quality Standards for Carbon Monoxide; 
Final Rule

Federal Register / Vol. 76 , No. 169 / Wednesday, August 31, 2011 / 
Rules and Regulations

[[Page 54294]]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Parts 50, 53 and 58

[EPA-HQ-OAR-2008-0015; FRL-9455-2]
RIN 2060-AI43


Review of National Ambient Air Quality Standards for Carbon 
Monoxide

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: This rule is being issued at this time as required by a court 
order governing the schedule for completion of this review of the air 
quality criteria and the national ambient air quality standards (NAAQS) 
for carbon monoxide (CO). Based on its review, the EPA concludes the 
current primary standards are requisite to protect public health with 
an adequate margin of safety, and is retaining those standards. After 
review of the air quality criteria, EPA further concludes that no 
secondary standard should be set for CO at this time. EPA is also 
making changes to the ambient air monitoring requirements for CO, 
including those related to network design, and is updating, without 
substantive change, aspects of the Federal reference method.

DATES: This final rule is effective on October 31, 2011.

ADDRESSES: EPA has established a docket for this action under Docket ID 
No. EPA-HQ-OAR-2008-0015. Incorporated into this docket is a separate 
docket established for the 2010 Integrated Science Assessment for 
Carbon Monoxide (Docket ID No. EPA-HQ-ORD-2007-0925. All documents in 
these dockets are listed on the https://www.regulations.gov Web site. 
Although listed in the docket index, some information is not publicly 
available, e.g., confidential business information (CBI) or other 
information whose disclosure is restricted by statute. Certain other 
material, such as copyrighted material, is not placed on the Internet 
and will be publicly available for viewing at the Public Reading Room. 
Abstracts of scientific studies cited in the review are also available 
on the Internet at EPA's HERO Web site: https://hero.epa.gov/, by 
clicking on the box on the right side of the page labeled ``Search 
HERO.'' Publicly available docket materials are available 
electronically through www.regulations.gov or may be viewed at the 
Public Reading Room 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: Dr. Deirdre Murphy, Health and 
Environmental Impacts Division, Office of Air Quality Planning and 
Standards, Mail code C504-06, U.S. Environmental Protection Agency, 
Research Triangle Park, NC 27711; telephone number: 919-541-0729; fax 
number: 919-541-0237; e-mail address: murphy.deirdre@epa.gov. For 
further information specifically with regard to section IV of this 
notice, contact Mr. Nealson Watkins, Air Quality Analysis Division, 
Office of Air Quality Planning and Standards, Mail code C304-06, U.S. 
Environmental Protection Agency, Research Triangle Park, NC 27711; 
telephone number: 919-541-5522; fax number: 919-541-1903; e-mail 
address: watkins.nealson@epa.gov.

SUPPLEMENTARY INFORMATION:

Table of Contents

    The following topics are discussed in this preamble:

I. Background
    A. Legislative Requirements
    B. Related Carbon Monoxide Control Programs
    C. Review of the Air Quality Criteria and Standards for Carbon 
Monoxide
    D. Summary of Proposed Decisions on Standards for Carbon 
Monoxide
    E. Organization and Approach to Final Decisions on Standards for 
Carbon Monoxide
II. Rationale for Decisions on the Primary Standards
    A. Introduction
    1. Overview of Air Quality Information
    2. Overview of Health Effects Information
    a. Carboxyhemoglobin as Biomarker of Exposure and Toxicity
    b. Nature of Effects and At-Risk Populations
    c. Cardiovascular Effects
    3. Overview of Human Exposure and Dose Assessment
    B. Adequacy of the Current Primary Standards
    1. Rationale for Proposed Decision
    2. Comments on Adequacy
    3. Conclusions Concerning Adequacy of the Primary Standards
III. Consideration of a Secondary Standard
    A. Introduction
    B. Rationale for Proposed Decision
    C. Comments on Consideration of Secondary Standard
    D. Conclusions Concerning a Secondary Standard
IV. Amendments to Ambient Monitoring Requirements
    A. Monitoring Methods
    1. Proposed Changes to Parts 50 and 53
    2. Public Comments
    3. Decisions on Methods
    B. Network Design
    1. Proposed Changes
    2. Public Comments
    a. Near-Road Monitoring and Collocation With Near-Road Nitrogen 
Dioxide Monitors
    b. Population Thresholds for Requiring Near-Road Carbon Monoxide 
Monitors
    c. Implementation Schedule
    d. Siting Criteria
    e. Area-Wide Monitoring
    f. Regional Administrator Authority
    3. Conclusions on the Network Design
V. Statutory and Executive Order Reviews
    A. Executive Order 12866: Regulatory Planning and Review and 
Executive Order 13563: Improving Regulation and Regulatory 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
    K. Congressional Review Act 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 certain air pollutants and then to 
issue air quality criteria for those pollutants. The Administrator is 
to list those air pollutants that in her ``judgment, cause or 
contribute to air pollution which may reasonably be anticipated to 
endanger public health or welfare;'' ``the presence of which in the 
ambient air results from numerous or diverse mobile or stationary 
sources;'' and ``for which * * * [the Administrator] plans to issue air 
quality criteria * * * '' 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 * * *'' 42 U.S.C. 7408(b). Section 109 (42 
U.S.C. 7409) directs the Administrator to propose and promulgate 
``primary'' and ``secondary'' NAAQS for pollutants for which air

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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 [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 provide 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. See 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); American Farm Bureau Federation v. EPA, 559 F.3d 
512, 533 (DC Cir. 2009); Association of Battery Recyclers v. EPA, 604 
F.3d 613, 617-18 (DC Cir. 2010). 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 provide 
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 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, the 
EPA considers such factors as the nature and severity of the health 
effects involved, the size of sensitive 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. See Lead Industries Association v. EPA, 647 F.2d at 1161-62; 
Whitman v. American Trucking Associations, 531 U.S. 457, 495 (2001).
    In setting primary and secondary standards that are ``requisite'' 
to protect public health and welfare, respectively, 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. In so doing, 
EPA may not consider the costs of implementing the standards. See 
generally, Whitman v. American Trucking Associations, 531 U.S. 457, 
465-472, 475-76 (2001). Likewise, ``[a]ttainability and technological 
feasibility are not relevant considerations in the promulgation of 
national ambient air quality standards.'' American Petroleum Institute 
v. Costle, 665 F. 2d at 1185.
    Section 109(d)(1) 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. * * *'' Since the early 
1980's, this independent review function has been performed by the 
Clean Air Scientific Advisory Committee (CASAC).\3\
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    \3\ Lists of CASAC members and of members of the CASAC CO Review 
Panel are available at: https://yosemite.epa.gov/sab/sabproduct.nsf/WebCASAC/CommitteesandMembership?OpenDocument.
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B. Related Carbon Monoxide Control Programs

    States are primarily responsible for ensuring attainment and 
maintenance of ambient air quality standards once EPA has established 
them. Under section 110 of the Act, 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 sources of the pollutants involved. The 
states, in conjunction with EPA, also administer the prevention of 
significant deterioration program. See CAA sections 160-169. In 
addition, Federal programs provide for nationwide reductions in 
emissions of these and other air pollutants through the Federal motor 
vehicle and motor vehicle fuel control program under title II of the 
Act (CAA sections 202-250), which involves controls for emissions from 
moving sources and controls for the fuels used by these sources and new 
source performance standards for stationary sources under section 111.

C. Review of the Air Quality Criteria and Standards for Carbon Monoxide

    EPA initially established NAAQS for CO on April 30, 1971. The 
primary standards were established to protect against the occurrence of 
carboxyhemoglobin levels in human blood associated with health effects 
of concern. The standards were set at 9 parts per million (ppm), as an 
8-hour average, and 35 ppm, as a 1-hour average, neither to be exceeded 
more than once per year (36 FR 8186). In the 1971 decision, the 
Administrator judged that attainment of these standards would provide 
the requisite protection of public health with an adequate margin of 
safety and would also provide requisite protection against known and 
anticipated adverse effects on public welfare, and accordingly set the 
secondary (welfare-based) standards identical to the primary (health-
based) standards.
    In 1985, EPA concluded its first periodic review of the criteria 
and standards for CO (50 FR 37484). In that review, EPA updated the 
scientific criteria upon which the initial CO standards were based 
through the publication of the 1979 Air Quality Criteria Document for 
Carbon Monoxide (AQCD; USEPA, 1979a) and prepared a Staff Paper (USEPA, 
1979b), which, along with the 1979 AQCD, served as the basis for the 
development of the notice of proposed rulemaking which was published on 
August 18, 1980 (45 FR 55066). Delays due to uncertainties

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regarding the scientific basis for the final decision resulted in EPA's 
announcing a second public comment period (47 FR 26407). Following 
substantial reexamination of the scientific data, EPA prepared an 
Addendum to the 1979 AQCD (USEPA, 1984a) and an updated Staff Paper 
(USEPA, 1984b). Following review by CASAC (Lippmann, 1984), EPA 
announced its decision not to revise the existing primary standards and 
to revoke the secondary standard for CO on September 13, 1985, due to a 
lack of evidence of effects on public welfare at ambient concentrations 
(50 FR 37484).
    On August 1, 1994, EPA concluded its second periodic review of the 
criteria and standards for CO by deciding that revisions to the CO 
NAAQS were not warranted at that time (59 FR 38906). This decision 
reflected EPA's review of relevant scientific information assembled 
since the last review, as contained in the 1991 AQCD (USEPA, 1991) and 
the 1992 Staff Paper (USEPA, 1992). Thus, the primary standards were 
retained at 9 ppm with an 8-hour averaging time, and 35 ppm with a 1-
hour averaging time, neither to be exceeded more than once per year (59 
FR 38906).
    EPA initiated the next periodic review in 1997 and released the 
final 2000 AQCD (USEPA, 2000) in August 2000. After release of the 
AQCD, Congress requested that the National Research Council (NRC) 
review the impact of meteorology and topography on ambient CO 
concentrations in high altitude and extreme cold regions of the U.S. 
The NRC convened the Committee on Carbon Monoxide Episodes in 
Meteorological and Topographical Problem Areas, which focused on 
Fairbanks, Alaska, as a case-study.
    A final report, ``Managing Carbon Monoxide Pollution in 
Meteorological and Topographical Problem Areas,'' was published in 2003 
(NRC, 2003) and offered a wide range of recommendations regarding 
management of CO air pollution, cold start emissions standards, 
oxygenated fuels, and CO monitoring. Following completion of the NRC 
report, EPA did not conduct rulemaking to complete the review.
    On September 13, 2007, EPA issued a call for information from the 
public (72 FR 52369) requesting the submission of recent scientific 
information on specified topics. On January 28-29, 2008, a workshop was 
held to discuss policy-relevant scientific and technical information to 
inform EPA's planning for the CO NAAQS review (73 FR 2490). Following 
the workshop, a draft Integrated Review Plan (IRP) (USEPA, 2008a) was 
made available in March 2008 for public comment and was discussed by 
the CASAC via a publicly accessible teleconference consultation on 
April 8, 2008 (73 FR 12998; Henderson, 2008). EPA made the final IRP 
available in August 2008 (USEPA, 2008b).
    In preparing the Integrated Science Assessment for Carbon Monoxide 
(ISA or Integrated Science Assessment), EPA held an authors' 
teleconference in November 2008 with invited scientific experts to 
discuss preliminary draft materials prepared as part of the ongoing 
development of the CO ISA and its supplementary annexes. The first 
draft ISA (USEPA, 2009a) was made available for public review on March 
12, 2009 (74 FR 10734), and reviewed by CASAC at a meeting held on May 
12-13, 2009 (74 FR 15265). A second draft ISA (USEPA, 2009b) was 
released for CASAC and public review on September 23, 2009 (74 FR 
48536), and it was reviewed by CASAC at a meeting held on November 16-
17, 2009 (74 FR 54042). The final ISA was released in January 2010 
(USEPA, 2010a).
    In May 2009, OAQPS released a draft planning document, the draft 
Scope and Methods Plan (USEPA, 2009c), for consultation with CASAC and 
public review at the CASAC meeting held on May 12-13, 2009. Taking into 
consideration comments on the draft Scope and Methods Plan from CASAC 
(Brain, 2009) and the public, OAQPS staff developed and released for 
CASAC review and public comment a first draft Risk and Exposure 
Assessment (REA) (USEPA, 2009d), which was reviewed at the CASAC 
meeting held on November 16-17, 2009. Subsequent to that meeting and 
taking into consideration comments from CASAC (Brain and Samet, 2010a) 
and public comments on the first draft REA, a second draft REA (USEPA, 
2010d) was released for CASAC review and public comment in February 
2010, and reviewed at a CASAC meeting held on March 22-23, 2010. 
Drawing from information in the final CO ISA and the second draft REA, 
EPA released a draft Policy Assessment (PA) (USEPA, 2010e) in early 
March 2010 for CASAC review and public comment at the same meeting. 
Taking into consideration comments on the second draft REA and the 
draft PA from CASAC (Brain and Samet, 2010b, 2010c) and the public, 
staff completed the quantitative assessments which are presented in the 
final REA (USEPA, 2010b). Staff additionally took into consideration 
those comments and the final REA analyses in completing the final 
Policy Assessment (USEPA, 2010c) which was released in October 2010.
    The proposed decision (henceforth ``proposal'') on the review of 
the CO NAAQS was signed on January 28, 2011, and published in the 
Federal Register on February 11, 2011. The EPA held a public hearing to 
provide direct opportunity for oral testimony by the public on the 
proposal. The hearing was held on February 28, 2011, in Arlington, 
Virginia. At this public hearing, EPA heard testimony from five 
individuals representing themselves or specific interested 
organizations. Transcripts from this hearing and written testimony 
provided at the hearing are in the docket for this review. 
Additionally, written comments were received from various commenters 
during the public comment period on the proposal. Significant issues 
raised in the public comments are discussed in the preamble of this 
final action. A summary of all other significant comments, along with 
EPA's responses (henceforth ``Response to Comments'') can be found in 
the docket for this review.
    The schedule for completion of this review is governed by a court 
order resolving a lawsuit filed in March 2003 by a group of plaintiffs 
who alleged that EPA had failed to perform its mandatory duty, under 
section 109(d)(1), to complete a review of the CO NAAQS within the 
period provided by statute. The court order that governs this review, 
entered by the court on November 14, 2008, and amended on August 30, 
2010, provides that EPA will sign for publication a notice of final 
rulemaking concerning its review of the CO NAAQS no later than August 
12, 2011.
    Some commenters have referred to and discussed individual 
scientific studies on the health effects of CO that were not included 
in the ISA (USEPA, 2010a) (``'new' studies''). In considering and 
responding to comments for which such ``new'' studies were cited in 
support, EPA has provisionally considered the cited studies in the 
context of the findings of the ISA.
    As in prior NAAQS reviews, EPA is basing its decision in this 
review on studies and related information included in the ISA, REA and 
Policy Assessment, which have undergone CASAC and public review. The 
studies assessed in the ISA and Policy Assessment, and the integration 
of the scientific evidence presented in them, have undergone extensive 
critical review by EPA, CASAC, and the public. The rigor of that review 
makes these studies, and their integrative assessment, the most 
reliable source of scientific information on which to base decisions on 
the NAAQS, decisions that all parties recognize as of great import.

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NAAQS decisions can have profound impacts on public health and welfare, 
and NAAQS decisions should be based on studies that have been 
rigorously assessed in an integrative manner not only by EPA but also 
by the statutorily mandated independent advisory committee, as well as 
the public review that accompanies this process. EPA's provisional 
consideration of these studies did not and could not provide that kind 
of in-depth critical review.
    This decision is consistent with EPA's practice in prior NAAQS 
reviews and its interpretation of the requirements of the CAA. Since 
the 1970 amendments, the EPA has taken the view that NAAQS decisions 
are to be based on scientific studies and related information that have 
been assessed as a part of the pertinent air quality criteria, and has 
consistently followed this approach. This longstanding interpretation 
was strengthened by new legislative requirements enacted in 1977, which 
added section 109(d)(2) of the Act concerning CASAC review of air 
quality criteria. See 71 FR 61144, 61148 (October 17, 2006) (final 
decision on review of NAAQS for particulate matter) for a detailed 
discussion of this issue and EPA's past practice.
    As discussed in EPA's 1993 decision not to revise the NAAQS for 
ozone, ``new'' studies may sometimes be of such significance that it is 
appropriate to delay a decision on revision of a NAAQS and to 
supplement the pertinent air quality criteria so the studies can be 
taken into account (58 FR at 13013-13014, March 9, 1993). In the 
present case, EPA's provisional consideration of ``new'' studies 
concludes that, taken in context, the ``new'' information and findings 
do not materially change any of the broad scientific conclusions 
regarding the health effects and exposure pathways of ambient CO made 
in the air quality criteria. For this reason, reopening the air quality 
criteria review would not be warranted even if there were time to do so 
under the court order governing the schedule for this rulemaking.
    Accordingly, EPA is basing the final decisions in this review on 
the studies and related information included in the CO air quality 
criteria that have undergone CASAC and public review. EPA will consider 
the ``new'' studies for purposes of decision-making in the next 
periodic review of the CO NAAQS, which EPA expects to begin soon after 
the conclusion of this review and which will provide the opportunity to 
fully assess these studies through a more rigorous review process 
involving EPA, CASAC, and the public. Further discussion of these 
``new'' studies can be found in the Response to Comments document.

D. Summary of Proposed Decisions on Standards for Carbon Monoxide

    For reasons discussed in the notice of proposed rulemaking, the 
Administrator proposed to retain the current primary CO standards. With 
regard to consideration of a secondary standard, the Administrator 
proposed to conclude that no secondary standards should be set at this 
time.

E. Organization and Approach to Final Decisions on Standards for Carbon 
Monoxide

    This action presents the Administrator's final decisions in this 
review of the CO standards. Decisions regarding the primary CO 
standards are addressed below in section II. Consideration of a 
secondary CO standard is addressed below in section III. Ambient 
monitoring methods and network design related to implementation of the 
CO standards are addressed below in section IV. A discussion of 
statutory and executive order reviews is provided in section V.
    Today's final decisions are based on a thorough review in the 
Integrated Science Assessment of the latest scientific information on 
known and potential human health and welfare effects associated with 
exposure to CO in the environment. These final decisions also take into 
account: (1) Assessments in the Policy Assessment of the most policy-
relevant information in the Integrated Science Assessment as well as 
quantitative exposure, dose and risk assessments based on that 
information presented in the Risk and Exposure Assessment; (2) CASAC 
Panel advice and recommendations, as reflected in its letters to the 
Administrator and its discussions of drafts of the Integrated Science 
Assessment, Risk and Exposure Assessment and Policy Assessment at 
public meetings; (3) public comments received during the development of 
these documents, either in connection with CASAC Panel meetings or 
separately; and (4) public comments received on the proposed 
rulemaking.

II. Rationale for Decisions on the Primary Standards

A. Introduction

    This section presents the rationale for the Administrator's 
decision that the current primary standards are requisite to protect 
public health with an adequate margin of safety, and that they should 
be retained. In developing this rationale, EPA has drawn upon an 
integrative synthesis in the Integrated Science Assessment of the 
entire body of evidence published through mid-2009 on human health 
effects associated with the presence of CO in the ambient air. The 
research studies evaluated in the ISA have undergone intensive scrutiny 
through multiple layers of peer review, with extended opportunities for 
review and comment by the CASAC Panel and the public. As with virtually 
any policy-relevant scientific research, there is uncertainty in the 
characterization of health effects attributable to exposure to ambient 
CO. While important uncertainties remain, the review of the health 
effects information has been extensive and deliberate. In the judgment 
of the Administrator, this intensive evaluation of the scientific 
evidence provides an adequate basis for regulatory decision making at 
this time. This review also provides important input to EPA's research 
plan for improving our future understanding of the relationships 
between exposures to ambient CO and health effects.
    The health effects information and quantitative exposure/dose 
assessment were summarized in sections II.B and II.C of the proposal 
(76 FR at 8162-8172) and are only briefly outlined in sections II.A.2 
and II.A.3 below. Responses to public comments specific to the material 
presented in sections II.A.1 through II.A.3 below are provided in the 
Response to Comments document.
    Subsequent sections of this preamble provide a more complete 
discussion of the Administrator's rationale, in light of key issues 
raised in public comments, for concluding that the current standards 
are requisite to protect public health with an adequate margin of 
safety and that it is appropriate to retain the current primary CO 
standards to continue to provide requisite public health protection 
(section II.B).
1. Overview of Air Quality Information
    This section briefly summarizes the information on CO sources, 
emissions, ambient air concentrations and aspects of associated 
exposure presented in section II.A of the proposal, as well as in 
section 1.3 of the Policy Assessment and chapter 2 of the Risk and 
Exposure Assessment.
    Carbon monoxide in ambient air is formed by both natural and 
anthropogenic processes. In areas of human activity such as urban 
areas, it is formed primarily by the incomplete combustion of carbon-
containing fuels with the combustion conditions influencing the rate of 
formation. For example, as a result of the combustion

[[Page 54298]]

conditions, CO emissions from large fossil-fueled power plants are 
typically very low because optimized fuel consumption conditions make 
boiler combustion highly efficient. In contrast, internal combustion 
engines used in many mobile sources have widely varying operating 
conditions. As a result, higher and more varying CO formation results 
from the operation of mobile sources, which continue to be a 
significant source sector for CO in ambient air (ISA, sections 3.4 and 
3.5; 2000 AQCD, section 7.2; REA, section 2.2 and 3.1.3).
    Mobile sources are a substantial contributor to total CO emissions, 
particularly in urban areas (ISA, section 3.5.1.3; REA, section 3.1.3). 
Highest ambient concentrations in urban areas occur on or near 
roadways, particularly highly travelled roadways, and decline somewhat 
steeply with distance (ISA, section 3.5.1.3; REA, section 3.1.3; 
Baldauf et al., 2008a,b; Zhu et al., 2002). For example, as described 
in the ISA, a study by Zhu et al., (2002) documented CO concentrations 
at an interstate freeway to be ten times as high as an upwind 
monitoring site; concentrations declined rapidly in the downwind 
direction to levels only approximately one half roadway concentrations 
within 100 to 300 meters (ISA, section 3.5.1.3, Figure 3-29; Zhu et 
al., 2002). Factors that can influence the steepness of the gradient 
include wind direction and other meteorological variables, and on-road 
vehicle density (ISA, section 3.5.1.3, Figures 3-29 and 3-30; Zhu et 
al., 2002; Baldauf et al., 2008a, b). These traffic-related ambient 
concentrations contribute to the higher short-term ambient CO exposures 
experienced near busy roads and particularly in vehicles, as described 
in more detail in the REA and PA.
2. Overview of Health Effects Information
    This section summarizes information presented in section II.B of 
the proposal pertaining to health endpoints associated with the range 
of exposures considered to be most relevant to current ambient CO 
exposure levels. In recognition of the use of an internal biomarker in 
evaluating health risk for CO, the following section summarizes key 
aspects of the use of carboxyhemoglobin as an internal biomarker 
(section II.A.2.a). This is followed first by a summary of the array of 
CO-induced health effects and recognition of at-risk subpopulations 
(section II.A.2.b) and then by a summary of the evidence regarding 
cardiovascular effects (section II.A.2.c).
a. Carboxyhemoglobin as Biomarker of Exposure and Toxicity
    This section briefly summarizes the current state of knowledge, as 
described in the Integrated Science Assessment, of the role of 
carboxyhemoglobin in mediating toxicity and as a biomarker of exposure. 
The section also summarizes the roles of endogenously produced CO and 
exposure to ambient and nonambient CO in influencing internal CO 
concentrations and carboxyhemoglobin (COHb) levels.
    At this time, as during past reviews, the best characterized 
mechanism of action of CO is tissue hypoxia caused by binding of CO to 
hemoglobin to form COHb in the blood (e.g., USEPA, 2000; USEPA, 1991; 
ISA). Increasing levels of COHb in the blood stream with subsequent 
decrease in oxygen availability for organs and tissues are of concern 
in people who have compromised compensatory mechanisms (e.g., lack of 
capacity to increase blood flow in response to hypoxia), such as those 
with pre-existing heart disease. For example, the integrative review of 
health effects of CO indicates that ``the clearest evidence indicates 
that individuals with CAD [coronary artery disease] are most 
susceptible to an increase in CO-induced health effects'' (ISA, section 
5.7.8).
    Carboxyhemoglobin is formed in the blood both from CO originating 
in the body (endogenous CO) \4\ and from CO that has been inhaled into 
the body (exogenous CO).\5\ The amount of COHb that occurs in the blood 
depends on factors specific to both the physiology of the individual 
(including disease state) and the exposure circumstances. These include 
factors associated with an individual's rate of COHb elimination and 
production of endogenous CO, as well as those that influence the intake 
of exogenous CO into the blood, such as the differences in CO 
concentration (and partial pressure) in inhaled air, exhaled air, and 
blood; duration of a person's exposure to changed CO concentrations in 
air; and exertion level or inhalation rate (ISA, chapter 4).
---------------------------------------------------------------------------

    \4\ Endogenous CO is produced from biochemical reactions 
associated with normal breakdown of heme proteins (ISA, section 
4.5).
    \5\ Exogenous CO includes CO emitted to ambient air, CO emitted 
to ambient air that has infiltrated indoors and CO that originates 
indoors from sources such as gas stoves, tobacco smoke and gas 
furnaces (ISA, section 3.6; REA, section 2.2).
---------------------------------------------------------------------------

    Apart from the impairment of oxygen delivery to tissues related to 
COHb formation, toxicological studies also indicate several other 
pathways by which CO acts in the body, which involve a wide range of 
molecular targets and internal CO concentrations (2000 AQCD, sections 
5.6-5.9; ISA, section 5.1.3). The role of these alternative less-well-
characterized mechanisms in CO-induced health effects at concentrations 
relevant to the current NAAQS, however, is not clear. New research 
based on this evidence is needed to further understand these pathways 
and their linkage to CO-induced effects in susceptible populations. 
Accordingly, COHb level in blood continues to be well recognized and 
most commonly used as an important internal dose metric, and is 
supported by the evidence as the most useful indicator of CO exposure 
that is related to CO health effects of major concern (ISA, p. 2-4, 
sections 4.1, 4.2, 5.1.1; 1991 AQCD; 2000 AQCD; 2010 ISA).
b. Nature of Effects and At-Risk Populations
    The long-standing body of evidence that has established many 
aspects of the biological effects of CO continues to contribute to our 
understanding of the health effects of ambient CO (PA, section 2.2.1). 
Inhaled CO elicits various health effects through binding to, and 
associated alteration of the function of, a number of heme-containing 
molecules, mainly hemoglobin (see e.g., ISA, section 4.1). The best 
characterized health effect associated with CO levels of concern is 
decreased oxygen availability to critical tissues and organs, 
specifically the heart, induced by increased COHb levels in blood (ISA, 
section 5.1.2). Consistent with this, medical conditions that affect 
the biological mechanisms which compensate for this effect (e.g., 
vasodilation and increased coronary blood flow with increased oxygen 
delivery to the myocardium) can contribute to a reduced amount of 
oxygen available to key body tissues, potentially affecting organ 
system function and limiting exercise capacity (2000 AQCD, section 
7.1).\6\
---------------------------------------------------------------------------

    \6\ For example, people with peripheral vascular diseases and 
heart disease patients often have markedly reduced circulatory 
capacity and reduced ability to compensate for increased circulatory 
demands during exercise and other stress (2000 AQCD, p. 7-7).
---------------------------------------------------------------------------

    This evidence newly available in this review provides additional 
detail and support to our prior understanding of CO effects and 
population susceptibility. In this review, the clearest evidence for 
ambient CO-related effects is available for cardiovascular effects. 
Using an established framework to characterize the evidence as to 
likelihood of causal relationships between exposure to ambient CO and

[[Page 54299]]

specific health effects (ISA, chapter 1), the ISA states that ``Given 
the consistent and coherent evidence from epidemiologic and human 
clinical studies, along with biological plausibility provided by CO's 
role in limiting oxygen availability, it is concluded that a causal 
relationship is likely to exist between relevant short-term CO 
exposures and cardiovascular morbidity'' (ISA, p. 2-6, section 2.5.1). 
Using the same established framework, the ISA describes the evidence as 
suggestive of causal relationships between relevant ambient CO exposure 
and several other health effects: Relevant short- and long-term CO 
exposures and central nervous system (CNS) effects, birth outcomes and 
developmental effects following long-term exposure, respiratory 
morbidity following short-term exposure, and mortality following short-
term exposure (ISA, section 2.5). However, there is only limited 
evidence for these relationships, and the current body of evidence 
continues to indicate cardiovascular effects, particularly effects 
related to the role of CO in limiting oxygen availability to tissues, 
as those of greatest concern at low exposures with relevance to ambient 
concentrations (ISA, chapter 2). The evidence for these effects is 
further described in section II.A.2.c below.
    As described in the proposal, the terms susceptibility, 
vulnerability, sensitivity, and at-risk are commonly employed in 
identifying population groups or life stages at relatively higher risk 
for health risk from a specific pollutant. In the ISA for this review, 
the term susceptibility has been used broadly to recognize populations 
that have a greater likelihood of experiencing effects related to 
ambient CO exposure, with use of the term susceptible populations, as 
used in the ISA, defined as follows (ISA, section 5.7, p. 5-115):

    Populations that have a greater likelihood of experiencing 
health effects related to exposure to an air pollutant (e.g., CO) 
due to a variety of factors including, but not limited to: Genetic 
or developmental factors, race, gender, lifestage, lifestyle (e.g., 
smoking status and nutrition) or preexisting disease, as well as 
population-level factors that can increase an individual's exposure 
to an air pollutant (e.g., CO) such as socioeconomic status [SES], 
which encompasses reduced access to health care, low educational 
attainment, residential location, and other factors.

Thus, susceptible populations are at greater risk of CO effects and are 
also referred to as at-risk in the summary below.
    As described in the proposal, the population with pre-existing 
cardiovascular disease continues to be the best-characterized 
population at risk of adverse CO-induced effects, with CAD recognized 
as ``the most important susceptibility characteristic for increased 
risk due to CO exposure'' (ISA, section 2.6.1). An important factor 
determining the increased susceptibility of this population is their 
inability to compensate for the reduction in tissue oxygen levels due 
to an already compromised cardiovascular system. Individuals with a 
healthy cardiovascular system (i.e., with healthy coronary arteries) 
have operative physiologic compensatory mechanisms (e.g., increased 
blood flow and oxygen extraction) for CO-induced tissue hypoxia and are 
unlikely to be at increased risk of CO-induced effects (ISA, p. 2-
10).\7\ In addition, the high oxygen consumption of the heart, together 
with the inability to compensate for tissue hypoxia, makes the cardiac 
muscle of a person suffering from CAD a critical target for CO.
---------------------------------------------------------------------------

    \7\ The other well-studied individuals at the time of the last 
review were healthy male adults that experienced decreased exercise 
duration at similar COHb levels during short term maximal exercise. 
This population was of lesser concern since it represented a smaller 
sensitive group, and potentially limited to individuals that would 
engage in vigorous exercise such as competing athletes (1991 AQCD, 
section 10.3.2).
---------------------------------------------------------------------------

    Thus, the current evidence continues to support the identification 
of people with cardiovascular disease as susceptible to CO-induced 
health effects (ISA, 2-12) and those having CAD as the population with 
the best-characterized susceptibility (ISA, sections 5.7.1.1 and 
5.7.8).\8\ An important susceptibility consideration for this 
population is the inability to compensate for CO-induced hypoxia since 
individuals with CAD have an already compromised cardiovascular system. 
This population includes those with angina pectoris (cardiac chest 
pain), those who have experienced a heart attack, and those with silent 
ischemia or undiagnosed ischemic heart disease (AHA, 2003). People with 
other cardiovascular diseases, particularly heart diseases, are also at 
risk of CO-induced health effects.
---------------------------------------------------------------------------

    \8\ As recognized in the ISA, ``Although the weight of evidence 
varies depending on the factor being evaluated, the clearest 
evidence indicates that individuals with CAD are most susceptible to 
an increase in CO-induced health effects'' (ISA, p. 2-12).
---------------------------------------------------------------------------

    Cardiovascular disease comprises many types of medical disorders, 
including heart disease, cerebrovascular disease (e.g., stroke), 
hypertension (high blood pressure), and peripheral vascular diseases. 
Heart disease, in turn, comprises several types of disorders, including 
ischemic heart disease (coronary heart disease [CHD] or CAD, myocardial 
infarction, angina), congestive heart failure, and disturbances in 
cardiac rhythm (2000 AQCD, section 7.7.2.1).\9\ Other types of 
cardiovascular disease may also contribute to increased susceptibility 
to the adverse effects of low levels of CO (ISA, section 5.7.1.1). For 
example, evidence with regard to other types of cardiovascular disease 
such as congestive heart failure, arrhythmia, and non-specific 
cardiovascular disease, and more limited evidence for peripheral 
vascular and cerebrovascular disease, indicates that ``the continuous 
nature of the progression of CAD and its close relationship with other 
forms of cardiovascular disease suggest that a larger population than 
just those individuals with a prior diagnosis of CAD may be susceptible 
to health effects from CO exposure'' (ISA, p. 5-117).
---------------------------------------------------------------------------

    \9\ Coronary artery disease (CAD), often also called coronary 
heart disease or ischemic heart disease, is a category of 
cardiovascular disease associated with narrowed heart arteries. 
Individuals with this disease may have myocardial ischemia, which 
occurs when the heart muscle receives insufficient oxygen delivered 
by the blood. Exercise-induced angina pectoris (chest pain) occurs 
in many of them. Among all patients with diagnosed CAD, the 
predominant type of ischemia, as identified by electrocardiogram ST 
segment depression, is asymptomatic (i.e., silent). Patients who 
experience angina typically have additional ischemic episodes that 
are asymptomatic (2000 AQCD, section 7.7.2.1). In addition to such 
chronic conditions, CAD can lead to sudden episodes, such as 
myocardial infarction (ISA, p. 5-24).
---------------------------------------------------------------------------

    As described in the proposal, several other populations are 
potentially at risk of CO-induced effects, including: Those with other 
pre-existing diseases that may already have limited oxygen 
availability, increased COHb levels or increased endogenous CO 
production, such as people with obstructive lung diseases, diabetes and 
anemia; older adults; fetuses during critical phases of development and 
young infants or newborns; those who spend a substantial time on or 
near heavily traveled roadways; visitors to high-altitude locations; 
and people ingesting medications and other substances that enhance 
endogenous or metabolic CO formation (ISA, section 2.6.1). While the 
evidence suggests a potential susceptibility of these populations, 
information characterizing susceptibility for these groups is limited. 
For example, information is lacking on specific CO exposures or COHb 
levels that may be associated with health effects in these other groups 
and the nature of those effects, as well as a way to relate the 
specific evidence

[[Page 54300]]

available for the CAD population to these other populations (PA, 
section 2.2.1).
c. Cardiovascular Effects
    Similar to the previous review, results from controlled human 
exposure studies of individuals with coronary artery disease (CAD) 
(Adams et al., 1988; Allred et al., 1989a, 1989b, 1991; Anderson et 
al., 1973; Kleinman et al., 1989, 1998; Sheps et al., 1987\10\) are the 
``most compelling evidence of CO-induced effects on the cardiovascular 
system'' (ISA, section 5.2). Additionally, the use of an internal dose 
metric, COHb, adds to the strength of the findings in these controlled 
exposure studies. As a group, these studies demonstrate the role of 
short-term CO exposures in increasing the susceptibility of people with 
CAD to incidents of exercise-associated myocardial ischemia.
---------------------------------------------------------------------------

    \10\ Statistical analyses of the data from Sheps et al., (1987) 
by Bissette et al. (1986) indicate a significant decrease in time to 
onset of angina at 4.1% COHb if subjects that did not experience 
exercise-induced angina during air exposure are also included in the 
analyses.
---------------------------------------------------------------------------

    Among the controlled human exposure studies, the ISA places 
principal emphasis on the study of CAD patients by Allred et al. 
(1989a, 1989b, 1991) \11\ (which was also considered in the previous 
review) for the following reasons: (1) Dose-response relationships were 
observed; (2) effects were observed at the lowest COHb levels tested 
(mean of 2-2.4% COHb \12\ following experimental CO exposure), with no 
evidence of a threshold; (3) objective measures of myocardial ischemia 
(ST-segment depression) \13\ were assessed, as well as the subjective 
measure of decreased time to induction of angina; (4) measurements were 
taken both by CO-oximetry (CO-Ox) and by gas chromatography (GC), which 
provides a more accurate measurement of COHb blood levels \14\; (5) a 
large number of study subjects were used; (6) a strict protocol for 
selection of study subjects was employed to include only CAD patients 
with reproducible exercise-induced angina; and (7) the study was 
conducted at multiple laboratories around the U.S. This study evaluated 
changes in time to exercise-induced onset of markers of myocardial 
ischemia resulting from two short (approximately 1-hour) CO exposures 
targeted to result in mean study subject COHb levels of 2% and 4%, 
respectively (ISA, section 5.2.4). In this study, subjects (n = 63) on 
three separate occasions underwent an initial graded exercise treadmill 
test, followed by 50 to 70-minute exposures under resting conditions to 
room air CO concentrations or CO concentrations targeted for each 
subject to achieve blood COHb levels of 2% and 4%. The exposures were 
to average CO concentrations of 0.7 ppm (room air concentration range 
0-2 ppm), 117 ppm (range 42-202 ppm) and 253 ppm (range 143-357 ppm). 
After the 50- to 70-minute exposures, subjects underwent a second 
graded exercise treadmill test, and the percent change in time to onset 
of angina and time to ST endpoint between the first and second exercise 
tests was determined. For the two CO exposures, the average post-
exposure COHb concentrations were reported as 2.4% and 4.7%, and the 
subsequent post-exercise average COHb concentrations were reported as 
2.0% and 3.9%.\15\
---------------------------------------------------------------------------

    \11\ Other controlled human exposure studies of CAD patients 
(listed in Table 2-2 of the PA, and discussed in more detail in the 
1991 and 2000 AQCDs) similarly provide evidence of reduced time to 
exercise-induced angina associated with elevated COHb resulting from 
controlled short-duration exposure to increased concentrations of 
CO.
    \12\ These levels and other COHb levels described for this study 
below are based on gas chromatography analysis unless otherwise 
specified. Matched measurements available for CO-oximetry (CO-Ox) 
and gas chromatography (GC) in this study indicate CO-Ox 
measurements of 2.65% (post-exercise mean) and 3.21% (post-exposure 
mean) corresponding to the GC measurement levels of 2.00% (post-
exercise mean) to 2.38% (post-exposure mean) for the lower exposure 
level assessed in this study (Allred et al., 1991).
    \13\ The ST-segment is a portion of the electrocardiogram, 
depression of which is an indication of insufficient oxygen supply 
to the heart muscle tissue (myocardial ischemia). Myocardial 
ischemia can result in chest pain (angina pectoris) or such 
characteristic changes in ECGs or both. In individuals with coronary 
artery disease, it tends to occur at specific levels of exercise. 
The duration of exercise required to demonstrate chest pain and/or a 
1-mm change in the ST segment of the ECG were key measurements in 
the multicenter study by Allred et al. (1989a, 1989b, 1991).
    \14\ As stated in the ISA, the gas chromatographic technique for 
measuring COHb levels ``is known to be more accurate than 
spectrophotometric measurements, particularly for samples containing 
COHb concentrations < 5%'' (ISA, p. 5-41). CO-oximetry is a 
spectrophotometric method commonly used to rapidly provide 
approximate concentrations of COHb during controlled exposures (ISA, 
p. 5-41). At the low concentrations of COHb (< 5%) more relevant to 
ambient CO exposures, co-oximeters are reported to overestimate COHb 
levels compared to GC measurements, while at higher concentrations, 
this method is reported to produce underestimates (ISA, p. 4-18).
    \15\ While the COHb blood level for each subject during the 
exercise tests was intermediate between the post-exposure and 
subsequent post-exercise measurements (e.g., mean 2.4-2.0% and 4.7-
3.9%), the study authors noted that the measurements at the end of 
the exercise test represented the COHb concentrations at the 
approximate time of onset of myocardial ischemia as indicated by 
angina and ST segment changes. The corresponding ranges of CO-Ox 
measurements for the two exposures were 2.7-3.2% and 4.7-5.6%. In 
this document, we refer to the GC-measured mean of 2.0% or 2.0-2.4% 
for the COHb levels resulting from the lower experimental CO 
exposure.
---------------------------------------------------------------------------

    Across all subjects, the mean time to angina onset for control 
(``room'' air) exposures was approximately 8.5 minutes, and the mean 
time to ST endpoint was approximately 9.5 minutes (Allred et al., 
1989b). Relative to room-air exposure that resulted in a mean COHb 
level of 0.6% (post-exercise), exposures to CO resulting in post-
exercise mean COHb concentrations of 2.0% and 3.9% were observed to 
decrease the exercise time required to induce ST-segment depression by 
5.1% (p = 0.01) and 12.1% (p < 0.001), respectively. These changes were 
well correlated with the onset of exercise-induced angina, the time to 
which was shortened by 4.2% (p = 0.027) and 7.1% (p = 0.002), 
respectively, for the two experimental CO exposures (Allred et al., 
1989a, 1989b, 1991).\16\ As at the time of the last review, while ST-
segment depression is recognized as an indicator of myocardial 
ischemia, the exact physiological significance of the observed changes 
among those with CAD is unclear (ISA, p. 5-48).
---------------------------------------------------------------------------

    \16\ Another indicator measured in the study was the combination 
of heart rate and systolic blood pressure which provides a clinical 
index of the work of the heart and myocardial oxygen consumption, 
since heart rate and blood pressure are major determinants of 
myocardial oxygen consumption (Allred et al., 1991). A decrease in 
oxygen to the myocardium would be expected to be paralleled by 
ischemia at lower heart rate and systolic blood pressure. This heart 
rate-systolic blood pressure indicator at the time to ST-endpoint 
was decreased by 4.4% at the 3.9% COHb dose level and by a 
nonstatistically-significant, smaller amount at the 2.0% COHb dose 
level.
---------------------------------------------------------------------------

    No controlled human exposure studies have been specifically 
designed to evaluate the effect of controlled short-term exposures to 
CO resulting in COHb levels lower than a study mean of 2% (ISA, section 
5.2.6). However, an important finding of the multi-laboratory study was 
the dose-response relationship observed between COHb and the markers of 
myocardial ischemia, with effects observed at the lowest increases in 
COHb tested, without evidence of a measurable threshold effect. As 
reported by the authors, the results comparing ``the effects of 
increasing COHb from baseline levels (0.6%) to 2 and 3.9% COHb showed 
that each produced further changes in objective ECG measures of 
ischemia'' implying that ``small increments in COHb could adversely 
affect myocardial function and produce ischemia'' (Allred et al., 
1989b, 1991).
    The epidemiological evidence has expanded considerably since the 
last review including numerous additional studies that are coherent 
with the evidence on markers of myocardial

[[Page 54301]]

ischemia from controlled human exposure studies of CAD patients (ISA, 
section 2.7). The most recent set of epidemiological studies in the 
U.S. have evaluated the associations between ambient concentrations of 
multiple pollutants (i.e., fine particles or PM2.5, nitrogen 
dioxide, sulfur dioxide, ozone, and CO) at fixed-site ambient monitors 
and increases in emergency department visits and hospital admissions 
for specific cardiovascular health outcomes including ischemic heart 
disease (IHD), myocardial infarction, congestive heart failure (CHF), 
and cardiovascular diseases (CVD) as a whole (Bell et al., 2009; Koken 
et al., 2003; Linn et al., 2000; Mann et al., 2002; Metzger et al., 
2004; Symons et al., 2006; Tolbert et al., 2007; Wellenius et al., 
2005). As noted by the ISA, ``[s]tudies of hospital admissions and 
[emergency department] visits for IHD provide the strongest 
[epidemiological] evidence of ambient CO being associated with adverse 
CVD outcomes'' (ISA, p. 5-40, section 5.2.3). With regard to studies 
for other measures of cardiovascular morbidity, the ISA notes that 
``[t]hough not as consistent as the IHD effects, the effects for all 
CVD hospital admissions (which include IHD admissions) and CHF hospital 
admissions also provide evidence for an association of cardiovascular 
outcomes and ambient CO concentrations'' (ISA, section 5.2.3). While 
noting the difficulty in determining the extent to which CO is 
independently associated with CVD outcomes in this group of studies as 
compared to CO as a marker for the effects of another traffic-related 
pollutant or mix of pollutants, the ISA concludes that the 
epidemiological evidence, particularly when considering the copollutant 
analyses, provides support to the clinical evidence for a direct effect 
of short-term ambient CO exposure on CVD morbidity (ISA, pp. 5-40 to 5-
41).
3. Overview of Human Exposure and Dose Assessment
    Our consideration of the scientific evidence in the current review, 
as at the time of the last review, is informed by results from a 
quantitative analysis of estimated population exposure and resultant 
COHb levels. This analysis provides estimates of the percentages of 
simulated at-risk populations expected to experience daily maximum COHb 
levels at or above a range of benchmark levels 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. The benchmark COHb levels 
were identified based on consideration of the evidence discussed in 
section II.A.2 above. In this section, we provide a short overview of 
key aspects of the assessment conducted for this review. The assessment 
is summarized more fully in section II.C of the proposal, discussed in 
detail in the REA and summarized in the PA (section 2.2.2). The results 
of the analyses as they relate to considerations of the adequacy of the 
current standards are discussed in section II.B.3 below.
    As noted in the proposal notice, people can be exposed to CO in 
ambient air when they are outdoors and also when they are in indoor 
locations into which ambient (outdoor) air has infiltrated (ISA, 
sections 3.6.1 and 3.6.5). Indoor locations may also contain CO from 
indoor sources, such as gas stoves and tobacco smoke. Where present, 
these indoor sources can be important contributors to total CO exposure 
and can contribute to much greater CO exposures and associated COHb 
levels than those associated with ambient sources (ISA, section 
3.6.5.2). For example, indoor source-related exposures, such as faulty 
furnaces or other combustion appliances, have been estimated in the 
past to lead to COHb levels on the order of twice as high as short-term 
elevations in ambient CO that were more likely to be encountered by the 
general public (2000 AQCD, p. 7-4). Further, some exposure/dose 
assessments performed for previous reviews have included modeling 
simulations both without and with indoor (nonambient) sources (gas 
stoves and tobacco smoke) to provide context for the assessment of 
ambient CO exposure and dose (e.g., USEPA, 1992; Johnson et al., 2000), 
and these assessments have found that nonambient sources have a 
substantially greater impact on the highest total exposures and COHb 
levels experienced by the simulated population than do ambient sources 
(Johnson et al., 2000; REA, sections 1.2 and 6.3). While recognizing 
this potential for indoor sources, where present, to play a role in CO 
exposures and COHb levels, the exposure modeling in the current review 
(described below) did not include indoor CO sources in order to focus 
on the impact of ambient CO on population COHb levels.
    The assessment estimated ambient CO exposure and associated COHb 
levels in simulated at-risk populations in two urban study areas in 
Denver and Los Angeles, in which current ambient CO concentrations are 
below the current standards. Estimates were developed for exposures to 
ambient CO associated with current ``as is'' conditions (2006 air 
quality) and also for higher ambient CO concentrations associated with 
air quality conditions simulated to just meet the current 8-hour 
standard,\17\ as well as for air quality conditions simulated to just 
meet several potential alternative standards. Although we consider it 
unlikely that air concentrations in many urban areas across the U.S. 
that are currently well below the current standards would increase to 
just meet the 8-hour standard, we recognize the potential for CO 
concentrations in some areas currently below the standard to increase 
to just meet the standard. We additionally recognize that this 
simulation can provide useful information in evaluating the current 
standard, although we recognize the uncertainty associated with 
simulating this hypothetical profile of higher CO concentrations that 
just meet the current 8-hour standard.
---------------------------------------------------------------------------

    \17\ As noted elsewhere, the 8-hour standard is the controlling 
standard for ambient CO concentrations.
---------------------------------------------------------------------------

    The exposure and dose modeling for the assessment, presented in 
detail in the REA, relied on version 4.3 of EPA's Air Pollutant 
Exposure model (APEX4.3), which estimates human exposure using a 
stochastic, event-based microenvironmental approach (REA, chapter 4). 
The review of the CO standards completed in 1994 relied on population 
exposure and dose estimates generated from the probabilistic NAAQS 
exposure model (pNEM), a model that, among other differences from the 
current modeling approach with APEX4.3, employed a cohort-based 
approach (Johnson et al., 1992; USEPA, 1992).18 19 Each of 
the model developments since the use of pNEM in that review have been 
designed to allow APEX to better represent human behavior, human 
physiology, and

[[Page 54302]]

microenvironmental concentrations and to more accurately estimate 
variability in CO exposures and COHb levels (REA, chapter 4).\20\
---------------------------------------------------------------------------

    \18\ When using the cohort approach, each cohort is assumed to 
contain persons with identical exposures during the specified 
exposure period. Thus, variability in exposure will be attributed to 
differences in how the cohorts are defined, not necessarily 
reflecting differences in how individuals might be exposed in a 
population. In the assessment for the review completed in 1994, a 
total of 420 cohorts were used to estimate population exposure based 
on selected demographic information (11 groups using age, gender, 
work status), residential location, work location, and presence of 
indoor gas stoves (Johnson, et al., 1992; USEPA, 1992).
    \19\ The use of pNEM in the prior review also (1) relied on a 
limited set of activity pattern data (approximately 3,600 person-
days), (2) used four broadly defined categories to estimate 
breathing rates, and (3) implemented a geodesic distance range 
methodology to approximate workplace commutes (Johnson et al., 1992; 
USEPA, 1992). Each of these approaches used by pNEM, while 
appropriate given the data available at that time, would tend to 
limit the ability to accurately model expected variability in the 
population exposure and dose distributions.
    \20\ APEX4.3 inc