[Federal Register Volume 76, Number 169 (Wednesday, August 31, 2011)]
[Rules and Regulations]
[Pages 54294-54343]
[FR Doc No: 2011-21359]

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

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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 http://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: http://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<PHONE_NUMBER> 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:<PHONE_NUMBER>; fax
number:<PHONE_NUMBER>; e-mail address<EMAIL_ADDRESS>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:<PHONE_NUMBER>; fax number:<PHONE_NUMBER>; e-mail
address<EMAIL_ADDRESS>
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

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: http://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

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.

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

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 <IP_ADDRESS>; 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 <IP_ADDRESS>; 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 <IP_ADDRESS>, 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 <IP_ADDRESS>, 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

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 <IP_ADDRESS> 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 <IP_ADDRESS>).\9\ Other types of
cardiovascular disease may also contribute to increased susceptibility
to the adverse effects of low levels of CO (ISA, section <IP_ADDRESS>). 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 <IP_ADDRESS>). 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

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

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
<IP_ADDRESS>). 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

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 includes new algorithms to (1) simulate
longitudinal activity sequences and exposure profiles for
individuals, (2) estimate activity-specific minute-by-minute oxygen
consumption and breathing rates, (3) address spatial variability in
home and work-tract ambient concentrations for commuters, and (4)
estimate event-based microenvironmental concentrations (PA, section
2.2.2).
---------------------------------------------------------------------------

    As used in the current assessment, APEX probabilistically generates
a sample of hypothetical individuals from an actual population database
and simulates each individual's movements through time and space (e.g.,
indoors at home, inside vehicles) to estimate his or her exposure to
ambient CO (REA, chapter 4). Based on exposure concentrations, minute-
by-minute activity levels, and physiological characteristics of the
simulated individuals (see REA, chapters 4 and 5), APEX estimates the
level of COHb in the blood for each individual at the end of each hour
based on a nonlinear solution to the Coburn-Forster-Kane equation (REA,
section 4.4.7).
    As discussed in section II.A.2.b above, people with cardiovascular
disease are the population of primary focus in this review, and, more
specifically, coronary artery disease, also known as coronary heart
disease, is the ``most important susceptibility characteristic for
increased risk due to CO exposure'' (ISA, p. 2-11). Controlled human
exposure studies have provided quantitative COHb dose-response
information for this specific population with regard to effects on
markers of myocardial ischemia. Accordingly, based on the current
evidence with regard to quantitative information of COHb levels and
association with specific health effects, the at-risk populations
simulated in the quantitative assessment were (1) adults with CHD (also
known as IHD or CAD), both diagnosed and undiagnosed, and (2) adults
with any heart diseases, including undiagnosed ischemia.\21\ Evidence
characterizing the nature of specific health effects of CO in other
populations is limited and does not include specific COHb levels
related to health effects in those groups. As a result, the
quantitative assessment does not develop separate quantitative dose
estimates for populations other than those with CHD or HD.
---------------------------------------------------------------------------

    \21\ As described in section1.2 above, this is the same
population group that was the focus of the CO NAAQS exposure/dose
assessments conducted previously (e.g., USEPA, 1992; Johnson et al.,
2000).
---------------------------------------------------------------------------

    APEX simulations performed for this review focused on exposures to
ambient CO occurring in eight microenvironments,\22\ absent any
contribution to microenvironment concentrations from indoor
(nonambient) CO sources. Previous assessments, that have included
modeling simulations both with and without certain indoor sources,
indicated that the impact of such sources can be substantial with
regard to the portion of the at-risk population experiencing higher
exposures and COHb levels (Johnson et al., 2000). While we are limited
with regard to information regarding CO emissions from indoor sources
today and how they may differ from the time of the 2000 assessment, we
note that ambient contributions have notably declined, and indoor
source contributions from some sources may also have declined. Thus, as
indicated in the Policy Assessment, we have no firm basis to conclude a
different role for indoor sources today with regard to contribution to
population CO exposure and COHb levels.
---------------------------------------------------------------------------

    \22\ The 8 microenvironments modeled in the REA comprised a
range of indoor and outdoor locations including residences as well
as motor vehicle-related locations such as inside vehicles, and
public parking and fueling facilities, where the highest exposures
were estimated (REA, sections 5.9 and 6.1).
---------------------------------------------------------------------------

    In considering the REA dose estimates in the Policy Assessment,
staff considered estimates of the portion of the simulated at-risk
populations estimated to experience daily maximum end-of-hour absolute
COHb levels above identified benchmark levels (at least once and on
multiple occasions), as well as estimates of the percentage of
population person-days (the only metric available from the modeling for
the 1994 review), and also population estimates of daily maximum
ambient contribution to end-of-hour COHb levels.\23\ In identifying
COHb benchmark levels of interest, primary attention was given to the
multi-laboratory study in which COHb was analyzed by the more accurate
GC method (Allred et al., 1989a, 1989b, 1991) discussed in section
II.A.2.c above. As summarized in the proposal, the Policy Assessment
recognized distinctions between the REA ``baseline'' (arising from
prior ambient exposure and endogenous CO production) and the pre-
exposure COHb levels in the controlled human exposure study (arising
from ambient and nonambient exposure history, as well as from
endogenous CO production), and also noted the impact of ``baseline''
COHb levels on COHb levels occurring in response to short ambient CO
exposure events such as those simulated in the REA.
---------------------------------------------------------------------------

    \23\ As summarized in the proposal and described more fully in
the REA and PA, absolute COHb refers to the REA estimates of COHb
levels resulting from endogenously produced CO and exposure to
ambient CO (in the absence of any nonambient sources). The
additional REA estimates of ambient CO exposure contribution to COHb
levels were calculated by subtracting COHb estimates obtained in the
absence of CO exposure--i.e., that due to endogenous CO production
alone (see REA, Appendix B.6)--from the corresponding end-of-hour
absolute COHb estimates for each simulated individual. Thus, the REA
reports estimates of the maximum end-of-hour ambient contributions
across the simulated year, in addition to the maximum absolute end-
of hour COHb levels.
---------------------------------------------------------------------------

    Numerous improvements have been made over the last decade that have
reduced the uncertainties associated with the models used to estimate
COHb levels resulting from ambient CO exposures under different air
quality conditions, including those associated with just meeting the
current CO NAAQS (REA, section 4.3). This progression in exposure model
development has led to the model currently used by the agency
(APEX4.3), which has an enhanced capacity to estimate population CO
exposures and more accurately predicts COHb levels in persons exposed
to CO. Our application of APEX4.3 in this review, using updated data
and new algorithms to estimate exposures and doses experienced by
individuals, better represents the variability in population exposure
and COHb dose levels than the model version used in previous CO
assessments.\24\ However, while APEX 4.3 is greatly improved when
compared with previously used exposure models, its application is still
limited with regard to data to inform our understanding of spatial
relationships in ambient CO concentrations and within microenvironments
of particular interest. Further information regarding model
improvements and exposure modeling uncertainties is summarized in
section 2.2.2 of the Policy Assessment and described in detail in
chapter 7 of the REA.
---------------------------------------------------------------------------

    \24\ APEX4.3 provides estimates for percent of population
projected to experience a single or multiple occurrences of a daily
maximum COHb level above the various benchmark levels, as well as
percent of person-days.
---------------------------------------------------------------------------

    Taking into consideration improvements in the model algorithms and
data since the last review, and having identified and characterized
these uncertainties, the Policy Assessment concludes that the estimates
associated with the current analysis, at a minimum, better reflect the
full distribution of exposures and dose as compared to results from the
1992 analysis. As noted in the Policy Assessment, however, potentially
greater uncertainty remains in our characterization of the upper and
lower

percentiles of the distribution of population exposures and COHb dose
levels relative to that of other portions of the respective
distribution. When considering the overall quality of the current
exposure modeling approach, the algorithms, and the input data used,
alongside the identified limitations and uncertainties, the REA and
Policy Assessment conclude that the quantitative assessment provides
reasonable estimates of CO exposure and COHb dose for the simulated
population the assessment is intended to represent (i.e., the
population residing within the urban core of each study area). The
Policy Assessment additionally notes the impact on the REA dose
estimates for ambient CO contribution to COHb of the lack of nonambient
sources in the model simulations. This aspect of the assessment design
may contribute to higher estimates of the contribution of short-
duration ambient CO exposures to total COHb than would result from
simulations that include the range of commonly encountered CO sources
beyond just those contributing to ambient air CO concentrations.
Although the specific quantitative impact of this on estimates of
population percentages discussed in this document is unknown,
consideration of COHb estimates from the 2000 assessment indicates a
potential for the inclusion of nonambient sources to appreciably affect
absolute COHb (REA, section 6.3) and accordingly implies the potential,
where present, for an impact on overall ambient contribution to a
person's COHb level. Key results of the exposure and dose analyses were
presented in the Policy Assessment and summarized in the proposal
(Tables 1 and 2 of the proposal).

B. Adequacy of the Current Primary Standards

    In considering the evidence and quantitative exposure and dose
estimates with regard to judgments on the adequacy afforded by the
current standards, the final decision is largely a public health policy
judgment. A final decision must draw upon scientific information and
analyses about health effects and risks, as well as judgments about how
to consider the range and magnitude of uncertainties that are inherent
in the scientific evidence and analyses. Our approach to informing
these judgments is based on the recognition that the available health
effects evidence generally reflects a continuum, consisting of ambient
levels at which scientists generally agree that health effects are
likely to occur, through lower levels at which the likelihood and
magnitude of the response become increasingly uncertain. This approach
is consistent with the requirements of the NAAQS provisions of the Act
and with how EPA and the courts have historically interpreted the Act.
These provisions require the Administrator to establish primary
standards that, in the Administrator's judgment, are requisite to
protect public health with an adequate margin of safety. In so doing,
the Administrator seeks to establish standards that are neither more
nor less stringent than necessary for this purpose. The Act does not
require that primary standards be set at a zero-risk level, but rather
at a level that avoids unacceptable risks to public health, including
the health of sensitive groups.\25\
---------------------------------------------------------------------------

    \25\ The sensitive population groups identified in a NAAQS
review may (or may not) be comprised of low income or minority
groups. Where low income/minority groups are among the sensitive
groups, the rulemaking decision will be based on providing
protection for these and other sensitive population groups. To the
extent that low income/minority groups are not among the sensitive
groups, a decision based on providing protection of the sensitive
groups would be expected to provide protection for the low income/
minority groups (as well as any other less sensitive population
groups).
---------------------------------------------------------------------------

    In evaluating whether it is appropriate to revise the current CO
standards, the Administrator's considerations build on the general
approach used in the last review and reflect the broader body of
evidence and information now available. The approach used is based on
an integration of information on health effects associated with
exposure to ambient CO; expert judgment on the adversity of such
effects on individuals; and policy judgments as to when the standards
are requisite to protect public health with an adequate margin of
safety, which are informed by air quality and related analyses,
quantitative exposure and risk assessments when possible, and
qualitative assessment of impacts that could not be quantified. The
Administrator has taken into account both evidence-based and
quantitative exposure- and risk-based considerations in developing
conclusions on the adequacy of the current primary CO standards.
    The Administrator's proposed conclusions on the adequacy of the
current primary standards are summarized below (section II.B.1),
followed by consideration of comments received on the proposal (section
II.B.2) and the Administrator's final decision with regard to the
adequacy of the current primary standards (II.B.3).
1. Rationale for Proposed Decision
    At the time of the proposal, in considering the adequacy of the
current standards, the Administrator carefully considered the available
evidence and conclusions contained in the Integrated Science
Assessment; the information, exposure/dose assessment, rationale and
conclusions presented in the Policy Assessment; the advice and
recommendations from CASAC; and public comments as of that date. In so
doing, the Administrator noted the following: (1) The long-standing
evidence base concerning effects associated with exposure to CO,
including the key role played by hypoxia (reduced oxygen availability)
induced by increased COHb blood levels, and the use of COHb as the
bioindicator and dose metric for evaluating CO exposure and the
potential for health effects; (2) the strong evidence of cardiovascular
effects of short-term CO exposures including the evidence from
controlled human exposure studies that demonstrate a reduction in time
to onset of exercise-induced markers of myocardial ischemia in response
to increased COHb, and the health significance of responses observed at
the 2% COHb level induced by 1-hour CO exposure, as compared to higher
COHb levels; and (3) the identification of people with cardiovascular
disease as a key population at risk from short-term ambient CO
exposures. In the proposal, as at the time of the last review, the
Administrator additionally considered and took particular note of the
exposure and dose modeling results, recognizing key limitations and
uncertainties, and in light of judgments noted above regarding the
health significance of findings from the controlled human exposure
studies, placing less weight on the health significance of infrequent
or rare occurrences of COHb levels at or just above 2% and more weight
to the significance of repeated such occurrences, as well as
occurrences of higher COHb levels.
    The Administrator also considered the newly available and much-
expanded epidemiological evidence, including the complexity associated
with quantitative interpretation of these studies with regard to CO,
particularly the few studies available in areas where the current
standards are met. Further, the Administrator considered the advice of
CASAC, including their overall agreement with the Policy Assessment
conclusion that the current evidence and quantitative exposure and dose
estimates provide support for retaining the current standards, their
view that, in

light of the epidemiological studies, revisions to lower the standards
should be considered and their preference for a lower standard, and
also their advice regarding the complications associated with
interpreting the epidemiological studies for CO. Although CASAC
expressed a preference for a lower standard, CASAC also indicated that
the current evidence provides support for retaining the current suite
of standards and CASAC's recommendations appear to recognize that their
preference for a lower standard was contingent on a judgment as to the
weight to be placed on the epidemiological evidence. For the reasons
explained in the proposal, after full consideration of CASAC's advice
and the epidemiological evidence, as well as its associated
uncertainties and limitations, the Administrator proposed to judge
those uncertainties and limitations to be too great for the
epidemiological evidence to provide a basis for revising the current
standards.
    Taking all these considerations together, the Administrator
proposed to conclude that the current suite of standards provides a
very high degree of protection for the COHb levels and associated
health effects of concern, as indicated by the extremely low estimates
of occurrences, and provides slightly less but a still high degree of
protection for the effects associated with lower COHb levels, the
physiological significance of which is less clear. The Administrator
additionally proposed to conclude that consideration of the
epidemiological studies does not lead her to identify a need for any
greater protection. Thus, the Administrator proposed to conclude that
the current suite of standards provides an adequate margin of safety
against adverse effects associated with short-term ambient CO
exposures. For these and all of the reasons discussed above, and
recognizing the CASAC conclusion that, overall, the current evidence
and REA results provide support for retaining the current standards,
the Administrator proposed to conclude that the current suite of
primary CO standards is requisite to protect public health with an
adequate margin of safety from effects of ambient CO.
2. Comments on Adequacy
    In considering comments on the adequacy of the current standards,
the Administrator first notes the advice and recommendations from
CASAC. In the context of CASAC's review of the documents prepared
during the course of the review, CASAC sent EPA five letters providing
advice regarding assessment and interpretation of the available
scientific evidence and the REA for the purposes of judging the
adequacy of the current CO standards (Brain and Samet, 2009; Brain and
Samet, 2010a; Brain and Samet, 2010b; Brain and Samet, 2010c; Brain and
Samet, 2010d). In conveying comments on the draft Policy Assessment,
CASAC agreed with the conclusion that the current evidence provides
support for retaining the current suite of standards, while they also
expressed a preference for a lower standard and stated that the
epidemiological evidence could indicate the occurrence of adverse
health effects at levels of the standards (Brain and Samet, 2010c).
With regard to the interpretation of epidemiological studies on CO,
CASAC's collective advice included recommendations regarding the weight
to be placed on the epidemiological evidence (Brain and Samet, 2010c),
as well as cautionary statements regarding interpretation of the
epidemiological studies. Such statements included the observation that
``[d]istinguishing the effects of CO per se from the consequences of CO
as a marker of pollution or vehicular traffic is a challenge, which
[the ISA] needs to confront as thoroughly as possible'' (Brain and
Samet, 2009, p. 2). In another letter CASAC further cautioned (Brain
and Samet, 2010d, p. 2):

    The problem of co-pollutants serving as potential confounders is
particularly problematic for CO. Since exposure levels for CO are
now low, consideration needs to be given to the possibility that in
some situations CO may be a surrogate for exposure to a mix of
pollutants generated by fossil fuel combustion. A better
understanding of the possible role of co-pollutants is relevant to
regulation and to the design, analysis, and interpretation of
epidemiologic studies on the health effects of CO.

CASAC additionally noted concerns regarding the spatial coverage of the
existing CO monitoring network and the sensitivity of deployed monitors
(Brain and Samet, 2009; Brain and Samet, 2010a; Brain and Samet, 2010b;
Brain and Samet, 2010d). On a related note, they cautioned that
``[u]nderstanding the extent of exposure measurement error is critical
for evaluating epidemiological evidence'' (Brain and Samet, 2009).
    General comments from the public based on relevant factors that
either support or oppose retention of the current primary CO standards
are addressed in this section. Other specific public comments related
to consideration of the adequacy of the current standards, as well as
general comments based on implementation-related factors that are not a
permissible basis for considering the need to revise the current
standards, are addressed in the Response to Comments document.
    The public comments received on the proposal were divided with
regard to support for the Agency's proposed conclusion as to the
adequacy of the current standards. All of the state and local
environmental agencies or governments that provided comments on the
standards concurred with EPA's proposed conclusions as did the three
industry commenters. All of these commenters generally noted their
agreement with the rationale provided in the proposal, with some
additionally citing CASAC's recognition of support in the evidence for
the adequacy of the current standards. Some of these commenters noted
agreement with the weight given to the epidemiological studies in the
proposal and also noted the little change in exposure/risk estimates
since the time of the last review. One commenter additionally stated
their view that the REA overstates the exposure and risk associated
with the current standards.
    As described in section II.B.3 below, the EPA generally agrees with
these commenters regarding the adequacy of the current CO standards and
with CASAC that the evidence provides support for the conclusion that
the current CO standards protect public health with an adequate margin
of safety. EPA additionally has given consideration to CASAC's advice
regarding interpretation of epidemiological evidence for CO,
recognizing the limitations associated with its use in drawing
quantitative interpretations regarding levels of ambient CO related to
health outcomes.
    Two submissions recommending revision of the standards were
received from national environmental or public health organizations.
Additional submissions recommending revision were received from a
private consultant; a group of scientists, physicians, and others; and
a group of private citizens. In support of their position, these
commenters variously cited CASAC comments regarding emphasis to give
epidemiological studies and CASAC's stated preference for a lower
standard. These submissions generally disagreed with EPA's
consideration of the epidemiological evidence in the proposal and
recommended that EPA give greater emphasis to epidemiological studies
of a range of endpoints, including developmental and respiratory
effects, based on the commenters' view that the epidemiological studies
provided evidence of harm associated with ambient CO levels below the
current

standards and inadequate protection for sensitive populations. Among
these submissions, those that specified levels for revised standards
recommended levels that were no higher than the lowest part of the
ranges for the two standards that were identified for consideration in
the Policy Assessment and the example options that CASAC suggested for
inclusion in the Policy Assessment. Additionally, one commenter
described the view that the CO standards should be revised to levels at
or below the range of CO concentrations in exhaled breath of healthy
non-smokers.
    EPA generally disagrees with these commenters regarding conclusions
that can be drawn from the evidence, including the epidemiological
studies, pertaining to the adequacy of the current CO standards. In
considering the adequacy of the current standards, it is important to
consider both the extent to which the evidence supports a causal
relationship between ambient CO exposures and adverse health effects,
as well as the extent to which there is evidence pertinent to such
effects under air quality conditions in which the current standards are
met. With regard to the latter point, and focusing on the
epidemiological evidence, it is the studies involving air quality
conditions in which the current standards were met that are most
informative in evaluating the adequacy of the standards (PA, p. 2-30).
We note that very few of the epidemiological studies observing an
association of cardiovascular disease-related outcomes with short-term
CO concentrations (or those observing associations for other health
effects) were conducted in areas that met the current standards
throughout the period of study, thus limiting their usefulness with
regard to judging the adequacy of the current standards (PA, pp. 2-33,
2-36).
    Further, as CASAC has cautioned, ``the problem of co-pollutants
serving as potential confounders is particularly problematic for CO''
(Brain and Samet, 2010d). While some CO epidemiological studies have
applied the commonly used statistical method, two-pollutant regression
models, to inform conclusions regarding CO as the pollutant eliciting
the effects in these studies, and while, in some studies, the CO
associations remain robust after adjustment for another traffic
combustion-related pollutant, such as PM2.5 or nitrogen
dioxide (NO2) (PA, pp. 2-36 to 2-37), the potential exists
for there to be etiologically relevant pollutants that are correlated
with CO yet absent from the analysis, particularly given the many
pollutants associated with fossil fuel combustion. The CASAC
specifically recognized this potential in stating that ``consideration
needs to be given to the possibility that in some situations CO may be
a surrogate for exposure to a mix of pollutants generated by fossil
fuel combustion'' and ``a better understanding of the possible role of
co-pollutants is relevant to * * * the interpretation of epidemiologic
studies on the health effects of CO'' (Brain and Samet, 2010d).
    In light of these issues related to potential confounding by co-
pollutants in the case of CO, uncertainty related to exposure error for
CO is of particular concern in quantitatively interpreting the
epidemiological evidence (e.g., with regard to ambient concentrations
contributing to health outcomes).\26\ As noted above, CASAC cautioned
the Agency on the importance of understanding the extent of exposure
error in evaluating the epidemiological evidence for CO (Brain and
Samet, 2009). There are two aspects to the epidemiological studies in
the specific case of CO (as contrasted with other pollutants such as PM
and NO2) that may contribute exposure error in the studies
(PA, pp. 2-34 to 2-38; 76 FR 8177-8178). The first relates to the
uncertainty associated with quantitative interpretation of the
epidemiological study results at low ambient concentrations in light of
the sizeable portion of ambient CO measurements that are at or below
monitor method detection limits (MDLs). As described in the proposal,
uncertainty related to the prevalence of ambient CO monitor
concentrations at or below MDLs is a greater concern for the more
recently available epidemiological studies in which the study areas
have much reduced ambient CO concentrations compared with those in the
past (PA, pp. 2-37 to 2-38). This complicates our interpretation of
specific ambient CO concentrations associated with health effects (ISA,
p. 3-91; Brain and Samet, 2010d), providing us with reduced confidence
in quantitative interpretations of epidemiological studies for CO.
Additionally, as described in the proposal, there is uncertainty and
potential error associated with exposure estimates in the CO
epidemiological studies that relate to the use of area-wide or central-
site monitor CO concentrations in light of information about the steep
gradient in CO concentrations with distance from source locations such
as highly-trafficked roadways (ISA, section <IP_ADDRESS>). As a result of
differences in factors related to pollutant formation, this gradient is
steeper for CO than for other traffic combustion-related pollutants,
such as PM2.5 and NO2, contributing to a greater
potential for exposure misclassification in the case of CO by the
reliance on central site monitors in the CO epidemiological studies.
Thus, as noted in the proposal, we recognize that the expanded body of
epidemiological evidence available in this review includes its own set
of uncertainties which complicates its interpretation, particularly
with regard to ambient concentrations that may be eliciting health
outcomes.
---------------------------------------------------------------------------

    \26\ In contrasting the strength of the epidemiological evidence
available for the 2000 AQCD with that in the current review, the ISA
notes that uncertainties identified in 2000 remain, including the
ability of community fixed-site monitors to represent spatially
variable ambient CO concentrations and personal exposures; the small
expected increase in COHb due to ambient CO concentrations; the lack
of biological plausibility for health effects to occur at such COHb
levels, even in diseased individuals; and the possibility that
ambient CO is serving as a surrogate for a mixture of combustion-
related pollutants. These uncertainties complicate the quantitative
interpretation of the epidemiologic findings, ``particularly
regarding the biological plausibility of health effects occurring at
COHb levels resulting from exposures to ambient CO concentrations
measured at AQS monitors'' (ISA, pp. 2-16 to 2-17).
---------------------------------------------------------------------------

    In our integrated assessment across all types of evidence in the
ISA for this review, we conclude that a causal relationship is likely
to exist for short-term exposures to ambient concentrations of CO and
cardiovascular morbidity. In reaching this conclusion, the ISA notes
that the most compelling evidence comes from the controlled human
exposure studies (ISA, p. 2-5), which also document a significant dose-
response relationship over a range of COHb concentrations relevant to
consideration of the NAAQS (ISA, p. 2-13). In considering the
epidemiological evidence for relevant cardiovascular outcomes, which
includes multiple studies reporting associations with ambient CO
concentrations under conditions when the current standards were not met
(PA, p. 2-30), the ISA notes that these studies are coherent with the
findings from the controlled human exposure studies (ISA, p. 2-17).
However, as summarized here, various aspects of the evidence complicate
quantitative interpretation of it with regard to ambient concentrations
that might be eliciting the reported health outcomes.
    An additional complication to our consideration of the CO
epidemiological evidence is that, in contrast to the health effects
evidence for all other criteria pollutants, the epidemiological studies
for CO use a different exposure/dose metric from that which is the
focus of the broader health evidence base, and

additional information that might be used to bridge this gap is
lacking. In the case of CO, the epidemiological studies use air
concentration as the exposure/dose metric, while much of the broader
health effects evidence for CO, and particularly that related to
cardiovascular effects, demonstrates and focuses on an internal
biomarker of CO exposure (COHb) which has been considered a critical
key to CO toxicity.\27\ The strong evidence describing the role of COHb
in CO toxicity is important to consider in interpreting the CO
epidemiological studies and contributes to the biological plausibility
of the ischemia-related health outcomes that have been associated with
ambient CO concentrations. Yet, we do not have information on the COHb
levels of epidemiological study subjects that we can evaluate in the
context of the COHb levels eliciting health effects in the controlled
human exposure studies. Further, we lack additional information on the
CO exposures of the epidemiological study subjects to both ambient and
nonambient sources of CO that might be used to estimate their COHb
levels and bridge the gap between the two study types. Additionally the
ISA recognizes that the changes in COHb that would likely be associated
with exposure to the low ambient CO concentrations assessed in some of
the epidemiological studies would be smaller than changes associated
with ``substantially reduced [oxygen] delivery to tissues,'' that might
plausibly lead to the outcomes observed in those studies, with
additional investigation needed to determine whether there may be
another mechanism of action for CO that contributes to the observed
outcomes at low ambient concentrations (ISA, p. 5-48). Thus, there are
uncertainties associated with the epidemiological evidence that
``complicate the quantitative interpretation of the epidemiologic
findings, particularly regarding the biological plausibility of health
effects occurring at COHb levels resulting from exposures to the
ambient CO concentrations'' assessed in these studies (ISA, p. 2-17).
---------------------------------------------------------------------------

    \27\ In the case of the only other criteria pollutant for which
the health evidence relies on an internal dose metric--lead--the
epidemiological studies also use that metric. For lead (Pb), in
contrast to CO, the epidemiological evidence is focused on
associations of Pb-related health effects with measurements of Pb in
blood, providing a direct linkage between the pollutant, via the
internal biomarker of dose, and the health effects. Thus, for Pb, as
compared to the case for CO, we have less uncertainty in our
interpretations of the epidemiological studies with regard to the
pollutant responsible for the health effects observed. For other
criteria pollutants, including PM and NO2, air
concentrations are used as the exposure/dose metric in both the
epidemiological studies and the other types of health evidence.
Thus, there is no comparable aspect in the PM or NO2
evidence base.
---------------------------------------------------------------------------

    With regard to health effects other than cardiovascular outcomes,
in addition to noting the complications cited above with regard to
quantitative interpretation of the epidemiological evidence, we note
that the evidence for these other categories of health effects is
considered limited and only suggestive of a causal relationship with
relevant exposures to CO in ambient air, or inadequate to infer such a
relationship, or it supports the conclusion that such a relationship is
not likely (see section II.A.2.b above). As described in the proposal
sections II.B.2 and II.D.2.a, with regard to categories of health
effects or outcomes for which the evidence is considered suggestive,
evidence is lacking that might lend biological plausibility to
epidemiological study results, and also sufficiently rule out the role
of chance, bias and confounding in the epidemiological associations
observed, for outcomes such as developmental or respiratory (ISA,
chapters 1 and 2).
    Thus, EPA disagrees with the commenters' conclusion that the
epidemiological evidence establishes that a range of health effects,
including developmental or respiratory effects, are occurring as a
result of exposures to CO in ambient air at or below the current
standards. We additionally disagree with commenters' statements that
imply EPA has inadequately considered the evidence with regard to
protection of sensitive populations and to the protection provided by
the CO standards. As noted in section II.A.2.b above, EPA's assessment
of the current evidence presented in the Integrated Science Assessment
concludes that ``the most important susceptibility characteristic for
increased risk due to CO exposure is [CAD or CHD]'' (ISA, p. 2-10).
Accordingly, the proposal recognized people with cardiovascular disease
as a key population at risk from short-term ambient CO exposures
(proposal, section II.D.4). However, based on assessment of the
evidence in the ISA, the proposal and other documents in this review
also recognize the potential for susceptibility for several other
populations and lifestages, including people with pre-existing diseases
that may already have limited oxygen availability to tissues, increased
COHb levels or increased endogenous CO production, older adults, and
fetuses during critical phases of development (as summarized in section
II.A.2.b above). For these groups and lifestages, the evidence is
incomplete with regard to specific CO exposures or COHb levels that may
be associated with health effects in these groups and the nature of
those effects, as well as a way to relate the specific evidence
available for the CAD population to the limited evidence for these
other populations. Further, the currently available evidence does not
indicate a greater susceptibility for any of the other populations or
lifestages recognized as potentially at risk from exposure to ambient
CO. In reaching a decision on the adequacy of the current standards in
protecting public health in section II.B.3 below, however, the
Administrator has considered EPA's conclusions with regard to the
effects likely to be causally associated with exposure to ambient CO
and population groups particularly at risk, as well as those regarding
the evidence with regard to the potential for other effects and
sensitive groups, and the associated uncertainty. In so doing, as
indicated below, the Administrator judges the current standards to
provide the requisite protection for public health, including the
health of sensitive populations, with an adequate margin of safety.
3. Conclusions Concerning Adequacy of the Primary Standards
    Having carefully considered the public comments, as discussed
above, the Administrator believes that the fundamental scientific
conclusions on the effects of CO in ambient air reached in the
Integrated Science Assessment and Policy Assessment, summarized in
sections II.B and II.D of the proposal remain valid. Additionally, the
Administrator believes the judgments she reached in the proposal
(section II.D.4) with regard to consideration of the evidence and
quantitative exposure/dose assessments and advice from CASAC remain
appropriate. Thus, as described below, the Administrator concludes that
the current primary standards provide the requisite protection of
public health with an adequate margin of safety and should be
retained.\28\
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    \28\ As explained below in section IV.A, EPA is repromulgating
the Federal Reference Method (FRM) for CO, as set forth in Appendix
C of 40 CFR part 50. Consistent with EPA's decision to retain the
standards, the recodification clarifies and updates the text of the
FRM, but does not make substantive changes to it.
---------------------------------------------------------------------------

    In considering the adequacy of the current suite of primary CO
standards, the Administrator has carefully considered the available
evidence and conclusions contained in the Integrated Science
Assessment; the information, exposure/dose assessment, rationale and
conclusions presented in the Policy

Assessment; the advice and recommendations from CASAC; and public
comments. The Administrator places primary consideration on the
evidence obtained from controlled human exposure studies that
demonstrates a reduction in time to onset of exercise-induced markers
of myocardial ischemia in response to increased COHb resulting from
short-term CO exposures, and recognizes the greater significance
accorded both to larger reductions in time to myocardial ischemia and
to more frequent occurrences of myocardial ischemia. As at the time of
the review completed in 1994, the Administrator also takes note of the
results for the modeling of exposures to ambient CO under conditions
simulated to just meet the current, controlling, 8-hour standard in two
study areas, as described in the REA and Policy Assessment, and the
public health significance of those results. She also considers the
newly available and much-expanded epidemiological evidence, including
the complexity associated with quantitative interpretation of these
studies, particularly the few studies available in areas where the
current standards are met. In so doing, she notes that in considering
the adequacy of the current standards, it is important to consider both
the extent to which the evidence supports a causal relationship between
ambient CO exposures and adverse health effects, as well as the extent
to which there is evidence pertinent to such effects under air quality
conditions in which the current standards are met. Further, the
Administrator considers the advice of CASAC, including both their
overall agreement with the Policy Assessment conclusion that the
current evidence and quantitative exposure and dose estimates provide
support for retaining the current standards, as well as their view that
in light of the epidemiological studies, revisions to lower the
standards should be considered and their preference for a lower
standard.
    As an initial matter, the Administrator places weight on the long-
standing evidence base that has established key aspects of CO toxicity
that are relevant to this review as they were to the review completed
in 1994. These aspects include the key role played by hypoxia (reduced
oxygen availability) induced by increased COHb blood levels, the
identification of people with cardiovascular disease as a key
population at risk from short-term ambient CO exposures, and the use of
COHb as the bioindicator and dose metric for evaluating CO exposure and
the potential for health effects. The Administrator also recognizes the
Integrated Science Assessment's conclusion that a causal relationship
is likely to exist between relevant short-term exposures to CO and
cardiovascular morbidity.
    In placing weight on the controlled human exposure studies, the
Administrator also recognizes the uncertain health significance
associated with the smaller responses to the lowest COHb level assessed
in the study given primary consideration in this review (Allred et al.,
1989a, 1989b, 1991) and with single occurrences of such responses. In
the study by Allred et al. (1989a, 1989b, 1991), a 4-5% reduction in
time (approximately 30 seconds) to the onset of exercise-induced
markers of myocardial ischemia was associated with the 2% COHb level
induced by 1-hour CO exposure. In considering the significance of the
magnitude of the time decrement to onset of myocardial ischemia
observed at the 2% COHb level induced by short-term CO exposure, as
well as the potential for myocardial ischemia to lead to more adverse
outcomes, the EPA generally places less weight on the health
significance associated with infrequent or rare occurrences of COHb
levels at or just above 2% as compared to that associated with repeated
occurrences and occurrences of appreciably higher COHb levels in
response to short-term CO exposures. For example, at the 4% COHb level,
the study by Allred et al., (1989a, 1989b, 1991) observed a 7-12%
reduction in time to the onset of exercise-induced markers of
myocardial ischemia. The Administrator places more weight on this
greater reduction in time to onset of exercise-induced markers compared
to the reduction in time to onset at 2% COHb. The Administrator also
notes that at the time of the 1994 review, an intermediate level of
approximately 3% COHb was identified as a level at which adverse
effects had been demonstrated in persons with angina. Now, as at the
time of the 1994 review, the Administrator primarily considers the 2%
COHb level, resulting from 1-hour CO exposure, in the context of a
margin of safety against effects of concern that have been associated
with higher COHb levels, such as 3-4% COHb.
    The Administrator additionally takes note of the now much-expanded
evidence base of epidemiological studies, including the multiple
studies that observe positive associations between cardiovascular
outcomes and short-term ambient CO concentrations across a range of CO
concentrations, including conditions above as well as below the current
NAAQS. She notes particularly the Integrated Science Assessment
conclusion that the findings of CO-associated cardiovascular effects in
these studies are logically coherent with the larger, long-standing
health effects evidence base for CO and the conclusions drawn from it
regarding cardiovascular disease-related susceptibility. In further
considering the epidemiological evidence base with regard to the extent
to which it provides support for conclusions regarding adequacy of the
current standards, the Administrator takes note of CASAC's conclusions
that ``[i]f the epidemiological evidence is given additional weight,
the conclusion could be drawn that health effects are occurring at
levels below the current standard, which would support the tightening
of the current standard'' (Brain and Samet, 2010c). Additionally, the
Administrator places weight on the final Policy Assessment
consideration of aspects that complicate quantitative interpretation of
the epidemiological studies with regard to ambient concentrations that
might be eliciting the reported health outcomes.
    For purposes of evaluating the adequacy of the current standards,
the Administrator takes note of the multiple complicating features of
the epidemiological evidence base, as described in more detail in the
final Policy Assessment and in section II.D.2.a of the proposal. First,
while a number of studies observed positive associations of
cardiovascular disease-related outcomes with short-term CO
concentrations, very few of these studies were conducted in areas that
met the current standards throughout the period of study. Additionally,
in CASAC's advice regarding interpretation of the currently available
evidence, they stated that ``[t]he problem of co-pollutants serving as
potential confounders is particularly problematic for CO'' and that
given the currently low ambient CO levels, there is a possibility that
CO is acting as a surrogate for a mix of pollutants generated by fossil
fuel combustion. The CASAC further stated that ``[a] better
understanding of the possible role of co-pollutants is relevant to
regulation'' (Brain and Samet, 2010d). As described in the Policy
Assessment and summarized in section II.B.2 above, there are also
uncertainties related to representation of ambient CO exposures given
the steep concentration gradient near roadways, as well as the
prevalence of measurements below the MDL across the database. The CASAC
additionally indicated the need to consider the potential for
confounding effects of

indoor sources of CO (Brain and Samet, 2010c). As discussed in section
II.D.2.a of the proposal, the interpretation of epidemiological studies
for CO is further complicated because, in contrast to the situation for
all other criteria pollutants, the epidemiological studies for CO use
an exposure/dose metric (air concentration) that differs from the
metric commonly used in the other key CO health studies (COHb).
    The Administrator notes that although CASAC expressed a preference
for a lower standard, CASAC also indicated that the current evidence
provides support for retaining the current suite of standards. CASAC's
recommendations appear to recognize that their preference for a lower
standard was contingent on a judgment as to the weight to be placed on
the epidemiological evidence. Further, as noted above and summarized in
section II.C.2, CASAC has provided a range of advice regarding
interpretation of the CO epidemiological studies in light of the
associated uncertainties. Accordingly, in consideration of the current
evidence with regard to conclusions to be drawn as to the adequacy of
the current standards, the Administrator gives consideration to the
full breadth of CASAC's advice.
    In considering the evidence and quantitative exposure and dose
estimates available in this review with regard to the adequacy of
public health protection provided by the current primary standards, the
Administrator recognizes that, as noted in section II.B. above, the
final decision on such judgments is largely a public health policy
judgment, which draws upon scientific information and analyses about
health effects and risks, as well as judgments about how to consider
the range and magnitude of uncertainties that are inherent in the
information and analyses. These judgments are informed by the
recognition that the available health effects evidence generally
reflects a continuum, consisting of ambient levels at which scientists
generally agree that health effects are likely to occur, through lower
levels at which the likelihood and magnitude of the response become
increasingly uncertain. Accordingly, the final decision requires
judgment based on an interpretation of the evidence and other
information that neither overstates nor understates the strength and
limitations of the evidence and information nor the appropriate
inferences to be drawn. As described in section I.A above, the Act does
not require that primary standards be set at a zero-risk level; the
NAAQS must be sufficient but not more stringent than necessary to
protect public health, including the health of sensitive groups, with
an adequate margin of safety.
    In considering the judgments to be made regarding adequacy of the
level of protection provided by the current standards, the
Administrator takes particular note of the findings of the exposure and
dose assessment in light of considerations discussed above regarding
the weight given to different COHb levels and their frequency of
occurrence. As described in the proposal, the exposure and dose
assessment results indicate that only a very small percentage of the
at-risk population is estimated to experience a single occurrence in a
year of daily maximum COHb at or above 3.0% COHb under conditions just
meeting the current 8-hour standard in the two study areas evaluated,
and no multiple occurrences are estimated. The Administrator also notes
the results indicating that only a small percentage of the at-risk
populations are estimated to experience a single occurrence of 2% COHb
in a year under conditions just meeting the standard, and still fewer
are estimated to experience multiple such occurrences. Additionally,
consistent with findings of the assessment performed for the review
completed in 1994, less than 0.1% of person-days for the at-risk
populations were estimated to include occurrences of COHb at or above
2% COHb. Taken together, the Administrator judges the current standard
to provide a very high degree of protection for the COHb levels and
associated health effects of concern, as indicated by the extremely low
estimates of occurrences, and to provide slightly less but a still high
degree of protection for the effects associated with lower COHb levels,
the physiological significance of which is less clear.
    In further considering the adequacy of the margin of safety
provided by the current standards, the Administrator has additionally
considered conclusions drawn in the Integrated Science Assessment and
Policy Assessment with regard to interpretation of the limited and less
certain information concerning a relationship between exposure to
relevant levels of ambient CO and health effects in other, potentially,
susceptible groups, and with regard to the uncertainties concerning
quantitative interpretation of the available epidemiological studies.
In so doing, the Administrator additionally judges the current
standards to provide adequate protection against the risk of other
health effects for which the evidence is less certain. Further, the
Administrator concludes that consideration of the epidemiological
studies does not lead her to identify a need for any greater
protection. For these and all of the reasons discussed above, and
recognizing the CASAC conclusion that, overall, the current evidence
and REA results provide support for retaining the current standards,
the Administrator concludes that the current suite of primary CO
standards is requisite to protect public health with an adequate margin
of safety from effects of ambient CO.

III. Consideration of a Secondary Standard

    As noted in section I.A. above, section 109(b) of the Clean Air Act
requires the Administrator to establish secondary standards that, in
the judgment of the Administrator, are requisite to protect the public
welfare from any known or anticipated adverse effects associated with
the presence of the pollutant in the ambient air. In so doing, the
Administrator seeks to establish standards that are neither more nor
less stringent than necessary for this purpose. The Act does not
require that secondary standards be set to eliminate all risk of
adverse welfare effects, but rather at a level requisite to protect
public welfare from those effects that are judged by the Administrator
to be adverse.
    This section presents the rationale for the Administrator's final
decision not to set a secondary NAAQS for CO. In considering the
current air quality criteria, evidence of CO-related welfare effects at
or near ambient levels that are unrelated to climate has not been
identified. Accordingly, in considering whether a secondary standard is
requisite to protect the public welfare, the Administrator has
primarily considered conclusions based on the evidence of a role for CO
in effects on climate. Evaluation of this evidence in the Integrated
Science Assessment and staff considerations in the Policy Assessment
highlighted the limitations in this evidence and provided information
indicating that this role for atmospheric CO is predominantly indirect,
through its role in chemical reactions in the atmosphere which result
in increased concentrations of pollutants with direct contributions to
the greenhouse effect or that deplete stratospheric ozone. Given the
evaluation of the evidence, as well as the views of CASAC, the
Administrator concludes that no secondary standard should be set at
this time because, as in the past reviews, having no standard is
requisite to protect public welfare from any known or anticipated
adverse effects from ambient CO exposures.
    In this section, we first summarize the evidence currently
available for welfare

effects to inform decisions in this review in section III.A. Next, the
rationale for the proposed conclusions is summarized in section III.B.
Public comments and CASAC advice regarding consideration of a secondary
standard in this review are summarized in section III.C. Lastly, the
Administrator's final conclusions with regard to a secondary standard
for CO are presented in section III.D.

A. Introduction

    In evaluating whether establishment of a secondary standard for CO
is appropriate at this time, we adopted an approach in this review that
builds upon the general approach used in the last review and reflects
the broader body of evidence and information now available.
Consideration of the evidence available in this review focuses on the
following overarching question: Does the currently available scientific
information provide support for considering the establishment of a
secondary standard for CO?
    In considering this overarching question, the Policy Assessment
first noted that the extensive literature search performed for the
current review did not identify any evidence of public welfare effects
of CO unrelated to climate at or near ambient levels (ISA, section 1.3
and p. 1-3). However, ambient CO has been associated with welfare
effects related to climate (ISA, section 3.3). Climate-related effects
of CO were considered for the first time in the 2000 AQCD and are given
somewhat greater focus in the current ISA relative to the 2000 AQCD in
reflection of comments from CASAC and increased attention to the role
of CO in climate forcing (Brain and Samet, 2009; ISA, section 3.3).
Based on the current evidence, the ISA concludes that ``a causal
relationship exists between current atmospheric concentrations of CO
and effects on climate'' (ISA, section 2.2). Accordingly, the
discussion in the Policy Assessment (summarized in the proposal)
focuses on climate-related effects of CO in addressing the question
posed above.
    The currently available information summarized in the ISA (ISA
section, 3.3) does not alter the current well-established understanding
of the role of urban and regional CO in continental and global-scale
chemistry, as outlined in the 2000 AQCD (PA, section 3.2). CO absorbs
outgoing thermal infrared radiation very weakly; thus, the direct
contribution of CO itself to climate forcing (or greenhouse warming) is
very small (ISA, p. 3-11). Rather, the most significant effects on
climate are indirect, resulting from CO's role as the major atmospheric
sink for hydroxyl radicals. Through this role of CO in global
atmospheric chemistry, CO influences the abundance of chemically
reactive, major greenhouse gases, such as methane and ozone, that
contribute directly to the greenhouse effect and of other gases that
exert their effect on climate through depletion of stratospheric ozone
(ISA, section 3.3 and p. 3-11). There is significant uncertainty
concerning this effect, and it appears to be highly variable, with the
ISA recognizing that climate effects of changes to emissions of a
short-lived pollutant such as CO are very likely dependent on localized
conditions (ISA section 3.3, pp. 3-12, 3-15, 3-16). As noted in the
ISA, however, ``the indirect [global warming potential] values
evaluated and summarized by [the Intergovernmental Panel on Climate
Change] are global and cannot reflect effects of localized emissions or
emissions changes'' (ISA at p. 3-16). Accordingly, the Policy
Assessment stated that, as a result of the spatial and temporal
variation in emissions and concentrations of CO and the localized
chemical interdependencies that cause the indirect climate effects of
CO, it is highly problematic to evaluate the indirect effects of CO on
climate (PA, p. 3-3).
    Based upon the information and considerations summarized above, the
Policy Assessment concluded as an initial matter that, with respect to
non-climate welfare effects, including ecological effects and impacts
to vegetation, there is no currently available scientific information
that supports a CO secondary standard (PA, section 3.4). Secondly, with
respect to climate-related effects, the Policy Assessment recognized
the evidence of climate forcing effects associated with CO, most
predominantly through its participation in chemical reactions in the
atmosphere which contribute to increased concentrations of other more
direct acting climate-forcing pollutants (ISA, sections 2.2 and 3.3).
The PA also noted, however, that the available information provides no
basis for estimating how localized changes in the temporal and spatial
patterns of ambient CO likely to occur across the U.S. with (or
without) a secondary standard would affect local, regional, or
nationwide changes in climate. Moreover, more than half of the indirect
forcing effect of CO is attributable to ozone (O3)
formation, and welfare-related effects of O3 are more
appropriately considered in the context of the review of the
O3 NAAQS, rather than in this CO NAAQS review (PA, section
3.4). For these reasons, the Policy Assessment concluded that there is
insufficient information at this time to support the consideration of a
secondary standard based on CO effects on climate processes (PA,
section 3.4).

B. Rationale for Proposed Decision

    In considering a secondary standard for CO, the proposed
conclusions presented in the proposal were based on the assessment and
integrative synthesis of the scientific evidence presented in the ISA,
building on the evidence described in the 2000 AQCD, as well as staff
consideration of this evidence in the Policy Assessment and CASAC
advice. As an initial matter, the proposal concluded that the currently
available scientific information with respect to non-climate welfare
effects, including ecological effects and impacts to vegetation, does
not support a CO secondary standard. Secondly, with respect to climate-
related effects, the proposal took note of staff considerations in the
Policy Assessment and concurred with staff conclusions that information
is insufficient at this time to provide support for a CO secondary
standard. Thus, based on consideration of the evidence, staff
considerations in the Policy Assessment, as well as the views of CASAC,
the Administrator proposed to conclude that no secondary standards
should be set at this time because, as in the past reviews, having no
standard is requisite to protect public welfare from any known or
anticipated adverse effects from ambient CO exposures.

C. Comments on Consideration of Secondary Standard

    In considering the need for a secondary standard, the Administrator
first notes the advice and recommendations from CASAC based on their
review of two drafts of the Integrated Science Assessment and of the
draft Policy Assessment. With regard to consideration of a secondary
standard for CO, CASAC noted without objection or disagreement the
staff's conclusions that there is insufficient information to support
consideration of a secondary standard at this time (Brain and Samet,
2010c). One public comment generally concerning EPA's proposed decision