[Federal Register Volume 80, Number 206 (Monday, October 26, 2015)]
[Rules and Regulations]
[Pages 65291-65468]
[FR Doc No: 2015-26594]

Vol. 80

Monday,

No. 206

October 26, 2015

Part II

Environmental Protection Agency

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40 CFR Part 50, 51, 52, et al.

 National Ambient Air Quality Standards for Ozone; Final Rule

Federal Register / Vol. 80 , No. 206 / Monday, October 26, 2015 /
Rules and Regulations

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Parts 50, 51, 52, 53, and 58

[EPA-HQ-OAR-2008-0699; FRL-9933-18-OAR]
RIN 2060-AP38

National Ambient Air Quality Standards for Ozone

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: Based on its review of the air quality criteria for ozone
(O3) and related photochemical oxidants and national ambient
air quality standards (NAAQS) for O3, the Environmental
Protection Agency (EPA) is revising the primary and secondary NAAQS for
O3 to provide requisite protection of public health and
welfare, respectively. The EPA is revising the levels of both standards
to 0.070 parts per million (ppm), and retaining their indicators
(O3), forms (fourth-highest daily maximum, averaged across
three consecutive years) and averaging times (eight hours). The EPA is
making corresponding revisions in data handling conventions for
O3 and changes to the Air Quality Index (AQI); revising
regulations for the prevention of significant deterioration (PSD)
program to add a transition provision for certain applications; and
establishing exceptional events schedules and providing information
related to implementing the revised standards. The EPA is also revising
the O3 monitoring seasons, the Federal Reference Method
(FRM) for monitoring O3 in the ambient air, Federal
Equivalent Method (FEM) analyzer performance requirements, and the
Photochemical Assessment Monitoring Stations (PAMS) network. Along with
exceptional events schedules related to implementing the revised
O3 standards, the EPA is applying this same schedule
approach to other future new or revised NAAQS and removing obsolete
regulatory language for expired exceptional events deadlines. The EPA
is making minor changes to the procedures and time periods for
evaluating potential FRMs and equivalent methods, including making the
requirements for nitrogen dioxide (NO2) consistent with the
requirements for O3, and removing an obsolete requirement
for the annual submission of Product Manufacturing Checklists by
manufacturers of FRMs and FEMs for monitors of fine and coarse
particulate matter. For a more detailed summary, see the Executive
Summary below.

DATES: The final rule is effective on December 28, 2015.

ADDRESSES: EPA has established a docket for this action (Docket ID No.
EPA-HQ-OAR-2008-0699) and a separate docket, established for the
Integrated Science Assessment (ISA) (Docket No. EPA-HQ-ORD-2011-0050),
which has been incorporated by reference into the rulemaking docket.
All documents in the docket are listed on the www.regulations.gov Web
site. Although listed in the docket index, some information is not
publicly available, e.g., confidential business information or other
information whose disclosure is restricted by statute. Certain other
material, such as copyrighted material, is not placed on the Internet
and may be viewed, with prior arrangement, at the EPA Docket Center.
Publicly available docket materials are available either electronically
in www.regulations.gov or in hard copy at the Air and Radiation Docket
and Information Center, EPA/DC, WJC West Building, Room 3334, 1301
Constitution Ave., NW., Washington, DC. The Public Reading Room is open
from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal
holidays. The telephone number for the Public Reading Room is (202)
566-1744 and the telephone number for the Air and Radiation Docket and
Information Center is<PHONE_NUMBER>. For additional information about
EPA's public docket, visit the EPA Docket Center homepage at: http://www.epa.gov/epahome/dockets.htm.

FOR FURTHER INFORMATION CONTACT: Ms. Susan Lyon Stone, Health and
Environmental Impacts Division, Office of Air Quality Planning and
Standards, U.S. Environmental Protection Agency, Mail code C504-06,
Research Triangle Park, NC 27711; telephone:<PHONE_NUMBER>; fax: (919)
541-0237; email<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

General Information

Availability of Related Information

    A number of the documents that are relevant to this action are
available through the EPA's Office of Air Quality Planning and
Standards (OAQPS) Technology Transfer Network (TTN) Web site (http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_index.html). These documents
include the Integrated Science Assessment for Ozone (U.S. EPA, 2013),
available at http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_isa.html; the Health Risk and Exposure Assessment and the
Welfare Risk and Exposure Assessment for Ozone, Final Reports (HREA and
WREA, respectively; U.S. EPA, 2014a, 2014b), available at http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_rea.html; and the
Policy Assessment for the Review of the Ozone National Ambient Air
Quality Standards (PA; U.S. EPA, 2014c), available at http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_2008_pa.html. These and
other related documents are also available for inspection and copying
in the EPA docket identified above.

Table of Contents

    The following topics are discussed in this preamble:

Executive Summary
I. Background
    A. Legislative Requirements
    B. Related Control Programs
    C. Review of Air Quality Criteria and Standards for
O3
    D. Ozone Air Quality
    E. Summary of Proposed Revisions to the O3 Standards
    F. Organization and Approach to Decisions in This O3
NAAQS Review
II. Rationale for Decision on the Primary Standard
    A. Introduction
    1. Overview of Health Effects Evidence
    2. Overview of Human Exposure and Health Risk Assessments
    B. Need for Revision of the Primary Standard
    1. Basis for Proposed Decision
    2. Comments on the Need for Revision
    3. Administrator's Conclusions on the Need for Revision
    C. Conclusions on the Elements of a Revised Primary Standard
    1. Indicator
    2. Averaging Time
    3. Form
    4. Level
    D. Decision on the Primary Standard
III. Communication of Public Health Information
    A. Proposed Revisions to the AQI
    B. Comments on Proposed Revisions to the AQI
    C. Final Revisions to the AQI
IV. Rationale for Decision on the Secondary Standard
    A. Introduction
    1. Overview of Welfare Effects Evidence
    2. Overview of Welfare Exposure and Risk Assessment
    3. Potential Impacts on Public Welfare
    B. Need for Revision of the Secondary Standard
    1. Basis for Proposed Decision
    2. Comments on the Need for Revision
    3. Administrator's Conclusions on the Need for Revision
    C. Conclusions on Revision of the Secondary Standard
    1. Basis for Proposed Revision
    2. Comments on Proposed Revision
    3. Administrator's Conclusions on Revision
    D. Decision on the Secondary Standard
V. Appendix U: Interpretation of the Primary and Secondary NAAQS for
O3

    A. Background
    B. Data Selection Requirements
    C. Data Reporting and Data Handling Requirements
    D. Exceptional Events Information Submission Schedule
VI. Ambient Monitoring Related to O3 Standards
    A. Background
    B. Revisions to the Length of the Required O3
Monitoring Seasons
    1. Proposed Changes to the Length of the Required O3
Monitoring Seasons
    2. Comments on the Length of the Required O3
Monitoring Seasons
    3. Final Decisions on the Length of the Required O3
Monitoring Seasons
    C. Revisions to the PAMS Network Requirements
    1. Network Design
    2. Speciated VOC Measurements
    3. Carbonyl Measurements
    4. Nitrogen Oxides Measurements
    5. Meteorology Measurements
    6. PAMS Season
    7. Timing and Other Implementation Issues
    D. Addition of a New FRM for O3
    1. Proposed Changes to the FRM for O3
    2. Comments on the FRM for O3
    E. Revisions to the Analyzer Performance Requirements
    1. Proposed Changes to the Analyzer Performance Requirements
    2. Comments on the Analyzer Performance Requirements
VII. Grandfathering Provision for Certain PSD Permits
    A. Summary of the Proposed Grandfathering Provision
    B. Comments and Responses
    C. Final Action and Rationale
VIII. Implementation of the Revised O3 Standards
    A. NAAQS Implementation Plans
    1. Cooperative Federalism
    2. Additional New Rules and Guidance
    3. Background O3
    4. Section 110 State Implementation Plans
    5. Nonattainment Area Requirements
    B. O3 Air Quality Designations
    1. Area Designation Process
    2. Exceptional Events
    C. How do the New Source Review (NSR) requirements apply to the
revised O3 NAAQS?
    1. NSR Requirements for Major Stationary Sources for the Revised
O3 NAAQS
    2. Prevention of Significant Deterioration (PSD) Program
    3. Nonattainment NSR
    D. Transportation and General Conformity
    1. What are Transportation and General Conformity?
    2. When would Transportation and General Conformity apply to
areas designated nonattainment for the revised O3 NAAQS?
    3. Impact of a Revised O3 NAAQS on a State's Existing
Transportation and/or General Conformity SIP
    E. Regional and International Pollution Transport
    1. Interstate Transport
    2. International Transport
IX. 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 & 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 (CRA)

References

Executive Summary

    This section summarizes information about the purpose of this
regulatory action, the major provisions of this action, and provisions
related to implementation.

Purpose of This Regulatory Action

    Sections 108 and 109 of the Clean Air Act (CAA) govern the
establishment, review, and revision, as appropriate, of the NAAQS to
protect public health and welfare. The CAA requires the EPA to
periodically review the air quality criteria--the science upon which
the standards are based--and the standards themselves. This rulemaking
is being conducted pursuant to these statutory requirements. The
schedule for completing this review is established by a federal court
order, which requires that the EPA make a final determination by
October 1, 2015.
    The EPA completed its most recent review of the NAAQS for
O3 in 2008. As a result of that review, EPA took four
principal actions: (1) Revised the level of the 8-hour primary standard
to 0.075 ppm; (2) expressed the standard to three decimal places; (3)
revised the 8-hour secondary standard by making it identical to the
revised primary standard; and (4) made conforming changes to the AQI.
    In subsequent litigation, the U.S. Court of Appeals for the
District of Columbia Circuit (DC Circuit) upheld the EPA's 2008 primary
standard but remanded the 2008 secondary standard (Mississippi v. EPA,
744 F. 3d 1334 [D.C. Cir. 2013]). With respect to the primary standard,
the court held that the EPA reasonably determined that the existing
primary standard, set in 1997, did not protect public health with an
adequate margin of safety and required revision. In upholding the EPA's
revised primary standard, the court dismissed arguments that the EPA
should have adopted a more stringent standard. The court remanded the
secondary standard to the EPA after finding that the EPA's
justification for setting the secondary standard identical to the
revised 8-hour primary standard violated the CAA because the EPA had
not adequately explained how that standard provided the required public
welfare protection. In remanding the 2008 secondary standard, the court
did not vacate it. The EPA has addressed the court's remand with this
final action.
    This final action reflects the Administrator's conclusions based on
a review of the O3 NAAQS that began in September 2008, and
also concludes the EPA's reconsideration of the 2008 decision that it
initiated in 2009 and subsequently consolidated with the current
review. In conducting this review, the EPA has carefully evaluated the
currently available scientific literature on the health and welfare
effects of O3, focusing particularly on the new literature
available since the conclusion of the previous review in 2008. Between
2008 and 2014, the EPA prepared draft and final versions of the
Integrated Science Assessment, the Health and Welfare Risk and Exposure
Assessments, and the Policy Assessment. Multiple drafts of these
documents were subject to public review and comment, and, as required
by the CAA, were peer-reviewed by the Clean Air Scientific Advisory
Committee (CASAC), an independent scientific advisory committee
established pursuant to the CAA and charged with providing advice to
the Administrator.
    The EPA proposed revisions to the primary and secondary
O3 NAAQS on December 17, 2014 (79 FR 75234), and provided a
3-month period for submission of comments from the public. In addition
to written comments submitted to EPA, comments were also provided at
public hearings held in Washington, DC, and Arlington, Texas, on
January 29, 2015, and in Sacramento, California, on February 2, 2015.
After consideration of public comments and the advice from the CASAC,
the EPA has developed this final rulemaking, which is the final step in
the review process.
    In this rulemaking, the EPA is revising the suite of standards for
O3 to provide requisite protection of public health and
welfare. In addition, the EPA is updating the AQI, and making changes
in the data handling conventions and ambient air monitoring, reporting,
and network

design requirements to correspond with the changes to the O3
NAAQS.

Summary of Major Provisions

    With regard to the primary standard, the EPA is revising the level
of the standard to 0.070 ppm to provide increased public health
protection against health effects associated with long- and short-term
exposures. The EPA is retaining the indicator (O3),
averaging time (8-hour) and form (annual fourth-highest daily maximum,
averaged over 3 years) of the existing standard. This action provides
increased protection for children, older adults, and people with asthma
or other lung diseases, and other at-risk populations against an array
of adverse health effects that include reduced lung function, increased
respiratory symptoms and pulmonary inflammation; effects that
contribute to emergency department visits or hospital admissions; and
mortality.
    The decisions on the adequacy of the current standard and the
appropriate level for the revised standard are based on an integrative
assessment of an extensive body of new scientific evidence, which
substantially strengthens what was known about O3-related
health effects in the last review. The revised standard also reflects
consideration of a quantitative risk assessment that estimates public
health risks likely to remain upon just meeting the current and various
alternative standards. Based on this information, the Administrator
concludes that the current primary O3 standard is not
requisite to protect public health with an adequate margin of safety,
as required by the CAA, and that revision of the level to 0.070 ppm is
warranted to provide the appropriate degree of increased public health
protection for at-risk populations against an array of adverse health
effects. In concluding that a revised primary standard set at a level
of 0.070 ppm is requisite to protect public health with an adequate
margin of safety, the Administrator relies on several key pieces of
information, including: (a) A level of 0.070 ppm is well below the
O3 exposure concentration shown to cause the widest range of
respiratory effects (i.e., 0.080 ppm) and is below the lowest
O3 exposure concentration shown to cause the adverse
combination of decreased lung function and increased respiratory
symptoms (i.e., 0.072 ppm); (b) a level of 0.070 ppm will eliminate, or
nearly eliminate, repeated occurrence of these O3 exposure
concentrations (this is important because the potential for adverse
effects increases with frequency of occurrence); (c) a level of 0.070
ppm will protect the large majority of the population, including
children and people with asthma, from lower exposure concentrations,
which can cause lung function decrements and airway inflammation in
some people (i.e., 0.060 ppm); and (d) a level of 0.070 ppm will result
in important reductions in the risk of O3-induced lung
function decrements as well as the risk of O3-associated
hospital admissions, emergency department visits, and mortality. In
addition, the revised level of the primary standard is within the range
that CASAC advised the Agency to consider.
    The EPA is also revising the level of the secondary standard to
0.070 ppm to provide increased protection against vegetation-related
effects on public welfare. The EPA is retaining the indicator
(O3), averaging time (8-hour) and form (annual fourth-
highest daily maximum, averaged over 3 years) of the existing secondary
standard. This action, reducing the level of the standard, provides
increased protection for natural forests in Class I and other similarly
protected areas against an array of vegetation-related effects of
O3. The Administrator is making this decision based on
judgments regarding the currently available welfare effects evidence,
the appropriate degree of public welfare protection for the revised
standard, and currently available air quality information on seasonal
cumulative exposures that may be allowed by such a standard.
    In making this decision on the secondary standard, the
Administrator focuses on O3 effects on tree seedling growth
as a proxy for the full array of vegetation-related effects of
O3, ranging from effects on sensitive species to broader
ecosystem-level effects. Using this proxy in judging effects to public
welfare, the Administrator has concluded that the requisite protection
will be provided by a standard that generally limits cumulative
seasonal exposures to 17 ppm-hours (ppm-hrs) or lower, in terms of a 3-
year W126 index. Based on air quality analyses which indicate such
control of cumulative seasonal exposures will be achieved with a
standard set at a level of 0.070 ppm (and the same indicator, averaging
time, and form as the current standard), the Administrator concludes
that a standard revised in this way will provide the requisite
protection. In addition to providing protection of natural forests from
growth-related effects, the revised standard is also expected to
provide increased protection from other effects of potential public
welfare significance, including crop yield loss and visible foliar
injury. Thus, based on all of the information available in this review,
the Administrator concludes that the current secondary O3
standard is not requisite to protect public welfare as required by the
CAA, and that this revision will provide appropriate protection against
known or anticipated adverse effects to the public welfare.

Provisions Related to Implementation

    As directed by the CAA, reducing pollution to meet NAAQS always has
been a shared task, one involving the federal government, states,
tribes and local air agencies. This partnership has proved effective
since the EPA first issued O3 standards more than three
decades ago, and is evidenced by significantly lower O3
levels throughout the country. To provide a foundation that helps air
agencies build successful strategies for attaining new O3
standards, the EPA will continue to move forward with federal
regulatory programs, such as the final Tier 3 motor vehicle emissions
standards. To facilitate the development of CAA-compliant
implementation plans and strategies to attain new standards, the EPA
intends to issue timely and appropriate implementation guidance and,
where appropriate and consistent with the law, new rulemakings to
streamline regulatory burdens and provide flexibility in
implementation. Given the regional nature of O3 air
pollution, the EPA will continue to work with states to address
interstate transport of O3 and O3 precursors. The
EPA also intends to work closely with states to identify locations
affected by high background concentrations on high O3 days
due to stratospheric intrusions of O3, wildfire
O3 plumes, or long-range transport of O3 from
sources outside the U.S. and ensure that the appropriate CAA regulatory
mechanisms are employed. To this end, the EPA will be proposing
revisions to the 2007 Exceptional Events Rule and related draft
guidance addressing the effects of wildfires.
    In addition to revising the primary and secondary standards, this
action is changing the AQI to reflect the revisions to the primary
standard and also making corresponding revisions in data handling
conventions for O3, extending the O3 monitoring
season in 33 states, revising the requirements for the PAMS network,
and revising regulations for the PSD permitting program to add a
provision grandfathering certain pending permits from certain
requirements with respect to the revised standards. The preamble also
provides schedules and information related to implementing the revised
standards.

The rule also contains revisions to the schedules associated with
exceptional events demonstration submittals for the revised
O3 standards and other future revised NAAQS, and makes minor
changes related to monitoring for other pollutants.

I. Background

A. Legislative Requirements

    Two sections of the 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 Mississippi v. EPA, 744 F. 3d 1334, 1353 (D.C. Cir.
2013); Lead Industries Association v. EPA, 647 F.2d 1130, 1154 (D.C.
Cir 1980); American Petroleum Institute v. Costle, 665 F.2d 1176, 1186
(D.C. Cir. 1981); American Farm Bureau Federation v. EPA, 559 F. 3d
512, 533 (D.C. Cir. 2009); Association of Battery Recyclers v. EPA, 604
F. 3d 613, 617-18 (D.C. 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 concentrations, see
Lead Industries v. EPA, 647 F.2d at 1156 n.51; Mississippi v. EPA, 744
F. 3d at 1351, 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, the size of sensitive population(s) \3\ at risk, and the kind
and degree of the uncertainties that must be addressed. The selection
of any particular approach for 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;
Mississippi, 744 F. 3d at 1353.
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    \3\ As used here with regard to human populations, and similarly
throughout this document, the term ``population'' refers to people
having a quality or characteristic in common, including a specific
pre-existing illness or a specific age or lifestage.
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    In setting primary and secondary standards that are ``requisite''
to protect public health and welfare, respectively, as provided in
section 109(b), the EPA's task is to establish standards that are
neither more nor less stringent than necessary for these purposes. In
so doing, the 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, the CASAC \4\ has performed this independent review function.
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    \4\ Lists of CASAC members and of members of the CASAC Ozone
Review Panel are accessible from: http://yosemite.epa.gov/sab/sabpeople.nsf/WebCommittees/CASAC.
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B. Related Control Programs

    States are primarily responsible for ensuring attainment and
maintenance of NAAQS once the EPA has established them. The EPA
performs an oversight function, and as necessary takes actions to
ensure CAA objectives are achieved. Under section 110 of the CAA, and
related provisions, states submit, for the EPA's approval, state
implementation plans (SIPs) that provide for the attainment and
maintenance of such standards through control programs directed to
sources of the relevant pollutants. The states, in conjunction with the
EPA, also administer the PSD program (CAA sections 160 to 169) which is
a pre-construction permit program designed to prevent significant
deterioration in air quality. In addition, federal programs provide for
nationwide reductions in emissions of O3 precursors and
other air pollutants through new source performance standards for
stationary sources under section 111 of the CAA and the federal motor
vehicle and motor vehicle fuel control program under title II of the
CAA (sections 202

to 250), which involves controls for emissions from mobile sources and
controls for the fuels used by these sources. For some stationary
sources, the national emissions standards for hazardous air pollutants
under section 112 of the CAA may provide ancillary reductions in
O3 precursors.
    After the EPA establishes a new or revised NAAQS, the CAA directs
the EPA and the states to take steps to ensure that the new or revised
NAAQS are met. One of the first steps, known as the initial area
designations, involves identifying areas of the country that are not
meeting the new or revised NAAQS along with the nearby areas that
contain emissions sources that contribute to the areas not meeting the
NAAQS. For areas designated ``nonattainment,'' the responsible states
are required to develop SIPs to attain the standards. In developing
their attainment plans, states first take into account projected
emission reductions from federal and state rules that have been already
adopted at the time of plan submittal. A number of significant emission
reduction programs that will lead to reductions of O3
precursors are in place today or are expected to be in place by the
time revised SIPs will be due. Examples of such rules include the
Nitrogen Oxides (NOX) SIP Call and Cross-State Air Pollution
Rule (CSAPR),\5\ regulations controlling on-road and non-road engines
and fuels, hazardous air pollutant rules for utility and industrial
boilers, and various other programs already adopted by states to reduce
emissions from key emissions sources. States will then evaluate the
level of additional emission reductions needed for each nonattainment
area to attain the O3 standards ``as expeditiously as
practicable,'' and adopt new state regulations as appropriate. Section
VIII of this preamble includes additional discussion of designation and
implementation issues associated with the revised O3 NAAQS.
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    \5\ The Cross-State Air Pollution Rule was upheld by the Supreme
Court in Environmental Protection Agency v. EME Homer City
Generation, L.P., 134 S. Ct. 1584 (2014), and remanded to the D.C.
Circuit for further proceedings. The D.C. Circuit issued its
decision on remand from the Supreme Court on July 28, 2015,
remanding CSAPR to EPA, without vacating the rule, for EPA to
reconsider certain emission budgets for certain States (EME Homer
City Generation, L.P. v. Environmental Protection Agency, No. 11-
1302, 2015 WL 4528137 [D.C. Cir. July 28, 2015]).
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C. Review of Air Quality Criteria and Standards for O3

    The EPA first established primary and secondary NAAQS for
photochemical oxidants in 1971 (36 FR 8186, April 30, 1971). The EPA
set both primary and secondary standards at 0.08 ppm,\6\ as a 1-hour
average of total photochemical oxidants, not to be exceeded more than
one hour per year. The EPA based the standards on scientific
information contained in the 1970 Air Quality Criteria for
Photochemical Oxidants (AQCD; U.S. DHEW, 1970). The EPA initiated the
first periodic review of the NAAQS for photochemical oxidants in 1977.
Based on the 1978 AQCD (U.S. EPA, 1978), the EPA published proposed
revisions to the original NAAQS in 1978 (43 FR 26962, June 22, 1978)
and final revisions in 1979 (44 FR 8202, February 8, 1979). At that
time, the EPA revised the level of the primary and secondary standards
from 0.08 to 0.12 ppm and changed the indicator from photochemical
oxidants to O3, and the form of the standards from a
deterministic (i.e., not to be exceeded more than one hour per year) to
a statistical form. This statistical form defined attainment of the
standards as occurring when the expected number of days per calendar
year with maximum hourly average concentration greater than 0.12 ppm
equaled one or less.
---------------------------------------------------------------------------

    \6\ Although the level of the 2008 O3 standards are
specified in the units of ppm (i.e., 0.075 ppm), O3
concentrations are described using the units of parts per billion
(ppb) in several sections of this notice (i.e., sections II, III, IV
and VI) for consistency with the common convention for information
discussed in those sections. In ppb, 0.075 ppm is equivalent to 75.
---------------------------------------------------------------------------

    Following the EPA's decision in the 1979 review, the city of
Houston challenged the Administrator's decision arguing that the
standard was arbitrary and capricious because natural O3
concentrations and other physical phenomena in the Houston area made
the standard unattainable in that area. The U.S. Court of Appeals for
the District of Columbia Circuit (D.C. Circuit) rejected this argument,
holding (as noted above) that attainability and technological
feasibility are not relevant considerations in the promulgation of the
NAAQS. The court also noted that the EPA need not tailor the NAAQS to
fit each region or locale, pointing out that Congress was aware of the
difficulty in meeting standards in some locations and had addressed
this difficulty through various compliance related provisions in the
CAA. See API v. Costle, 665 F.2d 1176, 1184-6 (D.C. Cir. 1981).
    In 1982, the EPA announced plans to revise the 1978 AQCD (47 FR
11561; March 17, 1982), and, in 1983, the EPA initiated the second
periodic review of the O3 NAAQS (48 FR 38009; August 22,
1983). The EPA subsequently published the 1986 AQCD (U.S. EPA, 1986)
and the 1989 Staff Paper (U.S. EPA, 1989). Following publication of the
1986 AQCD, a number of scientific abstracts and articles were published
that appeared to be of sufficient importance concerning potential
health and welfare effects of O3 to warrant preparation of a
Supplement (U.S. EPA, 1992). In August of 1992, under the terms of a
court order, the EPA proposed to retain the existing primary and
secondary standards based on the health and welfare effects information
contained in the 1986 AQCD and its 1992 Supplement (57 FR 35542, August
10, 1992). In March 1993, the EPA announced its decision to conclude
this review by affirming its proposed decision to retain the standards,
without revision (58 FR 13008, March 9, 1993).
    In the 1992 notice of its proposed decision in that review, the EPA
announced its intention to proceed as rapidly as possible with the next
review of the air quality criteria and standards for O3 in
light of emerging evidence of health effects related to 6- to 8-hour
O3 exposures (57 FR 35542, August 10, 1992). The EPA
subsequently published the AQCD and Staff Paper for the review (U.S.
EPA, 1996a,b). In December 1996, the EPA proposed revisions to both the
primary and secondary standards (61 FR 65716, December 13, 1996). With
regard to the primary standard, the EPA proposed to replace the then-
existing 1-hour primary standard with an 8-hour standard set at a level
of 0.08 ppm (equivalent to 0.084 ppm based on the proposed data
handling convention) as a 3-year average of the annual third-highest
daily maximum 8-hour concentration. The EPA proposed to revise the
secondary standard either by setting it identical to the proposed new
primary standard or by setting it as a new seasonal standard using a
cumulative form. The EPA completed this review in 1997 by setting the
primary standard at a level of 0.08 ppm, based on the annual fourth-
highest daily maximum 8-hour average concentration, averaged over three
years, and setting the secondary standard identical to the revised
primary standard (62 FR 38856, July 18, 1997). In reaching her decision
on the primary standard, the Administrator identified several reasons
supporting her decision to reject a potential alternate standard set at
0.07 ppm, including first the fact that no CASAC panel member supported
a standard level lower than 0.08 ppm and her consideration of the
scientific uncertainties with regard to the health effects evidence for
exposure concentrations below 0.08 ppm. In addition to those reasons,
the Administrator noted that a standard set

at a level of 0.07 ppm would be closer to peak background
concentrations that infrequently occur in some areas due to
nonanthropogenic sources of O3 precursors (62 FR 38856,
38868; July 18, 1997).
    On May 14, 1999, in response to challenges by industry and others
to the EPA's 1997 decision, the D.C. Circuit remanded the O3
NAAQS to the EPA, finding that section 109 of the CAA, as interpreted
by the EPA, effected an unconstitutional delegation of legislative
authority. American Trucking Assoc. vs. EPA, 175 F.3d 1027, 1034-1040
(D.C. Cir. 1999) (``ATA I''). In addition, the court directed that, in
responding to the remand, the EPA should consider the potential
beneficial health effects of O3 pollution in shielding the
public from the effects of solar ultraviolet (UV) radiation, as well as
adverse health effects. Id. at 1051-53. In 1999, the EPA petitioned for
rehearing en banc on several issues related to that decision. The court
granted the request for rehearing in part and denied it in part, but
declined to review its ruling with regard to the potential beneficial
effects of O3 pollution. 195 F. 3d 4, 10 (D.C Cir., 1999)
(``ATA II''). On January 27, 2000, the EPA petitioned the U.S. Supreme
Court for certiorari on the constitutional issue (and two other
issues), but did not request review of the ruling regarding the
potential beneficial health effects of O3. On February 27,
2001, the U.S. Supreme Court unanimously reversed the judgment of the
D.C. Circuit on the constitutional issue. Whitman v. American Trucking
Assoc., 531 U. S. 457, 472-74 (2001) (holding that section 109 of the
CAA does not delegate legislative power to the EPA in contravention of
the Constitution). The Court remanded the case to the D.C. Circuit to
consider challenges to the O3 NAAQS that had not been
addressed by that court's earlier decisions. On March 26, 2002, the
D.C. Circuit issued its final decision on remand, finding the 1997
O3 NAAQS to be ``neither arbitrary nor capricious,'' and so
denying the remaining petitions for review. American Trucking
Associations, Inc. v. EPA, 283 F.3d 355, 379 (D.C Cir., 2002) (``ATA
III'').
    Specifically, in ATA III, the D.C. Circuit upheld the EPA's
decision on the 1997 O3 standard as the product of reasoned
decision making. With regard to the primary standard, the court made
clear that the most important support for EPA's decision to revise the
standard was the health evidence of insufficient protection afforded by
the then-existing standard (``the record is replete with references to
studies demonstrating the inadequacies of the old one-hour standard''),
as well as extensive information supporting the change to an 8-hour
averaging time (283 F. 3d at 378). The court further upheld the EPA's
decision not to select a more stringent level for the primary standard
noting ``the absence of any human clinical studies at ozone
concentrations below 0.08 [ppm]'' which supported the EPA's conclusion
that ``the most serious health effects of ozone are `less certain' at
low concentrations, providing an eminently rational reason to set the
primary standard at a somewhat higher level, at least until additional
studies become available'' (283 F. 3d at 378, internal citations
omitted). The court also pointed to the significant weight that the EPA
properly placed on the advice it received from CASAC (283 F. 3d at
379). In addition, the court noted that ``although relative proximity
to peak background O3 concentrations did not, in itself,
necessitate a level of 0.08 [ppm], the EPA could consider that factor
when choosing among the three alternative levels'' (283 F. 3d at 379).
    Independently of the litigation, the EPA responded to the court's
remand to consider the potential beneficial health effects of
O3 pollution in shielding the public from effects of UV
radiation. The EPA provisionally determined that the information
linking changes in patterns of ground-level O3
concentrations to changes in relevant patterns of exposures to UV
radiation of concern to public health was too uncertain, at that time,
to warrant any relaxation in 1997 O3 NAAQS. The EPA also
expressed the view that any plausible changes in UV-B radiation
exposures from changes in patterns of ground-level O3
concentrations would likely be very small from a public health
perspective. In view of these findings, the EPA proposed to leave the
1997 primary standard unchanged (66 FR 57268, Nov. 14, 2001). After
considering public comment on the proposed decision, the EPA published
its final response to this remand in 2003, re-affirming the 8-hour
primary standard set in 1997 (68 FR 614, January 6, 2003).
    The EPA initiated the fourth periodic review of the air quality
criteria and standards for O3 with a call for information in
September 2000 (65 FR 57810, September, 26, 2000). The schedule for
completion of that review was ultimately governed by a consent decree
resolving a lawsuit filed in March 2003 by plaintiffs representing
national environmental and public health organizations, who maintained
that the EPA was in breach of a nondiscretionary duty to complete
review of the O3 NAAQS within a statutorily mandated
deadline. In 2007, the EPA proposed to revise the level of the primary
standard within a range of 0.075 to 0.070 ppm (72 FR 37818, July 11,
2007). The EPA proposed to revise the secondary standard either by
setting it identical to the proposed new primary standard or by setting
it as a new seasonal standard using a cumulative form. Documents
supporting these proposed decisions included the 2006 AQCD (U.S. EPA,
2006a) and 2007 Staff Paper (U.S. EPA, 2007) and related technical
support documents. The EPA completed the review in March 2008 by
revising the level of the primary standard from 0.08 ppm to 0.075 ppm,
and revising the secondary standard to be identical to the revised
primary standard (73 FR 16436, March 27, 2008).
    In May 2008, state, public health, environmental, and industry
petitioners filed suit challenging the EPA's final decision on the 2008
O3 standards. On September 16, 2009, the EPA announced its
intention to reconsider the 2008 O3 standards, and initiated
a rulemaking to do so. At the EPA's request, the court held the
consolidated cases in abeyance pending the EPA's reconsideration of the
2008 decision.
    On January 2010, the EPA issued a notice of proposed rulemaking to
reconsider the 2008 final decision (75 FR 2938, January 19, 2010). In
that notice, the EPA proposed that further revisions of the primary and
secondary standards were necessary to provide a requisite level of
protection to public health and welfare. The EPA proposed to revise the
level of the primary standard from 0.075 ppm to a level within the
range of 0.060 to 0.070 ppm, and to revise the secondary standard to
one with a cumulative, seasonal form. At the EPA's request, the CASAC
reviewed the proposed rule at a public teleconference on January 25,
2010 and provided additional advice in early 2011 (Samet, 2010, 2011).
After considering comments from CASAC and the public, the EPA prepared
a draft final rule, which was submitted for interagency review pursuant
to Executive Order 12866. On September 2, 2011, consistent with the
direction of the President, the Administrator of the Office of
Information and Regulatory Affairs, Office of Management and Budget
(OMB), returned the draft final rule to the EPA for further
consideration. In view of this return and the fact that the Agency's
next periodic review of the O3 NAAQS required under CAA
section 109 had already begun (as announced on September 29, 2008), the
EPA decided to consolidate the

reconsideration with its statutorily required periodic review.\7\
---------------------------------------------------------------------------

    \7\ This rulemaking concludes the reconsideration process. Under
CAA section 109, the EPA is required to base its review of the NAAQS
on the current air quality criteria, and thus the record and
decision for this review also serve for the reconsideration.
---------------------------------------------------------------------------

    In light of the EPA's decision to consolidate the reconsideration
with the current review, the D.C. Circuit proceeded with the litigation
on the 2008 final decision. On July 23, 2013, the court upheld the
EPA's 2008 primary O3 standard, but remanded the 2008
secondary standard to the EPA (Mississippi v. EPA, 744 F. 3d 1334).
With respect to the primary standard, the court first held that the EPA
reasonably determined that the existing standard was not requisite to
protect public health with an adequate margin of safety, and
consequently required revision. Specifically, the court noted that
there were ``numerous epidemiologic studies linking health effects to
exposure to ozone levels below 0.08 ppm and clinical human exposure
studies finding a causal relationship between health effects and
exposure to ozone levels at and below 0.08 ppm'' (Mississippi v. EPA,
744 F. 3d at 1345). The court also specifically endorsed the weight of
evidence approach utilized by the EPA in its deliberations (Mississippi
v. EPA, 744 F. 3d at 1344).
    The court went on to reject arguments that the EPA should have
adopted a more stringent primary standard. Dismissing arguments that a
clinical study (as properly interpreted by the EPA) showing effects at
0.06 ppm necessitated a standard level lower than that selected, the
court noted that this was a single, limited study (Mississippi v. EPA,
744 F. 3d at 1350). With respect to the epidemiologic evidence, the
court accepted the EPA's argument that there could be legitimate
uncertainty that a causal relationship between O3 and 8-hour
exposures less than 0.075 ppm exists, so that associations at lower
levels reported in epidemiologic studies did not necessitate a more
stringent standard (Mississippi v. EPA, 744 F. 3d at 1351-52).\8\
---------------------------------------------------------------------------

    \8\ The court cautioned, however, that ``perhaps more [clinical]
studies like the Adams studies will yet reveal that the 0.060 ppm
level produces significant adverse decrements that simply cannot be
attributed to normal variation in lung function,'' and further
cautioned that ``agencies may not merely recite the terms
`substantial uncertainty' as a justification for their actions.''
Id. at 1350, 1357 (internal citations omitted).
---------------------------------------------------------------------------

    The court also rejected arguments that an 8-hour primary standard
of 0.075 ppm failed to provide an adequate margin of safety, noting
that margin of safety considerations involved policy judgments by the
agency, and that by setting a standard ``appreciably below'' the level
of the current standard (0.08 ppm), the agency had made a reasonable
policy choice (Mississippi v. EPA, 744 F. 3d at 1351-52). Finally, the
court rejected arguments that the EPA's decision was inconsistent with
the CASAC's scientific recommendations because the CASAC had been
insufficiently clear in its recommendations whether it was providing
scientific or policy recommendations, and the EPA had reasonably
addressed the CASAC's policy recommendations (Mississippi v. EPA, 744
F. 3d at 1357-58).
    With respect to the secondary standard, the court held that the
EPA's justification for setting the secondary standard identical to the
revised 8-hour primary standard violated the CAA because the EPA had
not adequately explained how that standard provided the required public
welfare protection. The court thus remanded the secondary standard to
the EPA (Mississippi v. EPA, 744 F. 3d at 1360-62).
    At the time of the court's decision, the EPA had already completed
significant portions of its next statutorily required periodic review
of the O3 NAAQS. This review was formally initiated in 2008
with a call for information in the Federal Register (73 FR 56581, Sept.
29, 2008). On October 28-29, 2008, the EPA held a public workshop to
discuss the policy-relevant science, which informed identification of
key policy issues and questions to frame the review. Based in part on
the workshop discussions, the EPA developed a draft Integrated Review
Plan (IRP) outlining the schedule, process,\9\ and key policy-relevant
questions that would guide the evaluation of the air quality criteria
for O3 and the review of the primary and secondary
O3 NAAQS. A draft of the IRP was released for public review
and comment in September 2009 and was the subject of a consultation
with the CASAC on November 13, 2009 (74 FR 54562; October 22,
2009).\10\ After considering the comments received from that
consultation and from the public, the EPA completed and released the
IRP for the review in 2011 (U.S. EPA, 2011a).
---------------------------------------------------------------------------

    \9\ As of this review, the document developed in NAAQS reviews
to document the air quality criteria, previously the AQCD, is the
ISA, and the document describing the OAQPS staff evaluation,
previously the Staff Paper, is the PA. These documents are described
in the IRP.
    \10\ See http://yosemite.epa.gov/sab/sabproduct.nsf/WebProjectsbyTopicCASAC!OpenView for more information on CASAC
activities related to the current O3 NAAQS review.
---------------------------------------------------------------------------

    In preparing the first draft ISA, the EPA's National Center for
Environmental Assessment (NCEA) considered CASAC and public comments on
the IRP, and also comments received from a workshop held on August 6,
2010, to review and discuss preliminary drafts of key ISA sections (75
FR 42085, July 20, 2010). In 2011, the first draft ISA was released for
public comment and for review by CASAC at a public meeting on May 19-
20, 2011 (U.S. EPA, 2011b; 76 FR 10893, February 28, 2011; 76 FR 23809,
April 28, 2011). Based on CASAC and public comments, NCEA prepared a
second draft ISA, which was released for public comment and CASAC
review (U.S. EPA, 2011c; 76 FR 60820, September 30, 2011). The CASAC
reviewed this draft at a January 9-10, 2012, public meeting (76 FR 236,
December 8, 2011). Based on CASAC and public comments, NCEA prepared a
third draft ISA (U.S. EPA, 2012; 77 FR 36534, June 19, 2012), which was
reviewed at a CASAC meeting in September 2012. The EPA released the
final ISA in February 2013 (U.S. EPA, 2013).
    The EPA presented its plans for conducting Risk and Exposure
Assessments (REAs) for health risk and exposure (HREA) and welfare risk
and exposure (WREA) in two documents that outlined the scope and
approaches for use in conducting quantitative assessments, as well as
key issues to be addressed as part of the assessments (U.S. EPA, 2011d,
e). The EPA released these documents for public comment in April 2011,
and consulted with CASAC on May 19-20, 2011 (76 FR 23809, April 28,
2011). The EPA considered CASAC advice and public comments in further
planning for the assessments, issuing a memo that described changes to
elements of the REA plans and brief explanations regarding them (Samet,
2011; Wegman, 2012).
    In July 2012, the EPA made the first drafts of the Health and
Welfare REAs available for CASAC review and public comment (77 FR
42495, July 19, 2012; 77 FR 51798, August 27, 2012). The first draft PA
was made available for CASAC review and public comment in August 2012
(77 FR 42495, July 19, 2012; 77 FR 51798, August 27, 2012).\11\ The
first

draft REAs and PA were the focus of a CASAC public meeting in September
2012 (Frey and Samet, 2012a, 2012b). The second draft REAs and PA,
prepared with consideration of CASAC advice and public comments, were
made available for public comment and CASAC review in January 2014 (79
FR 4694, January 29, 2014). These documents were the focus of a CASAC
public meeting on March 25-27, 2014 (Frey, 2014a; Frey, 2014b; Frey,
2014c). The final versions of these documents were developed with
consideration of the comments and recommendations from CASAC, as well
as comments from the public on the draft documents, and were released
in August 2014 (U.S. EPA 2014a; U.S. EPA, 2014b; U.S. EPA, 2014c).
---------------------------------------------------------------------------

    \11\ The PA is prepared by the OAQPS staff. Formerly known as
the Staff Paper, it presents a staff evaluation of the policy
implications of the key scientific and technical information in the
ISA and REAs for the EPA's consideration. The PA provides a
transparent evaluation, and staff conclusions, regarding policy
considerations related to reaching judgments about the adequacy of
the current standards, and if revision is considered, what revisions
may be appropriate to consider. The PA is intended to help ``bridge
the gap'' between the agency's scientific assessments presented in
the ISA and REAs, and the judgments required of the EPA
Administrator in determining whether it is appropriate to retain or
revise the NAAQS.
---------------------------------------------------------------------------

    The proposed decision (henceforth ``proposal'') on this review of
the O3 NAAQS was signed on November 25, 2014, and published
in the Federal Register on December 17, 2014. The EPA held three public
hearings to provide direct opportunity for oral testimony by the public
on the proposal. The hearings were held on January 29, 2015, in
Arlington, Texas, and Washington, DC, and on February 2, 2015, in
Sacramento, California. At these public hearings, the EPA heard
testimony from nearly 500 individuals representing themselves or
specific interested organizations. Transcripts from these hearings and
written testimony provided at the hearings are in the docket for this
review. Additionally, approximately 430,000 written comments were
received from various commenters during the public comment period on
the proposal, approximately 428,000 as part of mass mail campaigns.
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 the EPA's responses, can be found in a separate
document (henceforth ``Response to Comments'') in the docket for this
review.
    The schedule for completion of this review is governed by a court
order resolving a lawsuit filed in January 2014 by a group of
plaintiffs who alleged that the EPA had failed to perform its mandatory
duty, under section 109(d)(1), to complete a review of the
O3 NAAQS within the period provided by statute. The court
order that governs this review, entered by the court on April 30, 2014,
provides that the EPA will sign for publication a notice of final
rulemaking concerning its review of the O3 NAAQS no later
than October 1, 2015.
    As in prior NAAQS reviews, the EPA is basing its decision in this
review on studies and related information included in the ISA, REAs and
PA, which have undergone CASAC and public review. The studies assessed
in the ISA and PA, and the integration of the scientific evidence
presented in them, have undergone extensive critical review by the EPA,
the 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 the EPA but also by the
statutorily mandated independent advisory committee, as well as the
public review that accompanies this process. Some commenters have
referred to and discussed individual scientific studies on the health
and welfare effects of O3 that were not included in the ISA
(USEPA, 2013) (`` `new' studies''). In considering and responding to
comments for which such ``new'' studies were cited in support, the EPA
has provisionally considered the cited studies in the context of the
findings of the ISA. The EPA's provisional consideration of these
studies did not and could not provide the kind of in-depth critical
review described above.
    The decision to rely on studies and related information included in
the ISA, REAs and PA, which have undergone CASAC and public review, is
consistent with the 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 the EPA
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 the EPA's past practice.
    As discussed in the EPA's 1993 decision not to revise the NAAQS for
O3, ``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, the 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 and welfare effects and exposure pathways of
ambient O3 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, the EPA is basing the final decisions in this review
on the studies and related information included in the O3
air quality criteria that have undergone CASAC and public review. The
EPA will consider the ``new'' studies for purposes of decision making
in the next periodic review of the O3 NAAQS, which the 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 the EPA, CASAC, and the public.
Further discussion of these ``new'' studies can be found in the
Response to Comments document, which is in the docket for this
rulemaking and also available on the web (http://www.epa.gov/ttn/naaqs/standards/ozone/s_o3_index.html).

D. Ozone Air Quality

    Ozone is formed near the earth's surface due to chemical
interactions involving solar radiation and precursor pollutants
including volatile organic compounds (VOCs) and NOX. Over
longer time periods, methane (CH4) and carbon monoxide (CO)
can also lead to O3 formation at the global scale. The
precursor emissions leading to O3 formation can result from
both man-made sources (e.g., motor vehicles and electric power
generation) and natural sources (e.g., vegetation and wildfires).
Occasionally, O3 that is created naturally in the
stratosphere can also contribute to O3 levels near the
surface. Once formed, O3 near the surface can be transported
by winds before eventually being removed from the atmosphere via
chemical reactions or deposition to surfaces. In sum, O3
concentrations are influenced by complex interactions between precursor
emissions, meteorological conditions, and surface characteristics (U.S.
EPA, 2014a).

    In order to continuously assess O3 air pollution levels,
state and local environmental agencies operate O3 monitors
at various locations and subsequently submit the data to the EPA. At
present, there are approximately 1,400 monitors across the U.S.
reporting hourly O3 averages during the times of the year
when local O3 pollution can be important (U.S. EPA, 2014c,
Section 2.1). Much of this monitoring is focused on urban areas where
precursor emissions tend to be largest, as well as locations directly
downwind of these areas, but there are also over 100 sites in rural
areas where high levels of O3 can also be measured. Based on
data from this national network, the EPA estimates that, in 2013,
approximately 99 million Americans lived in counties where
O3 design values \12\ were above the level of the existing
health-based (primary) NAAQS of 0.075 ppm. High O3 values
can occur almost anywhere within the contiguous 48 states, although the
poorest O3 air quality in the U.S. is typically observed in
California, Texas, and the Northeast Corridor, locations with some of
the most densely populated areas in the country. From a temporal
perspective, the highest daily peak O3 concentrations
generally tend to occur during the afternoon within the warmer months
due to higher solar radiation and other conducive meteorological
conditions during these times. The exceptions to this general rule
include 1) some rural sites where transport of O3 from
upwind areas of regional production can occasionally result in high
nighttime levels of O3, 2) high-elevation sites episodically
influenced by stratospheric intrusions which can occur in other months,
and 3) certain locations in the western U.S. where large quantities of
O3 precursors emissions associated with oil and gas
development can be trapped by strong inversions associated with snow
cover during the colder months and efficiently converted to
O3 (U.S. EPA, 2014c, Section 2.3).
---------------------------------------------------------------------------

    \12\ A design value is a statistic that describes the air
quality status of a given location relative to the level of the
NAAQS.
---------------------------------------------------------------------------

    One of the challenging aspects of developing plans to address high
O3 concentrations is that the response of O3 to
precursor reductions is nonlinear. In particular, NOX
emissions can lead to both increases and decreases of O3.
The net impact of NOX emissions on O3
concentrations depends on the local quantities of NOX, VOC,
and sunlight which interact in a set of complex chemical reactions. In
some areas, such as certain urban centers where NOX
emissions typically are high compared to local VOC emissions,
NOX can suppress O3 locally. This phenomenon is
particularly pronounced under conditions associated with low
O3 concentrations (i.e., during cool, cloudy weather and at
night when photochemical activity is limited or nonexistent). However,
while NOX emissions can initially suppress O3
levels near the emission sources, these same NOX emissions
ultimately react to form higher O3 levels downwind when
conditions are favorable. Photochemical model simulations suggest that,
in general, reductions in NOX emissions in the U.S. will
slightly increase O3 concentrations on days with lower
O3 concentrations in close proximity to NOX
sources (e.g., in urban core areas), while at the same time decreasing
the highest O3 concentrations in downwind areas. See
generally, U.S. EPA, 2014a (section 2.2.1).
    At present, both the primary and secondary NAAQS use the annual
fourth-highest daily maximum 8-hour concentration, averaged over 3
years, as the form of the standard. An additional metric, the W126
exposure index, is often used to assess impacts of O3
exposure on ecosystems and vegetation. W126 is a cumulative seasonal
aggregate of weighted hourly O3 values observed between 8
a.m. and 8 p.m. As O3 precursor emissions have decreased
across the U.S., annual fourth-highest 8-hour O3 maxima have
concurrently shown a modest downward trend. The national average change
in annual fourth-highest daily maximum 8-hour O3
concentrations between 2000 and 2013 was an 18% decrease. The national
average change in the annual W126 exposure index over the same period
was a 52% decrease. Air quality model simulations estimate that
O3 air quality will continue to improve over the next decade
as additional reductions in O3 precursors from power plants,
motor vehicles, and other sources are realized.
    In addition to being affected by changing emissions, future
O3 concentrations may also be affected by climate change.
Modeling studies in the EPA's Interim Assessment (U.S. EPA, 2009a) that
are cited in support of the 2009 Endangerment Finding under CAA section
202(a) (74 FR 66496, Dec. 15, 2009) as well as a recent assessment of
potential climate change impacts (Fann et al., 2015) project that
climate change may lead to future increases in summer O3
concentrations across the contiguous U.S.\13\ While the projected
impact is not uniform, climate change has the potential to increase
average summertime O3 concentrations by as much as 1-5 ppb
by 2030, if greenhouse gas emissions are not mitigated. Increases in
temperature are expected to be the principal factor in driving any
O3 increases, although increases in stagnation frequency may
also contribute (Jacob and Winner, 2009). If unchecked, climate change
has the potential to offset some of the improvements in O3
air quality, and therefore some of the improvements in public health,
that are expected from reductions in emissions of O3
precursors.
---------------------------------------------------------------------------

    \13\ These modeling studies are based on coupled global climate
and regional air quality models and are designed to assess the
sensitivity of U.S. air quality to climate change. A wide range of
future climate scenarios and future years have been modeled and
there can be variations in the expected response in U.S.
O3 by scenario and across models and years, within the
overall signal of higher summer O3 concentrations in a
warmer climate.
---------------------------------------------------------------------------

    Another challenging aspect of this air quality issue is the impact
from sources of O3 and its precursors beyond those from
domestic, anthropogenic sources. Modeling analyses indicate that
nationally the majority of O3 exceedances are predominantly
caused by anthropogenic emissions from within the U.S. However,
observational and modeling analyses have concluded that O3
concentrations in some locations in the U.S. on some days can be
substantially influenced by sources that cannot be addressed by
domestic control measures. In particular, certain high-elevation sites
in the western U.S. are impacted by a combination of non-U.S. sources
like international transport, or natural sources such as stratospheric
O3, and O3 originating from wildfire
emissions.\14\ Ambient O3 from these non-U.S. and natural
sources is collectively referred to as background O3. See
generally section 2.4 of the PA (U.S. EPA, 2014c). The analyses suggest
that, at these locations, there can be episodic events with substantial
background contributions where O3 concentrations approach or
exceed the level of the current NAAQS (i.e., 75 ppb). These events are
relatively infrequent, and the EPA has policies that allow for the
exclusion of air quality monitoring data from design value calculations
when they are substantially affected by certain background influences.
---------------------------------------------------------------------------

    \14\ Without global greenhouse gas mitigation efforts, climate
change is projected to dramatically increase the area burned by
wildfires across most of the contiguous U.S., especially in the West
(U.S. EPA, 2015 p. 72).
---------------------------------------------------------------------------

E. Summary of Proposed Revisions to the O3 Standards

    For reasons discussed in the proposal, the Administrator proposed
to revise the

current primary and secondary standards for O3. With regard
to the primary standard, the Administrator proposed to revise the level
from 75 ppb to a level within a range from 65 to 70 ppb. The EPA
proposed to revise the AQI for O3, consistent with revision
to the primary standard.
    With regard to the secondary standard, the Administrator proposed
to revise the level of the current secondary standard to within the
range of 0.065 to 0.070 ppm, which air quality analyses indicate would
provide cumulative, seasonal air quality or exposure values, in terms
of 3-year average W126 index values, at or below a range of 13-17 ppm-
hours.
    The EPA also proposed to make corresponding revisions in data
handling conventions for O3; to revise regulations for the
PSD permitting program to add a provision grandfathering certain
pending permits from certain requirements with respect to the proposed
revisions to the standards; and to convey schedules and information
related to implementing any revised standards. In conjunction with
proposing exceptional event schedules related to implementing any
revised O3 standards, the EPA also proposed to extend the
new schedule approach to other future NAAQS revisions and to remove
obsolete regulatory language associated with expired exceptional event
deadlines for historical standards for both O3 and other
pollutants for which NAAQS have been established. The EPA also proposed
to make minor changes to the procedures and time periods for evaluating
potential FRMs and equivalent methods, including making the
requirements for NO2 consistent with the requirements for
O3, and removing an obsolete requirement for the annual
submission of documentation by manufacturers of certain particulate
matter monitors.

F. Organization and Approach to Decisions in This O3 NAAQS Review

    This action presents the Administrator's final decisions in the
current review of the primary and secondary O3 standards.
The final decisions addressing standards for O3 are based on
a thorough review in the ISA of scientific information on known and
potential human health and welfare effects associated with exposure to
O3 at levels typically found in the ambient air. These final
decisions also take into account the following: (1) Staff assessments
in the PA of the most policy-relevant information in the ISA as well as
a quantitative health and welfare exposure and risk assessments based
on that information; (2) CASAC advice and recommendations, as reflected
in its letters to the Administrator and its discussions of drafts of
the ISA, REAs, and PA at public meetings; (3) public comments received
during the development of these documents, both in connection with
CASAC meetings and separately; and (4) extensive public comments
received on the proposed rulemaking.
    The primary standard is addressed in section II. Corresponding
changes to the AQI are addressed in section III. The secondary standard
is addressed in section IV. Related data handling conventions and
exceptional events are addressed in section V. Updates to the
monitoring regulations are addressed in section VI. Implementation
activities, including PSD-related actions, are addressed in sections
VII and VIII. Section IX addresses applicable statutory and executive
order reviews.

II. Rationale for Decision on the Primary Standard

    This section presents the Administrator's final decisions regarding
the need to revise the existing primary O3 standard and the
appropriate revision to the level of that standard. Based on her
consideration of the full body of health effects evidence and exposure/
risk analyses, the Administrator concludes that the current primary
standard for O3 is not requisite to protect public health
with an adequate margin of safety. In order to increase public health
protection, she is revising the level of the primary standard to 70
ppb, in conjunction with retaining the current indicator, averaging
time and form. The Administrator concludes that such a revised standard
will be requisite to protect public health with an adequate margin of
safety. As discussed more fully below, the rationale for these final
decisions draws from the thorough review in the ISA (U.S. EPA, 2013) of
the available scientific evidence, generally published through July
2011, on human health effects associated with the presence of
O3 in the ambient air. This rationale also takes into
account: (1) Analyses of O3 air quality, human exposures to
O3, and O3-associated health risks, as presented
and assessed in the HREA (U.S. EPA, 2014a); (2) the EPA staff
assessment of the most policy-relevant scientific evidence and
exposure/risk information in the PA (U.S. EPA, 2014c); (3) CASAC advice
and recommendations, as reflected in discussions of drafts of the ISA,
REA, and PA at public meetings, in separate written comments, and in
CASAC's letters to the Administrator; (4) public input received during
the development of these documents, either in connection with CASAC
meetings or separately; and (5) public comments on the proposal notice.
    Section II.A below summarizes the information presented in the
proposal regarding O3-associated health effects,
O3 exposures, and O3-attributable health risks.
Section II.B presents information related to the adequacy of the
current primary O3 standard, including a summary of the
basis for the Administrator's proposed decision to revise the current
standard, public comments received on the adequacy of the current
standard, and the Administrator's final conclusions regarding the
adequacy of the current standard. Section II.C presents information
related to the elements of a revised primary O3 standard,
including information related to each of the major elements of the
standard (i.e., indicator, averaging time, form, level). Section II.D
summarizes the Administrator's final decisions on the primary
O3 standard.

A. Introduction

    As discussed in section II.A of the proposal (79 FR 75243-75246,
December 17, 2014), the EPA's approach to informing decisions on the
primary O3 standard in the current review builds upon the
general approaches used in previous reviews and reflects the broader
body of scientific evidence, updated exposure/risk information, and
advances in O3 air quality modeling now available. This
approach is based most fundamentally on using the EPA's assessment of
the available scientific evidence and associated quantitative analyses
to inform the Administrator's judgments regarding a primary standard
for O3 that is ``requisite'' (i.e., neither more nor less
stringent than necessary) to protect public health with an adequate
margin of safety. Specifically, it is based on consideration of the
available body of scientific evidence assessed in the ISA (U.S. EPA,
2013), exposure and risk analyses presented in the HREA (U.S. EPA,
2014a), evidence- and exposure-/risk-based considerations and
conclusions presented in the PA (U.S. EPA, 2014c), advice and
recommendations received from CASAC (Frey, 2014a, c), and public
comments.
    Section II.A.1 below summarizes the information presented in the
proposal regarding O3-associated health effects. Section
II.A.2 summarizes the information presented in the proposal regarding
O3 exposures and O3-attributable health risks.

1. Overview of Health Effects Evidence
    The health effects of O3 are described in detail in the
ISA (U.S. EPA, 2013). Based on its assessment of the health effects
evidence, the ISA determined that a ``causal'' relationship exists
between short-term exposure to O3 in ambient air and effects
on the respiratory system \15\ and that a ``likely to be causal''
relationship exists between long-term exposure to O3 in
ambient air and respiratory effects \16\ (U.S. EPA, 2013, pp. 1-6 to 1-
7). The ISA summarizes the longstanding body of evidence for
O3 respiratory effects as follows (U.S. EPA, 2013, p. 1-5):
---------------------------------------------------------------------------

    \15\ In determining that a causal relationship exists for
O3 with specific health effects, the EPA has concluded
that ``[e]vidence is sufficient to conclude that there is a causal
relationship with relevant pollutant exposures'' (U.S. EPA, 2013, p.
lxiv).
    \16\ In determining a ``likely to be a causal'' relationship
exists for O3 with specific health effects, the EPA has
concluded that ``[e]vidence is sufficient to conclude that a causal
relationship is likely to exist with relevant pollutant exposures,
but important uncertainties remain'' (U.S. EPA, 2013, p. lxiv).

    The clearest evidence for health effects associated with
exposure to O3 is provided by studies of respiratory
effects. Collectively, a very large amount of evidence spanning
several decades supports a relationship between exposure to
O3 and a broad range of respiratory effects (see Section
6.2.9 and Section 7.2.8). The majority of this evidence is derived
from studies investigating short-term exposures (i.e., hours to
weeks) to O3, although animal toxicological studies and
recent epidemiologic evidence demonstrate that long-term exposure
---------------------------------------------------------------------------
(i.e., months to years) may also harm the respiratory system.

    Additionally, the ISA determined that the relationships between
short-term exposures to O3 in ambient air and both total
mortality and cardiovascular effects are likely to be causal, based on
expanded evidence bases in the current review (U.S. EPA, 2013, pp. 1-7
to 1-8). The ISA determined that the currently available evidence for
additional endpoints is ``suggestive'' of causal relationships with
short-term (central nervous system effects) and long-term exposures
(cardiovascular effects, reproductive and developmental effects,
central nervous system effects and total mortality) to ambient
O3.
    Consistent with emphasis in past reviews on O3 health
effects for which the evidence is strongest, in this review the EPA
places the greatest emphasis on studies of health effects that have
been determined in the ISA to be caused by, or likely to be caused by,
O3 exposures (U.S. EPA, 2013, section 2.5.2). This preamble
section summarizes the evidence for health effects attributable to
O3 exposures, with a focus on respiratory morbidity and
mortality effects attributable to short- and long-term exposures, and
cardiovascular system effects (including mortality) and total mortality
attributable to short-term exposures (from section II.B in the
proposal, 79 FR 75246-75271).
    The information highlighted here is based on the assessment of the
evidence in the ISA (U.S. EPA, 2013, Chapters 4 to 8) and consideration
of that evidence in the PA (U.S. EPA, 2014c, Chapters 3 and 4) on the
known or potential effects on public health which may be expected from
the presence of O3 in the ambient air. This section
summarizes: (1) Information available on potential mechanisms for
health effects associated with exposure to O3 (II.A.1.a);
(2) the nature of effects that have been associated directly with both
short- and long-term exposure to O3 and indirectly with the
presence of O3 in ambient air (II.A.1.b); (3) considerations
related to the adversity of O3-attributable health effects
(II.A.1.c); and (4) considerations in characterizing the public health
impact of O3, including the identification of ``at risk''
populations (II.A.1.d).
a. Overview of Mechanisms
    This section briefly summarizes the characterization of the key
events and pathways that contribute to health effects resulting from
O3 exposures, as discussed in the proposal (79 FR 75247,
section II.B.1) and in the ISA (U.S. EPA, 2013, section 5.3).
    Experimental evidence elucidating modes of action and/or mechanisms
contributes to our understanding of the biological plausibility of
adverse O3-related health effects, including respiratory
effects and effects outside the respiratory system (U.S. EPA, 2013,
Chapters 6 and 7). Evidence indicates that the initial key event is the
formation of secondary oxidation products in the respiratory tract
(U.S. EPA, 2013, section 5.3). This mainly involves direct reactions
with components of the extracellular lining fluid (ELF). Although the
ELF has inherent capacity to quench (based on individual antioxidant
capacity), this capacity can be overwhelmed, especially with exposure
to elevated concentrations of O3 (U.S. EPA 2014c, at 3-3, 3-
9). The resulting secondary oxidation products transmit signals to the
epithelium, pain receptive nerve fibers and, if present, immune cells
involved in allergic responses. The available evidence indicates that
the effects of O3 are mediated by components of ELF and by
the multiple cell types in the respiratory tract. Oxidative stress is
an implicit part of this initial key event.
    Secondary oxidation products initiate numerous responses at the
cellular, tissue, and whole organ level of the respiratory system.
These responses include the activation of neural reflexes which leads
to lung function decrements; initiation of pulmonary inflammation;
alteration of barrier epithelial function; sensitization of bronchial
smooth muscle; modification of lung host defenses; airways remodeling;
and modulation of autonomic nervous function which may alter cardiac
function (U.S. EPA, 2013, section 5.3, Figure 5-8).
    Persistent inflammation and injury, which are observed in animal
models of chronic and quasi-continuous exposure to O3, are
associated with airways remodeling (see section 7.2.3 of the ISA, U.S.
EPA, 2013). Chronic quasi-continuous exposure to O3 has also
been shown to result in effects on the developing lung and immune
system. Systemic inflammation and vascular oxidative/nitrosative stress
are also key events in the toxicity pathway of O3 (U.S. EPA,
2013, section 5.3.8). Extrapulmonary effects of O3 occur in
numerous organ systems, including the cardiovascular, central nervous,
reproductive, and hepatic systems (U.S. EPA, 2013, sections 6.3 to 6.5
and sections 7.3 to 7.5).
    Responses to O3 exposure are variable within the
population. Studies have shown a large range of pulmonary function
(i.e., spirometric) responses to O3 among healthy young
adults, while responses within an individual are relatively consistent
over time. Other responses to O3 have also been
characterized by a large degree of interindividual variability,
including airways inflammation. The mechanisms that may underlie the
variability in responses seen among individuals are discussed in the
ISA (U.S. EPA, 2013, section 5.4.2). Certain functional genetic
polymorphisms, pre-existing conditions or diseases, nutritional status,
lifestages, and co-exposures can contribute to altered risk of
O3-induced effects. Experimental evidence for such
O3-induced changes contributes to our understanding of the
biological plausibility of adverse O3-related health
effects, including a range of respiratory effects as well as effects
outside the respiratory system (e.g., cardiovascular effects) (U.S.
EPA, 2013, Chapters 6 and 7).
b. Nature of Effects
    This section briefly summarizes the information presented in the
proposal on respiratory effects attributable to short-term exposures
(II.A.1.b.i), respiratory effects attributable to long-

term exposures (II.A.1.b.ii), cardiovascular effects attributable to
short-term exposures (II.A.1.b.iii), and premature mortality
attributable to short-term exposures (II.A.1.b.iv) (79 FR 75247,
section II.B.2).
i. Respiratory Effects--Short-term Exposure
    Controlled human exposure, animal toxicological, and epidemiologic
studies available in the last review provided clear, consistent
evidence of a causal relationship between short-term O3
exposure and respiratory effects (U.S. EPA, 2006a). Recent studies
evaluated since the completion of the 2006 AQCD support and expand upon
the strong body of evidence available in the last review (U.S. EPA,
2013, section 6.2.9).
    Key aspects of this evidence are discussed below with regard to (1)
lung function decrements; (2) pulmonary inflammation, injury, and
oxidative stress; (3) airway hyperresponsiveness; (4) respiratory
symptoms and medication use; (5) lung host defense; (6) allergic and
asthma-related responses; (7) hospital admissions and emergency
department visits; and (8) respiratory mortality.\17\
---------------------------------------------------------------------------

    \17\ CASAC concurred that these were ``the kinds of identifiable
effects on public health that are expected from the presence of
ozone in the ambient air'' (Frey 2014c, p. 3).
---------------------------------------------------------------------------

Lung Function Decrements
    Lung function decrements are typically measured by spirometry and
refer to reductions in the maximal amount of air that can be forcefully
exhaled. Forced expiratory volume in 1 second (FEV1) is a
common index used to assess the effect of O3 on lung
function. The ISA summarizes the currently available evidence from
multiple controlled human exposure studies evaluating changes in
FEV1 following 6.6-hour O3 exposures in young,
healthy adults engaged in moderate levels of physical activity \18\
(U.S. EPA, 2013, section <IP_ADDRESS>, Figure 6-1). Exposures to an average
O3 concentration of 60 ppb results in group mean decrements
in FEV1 ranging from 1.8% to 3.6% (Adams, 2002; Adams, 2006;
\19\ Schelegle et al., 2009; \20\ Kim et al., 2011). The weighted
average group mean decrement was 2.7% from these studies. In some
analyses, these group mean decrements in lung function were
statistically significant (Brown et al., 2008; Kim et al., 2011), while
in other analyses they were not (Adams, 2006; Schelegle et al.,
2009).\21\ Prolonged exposure to an average O3 concentration
of 72 ppb results in a statistically significant group mean decrement
in FEV1 of about 6% (Schelegle et al., 2009).\22\ There is a
smooth dose-response curve without evidence of a threshold for
exposures between 40 and 120 ppb O3 (U.S. EPA, 2013, Figure
6-1). When these data are taken together, the ISA concludes that ``mean
FEV1 is clearly decreased by 6.6-hour exposures to 60 ppb
O3 and higher concentrations in [healthy, young adult]
subjects performing moderate exercise'' (U.S. EPA, 2013, p. 6-9).
---------------------------------------------------------------------------

    \18\ Table 6-1 of the ISA includes descriptions of the activity
levels evaluated in controlled human exposure studies (U.S. EPA,
2013).
    \19\ Adams (2006); (2002) both provide data for an additional
group of 30 healthy subjects that were exposed via facemask to 60
ppb O3 for 6.6 hours with moderate exercise. These
subjects are described on page 133 of Adams (2006) and pages 747 and
761 of Adams (2002). The facemask exposure is not expected to affect
the FEV1 responses relative to a chamber exposure.
    \20\ For the 60 ppb target exposure concentration, Schelegle et
al. (2009) reported that the actual mean exposure concentration was
63 ppb.
    \21\ Adams (2006) did not find effects on FEV1 at 60
ppb to be statistically significant. In an analysis of the Adams
(2006) data, Brown et al. (2008) addressed the more fundamental
question of whether there were statistically significant differences
in responses before and after the 6.6 hour exposure period and found
the average effect on FEV1 at 60 ppb to be small, but
highly statistically significant using several common statistical
tests, even after removal of potential outliers. Schelegle et al.
(2009) reported that, compared to filtered air, the largest change
in FEV1 for the 60 ppb protocol occurred after the sixth
(and final) exercise period.
    \22\ As noted above, for the 70 ppb exposure group, Schelegle et
al. (2009) reported that the actual mean exposure concentration was
72 ppb.
---------------------------------------------------------------------------

    As described in the proposal (79 FR 75250), the ISA focuses on
individuals with >10% decrements in FEV1 because (1) it is
accepted by the American Thoracic Society (ATS) as an abnormal response
and a reasonable criterion for assessing exercise-induced
bronchoconstriction, and (2) some individuals in the Schelegle et al.
(2009) study experienced 5-10% FEV1 decrements following
exposure to filtered air. The proportion of healthy adults experiencing
FEV1 decrements >10% following prolonged exposures to 80 ppb
O3 while at moderate exertion ranged from 17% to 29% and
following exposures to 60 ppb O3 ranged from 3% to 20%. The
weighted average proportion (i.e., based on numbers of subjects in each
study) of young, healthy adults with >10% FEV1 decrements is
25% following exposure to 80 ppb O3 and 10% following
exposure to 60 ppb O3, for 6.6 hours at moderate exertion
(U.S. EPA, 2013, page 6-18 and 6-19).\23\ Responses within an
individual tend to be reproducible over a period of several months,
reflecting differences in intrinsic responsiveness. Given this, the ISA
concludes that ``[t]hough group mean decrements are biologically small
and generally do not attain statistical significance, a considerable
fraction of exposed individuals [in the clinical studies] experience
clinically meaningful decrements in lung function'' when exposed for
6.6 hours to 60 ppb O3 during quasi-continuous, moderate
exertion (U.S. EPA, 2013, section <IP_ADDRESS>, p. 6-20).
---------------------------------------------------------------------------

    \23\ The ISA notes that by considering responses uncorrected for
filtered air exposures, during which lung function typically
improves (which would increase the size of the change, pre-and post-
exposure), 10% is an underestimate of the proportion of healthy
individuals that are likely to experience clinically meaningful
changes in lung function following exposure for 6.6 hours to 60 ppb
O3 during quasi-continuous moderate exertion (U.S. EPA,
2012, section <IP_ADDRESS>).
---------------------------------------------------------------------------

    This review has marked an advance in the ability to make reliable
quantitative predictions of the potential lung function response to
O3 exposure, and, thus, to reasonably predict the degree of
interindividual response of lung function to that exposure. McDonnell
et al. (2012) and Schelegle et al. (2012) developed models, described
in more detail in the proposal (79 FR 75250), that included
mathematical approaches to simulate the potential protective effect of
antioxidants in the ELF at lower ambient O3 concentrations,
and that included a dose threshold below which changes in lung function
do not occur. The resulting empirical models can estimate the frequency
distribution of individual responses and summary measures of the
distribution such as the mean or median response and the proportions of
individuals with FEV1 decrements >10%, 15%, and 20%.\24\ The
predictions of the models are consistent with the observed results from
the individual controlled human exposure studies of O3-
induced FEV1 decrements (79 FR 75250-51, see also U.S. EPA,
2013, Figures 6-1 and 6-3). CASAC agreed that these models mark a
significant technical advance over the exposure-response modeling
approach used for the lung function risk assessment in the last review
and explicitly found that ``[t]he MSS model to be scientifically and
biologically defensible'' (Frey, 2014a, pp. 8, 2). CASAC also stated
that ``the comparison of the MSS model results to those obtained with
the exposure-response model is of tremendous importance. Typically, the
MSS model gives a result about a factor of three higher . . . for
school-age children, which is expected because the MSS model includes

responses for a wider range of exposure protocols'' (Frey, 2014a, pp.
8, 2).
---------------------------------------------------------------------------

    \24\ One of these models, the McDonnell-Stewart-Smith (MSS)
model (McDonnell et al. 2012) was used to estimate the occurrences
of lung function decrements in the HREA.
---------------------------------------------------------------------------

    Epidemiologic studies have consistently linked short-term increases
in ambient O3 concentrations with lung function decrements
in diverse populations and lifestages, including children attending
summer camps, adults exercising or working outdoors, and groups with
pre-existing respiratory diseases such as asthmatic children (U.S. EPA,
2013, section <IP_ADDRESS>). Some of these studies reported O3-
associated lung function decrements accompanied by respiratory symptoms
\25\ in asthmatic children. In contrast, studies of children in the
general population have reported similar O3-associated lung
function decrements but without accompanying respiratory symptoms (79
FR 75251; U.S. EPA, 2013, section <IP_ADDRESS>). As noted in the PA (EPA,
2014c, pp. 4-70 to 4-71), additional research is needed to evaluate
responses of people with asthma and healthy people in the 40 to 70 ppb
range. Further epidemiologic studies and meta-analyses of the effects
of O3 exposure on children will help elucidate the
concentration-response functions for lung function and respiratory
symptom effects at lower O3 concentrations.
---------------------------------------------------------------------------

    \25\ Reversible loss of lung function in combination with the
presence of symptoms meets ATS criteria for adversity (ATS, 2000a).
---------------------------------------------------------------------------

    Several epidemiologic panel studies \26\ reported statistically
significant associations with lung function decrements at relatively
low ambient O3 concentrations. For outdoor recreation or
exercise, associations were reported in analyses restricted to 1-hour
average O3 concentrations less than 80 ppb, down to less
than 50 ppb. Among outdoor workers, Brauer et al. (1996) found a robust
association with daily 1-hour max O3 concentrations less
than 40 ppb. Ulmer et al. (1997) found a robust association in
schoolchildren with 30-minute maximum O3 concentrations less
than 60 ppb. For 8-hour average O3 concentrations,
associations with lung function decrements in children with asthma were
found to persist at concentrations less than 80 ppb in a U.S. multicity
study (Mortimer et al., 2002) and less than 51 ppb in a study conducted
in the Netherlands (Gielen et al., 1997).
---------------------------------------------------------------------------

    \26\ Panel studies include repeated measurements of health
outcomes, such as respiratory symptoms, at the individual level
(U.S. EPA, 2013, p. 1x).
---------------------------------------------------------------------------

    As described in the proposal (79 FR 75251), several epidemiologic
panel studies provided information on potential confounding by
copollutants and most O3 effect estimates for lung function
were robust to adjustment for temperature, humidity, and copollutants
such as particulate matter with mass median aerodynamic diameter less
than or equal to 2.5 micrometers (PM2.5), particulate matter
with mass median aerodynamic diameter less than or equal to 10
micrometers (PM10), NO2, or sulfur dioxide
(SO2) (Hoppe et al., 2003; Brunekreef et al., 1994; Hoek et
al. 1993; U.S. EPA, 2013, pp. 6-67 to 6-69). Although examined in only
a few epidemiologic studies, O3 also remained associated
with decreases in lung function with adjustment for pollen or acid
aerosols (79 F 75251; U.S. EPA, 2013, section <IP_ADDRESS>).
Pulmonary Inflammation, Injury and Oxidative Stress
    As described in detail in section II.B.2.a.ii of the proposal (79
FR 75252), O3 exposures can result in increased respiratory
tract inflammation and epithelial permeability. Inflammation is a host
response to injury, and the induction of inflammation is evidence that
injury has occurred. Oxidative stress has been shown to play a key role
in initiating and sustaining O3-induced inflammation. As
noted in the ISA (U.S. EPA, 2013, section 6.2.3), O3
exposures can initiate an acute inflammatory response throughout the
respiratory tract that has been reported to persist for at least 18-24
hours after exposure.
    Inflammation induced by exposure of humans to O3 can
have several potential outcomes, ranging from resolving entirely
following a single exposure to becoming a chronic inflammatory state,
as described in detail in section II.B.2.a.ii of the proposal (79 FR
75252) and in the ISA (U.S. EPA, 2013, section 6.2.3). Continued
cellular damage due to chronic inflammation ``may alter the structure
and function of pulmonary tissues'' (U.S. EPA, 2013, p. 6-161). Lung
injury and the resulting inflammation provide a mechanism by which
O3 may cause other more serious morbidity effects (e.g.,
asthma exacerbations) (U.S. EPA, 2013, section 6.2.3).\27\
---------------------------------------------------------------------------

    \27\ CASAC also addressed this issue: ``The CASAC believes that
these modest changes in FEV1 are usually associated with
inflammatory changes, such as more neutrophils in the
bronchoalveolar lavage fluid. Such changes may be linked to the
pathogenesis of chronic lung disease'' (Frey, 2014a p. 2).
---------------------------------------------------------------------------

    Building on the last review, recent studies continue to support the
evidence for airway inflammation and injury with new evidence for such
effects following exposures to lower concentrations than had been
evaluated previously. These studies include recent controlled human
exposure and epidemiologic studies and are discussed more below.
    An extensive body of evidence from controlled human exposure
studies, described in section II.B.2.a.ii of the proposal, indicates
that short-term exposures to O3 can cause pulmonary
inflammation and increases in polymorphonuclear leukocyte (PMN) influx
and permeability following 80-600 O3 ppb exposures,
eosinophilic inflammation following exposures at or above 160 ppb, and
O3-induced PMN influx following exposures of healthy adults
to 60 ppb O3, the lowest concentration that has been
evaluated for inflammation. A meta-analysis of 21 controlled human
exposure studies (Mudway and Kelly, 2004) using varied experimental
protocols (80-600 ppb O3 exposures; 1-6.6 hours exposure
duration; light to heavy exercise; bronchoscopy at 0-24 hours post-
O3 exposure) reported that PMN influx in healthy subjects is
linearly associated with total O3 dose.
    As with FEV1 responses to O3, inflammatory
responses to O3 are generally reproducible within
individuals, with some individuals experiencing more severe
O3-induced airway inflammation than indicated by group
averages. Unlike O3-induced decrements in lung function,
which are attenuated following repeated exposures over several days,
some markers of O3-induced inflammation and tissue damage
remain elevated during repeated exposures, indicating ongoing damage to
the respiratory system (79 FR 75252). Most controlled human exposure
studies have reported that asthmatics experience larger O3-
induced inflammatory responses than non-asthmatics.\28\
---------------------------------------------------------------------------

    \28\ When evaluated, these studies have also reported
O3-induced respiratory symptoms in asthmatics.
Specifically, Scannell et al. (1996), Basha et al. (1994), and
Vagaggini et al. (2001, 2007) reported increased symptoms in
addition to inflammation.
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    In the previous review (U.S. EPA, 2006a), the epidemiologic
evidence of O3-associated changes in airway inflammation and
oxidative stress was limited (79 FR 75253). Since then, as a result of
the development of less invasive test methods, there has been a large
increase in the number of studies assessing ambient O3-
associated changes in airway inflammation and oxidative stress, the
types of biological samples collected, and the types of indicators.
Most of these recent studies have evaluated biomarkers of inflammation
or oxidative stress in exhaled breath, nasal lavage fluid, or induced
sputum (U.S. EPA, 2013, section <IP_ADDRESS>). These recent studies form a
larger database to establish coherence with findings from controlled
human exposure and animal

studies that have measured the same or related biological markers.
Additionally, results from these studies provide further biological
plausibility for the associations observed between ambient
O3 concentrations and respiratory symptoms and asthma
exacerbations.
Airway Hyperresponsiveness (AHR)
    A strong body of controlled human exposure and animal toxicological
studies, most of which were available in the last review of the
O3 NAAQS, report O3-induced AHR after either
acute or repeated exposures (U.S. EPA, 2013, section <IP_ADDRESS>). People
with asthma often exhibit increased airway responsiveness at baseline
relative to healthy control subjects, and asthmatics can experience
further increases in responsiveness following exposures to
O3. Studies reporting increased airway responsiveness after
O3 exposure contribute to a plausible link between ambient
O3 exposures and increased respiratory symptoms in
asthmatics, and increased hospital admissions and emergency department
visits for asthma (section II.B.2.a.iii, 79 FR 75254; U.S. EPA, 2013,
section <IP_ADDRESS>).
Respiratory Symptoms and Medication Use
    Respiratory symptoms are associated with adverse outcomes such as
limitations in activity, and are the primary reason for people with
asthma to use quick relief medication and to seek medical care. Studies
evaluating the link between O3 exposures and such symptoms
allow a direct characterization of the clinical and public health
significance of ambient O3 exposure. Controlled human
exposure and toxicological studies have described modes of action
through which short-term O3 exposures may increase
respiratory symptoms by demonstrating O3-induced AHR (U.S.
EPA, 2013, section 6.2.2) and pulmonary inflammation (U.S. EPA, 2013,
section 6.2.3).
    The link between subjective respiratory symptoms and O3
exposures has been evaluated in both controlled human exposure and
epidemiologic studies, and the link with medication use has been
evaluated in epidemiologic studies. In the last review, several
controlled human exposure studies reported respiratory symptoms
following exposures to O3 concentrations at or above 80 ppb.
In addition, one study reported such symptoms following exposures to 60
ppb O3, though the increase was not statistically different
from filtered air controls. Epidemiologic studies reported associations
between ambient O3 and respiratory symptoms and medication
use in a variety of locations and populations, including asthmatic
children living in U.S. cities (U.S. EPA, 2013, pp. 6-1 to 6-2). In the
current review, additional controlled human exposure studies have
evaluated respiratory symptoms following exposures to O3
concentrations below 80 ppb and recent epidemiologic studies have
evaluated associations with respiratory symptoms and medication use
(U.S. EPA, 2013, sections 6.2.1, 6.2.4).
    As noted in section II.B.2.a.iv in the proposal (79 FR 75255), the
findings for O3-induced respiratory symptoms in controlled
human exposure studies, and the evidence integrated across disciplines
describing underlying modes of action, provide biological plausibility
for epidemiologic associations observed between short-term increases in
ambient O3 concentration and increases in respiratory
symptoms (U.S. EPA, 2013, section 6.2.4).
    Most epidemiologic studies of O3 and respiratory
symptoms and medication use have been conducted in children and/or
adults with asthma, with fewer studies, and less consistent results, in
non-asthmatic populations (U.S. EPA, 2013, section 6.2.4). The 2006
AQCD (U.S. EPA, 2006a; U.S. EPA, 2013, section 6.2.4) concluded that
the collective body of epidemiologic evidence indicated that short-term
increases in ambient O3 concentrations are associated with
increases in respiratory symptoms in children with asthma. A large body
of single-city and single-region studies of asthmatic children provides
consistent evidence for associations between short-term increases in
ambient O3 concentrations and increased respiratory symptoms
and asthma medication use in children with asthma (U.S. EPA, 2013,
Figure 6-12, Table 6-20, section <IP_ADDRESS>). Methodological differences,
described in section II.B.2.a.iv of the proposal, among studies make
comparisons across recent multicity studies of respiratory symptoms
difficult.
    Available evidence indicates that O3-associated
increases in respiratory symptoms are not confounded by temperature,
pollen, or copollutants (primarily PM) (U.S. EPA, 2013, section
<IP_ADDRESS>; Table 6-25). However, identifying the independent effects of
O3 in some studies was complicated due to the high
correlations observed between O3 and PM or different lags
and averaging times examined for copollutants. Nonetheless, the ISA
noted that the robustness of associations in some studies of
individuals with asthma, combined with findings from controlled human
exposure studies for the direct effects of O3 exposure,
provide substantial evidence supporting the independent effects of
short-term ambient O3 exposure on respiratory symptoms (U.S.
EPA, 2013, section <IP_ADDRESS>).
    In summary, both controlled human exposure and epidemiologic
studies have reported respiratory symptoms attributable to short-term
O3 exposures. In the last review, the majority of the
evidence from controlled human exposure studies in young, healthy
adults was for symptoms following exposures to O3
concentrations at or above 80 ppb. Although studies that have become
available since the last review have not reported increased respiratory
symptoms in young, healthy adults following exposures with moderate
exertion to 60 ppb, one recent study did report increased symptoms
following exposure to 72 ppb O3. As was concluded in the
last review, the collective body of epidemiologic evidence indicates
that short-term increases in ambient O3 concentration are
associated with increases in respiratory symptoms in children with
asthma (U.S. EPA, 2013, section 6.2.4). Recent studies of respiratory
symptoms and medication use, primarily in asthmatic children, add to
this evidence. In a smaller body of studies, increases in ambient
O3 concentration were associated with increases in
respiratory symptoms in adults with asthma.
Lung Host Defense
    The mammalian respiratory tract has a number of closely integrated
defense mechanisms that, when functioning normally, provide protection
from the potential health effects of exposures to a wide variety of
inhaled particles and microbes. Based on toxicological and human
exposure studies, in the last review EPA concluded that available
evidence indicates that short-term O3 exposures have the
potential to impair host defenses in humans, primarily by interfering
with alveolar macrophage function. Any impairment in alveolar
macrophage function may lead to decreased clearance of microorganisms
or nonviable particles. Compromised alveolar macrophage functions in
asthmatics may increase their susceptibility to other O3
effects, the effects of particles, and respiratory infections (U.S.
EPA, 2006a).
    Relatively few studies conducted since the last review have
evaluated the effects of O3 exposures on lung host defense.
As presented in section II.B.2.a.v of the proposal (79 FR 75256),

when the available evidence is taken as a whole, the ISA concludes that
acute O3 exposures impair the host defense capability of
animals, primarily by depressing alveolar macrophage function and
perhaps also by decreasing mucociliary clearance of inhaled particles
and microorganisms. Coupled with limited evidence from controlled human
exposure studies, this suggests that humans exposed to O3
could be predisposed to bacterial infections in the lower respiratory
tract.
Allergic and Asthma Related Responses
    Evidence from controlled human exposure and epidemiologic studies
available in the last review indicates that O3 exposure
skews immune responses toward an allergic phenotype and could also make
airborne allergens more allergenic, as discussed in more detail in the
proposal (79 FR 75257). Evidence from controlled human exposure and
animal toxicology studies available in the last review indicates that
O3 may also increase AHR to specific allergen triggers (75
FR 2970, January 19, 2010). When combined with NO2,
O3 has been shown to enhance nitration of common protein
allergens, which may increase their allergenicity (Franze et al.,
2005).
Hospital Admissions and Emergency Department Visits
    The 2006 AQCD concluded that ``the overall evidence supports a
causal relationship between acute ambient O3 exposures and
increased respiratory morbidity resulting in increased emergency
department visits and [hospital admissions] during the warm season''
\29\ (U.S. EPA, 2006a). This conclusion was ``strongly supported by the
human clinical, animal toxicologic[al], and epidemiologic evidence for
[O3-induced] lung function decrements, increased respiratory
symptoms, airway inflammation, and airway hyperreactivity'' (U.S. EPA,
2006a).
---------------------------------------------------------------------------

    \29\ Epidemiologic associations for O3 are more
robust during the warm season than during cooler months (e.g.,
smaller measurement error, less potential confounding by
copollutants). The rationale for focusing on warm season
epidemiologic studies for O3 can be found at 72 FR 37838-
37840.
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    The results of recent studies largely support the conclusions of
the 2006 AQCD (U.S. EPA, 2013, section 6.2.7). Since the completion of
the 2006 AQCD, relatively fewer studies, conducted in the U.S., Canada,
and Europe, have evaluated associations between short-term
O3 concentrations and respiratory hospital admissions and
emergency department visits, with a growing number of studies conducted
in Asia. This epidemiologic evidence is discussed in detail in the
proposal (79 FR 75258) and in the ISA (U.S. EPA, 2013, section
6.2.7).\30\
---------------------------------------------------------------------------

    \30\ The consideration of ambient O3 concentrations
in the locations of these epidemiologic studies are discussed in
sections II.D.1.b and II.E.4.a below, for the current standard and
for alternative standards, respectively.
---------------------------------------------------------------------------

    In considering this body of evidence, the ISA focused primarily on
multicity studies because they examine associations with respiratory-
related hospital admissions and emergency department visits over large
geographic areas using consistent statistical methodologies (U.S. EPA,
2013, section <IP_ADDRESS>). The ISA also focused on single-city studies
that encompassed a large number of daily hospital admissions or
emergency department visits, included long study-durations, were
conducted in locations not represented by the larger studies, or
examined population-specific characteristics that may impact the risk
of O3-related health effects but were not evaluated in the
larger studies (U.S. EPA, 2013, section <IP_ADDRESS>). When examining the
association between short-term O3 exposure and respiratory
health effects that require medical attention, the ISA distinguishes
between hospital admissions and emergency department visits because it
is likely that a small percentage of respiratory emergency department
visits will be admitted to the hospital; therefore, respiratory
emergency department visits may represent potentially less serious, but
more common outcomes (U.S. EPA, 2013, section <IP_ADDRESS>).
    The collective evidence across studies indicates a mostly
consistent positive association between O3 exposure and
respiratory-related hospital admissions and emergency department
visits. Moreover, the magnitude of these associations may be
underestimated to the extent members of study populations modify their
behavior in response to air quality forecasts, and to the extent such
behavior modification increases exposure misclassification (U.S. EPA,
2013, Section 4.6.6). Studies examining the potential confounding
effects of copollutants have reported that O3 effect
estimates remained relatively robust upon the inclusion of PM and
gaseous pollutants in two-pollutant models (U.S. EPA, 2013, Figure 6-
20, Table 6-29). Additional studies that conducted copollutant
analyses, but did not present quantitative results, also support these
conclusions (Strickland et al., 2010; Tolbert et al., 2007; Medina-
Ramon et al., 2006; U.S. EPA, 2013, section <IP_ADDRESS>).\31\
---------------------------------------------------------------------------

    \31\ The ISA concluded that, ``[o]verall, recent studies provide
copollutant results that are consistent with those from the studies
evaluated in the 2006 O3 AQCD [(U.S. EPA, 2006[a]),
Figure 7-12, page 7-80 of the 2006 O3 AQCD], which found
that O3 respiratory hospital admissions risk estimates
remained robust to the inclusion of PM in copollutant models (U.S.
EPA, 2013, pp. 6-152 to 6-153).
---------------------------------------------------------------------------

    In the last review, studies had not evaluated the concentration-
response relationship between short-term O3 exposure and
respiratory-related hospital admissions and emergency department
visits. As described in the proposal in section II.B.2.a.vii (79 FR
75257) and in the ISA (U.S. EPA, 2013, section <IP_ADDRESS>), a preliminary
examination of this relationship in studies that have become available
since the last review found no evidence of a deviation from linearity
when examining the association between short-term O3
exposure and asthma hospital admissions (Silverman and Ito, 2010;
Strickland et al., 2010). In addition, an examination of the
concentration-response relationship for O3 exposure and
pediatric asthma emergency department visits found no evidence of a
threshold at O3 concentrations as low as 30 ppb (for daily
maximum 8-hour concentrations) (U.S. EPA, 2013, section <IP_ADDRESS>).
However, in these studies there is uncertainty in the shape of the
concentration-response curve at the lower end of the distribution of
O3 concentrations due to the low density of data in this
range. Further studies at low-level O3 exposures might
reduce this uncertainty.
Respiratory Mortality
    Evidence from experimental studies indicates multiple potential
pathways of respiratory effects from short-term O3
exposures, which support the continuum of respiratory effects that
could potentially result in respiratory-related mortality in adults
(U.S. EPA, 2013, section 6.2.8).\32\ The evidence in the last review
was inconsistent for associations between short-term O3
concentrations and respiratory mortality (U.S. EPA, 2006a). New
epidemiologic evidence for respiratory mortality is discussed in detail
in the ISA (U.S. EPA, 2013, section 6.6) and summarized below. The
majority of recent multicity studies have reported positive
associations between short-term O3 exposures and respiratory
mortality, particularly during the summer months (U.S. EPA, 2013,
Figure 6-36).
---------------------------------------------------------------------------

    \32\ Premature mortality is discussed in more detail below in
section II.A.1.b.iv.

---------------------------------------------------------------------------

    Recent multicity studies from the U.S. (Zanobetti and Schwartz,
2008), Europe (Samoli et al., 2009), Italy (Stafoggia et al., 2010),
and Asia (Wong et al., 2010), as well as a multi-continent study
(Katsouyanni et al., 2009), reported associations between short-term
O3 concentrations and respiratory mortality (U.S. EPA, 2013,
Figure 6-37, page 6-259). With respect to respiratory mortality,
summer-only analyses were consistently positive and most were
statistically significant. All-year analyses had more mixed results,
but most were positive.
    Of the studies evaluated, only two studies analyzed the potential
for copollutant confounding of the O3-respiratory mortality
relationship (Katsouyanni et al., (2009); Stafoggia et al., (2010)).
Based on the results of these analyses, the O3 respiratory
mortality risk estimates appear to be moderately to substantially
sensitive (e.g., increased or attenuated) to inclusion of
PM10. However, in the APHENA study (Katsouyanni et al.,
2009), the mostly every-6th-day sampling schedule for PM10
in the Canadian and U.S. datasets greatly reduced their sample size and
limits the interpretation of these results (U.S. EPA, 2013, sections
6.2.8 and 6.2.9).
    The evidence for associations between short-term O3
concentrations and respiratory mortality has been strengthened since
the last review, with the addition of several large multicity studies.
The biological plausibility of the associations reported in these
studies is supported by the experimental evidence for respiratory
effects.
ii. Respiratory Effects--Long-Term Exposure
    Since the last review, the body of evidence indicating the
occurrence of respiratory effects due to long-term O3
exposure has been strengthened. This evidence is discussed in detail in
the ISA (U.S. EPA, 2013, Chapter 7) and summarized below for new-onset
asthma and asthma prevalence, asthma hospital admissions, pulmonary
structure and function, and respiratory mortality.
    Asthma is a heterogeneous disease with a high degree of temporal
variability. The onset, progression, and symptoms can vary within an
individual's lifetime, and the course of asthma may vary markedly in
young children, older children, adolescents, and adults. In the
previous review, longitudinal cohort studies that examined associations
between long-term O3 exposures and the onset of asthma in
adults and children indicated a direct effect of long-term
O3 exposures on asthma risk in adults and effect
modification by O3 in children. Since then, additional
studies have evaluated associations with new onset asthma, further
informing our understanding of the potential gene-environment
interactions, mechanisms, and biological pathways associated with
incident asthma.
    In children, the relationship between long-term O3
exposure and new-onset asthma has been extensively studied in the
Children's Health Study (CHS), a long-term study that was initiated in
the early 1990's which has evaluated effects in several cohorts of
children. For this review, recent studies from the CHS provide evidence
for gene-environment interactions in effects on new-onset asthma by
indicating that the lower risks associated with specific genetic
variants are found in children who live in lower O3
communities. Described in detail in the proposal (79 FR 75259) and in
the ISA (U.S. EPA, 2013, section 7.2.1), these studies indicate that
the risk for new-onset asthma is related in part to genetic
susceptibility, as well as behavioral factors and environmental
exposure. Cross-sectional studies by Akinbami et al. (2010) and Hwang
et al. (2005) provide further evidence relating O3 exposures
with asthma prevalence. Gene-environment interactions are discussed in
detail in Section <IP_ADDRESS> in the ISA (U.S. EPA, 2013).
    In the 2006 AQCD (U.S. EPA, 2006a), studies on O3-
related hospital discharges and emergency department visits for asthma
and respiratory disease mainly looked at short-term (daily) metrics.
Recent studies continue to indicate that there is evidence for
increases in both hospital admissions and emergency department visits
in children and adults related to all respiratory outcomes, including
asthma, with stronger associations in the warm months.
    In the 2006 AQCD (U.S. EPA, 2006a), few epidemiologic studies had
investigated the effect of chronic O3 exposure on pulmonary
function. As discussed in the proposal, epidemiologic studies of long-
term exposures in both children and adults provide mixed results about
the effects of long-term O3 exposure on pulmonary function
and the growth rate of lung function.
    Long-term studies in animals allow for greater insight into the
potential effects of prolonged exposure to O3 that may not
be easily measured in humans, such as structural changes in the
respiratory tract. Despite uncertainties, epidemiologic studies
observing associations of O3 exposure with functional
changes in humans can attain biological plausibility in conjunction
with long-term toxicological studies, particularly O3-
inhalation studies performed in non-human primates whose respiratory
systems most closely resemble that of the human. An important series of
studies, discussed in section <IP_ADDRESS> of the ISA (U.S. EPA, 2013), have
used nonhuman primates to examine the effect of O3 alone, or
in combination with an inhaled allergen, house dust mite antigen, on
morphology and lung function. Animals exhibit the hallmarks of allergic
asthma defined for humans (NHLBI, 2007). These studies and others have
demonstrated changes in pulmonary function and airway morphology in
adult and infant nonhuman primates repeatedly exposed to
environmentally relevant concentrations of O3 (U.S. EPA,
2013, section <IP_ADDRESS>). As discussed in more detail in the proposal,
the studies provide evidence of an O3-induced change in
airway resistance and responsiveness and provide biological
plausibility of long-term exposure, or repeated short-term exposures,
to O3 contributing to the effects of asthma in children.
    Collectively, evidence from animal studies strongly suggests that
chronic O3 exposure is capable of damaging the distal
airways and proximal alveoli, resulting in lung tissue remodeling and
leading to apparent irreversible changes. Potentially, persistent
inflammation and interstitial remodeling play an important role in the
progression and development of chronic lung disease. Further discussion
of the modes of action that lead to O3-induced morphological
changes and the mechanisms involved in lifestage susceptibility and
developmental effects can be found in the ISA (U.S. EPA, 2013, section
5.3.7, section <IP_ADDRESS>). The findings reported in chronic animal
studies offer insight into potential biological mechanisms for the
suggested association between seasonal O3 exposure and
reduced lung function development in children as observed in
epidemiologic studies (U.S. EPA, 2013, section <IP_ADDRESS>). Further
research could help fill in the gaps in our understanding of the
mechanisms involved in lifestage susceptibility and developmental
effects in children of seasonal or long-term exposure to O3.
    A limited number of epidemiologic studies have assessed the
relationship between long-term exposure to O3 and mortality
in adults. The 2006 AQCD concluded that an insufficient amount of
evidence existed ``to suggest a causal relationship between chronic
O3 exposure and increased risk for

mortality in humans'' (U.S. EPA, 2006a). Though total and cardio-
pulmonary mortality were considered in these studies, respiratory
mortality was not specifically considered.
    In a recent follow-up analysis of the American Cancer Society
cohort (Jerrett et al., 2009), cardiopulmonary deaths were separately
subdivided into respiratory and cardiovascular deaths, rather than
combined as in the Pope et al. (2002) work. Increased O3
exposure was associated with the risk of death from respiratory causes,
and this effect was robust to the inclusion of PM2.5.
Additionally, a recent multicity time series study (Zanobetti and
Schwartz, 2011), which followed (from 1985 to 2006) four cohorts of
Medicare enrollees with chronic conditions that might predispose to
O3-related effects, observed an association between long-