Review of the Ozone National Ambient Air Quality Standards

Federal RegisterAug 14, 2020

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 50

[EPA-HQ-OAR-2018-0279; FRL-10012-49-OAR]

RIN 2060-AU40

Review of the Ozone National Ambient Air Quality Standards

AGENCY:

Environmental Protection Agency (EPA).

ACTION:

Proposed action.

SUMMARY:

Based on the Environmental Protection Agency's (EPA's) review of the air quality criteria and the national ambient air quality standards (NAAQS) for photochemical oxidants including ozone (O

), the EPA is proposing to retain the current standards, without revision.

DATES:

Comments must be received on or before October 1, 2020.

Public hearings:

The EPA will hold two virtual public hearings on Monday, August 31, 2020, and Tuesday, September 1, 2020. Please refer to the

SUPPLEMENTARY INFORMATION

section for additional information on the public hearings.

ADDRESSES:

You may submit comments, identified by Docket ID No. EPA-HQ-OAR-2018-0279, by any of the following methods:

•

Federal eRulemaking Portal:

https://www.regulations.gov

(our preferred method). Follow the online instructions for submitting comments.

•

Email:

a-and-r-Docket@epa.gov.

Include the Docket ID No. EPA-HQ-OAR-2018-0279 in the subject line of the message.

•

Mail:

U.S. Environmental Protection Agency, EPA Docket Center, Air and Radiation Docket, Mail Code 28221T, 1200 Pennsylvania Avenue NW, Washington, DC 20460.

•

Hand Delivery or Courier (by scheduled appointment only):

EPA Docket Center, WJC West Building, Room 3334, 1301 Constitution Avenue NW, Washington, DC 20004. The Docket Center's hours of operations are 8:30 a.m.-4:30 p.m., Monday-Friday (except Federal Holidays).

Instructions:

All submissions received must include the Docket ID No. for this document. Comments received may be posted without change to

https://www.regulations.gov,

including any personal information provided. For detailed instructions on sending comments, see the

SUPPLEMENTARY INFORMATION

section of this document. Out of an abundance of caution for members of the public and our staff, the EPA Docket Center and Reading Room are closed to the public, with limited exceptions, to reduce the risk of transmitting COVID-19. Our Docket Center staff will continue to provide remote customer service via email, phone, and webform. We encourage the public to submit comments via

https://www.regulations.gov/

or email, as there may be a delay in processing mail and faxes. Hand deliveries and couriers may be received by scheduled appointment only. For further information on EPA Docket Center services and the current status, please visit us online at

https://www.epa.gov/dockets.

The two virtual public hearings will be held on Monday, August 31, 2020, and Tuesday, September 1, 2020. The EPA will announce further details on the virtual public hearing website at

https://www.epa.gov/ground-level-ozone-pollution/setting-and-reviewing-standards-control-ozone-pollution.

Refer to the

SUPPLEMENTARY INFORMATION

section below for additional information.

FOR FURTHER INFORMATION CONTACT:

For information or questions about the public hearing, please contact Ms. Regina Chappell, U.S. Environmental Protection Agency, Office of Air Quality Planning and Standards (OAQPS) (Mail Code C304-03), Research Triangle Park, NC 27711; telephone: (919) 541-3650; email address:

chappell.regina@epa.gov.

For information or questions regarding the review of the O

NAAQS, please contact Dr. Deirdre Murphy, Health and Environmental Impacts Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Mail Code C504-06, Research Triangle Park, NC 27711; telephone: (919) 541-0729; fax: (919) 541-0237; email:

murphy.deirdre@epa.gov.

SUPPLEMENTARY INFORMATION:

General Information

Participation in Virtual Public Hearings

Please note that the EPA is deviating from its typical approach because the President has declared a national emergency. Due to the current Centers for Disease Control and Prevention (CDC) recommendations, as well as state and local orders for social distancing to limit the spread of COVID-19, the EPA cannot hold in-person public meetings at this time. The EPA will begin pre-registering speakers for the hearings upon publication of this document in the

Federal Register

. To register to speak at a virtual hearing, please use the online registration form available at

https://www.epa.gov/ground-level-ozone-pollution/setting-and-reviewing-standards-control-ozone-pollution

or contact Ms. Regina Chappell at (919) 541-3650 or by email at

chappell.regina@epa.gov

to register to speak at the virtual hearing. The last day to pre-register to speak at one of the hearings will be August 27, 2020. On August 28, 2020, the EPA will post a general agenda for the hearings that will list preregistered speakers in approximate order at:

https://www.epa.gov/ground-level-ozone-pollution/setting-and-reviewing-standards-control-ozone-pollution.

The EPA will make every effort to follow the schedule as closely as possible on the day of each hearing; however, please plan for the hearing to run either ahead of schedule or behind schedule. Each commenter will have 5 minutes to provide oral testimony. The EPA may ask clarifying questions during the oral presentations but will not respond to the presentations at that time. The EPA encourages commenters to provide the EPA with a copy of their oral testimony electronically (via email) by emailing it to Dr. Deirdre Murphy and Ms. Regina Chappell. The EPA also recommends submitting the text of your oral testimony as written comments to the rulemaking docket. Written statements and supporting information submitted during the comment period will be considered with the same weight as oral testimony and supporting information presented at the public hearing. Please note that any updates made to any aspect of the hearing will be posted online at

https://www.epa.gov/ground-level-ozone-pollution/setting-and-reviewing-standards-control-ozone-pollution.

While the EPA expects the hearings to go forward as set forth above, please monitor our website or contact Ms. Regina Chappell at (919) 541-3650 or

chappell.regina@epa.gov

to determine if there are any updates. The EPA does not intend to publish a document in the

Federal Register

announcing updates. If you require the services of a translator or a special accommodation such as audio description, please preregister for the hearing with Ms. Regina Chappell and describe your needs by August 21, 2020. The EPA may not be able to arrange accommodations without advance notice.

Preparing Comments for the EPA

Follow the online instructions for submitting comments. Once submitted to the Federal eRulemaking Portal, comments cannot be edited or withdrawn. The EPA may publish any comment received to its public docket. Do not submit electronically any information you consider to be Confidential Business Information (CBI)

or other information whose disclosure is restricted by statute. Multimedia submissions (audio, video, etc.) must be accompanied by a written comment. The written comment is considered the official comment and should include discussion of all points you wish to make. The EPA will generally not consider comments or comment contents located outside of the primary submission (

i.e.,

on the web, the cloud, or other file sharing system). For additional submission methods, the full EPA public comment policy, information about CBI or multimedia submissions, and general guidance on making effective comments, please visit

http://www2.epa.gov/dockets/commenting-epa-dockets.

When submitting comments, remember to:

• Identify the action by docket number and other identifying information (subject heading,

Federal Register

date and page number).

• Explain why you agree or disagree, suggest alternatives, and substitute language for your requested changes.

• Describe any assumptions and provide any technical information and/or data that you used.

• Provide specific examples to illustrate your concerns and suggest alternatives.

• Explain your views as clearly as possible, avoiding the use of profanity or personal threats.

• Make sure to submit your comments by the comment period deadline identified.

Availability of Information Related to This Action

All documents in the dockets pertaining to this action are listed on the

www.regulations.gov

website. This includes documents in the docket for the proposed decision (Docket ID No. EPA-HQ-OAR-2018-0279) and a separate docket, established for the Integrated Science Assessment (ISA) for this review (Docket ID No. EPA-HQ-ORD-2018-0274) that has been incorporated by reference into the docket for this proposed decision. Although listed in the index, some information is not publicly available,

e.g.,

CBI or other information whose disclosure is restricted by statute. Certain other material, such as copyrighted material, is not placed on the internet and may be viewed with prior arrangement with the EPA Docket Center. Additionally, a number of the documents that are relevant to this proposed decision are available through the EPA's website at

https://www.epa.gov/naaqs/ozone-o3-air-quality-standards.

These documents include the Integrated Review Plan for the Review of the Ozone National Ambient Air Quality Standards (U.S. EPA, 2019b; hereafter IRP), available at

https://www.epa.gov/naaqs/ozone-o3-standards-planning-documents-current-review,

the Integrated Science Assessment for Ozone and Related Photochemical Oxidants (U.S. EPA, 2020a; hereafter ISA), available at

https://www.epa.gov/naaqs/ozone-o3-standards-integrated-science-assessments-current-review,

and the Policy Assessment for the Review of the Ozone National Ambient Air Quality Standards (U.S. EPA, 2020b; hereafter PA), available at

https://www.epa.gov/naaqs/ozone-o3-standards-policy-assessments-current-review.

Table of Contents

The following topics are discussed in this preamble:

Executive Summary

I. Background

A. Legislative Requirements

B. Related O

Control Programs

C. Review of the Air Quality Criteria and Standards for O

D. Air Quality Information

II. Rationale for Proposed Decision on the Primary Standard

A. General Approach

1. Background on the Current Standard

2. Approach for the Current Review

B. Health Effects Information

1. Nature of Effects

2. Public Health Implications and At-Risk Populations

3. Exposure Concentrations Associated With Effects

C. Summary of Exposure and Risk Information

1. Key Design Aspects

2. Key Limitations and Uncertainties

3. Summary of Exposure and Risk Estimates

D. Proposed Conclusions on the Primary Standard

1. Evidence- and Exposure/Risk-Based Considerations in the Policy Assessment

2. CASAC Advice

3. Administrator's Proposed Conclusions

III. Rationale for Proposed Decision on the Secondary Standard

A. General Approach

1. Background on the Current Standard

2. Approach for the Current Review

B. Welfare Effects Information

1. Nature of Effects

2. Public Welfare Implications

3. Exposures Associated With Effects

C. Summary of Air Quality and Exposure Information

1. Influence of Form and Averaging Time of Current Standard on Environmental Exposure

2. Environmental Exposures in Terms of W126 Index

D. Proposed Conclusions on the Secondary Standard

1. Evidence- and Exposure/Risk-Based Considerations in the Policy Assessment

2. CASAC Advice

3. Administrator's Proposed Conclusions

IV. Statutory and Executive Order Reviews

A. Executive Order 12866: Regulatory Planning and Review and Executive Order 13563: Improving Regulation and Regulatory Review

B. Executive Order 13771: Reducing Regulations and Controlling Regulatory Costs

C. Paperwork Reduction Act (PRA)

D. Regulatory Flexibility Act (RFA)

E. Unfunded Mandates Reform Act (UMRA)

F. Executive Order 13132: Federalism

G. Executive Order 13175: Consultation and Coordination With Indian Tribal Governments

H. Executive Order 13045: Protection of Children From Environmental Health and Safety Risks

I. Executive Order 13211: Actions That Significantly Affect Energy Supply, Distribution or Use

J. National Technology Transfer and Advancement Act

K. Executive Order 12898: Federal Actions To Address Environmental Justice in Minority Populations and Low-Income Populations

L. Determination Under Section 307(d)

V. References

Executive Summary

This document presents the Administrator's proposed decisions in the current review of the primary (health-based) and secondary (welfare-based) O

NAAQS. In so doing, this document summarizes the background and rationale for the Administrator's proposed decisions to retain the current standards, without revision. In reaching his proposed decisions, the Administrator has considered the currently available scientific evidence in the ISA, quantitative and policy analyses presented in the PA, and advice from the Clean Air Scientific Advisory Committee (CASAC). The EPA solicits comment on the proposed decisions described here and on the array of issues associated with review of these standards, including judgments of public health, public welfare and science policy inherent in the proposed decisions, and requests commenters also provide the rationales upon which views articulated in submitted comments are based.

This review of the O

standards, required by the Clean Air Act (CAA) on a periodic basis, was initiated in 2018. The last review of the O

NAAQS, completed in 2015 established the current primary and secondary standards (80 FR 65291, October 26, 2015). In that review, the EPA significantly strengthened the primary and secondary standards by revising both standards from 75 ppb to 70 ppb and retaining their indicators (O

), forms (fourth-highest daily maximum,

averaged across three consecutive years) and averaging times (eight hours). These revisions to the NAAQS were accompanied by revisions to the data handling procedures, ambient air monitoring requirements, the air quality index and several provisions related to implementation (80 FR 65292, October 26, 2015). In the decision on subsequent litigation on the 2015 decisions, the U.S. Court of Appeals for the District of Columbia Circuit (D.C. Circuit) upheld the 2015 primary standard but remanded the 2015 secondary standard to the EPA for further justification or reconsideration. The court's remand of the secondary standard has been considered in reaching the proposed decision, and the associated proposed conclusions and judgments, described in this document.

In this review as in past reviews of the NAAQS for O

and related photochemical oxidants, the health and welfare effects evidence evaluated in the ISA is focused on O

. Ozone is the most prevalent photochemical oxidant in the atmosphere and the one for which there is a large body of scientific evidence on health and welfare effects. A component of smog, O

in ambient air is a mixture of mostly tropospheric O

and some stratospheric O

. Tropospheric O

, forms in the atmosphere when precursor emissions of pollutants, such as nitrogen oxides and volatile organic compounds (VOCs), interact with solar radiation. Precursor emissions result from man-made sources (

e.g.,

motor vehicles, and power plants) and natural sources (

e.g.,

vegetation and wildfires). In addition, O

that is created naturally in the stratosphere also mixes with tropospheric O

near the tropopause, and, under more limited meteorological conditions and topographical characteristics, nearer the earth's surface.

The proposed decision to retain the current primary standard, without revision, has been informed by key aspects of the currently available health effects evidence and conclusions contained in the ISA, quantitative exposure/risk analyses and policy evaluations presented in the PA, advice from the CASAC and public input received as part of this ongoing review. The health effects evidence newly available in this review, in conjunction with the full body of evidence critically evaluated in the ISA, continues to support prior conclusions that short-term O

exposure causes and long-term O

exposure likely causes respiratory effects, with evidence newly available in this review also indicating a likely causal relationship of short-term O

with metabolic effects. The strongest evidence for health effects due to ozone exposure, however, continues to come from studies of short- and long-term ozone exposure and respiratory health, including effects related to asthma exacerbation in people with asthma, particularly children with asthma. The longstanding evidence base of respiratory effects, spanning several decades, documents the causal relationship between short-term exposure to O

and an array of respiratory effects. The clearest evidence for this conclusion comes from controlled human exposure studies, available at the time of the last review, of individuals, exposed for 6.6 hours during quasi-continuous exercise that report an array of respiratory responses including lung function decrements and respiratory symptoms. Epidemiologic studies include associations between O

exposures and hospital admissions and emergency department visits, particularly for asthma exacerbation in children. People at risk include people with asthma, children, the elderly, and outdoor workers.

The quantitative analyses of population exposure and risk, as well as policy considerations in the PA, also inform the proposed decision on the primary standard. The general approach and methodology for the exposure-based assessment used in this review is similar to that used in the last review. However, a number of updates and improvements have been implemented in this review which result in differences from the analyses in the prior review. These include a more recent period (2015-2017) of ambient air monitoring data in which O

concentrations in the areas assessed are at or near the current standard, as well as improvements and updates to models, model inputs and underlying databases. The analyses are summarized in this document and described in detail in the PA.

Based on the current evidence and quantitative information, as well as consideration of CASAC advice and public comment thus far in this review, the Administrator proposes to conclude that the current primary standard is requisite to protect public health, with an adequate margin of safety, from effects of O

in ambient air and should be retained, without revision. In its advice to the Administrator, the CASAC concurred with the draft PA that the currently available health effects evidence is generally similar to that available in the last review when the standard was set. Part of CASAC concluded that the primary standard should be retained. Another part of CASAC expressed concern regarding the margin of safety provided by the current standard, pointing to comments from the 2014 CASAC, who while agreeing that the evidence supported a standard level of 70 ppb, additionally provided policy advice expressing support for a lower standard. The advice from the CASAC has been considered by the Administrator in proposing to conclude that the current standard, with its level of 70 ppb, provides the requisite public health protection, with an adequate margin of safety. The EPA solicits comment on the Administrator's proposed conclusion, and on the proposed decision to retain the standard, without revision. The EPA also solicits comment on the array of issues associated with review of this standard, including public health and science policy judgments inherent in the proposed decision.

The proposed decision to retain the current secondary standard, without revision, has been informed by key aspects of the currently available welfare effects evidence and conclusions contained in the ISA, quantitative exposure/risk analyses and policy evaluations presented in the PA, advice from the CASAC and public input received as part of this ongoing review. The welfare effects evidence newly available in this review, in conjunction with the full body of evidence critically evaluated in the ISA, supports, sharpens and expands somewhat on the conclusions reached in the last review. Consistent with the evidence in the last review, the currently available evidence describes an array of O

effects on vegetation and related ecosystem effects, as well as the role of O

in radiative forcing and subsequent climate-related effects. Further, evidence newly available in this review augments more limited previously available evidence for some additional vegetation-related effects. As in the last review, the strongest evidence and the associated findings of causal or likely causal relationships with O

in ambient air, as well as the quantitative characterizations of relationships between O

exposure and occurrence and magnitude of effects, are for vegetation effects. The scales of these effects range from the individual plant scale to the ecosystem scale, with potential for impacts on the public welfare. While the welfare effects of O

vary widely with regard to the extent and level of detail of the available information that describes the exposure circumstances that may elicit them, such information is most advanced for growth-related effects such as growth and yield. For example, the information

on exposure metric and relationships for these effects with the cumulative, concentration-weighted exposure index, W126, is long-standing, having been first described in the 1997 review. Utilizing this information, reduced growth is considered as proxy or surrogate for the broader array of vegetation effects in reviewing the public welfare protection provided by the current standard.

Quantitative analyses of air quality and exposure, including use of the W126 index, as well as policy considerations in the PA, also inform the proposed decision on the secondary standard. For example, analyses of air quality monitoring data across the U.S., as well as in Class I areas, updated and expanded from analyses conducted in the last review, inform EPA's understanding of vegetation exposures in areas meeting the current standard. Based on the current evidence and quantitative information, as well as consideration of CASAC advice and public comment thus far in this review, the Administrator proposes to conclude that the current secondary standard is requisite to protect the public welfare from known or anticipated adverse effects of O

in ambient air, and should be retained, without revision. In its advice to the Administrator, the full CASAC concurred with the preliminary conclusions in the draft PA that the current evidence supports retaining the current standard without revision. The EPA solicits comment on the Administrator's proposed conclusion that the current standard is requisite to protect the public welfare, and on the proposed decision to retain the standard, without revision. The EPA also solicits comment on the array of issues associated with review of this standard, including public welfare and science policy judgments inherent in the proposed decision.

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 pollutants “emissions of which, in his 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 he “plans to issue air quality criteria. . . .” (42 U.S.C. 7408(a)(1)). 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(a)(2)).

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 [42 U.S.C. 7409(a)]. Section 109(b)(1) defines primary standards as ones “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.”

Under section 109(b)(2), a secondary standard 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.”

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).

Under CAA section 302(h) (42 U.S.C. 7602(h)), effects on welfare include, but are not limited to, “effects on soils, water, crops, vegetation, manmade 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.”

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. In so doing, the EPA may not consider the costs of implementing the standards. See generally,

Whitman

American Trucking Ass'ns,

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.” See

American Petroleum Institute

Costle,

665 F.2d 1176, 1185 (D.C. Cir. 1981);

accord Murray Energy Corp.

EPA,

936 F.3d 597, 623-24 (D.C. Cir. 2019). At the same time, courts have clarified the EPA may consider “relative proximity to peak background . . . concentrations” as a factor in deciding how to revise the NAAQS in the context of considering standard levels within the range of reasonable values supported by the air quality criteria and judgments of the Administrator. See

American Trucking Ass'ns,

EPA,

283 F.3d 355, 379 (D.C. Cir. 2002), hereafter referred to as “

ATA III.”

The requirement that primary standards provide an adequate margin of safety was intended to address uncertainties associated with inconclusive scientific and technical information available at the time of standard setting. It was also intended to provide a reasonable degree of protection against hazards that research has not yet identified. See

Lead Industries Ass'n

EPA,

647 F.2d 1130, 1154 (D.C. Cir 1980);

American Petroleum Institute

Costle,

665 F.2d at 1186;

Coalition of Battery Recyclers Ass'n

EPA,

604 F.3d 613, 617-18 (D.C. Cir. 2010);

Mississippi

EPA,

744 F.3d 1334, 1353 (D.C. Cir. 2013). Both kinds of uncertainties are components of the risk associated with pollution at levels below those at which human health effects can be said to occur with reasonable scientific certainty. Thus, in selecting primary standards that include an adequate margin of safety, the Administrator is seeking not only to prevent pollution levels that have been demonstrated to be harmful but also to prevent lower pollutant levels that may pose an unacceptable risk of harm, even if the risk is not precisely identified as to nature or degree. The CAA does not require the Administrator to establish a primary NAAQS at a zero-risk level or at background concentration levels (see

Lead Industries Ass'n

EPA,

647 F.2d at 1156 n.51,

Mississippi

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 involved, the size of the sensitive population(s), and the kind and degree of uncertainties. The selection of any particular approach to providing an adequate margin of safety is a policy choice left specifically to the Administrator's judgment. See

Lead Industries Ass'n

EPA,

647 F.2d at 1161-62;

Mississippi

EPA,

744 F.3d at 1353.

Section 109(d)(1) of the Act requires periodic review and, if appropriate, revision of existing air quality criteria to reflect advances in scientific knowledge concerning the effects of the pollutant on public health and welfare. Under the same provision, the EPA is also to periodically review and, if appropriate,

revise the NAAQS, based on the revised air quality criteria.

This section of the Act requires the Administrator to complete these reviews and make any revisions that may be appropriate “at five-year intervals.”

Section 109(d)(2) addresses the appointment and advisory functions of an independent scientific review committee. Section 109(d)(2)(A) requires the Administrator to appoint this committee, which is to be composed of “seven members including at least one member of the National Academy of Sciences, one physician, and one person representing State air pollution control agencies.” Section 109(d)(2)(B) provides that the 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 1980s, this independent review function has been performed by the CASAC of the EPA's Science Advisory Board. A number of other advisory functions are also identified for the committee by section 109(d)(2)(C), which reads:

Such committee shall also (i) advise the Administrator of areas in which additional knowledge is required to appraise the adequacy and basis of existing, new, or revised national ambient air quality standards, (ii) describe the research efforts necessary to provide the required information, (iii) advise the Administrator on the relative contribution to air pollution concentrations of natural as well as anthropogenic activity, and (iv) advise the Administrator of any adverse public health, welfare, social, economic, or energy effects which may result from various strategies for attainment and maintenance of such national ambient air quality standards.

As previously noted, the Supreme Court has held that section 109(b) “unambiguously bars cost considerations from the NAAQS-setting process,” in

Whitman

American Trucking Ass'ns,

531 U.S. 457, 471 (2001). Accordingly, while some of the issues listed in section 109(d)(2)(C) as those on which Congress has directed the CASAC to advise the Administrator, are ones that are relevant to the standard setting process, others are not. Issues that are not relevant to standard setting may be relevant to implementation of the NAAQS once they are established.

Because some of these issues are not relevant to standard setting, some aspects of CASAC advice may not be relevant to EPA's process of setting primary and secondary standards that are requisite to protect public health and welfare. Indeed, were the EPA to consider costs of implementation when reviewing and revising the standards “it would be grounds for vacating the NAAQS.”

Whitman

American Trucking Ass'ns,

531 U.S. 457, 471 n.4 (2001). At the same time, the CAA directs CASAC to provide advice on “any adverse public health, welfare, social, economic, or energy effects which may result from various strategies for attainment and maintenance” of the NAAQS to the Administrator under section 109(d)(2)(C)(iv). In

Whitman,

the Court clarified that most of that advice would be relevant to implementation but not standard setting, as it “enable[s] the Administrator to assist the States in carrying out their statutory role as primary

implementers

of the NAAQS” (

id.

at 470 [emphasis in original]). However, the Court also noted that CASAC's “advice concerning certain aspects of `adverse public health . . . effects' from various attainment strategies is unquestionably pertinent” to the NAAQS rulemaking record and relevant to the standard setting process (

id.

at 470 n.2).

B. Related O

Control Programs

States are primarily responsible for ensuring attainment and maintenance of ambient air quality standards once the EPA has established them. Under sections 110 and 171 through 185 of the CAA, and related provisions and regulations, states are to 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 pollutants involved. The states, in conjunction with the EPA, also administer the prevention of significant deterioration of air quality program that covers these pollutants.

See

42 U.S.C. 7470-7479. In addition, federal programs provide for nationwide reductions in emissions of O

precursors and other air pollutants under Title II of the Act, 42 U.S.C. 7521-7574, which involves controls for automobile, truck, bus, motorcycle, nonroad engine and equipment, and aircraft emissions; the new source performance standards under section 111 of the Act, 42 U.S.C. 7411; and the national emissions standards for hazardous air pollutants under section 112 of the Act, 42 U.S.C. 7412.

C. Review of the Air Quality Criteria and Standards for O

Primary and secondary NAAQS were first established for photochemical oxidants in 1971 (36 FR 8186, April 30, 1971) based on the air quality criteria developed in 1970 (U.S. DHEW, 1970; 35 FR 4768, March 19, 1970). The EPA set both primary and secondary standards at 0.08 parts per million (ppm), as a 1-hour average of total photochemical oxidants, not to be exceeded more than one hour per year based on the scientific information in the 1970 air quality criteria document (AQCD). Since that time, the EPA has reviewed the air quality criteria and standards a number of times, with the most recent review being completed in 2015.

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 changed the indicator from photochemical oxidants to O

, revised the level of the primary and secondary standards from 0.08 to 0.12 ppm and revised the form of both standards from a deterministic (

i.e.,

not to be exceeded more than one hour per year) to a statistical form. With these changes, attainment of the standards was defined to occur when the average number of days per calendar year (across a 3-year period) with maximum hourly average O

concentration greater than 0.12 ppm equaled one or less (44 FR 8202, February 8, 1979; 43 FR 26962, June 22, 1978). Several petitioners challenged the 1979 decision. Among those, one claimed natural O

concentrations and other physical phenomena made the standard unattainable in the Houston area. The U.S. Court of Appeals for the District of Columbia Circuit (D.C. Circuit) rejected this argument, holding (as noted in section I.A above) that attainability and technological feasibility are not relevant considerations in the promulgation of the NAAQS (

American Petroleum Institute

Costle,

665 F.2d at 1185). 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 it through various compliance-related provisions in the CAA (

id.

at 1184-86).

The next periodic reviews of the criteria and standards for O

and other photochemical oxidants began in 1982 and 1983, respectively (47 FR 11561, March 17, 1982; 48 FR 38009, August 22, 1983). The EPA subsequently published the 1986 AQCD, 1989 Staff Paper, and a supplement to the 1986 AQCD (U.S. EPA, 1986; U.S. EPA, 1989; U.S. EPA, 1992). In August of 1992, the EPA proposed to retain the existing primary and secondary standards (57 FR 35542, August 10, 1992). In March 1993, the EPA concluded this review by finalizing its proposed decision to retain the standards, without revision (58 FR 13008, March 9, 1993).

In the 1992 decision in that review, the EPA announced its intention to proceed rapidly with the next review of the air quality criteria and standards for O

and other photochemical oxidants

(57 FR 35542, August 10, 1992). The EPA subsequently published the AQCD and Staff Paper for that next review (U.S. EPA, 1996a; U.S. EPA, 1996b). In December 1996, the EPA proposed revisions to both the primary and secondary standards (61 FR 65716, December 13, 1996). The EPA completed this review in 1997 by revising the primary and secondary standards to 0.08 ppm, as the annual fourth-highest daily maximum 8-hour average concentration, averaged over three years (62 FR 38856, July 18, 1997).

In response to challenges to the EPA's 1997 decision, the D.C. Circuit remanded the 1997 O

NAAQS to the EPA, finding that section 109 of the CAA, as interpreted by the EPA, effected an unconstitutional delegation of legislative authority. See

American Trucking Ass'ns

EPA,

175 F.3d 1027, 1034-1040 (D.C. Cir. 1999). The court also directed that, in responding to the remand, the EPA should consider the potential beneficial health effects of O

pollution in shielding the public from the effects of solar ultraviolet (UV) radiation, as well as adverse health effects (

id.

at 1051-53). See

American Trucking Ass'ns

EPA,

195 F.3d 4, 10 (D.C. Cir. 1999) (granting panel rehearing in part but declining to review the ruling on consideration of the potential beneficial effects of O

pollution). After granting petitions for

certiorari,

the U.S. Supreme Court unanimously reversed the judgment of the D.C. Circuit on the constitutional issue, holding that section 109 of the CAA does not unconstitutionally delegate legislative power to the EPA. See

Whitman

American Trucking Ass'ns,

531 U.S. 457, 472-74 (2001). The Court remanded the case to the D.C. Circuit to consider challenges to the 1997 O

NAAQS that had not yet been addressed. On remand, the D.C. Circuit found the 1997 O

NAAQS to be “neither arbitrary nor capricious,” and so denied the remaining petitions for review. See

ATA III,

283 F.3d at 379.

Coincident with the continued litigation of the other issues, the EPA responded to the court's 1999 remand to consider the potential beneficial health effects of O

pollution in shielding the public from effects of UV radiation (66 FR 57268, Nov. 14, 2001; 68 FR 614, January 6, 2003). In 2001, 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 O

and other photochemical oxidants with a call for information in September 2000 (65 FR 57810, September 26, 2000). Documents developed for the review included the 2006 AQCD (U.S. EPA, 2006) and 2007 Staff Paper (U.S. EPA, 2007) and related technical support documents. In 2007, the EPA proposed revisions to the primary and secondary standards (72 FR 37818, July 11, 2007). The EPA completed the review in March 2008 by revising the levels of both the primary and secondary standards from 0.08 ppm to 0.075 ppm while retaining the other elements of the prior standards (73 FR 16436, March 27, 2008). A number of petitioners filed suit challenging this decision.

In September 2009, the EPA announced its intention to reconsider the 2008 O

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. In January 2010, the EPA issued a notice of proposed rulemaking to reconsider the 2008 final decision (75 FR 2938, January 19, 2010). Later that year, in view of the need for further consideration and the fact that the Agency's next periodic review of the O

NAAQS required under CAA section 109 had already begun (as announced on September 29, 2008),

the EPA consolidated the reconsideration with its statutorily required periodic review.

The press release of this announcement is available at:

https://archive.epa.gov/epapages/newsroom_archive/newsreleases/85f90b7711acb0c88525763300617d0d.html.

The “Call for Information

”

initiating the new review was announced in the

Federal Register

(73 FR 56581, September 29, 2008).

This rulemaking, completed in 2015, concluded the reconsideration process.

In light of the EPA's decision to consolidate the reconsideration with the review then ongoing, the D.C. Circuit proceeded with the litigation on the 2008 O

NAAQS decision. On July 23, 2013, the court upheld the EPA's 2008 primary standard, but remanded the 2008 secondary standard to the EPA. See

Mississippi

EPA,

744 F.3d 1334 (D.C. Cir. 2013). With respect to the primary standard, the court rejected petitioners' arguments, upholding the EPA's decision. With respect to the secondary standard, the court held that the EPA's explanation for the setting of the secondary standard identical to the revised 8-hour primary standard was inadequate under the CAA because the EPA had not adequately explained how that standard provided the required public welfare protection.

At the time of the court's decision, the EPA had already completed significant portions of its next statutorily required periodic review of the O

NAAQS, which had been formally initiated in 2008, as summarized above. The documents developed for this review included the ISA,

Risk and Exposure Assessments (REAs) for health and welfare, and PA.

In late 2014, the EPA proposed to revise the 2008 primary and secondary standards (79 FR 75234, December 17, 2014; Frey, 2014a, Frey, 2014b, Frey, 2014c, U.S. EPA, 2014a, U.S. EPA, 2014b, U.S. EPA, 2014c). The EPA's final decision in this review was published in October 2015, establishing the now-current standards (80 FR 65292, October 26, 2015). In this decision, based on consideration of the health effects evidence on respiratory effects of O

in at-risk populations, the EPA revised the primary standard from a level of 0.075 ppm to a level of 0.070 ppm, while retaining all other elements of the standard (80 FR 65292, October 26, 2015). The EPA's decision on the level for the standard was based on the weight of the scientific evidence and quantitative exposure/risk information. The level of the secondary standard was also revised from 0.075 ppm to 0.070 ppm based on the scientific evidence of O

effects on welfare, particularly the evidence of O

impacts on vegetation, and quantitative analyses available in the review.

The other elements of the standard were retained. This decision on the secondary standard also incorporated the EPA's response to the D.C. Circuit's remand of the 2008 secondary standard in

Mississippi

EPA,

744 F.3d 1344 (D.C. Cir. 2013).

The ISA serves the same purpose, in reviewing the air quality criteria, as the AQCD did in prior reviews.

The PA presents an evaluation, for consideration by the Administrator, of the policy implications of the currently available scientific information, assessed in the ISA; the quantitative air quality, exposure or risk analyses presented in the PA and developed in light of the ISA findings; and related limitations and uncertainties. The role of the PA is to help “bridge the gap” between the Agency's scientific assessment and quantitative technical analyses, and the judgments required of the Administrator in his decisions in the review of the O

NAAQS.

These standards, set in 2015, are specified at 40 CFR 50.19.

The 2015 revisions to the NAAQS were accompanied by revisions to the data handling procedures, ambient air monitoring requirements, the air quality index and several provisions related to implementation (80 FR 65292, October 26, 2015).

After publication of the final rule, a number of industry groups, environmental and health organizations, and certain states filed petitions for judicial review in the D.C. Circuit. The

industry and state petitioners argued that the revised standards were too stringent, while the environmental and health petitioners argued that the revised standards were not stringent enough to protect public health and welfare as the Act requires. On August 23, 2019, the court issued an opinion that denied all the petitions for review with respect to the 2015 primary standard while also concluding that the EPA had not provided a sufficient rationale for aspects of its decision on the 2015 secondary standard and remanding that standard to the EPA. See

Murray Energy Corp.

EPA,

936 F.3d 597 (D.C. Cir. 2019). The court's decision on the secondary standard focused on challenges to particular aspects of EPA's decision. The court concluded that EPA's identification of particular benchmarks for evaluating the protection the standard provided against welfare effects associated with tree growth loss was reasonable and consistent with CASAC's advice. However, the court held that EPA had not adequately explained its decision to focus on a 3-year average for consideration of the cumulative exposure, in terms of W126, identified as providing requisite public welfare protection, or its decision to not identify a specific level of air quality related to visible foliar injury. The EPA's decision not to use a seasonal W126 index as the form and averaging time of the secondary standard was also challenged, but the court did not reach that issue, concluding that it lacked a basis to assess the EPA's rationale on this point because the EPA had not yet fully explained its focus on a 3-year average W126 in its consideration of the standard. See

Murray Energy Corp.

EPA,

936 F.3d 597, 618 (D.C. Cir. 2019). Accordingly, the court remanded the secondary standard to EPA for further justification or reconsideration. The court's remand of the secondary standard has been considered in reaching the proposed decision, and associated proposed conclusions and judgments, described in section III.D.3 below.

In the August 2019 decision, the court additionally addressed arguments regarding considerations of background O

concentrations, and socioeconomic and energy impacts. With regard to the former, the court rejected the argument that the EPA was required to take background O

concentrations into account when setting the NAAQS, holding that the text of CAA section 109(b) precluded this interpretation because it would mean that if background O

levels in any part of the country exceeded the level of O

that is requisite to protect public health, the EPA would be obliged to set the standard at the higher nonprotective level (

id.

at 622-23). Thus, the court concluded that the EPA did not act unlawfully or arbitrarily or capriciously in setting the 2015 NAAQS without regard for background O

(

id.

at 624). Additionally, the court denied arguments that the EPA was required to consider adverse economic, social, and energy impacts in determining whether a revision of the NAAQS was “appropriate” under section 109(d)(1) of the CAA (

id.

at 621-22). The court reasoned that consideration of such impacts was precluded by

Whitman's

holding that the CAA “unambiguously bars cost considerations from the NAAQS-setting process” (531 U.S. at 471, summarized in section 1.2 above). Further, the court explained that section 109(d)(2)(C)'s requirement that CASAC advise the EPA “of any adverse public health, welfare, social, economic, or energy effects which may result from various strategies for attainment and maintenance” of revised NAAQS had no bearing on whether costs are to be considered in setting the NAAQS (

Murray Energy Corp.

EPA,

936 F.3d at 622). Rather, as described in

Whitman

and discussed further in section I.A above, most of that advice would be relevant to implementation but not standard setting (

id.

In May 2018, the Administrator directed his Assistant Administrators to initiate this current review of the O

NAAQS (Pruitt, 2018). In conveying this direction, the Administrator further directed the EPA staff to expedite the review, implementing an accelerated schedule aimed at completion of the review within the statutorily required period (Pruitt, 2018). Accordingly, the EPA took immediate steps to proceed with the review. In June 2018, the EPA announced the initiation of the current periodic review of the air quality criteria for photochemical oxidants and the O

NAAQS and issued a call for information in the

Federal Register

(83 FR 29785, June 26, 2018). Two types of information were called for: Information regarding significant new O

research to be considered for the ISA for the review, and policy-relevant issues for consideration in this NAAQS review. Based in part on the information received in response to the call for information, the EPA developed a draft IRP, which was made available for consultation with the CASAC and for public comment (83 FR 55163, November 2, 2018; 83 FR 55528, November 6, 2018). Comments from the CASAC (Cox, 2018) and the public were considered in preparing the final IRP (U.S. EPA, 2019b).

Under the plan outlined in the IRP and consistent with revisions to the process identified by the administrator in his 2018 memo directing initiation of the review, the current review of the O

NAAQS is progressing on an accelerated schedule (Pruitt, 2018). The EPA is incorporating a number of efficiencies in various aspects of the review process, as summarized in the IRP, to support completion within the statutorily required period (Pruitt, 2018). As one example of such an efficiency, rather than produce two separate documents, the exposure and risk analyses for the primary standard are included as an appendix in the PA, along with a number of other technical appendices. The draft PA (including these analyses as appendices) was reviewed by the CASAC and made available for public comment while the draft ISA was also being reviewed by the CASAC and was available for public comment (84 FR 50836, September 26, 2019; 84 FR 58711, November 1, 2019).

The CASAC was assisted in its review by a pool of consultants with expertise in a number of fields (84 FR 38625, August 7, 2019). The approach employed by the CASAC in utilizing outside technical expertise represents an additional modification of the process from past reviews. Rather than join with some or all of the CASAC members in a CASAC review panel as has been common in other NAAQS reviews in the past, in this O

NAAQS review (and also in the recent CASAC review of the PA for the particulate matter NAAQS), the consultants comprised a pool of expertise that CASAC members drew on through the use of specific questions, posed in writing prior to the public meeting, regarding aspects of the documents being reviewed, obtaining subject matter expertise for its document review in a focused, efficient and transparent manner.

The draft ISA and draft PA were released for public comment and CASAC review on September 26, 2019 and October 31, 2019, respectively. The charges for the CASAC review summarized the overarching context for the document review (including reference to Pruitt [2018], and the CASAC's role under section 109(d)(2)(C) of the Act), as well as specific charge questions for review of each of the documents.

The CASAC discussed its review of both the draft ISA and the draft PA over three days at a public meeting in December 2019 (84 FR 58713, November 1, 2019).

The CASAC discussed its

draft letters describing its advice and comments on the documents in a public teleconference in early February 2020 (85 FR 4656; January 27, 2020). The letters to the Administrator conveying the CASAC advice and comments on the draft PA and draft ISA were released later that month (Cox, 2020a, Cox, 2020b).

While simultaneous review of first drafts of both documents has not been usual in past reviews, there have been occurrences of the CASAC review of a draft PA (or draft REA when the process

involved a policy assessment being included within the REA document) simultaneous with review of a second (or later) draft ISA (

e.g.,

73 FR 19835, April 11, 2008; 73 FR 34739, June 18, 2008; 77 FR 64335, October 19, 2020; 78 FR 938, January 7, 2013).

The letters from the CASAC and public comment on the draft ISA and draft PA have informed completion of the final documents and further inform development of the Administrator's proposed decision in this review. Comments from the CASAC on the draft ISA have been considered by the EPA and led to a number of revisions in developing the final document. The CASAC review and the EPA's consideration of CASAC comments are described in Appendix 10, section 10.4.5 of the final ISA. In his reply to the CASAC letter conveying its review, “Administrator Wheeler noted, `for those comments and recommendations that are more significant or cross-cutting and which were not fully addressed, the Agency will develop a plan to incorporate these changes into future Ozone ISAs as well as ISAs for other criteria pollutant reviews' ” (ISA, p. 10-28; Wheeler, 2020). The ISA was completed and made available to the public in April 2020 (85 FR 21849, April 20, 2020). Based on the rigorous scientific approach utilized in its development, summarized in Appendix 10 of the final ISA, the EPA considers the final ISA 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 [O

] in the ambient air, in varying quantities” as required by the CAA (42 U.S.C. 7408(a)(2)).

The CASAC comments additionally provided advice with regard to the primary and secondary standards, as well as a number of comments intended to improve the PA. These comments were considered in completing that document, which was completed in May 2020 (85 FR 31182, May 22, 2020). The CASAC advice to the Administrator regarding the O

standards has also been described and considered in the PA, and in sections II and III below. The CASAC advice on the primary standard is summarized in II.D.2 below and its advice on the secondary standard is summarized in section III.D.2.

Materials upon which this proposed decision is based, including the documents described above, are available to the public in the docket for the review.

Following a public comment period on the proposed decision, a final decision in the review is projected for late in 2020.

The docket for the current O

NAAQS review is identified as EPA-HQ-OAR-2018-0279. This docket has incorporated the ISA docket (EPA-HQ-ORD-2018-0274) by reference. Both dockets are publicly accessible at

www.regulations.gov.

D. Air Quality Information

Ground level ozone concentrations are a mix of mostly tropospheric ozone and some stratospheric ozone. Tropospheric ozone is formed due to chemical interactions involving solar radiation and precursor pollutants including volatile organic compounds (VOCs) and nitrogen oxides (NO

). Methane (CH

) and carbon monoxide (CO) are also important precursors, particularly at the regional to global scale. The precursor emissions leading to tropospheric O

formation can result from both man-made sources (

e.g.,

motor vehicles and electric power generation) and natural sources (

e.g.,

vegetation and wildfires). In addition, O

that is created naturally in the stratosphere also contributes to O

levels near the surface. The stratosphere routinely mixes with the troposphere high above the earth's surface and, less frequently, there are intrusions of stratospheric air that reach deep into the troposphere and even to the surface. Once formed, O

near the surface can be transported by winds before eventually being removed from the atmosphere via chemical reactions or deposition to surfaces. In sum, O

concentrations are influenced by complex interactions between precursor emissions, meteorological conditions, and topographical characteristics (PA, section 2.1; ISA, Appendix 1).

For compliance and other purposes, state and local environmental agencies operate O

monitors across the U.S. and submit the data to the EPA. At present, there are approximately 1,300 monitors across the U.S. reporting hourly O

averages during the times of the year when local O

pollution can be important (PA, section 2.3.1).

Most of this monitoring is focused on urban areas where precursor emissions tend to be largest, as well as locations directly downwind of these areas. There are also over 100 routine monitoring sites in rural areas, including sites in the Clean Air Status and Trends Network (CASTNET) which is specifically focused on characterizing conditions in rural areas. Based on the monitoring data for the most recent 3-year period (2016-2018), the EPA identified 142 counties, in which together approximately 106 million Americans reside where O

design values

were above 0.070, the level of the existing NAAQS (PA, section 2.4.1). Across these areas, the highest design values are typically observed in California, Texas, and the Northeast Corridor, locations with some of the most densely populated areas in the country (

e.g.,

PA, Figure 2-8).

monitoring seasons vary by state from five months (May to September in Oregon and Washington) to all twelve months (in 11 states), with the most common season being March to October (in 27 states).

A design value is a statistic that summarizes the air quality data for a given area in terms of the indicator, averaging time, and form of the standard. Design values can be compared to the level of the standard and are typically used to designate areas as meeting or not meeting the standard and assess progress towards meeting the NAAQS.

From a temporal perspective, the highest daily peak O

concentrations generally tend to occur during the afternoon and within the warmer months of the year due to higher levels of solar radiation and other conducive meteorological conditions during these times. The exceptions to this general rule include (1) some rural sites where transport of O

from upwind urban areas can occasionally result in high nighttime levels of O

, (2) high-elevation sites which can be episodically influenced by stratospheric intrusions in other months of the year, and (3) mountain basins in the western U.S. where large quantities of O

precursors emissions associated with oil and gas development can be trapped in a shallow inversion layer and form O

under clear, calm skies with snow cover during the colder months (PA, section 2.1; ISA, Appendix 1).

Monitoring data indicate long-term reductions in short-term O

concentrations. For example, monitoring sites operating since 1980 indicate a 32% reduction in the national average annual fourth highest daily maximum 8-hour concentration from 1980 to 2018. (PA, Figure 2-10). This has been accompanied by appreciable reductions in peak 1-hour concentrations (PA, Figure 2-17).

Concentrations of O

in ambient air that result from natural and non-U.S. anthropogenic sources are collectively referred to as U.S. background O

(USB; PA, section 2.5). As in the last review, we generally characterize O

concentrations that would exist in the absence of U.S. anthropogenic emissions as U.S. background (USB). Findings from modeling analyses performed for this review to investigate

patterns of USB in the U.S. are largely consistent with conclusions reached in the last review (PA, section 2.5.4). The current modeling analysis indicates spatial variation in USB O

that is related to geography, topography and proximity to international borders and is also influenced by seasonal variation, with long-range international anthropogenic transport contributions peaking in the spring while U.S. anthropogenic contributions tend to peak in summer. The West is predicted to have higher USB concentrations than the East, with higher contributions from natural and international anthropogenic sources that exert influences in western high-elevation and near-border areas. The modeling predicts that for both the West and the East, days with the highest 8-hour concentrations of O

generally occur in summer and are likely to have substantially greater concentrations due to U.S. anthropogenic sources. While the USB contributions to O

concentrations on days with the highest 8-hour concentrations are generally predicted to come largely from natural sources, the modeling also indicates that a small area near the Mexico border may receive appreciable contributions from a combination of natural and international anthropogenic sources on these days. In such locations, the modeling suggests the potential for episodic and relatively infrequent events with substantial background contributions where daily maximum 8-hour O

concentrations approach or exceed the level of the current NAAQS (

i.e.,

70 ppb). This contrasts with most monitor locations in the U.S. for which international contributions are predicted to be the lowest during the season with the most frequent occurrence of daily maximum 8-hour O

concentrations above 70 ppb. This is generally because, except for in near-border areas, larger international contributions are associated with long-distance transport and that is most efficient in the springtime (PA, section 2.5.4).

II. Rationale for Proposed Decision on the Primary Standard

This section presents the rationale for the Administrator's proposed decision to retain the current primary O

standard. This rationale is based on a thorough review of the latest scientific information generally published between January 2011 and March 2018, as well as more recent studies identified during peer review or by public comments (ISA, section IS.1.2),

integrated with the information and conclusions from previous assessments and presented in the ISA, on human health effects associated with photochemical oxidants including O

and pertaining to their presence in ambient air. The Administrator's rationale also takes into account: (1) The PA evaluation of the policy-relevant information in the ISA and presentation of quantitative analyses of air quality, human exposure and health risks; (2) CASAC advice and recommendations, as reflected in discussions of drafts of the ISA and PA at public meetings and in the CASAC's letters to the Administrator; and (3) public comments received during the development of these documents.

In addition to the review's opening “Call for Information” (83 FR 29785, June 26, 2018), systematic review methodologies were applied to identify relevant scientific findings that have emerged since the 2013 ISA, which included peer reviewed literature published through July 2011. Search techniques for the current ISA identified and evaluated studies and reports that have undergone scientific peer review and were published or accepted for publication between January 1, 2011 (providing some overlap with the cutoff date for the last ISA) and March 30, 2018. Studies published after the literature cutoff date for this ISA were also considered if they were submitted in response to the Call for Information or identified in subsequent phases of ISA development, particularly to the extent that they provide new information that affects key scientific conclusions (ISA, Appendix 10, section 10.2). References that are cited in the ISA, the references that were considered for inclusion but not cited, and electronic links to bibliographic information and abstracts can be found at:

https://hero.epa.gov/hero/index.cfm/project/page/project_id/2737.

In presenting the rationale for the Administrator's proposed decision and its foundations, section II.A provides background and introductory information for this review of the primary O

standard. It includes background on the establishment of the current standard in 2015 (section II.A.1) and also describes the general approach for the current review (section II.A.2). Section II.B summarizes the currently available health effects evidence, focusing on consideration of key policy-relevant aspects. Section II.C summarizes the exposure and risk information for this review, drawing on the quantitative analyses for O

, presented in the PA. Section II.D presents the Administrator's proposed conclusions on the current standard (section II.D.3), drawing on both evidence-based and exposure/risk-based considerations (section II.D.1) and advice from the CASAC (section II.D.2).

A. General Approach

The past and current approaches described below are both based, most fundamentally, on using the EPA's assessments of the current scientific evidence and associated quantitative analyses to inform the Administrator's judgment regarding a primary standard for photochemical oxidants that is requisite to protect the public health with an adequate margin of safety. The EPA's assessments are primarily documented in the ISA and PA, all of which have received CASAC review and public comment (84 FR 50836, September 26, 2019; 84 FR 58711, November 1, 2019; 84 FR 58713, November 1, 2019; 85 FR 21849, April 20, 2020; 85 FR 31182, May 22, 2020). In bridging the gap between the scientific assessments of the ISA and the judgments required of the Administrator in his decisions on the current standard, the PA evaluates policy implications of the evaluation of the current evidence in ISA and the quantitative exposure and risk analyses documented in appendices of the PA. In evaluating the public health protection afforded by the current standard, the four basic elements of the NAAQS (indicator, averaging time, level, and form) are considered collectively.

The final decision on the adequacy of the current primary standard is a public health policy judgment to be made by the Administrator. In reaching conclusions with regard to the standard, the decision will draw on the scientific information and analyses about health effects, population exposure and risks, as well as judgments about how to consider the range and magnitude of uncertainties that are inherent in the scientific evidence and analyses. This approach is based on the recognition that the available health effects evidence generally reflects a continuum, consisting of levels at which scientists generally agree that health effects are likely to occur, through lower levels at which the likelihood and magnitude of the response become increasingly uncertain. This approach is consistent with the requirements of the NAAQS provisions of the Clean Air Act and with how the EPA and the courts have historically interpreted the Act (summarized in section I.A. above). These provisions require the Administrator to establish primary standards that, in the judgment of the Administrator, are requisite to protect public health with an adequate margin of safety. In so doing, the Administrator seeks to establish standards that are neither more nor less stringent than necessary for this purpose. The Act does not require that primary standards be set at a zero-risk level, but rather at a level that avoids unacceptable risks to public

health, including the health of sensitive groups.

As noted in section I.A above, the legislative history describes such protection for the sensitive group of individuals and not for a single person in the sensitive group (see S. Rep. No. 91-1196, 91st Cong., 2d Sess. 10 [1970]).

The subsections below provide background and introductory information. Background on the establishment of the current standard in 2015, including the rationale for that decision, is summarized in section II.A.1. This is followed, in section II.A.2, by an overview of the general approach for the current review of the 2015 standard. Following this introductory section and subsections, the subsequent sections summarize current information and analyses, including that newly available in this review. The Administrator's proposed conclusions on the standard set in 2015, based on the current information, are provided in section II.D.3.

1. Background on the Current Standard

The current primary standard was set in 2015 based on the scientific evidence and quantitative exposure and risk analyses available at that time, and on the Administrator's judgments regarding the available scientific evidence, the appropriate degree of public health protection for the revised standard, and the available exposure and risk information regarding the exposures and risk that may be allowed by such a standard (80 FR 65292, October 26, 2015). The 2015 decision revised the level of the primary standard from 0.075 to 0.070 ppm,

in conjunction with retaining the indicator (O

), averaging time (eight hours), and form (annual fourth-highest daily maximum 8-hour average concentration, averaged across three consecutive years). This action provided increased protection for at-risk populations,

such as children and people with asthma, against an array of adverse health effects. The 2015 decision drew upon the available scientific evidence assessed in the 2013 ISA, the exposure and risk information presented and assessed in the 2014 health REA (HREA), the consideration of that evidence and information in the 2014 PA, the advice and recommendations of the CASAC, and public comments on the proposed decision (79 FR 75234, December 17, 2014).

Although ppm are the units in which the level of the standard is defined, the units, ppb, are more commonly used throughout this document for greater consistency with their use in the more recent literature. The level of the current primary standard, 0.070 ppm, is equivalent to 70 ppb.

As used here and similarly throughout the document, the term population refers to persons having a quality or characteristic in common, such as, and including, a specific pre-existing illness or a specific age or lifestage. A lifestage refers to a distinguishable time frame in an individual's life characterized by unique and relatively stable behavioral and/or physiological characteristics that are associated with development and growth. Identifying at-risk populations includes consideration of intrinsic (

e.g.,

genetic or developmental aspects) or acquired (

e.g.,

disease or smoking status) factors that increase the risk of health effects occurring with exposure to a substance (such as O

) as well as extrinsic, nonbiological factors, such as those related to socioeconomic status, reduced access to health care, or exposure.

The health effects evidence base available in the 2015 review included extensive evidence from previous reviews as well as the evidence that had emerged since the prior review had been completed in 2008. This evidence base, spanning several decades, documents the causal relationship between exposure to O

and a broad range of respiratory effects (2013 ISA, p. 1-14). Such effects range from small, reversible changes in pulmonary function and pulmonary inflammation (documented in controlled human exposure studies involving exposures ranging from 1 to 8 hours) to more serious health outcomes such as emergency department visits and hospital admissions, which have been associated with ambient air concentrations of O

in epidemiologic studies (2013 ISA, section 6.2). In addition to extensive controlled human exposure and epidemiologic studies, the evidence base includes experimental animal studies that provide insight into potential modes of action for these effects, contributing to the coherence and robust nature of the evidence. Based on this evidence, the 2013 ISA concluded there to be a causal relationship between short-term O

exposures and respiratory effects, and also concluded that the relationship between longer-term exposure and respiratory effects was likely to be causal (2013 ISA, p. 1-14).

The 2013 ISA also concluded there likely to be causal relationship between short-term exposure and mortality, as well as short-term exposure and cardiovascular effects, including related mortality, and that the evidence was suggestive of causal relationships between long-term O

exposures and total mortality, cardiovascular effects and reproductive and developmental effects, and between short-term and long-term O

exposure and nervous system effects (2013 ISA, section 2.5.2).

With regard to the short-term respiratory effects that were the primary focus of the 2015 decision, the controlled human exposure studies were recognized to provide the most certain evidence indicating the occurrence of health effects in humans following specific O

exposures (80 FR 65343, October 26, 2015; 2014 PA, section 3.4). These studies additionally illustrate the role of ventilation rate

and exposure duration in eliciting responses to O

exposure at the lowest studied concentrations. The exposure concentrations eliciting a given level of response in subjects at rest are higher than those eliciting a response in subjects exposed while at elevated ventilation, such as while exercising (2013 ISA, section 6.2.1.1).

Ventilation rate (V

) is a specific technical term referring to breathing rate in terms of volume of air taken into the body per unit of time. The units for V

are usually liters (L) per minute (min). Another related term is equivalent ventilation rate (EVR), which refers to V

normalized by a person's body surface area in square meters (m

). Accordingly, the units for EVR are generally L/min-m

. For different activities, a person will experience different levels of exertion and different ventilation rates.

In the controlled human exposure studies, the magnitude or severity of the respiratory effects induced by O

is influenced by ventilation rate and exposure duration, as well as exposure concentration, with physical activity increasing ventilation and potential for effects. In studies of generally healthy adults exposed while at rest for 2 hours, 500 ppb is the lowest concentration eliciting a statistically significant O

-induced reduction in group mean lung function measures, while a much lower concentration produces such result when the study subject ventilation rates are sufficiently increased with exercise (2013 ISA, section 6.2.1.1). The lowest exposure concentration found to elicit a statistically significant O

-induced reduction in group mean lung function in an exposure of 2 hours or less was 120 ppb after a 1-hour exposure (continuous, very heavy exercise) of trained cyclists (2013 ISA, section 6.2.1.1; Gong et al., 1986) and after 2-hour exposure (intermittent heavy exercise) of young healthy adults (2013 ISA, section 6.2.1.1; McDonnell et al., 1983).

The exposure and risk information available in the 2015 review included exposure and risk estimates for air quality conditions just meeting the then-existing standard, and also for air quality conditions just meeting potential alternative standards (U.S. EPA, 2014a, hereafter 2014 HREA). Estimates were derived for two exposure-based analyses, as well as for an analysis based on epidemiologic study associations. The first of the exposure-based analyses involved comparison of population exposure estimates at elevated exertion to exposure benchmark concentrations (exposures of concern).

These benchmark concentrations are based on exposure concentrations from controlled human exposure studies in which lung function changes and other effects were measured in healthy, young adult volunteers exposed to O

while engaging in quasi-continuous moderate physical activity for a defined period (generally 6.6 hours).

The second

exposure-based analysis provided population risk estimates of the occurrence of days with O

-attributable lung function reductions of varying magnitudes by using the exposure-response (E-R) information in the form of E-R functions or other quantitative descriptions of biological processes.

In the epidemiologic study-based analysis, risk estimates were also derived from ambient air concentrations using concentration-response (C-R) functions derived from epidemiologic studies. These latter estimates were given less weight by the Administrator in her decision on the standard in light of conclusions reached in the 2014 PA and the HREA, which reflected lower confidence in these estimates (80 FR 65316-17, October 26, 2015).

The benchmark concentrations to which exposure concentrations experienced while at moderate or greater exertion were compared were 60, 70 and 80 ppb.

The studies given primary focus were those for which O

exposures occurred over the course of 6.6

hours during which the subjects engaged in six 50-minute exercise periods separated by 10-minute rest periods, with a 35-minute lunch period occurring after the third hour (

e.g.,

Folinsbee et al., 1988 and Schelegle et al., 2009). Responses after O

exposure were compared to those after filtered air exposure.

The E-R information and quantitative models derived from it are based on controlled human exposure studies.

The 2014 HREA developed exposure-based estimates for several population groups including all children and all adults. The type of exposure-based estimates that involved comparison of exposures to benchmarks was also derived for children with asthma and adults with asthma. The estimates of percentages of all children with exposures at or above benchmarks were virtually indistinguishable from the corresponding estimates for children with asthma.

When considered in terms of the number of children (rather than percentages of the child populations), the estimates for all children were much higher than those for children with asthma, with the magnitude of the differences varying based on asthma prevalence in each study area (2014 HREA, sections 5.3.2, 5.4.1.5 and section 5F-1). The estimates for percent of children experiencing an exposure at or above the benchmarks were higher than percent of adults due to the greater time that children spend outdoors and engaged in activities at elevated exertion (2014 HREA, section 5.3.2). Thus, consideration of the exposure-based results in the 2015 decision focused on the results for all children and children with asthma.

This reflects use of the same time-location-activity diary pool to construct each simulated individual's time-activity series, which is based on the similarities observed in the available diary data with regard to time spent outdoors and exertion levels (2014 HREA, sections 5.3.2 and 5.4.1.5).

In weighing the 2013 ISA conclusions with regard to the health effects evidence and making judgments regarding the public health significance of the quantitative estimates of exposures and risks allowed by the then-existing standard and potential alternative standards considered, as well as judgments regarding margin of safety, the Administrator considered the currently available information and commonly accepted guidelines or criteria within the public health community, including statements of the American Thoracic Society (ATS), an organization of respiratory disease specialists,

advice from the CASAC and public comments. In so doing, she recognized that the determination of what constitutes an adequate margin of safety is expressly left to the judgment of the EPA Administrator. See

Lead Industries Ass'n

EPA,

647 F.2d 1130, 1161-62 (D.C. Cir. 1980);

Mississippi

EPA,

744 F.3d 1334, 1353 (D.C. Cir. 2013). In NAAQS reviews generally, evaluations of how particular primary standards address the requirement to provide an adequate margin of safety include consideration of such factors as the nature and severity of the health effects, the size of the sensitive population(s) at risk, and the kind and degree of the uncertainties present. Consistent with past practice and long-standing judicial precedent, the Administrator took the need for an adequate margin of safety into account as an integral part of her decision-making.

In this regard, the 2014 PA considered statements issued by the ATS that had also been considered in prior reviews (ATS, 2000; ATS, 1985).

In the 2015 decision, the Administrator first addressed the adequacy of protection provided by the then-existing primary standard and decided that the standard should be revised. Considerations related to that decision are summarized in section II.A.1.a below. The considerations and decisions on the revisions to the then-existing standard in order to provide the requisite protection under the Act, including an adequate margin of safety, are summarized in section II.A.1.b.

a. Considerations Regarding Adequacy of the Prior Standard

In the decision that the primary standard that existed at the time of the last review should be revised, the Administrator at that time gave primary consideration to the evidence of respiratory effects from controlled human exposure studies, including those newly available in the review, and for which the exposure concentrations were at the lower end of those studied (80 FR 65343, October 26, 2015). This emphasis was consistent with comments from the CASAC at that time on the strength of this evidence (Frey, 2014b, p. 5). In placing weight on these studies, the Administrator took note of the variety of respiratory effects reported from the studies of healthy adults engaged in six 50-minute periods of moderate exertion within a 6.6-hour exposure to O

concentrations of 60 ppb and higher. The lowest exposure concentration in such studies for which a combination of statistically significant reduction in lung function and increase in respiratory symptoms was reported was 72 ppb (during the exercise periods),

while reduced lung function and increased pulmonary inflammation were reported following such exposures to O

concentrations as low as 60 ppb. In considering these findings, the Administrator noted that the combination of O

-induced lung function decrements and respiratory symptoms met ATS criteria for an adverse response.

She additionally noted the CASAC comments on this point and also its caution that these study findings were for healthy adults and thus indicated the potential for such effects in some groups of people, such as people with asthma, at lower exposure concentrations (Frey, 2014b, pp. 5-6; 80 FR 65343, October 26, 2015).

For the 70 ppb target exposure, Schelegle et al. (2009) reported, based on O

measurements during the six 50-minute exercise periods, that the mean O

concentration during the exercise portion of the study protocol was 72 ppb. Based on the measurements for the six exercise periods, the time weighted average concentration across the full 6.6-hour exposure was 73 ppb (Schelegle et al., 2009).

The most recent statement from the ATS available at the time of the 2015 decision stated that “[i]n drawing the distinction between adverse and nonadverse reversible effects, this committee recommended that reversible loss of lung function in combination with the presence of symptoms should be considered as adverse” (ATS, 2000).

The 2013 ISA indicated that the pattern of effects observed across the range of exposures assessed in the controlled human exposure studies, increasing with severity at higher exposures, is coherent with (

i.e.,

reasonably related to) the health outcomes reported to be associated with ambient air concentrations in epidemiologic studies (

e.g.,

respiratory-related hospital admissions, emergency department visits). With regard to the available epidemiologic studies, while analyses of O

air quality in the 2014 PA indicated that most O

epidemiologic studies reported health effect associations with O

concentrations in ambient air that violated the then-current (75 ppb) standard, the Administrator took particular note of a study that reported associations

between short-term O

concentrations and asthma emergency department visits in children and adults in a U.S. location that would have met the then-current standard over the entire 5-year study period (80 FR 65344, October 26, 2015; Mar and Koenig, 2009).

While uncertainties limited the Administrator's conclusions on air quality in locations of multicity epidemiologic studies,

in looking across the body of epidemiologic evidence, the Administrator reached the conclusion that analyses of air quality in some study locations supported the occurrence of adverse O

-associated effects at O

concentrations in ambient air that met, or are likely to have met, the then-current standard (80 FR 65344, October 26, 2016). Taken together, the Administrator concluded that the scientific evidence from controlled human exposure and epidemiologic studies called into question the adequacy of the public health protection provided by the 75 ppb standard that had been set in 2008.

The design values in this location over the study period were at or somewhat below 75 ppb (Wells, 2012).

Compared to the single-city epidemiologic studies, the Administrator noted additional uncertainty that applied specifically to interpreting air quality analyses within the context of multicity effect estimates for short-term O

concentrations, where effect estimates for individual study cities are not presented (80 FR 65344; October 26, 2015).

In considering the exposure and risk information, the Administrator gave particular attention to the exposure-based comparison-to-benchmarks analysis, focusing on the estimates of exposures of concern for children, in 15 urban study areas for air quality conditions just meeting the then-current standard. Consistent with the finding that larger percentages of children than adults were estimated to experience exposures at or above benchmarks, the Administrator focused on the results for all children and for children with asthma, noting that the results for these two groups, in terms of percent of the population group, are virtually indistinguishable (2014 HREA, sections 5.3.2, 5.4.1.5 and section 5F-1). In considering these estimates, she placed the greatest weight on estimates of two or more days with occurrences of exposures at or above the benchmarks, in light of her increased concern about the potential for adverse responses with repeated occurrences of such exposures. In particular, she noted that the types of effects shown to occur following exposures to O

concentrations from 60 ppb to 80 ppb, such as inflammation, if occurring repeatedly as a result of repeated exposure, could potentially result in more severe effects based on the ISA conclusions regarding mode of action (80 FR 65343, 65345, October 26, 2015; 2013 ISA, section 6.2.3).

While generally placing the greatest weight on estimates of repeated exposures, the Administrator also considered estimates for single exposures at or above the higher benchmarks of 70 and 80 ppb (80 FR 65345, October 26, 2015). Further, while the Administrator recognized the effects documented in the controlled human exposure studies for exposures to 60 ppb to be less severe than those associated with exposures to higher O

concentrations, she also recognized there to be limitations and uncertainties in the evidence base with regard to unstudied population groups. As a result, she judged it appropriate for the standard, in providing an adequate margin of safety, to provide some control of exposures at or above the 60 ppb benchmark (80 FR 65345-65346, October 26, 2015).

In addition to recognizing the potential for continued inflammation to evolve into other outcomes, the 2013 ISA also recognized that inflammation induced by a single exposure (or several exposures over the course of a summer) can resolve entirely (2013 ISA, p. 6-76; 80 FR 65331, October 26, 2015).

In considering the exposure estimates from the 2014 HREA with regard to public health implications, the Administrator concluded that the exposures and risks projected to remain upon meeting the then-current (75 ppb) standard could reasonably be judged to be important from a public health perspective. In particular, this conclusion was based on her judgment that it is appropriate to set a standard that would be expected to eliminate, or almost eliminate, the occurrence of exposures, while at moderate exertion, at or above 70 and 80 ppb (80 FR 65346, October 26, 2015). In addition, given that the average percent of children estimated to experience two or more days with exposures at or above the 60 ppb benchmark approaches 10% in some urban study areas (on average across the analysis years), the Administrator concluded that the then-current standard did not incorporate an adequate margin of safety against the potentially adverse effects that could occur following repeated exposures at or above 60 ppb (80 FR 65345-46, October 26, 2015). Further, although the Administrator recognized increased uncertainty in and placed less weight on the HREA estimates for lung function risk and for the epidemiologic-study-based risk analyses, she found them supportive of a conclusion that the O

-associated health effects estimated to remain upon just meeting the then-current standard are an issue of public health importance on a broad national scale. Thus, she concluded that O

exposure and risk estimates, taken together, supported a conclusion that the exposures and health risks associated with just meeting the then-current standard could reasonably be judged to be of public health significance, such that the then-current standard was not sufficiently protective and did not incorporate an adequate margin of safety.

In consideration of all of the above, as well as the CASAC advice, which included the unanimous recommendation “that the Administrator revise the current primary ozone standard to protect public health” (Frey, 2014b, p. 5),

the Administrator concluded that the then-current primary O

standard (with its level of 75 ppb) was not requisite to protect public health with an adequate margin of safety, and that it should be revised to provide increased public health protection. This decision was based on the Administrator's conclusions that the available evidence and exposure and risk information clearly called into question the adequacy of public health protection provided by the then-current primary standard such that it was “not appropriate, within the meaning of section 109(d)(1) of the CAA, to retain the current standard” (80 FR 65346, October 26, 2015).

The Administrator also noted that CASAC for the prior, 2008, review likewise recommended revision of the standard to one with a level below 75 ppb. This earlier recommendation was based entirely on the evidence and information in the record for the 2008 decision, which had been expanded in the 2015 review (Samet, 2011; Frey and Samet, 2012).

b. Considerations for the Revised Standard

With regard to the most appropriate indicator for a revised standard, the Administrator considered findings and assessments in the 2013 ISA and 2014 PA, as well as advice from the CASAC and public comment. These include the finding that O

is the only photochemical oxidant (other than nitrogen dioxide) that is routinely monitored and for which a comprehensive database exists, and the consideration that, since the precursor emissions that lead to the formation of O

also generally lead to the formation of other photochemical oxidants, measures leading to reductions in population exposures to O

can generally be expected to lead to reductions in other photochemical oxidants (2013 ISA, section 3.6; 80 FR

65347, October 26, 2015). The CASAC indicated its view that O

is the appropriate indicator “based on its causal or likely causal associations with multiple adverse health outcomes and its representation of a class of pollutants known as photochemical oxidants” (Frey, 2014c, p. ii). Based on all of these considerations and public comments, the Administrator concluded that O

remained the most appropriate indicator for a standard meant to provide protection against photochemical oxidants in ambient air, and she retained O

as the indicator for the primary standard (80 FR 65347, October 26, 2015).

The 8-hour averaging time for the primary O

standard was established in 1997 with the decision to replace the then-existing 1-hour standard with an 8-hour standard (62 FR 38856, July 18, 1997). The decision in that review was based on evidence from numerous controlled human exposure studies of healthy adults of adverse respiratory effects resulting from 6- to 8-hour exposures, as well as quantitative analyses indicating the control provided by an 8-hour averaging time of both 8-hour and 1-hour peak exposures and associated health risk (62 FR 38861, July 18, 1997; U.S. EPA, 1996b). The 1997 decision was also consistent with advice from the CASAC (62 FR 38861, July 18, 1997; 61 FR 65727, December 13, 1996). The EPA reached similar conclusions in the subsequent 2008 review in which the 8-hour averaging time was retained (73 FR 16436, March 27, 2008). In the review completed in 2015, the Administrator concluded, in consideration of the then-available health effects information, that an 8-hour averaging time remained appropriate for addressing health effects associated with short-term exposures to ambient air O

and that it could effectively limit health effects attributable to both short- and long-term O

exposures (80 FR 65348, October 26, 2015). Thus, she found it appropriate to retain this averaging time (80 FR 65350, October 26, 2015).

While giving foremost consideration to the adequacy of public health protection provided by the combination of all elements of the standard, including the form, the Administrator additionally considered the appropriateness of retaining the

th-high metric as the form for the revised standard (80 FR 65350-65352, October 26, 2015). In so doing, she considered findings from prior reviews, including the 1997 review, in which it was recognized that a concentration-based form, by giving proportionally more weight to years when 8-hour O

concentrations are well above the level of the standard than years when concentrations are just above the level, better reflects the continuum of health effects associated with increasing O

concentrations than does an expected exceedance form, which had been the form of the standard prior to 1997.

Although the subsequent 2008 review considered the potential value of a percentile-based form, the EPA concluded at that time that, because of the differing lengths of the monitoring season for O

across the U.S., a percentile-based statistic would not be effective in ensuring the same degree of public health protection across the country (73 FR 16474-75, March 27, 2008). The 2008 review additionally recognized the importance of a form that provides stability to ongoing control programs and insulation from the impacts of extreme meteorological events that are conducive to O

occurrence (73 FR 16474-16475, March 27, 2008). Based on all of these considerations, and including advice from the CASAC, which stated that this form “provides health protection while allowing for atypical meteorological conditions that can lead to abnormally high ambient ozone concentrations which, in turn, provides programmatic stability” (Frey, 2014b, p. 6), the 2015 decision was to retain the existing form (the annual fourth-highest daily maximum 8-hour O

average concentration, averaged over three consecutive years), without revision (80 FR 65352, October 26, 2015).

With regard to a specific concentration-based form, the fourth-highest daily maximum was selected in 1997, recognizing that a less restrictive form (

e.g.,

fifth highest) would allow a larger percentage of sites to experience O

peaks above the level of the standard, and would allow more days on which the level of the standard may be exceeded when the site attains the standard (62 FR 38868-38873, July 18, 1997), and there was no basis identified for selection of a more restrictive form (62 FR 38856, July 18, 1997).

The 2015 decision to set the level of the revised primary O

standard at 70 ppb built upon the Administrator's conclusion (summarized in section II.A.1.a above) that the overall body of scientific evidence and exposure/risk information called into question the adequacy of the public health protection afforded by the then-current standard, particularly for at-risk populations and lifestages (80 FR 65362, October 26, 2015). In her decision on level, the Administrator placed the greatest weight on the results of controlled human exposure studies and on quantitative analyses based on information from these studies, particularly analyses of O

exposures of concern.

In so doing, the Administrator noted that controlled human exposure studies provide the most certain evidence indicating the occurrence of health effects in humans following specific O

exposures, noting in particular that the effects reported in the controlled human exposure studies are due solely to O

exposures, and are not complicated by the presence of co-occurring pollutants or pollutant mixtures (as is the case in epidemiologic studies). The Administrator's emphasis on the information from the controlled human exposure studies was consistent with the CASAC's advice and interpretation of the scientific evidence (80 FR 65362, October 26, 2015; Frey, 2014b). In this regard, the Administrator recognized that: (1) The largest respiratory effects, and the broadest range of effects, have been studied and reported following exposures to 80 ppb O

or higher (

i.e.,

decreased lung function, increased airway inflammation, increased respiratory symptoms, airway hyperresponsiveness, and decreased lung host defense); (2) exposures to O

concentrations somewhat above 70 ppb have been shown to both decrease lung function and to result in respiratory symptoms; and (3) exposures to O

concentrations as low as 60 ppb have been shown to decrease lung function and to increase airway inflammation (80 FR 65363, October 26, 2015). The Administrator also considered both ATS recommendations and CASAC advice to inform her judgments on the potential adversity to public health associated with O

effects reported in controlled human exposure studies (80 FR 65363, October 26, 2015).

The Administrator viewed the results of the lung function risk assessment, analyses of O

air quality in locations of epidemiologic studies, and epidemiologic-study-based quantitative health risk assessment as being of less utility for selecting a particular standard level among a range of options (80 FR 65362, October 26, 2015).

In so doing, the Administrator recognized that a standard level of 70 ppb would be well below the O

exposure concentration documented to result in the widest range of respiratory effects (

i.e.,

80 ppb), and below the lowest O

exposure concentration shown to result in the adverse combination of lung function decrements and respiratory symptoms (80 FR 65363, October 26, 2015).

In considering the degree of protection provided by a revised primary O

standard, and the extent to which that standard would be expected to limit population exposures to the broad range of O

exposures shown to result in health effects, the Administrator considered the exposure estimates from the HREA, focusing particularly on the estimates of two or more exposures of concern. In so doing,

she placed the most emphasis on setting a standard that appropriately limits repeated occurrences of exposures at or above the 70 and 80 ppb benchmarks, while at elevated ventilation. She noted that a revised standard with a level of 70 ppb was estimated to eliminate the occurrence of two or more days with exposures at or above 80 ppb and to virtually eliminate the occurrence of two or more days with exposures at or above 70 ppb for all children and children with asthma, even in the worst-case year and location evaluated.

Given the considerable protection provided against repeated exposures of concern for all benchmarks evaluated in the HREA, the Administrator judged that a standard with a level of 70 ppb incorporated a margin of safety against the adverse O

-induced effects shown to occur in the controlled human exposure studies (80 FR 65364, October 26, 2015).

Under conditions just meeting an alternative standard with a level of 70 ppb across the 15 urban study areas, the estimate for two or more days with exposures at or above 70 ppb was 0.4% of children, in the worst year and worst area (80 FR 65313, Table 1, October 26, 2015).

In so judging, she noted that the CASAC had recognized the choice of a standard level within the range it recommended based on the scientific evidence (which is inclusive of 70 ppb) to be a policy judgment (80 FR 65355, October 26, 2015; Frey, 2014).

While she was less confident that adverse effects would occur following exposures to O

concentrations as low as 60 ppb,

as discussed above, the Administrator also considered estimates of exposures (while at moderate or greater exertion) for the 60 ppb benchmark (80 FR 65363-64, October 26, 2015). In so doing, she recognized that while CASAC advice regarding the potential adversity of effects observed in studies of 60 ppb was less definitive than for effects observed at the next higher concentration studied, the CASAC did clearly advise the EPA to consider the extent to which a revised standard is estimated to limit the effects observed in studies of 60 ppb exposures (80 FR 65364, October 26, 2015; Frey, 2014b). The Administrator's consideration of exposures at or above the 60 ppb benchmark, and particularly consideration of multiple occurrences of such exposures, was primarily in the context of considering the extent to which the health protection provided by a revised standard included a margin of safety against the occurrence of adverse O

-induced effects (80 FR 65464, October 26, 2015). In this context, the Administrator noted that a revised standard with a level of 70 ppb was estimated to protect the vast majority of children in urban study areas (

i.e.,

about 96% to more than 99% of children in individual areas) from experiencing two or more days with exposures at or above 60 ppb (while at moderate or greater exertion). Compared to the estimates for the then-current standard (with its level of 75 ppb), this represented a reduction in repeated exposures of more than 60%. Given the considerable protection provided against repeated exposures of concern for all of the benchmarks evaluated, including the 60 ppb benchmark, the Administrator judged that a standard with a level of 70 ppb would incorporate a margin of safety against the adverse O

-induced effects shown to occur following exposures (while at moderate or greater exertion) to a somewhat higher concentration. The Administrator also judged the HREA results for one or more exposures at or above 60 ppb to provide further support for her somewhat broader conclusion that “a standard with a level of 70 ppb would incorporate an adequate margin of safety against the occurrence of O

exposures that can result in effects that are adverse to public health” (80 FR 65364, October 26, 2015).

The Administrator was “notably less confident in the adversity to public health of the respiratory effects that have been observed following exposures to O

concentrations as low as 60 ppb,” based on her consideration of the ATS recommendation on judging adversity from transient lung function decrements alone, the uncertainty in the potential for such decrements to increase the risk of other, more serious respiratory effects in a population (per ATS recommendations on population-level risk), and the less clear CASAC advice regarding potential adversity of effects at 60 ppb compared to higher concentrations studied (80 FR 65363, October 26, 2015).

While the Administrator was less concerned about single occurrences of O

exposures of concern, especially for the 60 ppb benchmark, she judged that estimates of one or more exposures of concern can provide further insight into the margin of safety provided by a revised standard. In this regard, she noted that “a standard with a level of 70 ppb is estimated to (1) virtually eliminate all occurrences of exposures of concern at or above 80 ppb; (2) protect the vast majority of children in urban study areas from experiencing any exposures of concern at or above 70 ppb (

i.e.,

≥ about 99%, based on mean estimates; Table 1); and (3) to achieve substantial reductions, compared to the then-current standard, in the occurrence of one or more exposures of concern at or above 60 ppb (

i.e.,

about a 50% reduction; Table 1)” (80 FR 65364, October 26, 2015).

In the context of considering a standard with a level of 70 ppb, the Administrator additionally considered the lung function risk estimates, epidemiologic evidence and quantitative estimates based on information from the epidemiologic studies. Although she placed less weight on these estimates and information in light of associated uncertainties,

she judged that a standard with a level of 70 ppb would be expected to result in important reductions in the population-level risk of endpoints on which these types of information are focused and provide associated additional public health protection, beyond that provided by the then-current standard (80 FR 65364, October 26, 2015).

The Administrator noted important uncertainties in using lung function risk estimates as a basis for considering the occurrence of adverse effects in the population (also recognized in the prior review) that limited her reliance on these estimates in reaching judgments on health protection of a standard level of 70 ppb versus lower levels. Additionally, with regard to epidemiologic studies, while the Administrator recognized there to be support for a standard level at least as low as 70 ppb from a single-epidemiologic study (Mar and Koenig, 2009) that reported health effect associations in a location that met the then-current standard over the entire study period but that would have violated a revised standard with a level of 70 ppb, she found these studies to be of more limited utility for distinguishing between the appropriateness of health protection estimated for a standard level of 70 ppb and that estimated for lower levels (80 FR 65364, October 26, 2015).

In summary, given her consideration of the evidence, exposure and risk information, advice from the CASAC, and public comments, the Administrator in 2015 judged a revised primary standard of 70 ppb, in terms of the 3-year average of annual fourth-highest daily maximum 8-hour average O

concentrations, to be requisite to protect public health, including the health of at-risk populations, with an adequate margin of safety (80 FR 65365, October 26, 2015).

2. Approach for the Current Review

To evaluate whether it is appropriate to consider retaining the current primary O

standard, or whether consideration of revision is appropriate, the EPA has adopted an approach in this review that builds upon the general approach used in the last review and reflects the body of evidence and information now available. Accordingly, the approach in this review takes into consideration the approach used in the last review, addressing key policy-relevant questions in light of currently available scientific and technical information. As summarized above, the Administrator's decisions in the prior review were based on an integration of O

health effects information with judgments on the adversity and public health significance of key health effects, policy judgments as to when the standard is requisite to protect public health with an adequate margin of safety, consideration of CASAC advice, and consideration of public comments.

Similarly, in this review, we draw on the current evidence and quantitative assessments of exposure pertaining to

the public health risk of O

in ambient air. In considering the scientific and technical information here, we consider both the information available at the time of the last review and information newly available since the last review, including that which has been critically analyzed and characterized in the current ISA. The quantitative exposure and risk analyses provide a context for interpreting the evidence of respiratory effects in people breathing at elevated rates and the potential public health significance of exposures associated with air quality conditions that just meet the current standard. The overarching purpose of these analyses is to inform the Administrator's conclusions on the public health protection afforded by the current primary standard, with an important focus on the potential for exposures and risks beyond those indicated by the information available at the time the standard was established.

B. Health Effects Information

The information summarized here is based on our scientific assessment of the health effects evidence available in this review; this assessment is documented in the ISA and its policy implications are further discussed in the PA. In this review, as in past reviews, the health effects evidence evaluated in the ISA for O

and related photochemical oxidants is focused on O

(ISA, section IS.1.1). Ozone is concluded to be the most prevalent photochemical oxidant present in the atmosphere and the one for which there is a very large, well-established evidence base of its health and welfare effects. Further, “the primary literature evaluating the health and ecological effects of photochemical oxidants includes ozone almost exclusively as an indicator of photochemical oxidants” (ISA, section IS.1.1). Thus, the current health effects evidence and the Agency's review of the evidence, including the evidence newly available in this review, continues to focus on O

More than 1600 studies are newly available and considered in the ISA, including more than 1000 health studies (ISA, Appendix 10, Figure 10-2). As in the last review, the key evidence comes from the body of controlled human exposure studies that document respiratory effects in people exposed for short periods (6.6 to 8 hours) during quasi-continuous exercise. Policy implications of the currently available evidence are discussed in the PA (as summarized in section II.D.1 below). The subsections below briefly summarize the following aspects of the evidence: The nature of O

-related health effects (section II.B.1), the potential public health implications and populations at risk (section II.B.2), and exposure concentrations associated with health effects (section II.B.3).

1. Nature of Effects

The evidence base available in the current review includes decades of extensive evidence that clearly describes the role of O

in eliciting an array of respiratory effects and recent evidence suggests the potential for relationships between O

exposure and other effects. As was established in prior reviews, the most commonly observed effects, and those for which the evidence is strongest, are transient decrements in pulmonary function and respiratory symptoms, such as coughing and pain on deep inspiration, as a result of short-term exposures (ISA, section IS.4.3.1; 2013 ISA, p. 2-26). These effects are demonstrated in the large, long-standing evidence base of controlled human exposure studies

(1978 AQCD, 1986 AQCD, 1996 AQCD, 2006 AQCD, 2013 ISA, ISA). The lung function effects are also positively associated with ambient air O

concentrations in epidemiologic panel studies, available in past reviews, that describe these associations for outdoor workers and children attending summer camps in the 1980s and 1990s (2013 ISA, section 6.2.1.2; ISA, Appendix 3, section 3.1.4.1.3). The epidemiologic evidence base additionally documents associations of O

concentrations in ambient air with more severe health outcomes, including asthma-related emergency department visits and hospital admissions (2013 ISA, section 6.2.7; ISA, Appendix 3, sections 3.1.5.1 and 3.1.5.2). Extensive experimental animal evidence informs a detailed understanding of mechanisms underlying the respiratory effects of short-term exposures (ISA, Appendix 3, section 3.1.11), and studies in animal models also provide evidence for effects of longer-term O

exposure on the developing lung (ISA, Appendix 3, section 3.2.6).

The vast majority of the controlled human exposure studies (and all of the studies conducted at the lowest exposures) involved young healthy adults (typically 18-13 years old) as study subjects (2013 ISA, section 6.2.1.1). There are also some controlled human exposure studies of one to eight hours duration in older adults and adults with asthma, and there are still fewer controlled human exposure studies in healthy children (

i.e.,

individuals aged younger than 18 years) or children with asthma (See, for example, PA, Appendix 3A, Table 3A-3).

The current evidence continues to support our prior conclusion that short-term O

exposure causes respiratory effects. Specifically, the full body of evidence continues to support the conclusion of a causal relationship of respiratory effects with short-term O

exposures and the conclusion that the relationship of respiratory effects with longer-term exposures is likely to be causal (ISA, sections IS.4.3.1 and IS.4.3.2). The current evidence base for short-term O

exposure and metabolic effects,

which was not evaluated as a separate category of effects in the last review when less evidence was available, is expanded by evidence newly available in this review. The ISA determines the current evidence sufficient to conclude that the relationship between short-term O

exposure and metabolic effects is likely to be causal (ISA, section IS.4.3.3). The newly available evidence is primarily from experimental animal research. For other types of health effects, new evidence has led to different conclusions from those reached in the prior review. Specifically, the current evidence, particularly in light of the additional controlled human exposure studies, is less consistent than what was previously available and less indicative of O

-induced cardiovascular effects. This evidence has altered conclusions from the last review with regard to relationships between short-term O

exposures and cardiovascular effects and mortality, such that the evidence is no longer concluded to indicate that the relationships are likely to be causal.

Thus, while conclusions have changed for some effects based on the new evidence, the conclusions reached in the last review on respiratory effects are supported by the current evidence, and conclusions are also newly reached for an additional category of health effects.

The term metabolic effects is used in the ISA to refer metabolic syndrome (a collection of risk factors including high blood pressure, elevated triglycerides and low high density lipoprotein cholesterol), diabetes, metabolic disease mortality, and indicators of metabolic syndrome that include alterations in glucose and insulin homeostasis, peripheral inflammation, liver function, neuroendocrine signaling, and serum lipids (ISA, section IS.4.3.3).

The currently available evidence for cardiovascular, reproductive and nervous system effects, as well as mortality, is “suggestive of, but not sufficient to infer” a causal relationship with short- or long-term O

exposures (ISA, Table IS-1). The evidence is inadequate to infer the presence or absence of a causal relationship between long-term O

exposure and cancer (ISA, section IS.4.3.6.6).

a. Respiratory Effects

As in the last review, the currently available evidence in this review supports the conclusion of a causal relationship between short-term O

exposure and respiratory effects (ISA, section IS.1.3.1). The strongest evidence for this comes from controlled human

exposure studies, also available in the last review, demonstrating O

-related respiratory effects in generally healthy adults.

Experimental studies in animals also document an array of respiratory effects resulting from short-term O

exposure and provide information related to underlying mechanisms (ISA, Appendix 3, section 3.1). The potential for O

exposure to elicit health outcomes more serious than those assessed in the controlled human exposure studies continues to be indicated by the epidemiologic evidence of associations of O

concentrations in ambient air with increased incidence of hospital admissions and emergency department visits for an array of health outcomes, including asthma exacerbation, COPD exacerbation, respiratory infection, and combinations of respiratory diseases (ISA, Appendix 3, sections 3.1.5 and 3.1.6). The strongest such evidence is for asthma-related outcomes and specifically asthma-related outcomes for children, indicating an increased risk for people with asthma and particularly children with asthma (ISA, Appendix 3, section 3.1.5.7).

The phrases “healthy adults” or “healthy subjects” are used to distinguish from subjects with asthma or other respiratory diseases, for which there are many fewer controlled human exposure studies. For studies of healthy subjects “the study design generally precludes inclusion of subjects with serious health conditions,” such as individuals with severe respiratory diseases (2013 ISA, p. lx).

Respiratory responses observed in human subjects exposed to O

for periods of 8 hours or less, while intermittently or quasi-continuously, exercising, include reduced lung function,

respiratory symptoms, increased airway responsiveness, mild bronchoconstriction (measured as an increase in specific airway resistance [sRaw]), and pulmonary inflammation, with associated injury and oxidative stress (ISA, Appendix 3, section 3.1.4; 2013 ISA, sections 6.2.1 through 6.2.4). The available mechanistic evidence, discussed in greater detail in the ISA, describes pathways involving the respiratory and nervous systems by which O

results in pain-related respiratory symptoms and reflex inhibition of maximal inspiration (inhaling a full, deep breath), commonly quantified by decreases in forced vital capacity (FVC) and total lung capacity. This reflex inhibition of inspiration combined with mild bronchoconstriction contributes to the observed decrease in FEV

, the most common metric used to assess O

-related lung function effects. The evidence also indicates that the additionally observed inflammatory response is correlated with mild airway obstruction, generally measured as an increase in sRaw (ISA, Appendix 3, section 3.1.3). As described in section II.B.3 below, the prevalence and severity of respiratory effects in controlled human exposure studies, including symptoms (

e.g.,

pain on deep inspiration, shortness of breath, and cough), increases with increasing O

concentration, exposure duration, and ventilation rate of exposed subjects (ISA, Appendix 3, sections 3.1.4.1 and 3.1.4.2).

In summarizing FEV

responses from controlled human exposure studies, an O

-induced change in FEV

is typically the difference between the change observed with O

exposure (post-exposure FEV

minus pre-exposure FEV

) and what is generally an improvement observed with filtered air (FA) exposure (post-exposure FEV

minus pre-exposure FEV

). As explained in the 2013 ISA, “[n]oting that some healthy individuals experience small improvements while others have small decrements in FEV

following FA exposure, investigators have used the randomized, crossover design with each subject serving as their own control (exposure to FA) to discern relatively small effects with certainty since alternative explanations for these effects are controlled for by the nature of the experimental design” (2013 ISA, pp. 6-4 to 6-5).

Within the evidence base from controlled human exposure studies, the majority of studies involve healthy adult subjects (generally 18 to 35 years), although there are studies involving subjects with asthma, and a limited number of studies, generally of durations shorter than four hours, involving adolescents and adults older than 50 years. A summary of salient observations of O

effects on lung function, based on the controlled human exposure study evidence reviewed in the 1996 and 2006 AQCDs, and recognized in the 2013 ISA, continues to pertain to this evidence base as it exists today: “(1) young healthy adults exposed to ≥80 ppb ozone develop significant reversible, transient decrements in pulmonary function and symptoms of breathing discomfort if minute ventilation (Ve) or duration of exposure is increased sufficiently; (2) relative to young adults, children experience similar spirometric responses [

i.e.,

as measured by FEV

and/or FVC] but lower incidence of symptoms from O

exposure; (3) relative to young adults, ozone-induced spirometric responses are decreased in older individuals; (4) there is a large degree of inter-subject variability in physiologic and symptomatic responses to O

, but responses tend to be reproducible within a given individual over a period of several months; and (5) subjects exposed repeatedly to O

for several days experience an attenuation of spirometric and symptomatic responses on successive exposures, which is lost after about a week without exposure” (ISA, Appendix 3, section 3.1.4.1.1, p. 3-11).

A spirometric response refers to a change in the amount of air breathed out of the body (forced expiratory volumes) and the associated time to do so (

e.g.,

FEV

The evidence is most well established with regard to the effects, reversible with the cessation of exposure, that are associated with short-term exposures of several hours. For example, the evidence indicates a rapid recovery from O

-induced lung function decrements (

e.g.,

reduced FEV

) and respiratory symptoms (2013 ISA, section 6.2.1.1). However, in some cases, such as after exposure to higher concentrations such as 300 ppb, the recovery phase may be slower and involve a longer time period (

e.g.,

at least 24 hours). Repeated daily exposure studies at such higher concentrations also have found FEV

response to be enhanced on the second day of exposure. This enhanced response is absent, however, with repeated exposure at lower concentrations, perhaps as a result of a more complete recovery or less damage to pulmonary tissues (2013 ISA, section pp. 6-13 to 6-14; Folinsbee et al., 1994).

With regard to airway inflammation and the potential for repeated occurrences to contribute to further effects, 2013 ISA indicates that O

-induced respiratory tract inflammation “can have several potential outcomes: (1) Inflammation induced by a single exposure (or several exposures over the course of a summer) can resolve entirely; (2) continued acute inflammation can evolve into a chronic inflammatory state; (3) continued inflammation can alter the structure and function of other pulmonary tissue, leading to diseases such as fibrosis; (4) inflammation can alter the body's host defense response to inhaled microorganisms, particularly in potentially at-risk populations such as the very young and old; and (5) inflammation can alter the lung's response to other agents such as allergens or toxins” (2013 ISA, p. 6-76). With regard to O

-induced increases in airway responsiveness, the controlled human exposure study evidence for healthy adults generally indicates resolution within 18 to 24 hours after exposure (ISA, Appendix 3, section 3.1.4.3.1).

The extensive evidence base for O

health effects, compiled over several decades, continues to indicate respiratory responses to short exposures as the most sensitive effects of O

. Such

effects are well documented in controlled human exposure studies, most of which involve healthy adult study subjects. These studies have documented an array of respiratory effects, including reduced lung function, respiratory symptoms, increased airway responsiveness, and inflammation, in study subjects following 1- to 8-hour exposures, primarily while exercising. Such effects are of increased significance to people with asthma given aspects of the disease that contribute to a baseline status that includes chronic airway inflammation and greater airway responsiveness than people without asthma (ISA, section 3.1.5). For example, due to the latter characteristic, O

exposure of a magnitude that increases airway responsiveness may put such people at potential increased risk for prolonged bronchoconstriction in response to asthma triggers (ISA, p. IS-22; 2013 ISA, section 6.2.9; 2006 AQCD, section 8.4.2). Further, children are the age group most likely to be outdoors at activity levels corresponding to those that have been associated with respiratory effects in the human exposure studies (as recognized below in sections II.B.2 and II.C). The increased significance of effects in people with asthma and risk of increased exposure for children is illustrated by the epidemiologic findings of positive associations between O

exposure and asthma-related ED visits and hospital admissions for children with asthma. Thus, the evidence indicates O

exposure to increase the risk of asthma exacerbation, and associated outcomes, in children with asthma.

With regard to an increased susceptibility to infectious diseases, the experimental animal evidence continues to indicate, as described in the 2013 ISA and past AQCDs, the potential for O

exposures to increase susceptibility to infectious diseases through effects on defense mechanisms of the respiratory tract (ISA, section 3.1.7.3; 2013 ISA, section 6.2.5). The evidence base regarding respiratory infections and associated effects has been augmented in this review by a number of epidemiologic studies reporting positive associations between short-term O

concentrations and emergency department visits for a variety of respiratory infection endpoints (ISA, Appendix 3, section 3.1.7).

Although the long-term exposure conditions that may contribute to further respiratory effects are less well understood, the conclusion based on the current evidence base remains that the relationship for such exposure conditions with respiratory effects is likely to be causal (ISA, section IS.4.3.2). Most notably, experimental studies, including with nonhuman infant primates, have provided evidence relating O

exposure to asthma-like effects, and epidemiologic cohort studies have reported associations of O

concentrations in ambient air with asthma development in children (ISA, Appendix 3, sections 3.2.4.1.3 and 3.2.6). The biological plausibility of such a role for O

has been indicated by animal toxicological evidence on biological mechanisms (ISA, Appendix 3, sections 3.2.3 and 3.2.4.1.2). Specifically, the animal evidence, including the nonhuman primate studies of early life O

exposure, indicates that such exposures can cause “structural and functional changes that could potentially contribute to airway obstruction and increased airway responsiveness,” which are hallmarks of asthma (ISA, Appendix 3, section 3.2.6, p. 3-113).

Overall, the respiratory effects evidence newly available in this review is generally consistent with the evidence base in the last review (ISA, Appendix 3, section 3.1.4). A few recent studies provide insights in previously unexamined areas, both with regard to human study groups and animal models for different effects, while other studies confirm and provide depth to prior findings with updated protocols and techniques (ISA, Appendix 3, sections 3.1.11 and 3.2.6). Thus, our current understanding of the respiratory effects of O

is similar to that in the last review.

One aspect of the evidence that has been augmented concerns pulmonary function in adults older than 50 years of age. Previously available evidence in this age group indicated smaller O

-related decrements in middle-aged adults (35 to 60 years) than in adults 35 years of age and younger (2006 AQCD, p. 6-23; 2013 ISA, p. 6-22; ISA, Appendix 3, section 3.1.4.1.1.2). A recent multicenter study of 55- to 70-year old subjects (average age of 60 years), conducted for a 3-hour duration involving alternating 15-minute rest and exercise periods and a 120 ppb exposure concentration, reported a statistically significant O

FEV

response (ISA, Appendix 3, section 3.1.4.1.1.2; Arjomandi et al., 2018). While there is not a study in younger adults of precisely comparable design, the mean response for the 55- to 70-year olds, 1.2% O

-related FEV

decrement, is lower than results for somewhat comparable exposures in adults aged 18 to 35 years, suggesting somewhat reduced responses to O

exposure in this older age group (ISA, Appendix 3, section 3.1.4.1.1.2; Arjomandi et al., 2018; Adams, 2000; Adams, 2006b).

Such a reduced response in middle-aged and older adults compared to young adults is consistent with conclusions in previous reviews (2013 ISA, section 6.2.1.1; 2006 AQCD, section 6.4).

For the same exposure concentration of 120 ppb, Adams (2006b) observed an average 3.2%, statistically significant, O

-related FEV

decrement in young adults (average age 23 years) at the end of the third hour of an 8-hour protocol that alternated 30 minutes of exercise and rest, with the equivalent ventilation rate (EVR) averaging 20 L/min-m

during the exercise periods (versus 15 to 17 L/min-m

in.Arjomandi et al.[2018]). For the same concentration with a lower EVR during exercise (17 L/min-m

), although with more exercise, Adams (2000) observed a 4%, statistically significant, O

-related FEV

decrement in young adults (average age 22 years) after the third hour of a 6.6-hour protocol (alternating 50 minutes exercise and 10 minutes rest).

The strongest evidence of O

-related health effects, as was the case in the last review, continues to be that for respiratory effects of O

(ISA, section ES.4.1). Among the newly available studies, there are several controlled human exposure studies that investigated lung function effects of higher exposure concentrations (

e.g.,

100 to 300 ppb) in healthy individuals younger than 35 years old, with findings generally consistent with previous studies (ISA, Appendix 3, section 3.1.4.1.1.2, p. 3-17). No studies are newly available in this review of 6.6-hour controlled human exposures (with exercise) to O

concentrations below those previously studied.

The newly available animal toxicological studies augment the previously available information concerning mechanisms underlying the effects documented in experimental studies. Newly available epidemiologic studies of hospital admissions and emergency department visits for a variety of respiratory outcomes supplement the previously available evidence with additional findings of consistent associations with O

concentrations across a number of study locations (ISA, Appendix 3, sections 3.1.4.1.3, 3.1.5, 3.1.6.1.1, 3.1.7.1 and 3.1.8). These studies include a number that report positive associations for asthma-related outcomes, as well as a few for COPD-related outcomes. Together these studies in the current epidemiologic evidence base continue to indicate the potential for O

exposures to contribute to such serious health outcomes, particularly for people with asthma.

The recent 3-hour study of 55- to 70-year old subjects included a target exposure of 70 ppb, as well as 120 ppb, with only the latter eliciting a statistically significant FEV

decrement in this age group of subjects (ISA, Appendix 3, section 3.1.4.1.1.2).

b. Other Effects

As was the case for the evidence available in the last review, the currently available evidence for health effects other than those of O

exposures on the respiratory system is more uncertain than that for respiratory effects. For some of these other categories of effects, the evidence now available has contributed to changes in conclusions reached in the last review. For example, the current evidence for cardiovascular effects and mortality, expanded from that in the last review, is no longer considered sufficient to conclude that the relationships of short-term exposure with these effects are likely to be causal (ISA, sections IS.4.3.4 and IS.4.3.5). These changes stem from newly available evidence in combination with the uncertainties recognized for the evidence available in the last review. Additionally, newly available evidence has also led to conclusions for another category, metabolic effects, for which formal causal determinations were previously not articulated.

The ISA finds the evidence for metabolic effects sufficient to conclude that the relationship with short-term O

exposures is likely to be causal (ISA, section IS.4.3.3). The evidence of metabolic effects of O

comes primarily from experimental animal study findings that short-term O

exposure can impair glucose tolerance, increase triglyceride levels and elicit fasting hyperglycemia, and increase hepatic gluconeogenesis (ISA, Appendix 5, section 5.1.8 and Table 5-3). The exposure conditions from these studies generally involve much higher O

concentrations than those commonly occurring in areas of the U.S. where the current standard is met. For example, the animal studies include 4-hour concentrations of 400 to 800 ppb (ISA, Appendix 5, Tables 5-8 and 5-10). The concentration in the available controlled human exposure study is similarly high, at 300 ppb; this study reported increases in two biochemicals suggestive of some liver biomarkers and no change in a number of other biochemicals associated with metabolic effects (ISA, sections 5.1.3, 5.1.5 and 5.1.8, Table 5-3). A limited number of epidemiologic studies is also available (ISA, section IS.4.3.3; Appendix 5, sections 5.1.3 and 5.1.8).

The ISA additionally concludes that the evidence is suggestive of, but not sufficient to infer, a causal relationship between long-term O

exposures and metabolic effects (ISA, section IS.4.3.6.2). As with metabolic effects and short-term O

, the primary evidence is from experimental animal studies in which the exposure concentrations are appreciably higher than those commonly occurring in the U.S. For example, the animal studies include exposures over several weeks to concentrations of 250 ppb and higher (ISA, Appendix 5, section 5.2.3.1.1). The somewhat limited epidemiologic evidence related to long-term O

concentrations and metabolic effects includes studies reporting increased odds of being overweight or obese or having metabolic syndrome and increased hazard ratios for diabetes incidence with increased O

concentrations (ISA, Appendix 5, sections 5.2.3.4.1, 5.2.5 and 5.2.9, Tables 5-12 and 5-15).

With regard to cardiovascular effects and total (nonaccidental) mortality and short-term O

exposures, the conclusions regarding the potential for a causal relationship have changed from what they were in the last review after integrating the previously available evidence with newly available evidence. The relationships are now characterized as suggestive of, but not sufficient to infer, a causal relationship (ISA, Appendix 4, section 4.1.17; Appendix 6, section 6.1.8). This reflects several aspects of the current evidence base: (1) A now-larger body of controlled human exposure studies providing evidence that is not consistent with a cardiovascular effect in response to short-term O

exposure; (2) a paucity of epidemiologic evidence indicating more severe cardiovascular morbidity endpoints (

e.g.,

emergency department visits and hospital visits for cardiovascular endpoints including myocardial infarctions, heart failure or stroke) that could connect the evidence for impaired vascular and cardiac function from animal toxicological studies with the evidence from epidemiologic studies of cardiovascular mortality; and (3) the remaining uncertainties and limitations recognized in the 2013 ISA (

e.g.,

lack of control for potential confounding by copollutants in epidemiologic studies) that still remain. Although there exists consistent or generally consistent evidence for a limited number of O

-induced cardiovascular endpoints in animal toxicological studies and cardiovascular mortality in epidemiologic studies, there is a general lack of coherence between these results and findings in controlled human exposure and epidemiologic studies of cardiovascular health outcomes (ISA, section IS.1.3.1, Appendix 6, section 6.1.8). Related to the updated evidence for cardiovascular effects, the evidence for short-term O

concentrations and mortality is also updated (ISA, section 4.3.5 and Appendix 6, section 6.1.8). While epidemiologic studies show positive associations between short-term O

concentrations and total (nonaccidental) and cardiovascular mortality (and there are some studies reporting associations that remain after controlling for PM

and NO

), the full evidence base does not describe a continuum of effects that could lead to cardiovascular mortality.

The category of total mortality includes all contributions to mortality, including both respiratory and cardiovascular mortality, as well as other causes of death, such as cancer or other chronic diseases. The evidence base supporting a continuum of effects of short-term O

concentrations that could potentially lead to respiratory mortality is more consistent and coherent as compared to that for cardiovascular mortality (ISA, sections 3.1.11 and 4.1.17; 2013 ISA, section 6.2.8). However, because cardiovascular mortality is the largest contributor to total mortality, the relatively limited biological plausibility and coherence within and across disciplines for cardiovascular effects (including mortality) is the dominant factor which contributes to a revised causality determination for total mortality (ISA, section IS.4.3.5). The ISA concludes that the currently available evidence for cardiovascular effects and total mortality is suggestive of, but not sufficient to infer, a causal relationship with short-term (as well as long-term) O

exposures (ISA, sections IS.4.3.4 and IS.4.3.5).

Due to findings from controlled human exposure studies examining clinical endpoints (

e.g.,

blood pressure) that do not indicate an O

effect and from epidemiologic studies examining cardiovascular-related hospital admissions and ED visits that do not find positive associations, a continuum of effects that could lead to cardiovascular mortality is not apparent (ISA, Appendices 4 and 6).

For other health effect categories, conclusions in this review are largely unchanged from those in the last review. The available evidence for reproductive and developmental effects, as well as for effects on the nervous system, is suggestive of, but not sufficient to infer, a causal relationship, as was the case in the last review (ISA, section IS.4.3.6.5 and Table IS-1). Additionally, the evidence is inadequate to determine if a causal relationship exists between O

exposure and cancer (ISA, section IS.4.3.6.6 and Table IS-1).

2. Public Health Implications and At-Risk Populations

The public health implications of the evidence regarding O

-related health

effects, as for other effects, are dependent on the type and severity of the effects, as well as the size of the population affected. Such factors are discussed here in the context of our consideration of the health effects evidence related to O

in ambient air. Additionally, we summarize the currently available information related to judgments or interpretative statements developed by public health experts, particularly experts in respiratory health. This section also summarizes the current information on population groups at increased risk of the effects of O

in ambient air.

With regard to O

in ambient air, the potential public health impacts relate most importantly to the role of O

in eliciting respiratory effects, the category of effects that the ISA concludes to be causally related to O

exposure (short-term). Controlled human exposure studies have documented reduced lung function, respiratory symptoms, increased airway responsiveness, and inflammation, among other effects, in healthy adults exposed while at elevated ventilation, such as while exercising. Ozone effects in individuals with compromised respiratory function, such as individuals with asthma, are plausibly related to emergency department visits and hospital admissions for asthma which have been associated with ambient air concentrations of O

in epidemiologic studies (as summarized in section II.B.1 above; 2013 ISA, section 6.2.7; ISA, Appendix 3, sections 3.1.5.1 and 3.1.5.2).

The clinical significance of individual responses to O

exposure depends on the health status of the individual, the magnitude of the changes in pulmonary function, the severity of respiratory symptoms, and the duration of the response. With regard to pulmonary function, the greater impact of larger decrements on affected individuals can be described. For example, moderate effects on pulmonary function, such as transient FEV

decrements smaller than 20% or transient respiratory symptoms, such as cough or discomfort on exercise or deep breath, would not be expected to interfere with normal activity for most healthy individuals, while larger effects on pulmonary function (

e.g.,

FEV

decrements of 20% or larger lasting longer than 24 hours) and/or more severe respiratory symptoms are more likely to interfere with normal activity for more of such individuals (

e.g.,

2014 PA, p. 3-53; 2006 AQCD, Table 8-2).

In addition to the difference in severity or magnitude of specific effects in healthy people, the same reduction in FEV

or increase in inflammation or airway responsiveness in a healthy group and a group with asthma may increase the risk of a more severe effect in the group with asthma. For example, the same increase in inflammation or airway responsiveness in individuals with asthma could predispose them to an asthma exacerbation event triggered by an allergen to which they may be sensitized (

e.g.,

2013 ISA, sections 6.2.3 and 6.2.6). Duration and frequency of documented effects is also reasonably expected to influence potential adversity and interference with normal activity. In summary, consideration of differences in magnitude or severity, and also the relative transience or persistence of such FEV

changes and respiratory symptoms, as well as pre-existing sensitivity to effects on the respiratory system, and other factors, are important to characterizing implications for public health effects of an air pollutant such as O

(ATS, 2000; Thurston et al., 2017).

Decisions made in past reviews of the O

primary standard and associated judgments regarding adversity or health significance of measurable physiological responses to air pollutants have been informed by guidance, criteria or interpretative statements developed within the public health community, including the ATS, an organization of respiratory disease specialists, as well as the CASAC. The ATS released its initial statement (titled

Guidelines as to What Constitutes an Adverse Respiratory Health Effect, with Special Reference to Epidemiologic Studies of Air Pollution

) in 1985 and updated it in 2000 (ATS, 1985; ATS, 2000). The ATS described its 2000 statement, considered in the last review of the O

standard, as being intended to “provide guidance to policy makers and others who interpret the scientific evidence on the health effects of air pollution for the purposes of risk management” (ATS, 2000). The ATS described the statement as not offering “strict rules or numerical criteria,” but rather proposing “principles to be used in weighing the evidence and setting boundaries,” and stated that “the placement of dividing lines should be a societal judgment” (ATS, 2000). Similarly, the most recent policy statement by the ATS, which once again broadens its discussion of effects, responses and biomarkers to reflect the expansion of scientific research in these areas, reiterates that concept, conveying that it does not offer “strict rules or numerical criteria, but rather proposes considerations to be weighed in setting boundaries between adverse and nonadverse health effects,” providing a general framework for interpreting evidence that proposes a “set of considerations that can be applied in forming judgments” for this context (Thurston et al., 2017).

With regard to pulmonary function decrements, the earlier ATS statement concluded that “small transient changes in forced expiratory volume in 1 s[econd] (FEV

) alone were not necessarily adverse in healthy individuals, but should be considered adverse when accompanied by symptoms” (ATS, 2000). The more recent ATS statement continues to support this conclusion and also gives weight to findings of such lung function changes in the absence of respiratory symptoms in individuals with pre-existing compromised function, such as that resulting from asthma (Thurston et al., 2017). More specifically, the recent ATS statement expresses the view that the occurrence of “small lung function changes” in individuals with pre-existing compromised function, such as asthma, “should be considered adverse . . . even without accompanying respiratory symptoms” (Thurston et al., 2017). In keeping with the intent of these statements to avoid specific criteria, neither statement provides more specific descriptions of such responses, such as with regard to magnitude, duration or frequency, for consideration of such conclusions. The earlier ATS statement, in addition to emphasizing clinically relevant effects, also emphasized both the need to consider changes in “the risk profile of the exposed population,” and effects on the portion of the population that may have a diminished reserve that puts its members at potentially increased risk if affected by another agent (ATS, 2000). These concepts, including the consideration of the magnitude of effects occurring in just a subset of study subjects, continue to be recognized as important in the more recent ATS statement (Thurston et al., 2017) and continue to be relevant to the evidence base for O

The information newly available in this review has not altered our understanding of human populations at particular risk of health effects from O

exposures (ISA, section IS.4.4). For example, as recognized in prior reviews, people with asthma are the key population at risk of O

-related effects. The respiratory effects evidence, extending decades into the past and augmented by new studies in this review, supports this conclusion (ISA, sections IS.4.3.1). For example, numerous epidemiological studies document associations with O

with asthma exacerbation. Such studies

indicate the associations to be strongest for populations of children which is consistent with their generally greater time outdoors while at elevated exertion. Together, these considerations indicate people with asthma, including particularly children with asthma, to be at relatively greater risk of O

-related effects than other members of the general population (ISA, section IS.4.4.2 and Appendix 3).

Populations or lifestages can be at increased risk of an air pollutant-related health effect due to one or more of a number of factors. These factors can be intrinsic, such as physiological factors that may influence the internal dose or toxicity of a pollutant, or extrinsic, such as sociodemographic, or behavioral factors.

With respect to people with asthma, the limited evidence from controlled human exposure studies (which are primarily in adult subjects) indicates similar magnitude of FEV

decrements as in people without asthma (ISA, Appendix 3, section 3.1.5.4.1). Across other respiratory effects of O

(

e.g.,

increased respiratory symptoms, increased airway responsiveness and increased lung inflammation), the evidence has also found the observed responses to generally not differ due to the presence of asthma, although the evidence base is more limited with regard to study subjects with asthma (ISA, Appendix 3, section 3.1.5.7). However, the features of asthma (

e.g.,

increased airway responsiveness) contribute to a risk of asthma-related responses, such as asthma exacerbation in response to asthma triggers, which may increase the risk of more severe health outcomes (ISA, section 3.1.5). For example, a particularly strong and consistent component of the epidemiologic evidence is the appreciable number of epidemiologic studies that demonstrate associations between ambient O

concentrations and hospital admissions and emergency department visits for asthma (ISA, section IS.4.4.3.1).

We additionally recognize that in these studies, the strongest associations (

e.g.,

highest effect estimates) or associations more likely to be statistically significant are those for childhood age groups, which are recognized in section II.C.1 as age groups most likely to spend time outdoors during afternoon periods (when O

may be highest) and at activity levels corresponding to those that have been associated with respiratory effects in the human exposure studies (ISA, Appendix 3, sections 3.1.4.1 and 3.1.4.2).

The epidemiologic studies of hospital admissions and emergency department visits are augmented by a large body of individual-level epidemiologic panel studies that demonstrated associations of short-term ozone concentrations with respiratory symptoms in children with asthma. Additional support comes from epidemiologic studies that observed ozone-associated increases in indicators of airway inflammation and oxidative stress in children with asthma (ISA, section IS.4.3.1). Together, this evidence continues to indicate the increased risk of population groups with asthma (ISA, Appendix 3, section 3.1.5.7).

In addition to asthma exacerbation, the epidemiologic evidence also includes findings of positive associations of increased O

concentrations with hospital admissions or emergency department visits for COPD exacerbation and other respiratory diseases (ISA, Appendix 3, sections 3.1.6.1.3 and 3.1.8).

There is limited data on activity patterns by health status. An analysis in the 2014 HREA indicated that asthma status had little to no impact on the percent of people participating in outdoor activities during afternoon hours, the amount of time spent, and whether they performed activities at elevated exertion levels (2014 HREA, section 5.4.1.5). Based on an updated evaluation of recent activity pattern data we found children, for days having some time spent outdoors spend, on average, approximately 2

1/4

hours of afternoon time outdoors, 80% of which is at a moderate or greater exertion level, regardless of their asthma status (see Appendix 3D, section 3D.2.5.3). Adults, for days having some time spent outdoors, also spend approximately 2

1/4

hours of afternoon time outdoors regardless of their asthma status but the percent of afternoon time at moderate or greater exertion levels for adults (about 55%) is lower than that observed for children.

Children, and also outdoor adult workers, are at increased risk largely due to their generally greater time spent outdoors while at elevated exertion rates (including in the summer when O

levels may be higher). This behavior makes them more likely to be exposed to O

in ambient air, under conditions contributing to increased dose due to greater air volumes taken into the lungs (2013 ISA, section 5.2.2.7). In light of the evidence summarized in the prior paragraph, children and outdoor workers with asthma may be at increased risk of more severe outcomes, such as asthma exacerbation. Further, there is experimental evidence from early life exposures of nonhuman primates that indicates potential for effects in childhood when human respiratory systems are under development (ISA, section IS.4.4.4.1). Overall, the evidence available in the current review, while not increasing our knowledge about susceptibility of these population groups, is consistent with that in the last review.

Older adults have also been identified as being at increased risk. That identification, based on the assessment in the 2013 ISA, was based largely on studies of short-term O

exposure and mortality, which are part of the larger evidence base that is now concluded to be suggestive, but not sufficient to infer a causal relationship (ISA, sections IS.4.3.5 and IS.4.4.4.2, Appendix 4, section 4.1.16.1 and 4.1.17).

Other evidence available in the current review adds little to the evidence available at the time of the last review for older adults (ISA, sections IS.4.4.2 and IS.4.4.4.2).

As noted in the ISA, “[t]he majority of evidence for older adults being at increased risk of health effects related to ozone exposure comes from studies of short-term ozone exposure and mortality evaluated in the 2013 Ozone ISA” (ISA, p. IS-52).

The ISA in the last review concluded that the information available at the time for low socioeconomic status (SES) as a factor associated with the risk of O

-related health effects, provided suggestive evidence of potentially increased risk (2013 ISA, section 8.3.3 and p. 8-37). The 2013 ISA concluded that “[o]verall, evidence is suggestive of SES as a factor affecting risk of O

-related health outcomes based on collective evidence from epidemiologic studies of respiratory hospital admissions but inconsistency among epidemiologic studies of mortality and reproductive outcomes,” additionally stating that “[f]urther studies are needed to confirm this relationship, especially in populations within the U.S.” (2013 ISA, p. 8-28). The evidence available in the current review adds little to the evidence available at the time of the last review in this area (ISA, section IS.4.4.2 and Table IS-10). The ISA in the last review additionally identified a role for dietary anti-oxidants such as vitamins C and E in influencing risk of O

-related effects, such as inflammation, as well as a role for genetic factors to also confer either an increased or decreased risk (2013 ISA, sections 8.1 and 8.4.1). No newly available evidence has been evaluated that would inform or change these prior conclusions (ISA, section IS.4.4 and Table IS-10).

The magnitude and characterization of a public health impact is dependent upon the size and characteristics of the populations affected, as well as the type or severity of the effects. As summarized above, a key population most at risk of health effects associated with O

in ambient air is people with asthma. The National Center for Health Statistics data for 2017 indicate that approximately 7.9% of the U.S. populations has asthma (CDC, 2019; PA, Table 3-1). This is one of the principal populations that the primary O

NAAQS is designed to protect (80 FR 65294, October 26, 2015).

The age group for which the prevalence documented by these data is greatest is children aged five to 19 years old, with 9.7% of children aged five to

14 and 9.4% of children aged 15 to 19 years old having asthma (CDC, 2019, Tables 3-1 and 4-1; PA, Table 3-1). In 2012 (the most recent year for which such an evaluation is available), asthma was the leading chronic illness affecting children (Bloom et al., 2013). The prevalence is greater for boys than girls (for those less than 18 years of age). Among populations of different races or ethnicities, black non-Hispanic children aged five to 14 have the highest prevalence, at 16.1%. Asthma prevalence is also increased among populations in poverty. For example, 11.7% of people living in households below the poverty level have asthma compared to 7.3%, on average, of those living above it (CDC, 2019, Tables 3-1 and 4-1; PA, Table 3-1). Population groups with relatively greater asthma prevalence might be expected to have a relatively greater potential for O

-related health impacts.

As summarized in section II.A.1 above, the current standard was set to protect at-risk populations, which include people with asthma. Accordingly, populations with asthma living in areas not meeting the standard would be expected to be at increased risk of effects than others in those areas.

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