National Ambient Air Quality Standards for Ozone

Federal RegisterMar 27, 2008

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Parts 50 and 58

[EPA-HQ-OAR-2005-0172; FRL-8544-3]

RIN 2060-AN24

National Ambient Air Quality Standards for Ozone

AGENCY:

Environmental Protection Agency (EPA).

ACTION:

Final rule.

SUMMARY:

Based on its review of the air quality criteria for ozone (O

) and related photochemical oxidants and national ambient air quality standards (NAAQS) for O

, EPA is making revisions to the primary and secondary NAAQS for O

to provide requisite protection of public health and welfare, respectively. With regard to the primary standard for O

, EPA is revising the level of the 8-hour standard to 0.075 parts per million (ppm), expressed to three decimal places. With regard to the secondary standard for O

, EPA is revising the current 8-hour standard by making it identical to the revised primary standard. EPA is also making conforming changes to the Air Quality Index (AQI) for O

, setting an AQI value of 100 equal to 0.075 ppm, 8-hour average, and making proportional changes to the AQI values of 50, 150 and 200.

DATES:

This final rule is effective on May 27, 2008.

ADDRESSES:

EPA has established a docket for this action under Docket ID No. EPA-HQ-OAR-2005-0172. All documents in the docket are listed on the

www.regulations.gov

Web site. Although listed in the index, some information is not publicly available, e.g., confidential business information or other information whose disclosure is restricted by statute. Certain other material, such as copyrighted material, is not placed on the Internet and will be publicly available only in hard copy form. Publicly available docket materials are available either electronically through

www.regulations.gov

or in hard copy at the Air and Radiation Docket and Information Center, EPA/DC, EPA West, Room 3334, 1301 Constitution Ave., NW., Washington, DC. This Docket Facility is open from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal holidays. The Docket telephone number is 202-566-1742. The telephone number for the Public Reading Room is 202-566-1744.

FOR FURTHER INFORMATION CONTACT:

Dr. David J. McKee, Health and Environmental Impacts Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Mail Code C504-06, Research Triangle Park, NC 27711;

telephone:

919-541-5288;

fax:

919-541-0237;

e-mail: mckee.dave@epa.gov

SUPPLEMENTARY INFORMATION:

Table of Contents

The following topics are discussed in this preamble:

I. Background

A. Summary of Revisions to the O

NAAQS

B. Legislative Requirements

C. Review of Air Quality Criteria and Standards for O

D. Summary of Proposed Revisions to the O

NAAQS

E. Organization and Approach to Final Decision on O

NAAQS

II. Rationale for Final Decision on the Primary O

Standard

A. Introduction

1. Overview

2. Overview of Health Effects

3. Overview of Human Exposure and Health Risk Assessments

B. Need for Revision of the Current Primary O

Standard

1. Introduction

2. Comments on the Need for Revision

3. Conclusions Regarding the Need for Revision

C. Conclusions on the Elements of the Primary O

Standard

1. Indicator

2. Averaging Time

3. Form

4. Level

D. Final Decision on the Primary O

Standard

III. Communication of Public Health Information

IV. Rationale for Final Decision on the Secondary O

Standard

A. Introduction

1. Overview

2. Overview of Vegetation Effects Evidence

3. Overview of Biologically Relevant Exposure Indices

4. Overview of Vegetation Exposure and Risk Assessments

B. Need for Revision of the Current Secondary O

Standard

1. Introduction

2. Comments on the Need for Revision

3. Conclusions Regarding the Need for Revision

C. Conclusions on the Secondary O

Standard

1. Staff Paper Evaluation

2. CASAC Views

3. Administrator's Proposed Conclusions

4. Comments on the Secondary Standard Options

5. Administrator's Final Conclusions

D. Final Decision on the Secondary O

Standard

V. Creation of Appendix P—Interpretation of the NAAQS for O

A. General

B. Data Completeness

C. Data Reporting and Handling and Rounding Conventions

VI. Ambient Monitoring Related to Revised O

Standards

VII. Implementation and Related Control Requirements

A. Future Implementation Steps

1. Designations

2. State Implementation Plans

3. Trans-boundary Emissions

4. Monitoring Requirements

B. Related Control Requirements

VIII. Statutory and Executive Order Reviews

A. Executive Order 12866: Regulatory Planning and Review

B. Paperwork Reduction Act

C. Regulatory Flexibility Act

D. Unfunded Mandates Reform Act

E. Executive Order 13132: Federalism

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

G. Executive Order 13045: Protection of Children From Environmental Health & Safety Risks

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

I. National Technology Transfer and Advancement Act

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

K. Congressional Review Act

References

I. Background

A. Summary of Revisions to the O

NAAQS

Based on its review of the air quality criteria for O

and related photochemical oxidants and national ambient air quality standards (NAAQS) for O

, EPA is making revisions to the primary and secondary NAAQS for O

to provide protection of public health and welfare, respectively, that is appropriate under section 109, and is making corresponding revisions in data handling conventions for O

With regard to the primary standard for O

, EPA is revising the level of the 8-hour standard to a level of 0.075 parts per million (ppm), to provide increased protection for children and other “at risk” populations against an array of O

-related adverse health effects that range from decreased lung function and increased respiratory symptoms to serious indicators of respiratory morbidity including emergency department visits and hospital admissions for respiratory causes, and possibly cardiovascular-related morbidity as well as total nonaccidental and cardiorespiratory mortality. EPA is specifying the level of the primary standard to the nearest thousandth ppm.

With regard to the secondary standard for O

, EPA is revising the standard by making it identical to the revised primary standard.

B. Legislative Requirements

Two sections of the Clean Air Act (CAA) govern the establishment and revision of the NAAQS. Section 108 (42 U.S.C. 7408) directs the Administrator to identify and list “air pollutants” emissions of which “in his judgment, cause or contribute to air pollution which may reasonably be anticipated to endanger public health or welfare,” whose “presence * * * in the ambient air results from numerous or diverse mobile or stationary sources,” and for which the Administrator plans to issue air quality criteria, and to issue air quality criteria for those that are listed. Air quality criteria are to “accurately reflect the latest scientific knowledge useful in indicating the kind and extent of identifiable effects on public health or welfare which may be expected from the presence of [a] pollutant in ambient air, in varying quantities * * *.” Section 109 (42 U.S.C. 7409) directs the Administrator to propose and promulgate “primary” and “secondary” NAAQS for pollutants listed under section 108. Section 109(b)(1) defines a primary standard as one “the attainment and maintenance of which in the judgment of the Administrator, based on such criteria and allowing an adequate margin of safety, are requisite to protect the public health.”

A secondary standard, as defined in section 109(b)(2), must “specify a level of air quality the attainment and maintenance of which in the judgment of the Administrator, based on such criteria, is requisite to protect the public welfare from any known or anticipated adverse effects associated with the presence of [the] pollutant in the ambient air.”

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)].

Welfare effects as defined in section 302(h) (42 U.S.C. 7602(h)) include, but are not limited to, “effects on soils, water, crops, vegetation, 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.”

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.

Lead Industries Association

EPA

, 647 F.2d 1130, 1154 (DC Cir 1980),

cert. denied

, 449 U.S. 1042 (1980);

American Petroleum Institute

Costle

, 665 F.2d 1176, 1186 (DC Cir. 1981),

cert. denied

, 455 U.S. 1034 (1982). Both kinds of uncertainties are components of the risk associated with pollution at levels below those at which human health effects can be said to occur with reasonable scientific certainty. Thus, in selecting primary standards that provide an adequate margin of safety, the Administrator is seeking not only to prevent pollution levels that have been demonstrated to be harmful but also to prevent lower pollutant levels that may pose an unacceptable risk of harm, even if the risk is not precisely identified as to nature or degree. The CAA does not require the Administrator to establish a primary NAAQS at a zero-risk level or at background concentration levels,

see Lead Industries Association

EPA

, 647 F.2d at 1156 n. 51, but rather at a level that reduces risk sufficiently so as to protect public health with an adequate margin of safety.

The selection of any particular approach to providing an adequate margin of safety is a policy choice left specifically to the Administrator's judgment.

Lead Industries Association

EPA

, 647 F.2d at 1161-62. In addressing the requirement for an adequate margin of safety, EPA considers such factors as the nature and severity of the health effects involved, the size of the population(s) at risk, and the kind and degree of the uncertainties that must be addressed.

In setting standards that are “requisite” to protect public health and welfare, as provided in section 109(b), EPA's task is to establish standards that are neither more nor less stringent than necessary for these purposes.

Whitman

America Trucking Associations

, 531 U.S. 457, 473. Further the Supreme Court ruled that “[t]he text of § 109(b), interpreted in its statutory and historical context and with appreciation for its importance to the CAA as a whole, unambiguously bars cost considerations from the NAAQS-setting process * * *”

Id.

at 472.

In considering whether the CAA allowed for economic considerations to play a role in the promulgation of the NAAQS, the Supreme Court rejected arguments that because many more factors than air pollution might affect public health, EPA should consider compliance costs that produce health losses in setting the NAAQS. 531 U.S. at 466. Thus, EPA may not take into account possible public health impacts from the economic cost of implementation.

Id.

Section 109(d)(1) of the CAA requires that “not later than December 31, 1980, and at 5-year intervals thereafter, the Administrator shall complete a thorough review of the criteria published under section 108 and the national ambient air quality standards * * * and shall make such revisions in such criteria and standards and promulgate such new standards as may be appropriate in accordance with section 108 and [109(b)].” Section 109(d)(2) requires that an independent scientific review committee “shall complete a review of the criteria * * * and the national primary and secondary ambient air quality standards * * * and shall recommend to the Administrator any new * * * standards and revisions of existing criteria and standards as may be appropriate under section 108 and [section 109(b)].” This independent review function is performed by the Clean Air Scientific Advisory Committee (CASAC) of EPA's Science Advisory Board.

C. Review of Air Quality Criteria and Standards for O

Ground-level O

is formed from biogenic and anthropogenic precursor emissions. Naturally occurring O

in the troposphere can result from biogenic organic precursors reacting with naturally occurring nitrogen oxides (NO

) and by stratospheric O

intrusion into the troposphere. Anthropogenic precursors of O

, specifically NO

and volatile organic compounds (VOC), originate from a wide variety of stationary and mobile sources. Ambient O

concentrations produced by these emissions are directly affected by temperature, solar radiation, wind speed and other meteorological factors.

The last review of the O

NAAQS was completed on July 18, 1997, based on the 1996 O

Air Quality Criteria Document (EPA, 1996a) and 1996 O

Staff Paper (EPA, 1996b). EPA revised the primary and secondary O

standards on the basis of the then latest scientific evidence linking exposures to ambient O

to adverse health and welfare effects at levels allowed by the 1-hour average standards (62 FR 38856). The O

standards were revised by replacing the existing primary 1-hour average standard with an 8-hour average O

standard set at a level of 0.08 ppm, which is equivalent to 0.084 ppm using the standard rounding conventions. The form of the primary standard was changed to the annual fourth-highest daily maximum 8-hour average concentration, averaged over 3 years. The secondary O

standard was changed by making it identical in all respects to the revised primary standard.

EPA initiated this current review in September 2000 with a call for information (65 FR 57810) for the development of a revised Air Quality

Criteria Document for O

and Other Photochemical Oxidants (henceforth the “Criteria Document”). A project work plan (EPA, 2002) for the preparation of the Criteria Document was released in November 2002 for CASAC O

Panel

(henceforth, “CASAC Panel”) and public review. EPA held a series of workshops in mid-2003 on several draft chapters of the Criteria Document to obtain broad input from the relevant scientific communities. These workshops helped to inform the preparation of the first draft Criteria Document (EPA, 2005a), which was released for CASAC Panel and public review on January 31, 2005; a CASAC Panel meeting was held on May 4-5, 2005 to review the first draft Criteria Document. A second draft Criteria Document (EPA, 2005b) was released for CASAC Panel and public review on August 31, 2005, and was discussed along with a first draft Staff Paper (EPA, 2005c) at a CASAC Panel meeting held on December 6-8, 2005. In a February 16, 2006 letter to the Administrator, the CASAC Panel offered final comments on all chapters of the Criteria Document (Henderson, 2006a), and the final Criteria Document (EPA, 2006a) was released on March 21, 2006. In a June 8, 2006 letter (Henderson, 2006b) to the Administrator, the CASAC Panel offered additional advice to the Agency concerning chapter 8 of the final Criteria Document (Integrative Synthesis) to help inform the second draft Staff Paper.

The CASAC O

Review Panel includes the seven members of the chartered CASAC, supplemented by fifteen subject-matter experts appointed by the Administrator to provide additional scientific expertise relevant to this review of the O

NAAQS.

A second draft Staff Paper (EPA, 2006b) was released on July 17, 2006 and reviewed by the CASAC Panel on August 24 and 25, 2006. In an October 24, 2006 letter to the Administrator, CASAC Panel provided advice and recommendations to the Agency concerning the second draft Staff Paper (Henderson, 2006c). A final Staff Paper (EPA, 2007a) was released on January 31, 2007. Around the time of the release of the final Staff Paper in January 2007, EPA discovered a small error in the exposure model that when corrected resulted in slight increases in the human exposure estimates. Since the exposure estimates are an input to the lung function portion of the health risk assessment, this correction also resulted in slight increases in the lung function risk estimates as well. The exposure and risk estimates discussed in this final rule reflect the corrected estimates, and thus are slightly different than the exposure and risk estimates cited in the January 31, 2007 Staff Paper.

In a March 26, 2007 letter (Henderson, 2007), the CASAC Panel offered additional advice to the Administrator with regard to recommendations and revisions to the primary and secondary O

NAAQS.

EPA made available corrected versions of the final Staff Paper (EPA, 2007b, henceforth, “Staff Paper”) and the human exposure and health risk assessment technical support documents on July 31, 2007 on the EPA Web site

http://www.epa.gov/ttn/naaqs

The schedule for completion of this review has been governed by a consent decree resolving a lawsuit filed in March 2003 by a group of plaintiffs representing national environmental and public health organizations, alleging that EPA had failed to complete the current review within the period provided by statute.

The modified consent decree that currently governs this review provides that EPA sign for publication notices of proposed and final rulemaking concerning its review of the O

NAAQS no later than June 20, 2007 and March 12, 2008, respectively. The proposed decision (henceforth “proposal”) was signed on June 20, 2007 and published in the

Federal Register

on July 11, 2007.

American Lung Association

Whitman

(No. 1:03CV00778, D.D.C. 2003).

A large number of comments were received from various commenters on the proposed revisions to the O

NAAQS. Significant issues raised in the public comments are discussed throughout the preamble of this final action. A comprehensive summary of all significant comments, along with EPA's responses (henceforth “Response to Comments”), can be found in the docket for this rulemaking.

Various commenters have referred to and discussed a number of new scientific studies on the health effects of O

that had been published recently and therefore were not included in the Criteria Document (EPA, 2006a, henceforth “Criteria Document).

EPA has provisionally considered any significant “new” studies, including those submitted during the public comment period. The purpose of this effort was to ensure that the Administrator was fully aware of the “new” science before making a final decision on whether to revise the current O

NAAQS. EPA provisionally considered these studies to place their results in the context of the findings of the Criteria Document.

For ease of reference, these studies will be referred to as “new” studies or “new” science, using quotation marks around the word new. Referring to studies that were published too recently to have been included in the 2004 Criteria Document as “new” studies is intended to clearly differentiate such studies from those that have been published since the last review and are included in the 2004 Criteria Document (these studies are sometimes referred to as new (without quotation marks) or more recent studies, to indicate that they were not included in the 1996 Criteria Document and thus are newly available in this review.

As in prior NAAQS reviews, EPA is basing its decision in this review on studies and related information included in the Criteria Document and Staff Paper, which have undergone CASAC and public review. The studies assessed in the Criteria Document, and the integration of the scientific evidence presented in that document, have undergone extensive critical review by EPA, CASAC, and the public during the development of the Criteria Document. The rigor of that review makes these studies, and their integrative assessment, the most reliable source of scientific information on which to base decisions on the NAAQS, decisions that all parties recognize as of great import. NAAQS decisions can have profound impacts on public health and welfare, and NAAQS decisions should be based on studies that have been rigorously assessed in an integrative manner not only by EPA but also by the statutorily mandated independent advisory committee, as well as the public review that accompanies this process. As described above, EPA's provisional consideration of these studies did not and could not provide that kind of in-depth critical review.

This decision is consistent with EPA's practice in prior NAAQS reviews. Since the 1970 amendments, the EPA has taken the view that NAAQS decisions are to be based on scientific studies and related information that have been assessed as a part of the pertinent air quality criteria, and has consistently followed this approach. See 71 FR 61144, 61148 (October 17, 2006) (final decision on review of PM NAAQS) for a detailed discussion of this issue and EPA's past practice.

As discussed in EPA's 1993 decision not to revise the NAAQS for O

“new” studies may sometimes be of such significance that it is appropriate to delay a decision on revision of a NAAQS and to supplement the pertinent air quality criteria so the studies can be taken into account (58 FR at 13013-13014, March 9, 1993). In the present case, EPA's provisional consideration of “new” studies concludes that, taken in context, the “new” information and findings do not materially change any of the broad scientific conclusions regarding the health effects of O

exposure made in the Criteria Document. For this reason, reopening the air quality criteria review would not be warranted even if there were time to do so under the court order

governing the schedule for this rulemaking. Accordingly, EPA is basing the final decisions in this review on the studies and related information included in the O

air quality criteria that have undergone CASAC and public review. EPA will consider the newly published studies for purposes of decision making in the next periodic review of the O

NAAQS, which will provide the opportunity to fully assess them through a more rigorous review process involving EPA, CASAC, and the public. Further discussion of these “new” studies can be found in the Response to Comments document.

This action presents the Administrator's final decisions on the review of the current primary and secondary O

standards. Throughout this preamble a number of conclusions, findings, and determinations made by the Administrator are noted. They identify the reasoning that supports this final decision and are intended to be final and conclusive.

D. Summary of Proposed Revisions to the O

NAAQS

For reasons discussed in the proposal, the Administrator proposed to revise the current primary and secondary O

standards. With regard to the primary O

standard, the Administrator proposed to revise the level of the 8-hour O

standard to a level within the range of 0.070 ppm to 0.075 ppm, based on a 3-year average of the fourth-highest maximum 8-hour average concentration. Related revisions for O

data handling conventions and for the reference method for monitoring O

were also proposed. These revisions were proposed to provide increased protection for children and other “at risk” populations against an array of O

-related adverse health effects that range from decreased lung function and increased respiratory symptoms to serious indicators of respiratory morbidity, including emergency department visits and hospital admissions for respiratory causes, and possibly cardiovascular-related morbidity, as well as total nonaccidental and cardiorespiratory mortality. EPA also proposed to specify the level of the primary standard to the nearest thousandth ppm. EPA solicited comment on alternative levels down to 0.060 ppm and up to and including retaining the current 8-hour standard of 0.08 ppm (effectively 0.084 ppm using current data rounding conventions).

With regard to the secondary standard for O

, EPA proposed to revise the current 8-hour standard with one of two options to provide increased protection against O

-related adverse impacts on vegetation and forested ecosystems. One option was to replace the current standard with a cumulative, seasonal standard expressed as an index of the annual sum of weighted hourly concentrations, cumulated over 12 hours per day (8 am to 8 pm) during the consecutive 3-month period within the O

season with the maximum index value, set at a level within the range of 7 to 21 ppm-hours. The other option was to make the secondary standard identical to the proposed primary 8-hour standard. EPA solicited comment on specifying a cumulative, seasonal standard in terms of a 3-year average of the annual sums of weighted hourly concentrations; on the range of alternative 8-hour standard levels for which comment was being solicited for the primary standard, including retaining the current secondary standard, which is identical to the current primary standard; and on an alternative approach to setting a cumulative, seasonal secondary standard.

E. Organization and Approach to Final O

NAAQS Decisions

This action presents the Administrator's final decisions regarding the need to revise the current primary and secondary O

standards. Revisions to the primary standard for O

are addressed below in section II, and a discussion on communication of public health information regarding revisions to the primary O

standard is presented in section III. The secondary O

standard is addressed below in section IV. Related data completeness and data handling and rounding conventions are addressed in section V, and federal reference methods for monitoring O

are addressed below in section VI. Future implementation steps and related control requirements are discussed in section VII. A discussion of statutory and executive order reviews is provided in section VIII.

Today's final decisions are based on a thorough review in the Criteria Document of scientific information on known and potential human health and welfare effects associated with exposure to O

at levels typically found in the ambient air. These final decisions also take into account: (1) Staff assessments in the Staff Paper of the most policy-relevant information in the Criteria Document as well as quantitative exposure and risk assessments based on that information; (2) CASAC Panel advice and recommendations, as reflected in its letters to the Administrator, its discussions of drafts of the Criteria Document and Staff Paper at public meetings, and separate written comments prepared by individual members of the CASAC Panel; (3) public comments received during the development of these documents, either in connection with CASAC Panel meetings or separately; and (4) extensive public comments received on the proposed rulemaking.

II. Rationale for Final Decisions on the Primary O

Standard

A. Introduction

1. Overview

This section presents the Administrator's final decisions regarding the need to revise the current primary O

NAAQS, and the appropriate revision to the level of the 8-hour standard. As discussed more fully below, the rationale for the final decision on appropriate revisions to the primary O

NAAQS includes consideration of: (1) Evidence of health effects related to short-term exposures to O

; (2) insights gained from quantitative exposure and health risk assessments; (3) public and CASAC Panel comments received during the development and review of the Criteria Document, Staff Paper, exposure and risk assessments and on the proposal notice.

In developing this rationale, EPA has drawn upon an integrative synthesis of the entire body of evidence

relevant to examining associations between exposure to ambient O

and a broad range of health endpoints (EPA, 2006a, Chapter 8), focusing on those health endpoints for which the Criteria Document concluded that the associations are causal or likely to be causal. This body of evidence includes hundreds of studies conducted in many countries around the world. In its assessment of the evidence judged to be most relevant to decisions on elements of the primary O

standards, EPA has placed greater weight on U.S. and Canadian studies, since studies conducted in other countries may well reflect different demographic and air pollution characteristics.

The word “evidence” is used in this notice to refer to studies that provide information relevant to an area of inquiry, which can include studies that report positive or negative results or that provide interpretative information.

As discussed below, a significant amount of new research has been conducted since the last review, with important new information coming from epidemiological, toxicological, controlled human exposure, and dosimetric studies. Moreover, the newly available research studies evaluated in the Criteria Document have undergone intensive scrutiny through multiple layers of peer review, with extended

opportunities for review and comment by CASAC Panel and the public. As with virtually any policy-relevant scientific research, there is uncertainty in the characterization of health effects attributable to exposure to ambient O

, most generally with regard to whether observed health effects and associations are causal or likely causal in nature and, if so, the certainty of causal associations at various exposure levels. While important uncertainties remain, the review of the health effects information has been extensive and deliberate. In the judgment of the Administrator, this intensive evaluation of the scientific evidence provides an adequate basis for regulatory decision making at this time. This review also provides important input to EPA's research plan for improving our future understanding of the relationships between exposures to ambient O

and health effects.

The health effects information and quantitative exposure and health risk assessment were summarized in sections II.A and II.B of the proposal (72 FR at 37824-37862) and are only briefly outlined below in sections II.A.2 and II.A.3. Subsequent sections of this preamble provide a more complete discussion of the Administrator's rationale, in light of key issues raised in public comments, for concluding that the current standard is not requisite to protect public health with an adequate margin of safety, and it is appropriate to revise the current primary O

standards to provide additional public health protection (section II.B), as well as a more complete discussion of the Administrator's rationale for retaining or revising the specific elements of the primary O

standards (section II.C), namely the indicator (section II.C.1); averaging time (section II.C.2); form (section II.C.3); and level (section II.C.4). A summary of the final decisions on revisions to the primary O

standards is presented in section II.D.

2. Overview of Health Effects

This section outlines the information presented in Section II.A of the proposal on known or potential effects on public health which may be expected from the presence of O

in ambient air. The decision in the last review focused primarily on evidence from short-term (e.g., 1 to 3 hours) and prolonged ( 6 to 8 hours) controlled-exposure studies reporting lung function decrements, respiratory symptoms, and respiratory inflammation in humans, as well as epidemiology studies reporting excess hospital admissions and emergency department visits for respiratory causes. The Criteria Document prepared for this review emphasizes a large number of epidemiological studies published since the last review with these and additional health endpoints, including the effects of acute (short-term and prolonged) and chronic exposures to O

on lung function decrements and enhanced respiratory symptoms in asthmatic individuals, school absences, and premature mortality. It also emphasizes important new information from toxicology, dosimetry, and controlled human exposure studies. Highlights of the evidence include:

(1) Two new controlled human-exposure studies are now available that examine respiratory effects associated with prolonged O

exposures at levels at and below 0.080 ppm, which was the lowest exposure level that had been examined in the last review.

(2) Numerous recent controlled human-exposure studies have examined indicators of O

-induced inflammatory response in both the upper respiratory tract (URT) and lower respiratory tract (LRT), while other studies have examined changes in host defense capability following O

exposure of healthy young adults and increased airway responsiveness to allergens in subjects with allergic asthma and allergic rhinitis exposed to O

(3) New evidence from controlled human exposure studies showing that asthmatics have greater respiratory-related physiological responses than healthy subjects and new evidence from epidemiological studies showing associations between O

exposure and lung function and respiratory symptom responses; these findings differ from the presumption in the last review that people with asthma had generally the same magnitude of respiratory responses to O

as those experienced by healthy individuals.

(4) Animal toxicology studies provide new information regarding potential mechanisms of action, increased susceptibility to respiratory infection, and biological plausibility of acute effects as well as chronic, irreversible respiratory damage observed in animals.

(5) Numerous epidemiological studies published during the past decade offer added evidence of associations between acute ambient O

exposures and lung function decrements and respiratory symptoms in physically active healthy subjects and asthmatic subjects, as well as new evidence regarding additional health endpoints, including relationships between ambient O

concentrations and school absenteeism and between ambient O

and cardiac-related physiological endpoints.

(6) Several additional studies have been published over the last decade examining the temporal associations between acute O

exposures and both emergency department visits for respiratory diseases and respiratory-related hospital admissions.

(7) A large number of newly available epidemiological studies have examined the effects of acute exposure to PM and O

on premature mortality, notably including large multi-city studies that provide much more robust information than was available in the last review, as well as recent meta-analyses that have evaluated potential sources of heterogeneity in O

-mortality associations.

Section II.A of the proposal provides a detailed summary of key information contained in the Criteria Document (chapters 4-8) and in the Staff Paper (chapter 3), on the known and potential effects of O

exposure and information on the effects of O

exposure in combination with other pollutants that are routinely present in the ambient air (72 FR 37824-37851). The information there summarizes:

(1) New information available on potential mechanisms for morbidity and mortality effects associated with exposure to O

, including potential mechanisms or pathways related to direct effects on the respiratory system, systemic effects that are secondary to effects in the respiratory system (e.g., cardiovascular effects);

(2) The nature of effects that have been associated directly with exposure to O

or indirectly with the presence of O

in ambient air, including premature mortality, aggravation of respiratory and cardiovascular disease (as indicated by increased hospital admissions and emergency department visits), changes in lung function and increased respiratory symptoms, as well as new evidence for more subtle indicators of cardiovascular health;

(3) An integrative interpretation of the health effects evidence, focusing on the biological plausibility and coherence of the evidence and key issues raised in interpreting epidemiological studies, along with supporting evidence from experimental (e.g., dosimetric and toxicological) studies as well as the limitations of the evidence; and

(4) Considerations in characterizing the public health impact of O

, including the identification of sensitive and vulnerable subpopulations that are potentially at risk to such effects, including active people, people with pre-existing lung and heart diseases, children and older adults, and people with increased responsiveness to O

3. Overview of Human Exposure and Health Risk Assessments

To put judgments about health effects that are adverse for individuals into a broader public health context, EPA developed and applied models to estimate human exposures and health risks. This broader public health context included consideration of the size of particular population groups at risk for various effects, the likelihood that exposures of concern would occur for individuals in such groups under varying air quality scenarios, estimates of the number of people likely to experience O

-related effects, the variability in estimated exposures and risks, and the kind and degree of uncertainties inherent in assessing the exposures and risks involved.

As discussed in more detail in section II.B of the proposal, there are a number of important uncertainties that affect the exposure and health risk estimates. It is also important to note that there have been significant improvements since the last review in both the exposure and health risk models. The CASAC Panel expressed the view that the exposure analysis represents a state-of-the-art modeling approach and that the health risk assessment was “well done, balanced and reasonably communicated” (Henderson, 2006c).

In modeling exposures and health risks associated with just meeting the current and alternative O

standards, EPA simulated air quality just meeting these standards based on O

air quality patterns in several recent years and on how the shape of the O

air quality distributions has changed over time based on historical trends in monitored O

air quality data. As discussed in the proposal notice and in the Staff Paper (section 4.5.8), recent O

air quality distributions were statistically adjusted to simulate just meeting the current and selected alternative standards. Specifically, the exposure and risk assessment included estimates for a recent year of air quality and for air quality adjusted to simulate just meeting the current and alternative standards based on O

season data from a recent three-year period (2002-2004). The O

season in each area included the period of the year for which routine hourly O

monitoring data are available. Typically this period spans from March or April through September or October, although in some areas it includes the entire year. Three years were modeled to reflect the substantial year-to-year variability that occurs in O

levels and related meteorological conditions, and because the standard is specified in terms of a three-year period. The year-to-year variability observed in O

levels is due to a combination of different weather patterns and the variation in emissions of O

precursors. Nationally, 2002 was a relatively high year with respect to the 4th highest daily maximum 8-hour O

levels observed in urban areas across the U.S. (see Staff Paper, Figure 2-16), with the mean of the distribution of annual 4th highest daily maximum 8-hour O

levels for urban monitors nationwide being in the upper third among the years 1990 through 2004. In contrast, on a national basis, 2004 was the lowest year on record with respect to the mean of the distribution of annual 4th highest daily maximum 8-hour O

levels for this same 15 year period. The 4th highest daily maximum 8-hour levels observed in most, but not all of the 12 urban areas included in the exposure and risk assessment, were relatively low in 2004 compared to other recent years. The 4th highest daily maximum 8-hour O

levels observed in 2003 in the 12 urban areas and nationally generally were between those observed in 2002 and 2004. As a result of the variability in air quality, the exposure and risk estimates associated with just meeting the current or any alternative standard also will vary depending on the year chosen for the analysis. Thus, exposure and risk estimates based on 2002 air quality generally show relatively higher numbers of children affected and the estimates based on 2004 air quality generally show relatively fewer numbers of children affected.

These simulations do not reflect any consideration of specific control programs or strategies designed to achieve the reductions in emissions required to meet the specified standards. Further, these simulations do not represent predictions of when, whether, or how areas might meet the specified standards.

Instead these simulations represent a projection of the kind of air quality levels that would be likely to occur in areas just attaining various alternative standards, when historical patterns of air quality, reflecting averages over many areas, are applied in the urban areas examined.

For informational purposes only, modeling that projects how areas might attain alternative standards in a future year as a result of Federal, State, local, and Tribal efforts is presented in the final Regulatory Impact Analysis being prepared in connection with this decision.

a. Exposure Analyses

As discussed in section II.B.1 of the proposal, EPA conducted human exposure analyses using a simulation model to estimate O

exposures for the general population, school age children (ages 5-18), and school age children with asthma living in 12 U.S. metropolitan areas representing different regions of the country where the current 8-hour O

standard is not met. The emphasis on children reflected the finding of the last review that children are an important at-risk group. Exposure estimates were developed using a probabilistic exposure model that is designed to explicitly model the numerous sources of variability that affect people's exposures. This exposure assessment is more fully described and presented in the Staff Paper and in a technical support document,

Ozone Population Exposure Analysis for Selected Urban Areas

(EPA, 2007c; henceforth “Exposure Analysis TSD”). As noted in the proposal, the scope and methodology for this exposure assessment were developed over the last few years with considerable input from the CASAC Panel and the public.

As discussed in the proposal notice and in greater detail in the Staff Paper (chapter 4) and Exposure Analysis TSD, EPA recognized that there are many sources of variability and uncertainty inherent in the input to this assessment and that there was uncertainty in the resulting O

exposure estimates. In EPA's judgment, the most important uncertainties affecting the exposure estimates are related to the modeling of human activity patterns over an O

season, the modeling of variations in ambient concentrations near roadways, and the modeling of air exchange rates that affect the amount of O

that penetrates indoors. Another important uncertainty that affects the estimation of how many exposures are associated with moderate or greater exertion is the characterization of energy expenditure for children engaged in various activities. As discussed in more detail in the Staff Paper (section 4.3.4.7), the uncertainty in energy expenditure values carries over to the uncertainty of the modeled breathing rates, which are important since they are used to classify exposures occurring at moderate or greater exertion. These are the relevant exposures since O

-related effects observed in clinical studies only are observed when individuals are engaged in some form of exercise. The uncertainties in the exposure model inputs and the estimated exposures have been assessed using quantitative uncertainty and sensitivity analyses. Details are discussed in the Staff Paper (section 4.6) and in a technical memorandum describing the exposure modeling uncertainty analysis (Langstaff, 2007).

The exposure assessment, which provided estimates of the number of people exposed to different levels of

ambient O

while at elevated exertion

, served two purposes. First, the entire range of modeled personal exposures to ambient O

was an essential input to the portion of the health risk assessment based on exposure-response functions from controlled human exposure studies, discussed in the next section. Second, estimates of personal exposures to ambient O

concentrations at and above specified benchmark levels while at elevated exertion provided some perspective on the public health impacts of health effects that we cannot currently evaluate in quantitative risk assessments but that may occur at current air quality levels, and the extent to which such impacts might be reduced by meeting the current and alternative standards. In the proposal, we referred to exposures at and above these benchmark levels while at elevated exertion as “exposures of concern.”

As discussed in section II.A of the proposal, O

health responses observed in controlled human exposure studies are associated with exposures while subjects are engaged in moderate or greater exertion on average over the exposure period (hereafter referred to as “elevated exertion”) and, therefore, these are the exposures of interest.

Based on the observation from the exposure analyses conducted in the prior review that children represented the population subgroup with the greatest exposure to ambient O

, EPA chose to model 8-hour exposures at elevated exertion for all school age children, and separately for asthmatic school age children, as well as for the general population in the current exposure assessment. While outdoor workers and other adults who engage in moderate or greater exertion for prolonged periods while outdoors during the day in areas experiencing elevated O

concentrations also are at risk for O

-related health effects, EPA did not focus on developing quantitative exposure estimates for these population subgroups due to the lack of information about the number of individuals who regularly work or exercise outdoors. Thus, as presented in the proposal and in the Staff Paper the exposure estimates are most useful for making relative comparisons of estimated exposures in school age children across alternative air quality scenarios. This assessment does not provide information on exposures for adult subgroups within the general population associated with the air quality scenarios.

EPA noted in the proposal key observations that were important to consider in comparing exposure estimates associated with just meeting the current NAAQS and alternative standards considered. These included:

(1) As shown in Table 6-1 of the Staff Paper, the patterns of exposures in terms of percentages of the population exceeding given exposure levels were very similar for the general population and for asthmatic and all school age (5-18) children, although children were about twice as likely as the general population to be exposed at any given level.

(2) As shown in Table 1 in the proposal (72 FR 37855), the number and percentage of asthmatic and all school age children aggregated across the 12 urban areas estimated to experience 1 or more exposures of concern declined from simulations of just meeting the current standard to simulations of alternative 8-hour standards by varying amounts, depending on the benchmark level, the population subgroup considered, and the air quality year chosen.

While the proposal notice stated in the text that “approximately 2 to 4 percent of all and asthmatic children” were estimated to experience exposures of concern at and above the 0.070 ppm benchmark level for standards in the range of 0.070 to 0.075 ppm (72 FR 37879), the correct range is about 1 to 5 perecent consistent with the estimates provided in Table 1 of the proposal (72 FR 37855).

(3) Substantial year-to-year variability in exposure estimates was observed over the three-year modeling period.

(4) There was substantial variability observed across the 12 urban areas in the percent of the population subgroups estimated to experience exposures at and above specified benchmark levels while at elevated exertion.

(5) Of particular note, there is high inter-individual variability in responsiveness such that only a subset of individuals who were exposed at and above a given benchmark level while at elevated exertion would actually be expected to experience any such potential adverse health effects.

(6) In considering these observations, it was important to take into account the variability, uncertainties, and limitations associated with this assessment, including the degree of uncertainty associated with a number of model inputs and uncertainty in the model itself.

b. Quantitative Health Risk Assessment

As discussed in section II.B.2 of the proposal, the approach used to develop quantitative risk estimates associated with exposures to O

builds upon the risk assessment conducted during the last review.

The expanded and updated assessment conducted in this review includes estimates of (1) risks of lung function decrements in all and asthmatic school age children, respiratory symptoms in asthmatic children, respiratory-related hospital admissions, and non-accidental and cardiorespiratory-related mortality associated with recent short-term ambient O

levels; (2) risk reductions and remaining risks associated with just meeting the current 8-hour O

NAAQS; and (3) risk reductions and remaining risks associated with just meeting various alternative 8-hour O

NAAQS in a number of example urban areas. The health risk assessment was discussed in the Staff Paper (chapter 5) and presented more fully in a technical support document,

Ozone Health Risk Assessment for Selected Urban Areas

(Abt Associates, 2007a). As noted in the proposal, the scope and methodology for this risk assessment was developed over several years with considerable input from the CASAC Panel and the public.

The methodology, scope, and results from the risk assessment conducted in the last review are described in Chapter 6 of the 1996 Staff Paper (EPA, 1996) and in several technical reports (Whitfield

et al.

, 1996; Whitfield, 1997) and publication (Whitfield

et al.

, 1998).

EPA recognized that there were many sources of uncertainty and variability inherent in the inputs to these assessments and that there was a high degree of uncertainty in the resulting O

risk estimates. Such uncertainties generally relate to a lack of clear understanding of a number of important factors, including, for example, the shape of exposure-response and concentration-response functions, particularly when, as here, effect thresholds can neither be discerned nor determined not to exist; issues related to selection of appropriate statistical models for the analysis of the epidemiologic data; the role of potentially confounding and modifying factors in the concentration-response relationships; and issues related to simulating how O

air quality distributions will likely change in any given area upon attaining a particular standard, since strategies to reduce emissions are not yet fully defined. While some of these uncertainties were addressed quantitatively in the form of estimated confidence ranges around central risk estimates, other uncertainties and the variability in key inputs were not reflected in these confidence ranges, but rather were partially characterized through separate sensitivity analyses or discussed qualitatively.

Key observations and insights from the O

risk assessment, together with important caveats and limitations, were discussed in section II.B of the proposal. In general, estimated risk reductions associated with going from current O

levels to just meeting the current and

alternative 8-hour standards show patterns of increasing estimated risk reductions associated with just meeting the lower alternative 8-hour standards considered. Furthermore, the estimated percentage reductions in risk were strongly influenced by the baseline air quality year used in the analysis (see Staff Paper, Figures 6-1 through 6-6)

Key observations important in comparing estimated health risks associated with attainment of the current NAAQS and alternative standards included:

(1) As discussed in the Staff paper (section 5.4.5), EPA has greater confidence in relative comparisons in risk estimates between alternative standards than in the absolute magnitude of risk estimates associated with any particular standard.

(2) Significant year-to-year variability in O

concentrations combined with the use of a 3-year design value to determine the amount of air quality adjustment to be applied to each year analyzed, results in significant year-to-year variability in the annual health risk estimates upon just meeting the current and potential alternative standards.

(3) There is noticeable city-to-city variability in estimated O

-related incidence of morbidity and mortality across the 12 urban areas analyzed for both recent years of air quality and for air quality adjusted to simulate just meeting the current and selected potential alternative standards. This variability is likely due to differences in air quality distributions, differences in estimated exposure related to many factors including varying activity patterns and air exchange rates, differences in baseline incidence rates, and differences in susceptible populations and age distributions across the 12 urban areas.

(4) With respect to the uncertainties about estimated policy-relevant background (PRB) concentrations,

as discussed in the Staff Paper (section 5.4.3), alternative assumptions about background levels had a variable impact depending on the health effect considered and the location and standard analyzed in terms of the absolute magnitude and relative changes in the risk estimates. There was relatively little impact on either absolute magnitude or relative changes in lung function risk estimates due to alternative assumptions about background levels.

With respect to O

-related non-accidental mortality, while notable differences (i.e., greater than 50 percent) were observed in some areas, particularly for more stringent standards, the overall pattern of estimated reductions, expressed in terms of percentage reduction relative to the current standard, was significantly less impacted.

PRB O

concentrations used in the O

risk assessment were defined in chapter 2 of the Staff Paper (EPA, 2007, pp. 2-48, 2-54) as the O

concentrations that would be observed in the U.S. in the absence of anthropogenic emissions of precursors (e.g., VOC, NO

, and CO) in the U.S., Canada, and Mexico. Based on runs of the GEOS-CHEM model (a global tropospheric O

model) applied for the 2001 warm season (i.e., April to September), monthly background daily diurnal profiles for each of the 12 urban areas for each month of the O

season were simulated using meteorology for the year 2001. Based on these model runs, the Criteria Document states that current estimates of PRB O

concentrations are generally in the range of 0.015 to 0.035 ppm in the afternoon, and they are generally lower under conditions conducive to high O

episodes. They are highest during spring due to contributions from hemispheric pollution and stratospheric intrusions. The Criteria Document states that the GEOS-CHEM model applied for the 2001 warm season reports PRB O

concentrations for afternoon surface air over the United States that are likely 10 ppbv too high in the southeast in summer, and accurate within 5 ppbv in other regions and seasons.

Sensitivity analyses examining the impact of alternative assumptions about PRB were only conducted for lung function decrements and non-accidental mortality.

(5) Concerning the part of the risk assessment based on effects reported in epidemiological studies, important uncertainties include uncertainties (1) surrounding estimates of the O

coefficients for concentration-response relationships used in the assessment, (2) involving the shape of the concentration-response relationship and whether or not a population threshold or non-linear relationship exists within the range of concentrations examined in the studies, (3) related to the extent to which concentration-response relationships derived from studies in a given location and time when O

levels were higher or behavior and /or housing conditions were different provide accurate representations of the relationships for the same locations with lower air quality distributions and/or different behavior and/or housing conditions, and (4) concerning the possible role of co-pollutants which also may have varied between the time of the studies and the current assessment period. An important additional uncertainty for the mortality risk estimates is the extent to which the associations reported between O

and non-accidental and cardiorespiratory mortality actually reflect causal relationships.

As discussed in the proposal, some of these uncertainties have been addressed quantitatively in the form of estimated confidence ranges around central risk estimates; others are addressed through separate sensitivity analyses (e.g., the influence of alternative estimates for policy-relevant background levels) or are characterized qualitatively. For both parts of the health risk assessment, statistical uncertainty due to sampling error has been characterized and is expressed in terms of 95 percent credible intervals. EPA recognizes that these credible intervals do not reflect all of the uncertainties noted above.

B. Need for Revision of the Current Primary O

Standard

1. Introduction

The initial issue to be addressed in this review of the primary O

standard is whether, in view of the advances in scientific knowledge reflected in the Criteria Document and Staff Paper, the current standard should be revised. As discussed in section II.C of the proposal, in evaluating whether it was appropriate to propose to retain or revise the current standard, the Administrator built upon the last review and reflected the broader body of evidence and information now available. In the proposal, EPA presented information, judgments, and conclusions from the last review, which revised the level, averaging time, and form of the standard, from the Staff Paper's evaluation of the adequacy of the current primary standard, including both evidence- and exposure/risk-based considerations, as well as from the CASAC Panel's advice and recommendations. The Staff Paper evaluation, CASAC Panel's views, and the Administrator's proposed conclusions on the adequacy of the current primary standard are presented below.

a. Staff Paper Evaluation

The Staff Paper considered the evidence presented in the Criteria Document as a basis for evaluating the adequacy of the current O

standard, recognizing that important uncertainties remain. The extensive body of human clinical, toxicological, and epidemiological evidence, highlighted above in section II.A.2 and discussed in section II.A of the proposal, serves as the basis for judgments about O

-related health effects, including judgments about causal relationships with a range of respiratory morbidity effects, including lung function decrements, increased respiratory symptoms, airway inflammation, increased airway responsiveness, and respiratory-related hospitalizations and emergency department visits in the warm season, and about the evidence being highly suggestive that O

directly or indirectly contributes to non-accidental and cardiorespiratory-related mortality.

These judgments take into account important uncertainties that remain in interpreting this evidence. For example, with regard to the utility of time-series epidemiological studies to inform judgments about a NAAQS for an individual pollutant, such as O

, within a mix of highly correlated pollutants, such as the mix of oxidants produced in photochemical reactions in the atmosphere, the Staff Paper noted that there are limitations especially at ambient O

concentrations below levels at which O

-related effects have been observed in controlled human exposure studies. The Staff Paper also recognized that the available epidemiological evidence neither supports nor refutes the existence of thresholds at the population level for effects such as increased hospital admissions and premature mortality. There are limitations in epidemiological studies that make discerning thresholds in populations difficult, including low data density in the lower concentration ranges, the possible influence of exposure measurement error, and variability in susceptibility to O

-related effects in populations.

While noting these limitations in the interpretation of the findings from the epidemiological studies, the Staff Paper concluded that if a population threshold level does exist, it would likely be well below the level of the current O

standard and possibly within the range of background levels. This conclusion is supported by several epidemiological studies that have explored the question of potential thresholds either by using a statistical curve-fitting approach to evaluate whether linear or non-linear models fit the data better using, or by analyzing, sub-sets of the data where days over or under a specific cutpoint (e.g., 0.080 ppm or even lower O

levels) were excluded and then evaluating the association for statistical significance. In addition to consideration of the epidemiological studies, findings from controlled human exposure studies indicate that prolonged exposures produced statistically significant group mean FEV

decrements and symptoms in healthy adult subjects at levels down to at least 0.060 ppm, with a small percentage of subjects experiencing notable effects (e.g., >10 percent FEV

decrement, pain on deep inspiration). Controlled human exposure studies evaluated in the last review also found significant responses in indicators of lung inflammation and cell injury at 0.080 ppm in healthy adult subjects. The effects in these controlled human exposure studies were observed in healthy young adult subjects, and it is likely that more serious responses, and responses at lower levels, would occur in people with asthma and other respiratory diseases. These physiological effects can lead to aggravation of asthma and increased susceptibility to respiratory infection. The observations provide support for the conclusion in the Staff Paper that the associations observed in the epidemiological studies, particularly for respiratory-related effects such as increased medication use, increased school and work absences, increased visits to doctors' offices and emergency departments, and increased hospital admissions, extend down to O

levels well below the current standard (i.e., 0.084 ppm) (p. 6-7).

The newly available information reinforces the judgments in the Staff Paper from the last review about the likelihood of causal relationships between O

exposures and respiratory effects and broadens the evidence of O

-related associations to include additional respiratory-related endpoints, newly identified cardiovascular-related health endpoints, and mortality. Newly available evidence also led the Staff Paper to conclude that people with asthma are likely to experience more serious effects than people who do not have asthma. The Staff Paper also concluded that substantial progress has been made since the last review in advancing the understanding of potential mechanisms by which ambient O

, alone and in combination with other pollutants, is causally linked to a range of respiratory-related health endpoints, and may be causally linked to a range of cardiovascular-related health endpoints. Thus, the Staff Paper found strong support in the evidence available since the last review, for consideration of an O

standard that is at least as protective as the current standard and finds no support for consideration of an O

standard that is less protective than the current standard. This conclusion is consistent with the advice and recommendations of the CASAC Panel and with the views expressed by all interested parties who provided comments on drafts of the Staff Paper. While the CASAC Panel and some commenters on drafts of the Staff Paper supported revising the current standard to provide increased public health protection and other such commenters supported retaining the current standard, no one who provided comments on drafts of the Staff Paper supported a standard that would be less protective than the current standard.

i. Evidence-Based Considerations

In looking more specifically at the controlled human exposure and epidemiological evidence, the Staff Paper first noted that controlled human exposure studies provide the clearest and most compelling evidence for an array of human health effects that are directly attributable to acute exposures to O

per se.

Evidence from such human studies, together with animal toxicological studies, help to provide biological plausibility for health effects observed in epidemiological studies. In considering the available evidence, the Staff Paper focused on studies that examined health effects that have been demonstrated to be caused by exposure to O

, or for which the Criteria Document judges associations with O

to be causal or likely causal, or for which the evidence is highly suggestive that O

contributes to the reported effects.

In considering the epidemiological evidence as a basis for reaching conclusions about the adequacy of the current standard, the Staff Paper focused on studies reporting effects in the warm season, for which the effect estimates are more consistently positive and statistically significant than those from all-year studies. The Staff Paper considered the extent to which such studies provide evidence of associations that extend down to ambient O

concentrations below the level of the current standard, which would thereby call into question the adequacy of the current standard. In so doing, the Staff Paper noted that if a population threshold level does exist for an effect observed in such studies, it would likely be at a level well below the level of the current standard. The Staff Paper also attempted to characterize whether the area in which a study was conducted likely would or would not have met the current standard during the time of the study, although it recognizes that the confidence that would appropriately be placed on the associations observed in any given study, or on the extent to which the association would likely extend down to relatively low O

concentrations, is not dependent on this distinction. Further, the Staff Paper considered studies that examined subsets of data that include only days with ambient O

concentrations below the level of the current O

standard, or below even lower O

concentrations, and continue to report statistically significant associations. The Staff Paper judged that such studies are directly relevant to considering the adequacy of the current standard, particularly in light of reported responses to O

levels below the current standard found in controlled human exposure studies.

The Staff Paper evaluation of such studies is discussed below and in section II.C.2.a of the proposal, focusing in turn on studies of (1) lung function, respiratory symptoms and other respiratory-related physiological effects, (2) respiratory hospital admissions and emergency department visits, and (3) mortality.

(1) Lung function, respiratory symptoms and other respiratory-related physiological effects. Health effects for which the Criteria Document continued to find clear evidence of causal associations with short-term O

exposures include lung function decrements, respiratory symptoms, pulmonary inflammation, and increased airway responsiveness. In the last review, these O

-induced effects were demonstrated with statistical significance down to the lowest level tested in controlled human exposure studies at that time (i.e., 0.080 ppm). Two new studies are notable in that they are the only controlled human exposure studies that examined respiratory effects, including lung function decrements and respiratory symptoms, in healthy adults at lower exposure levels than had previously been examined. EPA's reanalysis of the data from the most recent study shows small group mean decrements in lung function responses to be statistically significant at the 0.060 ppm exposure level, while the author's analysis did not yield statistically significant lung function responses but did yield some statistically significant respiratory symptom responses toward the end of the exposure period. These studies report a small percentage of subjects experiencing lung function decrements (≥ 10 percent) at the 0.060 ppm exposure level. These studies provide very limited evidence of O

-related lung function decrements and respiratory symptoms at this lower exposure level.

The Staff Paper noted that evidence from controlled human exposures studies indicates that people with moderate-to-severe asthma have somewhat larger decreases in lung function in response to O

relative to healthy individuals. In addition, lung function responses in people with asthma appear to be affected by baseline lung function (i.e., magnitude of responses increases with increasing disease severity). This newer information expands our understanding of the physiological basis for increased sensitivity in people with asthma and other airway diseases, recognizing that people with asthma present a different response profile for cellular, molecular, and biochemical responses than people who do not have asthma. New evidence indicates that some people with asthma have increased occurrence and duration of nonspecific airway responsiveness, which is an increased bronchoconstrictive response to airway irritants. Controlled human exposure studies also indicate that some people with allergic asthma and rhinitis have increased airway responsiveness to allergens following O

exposure. Exposures to O

exacerbated lung function decrements in people with pre-existing allergic airway disease, with and without asthma. Ozone-induced exacerbation of airway responsiveness persists longer and attenuates more slowly than O

-induced lung function decrements and respiratory symptom responses and can have important clinical implications for asthmatics.

The Staff Paper also concluded that newly available human exposure studies suggest that some people with asthma also have increased inflammatory responses, relative to non-asthmatic subjects, and that this inflammation may take longer to resolve. The new data on airway responsiveness, inflammation, and various molecular markers of inflammation and bronchoconstriction indicate that people with asthma and allergic rhinitis (with or without asthma) comprise susceptible groups for O

-induced adverse effects. This body of evidence qualitatively informs the Staff Paper's evaluation of the adequacy of the current O

standard in that it indicates that controlled human exposure and epidemiological panel studies of lung function decrements and respiratory symptoms that evaluate only healthy, non-asthmatic subjects likely underestimate the effects of O

exposure on asthmatics and other susceptible populations.

The Staff Paper noted that in addition to the experimental evidence of lung function decrements, respiratory symptoms, and other respiratory effects in healthy and asthmatic populations discussed above, epidemiological studies have reported associations of lung function decrements and respiratory symptoms in several locations. Two large U.S. panel studies which together followed over 1,000 asthmatic children on a daily basis (Mortimer

et al.

, 2002, the National Cooperative Inner-City Asthma Study, or NCICAS; and Gent

et al.

, 2003), as well as several smaller U.S. and international studies, have reported robust associations between ambient O

concentrations and measures of lung function, daily respiratory symptoms (e.g., chest tightness, wheeze, shortness of breath), and increased asthma medication use in children with moderate to severe asthma. Mortimer

et al.

(2002) found that of the pollutants measured (including O

, NO

, SO

and PM

), O

was the only one that had a statistically significant effect on lung function. (Mortimer

et al.

2002) also found associations between NO

, SO

and PM

and respiratory symptoms that were stronger than those between O

and respiratory symptoms. Gent

et al.

(2003) found that in co-pollutant models, O

but not PM

2.5

significantly predicted increased risk of respiratory symptoms and rescue medication use among children using asthma maintenance medication. Overall, the multi-city NCICAS (Mortimer

et al.

, 2002), (Gent

et al.

2003), and several other single-city studies indicate a robust positive association between ambient O

concentrations and increased respiratory symptoms and increased medication use in asthmatic children.

In considering the large number of single-city epidemiological studies reporting lung function or respiratory symptoms effects in healthy or asthmatic populations, the Staff Paper noted that most such studies that reported positive and often statistically significant associations in the warm season were conducted in areas that likely would not have met the current standard. In considering the large multi-city NCICAS (Mortimer

et al.

, 2002), the Staff Paper noted that the 98th percentile 8-hour daily maximum O

concentrations at the monitor reporting the highest O

concentrations in each of the study areas ranged from 0.084 ppm to > 0.10 ppm. However, the authors indicate that less than 5 percent of the days in the eight urban areas had 8-hour daily O

concentrations exceeding 0.080 ppm. Moreover, the authors observed that when days with 8-hour average O

levels greater than 0.080 ppm were excluded, similar effect estimates were seen compared to estimates that included all of the days. There are also a few other studies in which the relevant air quality statistics provide some indication that lung function and respiratory symptom effects may be occurring in areas that likely would have met the current standard (EPA, 2007b, p. 6-12).

(2) Respiratory hospital admissions and emergency department visits. At the time of the last review, many time-series studies indicated positive associations between ambient O

and increased respiratory hospital admissions and emergency room visits, providing strong evidence for a relationship between O

exposure and increased exacerbations of

preexisting lung disease extending below the level of the then current 1-hour O

standard (EPA 2007b, section 3.3.1.1.6). Analyses of data from studies conducted in the northeastern U.S. indicated that O

air pollution was consistently and strongly associated with summertime respiratory hospital admissions.

Since the last review, new epidemiological studies have evaluated the association between short-term exposures to O

and unscheduled hospital admissions for respiratory causes. Large multi-city studies, as well as many studies from individual cities, have reported positive and often statistically significant O

associations with total respiratory hospitalizations as well as asthma- and chronic obstructive pulmonary disease (COPD)-related hospitalizations, especially in studies analyzing the O

effect during the summer or warm season. Analyses using multipollutant regression models generally indicate that copollutants do not confound the association between O

and respiratory hospitalizations and that the O

effect estimates were robust to PM adjustment in all-year and warm-season only data. The Criteria Document concluded that the evidence supports a causal relationship between acute O

exposures and increased respiratory-related hospitalizations during the warm season.

In looking specifically at U.S. and Canadian respiratory hospitalization studies that reported positive and often statistically significant associations (and that either did not use GAM or were reanalyzed to address GAM-related problems), the Staff Paper noted that many such studies were conducted in areas that likely would not have met the current O

standard, with many providing only all-year effect estimates, and with some reporting a statistically significant association in the warm season. Of the studies that provide some indication that O

-related respiratory hospitalizations may be occurring in areas that likely would have met the current standard, the Staff Paper noted that some are all-year studies, whereas others reported statistically significant warm-season associations.

Emergency department visits for respiratory causes have been the focus of a number of new studies that have examined visits related to asthma, COPD, bronchitis, pneumonia, and other upper and lower respiratory infections, such as influenza, with asthma visits typically dominating the daily incidence counts. Among studies with adequate controls for seasonal patterns, many reported at least one significant positive association involving O

. However, inconsistencies were observed which were at least partially attributable to differences in model specifications and analysis approach among various studies. In general, O

effect estimates from summer-only analyses tended to be positive and larger compared to results from cool season or all-year analyses. Almost all of the studies that reported statistically significant effect estimates were conducted in areas that likely would not have met the current standard. The Criteria Document concluded that analyses stratified by season generally supported a positive association between O

concentrations and emergency department visits for asthma in the warm season. These studies provide evidence of effects in areas that likely would not have met the current standard and evidence of associations that likely extend down to relatively low ambient O

concentrations.

(3) Mortality. The 1996 Criteria Document concluded that an association between daily mortality and O

concentrations for areas with high O

levels (e.g., Los Angeles) was suggested. However, due to inconsistencies in the results from the very limited number of studies available at that time, there was insufficient evidence to determine whether the observed association was likely causal, and thus the possibility that O

exposure may be associated with mortality was not relied upon in the 1997 decision on the O

primary standard.

Since the last review, the body of evidence with regard to O

-related health effects has been expanded by animal, controlled human exposure, and epidemiological studies and now identifies biologically plausible mechanisms by which O

may affect the cardiovascular system. In addition, there is stronger information linking O

to serious morbidity outcomes, such as hospitalization, that are associated with increased mortality. Thus, there is now a coherent body of evidence that describes a range of health outcomes from lung function decrements to hospitalization and premature mortality.

Newly available large multi-city studies and related analyses (Bell

et al.

, 2004; Huang

et al.

, 2005; and Schwartz, 2005) designed specifically to examine the effect of O

and other pollutants on mortality have provided much more robust and credible information. Together these studies have reported significant associations between O

and mortality that were robust to adjustment for PM and different adjustment methods for temperature and suggest that the effect of O

on mortality may be immediate but may also persist for several days. Further analysis of one of these multi-city studies (Bell

et al.

, 2006) examined the shape of the concentration-response function for the O

-mortality relationship in 98 U.S. urban communities for the period 1987 to 2000 specifically to evaluate whether a threshold level exists. Results from various analytic methods all indicated that any threshold, if it exists, would likely occur at very low concentrations, far below the level of the current O

NAAQS and nearing background levels.

New data are also available from several single-city studies conducted worldwide, as well as from several meta-analyses that have combined information from multiple studies. Three recent meta-analyses evaluated potential sources of heterogeneity in O

-mortality associations. All three analyses reported common findings, including effect estimates that were statistically significant and larger in warm season analyses. Reanalysis of results using default GAM criteria did not change the effect estimates, and there was no strong evidence of confounding by PM.

Overall, the Criteria Document (p. 8-78) found that the results from U.S. multi-city time-series studies, along with the meta-analyses, provide relatively strong evidence for associations between short-term O

exposure and all-cause mortality even after adjustment for the influence of season and PM. The results of these analyses of studies considered in this review indicate that copollutants generally do not appear to substantially confound the association between O

and mortality. In addition, several single-city studies observed positive associations of ambient O

concentrations with total nonaccidental and cardiorespiratory mortality.

Finally, from those studies that included assessment of associations with specific causes of death, it appears that effect estimates for associations with cardiovascular mortality are larger than those for total mortality; effect estimates for respiratory mortality are less consistent in size, possibly due to reduced statistical power in this subcategory of mortality. For cardiovascular mortality, the Criteria Document (p. 7-106) suggested that effect estimates are consistently positive and more likely to be larger and statistically significant in warm season analyses. The Criteria Document (p. 8-78) concluded that these findings are highly suggestive that short-term O

exposure directly or indirectly contributes to nonaccidental and cardiorespiratory-related mortality, but

additional research is needed to more fully establish underlying mechanisms by which such effects occur.

In commenting on the Criteria Document, the CASAC Ozone Panel raised questions about the implications of these time-series results in a policy context, emphasizing that “* * * while the time-series study design is a powerful tool to detect very small effects that could not be detected using other designs, it is also a blunt tool” (Henderson, 2006b). They note that “* * * not only is the interpretation of these associations complicated by the fact that the day-to-day variation in concentrations of these pollutants is, to a varying degree, determined by meteorology, the pollutants are often part of a large and highly correlated mix of pollutants, only a very few of which are measured” (Henderson, 2006b). Even with these uncertainties, the CASAC Ozone Panel, in its review of the Staff Paper, found “* * * premature total non-accidental and cardiorespiratory mortality for inclusion in the quantitative risk assessment to be appropriate.” (Henderson, 2006b)

ii. Exposure- and Risk-Based Considerations

In evaluating the adequacy of the current standard, the Staff Paper also considered estimated quantitative exposures and health risks, and important uncertainties and limitations in those estimates, which are highlighted above in section II.A.3 and discussed in section II.B of the proposal. These estimates are derived from an EPA assessment of exposures and health risks associated with recent air quality levels and with air quality simulated to just meet the current standard to help inform judgments about whether or not the current standard provides adequate protection of public health.

The Staff Paper (and the CASAC Panel) recognized that the exposure and risk analyses could not provide a full picture of the O

exposures and O

-related health risks posed nationally. The Staff Paper did not have sufficient information to evaluate all relevant at-risk groups (e.g., outdoor workers, children under age 5) or all O

-related health outcomes (e.g., increased medication use, school absences, and emergency department visits that are part of a broader pyramid of effects), and the scope of the Staff Paper analyses was generally limited to estimating exposures and risks in 12 urban areas across the U.S., and to only five or just one area for some health effects included in the risk assessment. Thus, due to the limited geographic scope of the exposure and risk assessments, EPA recognizes that national-scale public health impacts of ambient O

exposures would be much larger than the quantitative exposure and risk estimates associated with recent air quality or air quality that just meets the current or alternative standards in the 12 urban areas analyzed. On the other hand, inter-individual variability in responsiveness means that only a subset of individuals in each group estimated to experience exposures at and above a given benchmark level while at elevated exertion would actually be expected to experience such adverse health effects.

The Staff Paper estimated exposures and risks for the three most recent years (2002-2004) for which data were available at the time of the analyses. As discussed above in section II.A.3.a, within this 3-year period, 2002 was a year with relatively higher O

levels in most, but not all, areas and simulation of just meeting the current standard based on 2002 air quality data provides a generally higher-end estimate of exposures and risks, while 2004 was a year with relatively lower O

levels in most, but not all, areas and simulation of just meeting the current standard using 2004 air quality data provides a generally lower-end estimate of exposures and risks.

The Staff Paper consideration of such exposure and risk analyses is discussed below and in section II.C.2.b of the proposal, focusing on both the exposure analyses and the human health risk assessment.

(1) Exposure analyses. EPA's exposure analysis estimated personal exposures to ambient O

levels at and above specific benchmark levels while at elevated exertion to provide some perspective on the potential public health impacts of respiratory symptoms and respiratory-related physiological effects that cannot currently be evaluated in quantitative risk assessments but that may occur at current air quality levels, and the extent to which such impacts might be reduced by meeting the current and alternative standards. As noted above in section II.A.3, the Staff Paper referred to exposures at and above these benchmark levels as “exposures of concern.” The Staff Paper noted that potential public health impacts likely occur across a range of O

exposure levels, such that there is no one exposure level that addresses all relevant public health impacts. Therefore, with the concurrence of the CASAC Panel, the Staff Paper estimated exposures of concern not only at 0.080 ppm O

, a level at which there are demonstrated effects, but also at 0.070 and 0.060 ppm O

. The Staff Paper recognized that there will be varying degrees of concern about exposures at each of these levels, based in part on the population subgroups experiencing them. Given that there is clear evidence of inflammation, increased airway responsiveness, and changes in host defenses in healthy people exposed to 0.080 ppm O

and reason to infer that such effects will continue at lower exposure levels, but with increasing uncertainty about the extent to which such effects occur at lower O

concentrations, the Staff Paper focused on exposures at or above benchmark levels of 0.070 and 0.060 ppm O

while at elevated exertion for purposes of evaluating the adequacy of the current standard.

Exposure estimates were presented in the Staff Paper and in section II.B (Table 1) of the proposal for the number and percent of all school age children and asthmatic school age children exposed, and the number of person-days (occurrences) of exposures, with daily 8-hour maximum exposures at or above several benchmark levels while at intermittent moderate or greater exertion. The percent of population exposed at any given level is very similar for all and asthmatic school age children. Substantial year-to-year variability in exposure estimates is observed, ranging to over an order of magnitude at the current standard level, in estimates of the number of children and the number of occurrences of exposures at both of these benchmark levels while at elevated exertion. The Staff Paper stated that it is appropriate to consider not just the average estimates across all years, but also to consider public health impacts in years with relatively higher O

levels. The Staff Paper also noted that there is substantial city-to-city variability in these estimates, and notes that it is appropriate to consider not just the aggregate estimates across all cities, but also to consider the public health impacts in cities where these estimates are higher than the average upon meeting the current standard.

About 50 percent of asthmatic of all school age children, representing nearly 1.3 million asthmatic children and about 8.5 million school age children in the 12 urban areas examined, are estimated to experience exposures at or above the 0.070 ppm benchmark level while at elevated exertion (i.e., these individuals are estimated to experience 8-hour O

exposures at or above 0.070 ppm while engaged in moderate or greater exertion 1 or more times during the O

season) associated with 2002 O

air quality levels. In contrast, about 17 percent of asthmatic and all school age children are estimated to experience exposures at or above the 0.070 ppm benchmark level while at elevated exertion associated with 2004 O

air quality levels. Just meeting the current standard results in an aggregate estimate of about 20 percent of asthmatic or 18 percent of all school age children likely to experience exposures at or above the

0.070 ppm benchmark level while at elevated exertion using the 2002 simulation. The exposure estimates for this benchmark level range up to about 40 percent of asthmatic or all school age children in the single city with the highest estimate among the cities analyzed. Just meeting the current standard based on the 2004 simulation, results in an aggregate estimate of about 1 percent of asthmatic or all school age children experiencing exposures exceeding the 0.070 ppm benchmark level while at elevated exertion.

At the benchmark level of 0.060 ppm, about 70 percent of all or asthmatic school age children are estimated to experience exposures at or above this benchmark level while at elevated exertion for the aggregate of the 12 urban areas associated with 2002 O

levels. Just meeting the current standard would result in an aggregate estimate of about 45 percent of asthmatic or all school age children likely to experience exposures at or above the 0.060 ppm benchmark level while at elevated exertion using the 2002 simulation. The exposure estimates for this benchmark level range up to nearly 70 percent of all or asthmatic school age children in the single city with the highest estimate among the cities analyzed associated with just meeting the current standard using the 2002 simulation. The Staff Paper indicated an aggregate estimate of about 10 percent of asthmatic or all school age children would experience exposures at or above the 0.060 ppm benchmark level while at elevated exertion associated with just meeting the current standard using the 2004 simulation.

(2) Risk assessment. The health risk assessment estimated risks for several important health endpoints, including: (1) Lung function decrements (i.e., ≥ 15 percent and ≥ 20 percent reductions in FEV

) in all school age children for 12 urban areas; (2) lung function decrements (i.e., ≥ 10 percent and ≥ 20 percent reductions in FEV

) in asthmatic school age children for 5 urban areas (a subset of the 12 urban areas); (3) respiratory symptoms (i.e., chest tightness, shortness of breath, wheeze) in moderate to severe asthmatic children for the Boston area; (4) respiratory-related hospital admissions for 3 urban areas; and (5) nonaccidental and cardiorespiratory mortality for 12 urban areas for three recent years (2002 to 2004) and for just meeting the current standard using a 2002 simulation and a 2004 simulation.

With regard to estimates of moderate lung function decrements, meeting the current standard substantially reduces the estimated number of school age children experiencing one or more occurrences of FEV

decrements ≥ 15 percent for the 12 urban areas, going from about 1.3 million children (7 percent of children) under 2002 air quality to about 610,000 (3 percent of children) based on the 2002 simulation, and from about 620,000 children (3 percent of children) to about 230,000 (1 percent of children) using the 2004 simulation. In asthmatic children, the estimated number of children experiencing one or more occurrences of FEV

decrements ≥ 10 percent for the 5 urban areas goes from about 250,000 children (16 percent of asthmatic children) under 2002 air quality to about 130,000 (8 percent of asthmatic children) using the 2002 simulation, and from about 160,000 (10 percent of asthmatic children) to about 70,000 (4 percent of asthmatic children) using the 2004 simulation. Thus, even when the current standard is met, about 4 to 8 percent of asthmatic school age children are estimated to experience one or more occurrences of moderate lung function decrements, resulting in about 1 million occurrences (using the 2002 simulation) and nearly 700,000 occurrences (using the 2004 simulation) in just 5 urban areas. Moreover, the estimated number of occurrences of moderate or greater lung function decrements per child is on average approximately 6 to 7 in all children and 8 to 10 in asthmatic children in an O

season, even when the current standard is met, depending on the year used to simulate meeting the current standard. In the 1997 review of the O

standard a general consensus view of the adversity of such moderate responses emerged as the frequency of occurrences increases, with the judgment that repeated occurrences of moderate responses, even in otherwise healthy individuals, may be considered adverse since they may well set the stage for more serious illness.

With regard to estimates of large lung function decrements, the Staff Paper noted that FEV

decrements > 20 percent would likely interfere with normal activities in many healthy individuals, therefore single occurrences would be considered to be adverse. In people with asthma, large lung function responses would likely interfere with normal activities for most individuals and would also increase the likelihood that these individuals would use additional medication or seek medical treatment. Single occurrences would be considered to be adverse to asthmatic individuals under the ATS definition. They also would be cause for medical concern in some individuals. While the current standard reduces the occurrences of large lung function decrements in all children and asthmatic children from about 60 to 70%, in a year with relatively higher O

levels (2002), there are estimated to be about 500,000 occurrences in all school children across the entire 12 urban areas, and about 40,000 occurrences in asthmatic children across just 5 urban areas. As noted above, it is clear that even when the current standard is met over a three-year period, O

levels in each year can vary considerably, as evidenced by relatively large differences between risk estimates based on 2002 to 2004 air quality. The Staff Paper expressed the view that it was appropriate to consider this yearly variation in O

levels allowed by the current standard in judging the extent to which impacts on members of at-risk groups in a year with relatively higher O

levels remain of concern from a public health perspective.

With regard to other O

-related health effects, the estimated risks of respiratory symptom days in moderate to severe asthmatic children, respiratory-related hospital admissions, and non-accidental and cardiorespiratory mortality, respectively, are not reduced to as great an extent by meeting the current standard as are lung function decrements. For example, just meeting the current standard reduces the estimated average incidence of chest tightness in moderate to severe asthmatic children living in the Boston urban area by 11 to 15%, based on 2002 and 2004 simulations, respectively, resulting in an estimated incidence of about 23,000 to 31,000 per 100,000 children attributable to O

exposure (Table 6-4). Just meeting the current standard is estimated to reduce the incidence of respiratory-related hospital admissions in the New York City urban area by about 16 to 18%, based on 2002 and 2004 simulations, respectively, resulting in an estimated incidence per 100,000 population of 4.6 to 6.4, respectively. Across the 12 urban areas, the estimates of non-accidental mortality incidence per 100,000 relevant population range from 0.4 to 2.6 (for 2002) and 0.5 to 1.5 (for 2004). Meeting the current standard results in a reduction of the estimated incidence per 100,000 population to a range of 0.3 to 2.4 based on the 2002 simulation and a range of 0.3 to 1.2 based on the 2004 simulation. Estimates for cardiorespiratory mortality show similar patterns.

In considering the estimates of the proportion of population affected and the number of occurrences of the health effects that are included in the risk assessment, the Staff Paper noted that

these limited estimates are indicative of a much broader array of potential O

-related health endpoints that we consider part of a “pyramid of effects” that include various indicators of morbidity that could not be included in the risk assessment (e.g., school absences, increased medication use, emergency department visits) and which primarily affect members of at-risk groups. While the Staff Paper had sufficient information to estimate and consider the number of symptom days in children with moderate to severe asthma, it recognized that there are many other effects that may be associated with symptom days, such as increased medication use, school and work absences, or visits to doctors' offices, for which there was not sufficient information to estimate risks but which are important to consider in assessing the adequacy of the current standard. The same is true for more serious, but less frequent effects. The Staff Paper estimated hospital admissions, but there was not sufficient information to estimate emergency department visits in a quantitative risk assessment. Consideration of such unquantified risks in the Staff Paper reinforced the Staff Paper conclusion that consideration should be given to revising the standard so as to provide increased public health protection, especially for at-risk groups such as people with asthma or other lung diseases, as well as children and older adults, particularly those active outdoors, and outdoor workers.

iii. Summary of Staff Paper Considerations

The Staff Paper concluded that the overall body of evidence clearly calls into question the adequacy of the current standard in protecting at-risk groups against an array of adverse health effects that range from decreased lung function and respiratory symptoms to serious indicators of respiratory morbidity including emergency department visits and hospital admissions for respiratory causes, nonaccidental mortality, and possibly cardiovascular effects. These at-risk groups notably include asthmatic children and other people with lung disease, as well as all children and older adults, especially those active outdoors, and outdoor workers.

The available information provides strong support for consideration of an O

standard that would provide increased health protection for these at-risk groups. The Staff Paper also concluded that risks projected to remain upon meeting the current standard are indicative of risks to at-risk groups that can be judged to be important from a public health perspective. This information reinforced the Staff Paper conclusion that consideration should be given to revising the level of the standard so as to provide increased public health protection.

In defining at-risk groups this way we are including both groups with greater inherent sensitivity and those more likely to be exposed.

b. CASAC Views

The CASAC Panel unanimously concluded in a letter to the Administrator that there is “no scientific justification for retaining” the current primary O

standard, and the current standard “needs to be substantially reduced to protect human health, particularly in sensitive subpopulations” (Henderson, 2006c, pp. 1-2). In its rationale for this conclusion, the CASAC Panel concluded that “new evidence supports and builds-upon key, health-related conclusions drawn in the 1997 O

NAAQS review” (id., p. 3). The Panel noted that several new single-city studies and large multi-city studies have provided more evidence for adverse health effects at concentrations lower than the current standard, and that these epidemiological studies are backed-up by evidence from controlled human exposure studies. The Panel specifically noted evidence from the recent Adams (2006) study that reported statistically significant decrements in the lung function of healthy, moderately exercising adults at a 0.080 ppm exposure level, and importantly, also reported adverse lung function effects in some healthy individuals at 0.060 ppm. The CASAC Panel concluded that these results indicate that the current standard “is not sufficiently health-protective with an adequate margin of safety,” noting that while similar studies in sensitive groups such as asthmatics have yet to be conducted, “people with asthma, and particularly children, have been found to be more sensitive and to experience larger decrements in lung function in response to O

exposures than would healthy volunteers (Mortimer

et al.

, 2002)” (Henderson, 2006c, p. 4).

The CASAC Panel also highlighted a number of O

-related adverse health effects that are associated with exposure to ambient O

, below the level of the current standard based on a broad range of epidemiological studies (Henderson, 2006c). These adverse health effects include increases in school absenteeism, respiratory hospital emergency department visits among asthmatics and patients with other respiratory diseases, hospitalizations for respiratory illnesses, symptoms associated with adverse health effects (including chest tightness and medication usage), and premature mortality (nonaccidental, cardiorespiratory deaths) reported at exposure levels well below the current standard. “The CASAC considers each of these findings to be an important indicator of adverse health effects” (Henderson, 2006c).

The CASAC Panel expressed the view that more emphasis should be placed on the subjects in controlled human exposure studies with FEV

decrements greater than 10 percent, which can be clinically significant, rather than on the relatively small average decrements. The Panel also emphasized significant O

-related inflammatory responses and markers of injury to the epithelial lining of the lung that are independent of spirometric responses. Further, the Panel expressed the view that the Staff Paper did not place enough emphasis on serious morbidity (e.g., hospital admissions) and mortality observed in epidemiological studies. On the basis of the large amount of recent data evaluating adverse health effects at levels at and below the current O

standard, it was the unanimous opinion of the CASAC Panel that the current primary O

standard is not adequate to protect human health, that the relevant scientific data do not support consideration of retaining the current standard, and that the current standard needs to be substantially reduced to be protective of human health, particularly in sensitive subpopulations (Henderson, 2006c, pp. 4-5).

Further, the CASAC letter noted that “there is no longer significant scientific uncertainty regarding the CASAC's conclusion that the current 8-hour primary NAAQS must be lowered” (Henderson, 2006c, p. 5). The Panel noted that a “large body of data clearly demonstrates adverse human health effects at the current level” of the standard, such that “[R]etaining this standard would continue to put large numbers of individuals at risk for respiratory effects and/or significant impact on quality of life including asthma exacerbations, emergency room visits, hospital admissions and mortality” (Henderson, 2006c).

c. Administrator's Proposed Conclusions

At the time of proposal, in considering whether the current primary standard should be revised, the Administrator carefully considered the conclusions contained in the Criteria Document, the rationale and recommendations contained in the Staff Paper, the advice and recommendations

from CASAC, and public comments to date on this issue. In so doing, the Administrator noted the following: (1) That evidence of a range of respiratory-related morbidity effects seen in the last review has been considerably strengthened, both through toxicological and controlled human exposure studies as well as through many new panel and epidemiological studies; (2) that new evidence from controlled human exposure and epidemiological studies identifies people with asthma (including children with asthma) as an important susceptible population for which estimates of respiratory effects in the general population likely underestimate the magnitude or importance of these effects; (3) that new evidence about mechanisms of toxicity further contributes to the biological plausibility of O

-induced respiratory effects and is beginning to suggest mechanisms that may link O

exposure to cardiovascular effects; (4) that there is now relatively strong evidence for associations between O

and total nonaccidental and cardiopulmonary mortality, even after adjustment for the influence of season and PM; and (5) the limits of the available evidence. Relative to the information that was available to inform the Agency's 1997 decision to set the current standard, the newly available evidence increased the Administrator's confidence that respiratory morbidity effects such as lung function decrements and respiratory symptoms are causally related to O

exposures, that indicators of respiratory morbidity such as emergency department visits and hospital admissions are causally related to O

exposures, and that the evidence is highly suggestive that O

exposures during the O

season contribute to premature mortality.

The Administrator judged that there is important new evidence demonstrating that exposures to O

at levels below the level of the current standard are associated with a broad array of adverse health effects, especially in at-risk populations that include people with asthma or other lung diseases who are likely to experience more serious effects from exposure to O

, children and older adults with increased susceptibility, as well as those who are likely to be vulnerable as a result of spending a lot of time outdoors engaged in physical activity, especially active children and outdoor workers. Examples of this important new evidence include demonstration of O

-induced lung function effects and respiratory symptoms in some healthy individuals down to the previously observed exposure level of 0.080 ppm, as well as very limited new evidence at exposure levels well below the level of the current standard. In addition, there is now epidemiological evidence of statistically significant O

-related associations with lung function and respiratory symptom effects, respiratory-related emergency department visits and hospital admissions, and increased mortality, in areas that likely would have met the current standard. There are also many epidemiological studies done in areas that likely would not have met the current standard but which nonetheless report statistically significant associations that generally extend down to ambient O

concentrations that are below the level of the current standard. Further, there are a few studies that have examined subsets of data that include only days with ambient O

concentrations below the level of the current standard, or below even much lower O

concentrations, and continue to report statistically significant associations with respiratory morbidity outcomes and mortality. The Administrator recognized that the evidence from controlled human exposure studies, together with animal toxicological studies, provides considerable support for the biological plausibility of the respiratory morbidity associations observed in the epidemiological studies and for concluding that the associations extend below the level of the current standard. However, the Administrator recognized that in the body of epidemiological evidence, many studies reported positive and statistically significant associations, while others reported positive results that were not statistically significant, and a few did not report any positive O

-related associations. In addition, the Administrator judged that evidence of a causal relationship between adverse health outcomes and O

exposures became increasingly uncertain at lower levels of exposure.

Based on the strength of the currently available evidence of adverse health effects, and on the extent to which the evidence indicates that such effects likely result from exposures to ambient O

concentrations below the level of the current standard, the Administrator judged that the current standard does not protect public health with an adequate margin of safety and that the standard should be revised to provide such protection, especially for at-risk groups, against a broad array of adverse health effects.

In reaching this judgment, the Administrator had also considered the results of both the exposure and risk assessments conducted for this review, to provide some perspective on the extent to which at-risk groups would likely experience “exposures of concern”

and on the potential magnitude of the risk of experiencing various adverse health effects when recent air quality data (from 2002 to 2004) are used to simulate meeting the current standard and alternative standards in a number of urban areas in the U.S.

In considering the results of the health risk assessment, as discussed in the proposal notice (section II.C.2), the Administrator noted that there were important uncertainties and assumptions inherent in the risk assessment and that this assessment was most appropriately used to simulate trends and patterns that could be expected, as well as providing informed, but still imprecise, estimates of the potential magnitude of risks.

As discussed in section II.A.3 above, “exposures of concern” are estimates of personal exposures while at moderate or greater exertion to 8-hour average ambient O

levels at and above specific benchmark levels which represent exposure levels at which O

-related health effects are known or can with varying degrees of certainty be inferred to occur in some individuals. Estimates of exposures of concern provide some perspective on the public health impacts of health effects that may occur in some individuals at recent air quality levels but cannot be evaluated in quantitative risk assessments, and the extent to which such impacts might be reduced by meeting the current and alternative standards.

As noted above in section II.A.3, recent O

air quality distributions have been statistically adjusted to simulate just meeting the current and selected alternative standards. These simulations do not represent predictions of when, whether, or how areas might meet the specified standards.

In considering the exposure assessment results at the time of proposal, the Administrator considered analyses that define “exposures of concern” by three benchmark exposure levels: 0.080, 0.070, and 0.060 ppm. Estimates of exposures in at-risk groups at and above these benchmark levels while at elevated exertion, using O

air quality data in 2002 and 2004, provide some indication of the potential magnitude of the incidence of health outcomes that cannot currently be evaluated in a quantitative risk assessment, such as increased airway responsiveness, increased pulmonary inflammation, increased cellular permeability, and decreased pulmonary defense mechanisms. These respiratory-related physiological effects have been demonstrated to occur in healthy people at O

exposures as low as 0.080 ppm, the lowest level tested for these effects. These physiological effects provide plausible mechanisms underlying observed associations with aggravation of asthma, increased medication use, increased school and work absences,

increased susceptibility to respiratory infection, increased visits to doctors' offices and emergency departments, and increased admissions to hospitals. In addition, these physiological effects, if repeated over time, have the potential to lead to chronic effects such as chronic bronchitis or long-term damage to the lungs that can lead to reduced quality of life.

In considering these various benchmark levels for exposures of concern at the time of proposal, the Administrator focused primarily on estimated exposures at and above the 0.070 ppm benchmark level while at elevated exertion as an important surrogate measure for potentially more serious health effects in at-risk groups such as people with asthma. This judgment was based on the strong evidence of effects in healthy people at the 0.080 ppm exposure level and the new evidence that people with asthma are likely to experience larger and more serious effects than healthy people at the same level of exposure. In the Administrator's view at the time of proposal, this evidence did not support a focus on exposures at and above the benchmark level of 0.080 ppm O

, as it would not adequately account for the increased risk of harm from exposure for members of at-risk groups, especially people with asthma. The Administrator also judged that the evidence of demonstrated effects is too limited to support a primary focus on exposures down to the lowest benchmark level considered of 0.060 ppm. The Administrator particularly noted that although the analysis of “exposures of concern” was conducted to estimate exposures at and above three discrete benchmark levels (0.080, 0.070, and 0.060 ppm) while at elevated exertion, the concept is appropriately viewed as a continuum. In so doing, the Administrator sought to balance concern about the potential for health effects and their severity with the increasing uncertainty associated with our understanding of the likelihood of such effects at lower O

exposure levels.

The Administrator observed that based on the aggregate exposure estimates for the 2002 simulation (summarized in section II.B.1, Table 1, of the proposal) for the 12 U.S. urban areas included in the exposure analysis, upon just meeting the current standard up to about 20 percent of asthmatic or all school age children are likely to experience one or more exposures at and above the 0.070 ppm benchmark level while at elevated exertion; the 2004 simulation yielded an estimate of about 1 percent of such children. The Administrator noted from this comparison that there is substantial year-to-year variability, ranging up to an order of magnitude or more in estimates of the number of people and the number of occurrences of exposures at and above this benchmark level while at elevated exertion. Moreover, within any given year, the exposure assessment indicates that there is substantial city-to-city variability in the estimates of the children exposed or the number of occurrences of exposure at and above this benchmark level while at elevated exertion. For example, city-specific estimates of the percent of asthmatic or all school age children likely to experience exposures at and above the benchmark level of 0.070 ppm while at elevated exertion ranges from about 1 percent up to about 40 percent across the 12 urban areas upon just meeting the current standard based on the 2002 simulation; the 2004 simulation yielded estimates that range from about 0 up to about 7 percent. The Administrator judged that it was important to recognize the substantial year-to-year and city-to-city variability in considering these estimates.

With regard to the results of the risk assessment, the Administrator focused on the risks estimated to remain upon just meeting the current standard. Based on the aggregate risk estimates (summarized in section II.B.2, Table 2, of the proposal), the Administrator observed that upon just meeting the current standard based on the 2002 simulation, approximately 8 percent of asthmatic school age children across 5 urban areas (ranging up to about 11 percent in the city with the highest estimate among the cities analyzed) would still be estimated to experience moderate or greater lung function decrements one or more times within an O

season. These estimated percentages would be approximately 3 percent of all school age children across 12 urban areas (ranging up to over 5 percent in the city with the highest estimate among the cities analyzed). The Administrator recognized that, as with the estimates of exposures of concern, there is substantial year-to-year and city-to-city variability in these risk estimates.

In addition to the percentage of asthmatic or all children estimated to experience one or more occurrences of an effect, the Administrator recognized that some individuals are estimated to have multiple occurrences. For example, across all the cities in the assessment, approximately 6 to 7 occurrences of moderate or greater lung function decrements per child are estimated to occur in all children and approximately 8 to 10 occurrences are estimated to occur in asthmatic children in an O

season, even upon just meeting the current standard. In the last review, a general consensus view of the adversity of such responses emerged as the frequency of occurrences increases, with the judgment that repeated occurrences of moderate responses, even in otherwise healthy individuals, may be considered adverse since they may well set the stage for more serious illness. The Administrator continued to support this view.

Large lung function decrements (i.e., ≥ 20 percent FEV

decrement) would likely interfere with normal activities in many healthy individuals, therefore single occurrences would be considered to be adverse. In people with asthma, large lung function responses (i.e., ≥ 20 percent FEV

decrement), would likely interfere with normal activities for most individuals and would also increase the likelihood that these individuals would use additional medication or seek medical treatment. Not only would single occurrences be considered to be adverse to asthmatic individuals under the ATS definition, but they also would be cause for medical concern for some individuals. Upon just meeting the current standard based on the 2002 simulation, close to 1 percent of asthmatic and all school age children are estimated to experience one or more occurrences of large lung function decrements in the aggregate across 5 and 12 urban areas, respectively, with close to 2 percent of both asthmatic and all school age children estimated to experience such effects in the city that receives relatively less protection from this standard. These estimates translate into approximately 500,000 occurrences of large lung function decrements in all children across 12 urban areas, and about 40,000 occurrences in asthmatic children across 5 urban areas upon just meeting the current standard based on the 2002 simulation; the 2004 simulation yielded estimates that translate into approximately 160,000 and 10,000 such occurrences in all children and asthmatic children, respectively.

Upon just meeting the current standard based on the 2002 simulation, the estimate of the O

-related risk of respiratory symptom days in moderate to severe asthmatic children in the Boston area is about 8,000 symptom days; the 2004 simulation yielded an estimate of about 6,000 such symptoms days. These estimates translate into as many as one symptom day in six, and one symptom day in eight, respectively, that are attributable to O

exposure during the O

season of the total number of symptom days associated with all

causes of respiratory symptoms in asthmatic children during those years.

The estimated O

-related risk of respiratory-related hospital admissions upon just meeting the current standard based on the 2002 simulation is greater than 500 hospital admissions in the New York City area alone, or about 1.5 percent of the total incidence of respiratory-related admissions associated with all causes; the 2004 simulation yielded an estimate of approximately 400 such hospital admissions. For nonaccidental mortality, just meeting the current standard based on the 2002 simulation results in an estimated incidence of from 0.3 to 2.4 per 100,000 population; the 2004 simulation resulted in an estimated incidence of from 0.3 to 1.2 per 100,000 population. Estimates for cardiorespiratory mortality show similar patterns (Abt Associates, 2007a, Table 4-26).

The Administrator recognized that in considering the estimates of the proportion of population affected and the number of occurrences of those specific health effects that are included in the risk assessment, these limited estimates based on 2002 and 2004 simulations are indicative of a much broader array of O

-related health endpoints that are part of a “pyramid of effects” (discussed in section II.A.4.d of the proposal) that include various indicators of morbidity that could not be included in the risk assessment (e.g., school absences, increased medication use, emergency department visits) and which primarily affect members of at-risk groups. Moreover, the Administrator noted that the CASAC Panel supported a qualitative consideration of the much broader array of O

-related health endpoints, and specifically referred to respiratory emergency department visits in asthmatics and people with other lung diseases, increased medication use, and increased respiratory symptoms reported at exposure levels well below the current standard.

The Administrator expressed the view in the proposal that the exposure and risk estimates discussed in the Staff Paper and summarized above are important from a public health perspective and indicative of potential exposures and risks to at-risk groups. In reaching this proposed judgment, the Administrator considered the following factors: (1) The estimates of numbers of persons exposed at and above the 0.070 ppm benchmark level; (2) the risk estimates of the proportion of the population and number of occurrences of various health effects in areas upon just meeting the current standard; (3) the year-to-year and city-to-city variability in both the exposure and risk estimates; (4) the uncertainties in these estimates; and (5) recognition that there is a broader array of O

-related adverse health outcomes for which risk estimates could not be quantified (that are part of a broader “pyramid of effects”) and that the scope of the assessment was limited to just a sample of urban areas and to some but not all at-risk populations, leading to an incomplete estimation of public health impacts associated with O

exposures across the country. The Administrator also noted that it was the unanimous conclusion of the CASAC Panel that there is no scientific justification for retaining the current primary O

standard, that the current standard is not sufficiently health-protective with an adequate margin of safety, and that the standard needs to be substantially reduced to protect human health, particularly in at-risk subpopulations.

Based on all of these considerations, the Administrator proposed that the current O

standard is not requisite to protect public health with an adequate margin of safety because it does not provide sufficient protection and that revision would result in increased public health protection, especially for members of at-risk groups.

2. Comments on the Need for Revision

The above section outlines the health effects evidence and assessments used by the Administrator to inform his proposed judgments about the adequacy of the current O

primary standard. General comments received on the proposal that either supported or opposed the proposed decision to revise the current O

primary standard are addressed in this section. Comments on the health effects evidence, which includes evidence from controlled human exposure and epidemiological studies, are considered in section II.B.2.a below. Comments on human exposure and health risk assessments are considered in section II.B.2.b, and comments on other policy-related issues are considered in section II.B.2.c, below. Comments on specific issues, health effects evidence, or the human exposure and health risk assessments that relate to consideration of the appropriate averaging time, form, or level of the O

standard are addressed below in sections II.C.3 and II.C.4. General comments based on implementation-related factors that are not a permissible basis for considering the need to revise the current standard are noted in the Response to Comments document.

a. Consideration of Health Effects Evidence

With regard to the need to revise the current primary O

standard, sharply divergent comments were received from two general sets of commenters. Many public comments received on the proposal asserted that the current O

standard is insufficient to protect public health, especially the health of sensitive groups, with an adequate margin of safety and revisions to the standard are appropriate. Among those calling for revisions to the current primary standard were medical groups, including for example, the American Medical Association (AMA), the American Thoracic Society (ATS), the American Academy of Pediatrics (AAP), and the American College of Chest Physicians (ACCP), as well as medical doctors and academic researchers. For example, the ATS stated:

We believe that the Administrator has correctly stated that, beyond any degree of scientific uncertainty, convincing and compelling evidence has demonstrated that exposure to ozone at levels below the current standard is responsible for measurable and significant adverse health effects, both in terms of morbidity and mortality. * * * The known respiratory, cardiac and perinatal effects of ozone pollution are each in their own right major public health issues. In combination they provide immediate, actionable information and require a meaningful public health policy response from the EPA. [ATS

et al.

pp. 1, 11]

Similar conclusions were also reached in comments by many national, State, and local public health organizations, including, for example, the American Lung Association (ALA) in a joint set of comments with several environmental groups, the American Heart Association (AHA), the American Nurses Association (ANA), the American Public Health Association (APHA), and the National Association of County and City Health Officials (NACCHO), as well as in letters to the Administrator from EPA's advisory panel on children's environmental health (Children's Health Protection Advisory Committee; Marty

et al.

, 2007a, 2007b). Environmental groups also commented in support of revising the standard, including the Sierra Club, Environmental Defense, the Natural Resources Defense Council (NRDC), Earthjustice, and the U.S. Public Interest Research Group (US PIRG). All of these medical, environmental and public health commenters stated that the current O

standard needs to be revised and that an even more protective standard than proposed by EPA is needed to protect the health of sensitive population

groups. Many individual commenters also expressed such views.

The majority of State and local air pollution control authorities who commented on the O

standard supported revision of the current O

standard, as did the National Tribal Air Association (NTAA). Environmental agencies that supported revising the standard include agencies from: Arkansas; California; Delaware; Iowa; Illinois; Michigan; North Carolina; New Mexico; New York; Oklahoma; Oregon; Pennsylvania; Utah; Wisconsin; and Washington, DC. State organizations, including the National Association of Clean Air Agencies (NACAA), Northeast States for Coordinated Air Use Management (NESCAUM), and the Ozone Transport Commission (OTC) urged that EPA revise the O

standard. All of these commenters supported revisions to the current standard, with most supporting a standard consistent with CASAC's recommendations.

In general, the commenters noted above primarily based their views on the body of evidence assessed in the Criteria Document, finding it to be stronger and more compelling than in the last review. Some specifically agreed with the weight of evidence approach taken by the Criteria Document. These commenters generally placed much weight on CASAC's interpretation of the body of available evidence and the results of EPA's exposure and risk assessments, both of which formed the basis for CASAC's recommendation to revise the O

standard to provide increased public health protection.

In recent years, a broad scientific consensus has emerged that EPA's current air quality standards for ozone are not sufficient to protect public health, and that the levels and form must be greatly tightened. This consensus is evidenced by the by the strong unanimous comments of the CASAC, which was backed by the endorsement of over 100 leading independent air quality scientists, EPA's Children's Health Protection Advisory Committee, and many others. In the face of this strong consensus, it is untenable to cite “uncertainty” as a rationale for failing to propose tighter standards. [ALA

et al.

, p. 15]

Medical and public health commenters also expressed the view that EPA must not use uncertainty in the scientific evidence as justification for retaining the current O

standard.

EPA generally agrees with these commenters' conclusion regarding the need to revise the current primary O

standard. The scientific evidence-related health effects to O

exposure noted by these commenters was generally the same as that assessed in the Criteria Document and the proposal. EPA agrees that this information provides a basis for concluding that the current O

standard is not adequately protective of public health. For reasons discussed below in sections II.C.3 and II.C.4, however, EPA disagrees with aspects of these commenters' views on the level of protection that is appropriate and supported by the available scientific information.

Another group of commenters representing industry associations and businesses opposed revising the current primary O

standard. These views were extensively presented in comments from the Utility Air Regulatory Group (UARG), representing a group of electric generating companies and organizations and several national trade associations, and in comments from other industry and business associations including, for example: Exxon Mobil Corporation; the Alliance of Automobile Manufacturers (AAM); the National Association of Manufacturers (NAM), the American Petroleum Institute (API). The API sponsored a workshop at the University of Rochester in June 2007 to review the scientific information and health risk assessment considered by EPA during the review of the O

NAAQS. Although the report (hereafter, “Rochester Report”) from this workshop does not offer judgments on the specific elements of the current or proposed standard, it has been cited in a number of public comments that opposed revision of the current 8-hour standard. The Annapolis Center for Science-Based Public Policy issued a report (hereafter, “Annapolis Center”) on the science and health effects of O

, which explicitly opposed revising the current O

primary standard. Several State environmental agencies also opposed revising the current O

primary standard, including agencies from: Georgia; Indiana; Kentucky; Louisiana; Nevada; and Texas.

As discussed more fully below in sections dealing with specific comments, these and other commenters in this group generally mentioned many of the same studies from the body of evidence in the Criteria Document that were cited by the commenters who supported revising the standards, but highlighted different aspects of these studies in reaching substantially different conclusions about their strength and the extent to which progress has been made in reducing uncertainties in the evidence since the last review. They then considered whether the evidence that has become available since the last review has established a more certain risk or a risk of effects that is significantly different in character from those that provided a basis for the current standards, or whether the evidence demonstrates that the risk to public health upon attainment of the current standards would be greater than was understood when EPA established the current O

standard in 1997. These commenters generally expressed the view that the current standard provides the requisite degree of public health protection.

In supporting their view that the present primary O

standard continues to provide the requisite public health protection and should not be revised, UARG and others generally stated: That the effects of concern have not changed significantly since 1997; that the uncertainties in the underlying health science are as great or greater than in 1997; that the estimated number of exposures of concern and health risks upon attainment of the current O

standard has not changed or decreased since 1997; and that “new” studies not included in the Criteria Document continue to demonstrate uncertainties about possible health risks associated with exposure to O

at levels below the current standard. As noted above, EPA disagrees with this general assessment, and agrees with the general position that the available information provides a basis for concluding that the current O

standard is not adequately protective of public health. The rationale for this position is discussed more fully in the responses to specific comments that are presented below.

More specific comments on the evidence and EPA's responses are discussed below. Section II.B.2.a.i contains comments on evidence from controlled human exposure studies; section II.B.2.a.ii contains comments on evidence from epidemiological studies, including interpretation of the evidence and specific methodological issues. Comments on evidence pertaining to at-risk subgroups for O

-related effects can be found in section II.B.2.a.iii below. EPA notes here that most of the issues and concerns raised by commenters concerning the health effects evidence, including both the interpretation of the evidence and specific technical or methodological issues, were essentially restatements of issues raised during the review of the Criteria Document and the Staff Paper. Most of these issues were highlighted and thoroughly discussed during the review of these documents by the CASAC. More detailed responses related to the interpretation of the health effects evidence and its role in the decision on the O

NAAQS are contained in the Response to Comments document.

i. Evidence from Controlled Human Exposure Studies

As noted in the overview of health effects evidence, section II.A.2 above, two new controlled human-exposure studies (Adams 2002, 2006) are now available that examine respiratory effects associated with prolonged O

exposures at levels at and below 0.080 ppm, which was the lowest exposure level that had been examined in the last review. One group of commenters that included national medical (e.g., ATS, AMA, ACCP) and national environmental and public health organizations (e.g., ALA in a joint set of comments with Environmental Defense, Sierra Club), agreed with EPA's reanalysis of the Adams' data while disagreeing with EPA's characterization of the evidence from the Adams studies as “very limited” (72 FR 37870). These commenters expressed the view that the Adams studies provide evidence of effects at lower concentrations than had previously been reported. They noted that Adams, while finding small group mean changes at 0.060 ppm, reported total subjective symptom scores reached statistical significance (relative to pre-exposure) at 5.6 and 6.6 hours, with the triangular exposure scenario, and that pain on deep inspiration values followed a similar pattern to total subjective symptoms scores. In addition, Adams (2002) reports that “some sensitive subjects experience notable effects at 0.060 ppm,” based on a greater than 10% reduction in FEV

. These commenters made the point that the responses of individuals are more important than group mean responses and that when the Adams (2002, 2006) study data are corrected for the effects of exercise in clean air, 7 percent of subjects experience FEV

decrements greater than 10% at the 0.040 and 0.060 ppm exposure levels. They expressed the view that while 2 of 30 tested subjects responding at the 0.060 ppm level may seem like a small number, a 7 percent response rate is far from trivial. Seven percent of the U.S. population is 21.2 million people (ALA

et al.

, p. 51). Noting that the subjects in the Adams' studies were all healthy adults, these groups expressed concern that “in some vulnerable populations the magnitude of the response would be greater and the exposure level at which responses are observed to occur would be lower” (ATS, p. 4).

These commenters generally supported EPA's reanalysis of the Adams' data, stating that EPA has undertaken a careful reanalysis of the underlying data in the Adams studies to assess the change in FEV

following exposure to 0.060 ppm O

and filtered air, and concluding that “the reanalysis employs the standard approach used by other researchers, and supported by CASAC” (ALA

et al.

, p. 49), and “we believe that the Adams study shows significant health effects at 0.06 ppm exposure levels” (ATS, p. 5). The American Thoracic Society, AMA and other medical organizations conclude:

The Adams study confirms our understanding that in healthy populations, an important fraction of the population will experience larger-than-average decrements in FEV

when exposed to low levels of ozone. It is reasonable to assume that these effects would be even greater when extrapolated to other populations known to have sensitivities to ozone (children, asthmatics, COPD patients). We feel the correct conclusion to draw from the Adams study is that there is a significant fraction of the population that will express significant responses to low levels of ozone. [ATS, p. 5]

EPA generally agrees with most of the comments summarized above, while placing more emphasis on the limited nature of the evidence addressing O

-related lung function and respiratory symptom responses at the 0.060 and 0.040 ppm exposure levels. As characterized in the proposal notice, EPA's reanalysis of the data from the most recent Adams study shows small group mean decrements in lung function responses to be statistically significant at the 0.060 ppm exposure level, while acknowledging that the author's analysis did not yield statistically significant lung function responses. The Adams studies report a small percentage of subjects experiencing lung function decrements (≥10 percent) at the 0.060 ppm exposure level. EPA disagrees with these commenters that the percent of subjects that experienced FEV

decrements greater than 10% in this study of 30 subjects can appropriately be generalized to the U.S. population. The Administrator concludes that these studies provide very limited evidence of O

-related lung function decrements and respiratory symptoms at this lower exposure level.

The second group of commenters, who opposed revision of the standard, raised many concerns about the role of the Adams studies and EPA's reanalysis of the Adams data in the decision. With regard to the results reported by Adams, these commenters expressed the view that the group mean FEV

decrement measured at 0.060 ppm was small, less than 3%, which is within the 3 to 5% range of normal measurement variability for an individual (UARG, p. 12). Moreover even the reported group mean FEV

decrements in Adams subjects when exposed to an O

concentration of 0.080 ppm were described as quite minimal, likely non-detectable by the subjects and within the range that the EPA would consider to be normal or mild (UARG, p. 13); With respect to the larger decrements in FEV

(≥ 10%) experienced by some subjects in the Adams studies, these commenters stated the view that such decrements would not be considered adverse in healthy individuals, and that “reliance on the individual responses of such a miniscule number of subjects (2 of 30) is woefully inadequate as any basis for a nationwide O

standard” (UARG, p.14). Some of these commenters put the results of the Adams studies (2002, 2006) in the context of the 1997 decision on the O

standard to reach the conclusion that there is no basis for revising that standard. They stated that the data from Adams (2002, 2006) on O

levels below 0.080 ppm was too limited to support a revised standard, and noted that responses reported in the Adams studies at 0.080 ppm were similar to responses reported previously (Horstmann

et al.

, 1990 and McDonnell

et al.

, 1991), and therefore, provided no new information on O

that was not known at the time of EPA's last review (Exxon Mobil, pp. 5-6).

These commenters raised one or more of the following concerns about EPA's reanalysis of the Adams data: (1) EPA's re-analysis was not published or peer-reviewed, and therefore neither the scientific community nor the public was afforded opportunity to appropriately review the analysis (Exxon Mobil, p. 6); (2) EPA has misinterpreted the studies of Dr. Adams, and over his objections used a different analytical methodology to reach a different conclusion; (3) EPA's reanalysis did not employ an appropriate statistical test; the ANOVA statistical test employed by Adams was preferred over the statistical test used in EPA's reanalysis (paired t-test); and (4) the reanalysis of the Adams data is evidence that EPA interpreted and presented scientific information in a systematically biased manner, reflecting purposeful bias because the reanalysis supported staff policy recommendations and Adams' own analysis did not, and the 10% decrement in FEV

was a post-hoc threshold chosen for compatibility with EPA staff policy recommendations (NAM, p. 19).

First, EPA agrees that the group mean lung function decrement observed in the Adams study at the 0.060 ppm exposure level is relatively small. However, EPA and the CASAC Panel observed that the study showed some individuals experienced lung function decrements ≥ 10 percent, which is the most

important finding from this study in terms of public health implications. The magnitude of changes in the group mean do not address whether a subset of the population is at risk of health effects. The clinical evidence to date makes it clear that there is significant variability in responses across individuals, so it is important to look beyond group mean to the response of subsets of the group to evaluate the potential impact for sensitive or susceptible parts of the population. The Administrator also agrees with both EPA staff and CASAC's views that this level of response may not represent an adverse health effect in healthy individuals but does represent a level that should be considered adverse for asthmatic individuals.

Second, EPA notes that its reanalysis of the Adams (2006) study was prepared in response to the issues and analysis raised by a public commenter who made a presentation to the CASAC Panel at its March 5, 2007 teleconference. EPA replicated the analysis and addressed issues raised in these public comments concerning the statistical significance of 0.060 ppm O

exposure on lung function response in the Adams (2006) publication. EPA documented its response in a technical memorandum (Brown, 2007), which was placed in the rulemaking docket prior to publication of the proposal. EPA has clearly stated that the additional statistical analyses conducted by both the public commenter and by EPA staff do not contradict or undercut the statistical analysis presented by Dr. Adams in his published study, as EPA and the author were addressing different questions. While the author of the original study was focused on determining whether the changes observed on an hour-by-hour basis were statistically significant for different exposure protocols, EPA's reanalysis was focused on the different question of whether there was a statistically significant difference in lung function decrement before and after the entire 6.6 hour exposure period between the 0.060 ppm exposure protocol and filtered air.

Third, with respect to the concerns raised by Dr. Adams and other commenters that EPA had used an inappropriate statistical approach to address the question regarding statistical significance of the average lung function response at 0.060 ppm, members of the CASAC Panel noted on the March 5, 2007 teleconference the very conservative nature of the approach used by Adams to evaluate the research questions posed by the author. These same CASAC Panel members also supported the use of the statistical approach (i.e., paired-t test) used in the analysis prepared by the public commenter, which was the same approach later used in EPA's reanalysis, as the preferred method for analyzing the pre-minus post-exposure lung function responses reported in this study. EPA agrees with the characterization of the Adams (2006) study in the Rochester Report, which stated, “Although these findings have not been confirmed or replicated, the responses to 0.06 ppm ozone in this [Adams] study are consistent with the presence of an exposure-response curve with responses that do not end abruptly below 0.08 ppm.” This same report also concluded,

The statistical test used in Adams (2006) did not identify the response of the 0.06 ppm exposure as statistically different from that of the filtered air exposure. However, alternative statistical tests suggest that the observed small group mean response in FEV

induced by exposure to 0.06 ppm compared to filtered air is not the result of chance alone. [Rochester Report, p. 56].

Fourth, EPA rejects the contention that the conduct and presentation of its reanalysis of the Adams (2006) study to address issues raised by public commenters represents purposeful bias and was developed only to support a pre-determined policy position. As discussed above, EPA's reanalysis addressed a different question than the author's analysis contained in the publication. Other controlled human exposure studies had routinely examined the same question EPA's reanalysis addressed, whether or not there was a statistically significant group mean response for the entire exposure period compared to filtered air.

ii Evidence from Epidemiological Studies

This section contains major comments on EPA's assessment of epidemiological studies in the proposal and the Agency's general responses to those comments. Many of the issues discussed below are addressed in more detail in the Response to Comments document. Comments on EPA's interpretation and assessment of the body of epidemiological evidence are discussed first and then comments on methodological issues and particular study designs are discussed. EPA notes here that most of the issues and concerns raised by commenters on the interpretation of the epidemiological evidence and methodological issues are essentially restatements of issues raised during the review of the Criteria Document and Staff Paper. EPA presented and the CASAC Panel reviewed the interpretation of the epidemiological evidence in the Criteria Document and the integration of the evidence with policy considerations in the development of the policy options presented in the Staff Paper for consideration by the Administrator. CASAC reviewed both the O

Criteria Document and O

Staff Paper and approved of the scientific content and accuracy of both documents. The CASAC chairman sent to the Administrator one letter (Henderson, 2006a) for the O

Criteria Document and another letter for the O

Staff Paper (Henderson, 2006c) indicating that these documents provided an appropriate basis for use in regulatory decision making regarding the O

NAAQS.

As with evidence from controlled human exposure studies, sharply divergent comments were received on the evidence from epidemiological studies, including EPA's interpretation of the evidence. One group of commenters from medical, public health and environmental organizations, in general, supported EPA's interpretation of the epidemiological evidence (72 FR 37838, section II.a.3.a-c) with regard to whether the evidence for associations is consistent and coherent and whether there is biological plausibility for judging whether exposure to O

is causally related to respiratory and cardiovascular morbidity and mortality effects. Comments of public health and environmental groups, including a joint set of comments from ALA and several environmental groups, note that more than 250 new epidemiological studies, published from 1996 to 2005, were included in the Criteria Document and point to a figure from the Staff Paper and proposal (72 FR 37842, Figure 1) of short-term O

exposures and respiratory health outcome showing consistency in an array of positive effects estimates and health endpoints observed in multiple locations in Canada and the U.S. Medical commenters, including ATS and AMA, stated that these “real world” studies support the findings of chamber studies to show adverse respiratory health effects at levels below the current 8-hour O

standard. These commenters generally expressed agreement with the weight of evidence approach taken by the Criteria Document and the conclusions reached, which were reviewed by CASAC, that the effects of O

on respiratory symptoms, lung function changes, emergency department visits for respiratory and cardiovascular effects, and hospital admissions can be considered causal.

EPA generally agrees with this interpretation of the epidemiological evidence. The Criteria Document concludes that positive and robust

associations were found between ambient O

concentrations and various respiratory disease hospitalization outcomes and emergency department visits for asthma, when focusing particularly on results of warm-season analyses. These positive and robust associations are supported by the human clinical, animal toxicological, and epidemiological evidence for lung function decrements, increased respiratory symptoms, airway inflammation, and increased airway responsiveness. Taken together, the overall evidence supports a causal relationship between acute ambient O

exposures and increased respiratory morbidity outcomes resulting in increased emergency department visits and hospitalizations during the warm season (EPA, 2006a, p. 8-77).

However, in contrast with EPA, these commenters from ALA and other environmental, medical and public health groups asserted that the causal associations extend down to the lowest ambient O

concentrations reported in these studies. These commenters also expressed the view that the respiratory and cardiovascular system effects are well-supported by the Hill criteria

of judging causality: strength of association, consistency between studies, coherence among studies, and biological plausibility (ALA

et al.

, pp. 51-52). They also noted that recent studies provide compelling evidence that exposure to O

results in adverse cardiovascular health effects (ATS, p. 6-7).

The Hill criteria, published by Sir Bradford Hill (1965), are commonly used criteria for reaching judgments about causality from observed associations, and these criteria were the basis for the critical assessment of the epidemiological evidence presented in the Criteria Document (pp. 7-3-7-4).

EPA disagrees with the assertion of these commenters that the causal associations extend down to the lowest ambient O

concentrations reported in these studies. The biological plausibility of the epidemiological associations is generally supported by controlled human exposure and toxicological evidence of respiratory morbidity effects for levels at and below 0.080 ppm, but that biological plausibility becomes increasingly uncertain at much lower levels. Further, at much lower levels, it becomes increasingly uncertain as to whether the reported associations are related to O

alone rather than to the broader mix of air pollutants present in the ambient air. With regard to cardiovascular health outcomes, the Criteria Document concludes that the generally limited body of evidence from animal toxicology, human controlled exposure, and epidemiologic studies is suggestive that O

can directly and/or indirectly contribute to cardiovascular-related morbidity, and that for cardiovascular mortality the Criteria Document suggests that effects estimates are more consistently positive and statistically significant in warm season analyses but that additional research is needed to more fully establish the underlying mechanisms by which such mortality effects occur (EPA, 2006a, pp. 8-77-78).

The second group of commenters, mostly representing industry associations and some businesses opposed to revising the primary O

standard, disagreed with EPA's interpretation of the epidemiological evidence. These commenters expressed the view that while many new epidemiological studies have been published since the current primary O

standard was promulgated, the inconsistencies and uncertainties inherent in these studies as a whole should preclude any reliance on them as justification for a more stringent primary O

NAAQS. They contend that the purported consistency is the result of inappropriate selectivity in focusing on specific studies and specific results within those studies (UARG, p. 15). With regard to daily mortality, the proposal emphasizes the multi-city studies, suggesting that they have the statistical power to allow the authors to reliably distinguish even weak relationships from the null hypothesis with statistical confidence. However, these commenters note that these studies are not consistent, with regard to the findings concerning individual cities analyzed in the multi-city analyses. One commenter asserted that each of the multi-city studies and meta-analyses cited by EPA involves cities for which the city-specific estimates of O

effects have been observed to vary over a wide range that includes negative [i.e., beneficial] effects (API, p. 15). To illustrate this point, many commenters point to EPA's use of the study by Bell

et al.

, 2004. They note that in focusing on the national estimate from Bell of the association between 24-hour average O

levels and daily mortality, the Administrator overlooks the very significant and heterogeneous information of the individual analyses of the 95 cities used to produce the national estimate and, based on this inconsistency, question whether what is being seen is actually an O

mortality association at all (UARG, p. 16).

EPA has accurately characterized the inconsistencies and uncertainties in the epidemiological evidence and strongly denies that it has inappropriately focused on specific positive studies or specific positive results within those studies. EPA's assessment of the health effects evidence in the Criteria Document has been reviewed by the CASAC Panel. EPA has appropriately characterized the heterogeneity in O

health effects in assessing the results of the single-city and multi-city studies and the meta-analyses, as discussed in section 7.6.6 of the Criteria Document. In general, in the proposal, the Administrator recognized that in the body of epidemiological evidence, many studies reported positive and statistically significant assoc

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