## Responses to Significant Comments on the 2007 Proposed Rule on the National Ambient Air Quality Standards

for Ozone
(July 11, 2007; 72 FR 37818)

Docket Number OAR-2005-0172

U.S. Environmental Protection Agency

March 2008ii 

## Table of Contents

List of Acronyms

Frequently Cited Documents

I. INTRODUCTION ................................................................................................................ .. 1

II. RESPONSES TO SIGNIFICANT COMMENTS ON PROPOSED O 3 STANDARDS........ 2 A. Primary O 3 Standards.......................................................................................................... 2 1. General Comments on Proposed Primary O 3 standard ................................................... 2 a. Support for Revising the Current Standard................................................................. 2 b. Support for Retaining the Current Standard ............................................................... 5 2. Specific Comments on Proposed Primary O 3 Standards................................................. 9 a. Averaging Time .......................................................................................................... 9

b. Form of the Standard ................................................................................................ 10

c. Level ....................................................................................................................... .. 11

i. Comments on Health Evidence Considerations.................................................... 12 ii. Comments on Exposure and Risk Considerations................................................ 16 3. Specific Comments on the Interpreta tion of Scientific Evidence................................. 20

a. Evidence from Controlled Human Exposure Studies ............................................... 20 b. Evidence from Epidemiological Studies................................................................... 28 c. Evidence Pertaining to At-Risk Subgroups for O 3 -Related Effects.......................... 56 d. Adversity of Health Effects ...................................................................................... 61

e. Comments on Role of Ground-Level O 3 in Solar Radiation-Related Health Effects66 4. Specific Comments on the Population Exposure Analyses .......................................... 68 5. Specific Comments on the Health Risk Assessment .................................................... 73 6. Specific Comments Related to Communicati on of Public Health Information.......... 101 B. Secondary O 3 Standards.................................................................................................. 104 1. General Comments on Proposed Alternative Secondary O 3 Standards ...................... 104

a

. Support for Distinct Cumulative, Seasonal Secondary Standard............................ 105 b. Support for Secondary Identical to Current or Revised 8-Hour Standard.............. 106 2. Specific Comments on Proposed Alternative Secondary O 3 Standards ..................... 108

a. Form........................................................................................................................ 108 b. Averaging Times..................................................................................................... 113

iii. Seasonal Window............................................................................................ 113

iv. Diurnal Window.............................................................................................. 114 v. Annual vs. Three Year Average.......................................................................... 115

c. Level ....................................................................................................................... 116 3. Specific Comments on the Interpreta tion of Scientific Evidence............................... 120 4. Specific Comments on the Vegetation Exposure and Risk Assessments................... 128 C. Specific Comments Related to Data Handling (Appendix P)......................................... 134 1. Specific Comments on Data Handling Related to the 8-hour Standard...................... 135 2. Specific Comments Related to Non-identi cal Secondary Standard Provisions of Appendix P..................................................................................................................... ..... 140 D. Comments Related to Monitoring................................................................................... 141iii 1. Specific Comments Related to Moni toring and the Primary Standard....................... 142 2. Specific Comments Related to Monito ring and the Secondary Standard................... 144 III. RESPONSES TO LEGAL, ADMINISTR ATIVE, AND PROCEDURAL ISSUES AND

MISPLACED COMMENTS ...................................................................................................... 146 A. Legal, Administrative and Procedural Issues.................................................................. 146 B. Misplaced Comments...................................................................................................... 164

References..................................................................................................................... .............. 169

Appendix - Provisional Consid eration of Recent Studiesiv 

### List of Acronyms

The following acronyms have been used for th e sake of brevity in this document:

Act Clean Air Act

AAM Alliance of Automobile Manufacturers AAP American Academy of Pediatrics ACC American Chemistry Council ACCP American College of Chest Physicians

AHA American Heart Association ALA American Lung Association

AMA American Medical Association

ANA American Nurses Association

APHA American Public Health Association

API American Petroleum Institute AQI Air Quality Index AQS Air Quality System ARMs Approved Regional Methods ATS American Thoracic Society

CAA Clean Air Act

CARB California Air Resources Board CASAC Clean Air Scientific Advisory Committee

CASTNET Clean Air Status and Trends Network

CDC Centers for Disease Control CFR Code of Federal Regulations CHPAC Children’s Health Protection Advisory Committee

CI Confidence interval

CO Carbon monoxide

COPD Chronic obstruc tive pulmonary disease EPA Environmental Protection Agency FEM Federal Equivalent Method

FEV 1 Forced Expiratory Volume for 1 second

FRM Federal Reference Method

GAM Generalized additive model

GLM Generalized linear model

HEI Health Effects Institute HML Highest measured level IQG Information Quality Guidelines

LML Lowest measured level MSA Metropolitan Statistical Area NACAA National Association of Clean Air Agencies

NACCHO National Association of C ounty and City Health Officials NAAQS National ambient air quality standards

NAM National Association of Manufacturers

NESCAUM Northeast States C oordinated Air Use Management NMMAPS National Morbidity, Mo rtality, and Air Pollution Studyv NO 2 Nitrogen Dioxide

NPS National Park Service

NRC National Research Council

NRDC Natural Resources Defense Council

NTAA National Tribal Air Association

O 3 Ozone OAP Office of Atmospheric Programs

OR Odds ratio OTC Ozone Transport Commission PAMS Photochemical Assessment Monitoring Stations PEFR Peak Expiratory Flow Rate ppm Parts per million ppb Parts per billion

PM Particulate matter

PM 2.5 Particles generally less than or equal to 2.5 μm in diameter

PM 10 Particles generally less than or equal to 10 micrometers (μm) in diameter PRB Policy relevant background QA Quality assurance RIA Regulatory Impact Analysis

RR Relative risk SAB Science Advisory Board

SO 2 Sulfur Dioxide TSD Technical support document UARG Utility Air Regulatory Group USDA U.S. Department of Agriculture US PIRG U.S. Public Interest Research Group WHO World Health Organizationvi 

### Frequently Cited Documents

The following documents are frequently cited throughout EPA = s response to comments, often by

means of the short names listed below:

Criteria Document: Environmenta l Protection Agency (2006) Air Quality Criteria for Ozone

and Related Photochemical Oxid ants (Final). Washington, DC,

EPA/600/R-05/004aB-cB. Available online at: http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=149923

.

Preamble to the final rule:

Preamble to the Final Rule on the Review of the National Ambient Air Quality Standards for Ozone; to be published in the Federal Register in

March 2008.

Proposal notice: National Ambient Air Quality Standards for Ozone: Proposed Rule. 72 FR 37818, July 11, 2007.

Staff Paper: Environmental Protection Agen cy (2007a) Review of the national ambient air quality standards for ozone: assess ment of scientific and technical information. OAQPS staff paper. (Final) July 2007. Research Triangle Park, NC: Office of Air Quality Planning and Standards; EPA report no.

EPA-452/R-07-003. Available online at: http://epa.gov/ttn/naaqs/standards/ozone/s_o3_cr_sp.html

.

Health Risk TSD: Abt Associates Inc. (20 07a) Ozone Health Risk Assessment for Selected Urban Areas. Prepared for Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, NC. July 2007. Available electronically on the internet at: http://www.epa.gov/ttn/naaqs/st andards/ozone/s_o3_cr_td.html

.

Human Exposure TSD: Environmental Protection Agency (2007b) Ozone Population Exposure Analysis for Selected Urban Areas. Office of Air Quality Planning and Standards, Research Triangle Park, NC. (Final) July 2007. Available

online at: http://www.epa.gov/ttn/naaqs/sta ndards/ozone/s_o 3_cr_td.html

.

Vegetation Risk TSD: Abt Associates Inc. (2 007b) Technical Report on Ozone Exposure, Risk, and Impacts Assessments for Vegetation: Final Report. Prepared for Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, NC. January 2007. Available

online at: http://www.epa.gov/ttn/naaqs/st andards/ozone/s _o3_cr_td.html

.1 

## Responses to Significant Comments on the 2007 Proposed Rule on the National Ambient Air Qu ality Standards for Ozone

I. INTRODUCTION

This document, together with the preamble to the final rule on the review of the national ambient air quality standards (NAAQS) for ozone (O 3 ), presents the responses of the Environmental Protection Agency (EPA) to some of the thousands of public comments received

on the 2007 O 3 NAAQS proposal notice (72 FR 37818). All significant issues raised in the public comments have been addressed.

Due to the large number of comments that a ddressed similar issues, as well as the sheer volume of the comments received, this res ponse-to-comments document does not generally cross-reference each response to the commenter(s ) who raised the partic ular issue involved, although commenters are identified in some cases where they provided particularly detailed comments that were used to frame the overall response on an issue.

The responses presented in this document are intended to augment the responses to comments that appear in the prea mble to the final rule or to address comments not discussed in the preamble to the final rule. Although porti ons of the preamble to the final rule are paraphrased in this document wh ere useful to add clarity to responses, the preamble itself

remains the definitive statement of the rationale fo r the revisions to the standards adopted in the

final rule.

In many instances, particular responses pr esented in this document include cross references to responses on related issues that are located either in the preamble to the O 3 NAAQS final rule, or in this Response to Comments docum ent. All issues on which the Administrator is taking final action in the O 3 NAAQS final rule are addressed in the O 3 NAAQS rulemaking

record. Issues on which the Administrator is ta king final action in the monitoring final rule are addressed in that rulemaking record.

Accordingly, this Response to Comments document, together with the preamble to the O 3 NAAQS final rule and the information contained in the Criteria Document (EPA, 2006) and the Staff Paper (EPA, 2007), should be considered co llectively as EPA’s response to all of the significant comments submitted on EPA’s 2007 O 3 NAAQS proposed rule. This document incorporates directly or by refe rence the significant public commen ts addressed in the preamble

to the O 3 NAAQS final rule as well as other significant pub lic comments that were submitted on the proposed rule.

Various commenters have referr ed to and discussed a number of “new” scientific studies

on the health and welfare effects of O 3 that had been published recently and therefore were not2 included in the Criteria Document. 1 EPA has provisionally cons idered 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 3 NAAQS. EPA provisionally considered these studies to place their results in the context of the findings of the Criteria Document. EPA’s provisional consideration of “new” studies is included as an Appendix to this document and is referred to throughout this document with regard to specific comments related to “new” studies. EPA concludes that, taken in context, the “n ew” information and findings do not materially change any of the broad scie ntific conclusions regardi ng the health effects of O 3 exposure made

in the Criteria Document.

Consistent with the final decisions presen ted in the notice of final rulemaking, comments on the primary O 3 standard are addressed in secti on II.A. Comments on the secondary O 3 standard are addressed below in section II.B. Comments on data handling procedures are addressed in II.C. Comments on monitoring related issues are addressed in section II.D. Section III includes responses to legal, administrati ve, procedural, or misplaced comments.

II. RESPONSES TO SIGNIFICANT COMMENTS ON PROPOSED O 3 STANDARDS

A. Primary O 3 Standards

1. General Comments on Proposed Primary O 3 standard

General comments based on relevant factors th at either support or oppose any change to

the current O 3 primary standard are addressed in this section. The respon ses to these comments are also discussed in section II.B.2 of the preamb le to the final rule. Specific comments on the proposed primary standard, including comments on the indicator, averaging time, form and level are addressed in sections II.C in the preamble to the final rule and discussed more fully below in section II.A.2. Specific comments about the health effects evidence and th e results of the human exposure and health risk assessments are addressed in sections II.B.2 in the preamble to the final rule and discussed in sections II.A.3 through II.A. 5 below. Incorporating responses contained in sections II.B of the preamble to the final rule , EPA provides the following responses to general

comments related to the need to revise the O 3 standard.

a. Support for Revising the Current Standard

1 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 incl uded in the 2004 Criteria Document as “new” studies is intended to clearly differentiate such studies from those that have been pub lished 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.3 Many public comments received on the proposal asserted that, based on the available scientific information, the current O 3 standard is insufficient to pr otect public health with an adequate margin of safety and revisions to th e standard are appropriate. Among those calling for

revisions to the current standards are medical groups, including the American Thoracic Society (and other health organizations, including Amer ican Medical Association (AMA), American College of Chest Physicians (ACCP), American College of Preventive Medicine, American Association of Cardiovascular and Pulmonary Re habilitation, American College of Occupational and Environmental Medicine, National Associat ion for the Medical Direction of Respiratory Care) (ATS et al.), and the American Academy of Pediatrics (AAP), as well as medical doctors and academic researchers. Similar conclusions were also submitted in comments from many national, state, and loca l public health organizations, includ ing, for example, the American Lung Association (and other environmen tal organizations, including E nvironmental Defense, Sierra Club, Earthjustice) (ALA et al.), the American Heart Association (and other health organizations, including, National Association of County and City Health O fficials (NACCHO), American Lung Association, American Nurses Association (ANA), American Public Health Association (APHA), Physicians for Social Responsibility ) (AHA et al.), and the American Nurses Association (ANA), as well as in letters to the Administrator from EPA’s Children’s Health Protection Advisory Committee (CHPAC) (Mart y, 2007a, 2007b). Environmental groups also commented in support of revising the standa rd, including the Sierra Club, Environmental Defense, the Natural Resources Defense Counc il (NRDC), Earthjustice, and the US Public Interest Research Group (US PIRG). All of these medical, public health and environmental

commenters stated that the current O 3 standard needs to be revi sed and that an even more protective standard than proposed by EPA is need ed to protect the health of sensitive population groups. Many individual commenters also expressed such views.

The majority of State and local air pollu tion control authorities who commented on the

O 3 standard supported revi sion of the current O 3 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; Pennsylva nia; Utah; Wisconsin; and Washington, DC. State organizations, including the National A ssociation of Clean Air Agencies (NACAA),

Northeast States for Coordinated Air Use Mana gement (NESCAUM), and the Ozone Transport Commission (OTC) urged th at EPA revise the O 3 standard. All of th ese commenters supported

revisions to the current standa rd, with most supporting a standa rd consistent with CASAC’s

recommendations.

Comment: Many public comments received on the pr oposal asserted that the current O 3 standard is insufficient to prot ect public health, especially th e health of sensitive groups, with an adequate margin of safety and revi sions to the standard are appropriate. For example, the ATS stated:

We believe that the Administrator has co rrectly stated that, beyond any degree of scientific uncertainty, convi ncing 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, ca rdiac and perinatal effects of ozone4 pollution are each in their own right major public health issues. In combination they provide immediate, actionable info rmation and require a meaningful public health policy response from the EPA. (ATS et al., pp. 1, 11)

All of these commenters supported revisions to the current standard, with most supporting a standard consiste nt with CASAC’s recommendations. In general, the commenters noted above primarily based their views on the body of evidence assessed in

the Criteria Document as articu lated in sections II.A and II. C of the preamble to proposal, finding it to be stronger and more compelling th an in the last review. Some specifically agreed with the weight of evidence appro ach 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 r ecommendation to revise the O 3 standard to provide increased public health protection.

These commenters also noted that in recent years, a broad scientific consensus has emerged that EPA's current air quality standa rds for ozone are not sufficient to protect public health, and that the leve ls and form must be greatly tightened. This consensus is evidenced 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 ma ny others. In the face of this strong scientific consensus, one commenter stated that 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 e xpressed the view that EPA must not use uncertainty in the scientific evidence as justification for retaining the current O 3 standard. For example, the ATS stated:

We note with concern that throughout the standard sett ing process, senior EPA officials have take a very conservative approach to reviewing the scientific

literature on the health effects of ozone. We find the science on the health effects of ozone to be robust and compelling. (ATS et al., p. 11)

Response: EPA generally agrees with these co mmenters’ conclusion regarding the need

to revise the O 3 primary standard. The scientific evidence noted by these commenters was generally the same as that assessed in th e Criteria Document a nd the Staff Paper, and EPA agrees that this evidence provides a basis for concluding that the current O 3 standard is not sufficient to protect public health with an adequate margin of safety. However, for reasons discussed in section II.B of the preambl e to the final rule and in sections II.A.2 and II.A.3 below, EPA disagrees with aspects of these commenters’ views on the level of protection that is appropriate and supported by the available scientific information. The

Administrator’s overall conc lusions about the need for revisions to the primary O 3 standard, which include consideration of th ese general comments, are presented in the response to comment (1) in section II.A.1.b below.5 b. Support for Retaining the Current Standard

Another group of commenter s representing industry associ ations and businesses opposed revising the current primary O 3 standard. These views were ex tensively presented in comments from the Utility Air Regulatory Group (UARG), representing a group of electric generating companies and organizations and several nationa l trade associations, and in comments from other industry and business associ ations including, for example: Exxon Mobil Corporation; the Alliance of Automobile Manufacturers (AAM); the National Association of Manufacturers (NAM), and the American Petroleum Institute (API). The API sponsored a workshop at the University of Rochester in June 2007 to review the scientific inform ation and health risk assessment considered by EPA during the review of the O 3 NAAQS. Although the report (hereafter, “Rochester Report”) from this wo rkshop does not offer j udgments 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 standa rd. The Annapolis Center for Science-Based Public Policy issued a report (h ereafter, “Annapolis Center”) on th e science and health effects of

O 3 , which explicitly opposed revising the current O 3 primary standard. Several State environmental agencies also opposed revising the current O 3 primary standard, including agencies from: Georgia; I ndiana; Kentucky; Louisiana; Nevada; and Texas.

As discussed more fully below in sections dealing with specific comments, these and other commenters in this group generally mentione d many of the same studies that were cited by the commenters noted above who supported revising the standard, as well as other studies, but highlighted different aspects of these studies in reaching substan tially different conclusions about their strength and the extent to which progress has been made in reducing uncertainties in the

evidence since the last review.

Comment: These commenters generally expresse d the view that the current standard provides the requisite degree of public health protection. In so doing, they considered

whether the evidence that has become availabl e since the last review has established a

more certain risk or a risk of effects that ar e significantly different in character to those that provided a basis for the current standar d, or whether the evidence demonstrates that the risk to public health upon attainment of the current stan dard would be greater than

was understood when EPA established the current standard in 1997.

In supporting their view th at the present primary O 3 standard continues to provide the requisite public health prot ection and should not be revise d, UARG and others generally

stated that:

• the effects of concern have not changed significantly since 1997

• the uncertainties in the underlying health sc ience are as great or greater than in

1997

• the estimated risk upon atta inment of the current O 3 standard has decreased since

1997

• “new” studies not included in the Crit eria Document continue to increase uncertainty about possible health ri sks associated with exposure to O 3.6 Response: As noted in the response to comm ent (1) in section II.A.1.a above, EPA, believes, contrary to the view fo the comment ers, that the available information provides a basis for concluding that the current O3 standard does not pr otect public health with an adequate margin of safety. EPA has responde d to the specific points noted above as well as additional specific issues raised by thos e contending that the current 8-hour primary

standard should not be revised in sect ions II.A.3 through II.A.5 below and in the Appendix to this document.

More generally, the ra tionale for EPA’s position regardi ng the need for revision of the current primary O 3 standard is necessarily based upon consideration of all the comments, including the specific comments that are presented in secti ons II.A.3 through II.A.5. The

Administrator’s overall conc lusions about the need for revisions to the primary O 3 standard, which include consideration of th ese general comments, are presented below.

Having carefully considered all of the public comment s related to the need for revision of

the current O 3 primary standard, the Administrator believes the fundamental scientific

conclusions on the effects of O 3 reached in the Criteria Document and Staff Paper, briefly

summarized below in section II.A.2 and disc ussed more fully in section II.A of the proposal, remain valid. In considering whether the primary O 3 standard should be revised, the Administrator places primar y consideration on the body of scientific

evidence available in this review on th e health effects associated with O 3 exposure, as summarized in section II.B.1 of the preamble to the final rule,. The Administrator notes

that there is much new evidence that has become available since the last review, including an especially larg e number of new epidemiological studies. The Administrator believes that this body of scien tific evidence is very robust, recognizing that it includes large numbers of various types of studies, including toxicological studies, controlled human exposure studies, field panel studies, and community epidemiological studies, that provide consistent and coherent evidence of an array of O 3 -related respiratory morbidity effects and possibly cardiovasc ular-related morbidity as well as total nonaccidental and cardiorespiratory mortality. The Administrato r observes that (1) the evidence of a range of respiratory-related morbidity effects seen in the last review has been considerably strengthened, both through toxi cological and controlled hum an exposure studies as well as through many new panel and epidemiological studies; (2) newly available evidence from controlled human exposure and epidem iological studies identifies people with asthma as an important susceptible populati on for which estimates of respiratory effects in the general population likely underestimate the magnitude or importance of these effects; (3) newly available evidence about mechanisms of toxicity more completely explains the biological plausibility of O 3 -induced respiratory eff ects and is beginning to suggest mechanisms that may link O 3 exposure to cardiovascular effects; and (4) there is now relatively strong evidence for associations between O 3 and total nonaccidental and cardiopulmonary mortality, even after adjustme nt for the influence of season and PM. The Administrator believes that this very robust body of evidence, taken together, enhances our understanding of O 3 -related effects relative to what was known at the time of the last review. Further, he believes th at the available evidence provides increased confidence that respiratory morbidity eff ects such as lung function decrements and respiratory symptoms are causally related to O 3 exposures, that indi cators of respiratory7 morbidity such as emergency department visits and hospital admissions are causally

related to O 3 exposures, and that the eviden ce is highly suggestive that O 3 exposures during the warm O 3 season contribute to premature mortality.

Further, the Administrator judge s that there is important new evidence demonstrating that exposures to O 3 at levels below the level of the cu rrent standard are associated with a broad array of adverse health e ffects. This is especially tr ue in at-risk populations that include people with asthma or other lung di seases, who are likely to experience more serious effects from exposure to O 3 , 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 activ ity, especially activ e children and outdoor

workers. The Administrator notes that th is important new evidence demonstrates O 3 - induced lung function effects and respirator y 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 th e level of the current standard. In addition, the Administrator notes that (1) there is now epidemiological evid ence of statistically significant O 3 -related associations with lung functi on and respiratory symptom effects, respiratory-related emergency department vi sits and hospital admissions, and increased mortality, in areas that likely would have met the current standard; (2) there are also many epidemiological studies done in areas th at likely would not have met the current

standard but which nonetheless re port statistical ly significant associa tions that generally

extend down to ambient O 3 concentrations that are below the level of the current standard; (3) there are a few studies that have examined subsets of data that include only days with ambient O 3 concentrations below the level of the current standard, or below

even much lower O 3 concentrations, and continue to report statistically significant associations with respiratory morbidity out comes and mortality; and (4) the evidence from controlled human exposure studies, toge ther with animal toxicological studies, provides considerable support for the biological plausibility of the respiratory morbidity associations observed in the epidemiologi cal studies and for concluding that the

associations extend below the level of the current standard.

Based on the available evidence, the Administ rator agrees with the CASAC Panel and the majority of public commenters that the current standard is not requis ite to protect public health with an adequate margin of safety because it is does not provide sufficient protection and that revi sion of the current O 3 standard is needed to provide increased public health protection. The Administrator not es that extensive critical review of this body of evidence and related uncertainties during the criteria a nd standard review process, including review by the CASAC Pane l and the public of the basis for EPA’s proposed decision to revise the primary O 3 standard, has identifie d a number of issues about which different reviewers disagree and fo r which additional research is warranted. Nonetheless, on balance, the Administrator be lieves that the remaining uncertainties in

the available evidence do not diminish confid ence in the causal relationships between O 3 exposures and indicators of se rious respiratory morbidity eff ects, or the hi ghly suggestive

evidence of associations between O 3 exposures and premature mortality, nor do they

diminish confidence in the conclusion that th e associations extend below the level of the

current standard.8 Beyond a primary consideration of the availa ble evidence, the Administrator has also taken into consideration the Agency’s exposur e and risk assessments to help inform his evaluation of the adequacy of the current st andard. As at the time of proposal, the

Administrator believes the results of t hose assessments inform his judgment on the adequacy of the current standard to protect against health effects of concern. In considering the exposure analysis results at this time, the Administ rator recognizes that

there is a risk of confusion in the term “exposure of concern” that was used at the time of proposal, as it could be read to imply a dete rmination that a certain benchmark level of exposure has been shown to be causally associ ated with adverse health effects. As a consequence, the Administrator believes that it is more appropriate to consider such exposure estimates in the context of a conti nuum rather than focusing on any one discrete benchmark level, as was done at the time of proposal, since the Administrator does not believe that the underlying scie ntific evidence is certain e nough to support a focus on any bright-line benchmark level. In so doing, th e Administrator recognize s that associations

between O 3 exposures and health effects of conc ern become increasingly uncertain at

lower O 3 exposure levels. Thus, the Administra tor has taken into consideration the pattern of such exposure estimates across the range of discrete benchmark levels considered in EPA’s exposure assessment to provide some indication of the potential magnitude of the incidence of health outco mes that could not be evaluated in the Agency’s quantitative risk assessment but wh ich have been demonstrated to occur in healthy people at O 3 exposures as low as 0.080 ppm, th e lowest level at which such

health outcomes have been tested. 2

More specifically, the Administrator has cons idered the pattern of reductions in such exposures across the benchmark levels of 0.080, 0.070, and 0.060 ppm, which span the level at which there is strong evidence of effects in healthy people down to a level at which the Administrator judges the evidence of effects to be very limited. The

Administrator observes that based on the aggregated exposure estimates for the 2002

simulation for the 12 urban areas included in the exposure analysis, upon just meeting the current standard, the percentages of asthma tic or all school age children likely to experience one of more exposures at a nd above these benchmark levels of 0.080, 0.070, and 0.060 ppm (while at moderate or greater exertion) are approxi mately 4%, 20%, and 45%, respectively. As noted at the time of proposal, the Administ rator recognizes that there is substantial year-to-year and city-to-city variability in these estimates and that it is important to recognize this variability in c onsidering these estimates. For example, for the 0.080, 0.070, and 0.060 ppm benchmark levels, these percentages are estimated to range from approximately 1 to 10%, 1 to 40%, and 7 to 65%, respectiv ely, across each of

2 As noted above, such health outcomes include increased airw ay responsiveness, increased pulmonary inflammation, increased cel lular permeability, and decreased pulmonary defense mechanisms, which have been associat ed with aggravation of asthma, increased medication use, increased school and work absen ces, increased susceptibility to respiratory infection, increased visits to doctors’ offices and emergency de partments, increased admissions to hospitals, and possibly to cardi ovascular system effects and ch ronic effects such as chronic bronchitis or long-term damage to the lungs that can lead to reduced quality of life.9 the 12 urban areas based on the 2002 simulation, and from approximately 0 to 1%, 0 to 7%, and 1 to 25%, respectively, based on the 2004 simulation.

With regard to the results of the risk asse ssment, the Administrato r again considered the risks estimated to remain upon just meeting the current standard. The Administrator

takes note of the estimated magnitudes of such risks, which are presented in section II.B.1.c of the preamble to the final rule for a range of health effects including moderate and large lung function decrem ents (including percentages of children and number of occurrences), respiratory symptom days, re spiratory-related hospital admissions, and nonaccidental and cardiorespiratory mortality, as well as year-to-ye ar and city-to-city variability, and the uncertainties in these estima tes. Further, the Ad ministrator recognizes that these estimated risks for the specific he alth effects that coul d be analyzed in the Agency’s risk assessment are indica tive of a much broader array of O 3 -related health endpoints that are part of a “pyramid of effects” that include various indicators of morbidity that could not be included in the risk as sessment (e.g., school absences, increased medication use, emergency depart ment visits) and which primarily affect members of at-risk groups.

In considering these quantitative exposure and risk estimates, as well as the broader array

of O 3 -related health endpoints th at could not be quantified, the Administrator believes that they are important from a public hea lth perspective and indicative of potential exposures and risks to at-risk groups. The Ad ministrator thus finds that the exposure and risk estimates provide additional support to the evidence-based conclusion, reached above, that the current standard needs to be revised. Based on these considerations, and

consistent with CASAC Panel’s unanimous conclusion that ther e is no scientific justification for retaining th e current standard, the Admini strator concludes that the current primary O 3 standard is not sufficient and thus not requisite to protect public health with an adequate margin of safety, and that revision is needed to provide increased public health protection. It is impor tant to note that this conclu sion, and the reasoning on which it is based, do not address the question of wh at specific revisions are appropriate. That requires looking specifically at the current i ndicator, averaging time, form, and level of

the O 3 standard, and evaluating the evidence releva nt to determining whether and to what extent any of these elements should be revi sed. Comments on the proposed elements of the primary standard are addr essed below in section II.A.2.

2. Specific Comments on Proposed Primary O 3 Standards

a. Averaging Time

The EPA received limited public comments on the issue of averaging time for the O 3 primary standard. In addition to the discussion co ntained in section II.C.2 of the preamble to the final rule, EPA provides the following response to a specific issue relate d to the averaging time

for O 3

.

Comment: A few comments specifically support ed keeping only the 8-hour averaging time. However, there were other comment s in support of setting a separate 1-hour10 standard along with am 8-hour standard to better protect agai nst peak exposures (California EPA, ALA et al.).

Response: EPA has conducted extensive air quality analyses to determine the extent to which meeting the 8-hour standard provide s protection from 1-hour and longer-term

ambient air concentrations of O 3 . It was concluded from these analyses that adequate protection from both 1-hour and longer-term ambient O 3 concentrations would be provided in areas meeting th e 8-hour primary standard.

b. Form of the Standard

The EPA received a limited number of public comments on the appropriate form for the

O 3 standard. Incorporating responses contained in sections II.C.3 of the preamble to the final rule, EPA provides the following responses to sp ecific comments related to the form of the 8-

hour O 3 standard.

(1) Comment: Some public commenters that expresse d the view that the current primary O 3 standard is not adequate also submitted comments that supported a more healthprotective form of the standa rd than the current form (e .g., a second- or third-highest daily maximum form)(e.g., ALA et al.). Most commenters who expressed the view that

the current standard should not be revised did not provide any view s on alternative forms that would be appropriate for consideration should the Administrator consider revisions to the standard. A few industry associat ion and business commenters supported changing

to a 5 th highest form (e.g., Dow Chemical, AAM). One commenter (Oklahoma Department of Transportation) suggested the use of a 6 th or 7 th highest daily maximum

form.

Response: There is not a clear health-based th reshold for selecti ng a particular nthhighest daily maximum form of the standard from among the ones analyzed in the Staff Paper, recognizing that the 4 th -highest daily maximum, 8-hour average concentration form of the standard provides a stable ta rget for implementing programs to improve air quality. The principal advantage of the concentra tion-based form is that it is more directly

related to the ambient O 3 concentrations that are associated with the health effects. With a concentration-based form, days on which higher O 3 concentrations occur would weigh proportionally more than days with lower con centrations, since the ac tual concentrations are used in determining whether the standard is attained. That is, given that there is a

continuum of effects associated with exposures to varying levels of O 3 , the extent to which public health is affected by exposure to ambient O 3 is related to the actual magnitude of the O 3 concentration, not just whether the concentration is above a specified level. EPA also believes that the adequacy of the public health protection provided by

the combination of the level and form is a foremost consideration. Based on this, EPA detemined that the form of the current standard, 4 th -highest daily maximum 8-hour average concentration, averaged over 3 years, should be reta ined, recognizing that the public health protection that w ould be provided by this standard is based on combining11 this form with the increased health protecti on provided by the lower level of the standard

discussed in the section below.

(2) Comment: While the CASAC Panel unanimously supported specifying the level of the standard to a three decimal places (i.e., ppb) degree of precision, public comments were mixed. Environmental organizations (e.g., ALA et al.) and some St ate/regional agencies (e.g., NESCAUM, PA Department of Environm ental Protection) supported the proposed increased precision but did not support truncatin g to the third decimal. However, several industry associations (e.g., API, EMA, AAM ) suggested that ther e is not sufficient evidence to modify the 1997 decision to round to two decimal places.

Response: EPA concludes that the level of th e standard should be specified to the thousandth ppm (three decimal places), based on the staff’s analysis and conclusions discussed in the Staff Paper that current monitoring technology allows accurate

measurement of O 3 to support specifying the 8-hour sta ndard to this degree of precision, and on the CASAC Panel’s reasoning and recomme ndation with respect to this aspect of

the standard. A discussion of the issue of truncating vs. rounding can be found in section II.C.1 of this Response to Comments document.

c. Level

A large number of comments on the propos ed range of levels for the primary O 3 standard basically expressed one of two substantively di fferent views: (1) support for a more health protective standard at or belo w the range of levels proposed by EPA or (2) opposition to any

modification of the current O 3 standard. Many of these comme nters simply expressed their views without stating any rationale , while others gave general reas ons for their views but without

reference to the factual evidence or rationale presented in the pr oposal notice as a basis for the Agency’s proposed decision regard ing the level of the primary O 3 standard.

With regard to the evaluation and considera tion of the health effects evidence and how

such information should be considered in the de cision on the standard leve l, EPA notes that the commenters fell into the same two groups discussed in section II.B.2 of the preamble to the final rule. The two groups often cited the same st udies and evidence, but they reached sharply divergent conclusions as to what standard level is supported by th e health effects evidence. The general views of both groups on the interpretation and use of the health effects evidence are presented in section II.B.2.a of the preamble, with most comments from one group arguing that this evidence supports a decision to revise the 8-hour standard to 0.060 ppm or below, and the other group arguing that it supports a decision not to revise the current 8-hour standard.

A number of commenters, in cluding many States and Trib es, who supported selecting a standard in the range 0.060 to 0.070 ppm generall y placed great weight on the recommendation of CASAC. Section II.C.4 of the preamble to th e final rule presents the Agency’s response to these very general views. In addition to the discussion contained in th at section, EPA provides the following responses to specific issues related to the level for the primary O 3 standard. The

first section below addresses comments on health evidence considerations, and the next section12 addresses comments on exposure and ri sk considerations related to consideration of the level for the primary standard. Additional specific comments on the exposure analysis and health risk

assessment are included in sec tions II.A.4 and II.A.5 below.

i. Comments on Health Evidence Considerations

(1) Comment: With regard to the evidence from controlled human exposure studies, commenters that included public health and environmental groups who supported revising the current standard expressed the vi ew that the large body of evidence available at the time of the last review, demonstrati ng an array of adverse health effects (i.e., reduced lung function, respiratory sympto ms, increased airway responsiveness, inflammation, and increased susceptibility to re spiratory infection), at concentrations of 0.080 ppm O 3 , indicated that the standa rd should have been set at a lower level. These

commenters noted that standards must be set below the level shown to cause effects in healthy subjects in order to pr otect sensitive populations with an adequate margin of safety. As discussed in section II.B.2.a a bove, these commenters focused on the results of the Adams studies (2002, 2006) as evidence that exposure to 0.060 ppm O 3 will result in a significant proportion (i.e ., 7%) of the adult population who do not have asthma or other lung diseases experiencing no table lung function decrements (FEV 1 decrement ≥ 10%), and furthermore that larger decrements in FEV 1 would be expected in more susceptible populations. This evidence cau sed these commenters to reject EPA’s proposed range:

Clearly, EPA’s proposed standard of 0.070 to 0.075 ppm cannot be considered protective of public health in light of experimental evidence demonstrating adverse respiratory effects in healthy i ndividuals exposed to 0.060 ppm, and the legal requirements to protect sensitive populations with an adequate margin of safety. (ALA et al., p. 51)

The second group of commenters, who opposed revision of the standard, expressed the view that the group mean changes reporte d in the Adams studies (2002, 2006) were small, that such decrements should not be considered to be adverse, and that the individuals who experienced la rger responses were too few to serve as a basis for a

revised O 3 standard. This group incl uded virtually all commente rs representing industry associations and businesses. These genera l comments are also addressed in section II.B.2.a in the preamble to the final rule.

Response: In considering comments received on controlled human exposure studies, and how these studies support a focus on particul ar standard levels, the Administrator observes that in general the comments support hi s original view that these studies provide

the most certain evidence of adverse health effects, and that the large bulk of evidence derives from studies of exposures at leve ls of 0.080 ppm and above. The Administrator notes that since the last review important new evidence includes demonstration of O 3 - induced lung function effects and respiratory symptoms in some healthy adults down to the previously observed exposure level of 0.080 ppm, as well as very limited new evidence of the same effects at exposure le vels well below the le vel of the current13 standard (Adams, 2002, 2006). Based on careful consideration of the comments, the Administrator again concludes that while th e Adams studies provide evidence that some healthy individuals will expe rience lung function decrements and respiratory symptoms at the 0.060 ppm exposure level, this evidence is too limited to support a primary focus at this level. Moreover, the Administrator notes that while the CASAC panel supported a level of 0.060 ppm, they also supported a le vel above 0.060, indicating that they disagree

with the commenters view that the results of Adams studies mean that the level of the standard has to be set at 0.060 ppm.

(2) Comment: With regard to the information fr om epidemiological studies, commenters representing public health, e nvironmental, and medical orga nizations generally asserted that the large body of new epidemiological studies provides evidence of causal

associations between O 3 exposures and a wide array of respiratory and cardiovascular morbidity effects, including emergency depart ment visits and hospital admissions. They expressed the view that a si gnificant body of strong, consistent evidence links short-term exposures to premature mortality and noted that this evidence is supported by new research that provides biological plausibility for such effects. These commenters noted that various approaches, includ ing air quality assessments which show that statistically significant associations occurred in areas that likely would ha ve met the current standard, or statistical approaches that examined subsets of the data which indica te that statistically significant associations remain down to very low ambient O 3 levels, show effects well

below the level of the current standard. Mo reover they identified particular studies, including some “new” studies not considered in the Criteria Document, that indicated there are additional sub-populations that are likely to be sensitive to O 3 , including infants, women, and African-Americans, that should be considered in deciding the requisite level of protection. They asserted that this info rmation supports a standard set at a level no higher than 0.060 ppm O 3

.

With regard to the information from epidemiological studies, the second group of commenters focused strongly on EPA’s interpre tation of the epidemiological evidence and the uncertainties they saw in this eviden ce as a basis for concl uding that no change to

the current level of the 8-hour O 3 standard is warranted. In commenting on the proposed range of levels, these commenters generally relied on the same arguments presented above in section II.A.1.b as to why they beli eved it would be inappropriate for EPA to make any revisions to the primary O 3 standard. That is, they asserted that the health

effects of concern associ ated with short-term or prolonged exposures to O 3 have not changed significantly since 1997; that the in consistencies and uncer tainties inherent in these studies as a whole should preclude any reliance on them as just ification for a more stringent standard; and that “new” scien ce not included in the Criteria Document continues to increase uncertainty about possibl e health risks associat ed with exposure to

O 3 . Specific methodological i ssues cited as additional support for their conclusions included: adequacy of exposure data; potential confounding by c opollutants; model selection; inconsistent evidence relating O 3 exposure to mortality, and “new” studies that provide additional evidence of inconsistenc ies. These general comments are also

addressed in section II.B.2.a of the preamble to the final rule.14 Response: In considering these comments on the epidemiological evidence with regard to the interpretation of the epidemiological eviden ce and methodological issues, the Administrator notes that in ge neral, most of the issues a nd concerns raised by those who do not support any revisions to the primary O 3 standard with regard to the interpretation of the epidemiological evidence and methodological issues, are essentia lly restatements if issues raised during the review of the Criteria Document and Staff Paper. The same is true of the views of commenters who supporte d a level of the sta ndard no higher than 0.060 ppm O 3 . EPA presented and the CASAC Panel reviewed the interpretation of the epidemiological evidence in the Criteria Do cument 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 Ad ministrator. CASAC reviewed the scientific content of both the Criteria Document and Staff Paper and advised the Administrator that these documents provided an appropriate basis for use in regulatory decision making. Therefore, these comments do not provide a basis for the Administrator to reach fundamentally different conclusions than he reached at the time of proposal.

Moreover, the Administrator notes that epid emiological evidence is most appropriately

evaluated in the context of all available evidence, includ ing evidence from controlled human exposure and toxicological studies. The Administrator agrees with the weight of evidence approach used in the Criteria Document and believes that this body of scientific evidence is very robust, recognizing that it in cludes a large number of various types of studies that provide cons istent and coherent evid ence of an array of O 3 -related respiratory morbidity effects and possibly cardiovascul ar-related morbidity as well as total nonaccidental and cardiorespiratory mortality. Therefore, the Administrator judges that the body of epidemiological evidence indicating associations with a wide range of serious health effects, including respiratory emerge ncy department visits and hospital admissions and premature mortality, at and below 0.080 ppm supports revising the current standard to protect public health. Wh ile the great majority of ev idence concerning effects below 0.080 ppm was from epidemiological studies, the epidemiological studies do not identify any bright-line threshold level for effects. At the same time, the epidemiological studies

are not themselves direct evidence of a causal link betw een exposure to O 3 and the occurrence of the effects. Therefore, Admini strator has considered these studies in the

context of all the other available evidence in evaluating the degree of certainty that O 3 - related adverse health effects would occur at various ambient levels below 0.080 ppm. In that context, there is only quite limited evid ence from controlled human exposure studies at exposure levels below 0.080 ppm O 3 . The Administrator recogni zes that in the body of epidemiological evidence, many studies repo rted positive and statistically significant associations, while others reported positive results that were not statistically significant, and a few did not report any positive O 3 -related associations. In addition, the Administrator judged that ev idence of a causal relationshi p between adverse health

outcomes and O 3 exposures became increasingly uncerta in at lower levels of exposure.

Based on this the Administrator continues to believe that the b ody of epidemiological evidence does not support setting a standa rd as low as 0.060 as suggested by some

commenters.15 The Administrator also notes the many epidem iological studies done in areas that likely

would not have met the current standard but which nonetheless report statistically significant associations that gene rally extend down to ambient O 3 concentrations that

were below the level of the current standard. Further, there were a few studies that have

examined subsets of data that include only days with ambient O 3 concentrations below the level of the current standard, or below even much lower O 3 concentrations, and continued to report statistically significant associations with respiratory morbidity outcomes and mortality. In the context of the strong clinical evidence of adverse effect in healthy adults at 0.080, the Admi nistrator finds that the body of epidemiological evidence does not support retainin g a standard of 0.08, as suggested by commenters.

(3) Comment: Both groups of commenters also cons idered evidence from controlled human exposure and epidemiological studies of incr eased susceptibility in people with lung disease, especially people with asthma, but they reached sharply divergent conclusions about what standard level is supported by this evidence. As discussed above in section II.B.2.a, medical organizations and public heal th and environmental groups agreed with EPA that, based on evidence from controll ed human exposure and epidemiological studies, people with asthma, especially childr en, are likely to have greater lung function decrements and respiratory symptoms in response to O 3 exposure than people who do not have asthma, and are likely to respond at lower levels. Furthermore, these commenters noted that epidemiological studies have identified other potentially sensitive subpopulations, including for example, infant s, women and African-A mericans, and that effects in these groups should be part of the consideration in providing an adequate margin of safety. These commenters conclude d that the appropriate level for the primary

O 3 standard is 0.060 ppm, to provide pr otection for members of sensitive groups, especially people with asthma, who are likely to have more serious responses and to respond at lower levels that hea lthy people. They also contend that a standard set at this level also would provide prot ection against anticipated, but as yet unproven effects in the additional groups cited.

Response: The Administrator agrees with these commenters that important new evidence

shows that asthmatics have more serious re sponses, and are more likely to respond at

lower O 3 levels, than healthy individuals. Mo reover, he agrees that this evidence supports a standard set at a level below 0.080 ppm O 3 , based on the strong evidence from

human clinical studies in healt hy adults at this level. Howe ver, for the reasons described in preamble to the final rule and in the re sponse to comment number (2) above, he does not agree that the controlled human exposure and epidemiological evidence provide support for a standard set at 0.060 ppm.

(4) Comment: Industry association a nd business commenters assert ed that EPA is wrong to

claim that new evidence indicates that the current standard does not provide adequate health public health protection for people with asthma. In support of this position, these commenters made the following major comments : (1) the lung func tion decrements and respiratory symptoms observed in clinical studies of asthmatics are not clinically important; (2) EPA postulates that asthmatics would likely experience more serious responses and responses at lower levels than the subjects of controlled human exposure16 experiments, but that hypothesis is not s upported by scientific evidence; and, (3) EPA recognized asthmatics as a sensitive s ubpopulation in 1997, and new information does not suggest greater susceptibility th an was previously believed.

Response: EPA has specifically responded to these comments in the response to comment (2) in section II.3.c below. After careful consideration of these comments and based on the response given below, the Admini strator continues to judge that there is important new evidence demonstr ating that exposures to O 3 at levels below the level of

the current standard are associated with a broa d 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 3 , as well as children and older adults with increased susceptibility, a nd those who are likely to be vulnerable as a result of spending a lot of time outdoors e ngaged in physical activ ity, especially active

children and outdoor workers.

ii. Comments on Exposure and Risk Considerations

(1) Comment: With regard to considering how th e quantitative exposur e and health risk

assessments should factor into a decision on the standard level, EPA notes that the comments generally fell into two groups that reached sharply divergen t conclusions as to what standard level is supported by these asse ssments. The general views of both groups on the implications of the exposure and risk assessment are presented in the preamble to the final rule (section II.B.2.b), with one group arguing that it supports a decision to revise the 8-hour standard to 0.060 ppm or below, and the other group arguing that it supports a decision not to revise the current 8-hour standard.

A joint set of comments from ALA and seve ral environmental groups expressed the view that EPA cannot use exposures of concern to justify a standard in the range of 0.070 to 0.075 ppm. These commenters contend that standards in the proposed range would continue to expose too many asth matic children, as well as ot her at risk groups such as outdoor workers and preschool children, to “d emonstrably unhealt hy levels of ozone pollution” in only 12 cities which does not re present a national estimate (ALA et al., p. 106). These same commenters asserted that if EPA were to consider exposures of concern, then the benchmark level must be defined as 0.060 ppm based on the

considerable evidence of adverse health effects occurring at this level. They also cited various reasons why the exposure estimate s were underestimated, including: only 12 cities were included in the assessment, vari ous at risk groups including outdoor workers and preschool children were not include d in the assessment, and EPA’s exposure assessment underestimated exposures since it considers average children, not active children who spend more time outdoors and repeated exposures also were

underestimated.

In contrast, industry associat ion and business group commenter s expressed the view that the concept of exposures of c oncern should not be considered as a basis for revising the level of the standard because it provided no indication of the probability that individuals would actually experience an adverse health effect. These same commenters also17 provided various reasons why the exposure estimates were overestimated based on specific methodological choices made by EPA including, for example, O 3 measurements at fixed-site monitors can be higher than other locations where i ndividuals are exposed, the exposure estimates do not account for O 3 avoidance behaviors, and the exposure model overestimates elevated breathing rates. Finally, these comme nters also contend that the estimates of exposures of concern associated with just meeting the current standard, using the 0.080 ppm benchmark levels , have not appreciably changed since the prior review and, thus provide no sup port for revising the current standard.

Response: EPA has responded below to the critic isms from both groups of commenters

related to concerns that the exposure estimates are either und erestimated or overestimated

in sections II.A.4 and II.A.5 of this document. EPA also ha s addressed the issues raised by both groups of commenters concerning the appropriateness of considering exposures

at and above various benchmark levels as an element in the decision on the level of the standard in the preamble to the final rule (s ection II.C.4) and in the response to comment (2) below.

(2) Comment: Environmental and public health gro up comments expressed the view that if exposures of concern were considered, then the Administrator should focus only on the 0.060 ppm benchmark based on the contention th at adverse health effects had been

demonstrated down to this level. These commenters generally argued that significant exposure reductions could be achieved by setting the standa rd level at 0.060 ppm or lower. In contrast, other commenters, pr imarily industry and business groups focused on comparisons of the exposures of concern at the 0.080 ppm benchmark level based on

their view that there was no convincing evidence demonstrati ng adverse health effects at

levels below this benchmark.

Response: In view of the comments received rela ted to the definition and use of the term “exposure of concern” at the time of proposal , the Administrator recognizes that that there is a risk of confusion, as it could be read to imply a determination that a certain benchmark level of exposure has been show n to be causally associated with adverse health effects. As a consequen ce, the Administrator believes th at it is more appropriate to consider such exposure estimates in the cont ext of a continuum rather than focusing on any one discrete benchmark level, as wa s done at the time of proposal, since the

Administrator does not believe that the underlying scientific evidence is certain enough to support a focus on any single bright-line benc hmark level. Thus, the Administrator believes it is appropriate to consider a range of benchmark levels from 0.080 down to 0.060 ppm, recognizing that con centrations at and above sp ecified benchmark levels

while at elevated exertion must be consid ered in the context of a continuum of the potential for health effects of concern, and their severity, with increasing uncertainty

associated with the likelihood of such effects at lower O 3 exposure levels.

EPA recognizes that the 0.080 pp m benchmark level represents a level at which several health outcomes including lung inflammati on, increased airway responsiveness, and

decreased resistance to infection have been shown to occur in health adults. The Administrator places relatively great wei ght on the public health significance of18 exposures exceeding this benchmark level give n the greater certainty that these adverse health responses are likely to be observed in a significant fraction of the at-risk population. With respect to his decision on the level of the 8-hour standard, the Administrator notes that upon just meeting a standard within th e range of 0.070 to 0.075 ppm based on the 2002 simulation, the number of school age asthmatic children likely to experience exposures at and above the 0.080 ppm benchmark level in aggregate (for the 12 cities in the assessment) is estimated to range from 0.1 to 0.4 percent of asthmatic school age children. Based on the 2004 simulatio n, the estimates are even lower, with no asthmatic children estimated to experien ce exposures at and above the 0.080 ppm benchmark level. Similar patterns are obser ved for all school age children. Recognizing the uncertainties inherent in the exposure as sessment, the Administ rator concludes that the exposure assessment suggests that exposur es at and above the 0.080 ppm level, where

several health effects have been shown to o ccur in healthy individuals, are eliminated or nearly eliminated depending on the modeling year.

However, the Administrator does not agre e with those commenters who would only consider this single benchmar k level. While the Administ rator places less weight on exposures exceeding the 0.070 pm benchmark le vel, given the increased uncertainty about the fraction of the population and severity of the health responses that might occur associated with exposures above this level, he believes that it is a ppropriate to consider exposures at this benchmark as well in judgi ng what level will protect public health with an adequate margin of safety. Consid eration of the 0.070 ppm benchmark level recognizes that the effects observed at 0.080 ppm were in healthy adult subjects and sensitive population groups, su ch as asthmatics, are expe cted to respond at lower O 3 levels than healthy individuals. The Ad ministrator notes that upon just meeting a standard within the range of 0.070 to 0.075 ppm based on the 2002 simulation, the number of asthmatic school age children like ly to experience exposures at and above the 0.070 ppm benchmark level in aggregate (for the 12 cities in the asse ssment) is estimated to range from about 2 to 5 percent of as thmatic school age children. Based on the 2004 simulation, the estimates are substantially lo wer, with 0 to 0.6 percent of asthmatic children estimated to experience exposures at and above the 0.070 ppm benchmark level.

The Administrator considered but placed very l ittle weight on exposures at and above the 0.060 ppm benchmark given the very limited sc ientific evidence supporting a conclusion

that O 3 is causally related to various hea lth outcomes at this exposure level.

Considering the uncertainties associated with the exposure assessment, the Administrator concludes that the exposure estimates associat ed with each of the benchmark levels are not appreciably different, between a 0.070 or 0.075 ppm standard, and therefore, the exposure assessment does not provide a clear enough basis for choosing a specific level within the proposed range.

(3) Comment: With regard to considering how the quantitative risk assessment should factor into a decision on the standard level, both gr oups of commenters generally considered the risk assessment in their comments on the standard level, but they reached sharply19 divergent conclusions as to wh at standard level is supported by the risk assessment. More specifically, the envir onmental, public health, most medical organizations, and some State and regional air po llution agencies (e.g., California, NESCAUM) contend that EPA’s proposed range of 0.070 to 0.075 ppm woul d result in significant residual public health risks. As articulated most fully in the joint set of comments from ALA and several environmental organizations, these commente rs expressed the view that EPA’s risk assessment clearly demonstrates that a more stringent 8-hour O 3 standard of 0.065 ppm, the most stringent standard analyzed by EPA, would significantly decrease O 3 -related lung function decrements, respiratory sympto ms, hospital admissions, and mortality and that “EPA must adopt a more stringent ozone standard of 0.060 ppm or below – a level that incorporates a more adequate margin of safety” (ALA et al., p. 108). These same

commenters also cited various reasons for asserting that the risk assessment likely

underestimates health risks to a substantial degree, includi ng the limited nature of the assessment with respect to number of cities, populations covered, and health endpoints analyzed.

Response: EPA has responded to the comments concerning the scope of the risk

assessment and assertion that health risks ar e likely underestimated both in the preamble to the final rule (section II.B.2.b) and in more detail in section II.A.5 of this document. While the Administrator places less weight on th e results of the risk assessment, he notes

that the results indicate that a standard se t within the proposed range would likely reduce risks to at-risk groups from the O 3 -related health effects cons idered in the assessment, and by inference across the much broader array of O 3 -related health effects that can only be considered qualitatively, relative to th e level of protection afforded by the current standard. Moreover, he notes that the results of the assessment suggest a gradual reduction in risks with no clear breakpoint as increasingly lower standard levels are considered. However, in light of the importa nt uncertainties inherent in the assessment discussed above and in the proposal, the Admini strator concludes that the risk assessment does not provide a basis for choosing a level within the pr oposed 0.075 to 0.070 ppm

range.

(4) Comment: Industry association and business group commenters who supported not revising the level of the current 8-hour standard generally as serted the following points: (1) that risk estimates have not changed si gnificantly since the prior review in 1997; (2) that uncertainties and limitations underlyi ng the risk assessments make them too speculative to be used in supporting a decision to revise the standard; (3) that EPA should have defined PRB differently and that EPA underestimated PRB levels which results in

health risk reductions associated with more stringent standards being overestimated; and (4) that health risks are overestimated ba sed on specific methodological choices made by EPA including, for example, select ion of inappropriate effect estimates from health effect studies, EPA’s approach to addressing the sh ape of exposure-response relationships, and whether or not to incorporate thresholds into its models for the various health effects analyzed.20 Response: EPA has responded to the comments concerning the scope of the risk

assessment and assertion that health risks ar e likely underestimated both in the preamble to the final rule (section II.B.2.b) and in more detail in section II.A.5 of this document.

3. Specific Comments on the Interpretation of Scientific Evidence

More specific comments on the EPA’s interetation of the scientific evidence and EPA's responses are discussed below. The summary of comments and responses follows the discussion of these topics in the preamble to the final ru le. The first section be low contains comments on evidence from controlled human exposure stud ies (preamble section II.B.2.a.i); the second

section below contains comments on eviden ce from epidemiological studies, including interpretation of the evidence and specific me thodological issues (pream ble section II.B.2.a.ii);

the third section below contains comments on evidence pertaining to at-risk subgroups for O 3 - related effects (preamble section II.B.2.a.iii). A fourth section contains comments on the adversity of health effects, a topic that was disc ussed generally in the preamble and also as part of some responses to comments on at-risk subgroups for O 3 -related effects and the fifth section

below contains comments on the role of ground-level O 3 in solar radiation-related health effects.

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 Pape r. Most of these issu es were highlighted and thoroughly discussed during the re view of these documents by the CASAC. Incorporating responses contained in section II.B.2.a of the preamble to th e final rule, EPA provides the following responses to specific issues re lated to the need to revise the O 3 standard.

a. Evidence from Controlled Human Exposure Studies

(1) Comment: NAM contended that EPA did not disc lose critical studies and analyses (NAM, p. 17). This commenter stated that a noticeable instance of bi as is EPA’s failure

to disclose at least one critical collection of information within its control: its reanalysis of the data obtained by Adams (2006a). NAM c ontends that this r eanalysis (Brown 2007, "Brown Memorandum") is a crucial elemen t of Agency staff policy recommendations and that EPA did not disclose enough information to make it reproducible. NAM contends that it reaches conclusions opposite of the researcher, such that it is equivalent to a new study inserted into the record in a discriminatory fashion.

Response: EPA has disclosed all critical studies and analyses. As an initial matter, the

Brown Memorandum is not a crucial element of the staff’s policy recommendations, as it was prepared after completion of the Staff Pape r, or the Administrator’s final decision. The Brown Memorandum represents a logical progression in the inte rpretation of a study, not published until 2006, that was included in th e final Criteria Document in February 2006. In Chapter 8 of the Criteria Do cument, it was noted that the FEV 1 responses during exposure to 0.06 ppm ozone appeared to diverge away from the responses of21 filtered air and 0.04 ppm ozone after about 5.6 hr . Subsequently, in the Staff Paper, it was noted that a statistically significant difference in FEV 1 responses was suggested by a lack of overlap in the sta ndard error of the responses following 6.6 hours of exposure to 0.06 ppm ozone versus filtered air. That in terpretation of the data was supported by CASAC review. In late February 2007, public comments were submitted by a Dr. Richard Smith. In his comments, he pr ovided a table comparing changes in FEV 1 following all of the six exposure protocols ut ilized by Adams (2006) and the data for 0.04 ppm O 3 (corrected for filtered air responses) fr om Adams (2002). His table specifically

indicated that the FEV 1 responses, in the Adams (2006) study, following the two 0.06 ppm O 3 exposures were statistica lly different from the FEV 1 responses following filtered air exposures using a paired t test. Th e Brown Memorandum presents these same comparisons. The table provided in the Br own Memorandum discloses all information necessary to reproduce the standa rd statistical paired t test which was utilized. Thus, it was a public commenter that firs t placed the analysis of FEV 1 responses following exposure to 0.06 ppm O 3 versus filtered air in the public rulemaking docket. In short, the Brown Memorandum confirms Dr. Smith’s analys es, frames the analysis in terms of the analysis performed by Dr. Adams versus prior O 3 studies, and discu sses the biological significance of FEV 1 responses.

(2) Comment: NAM also contends that the Brown Memorandum itself exemplifies multiple types of violations of the information quali ty standard of objectivity (pp. 18-19). First, NAM contends that it is a post hoc statistic al analysis conducted on data whose initial analysis did not support the declared policy preferences of Agency staff. Second, NAM contends that it was prompted by a low-quality analytic review (“vi sual comparison” and “cursory evaluation,” p. 3). Io annidis (2005) shows that positi ve results are usually false

even when researchers exercise normal restrain t with respect to Type I error (rejecting the no-effect hypothesis when in fact it is true). NAM also contends that EPA has included

or excluded data or studies based on the extent to which th ey support stated or unstated risk management objectives (NAM, p. 19). In the proposal notice, NAM contends that EPA acknowledges implicitly that Agency staff used the Adams data for purposes that were never intended by the study design. It is reported that two of the 30 healthy adult subjects experienced exercise-adjusted FEV 1 decrements exceeding 10% at 0.060 ppm using one of the two exposure patterns ex amined (but not the other) (72 FR 37828, n. 16). It is inappropriate to obtain a sample, subject its members to a well designed test, learn that the sample does not yield hoped-for outcome , and in response, abandon the sample in favor of focusing on selected individuals within it. Federal information quality guidelines require transparency. When, as in this case, the disclosed portion of information shows the hallmarks of purpos eful bias, the only responsible default inference is that the reanalysis does not m eet applicable information quality standards. Unless EPA can show otherwise, the reanal ysis should not be disseminated and the

Brown Memorandum should be withdrawn.

Response: EPA rejects NAM’s contention that the Brown Memorandum exemplifies any violation of the information quality standard of objectivity. The API, which funded the Adams (2006) study, asked that the data from that study be included in the EPA risk assessment. Dr. Adams then provided his data to the EPA. Thus, the funding22 organization and the author provided their data for the express purpose that it be included in EPA’s analyses. Reporting that tw o of 30 subjects in the Adams (2006) study experienced exercise-adjusted FEV 1 decrements exceeding 10% at 0.060 ppm is merely a statement of fact by EPA. Adams (2002) repor ted that 6 of 30 subjects exposed to 0.06 ppm had greater than a 10% decrement in FEV 1 . API has refused to provide Dr. Adams technical report describing that data. In the reference cited by NAM, Ioannidis (2005) notes “... that true research findings may occasionally be annulled because of reverse bias. For example, with large measurement erro rs relationships are lo st in noise [12], or investigators use data inefficiently or fail to notice statistically si gnificant re lationships, or there may be conflicts of interest that tend to “bury” signifi cant findings [13].”

The Brown Memorandum confirms analyses completed by Dr. Smith who was funded by API to perform his analyses and to provide comments to CASAC. In the Brown Memorandum EPA used the same statistical appr oach as used by Dr. Smith. In both Dr. Brown’s and Dr. Smith’s analyses a standard st atistical test was used which is appropriate for the type of comparison made. EPA reject s NAM’s contention that this approach has the “peculiar quality of dramatically incr easing Type I error.” Thus, EPA has not

included or excluded data that has a stated policy purpose.

The Brown Memorandum objectively describes the FEV 1 responses following exposure to 0.06 ppm ozone relative to f iltered air in term s of both statistical and biological significance. The Brown Memorandum di scusses relevant public and CASAC comments. The table provided in the Br own Memorandum discloses all information necessary to reproduce the standa rd statistical paired t test which was utilized. In EPA’s judgment, its weight-of-the-evidence approach looks at all of the available evidence and the Brown Memorandum is transparen t and without purposeful bias.

(3) Comment: NAM contends that EPA draws infere nces from a study that are not supported by the data and analysis reported (NAM, p. 27 ). Five clinical studies have been performed since the last review, but only three involved exposures below the current standard level (Adams 2002, 2003b, 2006a). EPA’s interpretation of Adams’ work diverges, and is inconsistent with, that of the author (Adams 2007). Adams reports no statistically signifi cant effects from O 3 at 0.040 ppm, but EPA finds them in its reanalysis. This poses special information quali ty issues. EPA’s interpretation of Adams’ work does not enjoy a rebuttable presumpti on of objectivity. Moreover, to utilize Adams’ work in contrary ways, the Agen cy must first rebut the presumption of objectivity that attaches to these studies. Fu rthermore, EPA’s reanalysis of Adams’ data in the final Staff Paper and Brown Memorandu m is neither transparent nor capable of being substantially reproduced. This is an essential prerequisite for adherence to the objectivity standard and inconsistent with EPA’s information quality guidelines.

Response: EPA did not draw inferences that were not supported by the data and the reported analysis as NAM contends. The Adams (2007) teleconference comments to CASAC concerned the descrip tion of his 2006 publication in the Staff Paper. CASAC heard Dr. Adams comments and did not objec t to the discussion of the Adams (2006)23 publication in the Staff Paper. W ith regard to the effects of O 3 at 0.040 ppm, NAM is incorrect. Neither the Adams (2006) public ation nor EPA descri be statistically significant effects of exposure to 0.04 ppm O 3 on lung function. As already discussed, the table provided in the Brown Memorandum discloses all information necessary to reproduce the standard st atistical paired t test which was utilized.

(4) Comment: NAM also contends (NAM, p. 29) that EPA’s analysis of clinical data on cardiac effects is problematic with respect to information quality standards. In the proposed rule, NAM contends that EPA emphasi zes the increase in AaPO2 and interprets

it as evidence that O 3 exposure “result[s] in an overall increase in myocardial work and impairment in pulmonary gas exchange” (72 FR 38734). EPA says nothing about the relevance of the exposure level, which was 0.3 ppm -- 3.75 times greater than the current NAAQS, or the uncertainties implied by extrap olating to the populat ion clinical data obtained from a sample of 16.

Response: proposal notice. The quote provided by NAM, which appeared in the Staff Paper and proposal notice was based on the c onclusion of Dr. Henry Gong stated in the original article. Dr. Gong was a physician a nd first author of the study in question. The details of his study were provi ded in Chapter 6 and Annex 6 of the Criteria Document. Furthermore, in the paragraph to which NAM has referred (72 FR 38734), the EPA specifically states, "Since then, a very limited body of evidence from animal, controlled human exposure and epidemiologic studies has emerged that provides evidence for some potential plausible mechanisms for how O 3 exposures might exert cardiovascular system effects, however much needs to be done to substantiate these potential mechanisms ” (emphasis added). Absent evidence to the c ontrary, there is no reason to believe that

there would be a threshold O 3 concentration for such effect s. Additionally, the Gong et al. (1998) study was ethically rest ricted to patients with mild hypertension and could not

examine these effects in individuals more seve rely affected by cardiovascular disease. EPA explicitly stated that mechanistic data was limited and needed to be substantiated. In that context, no further discussion of limitations or extrapolations was warranted

(5) Comment: Some commenters cited the discussion of the controlled human exposure studies in the Rochester Report as supporting their views that the current standard should be retained. The following passages from th e Rochester Report summarize the points made in that report:

Adams (2006a), seeking differences in patterns of response among the different exposures, utilized a Scheffe post hoc test for controlling study-wide level of alpha while making multiple comparisons among the many data points. This test (which is not particularly powerful fo r detecting specific differences in the context of large numbers of comparisons) did not identify the response of the 0.06 ppm exposure as statistically different from that of the FA exposure. However,

alternative statistical test s suggest that the observed small group mean response in

FEV 1 induced by exposure to 0.06 ppm compar ed to FA is not the result of

chance alone. The mean difference in the FEV 1 decrements between the two exposures at 6.6 hours was approximately 2.9% which was statistically different24 (p<0.001) from zero when tested using a t- statistic without correction for multiple comparisons.

Further examination of the post-exposure FEV data and mean data at other time points and concentrations also suggest a pattern of response at 0.06 ppm that is consistent with a dose-response rather th an random variability. For example, the response at 5.6 hours was similar to that of the post-exposure 6.6 hour response and appeared to also differ from the FA response. The volunteers in this study did not appear to be more responsive to ozone than volunteers in previous studies as the observed response at 0.08 ppm in this study was similar to that of previous studies. Although of much smaller magn itude, the temporal pattern of the 0.06 ppm response was generally consistent with the temporal patterns of response to higher concentrations of ozone in this and other studies. Responses below 0.08 ppm ozone have not previously been obs erved, but this finding is not totally unexpected because the previously observ ed FEV responses to 0.08 ppm were in the range of 6-9% suggesti ng that exposure to lower concentrations of ozone would result in smaller, but real FEV decrements. The EPA re-analysis and reinterpretation of the studies of Adams has been questioned by Adams (2007) and by Smith (2007) in presentations to the Cl ean Air Scientific Advisory Committee. Thus, the public health si gnificance of responses at 0.06 ppm ozone is still being debated. The Panel recognizes that uncer tainty necessarily surrounds a secondary analysis and the integration of results from a single study in one laboratory with 0.06 ozone exposures and results obtained in studies at higher concentrations by other investigators. Resolution of this uncertainty will require that further research be conducted to clarify the i ssue. (Rochester Report, pp. 56-57)

Response: The EPA generally agrees with th e Rochester Report’s evaluation of the Adams (2006) study and the interpretation of th e EPA’s secondary analysis of the data. EPA agrees that there is a sm all group mean response in FEV 1 induced by exposure to 0.060 ppm ozone compared to FA and that the observed response is not the result of chance alone. Furthermore, EPA agrees that the pattern of res ponse at 0.060 ppm ozone

is consistent with a dose-res ponse curve rather th an random variability. Given that the 0.060 ozone exposures and results have not been replicated, some un certainty exists and EPA agrees that further research is needed to clarify the issue.

(6) Comment: One commenter submitted a sta tistical analysis and evaluation ( Exxon Mobil) of the Adams (2006) study and data by Dr. Nicolich. Dr. Nicolich reached four conclusions from his analysis: 1) Based on the additional statistical analyses detailed in this report, we have shown that the basic results of Adams (2006) ozone chamber study were replicated. 2) Based on analyses of the response patte rn over the 6.6 hours of experimentation, the only percent changes in FEV 1 responses that are statistica lly significantly different from the first period fresh air exposures were the 0.08 ppm triangle e xposure at hours 4.6, 5.6 and 6.6 hours and the 0.08 ppm square wave exposure at 6.6 hours. 3) The analysis of only the 6.6 hour readings indicated the 0.08 pp m square wave and 0.08 ppm triangle wave exposures were di fferent from the fresh air exposure.25 4) The magnitude of the estimated changes fo r all individuals in all exposure groups are less than the 15 percent decrement considered to be of clinica ll significance by the American Thoracic Society.

Response: Dr. Nicolich conducted a statistical rean alysis of the Adams (2006) data. To correct for the multiple comparisons, the sign ificance level was adju sted by the Dunnett’s

test which “is not as conservative as Scheffé’s te st or as extreme as individual t-tests.” It should be recognized that Dr. Nicolich ran multiple comparisons and had to correct for these multiple comparisons in order to avoi d type 1 error (falsely rejecting the null hypothesis when there is no effect). Thus, the probability of t ype 2 error (falsely accepting the null hypothesis when a real effect exists) was increased just as in the case of Dr. Adams’ analysis. Furthermore, Dr . Nicolich did not provide estimates of the power of his statistical analysis to detect an effect. Therefor e, the lack of being able to find a statistically significan t effect at 0.060 ppm ozone does not mean that no effect exists. On page A-3, Dr. Nicolich states “t hat the residuals are not normally distributed and the observations do not meet the assumpti ons required for the model” and that “the subject-based errors are not independently, identically and normally distributed and the subjects do not meet the assumptions require d for the model.” Later on page A-5, Dr.

Nicolich states that his “resu lts are essentially correct, but the significance levels may not be exactly correct.” Regardi ng the analysis of responses at 6.6 hours, Dr. Nicolich again stated that the “significance levels may not be exact because of the failure to meet the normality assumption.” Therefore, given th at the underlying statistical assumptions required for his analysis were not met and th at significance levels are questionable, in EPA’s judgment the analyses presented by Dr. Nicolich are ambiguous.

On page A-5 of his comments, Dr. Nicolich st ates that “The model predicted response for individuals in Figure 3 shows th at none of the predicted poin ts shows more than about a 6 percent decrement and the lower confidence inte rvals (not shown) ar e all greater than 10 percent and, therefore, do not include the 15 percent decrement c onsidered to be of clinical significance by the AT S (Wang and Petsonk 2004).” On inspection of the Adams (2006) data for the 0.080 ppm exposures, a great er than 15% ozone-induced decrement in

FEV 1 is seen in 2 individuals for the square-w ave exposure protocol and in 3 individuals for the triangular exposure protocol. It is unclear why Dr. Nicolich would utilize a

statistical model that violates basic statistical as sumptions to support his assertion. The commenter does not accurately characterize th e cited ATS guidelines on the magnitude of lung function (FEV 1 ) change. The cited gu idelines were not defining the magnitude of lung function (FEV 1 ) change that can be considered to be clinically adverse. The cited guidelines were established to help determin e whether a change in lung function, between two tests made a year or more apart, is “real” or only the result of test variability (ATS 1991). The guideline goes on to note that a ll lung function measurements tend to be more variable when made weeks to months ap art than when repeated at the same test session or even daily. EPA’s discussion of a dversity in the Staff Paper, NPRM, preamble to the final rule and this Response to Commen ts document appropriately characterizes the ATS adversity guidelines (ATS, 2000). Theref ore, Dr. Nicolich’s comment regarding clinical significance of FEV 1 responses in the Adams (2006) study is without merit.26 (7) Comment: Dr. Adams in his October 2007 comments states that the FEV 1 response in healthy young adults to 6.6 h exposure to 0.060 ppm O 3 in his study (Adams, 2006a) do not demonstrate a significant mean effect by ordinarily acceptable statistical analysis and then references the analysis of Dr. Mark Nicolich in support of this assertion. He considers the response to be in somewhat of a gray area, both in te rms of a biologically meaningful response and a statis tically significant response. Fu rther, he feels that more studies of human pulmonary function (and measurements of related physiological mechanisms) should be conduc ted in prolonged 0.060 ppm O 3 exposures as soon as possible.

Response: Both Dr. Adams and Dr. Nicolich ra n multiple comparisons which increases probability of type 2 error (fal sely accepting the null hypothesis when a true effect exists) when evaluating the simple issue of whet her post-exposure lung function was decreased in subjects exposed to 0.060 ppm ozone vers us filtered air in the Adams (2006) study. The two-factor analysis of variance and Scheffé method cited by Adams (2006) assumes that data are normally distributed and that variances are equal within cells. From previous studies of higher O 3 exposures, we know that FEV 1 responses become skewed and variance increases (McDonnell 1996). This increase in variance is clearly apparent in the Adams (2006) data with the standard deviation of FEV 1 responses increasing from

2.98% for filtered air to 4.24% for exposures at 0.060 ppm O 3 to 8.65% for exposures at 0.080 ppm. Dr. Nicolich’s analysis also found that the underlying st atistical assumptions of data normality required for Dr. Adams’ analysis were violated. Thus, it is very possible that the wide range in variances am ong the cells could have resulted in wider

confidence levels and inaccuracies of the reported p-values for a subset of the comparisons. Dr. Nicolich even stated that “significance levels may not be exact because of the failure to meet the normality assumption.” Therefore, as addressed in response to Dr. Nicolich’s comments, not finding a statis tically significant eff ect at 0.06 ppm ozone

does not mean that no effect exist.

Dr. Adams contends that, “it appears that paired t tests were applied to my data without

an initial ANOVA to examine whether there wa s statistical significance in pre- versus post-exposure FEV 1 response across multiple exposure conditions. If this were done, it would necessitate a post-hoc correction of the pa ired t test results that might or might not

result in the statistica l significance for the FEV 1 response reported in the memorandum. Statistical texts (e.g., Neter et al., 1996) routinely recommend that ANOVA is preferable because the t-test is too extreme (non-cons ervative)” (Adams, 2007, p. 2). Dr. Adams is not accurate with regard to the analysis presented in the Brown Memorandum. The effects of other exposure protocols (0.040 a nd 0.080 ppm) were not considered. The goal

of the memorandum was to address whether th ere was a pre- to postexposure change in the lung function of individuals exposed to 0.060 ppm ozone versus filtered air. A repeated measures ANOVA of the change in FEV 1 following exposure to 0.060 ppm ozone versus filtered air provides the same result as the paired t test which was utilized in the Brown Memorandum, i.e., a relatively small but statistically significant decrease in group mean FEV 1 responses following 6.6 h of exposure to 0.060 ppm ozone compared to filtered air. Dr. Adams’ comments (pag e 2) regarding the magnitude of lung function decrements due to exposure to 0.080 ppm versus 0.060 ppm ozone or other ozone27 exposure protocols are not relevant other than to establish that a trend in responses exists. Therefore, there was no need for an initial repeated measures ANOVA of all the exposure protocols in the Adams (2006) study to disc ern if ozone effected post-exposure lung function at 0.060 ppm versus filtered air.

As presented in the Brown Memorandum, paired t test were conducted for the two 0.060 ppm exposure protocols versus filtered air responses. The reported two-tailed significance levels were 0.009 and 0.001 for th e triangular and square-wave exposure protocols, respectively. Dr. Adams contends (Adams, 2007, p. 3) that “no correction for post hoc application is used (which would result in their increase by 5 times)” and thereby lead to a critical p-valu e of 0.01 (i.e., 0.05/5). Howeve r, it should be noted that in actuality, only two comparis ons were made in the Brow n Memorandum. Clearly, the significance levels reported in the Brown Memorandum which were <0.01 should remain statistically significant following any reas onable multiple comparison correction. Dr. Adams also generally objected to the use of a t test for evaluating the significance of results from his study. However, Dr. Richard Sm ith (a statistician at the University of North Carolina) also utilized t tests to evaluate the statis tical significance of the Adams data in his public comments to CASAC (Mar ch 5, 2007). Therefore, we conclude that ordinarily acceptable statisti cal analyses such as presen ted in the Brown Memorandum show that exposure to 0.060 ppm O 3 causes a relatively small but statistically significant decrease in group mean FEV 1 responses compared to filtered air.

Dr. Adams agrees in his October 2007 comme nts (p. 3) that pre- to postexposure responses may be an acceptable means of evaluating effects on lung function for the square-wave exposure protocols. He does not , however, consider it appropriate for analysis of triangular exposure protocols. Dr. Adams’ concern arises because during triangular exposures to 0.080 and 0.120 ppm oz one, subjects have been observed to experience their maximal pulmonary function de crements at one to two hours before the end of the exposure. Hence, by examining only pre- to postexposure pulmonary function changes, the maximal effects would be missed. However, as noted by Dr. Adams (Adams, 2007, p. 2) “no such tendency is apparent for FEV 1 response with time in thetwo 0.06 ppm exposures in Fig. 1 of the memorandum. Rather, there is a nonsignificantly greater drop from 4.6 h to 5.6 h for the 0.06 ppm square-wave exposure than for the 0.06 ppm triangular exposure.” Theref ore, for the 0.060 ppm ozone protocols, it appears that the use of pre- to postexpos ure responses are an acceptable means of evaluating effects on lung function for th e square-wave and triangular exposure protocols.

Dr. Adams did correctly note, contrary to what is stated in the Brown Memorandum, that Horstman et al. (1995) used an ANOVA for a sp lit-plot design to test the hypothesis that pre- minus post-exposur e differences in FEV 1 for the air and O 3 exposures were the same for a group of asthmatics as for a group of nonast hmatics. The t tests were used in the Horstman et al. (1995) study to evaluate the di fferences between an aerosol test of small airways function, not FEV 1 , between the asthmatics and nonasthmatics.28 Overall, there appears to be general agr eement among Dr. Adams, the Rochester Report,

and the EPA that the effects on pulmonary function at 0.060 ppm O 3 appear to be

consistent with the trend in FEV 1 responses observed for exposures ranging from to 0.04 ppm to 0.08 ppm O 3 and that further studies be low 0.08 ppm are warranted.

b. Evidence from Epidemiological Studies

This section contains comme nts on EPA’s assessment of ep idemiological studies in the proposal and the Agency’s general responses to those comments. Comments on EPA’s interpretation and assessment of the body of epidemiological ev idence are discussed first and then comments on methodological issues and partic ular study designs are discussed. EPA notes

here that most of the issues and concerns ra ised by commenters on the interpretation of the epidemiological evidence and methodological issues are essentially restatemen ts of issues raised during the review of the Criteria Document a nd Staff Paper. EPA presented and the CASAC Panel reviewed the interpretation of the epidem iological evidence in the Criteria Document and the integration of the evidence with policy cons iderations in the development of the policy options presented in the Staff Paper for consid eration by the Administra tor. CASAC reviewed both the Criteria Document and Staff Paper and approved of the scientif ic content and accuracy

of both documents. The CASAC chairman sent to the Administrator one letter (Henderson, 2006a) for the Criteria Document and another letter for the Staff Paper (Henderson, 2006c) indicating that these documents provided an appropriate basis for use in regulatory decision making regarding the O 3 NAAQS.

As with evidence from controlled human exposure studies, comments on the evidence from epidemiological studies, including EPA’s interpretation of the evidence, were highly polarized. One group of commenters from medical, public health and environmental organizations, in general, supported EPA’s interp retation of the epidemiological evidence (72 FR 37838, sections II.a.3.a-c) with regard to whether th e evidence for associations is consistent and coherent and whether there is biological plausibility for judging whether exposure to O 3 is causally related to respirator y and cardiovascular morbid ity and mortality effects.

(1) Comment: Comments of public health and enviro nmental groups, includ ing a joint set of comments from ALA and several environmental gr oups (ALA et al.), 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 3 exposures and respiratory hea lth 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 s how adverse respirator y health effects at

levels below the current 8-hour O 3 standard. These commenters generally expressed agreement with the weight of evidence appr oach taken by the Criteria Document and the conclusions reached, which were reviewed by CASAC, that the effects of O 3 on respiratory symptoms, lung function changes, emergency department visits for respiratory and cardiovascular e ffects, and hospital admissions can be considered causal.29 However, in contrast with EPA, these comm enters assert that th e causal associations

extend down to the lowest ambient O 3 concentrations reported in these studies. These commenters also expressed the view that th e respiratory and cardiovascular system effects are well-supported by the Hill criteria 3 of judging causality: strength of association, consistency between studies, coherence among studies, and biological plausibility (ALA et al., pp. 51-52). Me dical commenters, including ATS and AMA, state that these “real world” studies suppor t the findings of chamber studies to show adverse respiratory health effects at levels below the current 8-hour O 3 standard. They also note that recent studies provide compelling evidence that exposure to O 3 results in

adverse cardiovascular health effects (ATS, pp. 6-7).

Response: EPA generally agrees with this interp retation of the epidemiological evidence. The Criteria Document concludes that pos itive and robust associations were found

between ambient O 3 concentrations and various re spiratory disease hospitalization outcomes and emergency department visits fo r asthma, when focusing particularly on results of warm-season analyses. These posi tive and robust associations are supported by the human clinical, animal toxicological, a nd epidemiological evid ence for lung function decrements, increased respiratory symptoms, airway inflammation, and increased airway responsiveness. Taken toge ther, the overall evidence s upports a causal relationship

between acute ambient O 3 exposures and increased respiratory morbidity outcomes resulting in increased emergency department visits and hospitalizations during the warm season (Criteria Document, p. 8-77).

However, EPA disagrees with the asserti on of these commenters that the causal

associations extend down to the low ambient O 3 concentrations reported in these studies. The biological plausibility of the epidemiological associatio ns is generally supported by controlled human exposure and toxicological evidence of respiratory morbidity effects for levels at and below 0.080 ppm, but that bi ological plausibility becomes increasingly uncertain especially below 0.060 ppm, the lowest level at which effects were observed in controlled human exposure studies. Further, at lower levels, it becomes increasingly uncertain as to whether the reporte d associations are related to O 3 alone rather than to the broader mix of air pollutants present in the ambient air. EPA notes that the multi-city

times series studies evaluated in this review do not resolve this issue. It also becomes increasingly uncertain as to whether effect thresholds exist bu t can not be clearly discerned by statistical analyses. Thus, wh en considering the epidemiological evidence in light of the other available information, it is reasonable to judge th at at some point the epidemiological associations can not be interpreted with confidence as providing

evidence that the observed health effects can be attributed to O 3 alone. For a fuller discussion of EPA’s approach to making j udgments about causal relationships see response to comment 6 below.

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

.30 With regard to cardiovascular health outcome s, the Criteria Document concludes that the generally limited body of evidence from anim al toxicology, human controlled exposure, and epidemiologic studies is suggestive that O 3 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 a dditional research is n eeded 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 repr esenting industry asso ciations and some businesses opposed to revising the primary O 3 standard, disagreed with EPA’s interpretation of the epidemiological evidence.

(2) Comment: These commenters expressed the view that while many new epidemiological studies have been published since the current primary O 3 standard was promulgated, the

inconsistencies and uncertainties inherent in these studies as a whol e should preclude any reliance on them as justification for a more stringent primary O 3 NAAQS. They contend that the purported consistency is the result of inappropriate sel ectivity in focusing on specific studies and specific results within t hose studies (UARG, p. 15). With regard to daily mortality, the proposal emphasizes the mu lti-city studies, suggesting that they have the statistical power to allow the authors to reliably distinguish even weak relationships from the null hypothesis with st atistical confidence. Howe ver, these commenters note

that these studies are not cons istent, with regard to the fi ndings concerning individual cities analyzed in the multi-city analyses. On e commenter asserted th at each of the multicity studies and meta-analyse s cited by EPA involves cities for which the city-specific

estimates of O 3 effects have been observed to va ry 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 3 levels and daily mortality, the Administ rator overlooks the very si gnificant and heterogeneous information of the individual analyses of the 95 cities used to produce the national estimate and, based on this inc onsistency, question whether what is being seen is actually

an O 3 mortality association at all (UARG, p. 16).

Response: EPA has accurately characterized the in consistencies and uncertainties in the epidemiological evidence and strongly deni es that it has inappropriately focused on specific positive studies or specific positiv e 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 3 health effects in assessing the results of the singl e-city and multi-city studies and the metaanalyses, as discussed in section 7.6.6 of the Criteria Document In general, the Administrator recognizes that in the body of epidemiological evidence, many studies reported positive and statistically significant a ssociations, while others reported positive results that were not statistically signif icant, and a few did not report any positive O 3 - related associations. In a ddition, the Administrator judge s that eviden ce of a causal31 relationship between adverse health outcomes and O 3 exposures became increasingly uncertain at lower levels of exposure.

More specifically, the Bell et al. (2004) study observed a sta tistically significant, positive

association between short-term O 3 concentrations (24-hour average) and all-cause mortality using data from 95 U.S. National Morbidity, Mortality, and Air Pollution Study (NMMAPS) communities. The objective of the NMMAPS was to develop an overall national effect estimate using multi-city time-series analyses, by drawing on information from all of the individual cities. The strength of this approach is the use of a uniform analytic methodology, avoidance of selection bias, and larger statistical power. Significant intercity heterogeneity was noted in the Bell et al. and other multi-city studies, probably due to many factors, incl uding city-specific di fferences in pollution characteristics, the use of air conditioni ng, time spent indoors versus outdoors, and socioeconomic factors. Levy et al. (2005) found suggestive evidence that air conditioning prevalence was a pred ictor of heterogeneity in O 3 effect estimates in their meta-analysis.

(3) Comment: NAM contends that EPA has not considered publication bias in the presentation of reported results (NAM, pp. 11-13).

Response: Nam’s contention is not true, since EPA recognized the potential impact of publication bias on the conclusions that may be drawn from a body of studies, as

indicated in section 7.1.3.6 of the Criteria Document. NAM describes the theoretical basis for publication bias, but EPA was able to draw upon the findings of several studies that assessed the potential for publication bias for O 3 -related health effects studies. As

described in section 7.4.4 of the Criteria Do cument, two meta-analyses investigating the association between short-term exposure to O 3 and mortality also examined the evidence for publication bias in the availa ble literature. Bell et al. (200 5) concluded that the results provided strong evidence of an association between O 3 and mortality that was not sensitive to adjustment for PM or for model specifications. However, they suggested that, based on comparisons between the meta-analy sis results and NMMAPS results from 95 U.S. communities (Bell et al., 2004), there was evidence of publication bias (1.75% [95% CI: 1.10, 2.37] per 20 ppb increase in 24-h avg O 3 for meta-analysis versus 0.50% [95% CI: 0.24, 0.78] for NMMAPS 0-day lag results). Ito et al. (2005) also observed a statistically significant association between O 3 and mortality that wa s generally robust to adjustment for PM. They found suggestive ev idence of publication bi as (a significant asymmetry in the funnel plot), but adjusting for the asym metry reduced the combined estimate only slightly (from 1.6% [95% CI : 1.1, 2.0] to 1.4% [95% CI: 0.9, 1.9] per 20 ppb increase in 24-h avg O 3 ). The extent of potential bi as implicated in this study differed compared to that reported by Bell et al. (2005). The source of this difference is not clear, but Ito et al. stated that se nsitivity analyses comparing estimates from commonly used weather model specifications suggest that the stringent weather model used in NMMAPS may tend to yield smaller ri sk estimates than those used in other

studies.32 NAM also contends that EPA should, for each critical study, determine the extent to which nonpositive outcomes were not reported and include that information in its presentation. EPA rejects NAM’s contention th at it should determine the extent to which nonpositive outcomes were not repor ted and include that inform ation in its presentation of each critical study. First, there is no evidence to show that researchers are not reporting all results. Second, EPA can not includ e in its assessment results that were not reported. Third, EPA uses a weight of evidence approach to evaluate evidence that does not depend on a few critical studies.

Specifically, NAM (p. 13) cites three studies of respiratory symptoms (Gent et al., 2003; Korrick et al., 1998; Mortimer et al., 2002) as example of studies that “report only the most statistically significant results.” This is clearly not the case, as Gent et al. (2003), for example, reported that while effects were observed in asthmatic children using maintenance medication, no effects were observed among asthmatics not using

maintenance medication. In the Criteria Do cument, EPA recognized the post-hoc nature of the population stratification by medication use as one of th e limitations of this study.

NAM contends that Gent et al. (2003) exa ggerates their findings in their conclusions regarding the susceptibility of asthmatic children using maintenance medication. NAM states “Peak ozone exposures, which logica lly drive the results observed, exceeded current standards” (NAM, p. 13). However, th ere is no reason to believe that the peak O 3 concentrations drive the findings of this study. The Mortimer et al. (2002) study observed that excluding days when 8-h avg O 3 levels were greater than 80 ppb provided

effect estimates that were similar to those when all days were included in the analysis, indicating that the negative effect of O 3 on morning PEF were not driven by the peak O 3 concentrations.

NAM also contends that Mortimer et al . (2002) selectively re ported study results, by focusing on specific average lag periods for the various pollutants. However, as

discussed in section 7.2.3.2 of the Criteria Document, Mortimer et al. examined the

association between O 3 and respiratory effects using single day lags from lag day 1 to lag day 6. Small morning effects were observed at 1- and 2-day lags. The effect of O 3 on morning outcomes increased over several days . Examination of these single lag day effects led to the consideration of a multiday lag period of 1 to 5 days in the case of PEF and 1 to 4 days in the case of respiratory symptoms to estimate th e cumulative effect of

O 3 . The different multiday lag periods used for the various pollutants likely reflects the different relationship between the indivi dual pollutant and th e health effects.

NAM further states that the odds ratios in th e Mortimer et al. (2002) study were “barely statistically significant” and it cannot be discerned whethe r any of these ratios would have retained statistical signi ficance or declined in magnitude in a multipollutant model. In fact, Mortimer et al. does report multipollutant model results, as presented in section

7.2.4 of the Criteria Document. The odds rati os for the incidence of symptoms per 30 ppb increase in 8-h avg O 3 were 1.23 (95% CI: 0.94, 1.61) with SO 2 and 1.14 (95% CI: 0.85, 1.59) with NO 2 . In the three urban areas with PM 10 data, the odds ratios were 1.21 (95% CI: 0.61, 2.40) in the O 3 -only model and 1.08 (95% CI: 0.41, 2.40) when PM 10 also33 was included in the model. Though the O 3 effect was shown to be slightly diminished

and did not retain statisti cally significance in multipollutant models, there was considerable overlap in the 95% confidence intervals between the single-pollutant and multipollutant model results, leading EPA to c onclude that the asso ciation was generally

robust.

Finally, NAM contends that EPA did not recognize the fundame ntal data quality problems with self-reported re spiratory testing found by Kamps et al. (2001). In section 7.2.3 of the Criteria Document, EPA does in fact state that PEF measurements have been

shown to be more variable than FEV 1 in some studies (Vaughan et al., 1989; Cross and Nelson, 1991) and can have an element of uncer tain reliability when self-administered by study subjects. However, Lippmann and Spek tor (1998) state that PEF measurements from small inexpensive flow meters, which are more feasible to use in field studies, can produce similar results to PE F measured spirometrically.

In conclusion, EPA does not agree th at reported associ ations between O 3 and health effects are an artifact of publication bias. The EPA acknowledges that publication bias can result in potential overestimation of the estimated risk in a body of literature. However, for an individual study, factors such as exposure error or selection of results from an individual lag period from among seve ral positive associations can result in

underestimation of an effect estimate.

(4) Comment: NAM contends that EPA inappropriately assumes confidence intervals adequately describe variability and uncertainty (NAM, p. 49).

Response: EPA does not inappropriately assume th at confidence intervals fully describe variability and uncertainty. As an initial matter, EPA notes that while statistical significance (i.e., confidence intervals) is cons idered in the evaluation of the scientific evidence, EPA has emphasized the importance of examining the pattern of results across various studies and not focusing solely on sta tistical significance as a criterion (discussed in further detail in response to comments below and in section II.A.2 of the preamble to the proposed decision). Second, the point that the uncertainty ranges re ported in the risk assessment do not reflect all of the uncertainty in the risk estimates is explicitly discussed in the Staff Paper (section 5.3.2.5).

NAM contends that epidemiologists te nd to use convenience samples and other nonrandom research designs, which result in repor ted confidence interv als representing “best case” conditions. EPA disagrees that most of the epidemiologic literature evaluated in

the O 3 Criteria Document is based on non-random research designs. Not all epidemiologic studies evaluated in the O 3 Criteria Document use study populations that

are generalizable to the entire population, but th is does not mean that the study population was non-random. In fact, these epid emiologic studies tend to randomly select subjects into their st udy based on the study selection criteri a. The study selection criteria would limit the generalizability of the study results, for exam ple, results from a study of asthmatic children are likely not generalizable to healthy children or asthmatic adults, but this does not imply a lack of randomization. In time-series studi es that use population-34 level data, randomization is also not an issu e as the available data on the entire population (or within certain age groups of the population) in the sp ecified location are utilized.

(5) Comment: Several commenters argued that EP A overstates the probability of causal

links between health eff ects and exposure to O 3 , especially at the lower concentrations examined, and that the statistical associati ons found in the cited epidemiological studies do not automatically imply that a causal rela tionship exists. These commenters expressed

the view that the correlation between health effects and O 3 exposure must be rigorously evaluated according to a standa rd set of criteria before conc luding that there is a causal

link and that EPA fails to articulate and follo w the weight of the evidence or established causality criteria for evaluating epidemiologi cal studies in drawi ng conclusion regarding causality (Exxon Mobil, pp. 10-11).

Response: In the proposal, EPA explicitly stated that epidemiological studies are not themselves direct evidence of a causal link between exposure to O 3 and the occurrence of effects (72 FR 37879). Throughout the O 3 review, a standard set of criteria have been

used to evaluate evidence of a causal link. The critical assessment of epidemiological evidence presented in the Criteria Document was conceptually ba sed upon consideration of salient aspects of the eviden ce of associations so as to reach fundamental judgments as to the likely causal significance of the observe d associations in acco rdance with the Hill criteria (Criteria Document, pp. 7-3 - 7-4). Moreover, consistent with the proposal the Administrator has specifically considered ev idence from epidemiological studies in the

context of all the other available evidence in evaluating the degree of certainty that O 3 - related adverse health effect s occur at various levels at and below 0.080 ppm, including the strong evidence from controlled human e xposure studies and the toxicological studies that demonstrate biological plausibility and mechanisms for effects. More detailed

discussion of the criteria used to evaluate evidence with regard to judgments about causality can be found in section d. below.

(6) Comment: NAM contends that EPA uses polic y judgment, rather than scientific judgment in assessing causality (NAM, pp. 37-39).

Response : EPA strongly disagrees with this co mment by NAM that EPA’s approach to judging causality is “unambiguously and tran sparently policy dire cted” (NAM, p. 38) EPA’s approach to assessing the epidemiologic evidence is presented in section 7.1.2 of

the Criteria Document. The cr itical assessment of epidemiologic evidence presented in

the Criteria Document is con ceptually based upon consideration of salient aspects of the

evidence of associations so as to reach fundamental judgments as to the likely causal significance of the observe d associations, as described by Hill (1965).

NAM further alleges that EPA’s analysis and presentation of the scientific evidence does not follow a “plausibly objective analysis.” (p. 38) In developing an integrated

assessment of the health effects evidence for O 3 , EPA has emphasized the importance of examining the pattern of results across va rious studies, and not focusing solely on statistical significance as a criterion. In doing so, EPA recognizes th e distinction between evaluation of individual study re sults and integration of a body of evidence. Individual35 studies are discussed and evaluated to assess their relative scientific quality. Statistical significance is an indicator of the precision of that study’s results, which is influenced by the size of the study, as well as exposure and measurement error and other such factors. It is important not to focus the on results of statistical tests to the exclusion of other information. As observed by Rothman (1998):

Many data analysts appear to remain oblivious to the qualitative nature of significance testing. Although calculations based on m ountains of valuable quantitative information may go into it, statistical significan ce is itself only a dichotomous indicator. As it has only two values, significant or not significant, it cannot convey much useful information. . . . Nevertheless, P-values still confound effect size with study size, the two components of estimation that we believe need to be reported separately. Therefore, we prefer that P-values be omitted altogether, provided that point and interval estimates, or some equivalent, are available. (Rothman, 1998, p. 334)

The concepts underlying EPA’s approach to integrated assessment of statistical

associations have been discussed in nume rous publications, including a recent report by the U.S. Surgeon General on the health cons equences of smoking (Centers for Disease Control and Prevention, 2004). This report also cautions against over-reliance on statistical significance in evaluating the overall evidence for an exposure-response relationship.

Hill made a point of commenting on the value, or lack thereof, of statistical testing in the

determination of cause: “No formal tests of significance can answer those [causal] questions. Such tests can, and should, remind us of the effects the play of chance can create, and they will instruct us in the likely magnitude of those effects. Beyond that, they contribute nothing to the ‘proof’ of our hypothesis” (Hill, 1965, p. 299).

Hill’s warning was in some ways prescient, as the reliance on statistically significant testing as a substitute for judgment in causal inference remains today (Savitz et al., 1994; Holman et al., 2001; Poole 2001). To understand the basis for this warning, it is critical to recognize the difference between inductive inferences about the truth of underlying hypotheses, and deductive statistical calculations that are releva nt to those inferences, but

that are not inductive statements themselves . The latter includ e p values, confidence intervals, and hypothesis te sts (Greenland 1998; Goodma n 1999). The dominant approach to statistical inference today, which employs those statistical measures, obscures this important distinction between deductive and inductiv e inferences (Royall 1997), and has produced the mistaken view that inferences flow directly and inevitably

from data. There is no mathematic formula that can transform data into a probabilistic

statement about the truth of an associ ation without introducing some formal quantification of external know ledge, such as in Bayesian approaches to inference (Goodman 1993; Howson and Urbach 1993) . Significance testing and the complementary estimation of confidence interv als remain useful for characterizing the role of chance in producing the a ssociation in hand (CDC, pp. 23-24).36 Accordingly, the statistica l significance of individual study findings has played an important role in EPA’s evaluation of the study’s results, and EPA has placed greater emphasis on studies reporting st atistically significant results. However, in the broader evaluation of the evidence from many epidemiologic studies, EPA has also emphasized

the pattern of results for drawing conclusions on the relationship between air pollutants and health outcomes, as well as considera tion of the integrati on of epidemiologic evidence with findings of laboratory studies.

It is also important to reiterate that the EPA’s evaluation of the scientific evidence was reviewed in detail by CASAC and the public. Two drafts of the Criteria Document were released for CASAC and public review at public meetings, and an additional teleconference meeting was held with CASAC for review of Chapter 8. Evidence related to the substantive issues raised by the co mmenters were evaluated in the Criteria Document drafts, and discussed at length in public CASAC meetings. This process ensured that overemphasis or underempha sis on any study or group of studies was

addressed.

(7) Comment: Several commenters made the poi nt that the results of the new epidemiological studies included in this review are not cohere nt. They state that although

EPA notes that estimates of risk from cardi ovascular mortality are higher than those for total mortality and indicates that these findi ngs are highly suggestiv e that short-term O 3 exposure directly or indirectly contributes to cardiovascular mortalit y, the Agency fails to contrast the mortality studies to studies of hospital admissions for cardiovascular causes.

Most studies of cardiovascular causes have not found statisti cally significant associations

with O 3 exposures (UARG, pp. 16-17).

Response: EPA strongly disagrees th at it has failed to appr opriately characterize the

association between O 3 exposure and potential cardiova scular morbidity and mortality effects. As noted above, the Criteria Document characterizes the overall body of evidence as limited, but highly suggestive, and concludes that much needs to be done to more fully integrate links between ambient O 3 exposures and adverse cardiovascular outcomes (Criteria Document, p. 8-77). So me field/panel studies that examined

associations between O 3 and various cardiac physiologic e ndpoints have yielded limited epidemiological evidence suggestive of a potential association between acute O 3 exposure and altered HRV, ventricular arr hythmias, and incidence of myocardial infarction (Criteria Document, section 7.2.7). In addition, there we re approximately 20 single-city studies of emergency departme nt visits and hospital admissions for all cardiovascular diseases or specific diseases (i.e., myocardial infa rction, congestive heart failure, ischemic heart disease, dysrhythmias). In the studies using all year data, many showed positive results but few were statisti cally significant. Give n the strong seasonal

variations in O 3 concentrations and the ch anging relationship between O 3 and other copollutants by season, inadequate adjustment for seasonal effects might have masked or

underestimated the associations. In the limited number of studies that analyzed data by season (6 studies), statistically significant associations were observed in all but one study (Criteria Document, section 7.3.4). Newly av ailable animal toxicology data provide some plausibility for the observed associations between O 3 and cardiovascular outcomes.37 EPA believes that its character ization of the evidence for O 3 -related cardiovascular system effects is appropriate. It is clear that coherence is stronger in the much larger body of evidence of O 3 -related respiratory morbidity and mortality effects.

Many commenters who did not support revising the current O 3 primary standard also submitted comments on specific methodological issues related to the epid emiological evidence, including: the adequacy of exposure data; confounding by copollutants; model selection; evidence of mortality; and, new st udies not included in the Criteria Document. The comments on methodological issues rais ed by these commenters are discussed below.

(8) Comment: Many commenters, mostly represen ting industry associations and some businesses opposed to revising the primary O 3 standard, expressed concern about the adequacy of exposure data both for time-ser ies and panel studies. These commenters argued that almost all of the epidemiological studies on which EPA relies in recommending a more stringent O 3 standard are based on data from ambient monitors for which there is a poor correla tion with the actual persona l exposure subjects receive during their daily activities. They questione d the Administrator's c onclusion that in the absence of available data on personal O 3 exposure, the use of routinely monitored

ambient O 3 concentrations as a surrogate for pers onal exposures is not generally expected to change the principal conclusions from epidemiological studies. These commenters also note that, in its June 2006 letter, the CASAC Panel raised the issue of exposure error, concluding that it called into question whether observed associ ations could be attributed

to O 3 alone (API, p. 17). One of these commente rs cited studies (e.g., Sarnat et al., 2001; Sarnat et al., 2005) that show a lack of correlation between personal exposures and ambient concentrations (NAM, p. 22). A nother cited studies (Sarnat et al., 2001, 2005, and 2006; and Koutrakis et al., 2005) that ha ve found that the abil ity of ambient gas monitors to represent persona l exposure to such gases is similarly quite limited, including: (1) most personal exposures are so lo w as to be not detectable at a level of 5 parts per billion (ppb), resulti ng in very low correlation be tween concentrations reported from central ambient monitors and personal monitors; (2) O 3 measurements from ambient monitors are a better surrogate for personal exposure to PM 2.5 than to O 3 ; and (3) populations expected to be pot entially susceptible to O 3 , including children, the elderly, and those with COPD, are at the low end of the population exposure distribution (Exxon Mobil, pp. 15-16). These commenters contende d that without such a correlation there is no legitimate way for EPA to conclude that O 3 exposure has caused the reported health effects, or to conclude that us e of routinely monitored ambient O 3 concentrations as a surrogate for personal exposures is adequate. Some of these commenters also contended that EPA incorrectly concludes that the expos ure error in epidemiol ogical studies results in an underestimate of risk (Exxon Mobil, p. 20).

Response: With regard to the views on e xposure measurement error expressed by CASAC, while the commenter is correct that the CASAC Panel raised the question of exposure error and whether observed asso ciations could be attributed to O 3 alone, the

commenter failed to note that CASAC’s comment was focused on the association

between O 3 and mortality, at very low O 3 concentrations and in the group of people most susceptible to premature mortal ity. The CASAC Panel stated:38 The population that would be expected to be potentially susceptible to dying from exposure to ozone is likely to have ozone exposures that are at the lower end of the ozone population distribution, in wh ich case the population would be exposed to very low ozone concentrations, and especi ally so in winter. Therefore it seems unlikely that the observed associations be tween short-term ozone concentrations and daily mortality are due solely to ozone itself. (Henderson 2006b, pp. 3-4)

This section of the quote, which was not addressed in the comment submitted by API, together with the conclusions in the fina l CASAC letter (Henderson, 2007), leads EPA to conclude that contrary to the commenters ’ assertion, the CASAC Panel was not calling into question the a ssociation between O 3 exposure and the full range of morbidity effects found in panel or time-series studies that re ly on ambient monitoring data as a surrogate for personal exposure data. It is important to note that EPA agrees that the evidence is only highly suggestive that O 3 directly or indirectly contributes to mortality, as compared to the stronger evidence of causality for respiratory morbidity effects.

EPA agrees that exposure measurement erro r may result from the use of stationary ambient monitors as an indicator of personal exposure in population st udies. There is a

full discussion of measurement error and its e ffect on the estimates of relative risk in

section 7.1.3.1 of the Criteria Document. Howe ver, the possibility of measurement error does not preclude the use of ambient monitori ng data as a surrogate for personal exposure data in time-series or panel studies. It si mply means that in some situations where the

likelihood of measurement error is greatest, effects estimates must be evaluated carefully and that caution must be used in interpreti ng the results from these studies. Throughout this review, EPA has recognized this concern. The Criteria Document states that there is supportive evidence that ambient O 3 concentrations from central monitors may serve as valid surrogate measures for mean personal O 3 exposures experien ced by the population,

which is of most relevance to time-series stud ies, in which individual variations in factors affecting exposure tend to aver age out across the study population. This is especially true for respiratory hospital admission studies for wh ich much of the response is attributable

to O 3 effects on asthmatics. In children, for w hom asthma is more prevalent than adults, ambient monitors are more likely to correla te reasonably well with personal exposure to

O 3 of ambient origin because children tend to spend more time outdoors than adults in the warm season. EPA does not agree that th e correlation between personal exposure and ambient monitoring data is necessarily poor, especially in children. Moreover, the CASAC Panel supported this view as they noted that “[ p]ersonal exposures most likely

correlate better with central site values fo r those subpopulations that spend a good deal of time outdoors, which coincides, for example, with children actively engaged in outdoor activities, and which happens to be a group that the ozone risk assessment focuses upon.” (Henderson, 2006c. p. 10). However, the Criteria Docume nt notes that there is some concern in considering certain mortality and hospitalization time-series studies regarding

the extent to which ambient O 3 concentrations are representative of personal O 3 exposures in another particular ly susceptible group of individuals, the debilitated elderly,

as the correlation between th e two measurements has not been examined in this population. A better understanding of the rela tionship between ambient concentrations and personal exposures, as well as of the fact ors that affect the relationship, will improve39 the interpretation of observed associations between ambient concentration and population health response.

With regard to the specific comments that reference the findings of studies by Sarnat et al. (2001, 2005, 2006) and Koutrakis et al. (2005), the fact that personal exposure

monitors cannot detect O 3 levels of 5 ppb and below may in part explain why there was a poor correlation between pers onal exposure measurements and ambient monitoring data

in the winter relative to th e correlation in the warm s eason, along with differences in activity patterns and building ve ntilation. In one study conducted in Baltimore, Sarnat et al. (2001) observed that ambient O 3 concentrations showed st ronger associations with personal exposure to PM 2.5 than to O 3 ; however, in a later study conducted in Boston (Sarnat et al., 2005), ambient O 3 concentrations and personal O 3 exposures were found to be significantly associated in the summer. Another study cited by the commenter, but not included in the Criteria Document, conducted in Steubenville (Sarnat et al., 2006), also observed significant associ ations between ambient O 3 concentrations and personal O 3

. The authors noted that the city-specific discre pancy in the results may be attributable to differences in ventilation. Though the studies by Sarnat et al. (2001, 2005, and 2006) included senior citizens, the study selection criteria require d them to be nonsmoking and physically healthy. EPA is not relying on studies that are not in the Criteria Document, such as Sarnat et al. (2006), to refute the co mmenters. However, EPA notes that Sarnat et al. (2006) does not support the conclusion drawn by the commenters that this study shows very limited associations between ambient O 3 concentrations and personal

exposures.

Existing epidemiologic models may not fully ta ke into consideration all the biologically relevant exposure history or reflect the complexities of all the underlying biological processes. Using ambient concentrations to determine exposure generally overestimates true personal O 3 exposures (by approximately 2- to 4- fold in the various studies

described in the Criteria Do cument, section 3.9), which assuming the relationship is causal, would result in biased descrip tions of underlying c oncentration-response relationships (i.e., in attenuated effect estimates). From this perspective, the implication is that the effects being estimated in relati onship to ambient levels occur at fairly low personal exposures and the potency of O 3 is greater than these e ffect estimates indicate. On the other hand, as very few studies evaluating O 3 health effects with personal O 3 exposure measurements exist in the literature, eff ect estimates determined from ambient

O 3 concentrations must be evaluated and used with caution to assess the health risks of

O 3 (Criteria Document, pp. 7-8 to 7-10). Noneth eless, as noted in section II.C.3 of the proposal, the use of routinely monitored ambient O 3 concentrations as a surrogate for personal exposures is not generally expected to change the principal conclusions from O 3 epidemiologic studies. Therefore, populat ion risk estimates derived using ambient O 3 concentrations from currently available obs ervational studies, with appropriate caveats about personal exposure considerati ons, remain useful. (72 FR 37839)

(9) Comment: NAM contends that EPA characterizes a study as reporting something when it reports the opposite, specifical ly referring to the work by Sarnat and colleagues (2001, 2005) (NAM, pp. 22-23) NAM states that in Sa rnat et al. (2001), “t he authors concluded40 that ambient concentrations did not provide a surrogate fo r personal exposures, and in 2005 they reconfirmed that result” (NAM, p. 22). NAM then contends that EPA has “the study sites reversed and the result s reported incorrectly” (NAM, p. 23).

Response: EPA has correctly characterized the c onclusions of Sarnat et al. (2001) while NAM has the study sites reversed. Sarnat et al. (2001) was conducted in Baltimore, MD while the 2005 study was conducted in Bost on, MA. As reported in the Criteria Document, in the study conducted in Baltim ore, Sarnat et al. (2001) observed no relationship between ambient O 3 concentrations and personal O 3 exposures in both the

summer and winter. The ambient O 3 concentrations showed st ronger associations with personal exposure to PM 2.5 than to O 3 ; thus authors noted that “ambient concentrations of gaseous pollutants cannot be considered as surrogates for their respective personal exposure without site-specific evidence to support that assu mption.” They also noted, however, that a limitation of th eir study was that it was only conducted in one city. In the later study conducted in Boston (S arnat et al., 2005), ambient O 3 concentrations and personal O 3 exposures were found to be significantly associated in the summer. From this they noted that these results suggest that “there may be differences, by location in the strength of the personal-ambient association fo r the gases.” and that “it is incorrect to assume that ambient gas measurements are c onsistent surrogates for PM exposures.”

(10) Comment: Many commenters, mostly represen ting industry associations and some businesses opposed to revising the primary O 3 standard, argued that known confounders are inadequately controlled in the epidemiological studies of O 3 and various health

outcomes and that the health effects of O 3 are often not statistically significant when epidemiological studies consider the e ffects of confounding air pollutants (e.g., PM 2.5 , CO, nitrogen dioxide (NO 2 ) in multi-pollutant models. Many commenters cited Mortimer et al. (2002), a large multi-city asthma panel study as an example, and

indicated that it found that when othe r pollutants, i.e., sulfur dioxide (SO 2 ), NO 2 , and particles with an aerodynamic diameter less than or equal to a nominal 10 micrometers (PM 10 ), were placed in a multi-pollutant model with O 3 , the O 3 -related associations with respiratory symptoms and lung function became non-significant.

Response: EPA has thoroughly reviewed issues related to confoundi ng and the evidence of potential confounding by c opollutants in sections 7.1.3 and 7.6.4 of the Criteria Document. EPA recognizes that a ma jor methodological is sue affecting O 3 epidemiologic studies concerns the evaluation of the extent to which other air pollutants may confound or modify O 3 -related effect estimates, and that the changing relationship

between O 3 and copollutants across seasons further complicates the issue. The use of multipollutant regression models is the prevailing approach for controlling potential confounding by copollutants in O 3 health effects studies (Crite ria Document, p. 7-24). In section 7.6.4.2, the Criteria Document revi ews the evidence from studies that use multipollutant models to ev aluate confounding by copollutant s for effects ranging from mortality and respiratory hospitalizations to lung function measures and symptoms. It concluded that multipollutant regr ession analyses indicated that O 3 risk estimates, in general, were not sensitive to the inclusion of copollutants, including PM 2.5 and sulfate. As can be seen in the Figure 1 below (Figur e 7-22 from the Criteria Document) the ozone41 effect estimates for mortality are genera lly unchanged upon inclusion of PM in the models. These results sugge st that the effect of O 3 on respiratory health outcomes appears to be robust and independent of th e effects of other c opollutants (Criteria Document, p. 7-154).

Figure 1. All-cause (nonaccidental) O 3 excess mortality risk estimates (95% CI) with adjustment for PM indices for all-year analys es per standardized increment (see Section 7.1.3.2). Analyses include all ages unless otherwise noted.

The National Cooperative Inner-City Asthma Study (Mortimer et al., 2002) evaluated air pollution health effects in 846 asthmatic ch ildren in 8 urban areas. The pollutants

evaluated included O 3 , PM 10 , SO 2 , and NO 2 . Three effects were evaluated: (1) daily percent change in lung function, measured as peak expiratory fl ow rate (PEFR); (2)

incidence of ≥ 10% reduction in lung function (PEF R); and, (3) incidence of symptoms42 (i.e., cough, chest tightness, and wheeze) . EPA notes that in this study, O 3 was the only pollutant associated with reduction in lung function. Nitrogen dioxi de had the strongest effect on morning symptoms, and the authors concluded it "...may be a better marker for the summer-pollutant mix in these cities ” but had no association with morning lung function. In a two-pollutant model with NO 2 , the O 3 effect on morning symptoms remained relatively unchanged. Sulfur dioxide had statistically significant effects on morning symptoms but no association with morning lung function. Particulate matter (PM 10 ), which was measured daily in 3 cities, had no statistically significant effect on morning lung function. In a two-pollutant model with O 3 , the PM 10 estimate for morning symptoms was slightly reduced and there was a larger reduction in the O 3 estimate, which remained positive but not statistically significant.

(11) Comment: NAM contends that EPA did not cons ider non-air pollutant confounders that are not adequately controlled in the literature (NAM, pp. 32- 33). NAM cites a number of factors that have been reporte d to be associated with asth ma, and argues that failure to

control for all of these factors “yields upwardly biased estimates of risk.” (NAM, p. 32).

Response: Contrary to NAM’s contention, EPA thoroughly reviewed the issues related to confounding and the evidence of potentia l confounding in the Criteria Document. A number of the factors listed by NAM would not appropriately be id entified as potential confounders for a relationship between O 3 and health outcomes. For example, the NAM

comment discusses cockroach and house dust m ite allergens and exer cise, none of which would be likely to confo und a relationship with O 3 in a time-series study. To be a confounder, the variable must be correlat ed with both the health outcome and the exposure under study. In a time-series anal ysis, only variables that are temporally

correlated with O 3 can truly confound an O 3 -health outcome relationship. It is highly unlikely that exercise behaviors are correlated with O 3 concentrations – that people

choose to exercise when O 3 concentrations are highest. It is known that house dust mite and cockroach allergen concentrations in a home do not vary from day to day as do

ambient O 3 concentrations. Thus, these factors may be independently associated with exacerbation of asthma, but would not be c onfounders in a relationship between ozone

and asthma exacerbation.

NAM also observes that control for meteorol ogical variables is important. EPA agrees, and carefully evaluated the potential for confounding by temperatur e and humidity, as

discussed in section 7.1.3.4 and further in section 7.6.3 of the Criteria Document. EPA

concluded that O 3 risk estimates were generally more sensitive to alternative weather models than to varying degrees of freedom for temporal trend adjustment. In addition, careful consideration was given to whether studies had considered seasonality, as many epidemiologic studies observed differences in O 3 -related health effects in the warm versus cool season. Seasonality in fluences the relationship between O 3 and health outcomes, as it may serve as an indicator for time-varying factors, su ch as temperature, copollutant concentrations, infiltration, and human activity patterns. Given the potentially significant influence of season, EPA noted that season-specific analyses were more informative in assessing O 3 -related health risks and onl y estimated health risks for

the O3 warm season in its health risk assessment.43 The Administrator acknowledges that unc ertainties concerning other potential confounders may be an important source of uncertainty affecting the specific risk estimates included in EPA’s risk assessment and that these quantitative risk estimates must be used with appropriate caution, keepi ng in mind these important uncertainties. As discussed in the preamble to the final ru le, the Administrator is not relying on any specific quantitative effect estimates from th e time-series studies or any risk estimates

based on the time-series studies in reaching his judgment a bout the need to revise the

current 8-hour O 3 standard.

(12) Comment: Commenters who did not support revision of the primary O 3 standard raised issues regarding the adequacy of model specification includi ng control of temporal and weather variables in the time-series epid emiological studies that EPA has claimed support the finding of O 3 -related morbidity and mortality health outcomes. Specifically, concerns were expressed regarding the follo wing issues: (1) commenters noted that recent meta-analyses have confirmed the impor tant effects of model selection in the

results of the time-series st udies, including the choice of mo dels to address weather and the degree of smoothing, in direct contradict ion of the Staff Paper’s conclusion on the

robustness of the models used in the O 3 time-series studies (Exxon Mobil, p. 41); (2)

commenters contended that there were no criteria for how confounders such as temperature or other factors we re to be addressed, resulting in arbitrary model selection potentially impacting the resulting effect es timates; and (3) commenters expressed the view that to appropriately address co ncerns about model selection in the O 3 time-series studies, EPA should rely on an alternativ e statistical approach, Bayesian model averaging, that incorporates a range of models addr essing confounding variables, pollutants, and lags rather than a single model.

Response: In response to the first issue, EPA agr ees that the results of the meta-analyses do support the conclusion that there are importa nt effects of model selection and that, for example, alternative models to address weat her might make a differe nce of a factor of two in the effect estimates. However, as not ed in the Criteria Document, one of the metaanalyses (Ito et al., 2005) sugge sted that the stringent weathe r model used in the Bell et al. (2004) NMMAPS study may tend to yield smalle r effect estimates than those used in other studies (Criteria Document, p. 7-96), and, thus concerns about a ppropriate choice of models could result in either higher or lower effect estimates than reported. In addressing this issue, the Criteria Document concluded,

Considering the wide variability in po ssible study designs an d statistical model specification choices, the reported O 3 risk estimates for the various health outcomes are in reasonably good agreement. In the case of O 3 -mortality timeseries studies, combinations of choices in model specifications ... alone may explain the extent of difference in O 3 risk estimates across studies. (Criteria Document, p. 7-174)

Second, the issues surrounding sensitivity to model specifications were thoroughly

discussed in the Criteria Do cument (see section 7.1.3.6) and evaluated in some of the44 meta-analyses reviewed in the Criteria Docume nt and Staff Paper. As stated in the Criteria Document, O 3 effect estimates “were generall y more sensitive to alternative weather models than to varying degrees of freedom for temporal trend adjustment” (Criteria Document, p. 7-176). The Criteria Document also concluded that “although there is some concern regarding the use of multipollutant models ... results generally suggest that the inclusion of copollutants in to the models do not substantially affect O 3 risk estimates” and the results of the time-s eries studies are “robust and independent of the effects of other copollutants” (Criteria Document, p. 7-177). Overall, EPA continues to believe that based on its integrated assessm ent, the time-series studies provide strong support for concluding there are O 3 -related morbidity effect s, including respiratoryrelated hospital admissions and emergency depa rtment visits during the warm season and that the time-series studies provide findings th at are highly suggestiv e that short-term O 3 exposure directly or indirectly contributes to non-accidental and cardi orespiratory-related mortality. The Administrator acknowledges th at uncertainties concerning appropriate model selection are an importa nt source of uncertainty a ffecting the specific risk estimates included in EPA’s risk assessment and that these quantitative risk estimates must be used with appropriate caution, keepi ng in mind these important uncertainties. As discussed in the preamble to the final ru le, the Administrator is not relying on any specific quantitative effect estimates from th e time-series studies or any risk estimates

based on the time-series studies in reaching his judgment a bout the need to revise the

current 8-hour O 3 standard or on the appropria te level of the standard.

Third, in response to commenters who suggested that EPA adopt an al ternative statistical approach, i.e., Bayesian model averaging, to address concerns a bout potential arbitrary selection of models, the Crite ria Document evaluated the strengths and weaknesses of such methods in the context of air polluti on epidemiology. The Criteria Document noted several limitations, especially where there are many interaction terms and meteorological variables and where variables are highly correlated, as is the case for air pollution studies, which makes it very difficult to interpret the results using this alte rnative approach. EPA

believes further research is needed to addr ess concerns about m odel selection and to develop appropriate methods addressing these concerns.

(13) Comment: NAM asserts that EPA selected mode ls known to yield upw ardly biased risk estimates, such as single-pollutant models and models that do not control for known confounders (NAM, pp. 31-32, 34). NAM also cr iticizes the use of single-pollutant model results in EPA’s risk assessment, whic h is addressed in comme nt numbers (7) and (9) in section II.A.5.

Response: EPA rejects NAM’s asser tion that it selected mode ls known to yield upwardly biased risk estimates, such as single-pollutant models and models that do not correct for confounders in the Criteria Document, Staff Pape r, or risk assessment. EPA’s approach

in all of these documents was to include a nd discuss results from both single- and multipollutant models when available. EPA’ s Criteria Document ri gorously and thoroughly evaluated the potential for confounding in O 3 epidemiological studies. EPA discussed the merits and issues with both single- and multipollutant models in section 7.1.3.5 of the

Criteria Document. EPA further evaluated the potential confounding of the association45 between O 3 and various health outcomes by copo llutants in section 7.6.4 of the Criteria Document. EPA stated that although ther e was some concern regarding the use of multipollutant models given the varying conc urvity across pollutants, results generally suggested that the inclusion of copollutants into the models did not substantially affect O 3 risk estimates. From these findings , EPA concluded that effects of O 3 on various health outcomes were robust and independent of the effects of other copollutants. Additional response to this comment with respect to the issue of alleged upward bias in the context

of the health risk assessment is addresse d in the response to comment number (7) and number (9) in section II.A.5 of this document.

(14) Comment: NAM also contends that EPA disse minates results from models known to yield risk estimates that ar e upwardly biased and more un certain, such as Generalized

Additive Models conducted with insuffici ent convergence criteria (NAM, pp. 36-37).

Response: NAM incorrectly states “For year s EPA has relied on studies utilizing Generalized Additive Models (GAMs) and soft ware (S-PLUS) that yielded estimates of health effects from air pollution that were upwardly biased and excessively uncertain.” (p. 36). In fact, that has not been the case in recent years. NAM cites results from the Special Report prepared by the Health Effect s Institute (HEI, 2003); in fact EPA has been a leader in examining this issue. Upon fi rst learning of the questions surrounding the use of GAM, EPA funded a special workshop and s upported the HEI in a project to reanalyze dozens of studies to fully investigate this i ssue. EPA has always carefully evaluated the methodology used in epidemiologic studies in th e process of its scie ntific assessments.

EPA discusses the issue of GAM and othe r methodologies in section 7.1.3.7 of the Criteria Document. The Criteria Document ge nerally only includes results from studies

that used methods other than GAM or the newly developed converg ence criteria that

addressed the issues found with the initial use of GAM in SPlus. Thus EPA’s Criteria

Document and the risk assessment do not rely on studies that are impacted by the “GAM

issues.”

(15) Comment: NAM contends (NAM, pp. 34-35) that for la gs to be biologica lly plausible, at least three critical biological principles must be respected: (1) all health effects must occur after exposure; (2) for each health effect, the gradient of risk must be biologically appropriate; and (3) more severe health effect s must occur subsequent to minor effects.

NAM contends that the time-series studi es EPA relies upon do not respect these fundamental biological require ments. NAM specifically notes that biologically implausible lags are reported by Mortimer et al. (2002).

Response: EPA disagrees with NAM’s charge that lags for specific health effects have

been selected based on statis tical strength without regard for the underlying biology. All the epidemiologic studies included in the Criteria Document examined O 3 health effects associated with exposure from the same day or previous days; thus, in these studies the health effect did not preced e the exposure. In section 7.1.3.3 of the Criteria Document, EPA recognized that analyzing a large number of lags and simply choosing the largest and most significant results may bias the air pol lution risk estimates away from the null. However, most time-series analyses have shown that O 3 has a fairly consistent,46 immediate effect on emergency department visi ts, hospitalizations, a nd mortality. For the respiratory and cardiovascular outcomes inves tigated, the “most significant” lags were generally 0- or 1-day lags, suggesting that the majority of the si ngle-day associations were immediate, not a random pattern in whic h associations could be observed on any of the lags examined with equal probabilities.

EPA further recognized that effects can o ccur acutely with exposure on the same or previous day, cumulatively over several days, or after a delayed period of a few days. Several studies also observed significant O 3 effects over longer cumulative lag periods, suggesting that in addition to single-day la gs, multiday lags should be investigated to fully capture a delayed O 3 effect on health outcomes. Due to these findings, in the Criteria Document, discussion largely focuse d on effect estimates from same day and previous day exposures, with some considera tion of cumulative, multiday lag effects.

NAM specifically uses Mortimer et al. (2002) as an example to note that multiple lag times are used without biologi cal justification. As discus sed briefly in response to a previous comment #(7), Mortimer et al . examined the association between O 3 and respiratory effects using single day lags fr om lag day 1 to lag day 6. Small morning

effects were observed at a 1- day lag. The effect of O 3 on morning outcomes increased over several days. A single-day lag mode l calculates a risk estimate that assumes dependence only on exposure from the specified day. In contrast, a multiday lag model provides an estimate that is a summary meas ure of the cumulative lag effect from all included lag days. The effect estimates were not all statistically significant for each single-day lag, but the pattern of the effect estimates was generally consistent with considerable overlap in the confidence intervals for the multiple days considered, suggesting that the gradient of risk was, in general, biologically appropriate. Examination of these single lag day effects led to the consideration of a multiday lag period of 1 to 5 days in the case of PEF a nd 1 to 4 days in the case of respiratory symptoms to estimate the cumulative effect of O 3 . The selected cumulative lag period was biologically plausible and consistent with previous findings that asthma exacerbation is generally associated with pollutant exposures over a several day period. The observation of greater effect s in the morning and the change in effects following adjustment for copollutants were addresse d in responses to previous comments (see comments #(16) and #(10) in this section).

NAM also comments that more severe health effects must occur subsequent to more minor effects for a lag to be biologically plausible. NAM notes that respiratory symptoms should occur before emergency de partment visits and hospital admissions. Though not specified in the comments, NAM seems to be implying that the longer cumulative lag observed for respiratory sympto ms in the Mortimer et al. study compared to the shorter, more immediate lags observed in the time-series analyses of emergency department visits and hospital admissions indi cate that the observed association between respiratory health outcomes and O 3 is biologically implausibl e. EPA disagrees that a direct comparison can be made in the expos ure lags between thes e two very different types of studies. Mortimer et al. is a panel study of asthmatic children, in which

individual-level health outcome data is linked with ambient O 3 concentrations for a47 limited number of subjects. In contrast, time -series analyses link daily community-level health outcome data (i.e., counts of emergenc y department visits or hospitalizations) with ambient concentrations. By design, a populat ion with a much wider variability in susceptibility is considered in these time-seri es analyses. It is important to note that while several studies consistently observed associations between O 3 and respiratory emergency department visits and hospitalizations at lag 0- or 1-day, strong associations

were also observed in studies that examin ed longer multiday, cumulative exposures. In addition, it should be noted that there are pot entially different mechanisms between the different endpoints described above. For example, asthmatics may experience severe acute exacerbations that result in emergenc y department visits, or they may have inflammatory responses that develop over a l onger period of time. It is well known that asthma is a complex disease likely to have multiple etiologic pathways for health

responses.

(16) Comment: NAM contends that methodological erro rs, e.g., repeated statistical tests, biologically implausible lags, and inadequa te control for confounders, have not been properly considered by EPA in the evaluation of the evidence for O 3 health effects (NAM, pp. 14-16).

Response: In the Criteria Document, EPA condu cted a rigorous assessment of potential methodological error in epidemiologic analyses , as can be seen in section 7.1.3. Issues such as those cited by NAM, including cont rol for copollutants and other potential confounders, consideration of exposure lag periods, and measurement error, were evaluated by EPA in its assessment of the sc ientific evidence. EPA does not agree that methodological errors exist in th ese studies that are “so severe that they have a material effect on utility, particularly for re gulatory decision-making.” (p. 14).

With regard to NAM’s statement that repe ated statistical tests are performed without apparent regard for the resulting increase in the rate of false positive, EPA discusses the issue of multiple hypothesis testing in S ection 7.1.3.6 of the Criteria Document. In particular, EPA notes that multiple hypotheses may need to be developed for researchers to explore more thoroughly pot ential associations for an O 3 -related health effect. NAM specifically cites Korrick et al . (1998) and Mortimer et al. (2002) in reference to this

comment. In Korrick et al. (1998), though multiple hypot heses are tested, these hypotheses can be divided into confirmatory vs exploratory hypotheses. The main confirmatory hypothesis is whether O 3 concentrations are associated with pulmonary function. In their models adjusting for multip le covariates, they observe a clear inverse

association between O 3 and FEV 1 and FVC. In their sensitiv ity or exploratory analyses, they observe that the O 3 effect estimate is generally robust to adjustment for PM 2.5 and acidity. They further obser ved that the effect of O 3 may be modified by asthma status, but not by smoking status, gender, or age. In Mortimer et al. (2002) the issue pertains to the examination of multiple lags. As discu ssed above, the examination of multiple lags may be viewed as the testing of explorator y hypotheses. As noted in the response to comment (15) above, in section 7.1.3.3 of th e Criteria Document, EPA recognized that analyzing a large number of lags and simply choosing the largest and most significant results may bias the air pollution risk estimat es away from the null. In the response48 above and in the response to comment (3) the issue of lags is further discussed specifically with regard to Mortimer et al. (2002)

Other methodological errors that NAM me ntion include the reliability of selfadministered PEF testing (Mortimer et al., 2002), selective use of data from different times of day (Mortimer et al., 2002), reli ance on subjective symp toms rather than objective signs (Gent et al., 2003), and the us e of a nonstandard measure of incremental change (Korrick et al., 1998).

One issue that NAM discusses in some detail in this section is the error related to selfreported peak expiratory flow data. NAM pr esents the results of Kamps et al. (2001) which found that compliance and reliability of self-reported data was less than optimal. EPA recognizes that PEF measurements have be en shown to be more variable than FEV 1 in some studies (Vaughan et al., 1989; Cross and Nelson, 1991) and can have an element of uncertain reliability when self-administere d by study subjects. As increased variability

in the PEF measurement will add no ise to the relationship between O 3 and PEF, it will likely lead to bias towards the null rather than a spurious sign ificant association. Furthermore, the observed association between O 3 and PEF concur with the strong

associations found between O 3 and measures of spirometry, which is a more consistent test of lung function and typically conducted by a trained individual.

NAM also comments on the selective use of data from different times of day. In Mortimer et al. (2002), while a ssociations were found between O 3 and morning PEF and respiratory symptoms, no associations were observed with evening PEF or respiratory symptoms. The fact that associations we re more evident with asthma symptoms measured in the morning is consistent with the understanding that the development of asthma exacerbation through an inflammatory mechanism would occur over time, with symptoms manifested hours after the exposure period. Mortimer et al. further explain

that the most severe bronchoconstriction occurs in the morning, when measurable

differences between and within individuals may be greatest. Therefore, there are biologically plausible reasons as to why associ ations would be observe d at different times of day.

The NAM statement that Gent et al. (2003) relied on a subjective measure of symptoms rather than an objective measure is incorrect. In addition to respir atory symptoms, Gent

et al. also observed an association between O 3 and rescue medication use, which is an objective measure. Regardless, EPA deems respiratory symptoms to be a valuable health outcome, which considered in conjunction with various other more “objective” measures, allows a more complete depiction of the poten tial respiratory health effects of pollutants.

NAM further contends that Korrick et al. (1998) uses a nonstandard measure of incremental change (% per 50-100 ppb O 3 ) that is too large to ha ve any practical utility for making policy decisions ove r small exposure ranges. EPA disagrees with this

contention as these effect estimates can be st andardized to any incremental change based on the linear concentration-response function. Discussion of this approach can be found

in section 7.1.3.2 of the Criteria Docu ment (Criteria Document, p. 7-10).49 (17) Comment: With regard to evidence of O 3 -related mortality, many commenters, including those that argued for revising the current O 3 standard as well as those that argued against revisions, focused on the new evidence from multi-city time-series analyses and metaanalyses linking O 3 exposure with mortality. Agai n, sharply divergent comments were received. One group of commenters, includi ng medical, public health, and environmental organizations argued that recent published rese arch has provided more robust, consistent evidence linking O 3 to cardiovascular and respirator y mortality. The ATS, AMA, and others stated that data from single-city studies, multiple-city studies, and meta-analyses show a consistent relationship between O 3 exposure and mortality from respiratory and

cardiovascular causes. These commenters noted that this effect was observed after controlling for co-pollutants and seasonal im pacts. These commenters stated that research has demonstrated that exposure to O 3 pollution is causing premature deaths, and has also provided clues on the possible mechanisms that lead to premature mortality (ATS, p. 4). These commenters noted that people may die from O 3 exposure even when

the concentrations are well belo w the current standard. They pointed to a study (Bell et al., 2006) in which the authors followed up on their 2004 multi-city study to estimate the exposure-response curve for O 3 and the risk of mortality and to evaluate whether a

threshold exists below which there is no eff ect. The authors applied several statistical models to data on air pollution, weather, a nd mortality for 98 U.S. urban communities for the period 1987 to 2000. The study reported that O 3 and mortality results did not appear to be confounded by temperature or PM and showed that any threshold, if it existed, would have to be at very low concentrations , far below the current standard (ALA et al., p. 74). Another approach also indicated that the mortality effect is unlikely to be confounded by temperature. A case-crossove r study (Schwartz 2005) of over one million deaths in 14 U.S. cities, designed to control for the effect of temperature on daily deaths

attributable to O 3 , found that the association between O 3 and mortality risk reported in the multi-city studies is unlikely to be due to confounding by temperature (ALA et al., p. 76). These commenters argue that meta-analyses also provide compelling evidence that the

O 3 -mortality findings are consistent. They poi nt to three independent analyses conducted by separate research groups at Johns Hopki ns University, Harvard University and New York University, using their own met hods and study criteria, which reported a remarkably consistent link between daily O 3 levels and total mortality.

Response: In response, EPA notes that the Criteri a Document states that the results from the U.S. multi-city time-series studies provi de the strongest evidence to date for O 3 effects on acute mortality. Recent meta-analyses also indicate positive risk estimates that are unlikely to be confounded by PM; however , future work is needed to better understand the influence of model specificati ons on the risk coefficient (EPA, 2006a, p. 7-175). The Criteria Document concludes that these findings are hi ghly suggestive that

short-term O 3 exposure directly or indirectly contributes to non-accidental and cardiorespiratory-related mortality but that a dditional research is needed to more fully establish the underlying mechanisms by which such effects occur (72 FR 37836). Thus while EPA generally agrees with the dire ction of the comment, EPA believes the evidence supports a view as noted above. In addition, it must be noted that the Administrator did not focus on mortality as a basis for proposing that the current O 350 standard was not adequate or on determining th e appropriate level of the standard. In the proposal, the Administrator focused on the very strong evidence of respiratory morbidity effects in healthy people at the 0.080 ppm exposure level a nd new evidence that people with asthma are likely to experience larger and more serious effects than healthy people at the same level of exposu re and evidence that epidemiological studies indicated an

association with health effects at the current level of the standard (72 FR 37870). With regard to the ambient concentrations at which O 3 -related mortality effects may be occurring, EPA recognized in the proposal that evidence of a causal relationship between

adverse health effects and O 3 exposures becomes increasingly uncertain at lower levels of exposure (72 FR 37880). This is discussed more fully in other sections.

(18) Comment: Another group of comme nters, including severa l industry organizations argued against placing any reliance on the time -series epidemiological studies, especially

those studies related to mortal ity effects. The Annapolis Center (p. 46) makes the point that although there may be somewhat mo re positive associations than negative associations, there is so much noise or variability in the data that identifying which positive associations may be real health effects and which are not is beyond the capability of current methods. They cite the view th at the CASAC Panel expressed in a June 2006 letter (Henderson, 2006b), noting that “Because re sults of time-series studies implicate all of the criteria pollutants, findings of mortalit y time-series studies do not seem to allow us to confidently attribute observed effects specifically to individual pollutants.”

Several of these commenters focused on the O 3 mortality multi-city studies in particular, arguing that, although these studies have the statistical power to distinguish weak relationships between daily O 3 and mortality, they do not pr ovide reliable or consistent evidence implicating O 3 exposures as a cause of mortal ity. Several reasons were given, including: (a) the multi-city studies cited by EPA involve a wide ra nge of city-specific effects estimates, including some large cities th at have very slight or negligible effects (e.g., Los Angeles) (Bell et al., 2004), thus causing several commenters to question the

relevance of a “national” effect of O 3 on mortality and argue that a single national O 3 concentration-mortality coefficient should be used and interpreted with caution (Rochester Report p. 4); (b) the multi-city mo rtality studies did not sufficiently account for other pollutants, for example, Bell et al. (2004) adjusted for PM 10 but did not have the necessary air quality data to adequately adjust for PM 2.5 , which EPA has concluded also causes mortality and is correlated with O 3 , especially in the summer months (Annapolis Center, p. 42); and (c) these studies contain several finding s that are inconsistent or implausible, such as premature mortality report ed at such low levels as to imply that O 3 - related mortality is occurring at levels well within natural ba ckground, which is not biologically plausible (A nnapolis Center, p. 42).

Response: Evidence supporting an associ ation between short-term O 3 exposure and premature mortality is not limited to multi-c ity time-series studies. Most single-city

studies show elevated risk of total, non-acciden tal mortality, cardiorespiratory, and respiratory mortality (> 20 st udies), including one study in an area that would have met current standard (Vedal et al ., 2003). Three large meta-analyses, which pool data from many single-city studies to increase statisti cal power, reported st atistically significant

associations and examined sources of hetero geneity in those associ ations (Bell et al.,51 2005; Ito et al., 2005; Levy et al. 2005). These studies f ound: (1) larger and more significant effects in the warm season than in the cool season or all year; (2) no strong evidence of confounding by PM; and (3) suggest ive evidence of publication bias, but significant associations remain even af ter adjustment for the publication bias.

In the letter cited, the CASAC Panel did raise the issue of the utility of time-series studies in the standard setting process with regard to time-series mortality studies. Nevertheless, in a subsequent letter to the Administrato r, CASAC noted these mortality studies as evidence to support a recommendation to revise the current primary O 3 standard. “Several new single-city studies and large multi-city studies desi gned specifically to examine the effects of ozone and other pollutants on both morbidity and mortality have provided more evidence for adverse health e ffects at concentrations lower than the current standard (Henderson, 2006c, p. 3).”

With regard to the specific issues raised in the comments as to why the times-series mortality studies do not provi de reliable or consistent evidence implicating O 3 exposure as a cause of mortality, EPA has the following responses:

(1) The purpose of the NMMAPS approach is no t to single out indivi dual city results but rather to estimate the overall effect from the 95 communities. It was designed to provide a general, nationwide estimate. With regard to the very slight or negligible effects estimates for some large cities (e.g., Los Angeles) , an important factor to consider is that the Bell et al. (2004) study used all available data in their an alyses. Bell et al. reported

that the effect estimate for all available (including 55 cities with all year data) and warm season (April-October) analyses for the 95 U. S. cities were similar in magnitude; however, in most other studies , larger excess mortality risk s were reported in the summer season (generally June-August when O 3 concentrations are the highest) compared to all year or the cold season. Though the effect es timate for Los Angeles is small compared to some of the other communities, it should be not ed that all year data (combined warm and cool seasons) was used in the analyses for th is city, which likely resulted in a smaller effect estimate. Because all year data was used for Los Angeles, the median O 3 concentration for Los Angeles is fairly low compared to the other communities, ranked 23rd out of 95 communities. The median 24-hour average O 3 concentration for Los Angeles in this dataset was 22 ppb, with a 10 th percentile of 8 ppb to a 90 th percentile of 38 ppb. The importance of seasonal differences in O 3 -related health outcomes has been

well documented.

(2) In section 7.4.6, O 3 mortality risk estimates adjusti ng for PM exposure, the Criteria

Document states that the main confounders of interest for O 3 , especially for the northeast U.S., are “summer haze-type” pollutants such as acid aerosols and sulfates. Since very few studies included these chemical measurements, PM (especially PM 2.5 ) data, may serve as surrogates. However, due to the expected high correlation among the constituents of the “summer haze mix,” multi pollutant models including these pollutants may result in unstable coefficients; and, therefor e, interpretation of su ch results requires

some caution.52 In section 7.4.6 of the Criteria Document, Figure 7-22 shows the O 3 risk estimates with and without adjustment for PM indices using all-year data in studi es that conducted twopollutant analyses. Approximately half of the O 3 risk estimates increased slightly,

whereas the other half decreased slightly with the inclusion of PM in the models. In general, the O 3 mortality risk estimates were robust to adjustment for PM in the models.

The U.S. 95 communities study by Bell et al. (2 004) examined the sensitivity of acute O 3 - mortality effects to potential confounding by PM 10 . Restricting analysis to days when

both O 3 and PM 10 data were available, the community-specific O 3 -mortality effect

estimates as well as the national average results indicated that O 3 was robust to adjustment for PM 10 (Bell et al., 2004). As commenters noted, there were insufficient data available to examine potential confounding by PM 2.5 . One study (Lipfert et al., 2000) reported O 3 risk estimates with and without adju stment for sulfate, a component of

PM 2.5 . Lipfert et al. (2000a) calculated O 3 risk estimates based on mean (45 ppb) less background (not stated) le vels of 1-hour max O 3 in seven counties in Pennsylvania and New Jersey. The O 3 risk estimate was not substantially affected by the addition of sulfate in the model (3.2% versus 3.0% with sulfate) and remained statistically significant.

Several O 3 mortality studies examined the eff ect of confounding by PM indices in different seasons (Figure 7-23, section 7.4.6, Crit eria Document). In analyses using allyear data and warm-season only data, O 3 risk estimates were once again fairly robust to adjustment for PM indices, with values show ing both slight increases and decreases with

the inclusion of PM in the model. In th e analyses using cool season data only, the O 3 risk estimates all increased slightly with the ad justment of PM indices, although none reached statistical significance.

The three recent meta-analyse s (Bell et al., 2005; Ito et al ., 2005; Levy et al. 2005) all

examined the influence of PM on O 3 risk estimates. No substantial influence was observed in any of these studies. In the analysis by Bell et al. (2005), the combined estimate without PM adjustment was 1.75% (95% PI: 1.10, 2.37) from 41 estimates, and the combined estimate with PM adjustment was 1.95% (95% PI:

- 0.06, 4.00) from 11 estimates per 20 ppb increas e in 24-hour average O 3 . In the meta-analysis of 15 cities by Ito et al. (2005), the combined estimate wa s 1.6% (95% CI: 1.1, 2.2) and 1.5% (95% CI: 0.8, 2.2) per 20 ppb in 24-hour average O 3 without and with PM adjustment, respectively. The additional time-series analysis of six ci ties by Ito et al. found that the influence of PM by season varied across alternative weathe r models but was never substantial. Levy et al. (2005) examined the regr ession relationships between O 3 and PM indices (PM 10 and

PM 2.5 ) with O 3 -mortality effect estimates for all year and by season. Positive slopes, which might indicate potential confounding, were observed for PM 2.5 on O 3 risk estimates in the summer and all-year periods, but the relationships we re weak. The effect of one causal variable (i.e., O 3 ) is expected to be overestimated when a second causal variable (e.g., PM) is excluded from the analysis, if the two variables are positively

correlated and act in the same direction. Howe ver, EPA notes that the results from these meta-analyses, as well as several single- and multiple-city studies, indicate that copollutants, including PM, generally do not appear to substa ntially confound the

association between O 3 and mortality.53 (3) Moreover, EPA asserts that the biologi cal plausibility of the epidemiological mortality associations is generally supported by controlled human exposure and toxicological evidence of resp iratory morbidity effects for levels at and below 0.080 ppm, but that biological plausibility becomes increasingly uncertain especially below 0.060 ppm, the lowest level at which effects were observed in controlled human exposure studies. Further, at lower levels, it beco mes increasingly uncertain as to whether the reported associations are related to O 3 alone rather than to the broader mix of air pollutants present in the ambient air. EPA not es that the multi-city times series studies

evaluated in this review can not resolve this issue. It also becomes increasingly uncertain

as to whether effect thres holds exist but can not be cl early discerned by statistical analyses. Thus, when considering the epid emiological evidence in light of the other available information, it is reasonable to judge that at some poin t the epidemiological associations can not be interpreted with confidence as providing evidence that the

observed health effects can be attributed to O 3 alone.

(19) Comment: NAM contends that EPA assumes that associations observed in time-series studies are significant but the ab sence of associations in long- term cohort studies is not.

NAM states that EPA arrives at the conclusion that “ozone ca uses premature mortality in

the short-term that cannot be observed over th e long-term” by “leap of faith, not scientific inference” (NAM, p.50)

Response: EPA rejects NAM’s contention that it has reached inappropriate conclusions

about associations between O 3 exposure and premature mo rtality. In the Criteria Document, EPA presented numerous recent ep idemiologic studies conducted in the

United States and abroad which have invest igated the association between short-term exposure to O 3 and mortality. Results from several la rge U.S. multicity studies as well as several single-city studies indicated a positive association between increases in ambient

O 3 levels and excess risk of all-cause (nonaccidental) dail y mortality. Newly available experimental data from both animal and hum an studies provide evidence suggestive of plausible pathways by which risk of respiratory or cardiovascular morbidity and mortality could be increased by ambient O 3 either acting alone or in combination with copollutants in ambient air mixes. These overall findings led EPA to conclude that there is highly suggestive evidence that O 3 directly or indirectly c ontributes to non-accidental and cardiopulmonary-related mortality, but additi onal research is needed to more fully establish underlying mechanisms by which such effects occur. As few epidemiologic

studies were available on long-term exposure to O 3 and mortality, and the results from these studies were not consistent, EPA furt her concluded that there was insufficient evidence to suggest a causal re lationship between long-term O 3 exposure and increased risk for mortality in humans.

Kunzli et al. (2001) state th at air pollution may play a role both in increasing the decedent’s underlying susceptibility or frailt y and in triggering the event. In another case, the underlying frailty may be related to long term air pollution, but the event or the

occurrence of death itself is unrelated to the le vels of air pollution shortly before death. In the third case, reduced health status or fr ailty is not related to air pollution, but ambient54 air pollution experienced before death may tr igger the terminal event. Thus, mortality from long-term exposure to a pollutant is not simply the accumulation of mortality from short-term exposures. Different mechanisms are at play for mortality associated with short-term versus long-term e xposures; therefore, the inabilit y to assess causality of the effect of long-term O 3 exposure on mortality does not have bearing on the EPA’s finding that there is highly suggestive evid ence that short-term exposure to O 3 contributes to mortality.

Further, in a letter to the Administrato r, CASAC noted these mortality studies as evidence to support a recommendation to revise the current primary O 3 standard. “Several new single-city studies and large multi-city studies desi gned specifically to examine the effects of ozone and other pollutants on both morbidity and mortality have provided more evidence for adverse health e ffects at concentrations lower than the current standard” (Henderson, 2006c, p. 3).

(20) Comment: NAM contends that EPA characterizes in the proposal notice that results from “numerous” multi-city and single-city studies show that the association between O 3 and mortality do not appear to be change d in multipollutant models including PM 10 or PM 2.5 (72 FR 37839). NAM contends that these studies are NMMAPS st udies, none of which has daily PM 2.5 data. These associations “do not appe ar to be changed” because they only

measure PM 10 (NAM, pp. 21).

Response: EPA disagrees with NAM’s characteri zation of the basis for the statements made in the proposal notice with respect to what the scientific evidence shows with respect to the influence of PM in aff ecting the relationship observed between O 3 and mortality. NAM mistakenly states that the conclusion in the propos al notice was solely based on results of the NMMAPS; in fact, it is based on the results of many other studies as presented in Figures 7-22 and 7-23 in section 7.4.6 of the Cr iteria Document. The

studies used different PM indices, including PM 2.5 , PM 10 , BS, as well as TSP, to adjust for potential confounding by PM of the O 3 relationship with mortality. Furthermore, while not relying on “new” studies published since completion of the Criteria Document, EPA notes that specifically in response to the use of PM 10 by NMMAPS, a recently published study (not included in the Criteria Document) by Be ll et al. (2007) reported that the national and community-specific effect estimates of the shor t-term effects of O 3 on mortality were robus t to inclusion of PM 10 or PM 2.5 in time-series models.

(21) Comment: NAM contends that EPA has misinter preted two epidemiologic studies by Moolgavkar and colleagues (1995; 2000) in EPA’s risk assessment and that EPA’s interpretation is different than that of the pr imary author and states that “EPA represents the results of these studies in ways that the corresponding author says are says are incorrect (Moolgavkar 2007, 4-5)” (NAM, p.21).

Response: EPA disagrees with NAM’s contention that it has interpreted the two cited studies by Moolgavkar differently than the primary author. Mool gavkar (2007) on pages 4 and 5 states that EPA included the positiv e association that he reported in his 1995 Philadelphia paper but that EPA failed to ci te his 2000 study in Los Angeles. EPA notes55 that there is nothing on pp. 4- 5 of Moolgavkar that supports NAM’s contention that EPA has interpreted these two studies in a way different than the primary author. Furthermore,

there is no discussion of EPA’s risk assessmen t or the use of Moolgavkar’s studies in the risk assessment on pp.4-5 of the Moolgavkar (2007) document.

(22) Comment: Many commenters identified “new” studi es that were not included in the Criteria Document that they st ated support arguments both for and against the revision of

the current O 3 standard. Commenters who s upported revising the current O 3 standard

identified new studies that generally supported EPA’s conclu sions about the associations

between O 3 exposure and a range of respiratory and cardiovascu lar health outcomes.

These commenters also identified new studies that provide evidence for associations with

health outcomes that EPA has not linked to O 3 exposure, such as cancer, and populations

that EPA has not identified as bei ng susceptible or vulnerable to O 3 exposure, including

African-American and women. Commenters wh o did not support revision of the current

O 3 standard often submitted the same “new” st udies, but focused on different aspects of the findings. Commenters who did no t support revision of the current O 3 standard stated that these “new” studies provide inconsiste nt and sometimes conflicting findings that do little to resolve uncertainties regarding whether O 3 has a causal role in the reported associations with adverse health outcomes, including premature mortality and various morbidity outcomes.

Response: To the extent that these commenters included “new” scientific studies, studies that were published too late to be considered in the Criteria Docume nt, in support of their arguments for revising or not revising the sta ndards, EPA notes, as discussed in section II of the preamble to the final rule, that as in past NAAQS reviews, it is basing the final

decisions in this review on the studies and related information included in the O 3 air quality criteria that have undergone CASAC and public review and will consider newly published studies for purposes of decision making in the next O 3 NAAQS review. In provisionally evaluating commenters’ argum ents, EPA notes that its provisional

consideration of “new” science found that su ch studies did not materially change the

conclusions in the Criteria Document. Fo r more information about this provisional consideration see the Appendix.

(23) Comment: NAM contends that EPA displays a systematic preference for studies that show positive associations even among studies that have important information quality limitations (NAM, pp. 30-31). NAM asserts th at it has been unable to identify any epidemiological studies that EPA has identifi ed as dispositive but which did not find a positive association. NAM claims that EPA “consistently selects studies that show positive associations with ozone (e.g., Gent et al., 2003; Mortimer et al., 2002) over studies that do not (e.g., Schild crout et al., 2006) but does not establish an information quality basis for its selections” (NAM, p. 30).

Responses: EPA rejects NAM’s contention that it displays a systematic preference for studies that show positive associations. EPA has clearly presented the results of Mortimer et al. (2002) and Gent et al. (2003), including results that were not positive. EPA has described studies that do not report posit ive or statistically significant results.56 The reason that NAM is unable to find a ny epidemiological studies that EPA has identified as dispositive but which did not find a positive association is that there is no single study or group of studies th at is “dispositive.” EPA asse rts that this would be an inappropriate way to repres ent the entire body of evidence. EPA uses a weight of evidence approach that integrates evidence fr om different types of studies including: animal toxicology; controlled human e xposure; and epidemiological studies.

Schildcrout et al. (2006) is not included in the Criteria Do cument as it was published after the date specified for inclusion (new studies accepted for publication by December 2004). In fact, it was published on-line in June of 2006, after the Criteria Document had been finalized. As noted above, EPA is basing the final decisions in this review on the studies

and related information included in the O 3 air quality criteria that have undergone CASAC and public review and will consider the newly published studies for purposes of decision making in the next O 3 NAAQS review. This study has not been relied upon as it

is one of the “new” studies that have been published since the cutoff date.

NAM cites only the Schildcrout study to s upport its claim that “EPA’s risk assessment for ozone includes a large measure of study sel ection bias” (NAM, p. 31). In fact, clearly

the converse is true. EPA’s evaluation of th e scientific evidence has been rigorous and thorough, and the process for selec tion of studies for inclusion in the assessment has been transparent and subject to review by the CASAC and the public.

c. Evidence Pertaining to At-Risk Subgroups for O 3 -Related Effects

This section contains major comments on EPA’s assessment of the body of evidence, including controlled human expos ure and epidemiological studies, related to the effects of O 3 exposure on sensitive subpopulations . Since new information about the increased responsiveness of people with lung disease, especially childre n and adults with asthma, was an important

consideration in the Administrator’s proposed decision that the current O 3 standard is not adequate, many of the comments focused on this in formation and the conclusions drawn from it. There were also comments on other sensitive gr oups identified by EPA, as well as comments suggesting that additional groups should be considered at increased risk from O 3 exposure. As with the comments on controlled human expos ure and epidemiological studies, upon which judgments about sensitive subpopulations were based, the comments about EPA’s delineation of these groups were hi ghly polarized.

(1) Comment: In general, one group of commenter s who supported revising the current O 3 primary standard, including medical associ ations, public health and environmental groups, agreed in part with EPA’s assessment of the subpopulations th at are at increased

risk from O 3 exposure, but commented that there ar e additional groups that need to be

considered. A comment fr om ATS, AMA and other me dical associations noted:

Within this population exists a number of individuals uniquely at much higher

risk for adverse health effects from ozone exposures, including children, people57 with respiratory illness, the elderly, outdoor worker s and healthy children and adults who exercise outdoors. (ATS, p. 2)

These commenters agreed with EPA that, based on evidence from controlled human exposure and epidemiology studies, people with asthma, especially children, are likely to have greater lung function decrements and respiratory symptoms in response to O 3 exposure than people who do not have asthma, a nd are likely to respond at lower levels. Because of this, these commenters make the point that controlled human exposure studies that employ healthy subjects will underestimate the effects of O 3 exposures in people

with asthma.

These commenters also agreed with EPA’ s assessment that epidemiological studies provide evidence of increased morbidity e ffects, including lung function decrements, respiratory symptoms, emergency department visits and hospital admissions, in people with asthma and that controlled human expos ure studies provide biological plausibility for these morbidity outcomes. Further, the Ro chester Report evaluated some of the same

the studies that EPA did and found similar results with regard to the increased inflammatory responses and increased airw ay responsiveness of people with asthma when exposed to O 3 . The Rochester Report reached the same conclusion that EPA did, that this increased responsiveness provides bi ological plausibility for the respiratory morbidity effects found in epidemiological studies.

Several new studies have demonstrated th at exposure of individuals with atopic asthma to sufficient levels of ozone produces an increase in specific airway responsiveness to inhaled allergens.........These findings, in combination with previously observed effects of ozone on nonspecific airway responsiveness and airway inflammation, supports the idea that ambient ozone exposure could result in exacerbation of asthma several days following exposure, and provides biological plausibility fo r the epidemiologic studie s in which ambient ozone

concentration has been associated with increased asthma symptoms, medication use, emergency room visits, and hospitaliz ations for asthma. (Rochester Report, pp. 57-58)

Commenters also often mentioned the increas ed susceptibility of people with COPD and

in this case cited “new” studies not c onsidered in the Criteria Document.

They identify that one potentially suscep tible subpopulation that EPA did not focus on in the proposal is infants. Commenters from medical associations, and environmental and public health groups expr essed the view that O 3 exposure can have important effects on infants, including reduced birth weight, pr e-term birth, and increased respiratory morbidity effects in infants. Exposure to O 3 during pregnancy, es pecially during the second and third trimesters, was associated with reduced birth weight in full-term infants. Although this effect was noted at relatively low O 3 exposure levels, the ATS notes that, “...the reduced birth weight in infants in the highest ozone exposures communities equaled the reduced birth weight observed in pregnant women who smoke” (ATS, p. 7).58 Response: In general, EPA agrees with comments that there is very strong evidence from controlled human exposure and epidemiological studies that people with lung disease, especially children and adults wi th asthma, are susceptible to O 3 exposure and are likely to experience more serious effects than those people who do not have lung disease. This means that controlled human exposure studie s that employ subjects who do not have lung disease will likely underestimate effects in thos e people that do have asthma or other lung

diseases.

In summarizing the epidemiological evidence re lated to birth-related health outcomes, the Criteria Document (p. 7-133) concludes that O 3 was not an important predictor of several birth-related outcomes including premature birt hs and low birth weig ht. Birth-related outcomes generally appeared to be associated wi th air pollutants that tend to peak in the winter and are possibly traffic-related. However, given th at most of these studies did not analyze the data by season, seasonal confoundi ng may have therefore influenced the reported associations. One study reported some results suggestive of associations between exposures to O 3 in the second month of pregnanc y and birth defects, but further evaluation of such potential associations is needed. With regard to comments about effect in infants, EPA notes that some of the studies cited by commenters were “new”

studies too late for inclusion in the Criteria Document and thus were not considered in the

Criteria Document.

(2) Comment: The second group of commenters, mostly representing industry associations and some businesses opposed to revising the primary O 3 standard, asserted that EPA is wrong to claim that new evidence indicates th at the current standard does not provide adequate health public health protection for people with asthma. In support of this position, these commenters made the followi ng major comments: (1) lung function decrements and respiratory symptoms observe d in controlled human exposure studies of asthmatics are not clinically important; (2) EPA postulates that asthmatics would likely experience more serious responses and responses at lower levels than the subjects of controlled human exposure experi ments, but that hypothesis is not supported by scientific evidence; and, (3) EPA recognized asthmatic s as a sensitive s ubpopulation in 1997, and new information does not suggest greater sus ceptibility than was previously believed.

With regard to the first point, these commenters expressed the view that asthmatics are not likely to experience medically significan t lung function changes or respiratory symptoms at ambient O 3 concentrations at or even above the level of the cu rrent standard. Many of these commenters cited the opinion of one physician who was asked on behalf of a group of trade associations and comp anies to provide his views on the health significance for asthmatics of the types of respon ses that have been reported in controlled human exposure studies of O 3 . This commenter (McFadden) reviewed controlled human exposure studies of asthmatics from the last review as well as the recent controlled human exposure studies of healthy indi viduals (Adams 2002, 2003, and 2006) at 0.12, 0.08, 0.06, and 0.04 ppm and expressed the view that “...these studies on asthmatics indicate that ozone exposures at ~ 0.12 ppm do not produce medically significant functional changes and are right around the in flection point where one begins to see an increase in symptoms; however, that incr ease is small” (McFadden, p. 3). This59 commenter went on to express the view that responses to O 3 exposure at levels < 0 .08 ppm would be even less and that the available data are not su fficiently robust to indicate that such exposures would present a significant health concern even to sensitive people

like asthmatics.

With regard to the third point, commenters no te that there is no si gnificant new evidence establishing greater risk to asthmatics than was accepted in 1997, when EPA concluded that the existing NAAQS was sufficiently string ent to protect public health – including asthmatics – with and adequate margin of safety (UARG, pp. 22-23). To support this view, these commenters note the points made above, that the effects of O 3 at and below 0.080 ppm are not clinically significant and th at asthmatics do not have more serious responses and responses at lower levels. They also express the view that epidemiological studies of asthmatics that provide new evid ence of respiratory symptoms and medication use in asthmatic children are subject to th e limitations of epidemiological studies discussed above (e.g., confounding by co-pollutants, and heter ogeneity of results). In addition, these commenters identified a new, large multi-city panel study not included in the Criteria Document, by Schildcrout et al. (2006), which reported no association

between O 3 concentrations and exacerbation of asthma.

Response: With regard to the first point, EP A notes that this commenter based his comment on the group mean functional and resp iratory symptom changes in the studies he reviewed. EPA agrees that group mean chan ges at these levels ar e relatively small and has described them as such in both the prev ious review and this one (72 FR 37828). The importance of group mean changes is to eval uate the statistical significance of the association between the exposur es and the observed effects, to try to determine if the observed effects are likely due to O 3 exposure rather than chance. In the previous review as well as in this one, EPA has also focused on the fact that some individuals experience more severe effects that may be clinically si gnificant. With regard to the significance of individual responses, this commenter (McFadde n, p. 2) states “...transient decreases in

FEV 1 of 10-20% are not by themselves significan t or meaningful to asthmatics.... It has been my experience from examining and studyi ng thousands of patients for both clinical and research purposes that asthmatics typically will not begin to sense

bronchoconstriction until their FEV 1 falls about 50% from normal.” EPA strongly disagrees with this assessment. As stated in the Criteria Document (Table 8-3, p. 8-68) for people with lung disease, even moderate functional responses (e.g., FEV 1 decrements

≥ 10% but < 20%) would likely interfere with normal activities for many individuals, and would likely result in more fr equent medication use. EPA not es that in the context of standard setting, CASAC indicated (Henders on, 2006c) that a focus on the lower end of the range of moderate func tional responses (e.g., FEV 1 decrements ≥ 10%) is most appropriate for estimating potentially advers e lung function decrem ents in people with lung disease.

With regard to the second point, whether asthmatics would likely experience more serious responses and responses at lower levels than the subjects of controlled human exposure experiments and EPA’s discussion of the relationship of increased airway responsiveness and inflammation experienced by asthmatics to exacerbation of asthma,60 this commenter stated that “there simply ar e no data to support th e sequence described” and that “the assumption that these responses would lead to clinical manifestations in

terms of exacerbations of asthma or othe r adverse health effects remains unproven theory”(McFadden, p. 3). In the proposal (72 FR 37826, and 37846-37847), EPA describes the evidence that people with asthma are as sensitive as, if not more sensitive than, normal subjects in manifesting O 3 -induced pulmonary function decrements. Controlled human exposure studies show that asthmatics present a differential response profile for cellular, molecular, and biochemical parameters that are altered in response to

acute O 3 exposure. Asthmatics have greater O 3 -induced inflammatory responses and

increased O 3 -induced airway responsiveness (both incidence and duration) that could have important clinical implications.

There are two ways to interpret these comments. One way to interpret them is that because these controlled human exposure stud ies have not produced exacerbations of asthma in study subjects resul ting in the need for medical a ttention, there are no data to support the clinical sign ificance of the results. EPA rej ects this interpre tation because it would be unethical to knowingly conduct a controlled human exposure study that would

lead to exacerbation of asthma. Controll ed human exposure studies are specifically designed to avoid these types of responses . The other interpretation is that the commenter does not agree that the differe nces in lung function, inflammation and increased airway responsiveness found in these controlled hu man exposure studies support the inference that asthmatics are like ly to have more serious responses than healthy subjects, and that these responses c ould have important clinical implications. EPA rejects this interpretation as well. EPA did not base its increased concern for asthmatics solely on the results of the c ontrolled human exposur e studies, but has appropriately used a weight of evidence a pproach, integrating evidence from animal toxicological, controlled huma n exposure and epidemiological studies as a basis for this

concern. The Criteria Document evaluated a nu mber of epidemiological studies that have been conducted using asthmatic study populatio ns (72 FR 37847). These studies suggest

that O 3 exposure may be associated with incr eased respiratory symp toms and medication use in children with asthma, and also resp iratory symptoms, lung function decrements, emergency department visits and hospita l admissions for respiratory causes and respiratory mortality. The Criteria Document concludes that the positive and robust epidemiological associations between O 3 exposure and emergency department visits and hospitalizations in the warm season are supported by the human clinical, animal toxicological and epidemiological eviden ce for lung function decrements, increased respiratory symptoms, airway inflammation, a nd increased airway responsiveness (72 FR 37832). The CASAC Panel itself expressed the view that people with asthma, especially children, have been found to be more sensitive to O 3 exposure, and indicated that EPA should place more weight on inflammatory res ponses and serious morbidity effects, such as increased respiratory-related emergenc y department visits and hospitalizations (Henderson, p. 4). Moreover, the Rochester Report, cited above, reaches essentially the same conclusions as EPA did, that the eviden ce from controlled human exposure studies provides biological plausibility for the ep idemiological studies in which ambient O 3 concentrations have been associated with increased asthma symptoms, medication use, emergency room visits, and hospitalizations for asthma. Therefore, EPA continues to61 assert that there is strong evidence that asthmatics likely ha ve more serious responses to

O 3 exposure than people without asthma, and th at these responses have the potential to

lead to exacerbation of asthma as indicated by the serious morbidity effects, such as increased respiratory-related emergency depa rtment visits and hos pitalizations found in epidemiological studies.

With regard to the third point, at the time of the last review EPA concluded that people with asthma were at greater risk because the impact of O 3 -induced responses on alreadycompromised respiratory systems would noticeab ly impair an individual's ability to engage in normal activity or would be more likely to result in increased self-medication

or medical treatment. At that time there was little evidence that pe ople with pre-existing disease were more responsive than healthy individuals in terms of the magnitude of pulmonary function decrements or sympto matic responses. The new results from controlled exposure and epidemio logic studies indicate that individuals w ith preexisting lung disease, especially people with asthma, are likely to have more serious responses than people who do not have lung disease a nd therefore are at greater risk for O 3 health effects than previously judged in the 1997 review. EPA notes that comments on the limitations of epidemiological studies and th e evidence from “new” studies (not in the Criteria Document) have b een addressed above.

d. Adversity of Health Effects

This section contains comments on EP A’s assessment of the body of evidence particularly related to judgments about the adve rsity of the health effects associated with O 3 exposure, primarily estimates of mo derate lung function decrements (FEV 1 decrements ≥ 10%) from controlled human exposure studies.

(1) Comment: NAM contends that there is no consen sus concerning where to draw the line distinguishing adverse from non-adverse effects, such as effects that are transient and reversible over short periods of time.

NAM contends that EPA increasingly treats as adverse mere exposure and that when exposure cannot be detected, EPA increasi ngly looks for biomarkers of exposure - irrespective of whether they ar e associated with symptoms or signs; their selectivity with respect to the hazard of concern; or the capac ity to detect them without complex analytic techniques. As an example of this, the co mmenter points to the definition of a “key event” in EPA’s Guidelines of Carcinogenic Risk Assessment. A “key event” is an empirically observable precursor step that is itself a necessary element of the mode of action or is a biologically based marker for such an element. The term “mode of action” is defined as a sequence of key events and pro cesses, starting with interaction of an agent with a cell, proceeding through operational a nd anatomical changes, and resulting in

cancer formation. The scientific task is a very limited one, consisting only of the assignment of phenomena into categories defined by policy. Commenter notes that information quality guidelines require that th e Agency be transparent in its scientific description of these phenomena and the available data.62 NAM contends that this same problem infects EPA’s description of effects to asthmatics. Transient and reversible effects, such as chest tightness or wheezing, have a dozen reported triggers, including laughter. How similar are the effects of O 3 to the effects caused by exposure to humor? (NAM, p. 42)

Response: EPA strongly rejects NAM’s assert ion that there is no consensus in distinguishing adverse from non-adverse effect s, with regard to the Administrator’s judgments as to when O 3 -related effects become regarded as adverse to the health of individuals. Evaluating the a dversity of health effects in individuals and the resulting impacts on public health is a main focus of all NAAQS reviews. The issue of adversity was clearly addressed in this review and the judgments a bout adversity are consistent with the previous review. In this review, as in the 1997 review of the O 3 standard, the Administrator has looked to guidelines pub lished by ATS and the advice of the CASAC panel. While recognizing that perceptions of “medical signif icance” and “normal activity” may differ among physicians, lung physio logists and experimental subjects, the ATS (1985) 4 defined adverse respiratory health effects as “medically significant physiologic changes generally evidenced by one or more of the following: (1) interference with the normal activity of th e affected person or persons, (2) episodic respiratory illness, (3) incapacitating illness, (4) permanent respiratory injury, and/or (5) progressive respiratory dysf unction.” During the 1997 review, it was concluded that

there was evidence of causal associations from controlled human exposure studies for

effects in the first of these five ATS-de fined categories, evidence of statistically significant associations from epidemiological studies for effects in the second and third categories, and evidence from animal toxicol ogy studies, which could be extrapolated to humans only with a significant degree of uncertainty, for the last two categories.

For ethical reasons, clear causa l evidence from controlled human exposure studies still covers only effects in the first category. Ho wever, for this review there are results from epidemiological studies, upon which to base j udgments about adversity, for effects in all of the categories. Statistically significant a nd robust associations have been reported in epidemiology studies falling into the second and third categories. These more serious effects include respiratory events (e.g., tr iggering asthma attacks) that may require medication (e.g., asthma), but not necessarily hospitalization, as well as respiratory hospital admissions and emergency departme nt visits for respiratory causes.

Less conclusive, but still positive associations have been reported for school absences and cardiovascular hospital admissions. Huma n health effects for which associations have been suggested through evidence from epidemiological and animal toxicology

4 In 2000, the American Thoracic Society (ATS) published an official statement on “What

Constitutes an Adverse Health E ffect of Air Pollution?” (ATS , 2000), which updated its earlier guidance (ATS, 1985). Overall, the new guidance does not fundamentally change the approach previously taken to define a dversity, nor does it suggest a need at this time to change the

structure or content of the tabl es describing gradation of seve rity and adversity of effects

described below.63 studies, but have not been conclusively demonstr ated still fall primar ily into the last two categories. In the la st review of the O 3 standard, evidence for these more serious effects came from studies of effects in laboratory animals. Evidence from animal studies

evaluated in this Criteria Docu ment strongly suggests that O 3 is capable of damaging the distal airways and proximal alveoli, resu lting in lung tissue re modeling leading to apparently irreversible changes. Recent advancements of dosimetry modeling also provide a better basis for extr apolation from animals to humans. Information from epidemiological studies provides supporti ng, but limited evidence of irreversible respiratory effects in humans than was avai lable in the prior review. Moreover, the findings from single-city and multi-city tim e-series epidemiology studies and metaanalyses of these epidemiology studies are highly suggestive of an association between

short-term O 3 exposure and mortality particularly in the warm season.

While O 3 has been associated with effects that are clearly adverse, application of these guidelines, in particular to the least serious category of effects related to ambient O 3 exposures, involves judgments about which medical experts on the CASAC panel and public commenters have expressed diverse views in the past. It is these effects that are the focus of this comment, and have been an important focus in the current and the 1997 review of the primary O 3 standard. To help frame su ch judgments, EPA staff have defined specific ranges of functiona l responses (e.g., decrements in FEV 1 and airway responsiveness) and symptomatic responses (e.g., cough, chest pain, wheeze), together with judgments as to the potential impact on individuals experienci ng varying degrees of severity of these responses, that have been used in previous NAAQS reviews. These ranges of pulmonary responses and their asso ciated potential impacts are summarized in Tables 3-2 and 3-3 of the Staff Paper (EPA, 2007).

For active healthy people, moderate le vels of functional responses (e.g., FEV 1 decrements of > 10% but < 20%, lasting up to 24 hour s) and/or moderate symptomatic responses (e.g., frequent spont aneous cough, marked discomfort on exercise or deep breath, lasting up to 24 hours) would likely inte rfere with normal activity for relatively few responsive individuals. On the other hand, EPA staff determined that large functional responses (e.g., FEV 1 decrements > 20%, lasting longer th an 24 hours) and/or severe symptomatic responses (e.g., persiste nt uncontrollable cough, severe discomfort on exercise or deep breath, lasting longer than 24 hours) would likely interfere with normal activities for many responsive individu als. EPA staff determined that these would be considered adverse under ATS guidelines . In the context of standard setting, CASAC indicated that a focus on the mid to uppe r end of the range of moderate levels of functional responses (e.g., FEV 1 decrements ≥ 15% but < 20%) is appropriate for estimating potentially adverse lung function decrements in active healthy people. However, for people with lung disease, even moderate functional (e.g., FEV 1 decrements

> 10% but < 20%, lasting up to 24 hours) or symptomatic responses (e.g., frequent spontaneous cough, marked discomfort on exercise or with deep breath, wheeze accompanied by shortness of breath, lasting up to 24 hours) would likely interfere with normal activity for many individuals, and woul d likely result in more frequent use of medication. For people with lung disease, large functional responses (e.g., FEV 1 decrements > 20%, lasting longer than 24 hours) a nd/or severe symptomatic responses64 (e.g., persistent uncontrollable cough, severe discomfort on exercise or deep breath, persistent wheeze accompanied by shortness of breath, lasting longer than 24 hours) would likely interfere with normal activity fo r most individuals and would increase the

likelihood that these individuals would seek medi cal treatment. In the context of standard setting, the CASAC indicated (Henderson, 2006c) that a focu s on the lower end of the range of moderate levels of functional responses (e.g., FEV 1 decrements ≥ 10%) is most appropriate for estimating potentially advers e lung function decrem ents in people with lung disease. There is more discussion of th e focus on the lower end of moderate levels of functional responses (e.g., FEV 1 decrements ≥ 10%) in the next comment below.

In judging the extent to which these impacts re present effects that s hould be regarded as

adverse to the health status of individuals, an additional factor that has been considered in previous NAAQS reviews is whether such e ffects are experienced repeatedly during the course of a year or only on a single occasi on. While some experts would judge single occurrences of moderate respons es to be a “nuisance,” especi ally for healthy individuals, a more general consensus view of the advers ity of such moderate responses emerges as the frequency of occurrence increases. This is the reason that EPA focuses not only on single, but also on repeated occurrences of moderate lung function decrements in schoolage children.

As indicated by the discussion above and the additional discussions of adversity in the rationale for finding that the current standard needs revision and rationale for the level of the standard that is appropri ate, EPA has clearly addressed the issue of the adversity of

the transient and reversible effects attributable to O 3 exposure, specifically respiratory symptoms and lung function decrements, in bo th healthy people and people who have asthma. Moreover, EPA has evaluated the adve rsity of these effects in the context of daily activities. Its evaluation has been subjected to peer-review and supported by the

CASAC in both the 1997 and current reviews of the O 3 standard. In this review of the O 3 standard EPA has not evaluated the adversity of any biomarkers of exposure, so with regard to the discussion of biomarke rs the comment is not accurate.

(2) Comment: NAM contends that the 10% threshold for FEV 1 decrements is a post hoc threshold apparently chosen for compatibili ty with EPA staff policy recommendations in the Staff Paper. This threshold differs si gnificantly from the clinical thresholds recommended by the ATS (15%) and CASA C (15-20%). While EPA says CASAC agrees with its 10% threshold, there is “strong evidence sugges ting that any such agreement was at best a minority view based on policy considerations not science” (NAM, p.19). An individual CASAC panel member stated:

While most attributions to CASAC are correct, I don’t belie ve it was a written opinion of CASAC that “more emphasis shoul d be placed on numbers of subjects

in controlled human e xposure studies with FEV 1 decrements greater than 10%, which can be clinically significant, rather than on the relatively small decrements” (p. 6-43). While this may have merit in some (or even many) situation, for example when noting that 26% of indivi duals had > 10% FEV1 decrements at 0.08 ppm ..., in other cases, such as the specific case of 0.060 or 0.040 ppm exposures, this approach amounts to atte mpting to find effects in a very few65 individuals when the statistical tests ar e not significant, which is a dangerous precedent – especially in this case where we are looking at small effects in 3 of 30 vs. 1 of 30, a pitiful number on which to attempt to base policy ... (CASAC, 2007, C-30) (NAM, pp. 19-20)

NAM states that EPA did not correct the mi sstatement in the final Staff Paper on p.6-43.

Response: The focus on FEV 1 decrements ≥ 10% came up in the context of evaluation of the adversity of transient and reversible e ffects, as discussed in the comment above.

There was an extensive discussion of this topic at the August 24, 2006 meeting of the

CASAC O 3 Panel in Research Triangle Park, NC (see transcript p. 142-150). During the discussion of Chapter 3 of the Staff Paper, one of the CASAC Panel members noted that in Chapter 6 of the Staff Paper, EPA staff fo cused on the lower end of the moderate range (i.e., FEV 1 decrements ≥ 10%) as an indicator of adverse effects in people with asthma, given the new evidence that people with as thma have more serious responses to O 3 exposure than healthy people. The CASAC pane l, including Dr. Vedal the author of the opinion cited in the comment above, agreed th at this focus on a 10% reduction in FEV 1 was an appropriate one and should also be in cluded in the discussion of adversity in Chapter 3 of the Staff Paper. Clearly the CA SAC Panel agreed that more weight should be placed on lung function decrements (FEV 1 decrements ≥ 10%) as an indictor of adversity for people with asthma. Since FEV 1 is measured primarily in controlled human exposure studies, EPA asserts that this stat ement “more emphasis should be placed on numbers of subjects in controlled human exposure studies with FEV 1 decrements greater than 10%, which can be clinically significant, ” is appropriately attributed to the CASAC

Panel.

The commenter also incorrectly asserts that ATS has recommended a clinical threshold of

a 15% decrement in FEV 1 . In fact, ATS has not done this . The ATS guidelines indicate

that a reduction in FEV 1 or FVC associated with clinical symptoms is adverse. The guidelines also indicate that a small but significant reduction in a population mean FEV 1 is probably medically significant:

Exposure could also enhance risk for a population to an unacceptable degree, perhaps without shifting the risks of any pa rticular individuals to an unacceptable level. Effects on persons with asthma are illustrative. A population of children

with asthma could have a distribution of lung function such that no individual child has a level associated with signifi cant impairment. Exposure to air pollution

could shift the distribution toward lower levels without bringing any individual

child to a level that is associated with clinically relevant consequences

. Individuals within the p opulation would, however, ha ve diminished reserve function and are at potentially increased ri sk if affected by an other agent, e.g., a viral infection. Assuming that the relationship between the risk factor and the disease is causal, the committee considered that such a shift in the risk factor distribution, and hence the risk profile of the exposed population, should be considered adverse, even in the absen ce of the immediate occurrence of frank illness. (ATS, 2000)66 ATS also defines as adverse increased exacerb ations of disease (i.e ., shortness of breath) in people with chronic lung disease that could be reflected in a vari ety of ways, including for example, being less able to cope with daily activities. Clearly this is entirely

consistent with EPA’s definition of adversity, as discussed above.

e. Comments on Role of Ground-Level O 3 in Solar Radiation-Related Health Effects

Comment: A few commenters responded to EP A’s request for co mments, including

available studies or data that would be relevant to conducti ng a critical assessment with reasonable certainty of UV-induced health outcomes and how evidence of UV-induced health outcomes might inform the Agency’s review of the primary O 3 standard potential preventative effect ground level ozone may ha ve in reducing exposure to ultraviolet

radiation.

ATS, AMA and other medical organizations expressed the view that given the known adverse respiratory health effects of O 3 , it would appear more prudent to focus on current approaches to reducing ultraviolet radiati on by preventing UV exposures, rather than permitting the harmful respiratory effects of O 3 . These commenters conclude that there is “no compelling evidence that s hould persuade the Administra tor to consider this issue when setting the NAAQS O 3 standard.” (ATS et al., p. 9)

AAM and a few other commenters that did no t support revising the current primary O 3 standard expressed the opposite view that tropospheric O 3 has a beneficial effect along with stratospheric O 3 in protecting public health from solar UV radiation. A reduction in tropospheric O 3 would act to increase UV exposures and UV-induced health effects, including both non-melanoma and melanoma sk in cancer. These commenters noted that when EPA responded to a court’s remand ( 68 FR 614, Jan 2003) to consider UV-related effects of ground level O 3 there was no disagreement with the fact that ground-level O 3 has beneficial effects. The only disagreements centered on the magnitude of the effect or the certainty with which it can be estimated.

Response: EPA asserts that it has appropriately assessed the UV-B shielding effects of tropospheric O 3 . The Criteria Document has assessed pot ential indirect e ffects related to the presence of O 3 in the ambient air by consider ing the role of ground-level O 3 in mediating human health effects that may be di rectly attributable to exposure to solar ultraviolet radiation (UV–B). The Criteri a Document (chapter 10) focused this assessment on three key factors, including t hose factors that govern (1) UV–B radiation flux at the earth’s surface, (2) human expos ure to UV–B radiation, and (3) human health

effects due to UV–B radiation. In so doi ng, the Criteria Document provided a thorough analysis of the current unde rstanding of the relationshi p between reducing ground-level

O 3 concentrations and the potential impact these reductions might have on increasing UV–B surface fluxes and indirectly contri buting to UV–B related health effects.67 There are many factors that influence UV–B radi ation penetration to the earth’s surface, including latitude, altitude, cloud cove r, surface albedo, PM concentration and composition, and gas phase pollution. Of these, only latitude and altitude can be defined with small uncertainty in any effort to assess the changes in UV–B flux that may be attributable to any changes in tropospheric O 3 as a result of any revision to the O 3 NAAQS. Such an assessment of UV–B relate d health effects would also need to take into account human habits, such as outdoor activities (i ncluding age- and occupationrelated exposure patterns), dress and skin care to adequately estimate UV–B exposure levels. However, little is known about the im pact of these factors on individual exposure

to UV–B.

Moreover, detailed information does not exist re garding other factors th at are relevant to assessing changes in disease incidence, incl uding: Type (e.g., peak or cumulative) and time period (e.g., childhood, lifetime, current) of exposures related to various adverse health outcomes (e.g., damage to the skin, including skin cancer; damage to the eye, such as cataracts; and immune system suppressi on); wavelength depe ndency of biological responses; and interindividual va riability in UV–B resistance to such health outcomes. Beyond these well recognized adverse health e ffects associated with various wavelengths of UV radiation, the Criteria Document (section 10.2.3.6) also discusses protective

effects of UV–B radiation. R ecent reports indicate the necessity of UV–B in producing vitamin D, and that vitamin D deficien cy can cause metabolic bone disease among children and adults, and may also increase the risk of many common chronic diseases (e.g., type I diabetes and rheumatoid arthritis) as well as the risk of various types of cancers. Thus, the Criteria Document concludes that any assessment that attempts to quantify the consequences of increased UV–B exposure on humans due to reduced ground-level O 3 must include consideration of both negative and positive effects. However, as with other impacts of UV–B on hu man health, this beneficial effect of UV–

B radiation has not been studied in sufficient detail to allow for a credible health benefits or risk assessment. In conclusion, th e effect of changes in surface-level O 3 concentrations on UV-induced health outcomes cannot yet be critica lly assessed within reasonable uncertainty (Cr iteria Document, p. 10–36).

The Agency last considered indirect effects of O 3 in the ambient air in its 2003 final response to a remand of the Agency’s 1997 decision to revise the O 3 NAAQS. In so doing, based on the available information in the last review, the Administrator determined that the information linking (1) Changes in patte rns of ground-level O 3 concentrations likely to occu r as a result of programs impl emented to attain the 1997 O 3 NAAQS to (2) changes in relevant exposures to UV–B radiation of concern to public

health was too uncertain at that time to warra nt any relaxation in the level of public health protection previously determined to be requisite to protect ag ainst the demonstrated direct adverse respiratory effects of exposure to O 3 in the ambient air (68 FR 614). At that time, the more recent information on protec tive effects of UV–B radiation was not available, such that only adverse UV–B-relate d effects could be considered. Taking into

consideration the more recent information avai lable in this review, the Criteria Document and Staff Paper conclude that the e ffect of changes in ground-level O 3 concentrations, likely to occur as a result of revising the O 3 NAAQS, on UV-induced health outcomes,68 including whether these changes would ultima tely result in increased or decreased incidence of UV–B-related diseases, ca nnot yet be critically assessed.

4. Specific Comments on the Population Exposure Analyses

Comments related to the population exposure analyses conducted for O 3 are addressed in this section. Incorporating responses contained in section II.B.2.b and II. C.4 of the preamble to the final rule, EPA provides the following responses to specific issues related to the exposure analyses. Comments related to the overall weig ht placed on the exposur e analyses in reaching

decisions on the need to revise the current standard and on an appropriate standard level are addressed in the preamble to the final rule and in section II.A.2.c.ii of this document.

(1) Comment: Several commenters (e.g., UARG, API, AAM) contend that EPA has failed to adequately address the significant uncerta inties with its exposure assessment, including those associated with EPA’s APEX exposure model.

Response: As discussed in the proposal not ice, EPA recognizes that the exposure assessment necessarily contains many sources of uncertainty includ ing those noted by these commenters, and EPA has accounted for su ch uncertainties to the extent possible. EPA developed and presented an uncertainty analysis addressing the most significant uncertainties affecting the exposure estim ates (Langstaff, 2007). The CASAC Panel reviewed in detail the approach used to asse ss exposure and the presentation of the results in the Staff Paper. EPA believes, and the CASAC Panel concurred, that the model used to estimate exposures represents a state-of-the-a rt approach and that “t here is an explicit

discussion of the limitations of the APEX model in terms of variability and quality of the input data, which is appropriate and fine” (Henderson, 2006c, p. 11). Although EPA agrees that important limitati ons and uncertainties remain, and that future research directed toward addressing these uncertainti es is warranted, EPA believes that overall

uncertainties of short-term O 3 population exposure assessment have diminished since the last review. The Administrator has carefully considered the limitations and uncertainties associated with these quantitative assessments but continues to believe that they provide general support for concluding that exposures and health risks asso ciated with meeting the current 8-hour standard are important from a public health perspective and that the 8- hour standard needs to be revised to provide additional protection in order to protect public health with an adequate margin of safety.

(2) Comment: One commenter (AAM) stated that O 3 monitors are often sited so as to capture the highest O 3 concentrations expected in an area. Since downwind sites are usually the design value sites, they will dominate the upper tail of the O 3 distribution and yet may not reflect the overall outdoor expos ures in the area. This phenomenon will tend

to bias the modele d exposures high.

Response: EPA agrees that O 3 concentrations can vary spatia lly across an urban area. In the exposure modeling conducted, EPA used several O 3 monitors in each area to take into account the spatial variations of O 3 concentrations. The geographic variation of O 369 concentration is accounted for by usi ng measurements from the closest O 3 monitor to represent concentrations in a neighborhood and the measurements at downwind monitors are applied only to the downwind areas. Theref ore this is not a source of bias in the modeled exposures.

(3) Comment: One commenter (AAM) stated that O 3 concentrations are lower at person’s breathing height compared to measurement height. (Wisbeth et al. measured the

increment between O 3 at 2 and 10 meters and reported an average 13 percent difference.) This phenomenon will tend to bias the modeled exposures high.

Response: EPA recognizes that ther e can be differences in O 3 concentrations between breathing and monitor heights and that this wi ll result in some uncertainty in the modeled exposures, with some exposures underestimat ed and some overestimated as a result. However, as discussed in the exposure uncerta inty analysis, data we re not available to quantify the potential biases of differences between O 3 concentrations at a person’s breathing height compared to the heights of nearby monitors. EPA believes that these biases, to the extent that they exist, are relatively small during warm summer afternoons when the atmosphere is well-mixed and O 3 concentrations tend to be higher.

(4) Comment: One commenter (AAM) stated that if people spend time outdoors in closer proximity to streets or in areas with more surface area (buildings, etc.) to quench O 3 , their exposures will be below that measured at the monitor. This commenter contends that the

APEX model assumes that whatever O 3 is interpolated from the monitor measurement is

the actual O 3 exposure in the outdoor microenvironm ent, which will tend to bias the modeled exposures high.

Response: This statement about APEX is not true. The reduction in O 3 concentrations near roadways due to titration of O 3 from automobile emissions of NO is accounted for and explicitly modeled in APEX and thus doe s not bias estimates of exposures. This phenomenon was modeled through the use of “proximity factors,” which adjust the

monitored concentrations to account for the titration of O 3 by NO emissions (the monitored concentrations are multiplied by the proximity factors). Three proximity factor distributions were developed, one for local roads, one for urban roads, and one for interstates, with mean f actors of 0.75, 0.75, and 0.36 respectively (section 3.10.2, Human Exposure TSD). Furthermore, the uncertainty of these proximity factor distributions was included in the exposure uncertainty analysis.

(5) Comment: Some commenters (API, AAM) noted that the uppe r tail of the di stribution of breathing rates (equivalent vent ilation rates (EVR)) is particularly important because it is a critical factor in determining the number of exposures of concern. These commenters contend that the APEX model pr edicts more elevated ventilation rate occurrences than observed in real world data. They argue that this results in an overestimation of the number of exposures of concer n and of the risk estimates.

Response: EPA does not agree that the APEX model overestimates the number of exposures at specified exertion levels acr oss all age groups. EPA did a comparison70 (Langstaff, 2007) of ventilation rates predicte d by APEX to measurements which showed APEX over-predicting ventilation rates for ag es 5 to 10, under-predic ting ventilation rates for ages 11 to 29 and greater than 39, and in close agreement for ages 30 to 39. The overall agreement was judged favorable, and the errors of the predicted ventilation rates were partially incorporated into the over all uncertainty analysis as part of the uncertainties of the metabolic equivalent s (MET), which are the primary drivers of

ventilation rates.

(6) Comment: One set of comments (ALA et al., pp. 104-105) contends that school absences, increased use of asthma medication, emergency room visits, and hospital admissions are not accurately reflected in EPA’s use of “exposures of concern.” Contrary to EPA’s assertion, the exposure estimates cannot be generalized beyond the

effects studied in the controll ed human exposure studies -- th at is, primarily lung function decrements and respiratory symptoms. Other health endpoints, such as school absences, increased use of asthma medications, long-term deficits in lung function and associated risk of illness, emergency room visits, hos pital admissions, and premature deaths, have been characterized principally in epidemiological studies, where increased risks are a

function of the ambient concentrations. The exposure analysis, which relies on activity profiles to minimize assumed population exposures , is not relevant to the estimation of those health endpoints which have been re ported in epidemiological studies. This

limitation contradicts EPA’s desired use of th e exposure assessment to “provide some perspective on the public health impacts of health effects that we cannot currently evaluate in quantitative risk assessm ents.” 72 FR 37853. (ALA et al., pp. 104-105)

Response: The exposure analysis is not intende d to be used to characterize potential health risks for health endpoints which have be en reported in epidemiological studies. It also is not true that the exposure mode ling “relies on activity profiles to minimize assumed population exposures” (ALA, p. 105). In discussing exposures at specified

exertion levels EPA has referred to evid ence of inflammation, increased airway responsiveness, and changes in host defenses in healthy people exposed to 0.080 ppm O 3 in controlled huma n exposure studies.

(7) Comment: EPA’s exposure model underestimates repeated outdoor exposures. As EPA acknowledges, CHAD underestimates the freque ncy of occurrences of “repeated routine

behavior.” This results in underestimates of ex posures to children who spend large portions of their summers playing outside or in summer camps. The “exposures of

concern” assessment does not include outdoor workers or outdoor recreation enthusiasts who receive higher inhaled doses of O 3 due to their increased ve ntilation rates. Outdoor workers experience more frequent exposure to O 3 than the general pop ulation, due to the time spent outdoors, and the increased breat hing rate under physical exertion. Several

studies have examined the association between O 3 exposure and health outcomes in outdoor workers, including farm workers, mail carriers, and others. The Exposure Assessment and Risk Assessment completely ig nore health risks to outdoor workers, a population that is exposed to ambient O 3 while under exertion. In the United States, this population constitutes more than 9 million peopl e. Outdoor workers include a diverse set of occupations, ranging from construction worker s to farm workers. (ALA et al., p. 105)71 Response: This is discussed in th e assessment of uncertainty of the exposure analysis. While EPA has not conducted an exposure analysis for outdoor workers since it was judged that school aged children presented the greatest likelihood of being outdoors and exposed under moderate exertion averaged over an 8-hour period based on the exposure analyses conducted for outdoor wo rkers and children in the prior O 3 NAAQS review. EPA has recognized in the Staff Paper and in the final notice that outdoor workers would also be potentially affected by O 3 exposure. The Administra tor has concluded that the revised standard will protect th is population as well with an ad equate margin of safety.

(8) Comment: One set of comments (ALA et al ., p.105) contends that the exposure assessment focuses on the average child rather than the highly exposed and that active

children are not well ch aracterized. The exposure and risk assessments do not adequately capture risks to active children. EPA had initia lly profiled exposures of “active” children as a separate subpopulation, but subsequently dropped this category, and considers only exposures to average children. This analyti cal approach is then used to argue against adequate protection for those ac tive children or adu lts that spend a lot of time outdoors. Because EPA averages the activity patterns of active and sedentary people, standards may not protect the most exposed individuals. (ALA et al., p. 105)

Response: This assertion is incorrect; all ty pes of individuals are modeled, not the “average child.” The exposure modeling doe s not average activity patterns. Active

children are a subset of a ll children, which are modeled.

(9) Comment: The exposure analysis does not consider the effect of O 3 avoidance behavior on activity profiles. People living in the 12 cities examined experience frequent O 3 alerts warning them of unhealthy air quality and the need to avoid exercising outdoors. Schools, day cares and day camps routinely confin e children indoors on code red days. The analysis fails to consider the extent to which O 3 avoidance behavior has diminished the

estimates of outdoor exercise in children. (ALA et al., p. 105)

Response: EPA concurs that behavior changes in response to O 3 pollution or in response to AQI notification alerts (“avoidance behavior”) were not explicitly taken into account in the exposure modeling. EPA recognizes th at this is a limitation of the exposure analysis and discusses this in the exposure uncertainty analysis. There is not much information about the extent to which people cu rrently modify their activities in response

to O 3 alerts; in particular the activity data (CHAD) used in the analysis does not have

sufficient information to allow avoidance be havior to be modeled. However, under the scenarios modeled for just mee ting alternative standards, O 3 alerts would be infrequent

relative to the number of alerts that cu rrently occur in the nonatta inment areas modeled. Consequently, EPA does not feel that this is an influential factor in the estimation of exposure for the scenarios simulating just m eeting the current or proposed standards.

(10) Comment: Babies, toddlers, and preschoolers, an important segment of the population that spends lots of time playing outdoors, ar e not factored into the analysis. Only schoolaged children are included in EPA’s estimates. (ALA et al., p. 105)72 Response: The exposure analysis focused on school age children and adults due to the lack of health effects evidence explicitly addressing O 3 -related respiratory effects in preschool age children. In addition, there is a pa ucity of data for human activity data for

infants and toddlers that woul d make any exposure analysis applied to these populations very uncertain. The Administrator has ta ken into consideration that additional populations, including pre-school age childre n, are potentially at risk for the O 3 -related respiratory effects observe d in school-age children.

(11) Comment: Several commenters (e.g., ALA et al., p. 106) noted that most of the country is excluded from the analysis. The geographic sc ope of EPA’s analysis is limited to just 12 metropolitan areas.

Response: See response to comment (1) in section II.A.5.

(12) Comment: One set of comments (ALA et al., p. 106) noted that the exposure assessment does not account for exposures and h ealth impacts that result from O 3 transported from the 12 MSAs analyzed, which can actually re sult in people downwind being exposed to higher concentrations.

Response: The urban areas modeled are CSAs, not MSAs, and are large geographically (e.g., the Boston CSA extends into New Hamp shire). However, the increase in O 3 downwind may extend beyond the CSA for some of the areas modeled, and this is not captured in the analysis. The design of the exposure analysis intentionally focused on 12

urban areas.

(13) Comment: O 3 concentrations vary from year to year with different weather conditions. Estimates of “exposures of concern” are subj ect to great variability depending on whether the baseline year for comparison is 2002, a relatively dirty year, or 2004, a relatively clean year. The risk and exposure analysis mu st focus on 2002 as a baseline year. Use of a year with favorable meteorology as the base line year distorts exposure estimates. (ALA et al., p. 106)

Response: EPA accounted for this variability by analyzing all three years (2002-2004) with a focus on the year with higher exposures, 2002.

(14) Comment: One commenter (API) contends that “while EPA conducted an analysis of alternative adjustment procedures before c hoosing the quadratic over a linear one ... their two-parameter quadratic rollback procedure is stil l suspect” (API, p.27). API expressed concern that the quadratic method was devel oped from data spanning only six to eight years which would mean that ozone differen ces could have been caused more by extreme meteorologic events than from actual reducti ons in ozone precursor emissions. Thus, it was stated that air quality data spanning ten to fifteen years should be used. The commenter also cited an alternative analysis which utilized ten to fifteen years worth of data and proposed alternative optimized adjust ment procedures which better fit the ozone

data in four cities.73 Response: Regarding the commenter's objection that EPA's approach was developed from data spanning only six to eight years, EPA believes this time span was long enough

to reflect sizable emission reductions and thus was an appropriate period to use for developing the approach. Also, use of a longer time span would have introduced uncharacteristically high O 3 concentrations from the early part of the examined period when compared to those seen in more recen t years. Since the commenters analysis is based on a longer period, up to 15 years, it s conclusions about ra nking alternative air quality adjustment approaches may have introduced uncharacteristically high O 3 concentrations from the early part of the ex amined period. Further, EPA notes that the commenter’s analysis offered no evidence or analysis that its proposed alternative air quality adjustment procedures would have made any meaningful difference in the exposure or risk estimates associated with ju st meeting the current or alternative 8-hour

standards.

5. Specific Comments on the Health Risk Assessment

Comments related to the health risk assessment conducted for O 3 are addressed in this section. Incorporating responses contained in se ction II.B.2.b and II.C.4 of the preamble to the final rule, EPA provides the following responses to specific issues rela ted to the quantitative

health risk assessment. Comments related to the overall weight placed on the health risk assessment in reaching decisions on the need to re vise the current standard and on an appropriate

standard level are addressed in the preamble and in secti ons II.A.2.a and II.A.2.d above.

(1) Comment: Several commenters (ALA et al., NESCAUM) argued that EPA’s risk

assessment understated the total hea lth benefits of reducing the O 3 standard. Reasons given included:

• It considered only 12 metropolitan statistical areas (MSA), and didn’t consider benefits to adjacent areas beyond the MSA boundaries, that are likely because of the regional

character of O 3 ;

• It didn’t include all relevant health outcomes and populations; among the health outcomes and populations that were omitted are: lung function decrements and respiratory symptoms in adults; school abse nces for respiratory illness among children;

asthma-related ER visits and increased medi cation usage among asth matics; doctor visits, lung inflammation, and decreased resistance to infection among children and adults.

• A number of the health effects that EPA omitted in its risk assessment have been quantified in other an alyses, including EPA’s RIA, a nd in the benefits assessment conducted by California for the review of th e state ambient air quality standard for O 3 , both of which used EPA’s BenMAP model. They concluded that the methodology for quantitatively assessing these other h ealth endpoints is well established.

• EPA’s risk assessment excluded vulnerable subpopulations that are either more susceptible to O 3 health effects, experience gr eater exposure, or both. Specific populations they identified that are not quant itatively assessed incl ude children under five years old, active children, outdoor workers, and senior citizens.74 • One commenter expressed the concern that EPA’s risk assessment, being focused on 12 U.S. cities, may have underestimated O 3 impacts since it has been shown that O 3 concentrations downwind of an urban area are often higher than within a city. (Minister of the Environment, Province of Ontario, Canada)

Response: EPA agrees that the exposure and health risk assessments are limited to certain urban areas and do not capture all of the populations at risk for O 3 -related effects,

and that the risk assessment doe s not include all potential O 3 -related health effects. The

criteria and rationale for se lecting the populations and heal th outcomes included in the quantitative assessments were presented in th e draft Health Assessment Plan, Staff Paper, and technical support documents for the exposur e and health risk assessments that were reviewed by the CASAC Panel and the public. The CASAC Panel indicated in its letter that the health outcomes included in the quant itative risk assessment were appropriate, while recognizing that other health outcom es such as emergency department visits,

increased doctors’ visits s hould be addressed qualitatively (Henderson, 2006c). The Staff Paper (and the CASAC Panel) clearly recognized that the exposure and risk analyses could not provide a full picture of the O 3 exposures and O 3 -related health risks posed nationally. The proposal notice made note of this important point and stated that “national-scale public hea lth impacts of ambient O 3 exposures are clearly much larger than the quantitative estimates of O 3 -related incidences of adve rse health effects and the numbers of children likely to experience exposur es of concern associated with recent air quality or air quality that just meets the cu rrent or alternative st andards” (72 FR 37866). However, as stated in the proposal notice, EPA also recognizes that inter-individual variability in responsiveness to O 3 shown in controlled human exposure studies for a variety of effects means that only a s ubset of individuals in any population group estimated to experience exposures exceedi ng a given benchmark exposure of concern level would actually be expect ed to experience such adverse health effects. The Administrator continues to recognize that there is a broader array of O 3 -related adverse

health outcomes for which risk estimates co uld not be quantified (that are part of a broader “pyramid of effects”) and that the sc ope 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 3 exposures across the country. The Administrator is fully mind ful of these limitations, along with the uncertainties in these estimates, in reachi ng his conclusion that observations from the exposure and health risk assessments provide additional support for his judgment that the

current 8-hour standard does not protect public health with an adequate margin of safety

and must be revised.

In considering the level at which the primary O 3 standard should be set, the Administrator continues to place primary consideration on the body of scientific evidence available in

this review on the health effects associated with O 3 exposure, as summarized in section II.C.4.a of the preamble to the final rule, whil e viewing the results of exposure and risk assessment, as providing information in suppor t of his decision. While the Administrator places less weight on the results of the risk a ssessment, he notes that the results indicate that a standard set within the proposed range would likely reduce risk s to at-risk groups

from the O 3 -related health effects considered in the assessment, and by inference across75 the much broader array of O 3 -related health effects that can only be considered qualitatively, relative to the level of prot ection afforded by the current standard. Moreover, he notes that the results of the assessment suggest a gra dual reduction in risks with no clear breakpoint as incr easingly lower standard levels are considered. However, in light of the important uncertainties i nherent in the assessment discussed in the preamble to the final rule and in the proposal notice, the Administrato r concludes that the risk assessment does not provide a basis for c hoosing a level within the proposed range.

To the extent the commenters suggest that EPA is legally bound to base quantitative features of the standards (such as levels) on th e results of the risk assessment, or that the

standards must be established at a lower level because the risk assessment quantifies morbidity and mortality effects below the levels the Administrator selected, the

commenter is mistaken. See ATA III , 283 F. 3d at 373-74 (EPA not obliged to use the

numerical results of the risk a ssessment to establ ish the 24-hour PM 2.5 standard at a lower level when it provided a reasonable basis for not us ing the assessment).

(2) Comment: A group of commenters mostly represen ting industry associ ations, businesses, and some State and local officials opposed to revising the 8-hour standard, and most extensively presented in comments from UARG, API, Exxon-Mobil, AAM, NAM, and the Annapolis Center raised the concern th at exposures of concern and health risk estimates have not changed significan tly since the prior review in 1997.

Response: In asserting that the es timated exposures and risks associated with air quality just meeting the current standard have not appreciably changed si nce the prior review, comments from Exxon-Mobil, the Annapolis Cent er and others have compared results of EPA’s lung function risk assessment done in the last review with those from the Agency’s risk assessment done as part of this review and have concluded that lung function risks upon attainme nt of the current O 3 standard are below those that were predicted in 1997 and that uncertainties about other health effects based on epidemiological studies remain the same. Th ese commenters used this conclusion as the

basis for a claim that there is no reason to depart from the Admi nistrator’s 1997 decision

that the current 8-hour standard is requisite to protect public health.

EPA believes that this claim is fundamentally flawed for three reas ons, as discussed in turn below: (1) it is factually inappropriate to compare the quantitative risks estimated in

1997 with those estimated in the current rulemaking; (2) it fails to take into account that with similar risks, increased certa inty in the risk s presented by O 3 implies greater concern than in the last review, and (3) it fails to recognize that the Administrator has used these estimates in a supportive role, in light of signi ficant uncertainties inthe exposure and risk estimates, to inform the conclusions drawn primarily from integrative assessment of the controlled human exposure and epidemio logical evidence on whether ambient O 3 levels allowed under the current standard present a serious public health problem warranting

revision of the O 3 standard.

With respect to the first point, the 1997 risk estimates, or any comparison of the 1997 risk estimates to the current estimates, are irreleva nt for the purpose of judging the adequacy76 of the current 8-hour standard, as the 1997 estim ates reflect outdated analyses that have been updated in this review to reflect the curr ent science. Just co mparing the results for lung function decrements ignores these differences . In particular, as discussed in section 4.6.1 of the Staff Paper, there have been si gnificant improvements to the exposure model and the model inputs since the last review that make comparisons inappropriate between the prior and current review. For example, the geographic areas modeled are larger than in the previous review and when modeling a larger area, extending well beyond the urban core, there will be more people exposed, but a smaller percentage of the modeled population will be exposed at high levels, if O 3 concentrations are lower in the extended areas. In the prior review, only typical years, in terms of O 3 air quality were modeled,

while the current review used the most rece nt three year period (i.e., 2002-2004). Also, the prior review estimated exposures for ch ildren who spent more time outdoors, while

the assessment for the current review include d all school age and a ll asthmatic school age children. Therefore, the popul ation groups examined in the exposure assessment are

different between those considered in the 1997 and current review, making comparison of the resulting estimates inappropriate. A nother important difference making comparison

between the 1997 health risk assessment and th e current assessment in appropriate is that

a number of additional health effects were incl uded in the current review (e.g., respiratory symptoms in moderate/severe asthmatic ch ildren, non-accidental and cardiorespiratory mortality) based on health effects observed in epidemiological studies that were not included in the risk assessment for the prio r review. These commenters only compare the risk estimates with respect to lung function decrement and fail to account for differences in additional and more severe health endpoi nts not covered in the 1997 assessment, as

well as the fact that there are somewhat di fferent and more urban areas included in the

current assessment.

Second, it is important to take into account EPA’s increased level of confidence in the

associations between short-term O 3 exposures and morbidity a nd mortality effects. In comparing the scientific understanding of the risk presented by exposure to O 3 between the last and current reviews, one must examin e not only the quantitative estimate of risk from those exposures (e.g. the numbers of increased hospital admissions at various levels) but also the degree of confidence th at the Agency has that the observed health effects are causally linked to O 3 exposure at those levels. As documented in the Criteria

Document and the recommendations and c onclusions of CASAC, EPA recognizes significant advances in our understand ing of the health effects of O 3 based on new epidemiological studies, new human and an imal studies documenting effects, new laboratory studies identifying and inves tigating biological mechanisms of O 3 toxicity, and new studies addressing the utility of usi ng ambient monitors to assess population exposures to ambient O 3 . As a result of these advances, EPA is now more certain that

ambient O 3 , alone or in combination with other pollu tants, presents a significant risk to public health at levels at or above the range of levels that the Agency had considered for

these standards in 1997. From this more co mprehensive perspective, since the risks presented by O 3 are more certain and the current quantitative risk estimates include additional important health effects, O 3 -related risks for a wider ra nge of health effects are now of greater concern at the current level of the standard than in the last review.77 Third, quantitative risk estimates were not the only basis for EPA’s decision in setting a

level for the O 3 standard in 1997, and they do not se t any quantified “benchmark” for the Agency’s decision to revise the O 3 standard at this time. While EPA believes that confidence in the causal relationships between short-term exposures to O 3 and various health effects reported in epidemiological studies has increased markedly since 1997, the Administrator also recognizes th at the risk estimates for these effects must be considered in the light of uncertainties about whether or not these O 3 -related effects occur at very

low O 3 concentrations. The Administrator conti nues to believe that the exposure and risk estimates associated with just meeting the cu rrent standard discussed in the Staff Paper and summarized in the proposal notice are impor tant from a public health perspective and are indicative of potential expos ures and risks to at-risk gr oups. In considering the exposure and risk estimates, th e Administrator has consideredthe year-to-year and cityto-city variability in both the exposure and risk estimates, the uncertainties in these estimates, and recognition that th ere is a broader array of O 3 -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-r isk populations, leading to an incomplete estimation of public health impacts associated with O 3 exposures across the country.

(3) Comment: Several commenters, mostly represen ting industry associations, businesses, and some State and local officials opposed to revising the 8-hour standard (e.g., UARG, API, Exxon-Mobil, AAM), contend that, given the uncertainties and limitations underlying the risk assessments, the health risk estimates are too speculative to support lowering the primary standard level. Specific uncertainties and limitations cited include:

• uncertainties in the exposure estimates;

• uncertainties about the c oncentration-response relati onship (and especially the assumption of a linear non-threshold relationship between O 3 exposures and effects) particularly at levels below 0.08 ppm, so that the extrapolations assumed in the risk assessment may not be valid;

• uncertainties related to the us e of single pollutant models rather than multi-pollutant

models to estimate O 3 -related health risks;

• the risk estimates based on lung function decrements use a benchmark of FEV1

declines of ≥ 15% for healthy individuals and ≥ 10% for asthmatics; these types of changes are transient, routinely experien ced and well-tolerated, and not of adverse health consequence for either healthy or asthmatic individuals;

• the estimated risks of respiratory symp toms, hospital admissions, and non-accidental mortality are based on epidemiological st udies, which do not reliably implicate O 3 , and certainly not O 3 at any specific level, as the cau sal agent for the effects reported;

• the evidence for a causal relationship is particularly uncertain at lower O 3 levels; to the extent that the assumption of a causal link at lower O 3 levels is invalid, estimated

reductions in O 3 -related risk are artificially inflated;

• the evidence from single-city epidemiologi cal studies reporting relationships between O3 and cardiorespiratory mortality are too unreliable and mixed to be included in the

health risk assessment.78 Response: EPA’s response concerning uncerta inties in the exposure estimates is discussed in the previous s ection (II.A.4) on exposure an alysis. EPA’s response to comments concerning the assumption of a lin ear non-threshold concentration-response relationship is addressed under comment numbe r 5 in this section. EPA’s response to comments concerning the use of single vs . multi-pollutant models to estimate O 3 -related

health risks is addressed under comment numbe r (9) in this section. EPA’s response to comments asserting that the lung function decrement benchmarks included in the assessment do not represent adverse health cons equences for either healthy or asthmatic

individuals is addressed above in s ection II.A.3.d (comment number (2)).

In response to the assertion that the results of time-series studies should not be used at all in quantitative risk assessments, EPA notes that the selection of specific studies and

effect estimates was based on a careful evaluation of the evidence evaluated in the

Criteria Document and that the criteria and rationale for sel ection of studies and effect estimates were presented and extensively reviewed and discussed by the CASAC Panel and in public comments presented to the CASAC Panel. EPA notes that the CASAC Panel judged the selection of the endpoints based on the epidemiological studies for inclusion in the quantitative risk assessment to be “appropriate” and that the risk assessment chapter of the Staff Paper and its accompanying risk assessment were “well done, balanced and reasonably communicated” (Henderson, 2006c, p. 12).

In response to comments that O 3 -related risks for mortality and other endpoints based on the epidemiological evidence are artificially inflated due to the assumption of a causal relationship which is particularly uncertain at lower O 3 levels, EPA has responded to comments related to EPA’s characterization of the weight-of-the-evidence with respect to judgments about causality in section II.A .3 above. The Administrator has carefully considered the epidemiological evidence and has taken into consideration the implications of the uncertainties regarding wh ether or not there is a causal relationship

which extends to lower O 3 levels, particularly below 0.075 ppm. As discussed in the preamble to the final rule, this concern is one of the principle reasons that the Administrator has not placed much weight on th e results of the risk assessment in his

decision on the final level of the O 3 primary standard.

In response to the comments that risk estim ates from single-city time-series studies should not be used since they are highly heterogeneous and infl uenced by publication bias, EPA notes that while two of the meta-a nalyses, Bell et al. (2005) and Ito et al. (2005), provided suggestive evid ence of publication bias, O 3 -mortality associations remained after accounting for that potentia l bias. The Criteria Document (p. 7-97) concludes that the “positive O 3 effects estimates, along with th e sensitivity analyses in these three meta-analyses, provide evidence of a robust association between ambient O 3 and mortality.” Concerns about the heteroge neity of responses observed across different urban areas, particularly for O 3 -related mortality, are addresse d above in section II.A.3.b (comment number (2)).

As discussed in more detail in the Sta ff Paper (section 5.3.2.3), there are different advantages associated with use of single-city and multi-city effect estimates as the basis79 for estimating health risks in specific urba n areas. Therefore, the risk assessment included estimates based on both types of eff ect estimates where such information was

available.

(4) Comment: One commenter (NAM, pp. 10-11 and p. 28) argued that the portions of the health risk assessment that EPA generate d itself or sponsored are not sufficiently transparent, i.e., EPA does not provide e nough information for these results to be replicated.

Response: EPA strongly disagrees with this comment. EPA has carefully documented

the health risk assessment methods in the H ealth Risk TSD and has made available, upon request, the models and data inputs, incl uding the exposure-response data from the controlled human exposure studies, used to develop both the exposur e and health risk

assessments as indicated on EPA’s FERA website (http://www.epa.gov/ttn/fera/r isk_ozone.html) which states:

Program and input files used in the Health Risk Assessment: Because of the number and size of the program and data files, they are not available for

interactive download. To receive a DVD cont aining all of the code and data files, contact Harvey Richmond via email at Richmond.harvey@epa.gov

In fact, comments submitted from another industry group (UARG) i ndicating that it was able to closely replicate the risk assessme nt results reported in the Health Risk TSD (UARG, Attachment 3) clearly refute the claim made by NAM that the health risk assessment is not transparent enough to be replicated.

(5) Comment: Some commenters (e.g., AP I, Lefohn) contend that EPA’s risk assessment assumes a linear concentration-response relati onship but that there is ample evidence in the epidemiological literature that the relationship between ambient O 3 levels and health effects is nonlinear. Similarly, one comme nter contends, there is evidence that the relationship between O 3 and health endpoints in the human clinical literature is also nonlinear and that EPA’s assumption of linearity in its risk assessment is therefore invalid, it was argued, and the resulting risk estimates are also invalid (API, p.23) NAM

contends that EPA assumed a constant risk per unit of O 3 for all levels of O 3 exposure in

its health risk assessment and that this assu mption is not biologically plausible and that

EPA offers no scientific evidence to support this proposition (NAM, p.40).

Response: The portion of the risk assessment based on epidemiological studies used

studies that satisfied selecti on criteria that were clearly laid out (see section 4.1.5 in the Health Risk TSD), and the form of the c oncentration-response function was not one of the selection criteria – i.e., the risk asse ssment did not make its own assumptions about the form of the relationship between ambient O 3 levels and a given health endpoint but simply used the best epidemiological evid ence available. The vast majority of O 3 epidemiological studies estimat ed log-linear concen tration-response func tions. There is not “ample evidence” in the epidemiological literature of a non -linear relationship

between ambient O 3 levels and health effects (or, sp ecifically, of a threshold in that80 relationship). In fact, as discussed in th e Staff Paper (p. 6-15), one recent multi-city study (Bell et al., 2006) examined the threshold question for the O 3 -mortality concentration-response function using several different appr oaches and concluded that “all results indicate that any th reshold would exist at very low concentrations, far below current U.S. and international regulati ons and nearing background levels.”

The portion of the risk assessment based on controlled human exposure studies also did not assume linearity in the relations hip between personal exposure to O 3 and lung function response. In this portion of the risk assessment, EPA fit two different models – a linear (hockeystick) model and a logistic model – to the data from the available controlled human exposure studies. The hockeystick model was derived by fitting a linear regression to the data but not constraining the intercept to be ze ro. Thus, if the regression line crossed the x-axis, the data “dictated” a threshold value – EPA set the response rate to zero for all O 3 exposures less than or equal to the exposure at which the regression line crossed the x-axis in this m odel, forming a “hockeystick” model. The logistic model is also nonlin ear, and would constitute a smooth approximation to the hockeystick model. Both models allow for decreasing (or zero) re sponse rates at lower levels of exposure. Because of the uncerta inty about the correct functional form, EPA derived exposure-response functions that were mixtures of the two models. One such mixture hypothesized that the exposure-res ponse relationship is logistic with 90% probability and linear (hockeystick) with 10% probability. The other two mixtures were 80%/20% and 50%/50%. Thus, even if the line ar model was truly linear (i.e., even if it did not cross the x-axis), none of the final models used in this portion of the risk assessment were linear, because each assigned a substantial probability (90%, in the base case model) to the (nonlinear) logistic fo rm of the relationship between personal exposure to O 3 and lung function response.

In response to NAM’s comment, as indicated above, EPA did not assume a constant risk per unit of O 3 for the lung function portion of the health risk assessment. For the health outcomes based on epidemiological studies, as discussed above, EPA did not make its own assumptions about the form of the relationship between ambient O 3 levels and a given health endpoint but simply used the be st epidemiological evidence available. The vast majority of O 3 epidemiological studies estimated log-linear concentration-response

functions and EPA did offer scientific eviden ce, the analysis by Be ll et al. (2006) which found only a very small change in the size of the effect estimate down to very low O 3 levels (i.e., 10 ppb). EPA did acknowledge th e uncertainties about the shape of the concentration-response relationships for the health outcomes based on the epidemiological studies and stated in the St aff Paper that the risk estimates for these

effects “must be considered in the light of uncer tainties about whether or not these O 3 - related effects occur in the popul ation at very low concentrati ons” (Staff Paper, p.5-45).

(6) Comment: Several commenters (e.g., ACC) noted that only a single coefficient used in

the risk assessment is based on 8-hour O 3 concentrations, the averaging time of the current and proposed NAAQS. They argued that therefore the calculated excess risks are likely not relevant to se tting a NAAQS with an 8-hour averaging time.81 Response: As with many of the criteria air pollu tants, health effects have been reported in studies using a variety of averaging times. In this review, as in other NAAQS reviews, EPA has assessed risks arising from expos ure to the pollutant associated with concentrations or exposures for various aver aging times resulting from air quality just meeting the current and alternative standards for a specified averaging time. There is no requirement or logical argument that the averaging time of the models used to estimate specific health effects must be the same as the averaging time for the standard. It has long been recognized that air quality asso ciated with just meeting a NAAQS with a specific averaging time will also limit air qua lity and exposures for other averaging times as well. For example, in 1997 EPA and the CASAC clearly conclude d that an 8-hour O 3 standard set at an appropri ate level would provide protec tion against both 1-hour and 8-

hour O3-related effects. Ther efore, EPA does not agree th e calculated excess risks for health effects based on averaging times other than 8-hours are irrelevant to the setting of an 8-hour averaging time standard.

(7) Comment: One commenter (NAM, pp. 30-32) conte nds that both study selection bias (consistently selecting studies that show positive associations) and model selection bias (selecting models known to yield upwardly bias ed risk estimates, such as single-pollutant

models that do not control for known c onfounders) can be found in EPA’s risk

assessment. Several sources of bias were given, including

• publication bias (the predominance of positive studies reported);

• the choice of which study to emphasize (with preference given to those with larger risk coefficients);

• inadequate control for conf ounders (leading to their eff ects being attributed to O 3 );

• the choice of statistical me thods (with some more likel y to reject the no-effect hypothesis than others); and

• the choice of which estimate from which reported model to rely upon. The result, they contend, is “a cascade of bi as such that the resulting risk assessment is much higher than would have been obtained using objective methods.” Another comment (the Rocheste r Report) asserted that EPA ignored model uncertainty in

its health risk assessment.

Response: EPA has addressed the issues of a lleged publication bias, selection bias, control of confounders, and choice of statisti cal methods in section II.A.3 above and EPA does not agree with the conclusion that there is a “cascade of bias” resu lting in higher risk estimates. EPA takes exception to the impli cation that it used methods with some known bias. As stated in EPA’s IQG (p.22), “if data are subjected to formal, independent, external peer review the information may ge nerally be presumed to be of acceptable objectivity.” EPA’s risk assessment underwen t extensive peer review by the CASAC O 3 Panel, and in EPA’s judgment the commente r has not rebutted the presumed objectivity

of the methods used.

With respect to the selection of studies incl uded, it is important to recognize that EPA’s

criteria for selection of studi es and concentration-response relationships were described in the draft “Health Assessment Plan” (EPA, 2005) and in draft Health Risk TSD reports (Abt Associates, 2005; Abt Asso ciates, 2006) and drafts of the Staff Paper that were82 reviewed by the CASAC and made available to the public for comment at several stages during the review. The CASAC O 3 Panel did not express an y concerns about EPA’s

selection of studies to be included in the O 3 risk assessment and in its October 2006 letter (Henderson, 2006c, p. 12)) to the EPA Administ rator stated, “... the panel found Chapter 5 [the chapter in the Staff Paper that discu sses the risk assessment] and its accompanying risk assessment to be well done, balanced and reasonably communi cated.” The CASAC

O 3 Panel (Henderson, 2006c, p. 12) also explicitly stated that it judged the selection of

health outcomes “for inclusi on in the quantitative risk asse ssment to be appropriate.”

Contrary to the statement in the Rochester Report, EPA did not ignor e the issue of model uncertainty in its risk assessment. While we did not include a quant itative treatment of model uncertainty, EPA’s risk assessment and Staff Paper cl early discussed the potential impact of model uncertainty a nd the importance of consideri ng this issue in interpreting the results of the risk assessment. In pa rticular, EPA’s Staff Paper acknowledged that “other uncertainties, such as differences in study locat ion, time period, and model uncertainties are not represented by confidence or credible interval s presented” (p.5-44, OAQPS Staff Paper). As discussed further in the Staff Paper, “Based on the CD’s conclusions, we judge that there is insuffi cient evidence to suppor t use of potential threshold levels in the quantitative risk assessment [we note that CASAC supported this choice during its review of the scope and met hods to be used in the risk assessment], but we do recognize that there is increasing uncertainty about the concentration-response relationship at lower concentrations that is not captured by the ch aracterization of the statistical uncertainty due to sampling error . Therefore, ... the risk estimates for premature mortality, respiratory symptoms in moderate to severe asthmatic children, and respiratory-related hospital admission s associated with exposure to O 3 must be considered in the light of uncertain ties about whether or not these O 3 -related effects occur in the population at very low concentrations ” (p. 5-45, OAQPS Staff Paper, emphasis added).

With respect to choice of models to rely upon in the risk assess ment, EPA agrees that recent work on model sensitivity has raised new concerns and the Agency has given

much attention to this issue. In so doing, EPA recognizes, as does HEI and other researchers, that there is no clear consensus at this time as to what constitutes appropriate control of weather and temporal trends in time-series studies , and that no single statistical modeling approach is likely to be most appropriate in all cas es (EPA, 2004, p. 8-238).

The recent time-series epidemiologic studies evaluated in the Criteria Document have included some degree of contro l for variations in weathe r and seasonal variables. However, as summarized in the HEI review panel commentary, se lecting a level of control to adjust for time-varying factors, such as temperature, in time-series epidemiologic studies involves a trade-off. For example, if the model does not sufficiently adjust for the relationship between the health outcome a nd temperature, some effects of temperature could be falsely ascrib ed to the pollution vari able. Conversely, if an overly aggressive approach is used to control for temperat ure, the result would possibly underestimate the pollutio n-related effect and compromise the ability to detect a small but true pollution eff ect (EPA, 2004, p. 8-236; HEI, 2003, p. 266). The selection of83 approaches to address such variables depe nds in part on prior knowledge and judgments made by the investigators, for example, a bout weather patterns in the study area and expected relationships between weather a nd other time-varying factors and health outcomes considered in the study. EPA is una ware of any information that supports the

commenters’ contention that the models select ed by the original inve stigators are biased.

In considering these issues related to uncer tainties in the underlying health science, on balance, EPA believes that the available evidence interpreted in light of these remaining uncertainties does provide increased confidence re lative to the last review in the reported

associations between short-term O 3 exposures and mortality a nd morbidity effects, alone and in combination with other pollutants, and generally supports stronger inferences as to the causal nature of the associations. EPA also believes that this increased confidence, when taken in context of the entire body of available health effects evidence, adds support to its conclusion that the current 8-hour standard needs to be revised to provide increased public health protection.

(8) Comment: Several commenters contend that EPA inappropriately uses data from ambient monitors as proxies for personal expos ures in studies estimating effects that are used in the risk assessment. These commenters noted that the literature consistently shows that personal O 3 exposure is generally less than the values obtained from ambient monitors. Further, they stated that the only subpopulation for which ambient monitors may closely track personal exposur e are outdoor workers during the O 3 season and there is virtually no overlap between this subpopul ation and the sensitive subpopulations. To adhere to the information quality substantiv e objectivity standard, one commenter (NAM, p.32) contends that, “EPA must provide unbiased estimates of exposure for each subpopulation of concern.”

Response: Since the relationships used in the risk assessment for the health outcomes based on epidemiological studies are concentration-response relationships that relate ambient concentrations to a population response there is no bias introduced in the health risk estimates by not having an exposure assessment. The fact that ambient concentrations may overstate actual persona l exposure does not imply that the risk estimates are biased. EPA does not agree th at there is any requi rement to provide unbiased estimates of exposure for each s ubpopulation group of concern before it can use concentration-response relationships in its risk assessments.

(9) Comment: One commenter (NAM, p. 34) contends that EPA’s decision to disseminaterisk estimates derived from single-pollutant models as estimates of risk, even when multipollutant models are available, is an unam biguous violation of the objectivity standard.

NAM contends that EPA has utilized the study by Gent et al. ( 2003) in ways that systematically overstate risk estimates and that EPA assumes asthmatics are exposed at the same level as other children (NAM, p. 34).

Response: EPA rejects NAM’s cont ention that disseminating ri sk estimates derived from single-pollutant models is a violation of th e objectivity standard. As discussed in the

Criteria Document and section 3.3.2.1 of the Staff Paper, O 3 epidemiological studies have84 reported results based on both single and/or mu lti-pollutant models. As stated in the Staff Paper (p. 5-35), “To the extent that any of the co-polluants present in the ambient air may

have contributed to the hea lth effects attributed to O 3 in single pollutant models, risks

attributed to O 3 might be overestimated where concen tration-response functions are based on single pollutant models. However if co- pollutants are highly correlated with O 3 , their

inclusion in an O 3 health effects model can lead to misleading conclusi ons in identifying a specific causal pollutant. When collinearity exists, inclusion of multiple pollutants in models often produces unstable and statistica lly insignificant effect estimates for both O 3 and the co-pollutants. Given that single and multi-pollutant models each have both potential advantages and disa dvantages, with neither type clearly preferable over the other in all cases, risk estimates based on both single-and multiple-pollutant models have

been included in the risk assessment wh ere both are available.” The CASAC O 3 Panel generally agreed with this approach in its review of the risk assessment scope and methods plan, Health Risk TSD, and final Sta ff Paper. Further, EPA notes that CASAC’s

overall assessment of the risk assessment was that it was “well done, balanced and reasonably communicated” (Henderson, 2006c) which supports EPA’s view that the approach used did not violate the objectivity standard under the IQG.

For the reasons discussed in th e paragraph above, EPA does not agree that it has used the Gent et al. (2003) study in ways that systematically overstate risk estimates. Further, EPA did not make any assumption about the ex posure of asthmatics relative to other children. EPA applied concentr ation-response relationships reported in this study, which are relationships between levels observed at ambient monitors and a given response, to ambient data in the Boston area. Thus, NAM is incorrect in stating that EPA assumed asthmatics had the same exposure as ot her children in the risk assessment.

(10) Comment: Several commenters (e.g., AAM, NAM , p. 50) contend that, because EPA

failed to show that the associations between O 3 and health endpoints are causal, the risk assessment should include a probabilistic consid eration that the asso ciations may not be causal. They contend that, in contrast to the acute respiratory effects in clinical studies

where we know the observed effects are due to the exposure of the pollutant being assessed, “the most important uncertainty is th e extent to which the associations between

O 3 and the health endpoints included in the assessment actua lly reflect causal relationships” (AAM, citing Second Draft SP at 5-76). Noting the “biologically implausible” wide range of associations for mortality, one commenter questioned the practice of using Bayesian techniques to sh rink the (highly heter ogeneous) city-specific estimates towards the overall mean, especia lly when the heteroge neity includes both no effect and protective effects (AAM). They concluded that the risk assessment should include a probabilistic consider ation that the associations ma y not be causal, pointing out that the Regulatory Impact Analysis (R IA) does evaluate the case assuming that O 3 mortality associations are not causal.

Response: EPA does not agree that it must incl ude a probabilistic characterization of causality for the health effects included in th e risk assessment. EPA’s characterization of likely causality for the various O 3 -related health endpoi nts included in the risk assessment is presented in the Criteria Do cument and Staff Paper (see se ction 3.7.5). As stated in the85 Staff Paper, EPA has only included health e ndpoints in the quantitative risk assessment for which there is, “at a minimum, a likely cau sal relationship with either short-term O 3 exposure itself or with O 3 serving as an indicator for itself and other components of the photochemical oxidant mix, especially during the warm O 3 season” (p.5-42), EPA has not assigned a probability to causation. The Administrator has taken into consideration qualitatively uncertainties related to whethe r or not there is a causal relationship in general and particularly the ex tent to which there may or ma y not be a causal relationship at increasingly lower O 3 levels.

(11) Comment: One commenter (NAM) contends th at EPA abandoned its commitment “to provide the best possible scien tific characterization of risks based on a rigorous analysis of available information and knowledge” by decl aring, in the following statement, that its practices were biased, and pur posefully so: "EPA’s risk assessments are conducted in support of its mission to protect public h ealth and the environment. Given the uncertainty, variability, and da ta gaps encountered when conducting any risk assessment, a key objective for EPA's risk assessments is that they avoid both underestimation of risk and gross overestimation of risk. ... EPA seeks to adequately protect public and environmental health by ensuring that risk is not likely to be underestimated.” (NAM, pp. 39-40)

Response: Contrary to the claim made in the comment, EPA has not abandoned its commitment to provide the best possible scient ific characterization of risks. As noted previously, EPA’s approach a nd analytical assumptions were carefully documented and subject to review by the CASAC O 3 Panel and the public and were based on the scientifically peer-reviewed final Criteria Document. The CASAC O 3 Panel clearly supported EPA’s view that the health risk asse ssment was not biased when it stated that the assessment was “well done, balanced, and reasonably co mmunicated” and that the selection of health endpoint s for inclusion in the quant itative risk assessment was appropriate (Henderson, 2006c). As the quoted passage in the comment indicates, EPA

seeks to avoid both underestimation of risk a nd gross overestimation of risk. EPA notes that in conducting any health risk assessment, analytical c hoices have to be made and EPA has carefully discussed any known direct ional influences of these choices in the Health Risk TSD and Chapte r 5 of the Staff Paper.

(12) Comment: One commenter (NAM) contends that when EPA says that its estimates of

risk from O 3 (or a peer reviewed study on which it relies) has “contro lled for PM,” it is

not clear whether that control addressed only PM 10 or PM 2.5 as well. PM 2.5 is correlated in space and time with O 3 ; PM 10 is not. Thus, controlling for PM 10 is, in effect, functionally equivalent to no control at all (NAM, p. 41).

Response: For each concentration-response func tion used in the risk assessment, the specifics of the function, includ ing co-pollutants in the model, are listed in Table 4-2 of the Health Risk TSD. For those models that included a measure of PM, the exact measure used (i.e., PM 2.5 or PM 10 ) is given in Table 4-2, so there should be no lack of clarity about this.86 Moreover, there is some evidence th at the influence of PM on the O 3 -mortality effect estimate may not be very substantial. One study, Levy et al. (2005), ran univariate regressions at a numbe r of sites with O 3 as the dependent variable and another criteria pollutant as the independent variable, for each of the other criteria pollutants, including

PM 10 and PM 2.5 . They then examined the extent to which the relationship (correlation)

between O 3 and the other pollutant at a site influenced the O 3 -mortality effect estimate at the site. They found only a w eak relationship between the O 3 -PM 2.5 correlation at a site

and the O 3 -mortality effect estimate at the site . Further analysis of a possible PM 2.5 impact on the O 3 -mortality effect estimate did not a lter this finding (see Levy et al., 2005, p. 463).

(13) Comment: Several commenters (e.g., NAM, Roch ester Report, UARG) argued that EPA should conduct an “integrated uncertainty an alysis” – or, as it was described in one comment quoting the National Research C ouncil (NRC, 2002), “EPA should begin to

move the assessment of uncertainties from its ancillary analyses into its primary analyses by conducting probabilistic, multiple source unce rtainty analysis. This shift will require specification of probability distributions fo r major sources of uncertainty, which should be based on available data and expert judgm ent” (Rochester Report, p. 19; NAM, p.46) Such an “integrated uncertainty analysis” would include the effects of additional sources of uncertainty, “including m odel selection, non-linearity of the concentration response function at lower and lower concentrations, a nd the role of other pollutants” (UARG, p. 28). Additional related comments included:

• It was suggested that, the pre ponderant effect of all of the sources of uncertainty is to create an upward bias in EPA’s risk estimat es. “Even when leaving aside the uncertainty about causality, analyses produced by other re searchers have demonstr ated that when an integrated uncertainty analysis is performe d, the large majority of probability in the estimates falls far below the primary estimates that EPA reports (Rochester Report, p. 75).”

• EPA has presented the Administrator data and analyses that led him to be much more confident than is scientifically justified that O 3 exposure below the current NAAQS poses

actual human health risks. EPA’s risk estimates capture only statistical variability for the selected models, not scientific uncertainty about their validity and reliability as estimates

of human health risk. Information about va riability, which is small relative to the magnitude of variability and uncertainty co mbined, has no utility to the Administrator unless it is placed in proper context with information about uncertainty” (NAM, pp. 44- 45).

• One group of commenters contends that EPA sometimes reports “confidence bounds” or “uncertainty intervals” for its primary estimat es, but these ranges are based solely on the standard error of the single relative risk coefficient estimate. “In other words,” they contend, “EPA presents to the public a measure of variability as if it were a measure of uncertainty. This is highly misleading to the non-technical audience th at may not take the

time to learn all of the details of EPA’s an alysis methods. Thus, th is audience is easily swayed into believing that these ranges are a reasonably complete representation of the

uncertainties about the level of risk. Given that some of th ese ranges are very wide (in many cases falling into the negative numbers) it would be quite understandable if people87 were to think these ranges present a compre hensive view of uncertainty, but they do not even start to do so” (Rochester Report, p. 73).

Response: First, EPA notes that the 2002 NRC report cited by several commenters made recommendations with respect to EPA’s regul atory impact analyses which are required

under E.O. 120266 and not EPA’s health risk assessm ents. Even in this separate context, the NRC recognized that it would require a transition over time to implement its recommendations to incorporate more probabi listic assessments in health benefits

assessments.

Second, the point that th e uncertainty ranges reported in the risk assessment do not reflect all of the uncertainty in the risk estimates is explicitly discussed in the Staff Paper (EPA, 2007, section 5.3.2.5). As indicated in the Staff Paper, statistical uncertainty surrounding

the estimated O 3 coefficients in the reported concentr ation-response functions is reflected

in the confidence intervals and additiona l uncertainties “have been addressed quantitatively through sensitivity analyses and/ or have been discussed throughout section 5.3” (Staff Paper, p. 5-40). Given the existi ng data gaps in the scientific evidence and associated uncertainties, a more comprehens ive integrated assessment of uncertainties, would have be desirable, but in the staff’ s judgment would require use of techniques involving elicitation of probabilis tic judgments from health sc ientists. While the Agency is currently developing these approaches, such comprehensive assessments of uncertainty

are not available for the current O 3 risk assessment for this NAAQS review.

Third, EPA does not agree that the preponderant e ffect of all of the sources of uncertainty is to create an upward bias in EPA’s risk estimates and EPA does not agree that other researchers have presented a credible, bala nced, peer-reviewed integrated uncertainty analysis that shows the large majority of pr obability in the estimates falls far below the primary estimates that EPA reported. The analysis conducted by A. Smith for UARG cited by the commenter only examined one h ealth endpoint (i.e., premature mortality) and is based on the assumption that there is no O 3 -related response associ ated with levels below 0.070 ppm. As discussed in the Staff Paper (section 5.3.2.5) a nd section II.A.2 of the preamble to the final rule, there is no sc ientific basis to conc lude that a population

threshold exists at this level.

Fourth, EPA has defined very carefully in th e Staff Paper and Health Risk TSD (sections 3.1.5 and 4.1.9) the concepts of uncertainty and variability and has extensively discussed important sources of both uncertainty and vari ability and their impact on the health risk

assessment.

(14) Comment: One commenter (NAM) cont ends that EPA has violat ed the fundamental risk assessment principle that double counting is not acceptable by attributing to O 3 health risks that have been accounted for previous ly by EPA -- most prominently, premature mortality risks in its analysis of fine PM (NAM, pp. 51-52).

Response: In discussing the selection of concen tration-response functions to use in the portion of the O 3 risk assessment based on epidemiological studies, EPA noted that,88 “single and multi-pollutant models each have both potential advantages and disadvantages, with neither type clearly preferable over the ot her in all cases...” and, as a result, EPA made the decision to “report ri sk estimates based on both single- and multipollutant models where both are available” (Heal th Risk TSD, p. 4-11). It is possible that a single pollutant model could falsely attribut e some portion of mortality risk reduction (or avoided cases of mortality) to O 3 that should instead be attributed to fine PM, and if those avoided cases of mortality were already attributed to fine PM in a PM 2.5 analysis, then there would be some degree of double coun ting. However, the evidence that this is the case to any substantial degree for PM as the copollutant is weak. One study, Levy et al. (2005), ran univariate regression s at a number of sites with O 3 as the dependent variable and another criteria pollutant as the independent variable, for each of the other criteria pollutants, including PM 10 and PM 2.5 . They then examined the extent to which the relationship (cor relation) between O 3 and the other pollutant at a site influenced the

O 3 -mortality effect estimate at the site. Th ey found only a weak relationship between the

O 3 -PM 2.5 correlation at a site and the O 3 -mortality effect estimate at the site. Further analysis of a possible PM 2.5 impact on the O 3 -mortality effect estimate did not alter this finding (see Levy et al., 2005, p. 463). This s uggests that, if th ere is any “double counting” across EPA O 3 and PM 2.5 analyses, it will be fairly small. Given that there is a different price to be paid in using only multi- pollutant models (i.e., in reduced stability of

the O 3 coefficient estimate in such models), EP A continues to believe that the application of both single- and multi-pollutant models, wh ere both were available, is an appropriate approach.

(15) Comment: One commenter (UARG), “recognizing that the Administrator proposes to reject any possible standard level below 0.070 ppm because of the uncertainty about a

causal effect of low levels of O 3 ,” commissioned an analysis of the distribution of the risk

in EPA’s risk assessment attributable to O 3 exposures above and below 0.070 ppm. The analysis found that “v ery little of EPA’s estimated mo rtality and morbidity risk is attributable to days when the maximum 8-hour average level of O 3 is more than 70 ppb” and that attainment of the existing NAAQ S “would actually provi de very significant protection against exposures to O 3 right down to 70 ppb.” They concluded that there is no reason to believe that promulgation of a more stringent NAAQS would result in meaningful reduction in hea lth risk. (UARG, pp. 24-25)

Response: EPA had conducted its own analysis for non-accidental and cardiorespiratory mortality that partitioned th e contribution to overall O 3 -related risk estimates from specified O 3 concentration range intervals as displa yed in figure 5-15 of the Staff Paper (p.5-79) and figures 4-14 and 4-15 of the H ealth Risk TSD (pp. 4-70 to 4-71). UARG’s analysis makes the assumption that there is population threshold at 0.070 ppm. The Administrator is very mindful of the uncer tainties related to whether the observed

associations between O 3 concentrations at very low le vels, well below 0.080 ppm, and the health outcomes reported in the epidemiological studies reflect actual causal relationships

and has taken this into acc ount in considering the risk assessment estimates in his

decision.89 The Administrator does not agree with the co mmenter’s conclusion th at a more stringent NAAQS would not result in mean ingful reductions in health risk. The Administrator has

taken into consideration the pattern of exposure estimates across the range of discrete benchmark levels considered in EPA’s expos ure assessment to provide some indication of the potential magnitude of the inciden ce of health outcomes that could not be evaluated in the Agency’s quantitative risk a ssessment but which have been demonstrated to occur in healthy people at O 3 exposures as low as 0.080 ppm, the lowest level at which

such health outcomes have been tested. 5 As discussed in the pr eamble to the final rule, the Administrator concludes that the expos ure assessment suggests that exposures at above the 0.080 ppm benchmark level, where se veral health effects have been shown to occur in healthy individuals, are essentially eliminated for standards in the range 0.070 to 0.075 ppm. He also concludes that at the 0.070 ppm benchmark level, the exposures are substantially reduced and eliminated for the va st majority of people in at-risk groups, and that the very low estimates of such exposures are not appreciably di fferent, from a public health perspective, between those exposures asso ciated with just meeting a standard set at 0.070 ppm or 0.075 ppm. Further, the Administrato r places relatively li ttle weight on the exposures using the 0.060 ppm benchmark le vel given the very limited scientific evidence supporting a conclusion that O 3 is causally related to health outcomes at this exposure level. Considering the uncertainties associated with the exposure assessment, the Administrator concludes that the exposur e estimates associated with each of the benchmark levels are not appreciably diffe rent, between a 0.070 or 0.075 ppm standard, and therefore, the exposure assessment does not provide a basis for choosing a level within the proposed range.

While the Administrator places less weight on th e results of the risk assessment, he notes

that the results indicate that a standard se t within the proposed range would likely reduce risks to at-risk groups from the O 3 -related health effects cons idered in the assessment, and by inference across the much broader array of O 3 -related health effects that can only be considered qualitatively, relative to th e level of protection afforded by the current standard. Moreover, he notes that the results of the assessment suggest a gradual reduction in risks with no clear breakpoint as increasingly lower standard levels are considered. However, in light of the importa nt uncertainties inherent in the assessment discussed above and in the proposal, the Admini strator concludes that the risk assessment does not provide a basis for choosing a level within the proposed range.

(16) Comment: Several commenters (e.g., API, UARG, Rochester Report) contend that the approach EPA used to adjust hourly O 3 concentrations to simulate just attaining an alternative standard, the quadr atic rollback approach, may overstate the air quality

5 Such health outcomes include increased ai rway responsiveness, increased pulmonary inflammation, increased cellular permeability, and decreased pulmonary defense mechanisms, which have been associated 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, incr eased admissions to hospitals, and possibly to cardiovascular system effects and chronic effects such as chronic bronchitis or long-term damage to the lungs that can lead to reduced quality of life.90 improvements resulting from emissions reducti ons and thus overstate the benefits of stricter standards. One commenter (API) stat ed that the quadratic air quality adjustment approach “was still suspect” (API, p. 27) a nd submitted an analysis examining alternative air quality adjustment procedures. In a ddition, there is uncertain ty about whether the alternative standards in the proposed range ar e even attainable, given EPA’s focus on the mean background and failure to consider the extremes of background. One group of

commenters contends that cons iderable uncertainty remains on the impact of reducing the

8-hour O 3 standard from the current level of 0.08 ppm to a lower level, because EPA has assumed for its analysis that shifts in the probability distribution of exposure to O 3 will occur not just in the upp er tail of the distributi on (the days on which O 3 levels will exceed the existing 8-hour standard of 0.08 ppm or proposed alternative standards of 0.060 to 0.074 ppm), but also the lower and middle portions of this distribution, levels below 0.060 ppm. It is these changes in the lower and middle portio n of the distribution, they pointed out, that provide most of the calculated benefits in terms of reduced short termmortality and reduced hospital admissions associ ated with the more stringent alternative proposed standard (Rochester Report, p. 19) . One commenter contends that EPA’s “proportional rollback” approach assumes that States will reduce O3 levels by a “proportionate amount throughout the distri bution of 8-hour measurement periods” (NAM, p. 59).

Response: First, with respect to the air quality adjustment approach used in the current review to simulate air quality just meeting the current and alternative O 3 standards, as discussed in the Staff Paper (section 4.5.6) and in more de tail in a staff memorandum (Rizzo, 2006), EPA concluded that the quadr atic air quality adjustment approach generally best represented the pa ttern of reductions across the O 3 air quality distribution observed over an 8-year peri od in areas implementing contro l programs designed to attain

the O 3 NAAQS. See the response to comment num ber (14) in section II.A.4 in this document for additional response to API’s analysis of altern ative air quality adjustment procedures. While EPA recognizes that future changes in air quality distributions are area-specific, and will be affected by whatever specific control strategies are implemented in the future to attain a revi sed NAAQS, there is no empirical evidence to suggest that future reductions in ambient O 3 will be significantly different from past reductions with respect to imp acting the overall shape of the O 3 distribution.

Second, it is not permissible for EPA to cons ider whether or not a given alternative standard is or is not attainable under the pr ovisions of section 109 of the Clean Air Act.

Third, EPA believes that the commenters’ imp lied alternative approach of only reducing peak 8-hour daily maximum values that are at or near the standard level is unrealistic in

that most O 3 -related air pollution control measures ar e continuous in nature and have an impact on the entire distribution of 8-hour O 3 concentrations. In c ontrast, EPA’s use of a quadratic adjustment procedur e that reduces not only the upper end of the distribution,

but also to a lesser extent the middle and lowe r end of the distribution has been shown to

match reductions observed in O 3 concentrations over nearly a decade.91 Fourth, EPA rejects NAM’s contention that EP A used a “proportional rollback” approach and that the approach was not justified, when in fact, as described above, EPA used a quadratic air quality adjustment approach that reduced the upper end of the O 3 distribution more than the middle or lower-end of the distribution. Further, as discussed above, EPA’s air quality adjustment approach was based on an analysis of historical changes in O 3 concentrations and EPA’s approach is conistent with past changes in O 3 concentrations resulting from a myriad set of national, stat e, and local control programs reducing O 3 precursors.

Finally, some commenters appear to interpret attainment of the sta ndard using a single year. This is not consistent with the form of the current standard or the alternative standards that EPA analyzed. Thus, EPA doe s not agree that its approach assumed an arbitrary degree of further re duction, but rather EPA’s a pproach reflects that the reductions required are based on a three-y ear period, not just a single year.

(17) Comment: One commenter contends that, because a number of areas -- including some

of the cities involved in the risk assessment — will have difficulty in complying with the

current 8-hour standard within the next decad e, the full public health gains in these areas from a more stringent 8-hour st andard are unlikely to be real ized for a number of years. In light of this, this commenter questioned whether the Agency can or should consider these projected gains as a health-based criter ion for its decision making (Dow Chemical). Another commenter states that “it is technically infeasible to eliminate all U.S. anthropogentic emissions” and that “it is also technically infe asible to achieve the revised ozone standards proposed” (NAM, p. 63).

Response: EPA notes that the Administrator in reviewing and maki ng decisions with respect to the NAAQS is prohibited from consid ering the ability of areas to attain the NAAQS. In addition, while cost and technolog ical feasibility are taken into account in the implementation of the NAAQS – even if an area is delayed in meeting the standard due to cost or other implementation difficulties -- this does not reduce the benefits to public health that could be expected from fu ll attainment of a new standard, which is the

focus of EPA’s risk assessment.

(18) Comment: A group of environmental and health organizations contends that EPA “has illegally understated th e health effects of O 3 by basing its risk assessment solely on risks in excess of policy-related background levels. Section 109 of the [Clean Air] Act requires the primary NAAQS to be set at a leve l requisite to protect public health with an adequate margin of safety: it does not allo w EPA to protect only against health risks presented by O 3 attributable to anthropogenic sour ces. A person breathing the air is exposed to the total concentration of O 3 in the air, includ ing background, and the NAAQS must protect against that total exposure. There is noth ing in the Act that allows EPA to ignore or discount the risk pres ented by the background component of such exposures.” (ALA et al., p. 110)

Response: EPA does not agree that it is inapprop riate or impermissible to assess risks

that are in excess of PRB or that EPA mu st focus on total risks when using a risk assessment to inform decisions on the primary standard. Consistent with the approach92 used in the risk assessment for the prior O 3 standard review and consistent with the approach used in risk assessments for othe r prior NAAQS reviews, estimating risks in excess of PRB is judged to be relevant to policy decisions regarding the ambient air quality standard as it provides useful info rmation regarding the ri sks attributable to anthropogenic emissions. EPA also notes that wi th respect to the ade quacy of the current standard taking total risks into account would not impact the Administrator’s decision as he judges that the curr ent standard is not adequate even when risks in excess of PRB are considered. In addition, EPA notes that cons ideration of the eviden ce itself, as well as exposures at and above benchmark levels in the range of 0.060 to 0.080 ppm are not impacted at all by consideration of PRB. In this review, EPA’s use of PRB in the risk assessment had little impact on the Administra tor’s determination regarding the level of the standard given the relative weight placed on the risk assessment and the range of PRB values compared to the st andards under consideration.

(19) Comment: While disagreeing with EPA’s approach of estimating risks only above PRB, ALA et al. supported the use of the GEOS-CHE M model as the “best tool available to derive background concentrati ons” should EPA continue to pursue this approach.

Response: EPA agrees with this comment.

(20) Comment: Many industry commenters argued that EPA’s (flawed) approach to estimating PRB concentrations has lead to underestimates of PRB and thus to an

overestimation of the numbers of cases of health effects associated with O 3 concentrations above PRB. Some commenters also pointed out that the major difference between this review and the pr evious one is the lower bac kground level; others pointed out that if the same background level were use d, almost all the health benefits would be reduced by up to 90% – or, as one commenter put it, “the choice of the PRB dominates

EPA’s estimates of O 3 health risks” (NAM, p. 62). These commenters expressed

concerns that PRB levels were estimate d by EPA solely by modeling using the GEOSCHEM model, which they argue d underestimates PRB. Related arguments made related

to the role of PRB in the risk assessment included:

• A few commenters contend that EPA’s current PRB estimates inappropriately excluded

certain emissions contributions that s hould be included – notably, anthropogenic precursor emissions from Canada and Mexico. They argued that this approach artificially

inflates the risk estimates.

• One commenter argued that, based on EPA’s lim ited sensitivity analysis to examine how sensitive the risk estimates are to differing assumptions about PRB, the understatement of

PRB can result in substantial overstatement s of risk. For example, assuming PRB was 0.005 ppm higher than that pred icted by the GEOS-CHEM mode l decreased estimates of nonaccidental mortality by 50% or more – and resulted in a 62% decrease in predicted incidence of nonaccidental mortality in Lo s Angeles upon attainment of the present

standard when 2002 O 3 air quality data were used (API).

• One commenter contends that the risk estimat es were “highly sens itive (in the downward direction) to any of severa l alternative possible assumpti ons on PRB. The commenter found that using the monitored air quality data from the Trinidad Head site, “believed by many to represent PRB better than do the results of the GEOS-C HEM modeling,” when93 estimating the risk remaining after attain ment of the existing NAAQS reduced the average risk estimates by from 36% to 72% from the risk levels predicted in EPA’s analysis. For Sacramento and Los Angeles, the two cities considered in EPA’s risk

assessment that are closest to the Trinidad H ead site, the estimates of risk fell by 65% and 72%, respectively. The commenter concluded that the absolute risk estimates are highly sensitive to alternative plau sible PRB assumptions, preventing meaningful comparisons

of health risks at alternativ e possible standard levels to that upon attainment of the existing NAAQS (UARG, pp. 25-27).

• One commenter argued that the sensitiv ity to 0.005 ppm changes in background

demonstrates that the bulk of estimat ed mortality comes from days with O 3 concentrations that are very low. This commen ter contends that this is not biologically plausible (AAM).

• One commenter argued that EPA had ignored an important comment from the CASAC Panel which undermines the approach used in EPA’s risk assessment. Citing CASAC’s August teleconference, this commenter quoted the CASAC letter (Henderson, 2006b) which noted that PRB is highly problematic to calculate and is, in some sense, “unknowable.” CASAC went on to say, “One can avoid this problem, it was contended, by calculating the change in incidence of the h ealth effect associated with a change in

O 3 from the current standard to some other specified concentration. This approach, it was argued, would allow focus on the question, ‘What is the difference in the expected

number of health effects that will oc cur at various concentrations of O 3 , relative to the current standard of 0.08?’ A key advantage of th is approach is that it does not depend on the choice of PRB, and thus is free of the uncertainties surrounding estimation of PRB” (NAM, p. 26).

• One commenter argued that the sensitivity of clinical respiratory effects to background assumptions, while not as large as for other hea lth effects, is still very important. Citing Tables 3-28 and 3-31 in the Health Risk TSD, this commenter noted that the numbers of occurrences of lung function response of h ealthy and asthmatic children are reduced with a 0.005 ppm increase in PRB almost as much as a lowering of the standard from 0.084 to 0.074 ppm. The commenter concluded that, given the importance of the choiceof background, the Agency should reevaluate its assumed background and then reevaluate the clinical risks (AAM).

• One commenter contended that EPA had not considered one li terature review (Vingarzan, 2004) and one research study (Ortma ns et al., 2006) and that “both articles indicate that there is significant spatial a nd seasonal variability, with springtime peak” (NAM, p. 62).

Response: First, the U.S. government has influe nce over emissions at our borders that

affect ambient O 3 concentrations entering the U.S. from Canada and Mexico through either regulations or international agreem ents, and therefore EPA does not agree that

these emissions are uncontrollable. P RB is currently designed to identify O 3 levels that

result from emissions that are considered unc ontrollable because the U.S. has little if any influence on their control, a nd in that context anthropogeni c emissions from Mexico or

Canada should be excluded from PRB. EP A has consistently defined PRB as excluding anthropogenic emissions from Canada and Me xico in NAAQS reviews over more than

two decades and sees no basis in the comme nts to alter this current definition.94 Second, the criticisms raised concerning th e use of a modeling approach (GEOS-CHEM) and the potential alternative a pproach of using remote mon itoring data to estimate PRB were considered by EPA’s scie ntific staff and the CASAC Panel during the course of reviewing the Criteria Document. Both EPA’ s experts and CASAC endorsed the use of the peer-reviewed, thoroughly evaluated mode ling approach (GEOS-CHEM) described in the Criteria Document as the best appro ach for estimating PRB levels. The Criteria

Document reviewed detailed eval uations of GEOS-CHEM with O 3 observations at U.S. surface sites (Fiore et al., 2002, 2003) and comparisons of GEOS-CHEM predictions with observations at Trinidad Head, CA (Gol dstein et al., 2004) and found no significant differences between the model predictions and observations for all conditions, including those given in the current PRB definition. The Criteria Document (p. 3-49) states that the

current model estimates indicate that P RB in the U.S. is generally 0.015 to 0.035 ppm that declines from spring to summer and is generally < 0.025 ppm under conditions conducive to high O 3 episodes. The Criteria Document acknowledges that PRB can be higher, especially at elevated sites in the sp ring due to stratospheric exchange. However, unusually high springtime O 3 episodes tied to stratosphe ric intrusion are rare and generally occur at elevated locations and these can be r eadily identified and excluded under EPA’s exceptional events rule (72 FR 13560) to avoid any impact on

attainment/non-attainment status of an area.

Third, many of the commenters who raised the concern that EPA’s current estimates of PRB were too low and had the impact of ex aggerating the risks associated with the current standard ignored the f act that the risk assessment in cluded a sensitivity analysis which showed the potential impact of both lower and higher estimates of PRB or only focused on the impact of higher estimates of PRB. The choices of lower and higher

estimates of PRB included in the risk assessm ent sensitivity analyses were based on the peer-reviewed evaluation of the accuracy of GEOS-CHEM model. As discussed in the Staff Paper (p. 2-54), the Criteria Docume nt refers to a number of GEOS-CHEM publications (Bey et al., 2001; Liu et al., 2002; Martin et al., 2002; Fusco and Logan, 2003, Li et al., 2002; 2005), summarizing thei r conclusions as “results indicate no significant bias, and agreement to generally within 5 ppbv (parts per billion volume) for monthly mean concentrations at different al titudes”(Criteria Docume nt, p. 3-51 to 3-53). The Criteria Document (p. 3-53) also states "in conclusion, we estimate that the PRB O 3 values reported by Fiore et al . (2003) for afternoon surface ai r over the United States are likely 10 parts per billion by volume (ppbv) t oo high in the southeast in summer, and accurate within 5 ppbv in other regions and s easons." These error estimates are based on comparison of model output with observations for conditions which mo st nearly reflect those given in the PRB definition, i.e., at the lower end of the probabi lity distribution. As

discussed in the Criteria Do cument and Staff Paper, it can be seen that GEOS-CHEM

overestimates O 3 for the southeast and underestimates it by a small amount for the northeast. These commenters generally ignore d the scientific conclusion presented in the Criteria Document that for some regions of the country the eviden ce suggests that the model actually overestimates PRB. Thus, the influence of alternative estimates of PRB

on risks in excess of PRB associated with mee ting the current standard can be to lower or

increase the risk estimates. While the choice of estimates for PRB contributes to the95 uncertainty in the risk estimates, EPA does not agree that the approa ch currently used is biased since peer-reviewed evaluations of the model have shown relatively good agreement (i.e., generally within 5 ppb for most regions of the country).

Fourth, with respect to commenters who pointed to the CASAC comment (Henderson, 2006c, p. 12) that EPA could avoid problems about PRB by focusing on risk reductions relative to just meeting the current st andard, EPA notes the following. An O 3 risk

assessment calculates the risk reductions associated with changing from O 3 concentrations estimated to exist under one scenario to O 3 concentrations estimated to

exist under another scenario. Fo r example, we can calculate

• the risk reductions that would result from changing from “as is” (ambient) O 3 concentrations to PRB O 3 concentrations; or

• the risk reductions that would result from changing from O 3 concentrations under the

current standard to PRB O 3 concentrations; or

• the risk reductions that would result from changing from O 3 concentrations under the

current standard to O 3 concentrations under some more stringent standard.

EPA can avoid using estimates of PRB in its calculations only if all O 3 concentrations in both scenarios are above PRB. Since, by definition, we cannot get O 3 concentrations to

be less than PRB concentrati ons (i.e., we cannot get O 3 concentrations to be lower than what they would be in the absence of human activity), we must know what PRB concentrations are (or have estimates of these concentra tions) to know what the lower bound for feasibly reducing O 3 concentrations is.

The only way EPA could avoid using estimates of PRB concentrations in our risk assessment is if we were reasonably sure that all of the O 3 concentrations in both scenarios (i.e., before reduction and after re duction) were above PRB concentrations – i.e., even if we don’t know the P RB concentrations, our estimated O 3 concentrations are sufficiently high that we can be reasonabl y sure they are not below whatever PRB concentrations are. However, in practice, th is doesn’t happen – i.e ., we typically have O 3 concentrations that are sufficiently low that we cannot be sure they are above PRB.

EPA believes that some commenters have mi sread the CASAC Panel concern “that the current approach to determining PRB is th e best method to make this estimation” (Henderson, 2007, p. 2) as a cr iticism of the use of the GEOS-CHEM modeling approach and/or support for primary reliance on es timates based on remote monitoring sites. However, the CASAC Panel went on to state that one reason for its concern was that the contribution to PRB from beyond North Ameri ca was uncontrollable by EPA and that “a

better scientific unders tanding of intercontinen tal transport of air pollutants could serve

as the basis for a more concerted effort to control its growth ...” (Henderson, 2007, p. 3). Hence, CASAC’s concern appeared to be more with defining what emissions to include in defining PRB, and the role that PRB s hould play, as compared to the technical question of the best way to estimate PRB levels.96 In addition, EPA notes that Dr . Armistead Russell, the atmospheric modeling expert on

the CASAC O 3 Panel, stated the following about EPA’s current use of PRB in his comments on the second draft Staff Paper:

In regards to PRB, given the contentious nature of the issue, the use of the PRB should be discussed in Chapter 2, along with other measures. However, their current approach has been peer-reviewed, and is appropriate. They should, before the next analyses, continue to refine a nd evaluate their approach to setting the PRB, and how it is used in the assessment s. For example, might they use the PRB

in the roll-back formula? This could be done by analyzing CMAQ simulations where the boundary conditions are set to those conditions representative of PRB conditions (Henderson, 2006c, p. D-48).

Dr. Russell clearly endorsed EPA’s current approach to PRB and was discussing potential improvements for th e next review of the O 3 NAAQS. EPA notes that much of the spatial variability in O 3 concentrations is due to spatia l variability in the distribution of anthropogenic sources of O 3 precursors. This source of vari ability is not a factor in the PRB simulations using the GEOS-CHEM mode l. While Dr. Russell suggested that higher resolution models such as CMAQ might be needed, it is not clear that results will be significantly improved by going to the much higher spatial resolution used in regional scale air quality models given the good agreement of GEOS-CHEM estimates with

observations.

In conclusion, the model used, GEOS-CHEM ha s been extensively evaluated and is one of the key models used in major in ternational assessments including the Intergovernmental Panel on Climate Change and Long-Range Transboundary Air

Pollution Converntion assessments. As such it is highly suitable for gauging the influence

of intercontinental tran sport on air quality in the U.S. T hus, its predictions reflect state of the science estimates of intercontinental transp ort. In reviewing the Staff Paper, the atmospheric modeling expert on the CASA C Panel in his comments on how PRB had been estimated using the GEOS-CHEM model concluded that the “cu rrent approach has been peer-reviewed, and is appr opriate” (Henderson, 2006b, p. D-48).

Finally, in response to the NAM comment that EPA had ignored two studies related to PRB, the first study (Vingarzan, 2004) was co nsidered by EPA and is discussed in the Annex to the final Criteria Document (see p. AX3-136). The other study (Oltmans et al., 2006 – NAM misspelled the author of this study in its comment ) was published after completion of the Criteria Document. EPA has already discussed the fact that there is spatial and seasonal variability in PRB in th e Criteria Document and Staff Paper and the

GEOS-CHEM model runs also show th is spatial and seasonal variability.

(21) Comment: Some commenters (e.g., Lefohn, API) asserted that the EPA made an administrative (arbitrary) deci sion in its choice of methods for estimating PRB levels.

Response: EPA extensively evaluated the usefulne ss of different methods for estimating PRB levels. The methodology for estimating PRB levels was explained in section AX3.997 of the Criteria Document. EPA noted in the Criteria Document and Staff Paper that the GEOS-CHEM model has been extensively evaluated for O 3 and other species. Simulations at a number of relatively remote sites have indicated no significant bias in the model predictions (See comment #20 above). Ozone is a regional pollutant and it is thus highly problematic to se parate the regional pollution contribution from PRB. Even the Annapolis Report acknowledges this point – at least for the eastern U.S. However, the same considerations also appl y to the western U.S. As noted in the Criteria Document, it is impossible to tell whether or not a given site is subject to regional or continental anthropogenic influence without ancillary m easurements. These include measurements

of O 3 precursors from which photochemical produc tion rates can be calculated or of tracers of transport from source regions in No rth America. Either the requisite analyses have not been performed or data are not av ailable for the monitoring sites suggested in the comments. On the other hand, the GE OS-CHEM model has been evaluated with respect to O 3 precursors in addition to O 3 itself.

(22) Comment: One commenter (NAM, p. 63) contends that “presentational objectivity requires that EPA accurately a nd clearly state the proportion of reduced health effects properly attributable to each of the following factors: (a) the increase in EPA’s estimate of unit health risks; (b) the proposed reduction in the allowable peak O 3 level; (c) the rollback procedure; and (d) the lowering of the Policy Relevant Baseline.” Without such disaggregation, this commenter contends, polic ymakers and the public will be misled to believe that all or virtually al l of the projected health benefits are attributable to the

reduction in the standard.

Response: Contrary to the commenter’s contenti on, there is no requirement that EPA has to partition its risk estimates with respect to the factors cited. It is not clear what the commenter is referring to with respect to “t he increase in EPA’s estimate of unit health

risks.” Most of the health effects based on epidemiological studies were not included in the 1997 risk assessment, so these are new quantitative estimates, not increased risk estimates. EPA has appropriately discussed th e air quality adjustme nt procedure in the Health Risk TSD and Staff Paper. Simila rly, EPA has discussed its new estimates for PRB, which are based on the best available science as discussed in Chapter 2 of the Criteria Document (section 3.7) and has presente d the results of sensitivity analyses that show the impacts on the risk estimates of both lower and higher estimates for PRB in

several of the risk a ssessment locations.

(23) Comment: One commenter (NAM, p. 29) contends that EPA has used the data from the Adams’ clinical studies (Adams 2002 , 2003a, 2003b, 2006a, 2006b) for the purpose of estimating individual or populati on variability in response, which was not the original purpose of the authors. This commenter fu rther asserted that under the IQG EPA must provide an analysis supporting use of data for a purpose other than the original one.

Response: As in the 1997 risk assessment, EP A obtained individual data from several

6.6-hour O 3 controlled human exposur e studies from the author. API, the funding sponsor of the Adams studies, urged EPA to use the data from these studies, particularly the most recent study by Dr. Adams in its h ealth risk assessment in its comments on the98 draft Staff Paper and draft health risk assessment in January 2006 (API, 2006). EPA

obtained the individual data us ed in the health risk assessm ent directly from the author and explained that the data would be combined with othe r individual data from the Horstman, Folinsbee, and McDonnell 6.6-hour O 3 studies. The health risk assessment for lung function responses was reviewed by the CASAC O 3 Panel and there were no objections expressed by CASAC panel members or by Dr. Adams in either his oral or written comments to EPA concerning EPA’s use of the Adams data as part of the basis for estimating the exposure-response relationshi ps used in the hea lth risk assessment.

(24) Comment: One commenter (API) urged EPA to use a dynamic response model developed by McDonnell to estimate minute- by-minute FEV1 decrements in its health

risk assessment based on all of the co ntrolled human exposure study data. This commenter also urged EPA to break the wi de range of EVR cutpoints used in the exposure modeling into a number of smaller bins to test the hypothe sis that the use of such a wide EVR range biases the overall result. This commenter asserted that the sensitivity of the results to the use of the API model shoul d be evaluated prior to the

issuance of the final rule.

Response: The recommendation to replace the lung function exposure-response relationships developed for EPA’s risk assessment was first made in August 2006 in a presentation to the CASAC O3 Panel. EPA does not agree that it is appropriate or necessary to change the lung function exposur e-response model used in its health risk assessment for the following reasons: (1) th e proposed alternative model had not been peer-reviewed or published at the time EPA’ s assessment was completed; (2) while there are clearly described criteria about the re lative adversity of lu ng function decrements associated with 1- to 8-hour lung functi on decrements as discussed in the Criteria Document and Staff Paper and in the previ ous O3 NAAQS review, there is no consensus about the adversity of 1-minute decrements in lung function response, and (3) CASAC

reviewed two drafts of the Health Risk TSD and did not recommend that EPA adopt the alternative approach suggeste d by the commenter. In EPA’s judgment the alternative approach recommended by the commenter requi res further examination and review and should be investigated for potential use in the next O3 NAAQS review.

(25) Comment: EPA assumes that all exposures betw een 13 and 27 EVR respond as though they were at 20 EVR, substantially overesti mating the risk since there are many more 8-

hour occurrences of ozone at 13 EVR than at 20 and many more at 20 EVR than at 27.

This results in an overestimation of the numbe r of exposures of concern and of the risk estimates. (API, AAM)

Response: The commenter incorrectly asserts that EPA assumed that all exposures between 13 and 27 EVR respond as though they we re at 20 EVR. As in the lung function risk assessment conducted in the prior O 3 NAAQS review, EPA matched the exposureresponse relationships from cont rolled human exposure studies where the vast majority of subjects (>99% of subjects) had EVR’s in the range of 13 to 27 l-min -1 m 2 with 8-hour average exposures corresponding to averaged EV R’s in this same range. The individuals in the 6.6-hour controlled human exposure stud ies did not all have the same EVR and in99 fact there were individuals througho ut the range from 13 to 27 l-min -1 m 2 . In EPA’s judgment there is not adequate data from 6 to 8-hour exposure studies to justify specifying lung function decrements for a more detailed breakdown of EVRs. Therefore, EPA does not agree that there is necessar ily an overestimation of the number of exposures at specified exertion levels or th at the risk estimates are overstated. In addition, as noted in the response to comme nt number (23) above, CASAC reviewed two

drafts of the Health Risk TSD and di d not recommend changing the approach implemented by EPA in its risk assessment.

(26) Comment: One commenter contends that inform ation quality princi ples require that scientific information be presented “within a proper context” and that “a starting point for context would be to compare the severity of respiratory effects from ozone to effects

associated with the most relevant of perhaps a dozen confounders” (NAM, p.51)

Response: EPA believes it has provided sufficient c ontext in its discussion of respiratory effects in the Criteria Document and Staff Paper and that there is no specific requirement to make the type of comparison suggested by the commenter. Further, EPA is unaware

of scientific evidence that would allow it to present an equivalent difference in allergen exposure, exercise, temperature or humidity to a specified change in ozone levels.

(27) Comment: One commenter contends that EPA characterized its ri sk estimates as “primary” or “secondary” and that EPA’s pr imary estimates were those that tend to support a policy preference for a more stri ngent NAAQS and its secondary estimates

were those that did not. “To adhere to information quality requirements, EPA must accurately and clearly describe what distinguishes between these two classes of risk estimates” (NAM, p. 53). EPA’s treatment of a lternative risk estimates also show defects in presentational objectivity by “failing to carry forward al l risk estimates of similar likelihood – and in this case, giving greater pr esentational attention to risk estimates of lower likelihood” (NAM, p. 53).

Response: NAM’s contention that EPA’s risk esti mates are characterized as “primary” or “secondary” in the Staff Paper or proposal notice is incorrect. EPA did use the term “base case” for its lung function risk es timates and provided its rationale for distinguishing between its base case and alternative assumptions about the shape of the exposure-response relationshi p in the proposal notice:

EPA has chosen a model reflecting a 90 per cent weighting on a logistic form and a 10 percent weighting on a linear form as the base case for the current risk

assessment. The basis for this choice is that the logistic form provides a very good fit to the combined data set, but a li near model cannot be entirely ruled out since there are only very limited data (i.e ., 30 subjects) at the two lowest exposure levels (i.e., 0.040 and 0.060 ppm). EPA has conducted a sensitivity analysis which examines the impact on the lung func tion risk estimates of two alternative choices, an 80 percent logistic/20 percent linear split and a 50 percent logistic/50 percent linear spl it. (72 FR 37858)100 EPA strongly disagrees that its rationale fo r choosing its base cas e was influenced by a policy preference. As shown in Figures 5- 17 and 5-18 in the Staff Paper (pp. 5-88 to 5- 91), the pattern and, in many cases, the actual percent reduction in lung function risk is very similar across the base case and altern ative assumptions about the shape of the exposure-response relationship.

With respect to the risk estimates for the health outcomes based on epidemiological studies, EPA presented its rationale for presen ting certain risk estimates and noted where alternative estimates could be found in the Staff Paper and Risk Assessment TSD. For example, EPA stated in the proposal,

EPA has focused on estimates based on multi-city studies where available. The advantages of relying more heavily on c oncentration-response functions based on multi-city studies include: (1) More precise effect estimates due to larger data sets, reducing the uncertainty around th e estimated coefficient; (2) greater consistency in data handling and model sp ecification that can eliminate city-tocity variation due to stu dy design; and (3) less likeli hood of publication bias or exclusion of reporting of negative or nonsignificant findings (72 FR 37859).

In conclusion, EPA did not divide its risk estimates into “primary” and “secondary” categories: EPA clearly articulated its rationa le for presenting some risk estimates over risk estimates in the proposal notice; it s rationale was not influenced by any policy preference; and EPA discussed where alterna tive risk estimates could be found in its documents. Finally, the Administrator in his final decision focused on the overall pattern of the risk estimates, which is very similar between the base case estimates presented in the proposal notice and the alternative estimate s more fully presented in the Staff Paper

and Risk Assessment TSD.

(28) Comment: One commenter contends that EPA characterized its ri sk estimates as “primary” or “secondary” and that EPA’s pr imary estimates were those that tend to support a policy preference for a more stri ngent NAAQS and its secondary estimates

were those that did not. “To adhere to information quality requirements, EPA must accurately and clearly describe what distinguishes between these two classes of risk estimates” (NAM, p. 53). EPA’s treatment of a lternative risk estimates also show defects in presentational objectivity by “failing to carry forward al l risk estimates of similar likelihood – and in this case, giving greater pr esentational attention to risk estimates of lower likelihood” (NAM, p. 53).

Response: EPA rejects NAM’s contention that EP A characterized its risk estimates as “primary” or “secondary” in the Staff Paper or proposal notice. EPA did use the term “base case” for its lung function risk es timates and provided its rationale for distinguishing between its base case and alternative assumptions about the shape of the exposure-response relationshi p in the proposal notice:

EPA has chosen a model reflecting a 90 per cent weighting on a logistic form and a 10 percent weighting on a linear form as the base case for the current risk101 assessment. The basis for this choice is that the logistic form provides a very good fit to the combined data set, but a li near model cannot be entirely ruled out since there are only very limited data (i.e ., 30 subjects) at the two lowest exposure levels (i.e., 0.040 and 0.060 ppm). EPA has conducted a sensitivity analysis which examines the impact on the lung func tion risk estimates of two alternative choices, an 80 percent logistic/20 percent linear split and a 50 percent logistic/50 percent linear spl it. (72 FR 37858)

EPA strongly disagrees that its rationale fo r choosing its base cas e was influenced by a policy preference. As shown in Figures 5- 17 and 5-18 in the Staff Paper (pp. 5-88 to 5- 91), the pattern and, in many cases, the actual percent reduction in lung function risk is very similar across the base case and altern ative assumptions about the shape of the exposure-response relationship.

With respect to the risk estimates for the health outcomes based on epidemiological studies, EPA presented its rationale for presen ting certain risk estimates and noted where alternative estimates could be found in the Staff Paper and Risk Assessment TSD. For example, EPA stated in the proposal,

EPA has focused on estimates based on multi-city studies where available. The advantages of relying more heavily on c oncentration-response functions based on multi-city studies include: (1) More precise effect estimates due to larger data sets, reducing the uncertainty around th e estimated coefficient; (2) greater consistency in data handling and model sp ecification that can eliminate city-tocity variation due to stu dy design; and (3) less likeli hood of publication bias or exclusion of reporting of negative or nonsignificant fi ndings. (72 FR 37859)

In conclusion, EPA did not divide its risk estimates into “primary” and “secondary” categories, EPA cl early articulated its rati onale for presenting some

risk estimates over over risk estimates in the proposal notice and its rationale was not influenced by any policy preference, a nd EPA discussed where alternative risk

estimates could be found in its documents. Finally, the Administrator in his final decision focused on the overall pattern of th e risk estimates, which is very similar between the base case estimates presen ted in the proposal notice and the alternative estimates more fully presente d in the Staff Paper and Risk Assessment

TSD.

6. Specific Comments Related to Communica tion of Public Health Information

Information on the public health implicati ons of ambient concen trations of criteria pollutants is currently made available primarily through EPA's Air Qualit y Index (AQI) program (40 CFR 58.50). The current Air Quality Index has been in use since its inception in 1999 (64 FR 42530). It provides accurate, timely, and easily understandable information about daily levels of pollution. The Agency recognized th e importance of revising the AQI in a timely manner to be consistent with any revisions to the NAAQS. Therefore, EPA proposed to finalize conforming changes to the AQI, in connection with the Agency's final decision on the O 3102 NAAQS if revisions to the primary standard were promulgated. This section responds to comments received on the proposed conforming changes to the AQI.

Comment: EPA received relatively few comments on the proposed changes to the AQI. Three major issues came up in the comments, including: (1) whethe r the AQI should be revised at all, even if the primary standard is revised; (2) whet her the AQI should be revised in conjunction with this rulemaking, or in a separate rulemaking; and, (3) whether an AQI value of 100 should be set equal to or lower than the level of the short-term primary O 3 standard, and the other breakpoints adjusted accordingly. UARG asserted that EPA should not revise the AQI at all, even if EPA does revise the primary O 3 standard. In support of this view, UARG noted that there is no requirement for EPA to set an AQI value of 100 equal to the level of the short-term standa rd, and cited the 1999 decision to set the an AQI value of 100 for PM 2.5 equal to 40 μg/m 3 , when the level of the short-term standard was then 65 μg/m 3 . UARG also expressed the view that lowering the

ambient concentrations associated with diffe rent AQI values woul d confuse and mislead the public about actual trends in air quali ty, which UARG asserted are improving. ALA and other environmental groups in a joint se t of comments did not support revising the AQI in conjunction with this rulemaking. ALA et al. expressed the view that since EPA did not propose specific brea kpoints in its proposed revisi ons to the AQI, EPA should conduct a separate rulemaking, specifying the proposed breakpoints to allow the public an opportunity to comment on them. Several State agencies, including agencies from Pennsylvania, Wisconsin and Oklahoma, a nd State organizations, including NACAA and NESCAUM, supported revising the AQI at the same time that the standard is revised. NACAA expressed the view that: “The effectiveness of the AQI as a public health tool will be undermined if EPA undertakes regul atory changes to th e ozone NAAQS without simultaneously revising the AQI.” (NACAA, p. 5) The Wisconsin Department of Natural Resources (WI DNR) further noted that:

“...when the 24-hour PM 2.5 standard was revised, EP A missed an opportunity to adopt conforming changes to the AQI. The Administrator signed the Federal Register notice promulgati ng a revised fine-particle standard in September 2006, but EPA still has not changed the AQI to reflect the revised standard. We recommend that the AQI be amended to be consistent with the revised ozone and

PM 2.5 standards.” (WI DNR, p. 3)

Finally, ALA et al. and NESC AUM expressed the view that an AQI value of 100 should

be set at an ambient concentration below th e range for the proposed primary standard.

These commenters cited the health evidence showing adverse health effects below the proposed range of the standard, the recomme nded range of CASAC, and also cited the 1999 decision to set an AQI value of 100 for PM 2.5 equal to 40μg/m 3 when the level of the short-term standard was 65 μg/m 3 , as support for this view. Most other State commenters supported setting an AQI value of 100 equal to the level of the primary O 3 standard.

Response: Recognizing the importance of the AQI as a communication tool that allows the public to take exposure reduction measures when air quality may pose health risks,103 EPA agrees with State agenci es and organizations that fa vored revising the AQI at the same time as the primary standard. EPA also agrees with State agency commenters that its historical approach of setting an AQI va lue of 100 equal to the level of the revised primary standard is appropriate, both fr om a public health and a communication perspective.

Both UARG and ALA et al. cite the 1999 AQI rulemaking, which set an AQI value of

100 for PM 2.5 equal to 40 μg/m 3 a lower level than the level of the short-term PM 2.5 standard, as support for their vi ew that an AQI value of 100 does not need to be set at the

level of the revised O 3 standard. However, the sub-index for PM 2.5 was developed using an approach that was conceptually consistent with past practice for selecting the air quality concentrations associated with the AQI breakpoints. The Agency’s historical approach to selecting index breakpoints had been to simply set the AQI value of 100 at the level of the short-term standard (e.g., 24 hours) for a pollutant. This method of structuring the index is appropriate in the case where a short-term standard is set to protect against the health effects associated with short-term exposur es and/or an annual standard is set to protect agai nst health effects associated with long-term exposures. In such cases, the short-term standard in effect defines a level of health protection provided against short-term risks and thus can be a useful benchmark against which to compare daily air quality concentrations.

In the case of the 1997 PM 2.5 standards, EPA took a differe nt approach to protecting against the health risk s associated with short-term e xposures. The intended level of protection against short-term risk was not de fined by the 24-hour standard (set at a level of 65 μg/m 3 ) but by the combination of the 24-hour and the annual standards working in concert. In fact, the annual st andard (set at a level of 15 μg/m 3 ) was intended to serve as the principal vehicle for protecting agai nst both long-term and short-term PM 2.5 exposures by lowering the entire day-by-day distribution of PM 2.5 concentrations in an area throughout the year. See generally 62 FR at 38668-70 (July 18, 1997). Because the 24-hour standard served to provide additiona l protection against very high short-term concentrations, localized “hots pots,” or risks aris ing from seasonal emissions that would not be well-controlled by a national annual stan dard, EPA consequently concluded that it would be appropriate to caution members of sensitive groups exposed to concentrations

below the level of the 24-hour standard. EPA also concluded that it would be inappropriate to compare daily air quality conc entrations directly with the level of the annual standard by setting an AQI value of 100 at that level. EPA wanted to set the AQI value of 100 to reflect the ge neral level of health protec tion against short-term risks offered by the annual and 24-hour standards co mbined, consistent with the underlying logic of the historical approach to estab lishing AQI 100 levels. Therefore EPA set the AQI value of 100 at the midpoint of the range between the an nual and the 24-hour PM 2.5 standards (i.e., 40 μg/m 3 ) in order to reflect the combin ed role of the 24-hour and the

annual PM 2.5 standards in protecting ag ainst short-term risks. Therefore, this approach for defining and AQI value of 100 is conceptua lly consistent with the proposed decision to set an AQI value of 100 equa l to the level of the primary O 3 standard.104 Therefore, EPA is revising the AQI for O 3 by setting an AQI value of 100 equal to 0.075 ppm, 8-hour average, the level of the revised O 3 standard. EPA is also revising the following breakpoints: an AQI value of 50 is set at 0.059 ppm, an AQI value of 150 is set at 0.095 ppm; and an AQI value of 200 is set at 0.115 ppm. All these levels are averaged over 8 hours. As indicated in the proposal , these levels were developed by making proportional adjustments to the other AQI breakpoints (i.e., AQI values of 50, 150 and 200). The proportional adjustments were modified slightly to allow for each category to span at least a 0.015 ppm range to allow for more accurate forecasting. So, for example, simply making a proportional adjustment to th e level of an AQI value of 150 (0.104 ppm) would result in a level of about 0.092 ppm. Since most of these ranges are rounded to the nearest 5 thousandths of a ppm, that roundi ng would have resulted in a 0.014 ppm range (i.e., 0.076 to 0.090 ppm). So, the number was rounded upward to the nearest 5 thousandths of a ppm, to a llow for at least a 0.015 ppm ra nge for forecasting. The same principle applies to the calculation of an AQI value for 200 (0.115 ppm). EPA believes that the finalized breakpoints provide a ba lance between proportional adjustments to

reflect the revised O 3 standard and providing category ra nges that are large enough to be forecasted accurately, so that the new AQI for O 3 can be implemented more easily in the public forum for which the AQI ultimately exists.

B. Secondary O 3 Standards

Public comments on a range of issues related to the proposed secondary O 3 standard options are addressed in the preamble to the final rule and/or in this document. In particular, general public comments related to wh ether or not the current secondary O 3 standard should be

revised are addressed in secti on IV.B of the preamble and be low in section II.B.1. Specific comments addressing basic elements of the standar d, including form, averaging times, and level,

are addressed in section IV.C of the preamble and below in section II.B.2. Comments on the interpretation of the scientific evidence and EPA’s vegetation e xposure and risk assessments for

O 3 are addressed in sections IV .B and IV.C of the preamble and below in sections II.B.3 and

II.B.4.

1. General Comments on Proposed Alternative Secondary O 3 Standards

A large number of comments on the proposed secondary standards for O 3 were very general in nature, basically expressing one of two sharply divergent views: (1) support for revising the current secondary to provide additio nal protection for vegetation and ecosystems by establishing a separate and distinct cumulative, seasonal secondary standa rd with a biologically relevant form or (2) support for keeping the sec ondary standard identical to the 8-hour primary standard, either with revision as proposed, or without any revisi on. In general, commenters who supported a revised primary standard also suppor ted adopting a distinct cumulative, seasonal secondary standard. Commenters who supporte d retaining the current primary standard generally also supported retaining the current secondary standard. Many of these commenters simply expressed their views without stating any rationale, while others gave general reasons for105 their views but without reference to the factual evidence or rati onale presented in the proposal notice as a basis for the Agency’s proposed decision.

General comments based on relevant factors th at either support or oppose any change to

the current O 3 secondary standard are addressed in this section. The biggest difference between the two main groups of commenters related to th eir views regarding the form of the standard; that is, whether a secondary standard with a form separate and distin ct from that of the current or revised primary standard is appropriate, given the information available in this review.

a

. Support for Distinct Cumulative, Seasonal Secondary Standard

Many public comments received on the proposal asserted that, based on the available scientific information, the current secondary O 3 standard is insufficient in both form and level to protect vegetation and ecosystems fr om known or anticip ated adverse O 3 -induced effects and

revisions to the standard are nece ssary and appropriate. Among t hose calling for revisions to the current secondary standard are national a nd local environmental organizations (e.g., Environmental Defense, Appalachian Mount ain Club, Rocky Mountain Clean Air Action),

individual States and State e nvironmental/public health agenci es, State and local air pollution control authorities, NESCAUM, NACAA, Tribal Associations, and the National Park Service (NPS).

(1) Comment: These commenters stated that the av ailable science clearly showed that O 3 - induced vegetation and ecosystem effects are oc curring at and below levels that meet the current 8-hour standard and, therefore, provides a strong basi s and support for the conclusion that the current secondary standard is inadequate. In support of their view, these commenters relied on the entire body of ev idence available for co nsideration in this review, including evidence assess ed previously in the last review. These commenters pointed to the information and analyses in the Staff Paper and the conclusions and recommendations of CASAC as providing a cl ear basis for concluding that the current standard does not adequately prot ect vegetation from an array of O 3 -related effects. This group of commenters strongly supported revisi ng the current standard, not only because

in their view the available evidence conclusive ly demonstrates that the current standard is inadequate to protect sensitive vegetation, but also because the Staff Paper provides abundant evidence that it is ap propriate to establish an alte rnative cumulative, seasonal secondary standard that is distinctly different in form from the current or revised primary standard. For example, NESCAUM states that “... the option of equating the ozone secondary NAAQS with the 8-hour primary is inappropriate and clearly not supported by the weight of scientific evidence.”

Response: EPA agrees with these commenters that when evaluated as a whole, the information on vegetation and ecosystem effect s available in this review supports the need to revise the current standard to provi de increased protection from an array of O 3 - related effects on sensitive ve getation and ecosystems. For reasons discussed below in sections II.B.2, however, EPA disagrees with these commenters’ views that use of a106 cumulative form and related averaging time(s) an d level of such a standard is appropriate in light of all of the avai lable scientific information.

(2) Comment: These same commenters also presented new information for the Administrator’s consideration, including a number of “new” studies published after completion of the Criteria Document. Thes e commenters encouraged the Administrator

to consider these “new” studies in making his final decision.

Response: EPA notes, as discussed in section I of the preamble to the final rule and in section I above, that as in past NAAQS review s, it is basing the final decisions in this

review on the studies and related information included in the O 3 air quality criteria that have undergone CASAC and public review and will consider newly published studies for purposes of decision making in the next O 3 NAAQS review. In evaluating commenters’ arguments, as discussed below in secti on II.B.3, EPA notes that its provisional

consideration of “new” science found that su ch studies did not materially change the

conclusions in the Criteria Document (See further discussion in the Appendix.)

b. Support for Secondary Identical to Current or Revised 8-Hour Standard

The other main group of commenters, which included Exxon-Mobil, AAM, UARG, API, other industry groups, The Annapolis Center for Science Based Pub lic Policy, individual States and other organizations representi ng local energy, agriculture or business interests, expressed the contrasting view that the limite d number of studies publishe d since the last review and

addressed in the Criteria Do cument provided insufficient ev idence to support a conclusion

different than what was reached in the last revi ew. In addition, these commenters also generally

asserted that the evidence that has become ava ilable since the last revi ew does not materially reduce the uncertainties that were present and ci ted by the Administrator in the last review as important factors in her decision to set the seco ndary standard identical to the revised primary

standard.

(1) Comment: These commenters asserted that the types of vegetation effects evaluated in the last review have not changed, and that the Criteria Document, Staff Paper, and CASAC have acknowledged that the information that has become available since the last review does not fundamentally change the conc lusions reached in the last review. As a result, they argued that the currently availabl e evidence fails to show that revision to the standard is requisite to provi de additional protection from these effects. In particular,

UARG states that “...the effects of interest now are for all practical purposes, identical to

those that EPA considered in the last review ” and “...furthermore, recent science has not significantly changed what is known quantitatively about these effects in association with

O 3 .” Thus, UARG asserts that since “the record provides no new scientific insight concerning possible effects of O 3 on vegetation, it supplies no information to call into question the Agency’s determination duri ng the last review of the secondary O 3 NAAQS that the existing standard provides the requisite protection to public welfare.”107 Response: While EPA agrees with the above commenters that the array of known or anticipated vegetation effects evaluated in the la st review is generally the same as in the current review, EPA strongly disagrees with th e commenters’ assertion that the currently available evidence has not materially reduced key uncertainties present in the last review

that factored into the Administrator’s decisi on. EPA notes that the information that has become available since the last review, t hough limited, strengthens the scientific basis supporting the need for revision to the sec ondary standard. The recent expansion of field-based evidence across a broad array of ve getation effects categories, as discussed in the Criteria Document, Staff Pa per, and the preamble to the final rule, has significantly increased EPA’s confidence in extrapolating predictions based on chamber studies to the field. It was this uncertainty, e.g. applying ch amber results to the fi eld that in part, led

the Administrator to conclude that it was not appropriate to go beyond the increased level of protection that would be expected to occur from an 8-hour revised primary and secondary in the 1997 review. There wa s not, as implied by the above comment, important uncertainties remaining with respect to the types of O 3 -induced effects on vegetation at the time of the last review, though significant un certainties did and still do remain on the significance of these vegetati on effects at the ecosystem level. This

increased confidence in the likelihood that predicted effects based on open top chamber (OTC) data are and would continue to occur in the field at and below ambient levels was significant in forming EPA’s conclusion that revision to the secondary standard to provide increased protection to sensitive vegetation and asso ciated ecosystems, is both necessary and appropriate at this time.

A number of commenters also expressed the view that EPA has overstated conclusions that could be drawn from the vegetation data an d in particular, questioned the Administrator’s conclusion that the vegetation effects that are oc curring should be judged “adverse” to the public welfare. They assert that there remain consider able uncertainties about the degree to which and

levels at which O 3 produces adverse effects on the public welfare, as well as the extent to which the proposed revised secondary stan dard would protect the public welfare from such effects. These commenters make a number of specific poi nts related to this i ssue of adversity, as

described below.

(2) Comment: One commenter stated “The extent to which the predicted effects on vegetation from ozone exposure at levels below the current st andard would be adverse to the public welfare depends on the intended us e of the vegetation and its significance to the public. These factors have not been adequately explored.”

Response: EPA agrees that a judgmen t of adversity regarding any O 3 -induced vegetation effects takes in to account the intended use of the vegetation and the significance of any O 3 -induced impairment of that us e to the public (See following comment). However, EPA disagrees that these factors have not been adequately explored. EPA explicitly addressed the re lationship between adversity and intended use with respect to the definition of adversity in section IV.A.3 of the proposal notice. EPA further considered in the Staff Paper and described in the prop osal notice (72 FR 37902/3) what information could be brought to bear to help inform judgments pertaining to the adversity of various O 3 -induced levels of crop yield loss to the public welfare. In108 addition, EPA recognized in the proposal noti ce that “...the level se lected is largely a policy judgment as to the requisite level of protection needed, ....and that it is appropriate to weigh the importance of the predicted risks of these effects in th e overall context of public welfare protection.” Finally, EPA recognized in the proposal notice (72 FR 37903) that “... the public welfare significance of O 3 -related effects can vary significantly, depending on the nature of the effect, the intended use of the plant, and/or the type of environment or location in which the plant grows. Any given O 3 -related effect on vegetation ( e.g. , biomass loss, or foliar injury) ma y be judged to have a different degree of impact on public welfare depending, fo r example, on whether that effect occurs in a Class I area, commercial cropland, or a city park.”

(3) Comment: “The Administrator notes that ‘[ T]he Staff Paper concludes that a

determination of what constitutes an ‘adverse’ welfare effect in the context of the secondary NAAQS review’ can be viewed in the broader context of ‘linkages between stress-related effects ...at the species leve l and at higher levels with an ecosystem hierarchy.’ He does not, however, explicitly indicate that he is adopting this revised definition. Nor should he adopt it. The AQC [sic] is clear that we still lack sufficient scientific information to extrapolate meaningf ully from effects on individual plants to ecosystem effects.”

Response: EPA does not agree that it is inap propriate to expand considerations of adversity to include impacts on the intende d use of ecosystems or the associated ecosystem goods and services. Such impacts, at sufficient levels, could clearly prove adverse to the public welfare. The preamble to the final rule states EPA “...believes it is appropriate to continue to re ly on the definition of “adverse, ” discussed in section IV.A.3 of the proposal that imbeds the concept of “intended use” of the ecological receptors and resources that are affected, and applies th at concept beyond the species level to the ecosystem level.” EPA further believes that su ch a broad definition is in keeping with the

broad definition of welfare effects defined in section 302 (h) of the CAA, which includes effects on many interrelated components of ecosystems, (e.g., soils, water, wildlife, vegetation). Further, as stated in sec tion IV.A.3 of the proposal notice, “...a recent publication ...(Young and Sanzone, 2002) provi des additional support for expanding the

consideration of adversit y beyond the species level by making explicit the linkages

between stress-related effects ...at the species level and at higher levels within an ecosystem hierarchy.” While EPA agrees th at there still remains a high degree of uncertainty in assessing the linkages between O 3 effects on vegetation and those at the ecosystem level, including ecosystem servi ces, EPA believes such linkages have and continue to be made, and as such can reasonably be anticipated.

2. Specific Comments on Proposed Alternative Secondary O 3 Standards

a. Form

Comments received following proposal regardin g the appropriate form for the secondary standard fell generally into two groups. One group expressed support for a new, cumulative seasonal form while the other group expressed su pport for retaining the current 8-hour form.109 These comments were similar to those raised pr ior to the proposal during earlier phases of the NAAQS review. Discussions of these comments are included in sections IV.B.2 and IV.C.2 of the preamble to the final rule, a nd in more detail below.

(1) Comment: One group of commenters, includ ing the National Park Service, Environmental Defense, NESCAUM, NACAA, i ndividual States, Trib al Associations, and local environmental organizations, asserted that the weight of scientific evidence was unambiguous with regard to the need for a cumulative form, and specifically supported the proposed W126 exposure index. For exam ple, New York State DEC explained that “...scientific research recogni zes that exposure-based indi ces considering seasonal time period, exposure duration, diur nal dynamics, peak hourly ozone concentrations, and cumulative effects are important when asse ssing vegetation effects of ozone exposure (Musselman et al., 2006). The W126 exposur e index has long been recognized as a biologically meaningful and useful way to su mmarize hourly ozone data as a measure of ozone exposure to vegetation (Lefohn et al., 1989).” Similarly, Environmental Defense stated “...[f]or reasons amply explained by CA SAC and the Staff, neither the existing secondary standard for ozone nor the proposed primary standards are requisite to protect against adverse welfare effect s on vegetation and forested eco systems. CASAC and Staff further amply justified the need for a separa te cumulative seasonal welfare standard to protect against these effects, rather than relying solely on the primary standards to provide such protection.”

Response: For the reasons discussed in the pr eamble, EPA has determined that it is appropriate to adopt an 8- hour average secondary standa rd instead of a cumulative

seasonal standard.

(2) Comment: In addition to expressing strong supp ort for the W126 cumulative seasonal form, commenters in this group also expressed serious concerns with EPA’s other proposed option of setting the secondary standard equal to a revised primary standard. For example, NPS agreed with CASAC that “retaining the current form of the 8-hour standard for the secondary NAAQS is inappr opriate and inadequate for characterizing ozone exposures to vegetation.” NESCAUM stated “...we also strongly encourage EPA to avoid the flawed rationale employed in the previous 1997 ozone NAAQS review, i.e., that many of the benefits of a secondary NAAQS would be achieved if the primary NAAQS were attained. This rati onale is flawed in at least tw o ways: first, ozone damage to vegetation persists in areas that attain the primary NAAQS; and second, the relationship between short-term 8-hour peak concentrations and longer-term seasonal aggregations is not constant, but varies over space and time...as EPA notes at 72 FR 37904.... EPA should set a secondary NAAQS on its own independent merits based on

adverse welfare effects. Real or perceived relationships between primary and secondary

non-attainment areas are irrelevant to sett ing the appropriate form and level of the secondary NAAQS.”

Response: For the reasons discussed in the pr eamble, EPA has determined that it is appropriate to adopt an 8- hour average secondary standa rd instead of a cumulative

seasonal standard.110 (3) Comment: The other set of commenters, incl uding UARG, API, Exxon-Mobil, The Annapolis Center, ASL and Associates , and AAM, did not support adopting an alternative, cumulative form for the seconda ry standard. Some of these commenters, while agreeing that “directionally a cumulative form of the standard may better match the underlying data,” believe that further work is needed to determin e whether a cumulative exposure index for the form of the secondary standard is requisite to protect public

welfare.

Response: EPA agrees with the commenters who state that a cumulative form of the standard better matches the underlying data but for the reasons discu ssed in the preamble, EPA has determined that it is appropriate to adopt an 8-hour average secondary standard instead of a cumulative, seasonal standard.

(4) Comment: These commenters also asserted that EPA’s analysis of the impact of the

nation’s O 3 control program for the 8-hour st andard on W126 exposures is not scientifically sound due to the use of low es timates of PRB and an arbitrary rollback method that is uninformed by atmospheric chem istry from photochemical models. They argue that EPA must first realistically evaluate the total O 3 reductions that would occur by using a state-of-the-art photochemical mode l and perform an anal ysis of the exposureresponse data to determine if effects are observed for exposures which do not exceed the

8-hour standard.

Response: EPA disagrees that the methods used are not scientific ally sound and has provided a more detailed discus sion under section IV.B.2 in th e preamble to the final rule and in section II.A.4 of this Response to Comments document. Regarding the remaining uncertainties in the exposure and risk assessm ents and the reduction in uncertainties since the last review, these comments have alrea dy been addressed in section IV.B.2 of the preamble to the final rule and are furthe r discussed in sec tions II.B.4 below.

(5) Comment: These commenters also stated that without producing C-R functions for the 8- hour form of the standard, EPA has failed to show that the current 8-hour standard would provide less than requisite pr otection. These commenters asserted that substantial uncertainties remain in this review, and that the benefits of cha nging to a W126 form are too uncertain to warrant revising the form of the standard at this time.

Response: EPA emphasizes that the Criteria Document has reviewed hundreds of studies that support the conclusi on that cumulative metrics, such as W126, are the most biologically relevant concentration-based metr ics for vegetation available at this time (EPA 2006). EPA also notes that examples of crop concentration-response functions with the 8-hour form were provided (Staff Pa per, Figure 7E-1 of Appendix 7E) and refers

the reader to section II.B.3 below for a fuller discussion of this topic. For the reasons discussed in the preamble, EPA has determined that it is appropriate to adopt an 8-hour average secondary standard instead of a cumulative seasonal standard.111 (6) Comment: This group of commenters also addr essed perceived limitations associated

with selection of the W126 cumulative form. Commenters asserted that: (a) the W126 form lacks a biological basis, since it is me rely a mathematical expression of exposure that has been fit to specific responses in OTC studies, such that its relevance for real world biological responses is unclear; (b) a flux-based model would be a better choice

than a cumulative metric because it is an improvement over the many limitations and simplifications associated with the cumulative form; however, there is insufficient data to apply such a model at present; (c) th e European experience with cumulative O 3 metrics has been disappointing and now Europeans ar e working on their second level approach, which will be flux-based; and (d) the W 126 form cannot provide nationally uniform protection, as the same value of an exposur e index may relate to different vegetation

responses; some commenters support a dding a second index that reflects the accumulation of peaks at or above 0.10 ppm (called N100). These concerns are

addressed in turn below.

Response : (a) With respect to the comment that the W126 index lacks a biological basis, EPA disagrees. EPA conclude s that the vegetation effects science provides evidence that exposures of concern to plants are not based on discrete 8-hour periods but on the repeated occurrence of elevated O 3 levels throughout the pl ant’s growing season. The cumulative nature of the W126 is supported by the basic biological understanding of how most plants in the U.S. are most biologi cally active during the warm season and are exposed to ambient O 3 throughout this biologically activ e period. In addition, it has been clearly shown in the scientif ic literature that, all else being equal, plants respond disproportionately more to higher concen trations, though there continues to be no evidence of an exposure threshold for vegeta tion effects. The W126 sigmoidal weighting

function reflects both of thes e understandings, by not including a threshold below which

concentrations are not include d, and by differentially weighti ng concentrations to give greater weight to higher concen trations and less weight to lo wer ones. In addition, it has been clearly shown in the scientific literatu re that, all else bein g equal, plants respond more to higher concentrations, though there continues to be no evidence of an exposure threshold for vegetation effects. The W126 sigmoidal weighting f unction reflects both of these understandings, by not including a thre shold below which concentrations are not included, and by differentially weighting concentr ations to give grea ter weight to higher concentrations and less weight to lower ones. While recognizing that a cumulative, seasonal form is the most biologically releva nt way to relate exposure to plant growth response, EPA’s reasons for adopting an 8-hour average standard instead of a cumulative seasonal standard are expl ained in the preamble.

(b) With regard to the comment that a flux- based model would be a better choice, EPA acknowledges that flux models may produce a more accurate calculation of dose to a specific plant species in a specific area at a specific time, when detailed species-specific and site-specific information is known. Ho wever, flux calculations require large amounts of data on the physiology of each plant spec ies and the local growing conditions for the growing range of each plant species. The EPA recognizes that the selection of an appropriate form of exposure index that can be nationally applied will necessarily represent a simplification of the multiple fact ors that can potentially affect specific plant112 response across the wide variety of species and ecosystems/conditions that occur within

the U.S.

(c) With regard to European dissatisfacti on with the performance of a particular cumulative index in use in Europe 6 and growing interest in development of flux-based models, the Staff Paper (Appendix 7A) noted that “because of a lack of flux-response data, a cumulative, cutoff concentration-ba sed (e.g., AOT40) exposure index will remain in use in Europe for the near future for most crops and for forests and seminatural herbaceous vegetation (Ashmore et al., 2004a).”

(d) EPA disagrees with the comment that a W126 form, if it is to be used, must be coupled with a separate N100 index. EPA ha s found very little research on the N100 index or a coupled approach. The Criteria Do cument did not evaluate this approach in the discussion of exposure indices (EPA 2006) , and the CASAC, after reviewing all the information in the Criteria Document and the Staff Paper, did not recommend an

additional N100 index for consideration. Theref ore, the EPA has no basis at this time to judge the extent to which such a coupled W 126-N100 form would be a better choice than the proposed W126 form. In addition, EPA notes that the W126 form already has built in a weighting scheme that places greater wei ght on increasing concentrations and gives every concentration of 0.10 ppm and above an equal weight of 1, which is the highest weight in this sigmoidal wei ghting function. As has already been discussed, there is no threshold of exposure that is considered adverse to all plants under all conditions. By putting such an emphasis on concentrations at or above 0.10 ppm, the commenters seem to imply that there is a sudden shift in impor tance between concentrations that fall just below and above 0.10 ppm. This has not been shown in the vegetati on effects literature. In addition, in areas that typically have no o ccurrences of peaks above 0.10 ppm, yet still experience high cumulative exposures, it is not clear what purpose an N100 metric would serve, since it would not improve predictions of O 3 -induced effects.

With respect to the related concern that foliar injury in not well correlated with the W126 metric alone, EPA is aware that visible fo liar injury can be caused by both acute and chronic exposures. The proposal notice stat es that “cellular injury can and often does become visible. Acute injury usually appears within 24 hours after exposure to O 3 and, depending on species, can occur under a ra nge of exposures and durations from 0.040 ppm for a period of 4 hours to 0.410 ppm for 0.5 hours for crops and 0.060 ppm for 4 hours to 0.510 ppm for 1 hour for trees and sh rubs (Jacobson, 1977). Chronic injury may be mild to severe.” Clearly, with visible injury that occurs in response to an acute exposure, a 3-month cumulative value will have less meaning. However, as Jacobson, 1977 makes clear, foliar injury effects can also occur under chroni c low level exposure

conditions.

6 The AOT40 index used in Europe is a cumula tive index that incorpor ates a threshold at 0.04 ppm (40 ppb). This index is calculated as th e area over the threshold (AOT) by subtracting 40 ppb from the value of each hourly concentration above that threshold and then cumulating each hourly difference over a specified window.113 Several commenters, however, expressed the vi ew that a W126 coupled with an N100 is necessary to better predict visi ble foliar injury in the fi eld. EPA notes, however, that

none of these commenters makes a recommendation as to what number of N100 is important to protect against different degrees of foliar injury so as to inform judgments concerning what constitutes requisite protecti on. One commenter, A.S.L. and Associates also mentions numerous other modifying f actors that are important in accurately predicting levels of visible foliar injury observable in the field, including soil moisture,

diurnal/nocturnal variation in stomatal c onductance and detoxification potential. EPA was aware of these confounders. For example, the Criteria Document, Staff Paper, and proposal notice state that “a major confounding effect for O 3 induced visible foliar injury is the amount of soil moisture (local rainfall) available to a plant dur ing the year that the visible foliar injury is being a ssessed.” Given these complexiti es, it is not clear why this commenter concludes that adding the N100 alone will provide the stability this

commenter asserts is needed to make the W126 a more appropriate form for predicting foliar injury. Lacking additional data to the contrary, and given the full discussion of these issues above, EPA disagr ees that adding the N100 metric alone would significantly address the complexities and uncertainties that remain related to the relationship between available soil moisture, timing of peak O 3 exposures and plant.

b. Averaging Times

i. Seasonal Window

(1) Comment: Only a few commenters specifically st ated support for the 3-month seasonal window. In one example, the NPS stated that “...we agree that the maximum consecutive 3-month period within the ozone season is a reasonable averaging time for vegetation in many areas of the country.” Other commenters simply stated support for the recommendations of the Staff Paper a nd CASAC with regard to the W126 form

which included a 3-month seasonal window.

Response: For the reasons discussed in the pr eamble, EPA has determined that it is appropriate to adopt an 8- hour average secondary standa rd instead of a cumulative

seasonal standard.

(2) Comment: In contrast, other commenters r ecommended a longer seasonal averaging time. In particular, the Appalachian Mount ain Club stated that “...the ozone season for the secondary standard should range from May to September to fully protect plant and ecosystem health” and further, that “...the standard should be ba sed on the full growing season of a region and this should be re-e valuated over time. Growing seasons are expanding due to climate change.”

Response: EPA agrees that many plants, incl uding tree species, have growing seasons longer than three months and that the selecti on of any single seasonal exposure period for a national standard must necessarily repr esent a compromise, given the significant114 variability in growth patterns and lengths of growing seasons among the wide range of vegetation species occurring within the U. S. that may experience adverse effects

associated with O 3 exposures. For the reasons disc ussed in the preamble, EPA has determined that it is appropriate to adopt an 8-hour average secondary standard instead of

a cumulative seasonal standard.

ii. Diurnal Window

(1) Comment: With respect to the 12-hour diurna l window, the NPS stated that “...for many areas of the country, the daytime 12-hour window is an appropriate period over which to cumulate diurnal ozone exposures. However, as the Staff Paper points out, there is evidence to suggest that in some species in some areas, ozone uptake occurs outside this 12-hour window....Nevertheless, NPS agrees wi th EPA and CASAC that, for most areas and species, the 12-hour daytime period is su fficient and appropriate to characterize ozone uptake for the cumulative standard.” The NPS further noted that “...there may be specific areas (e.g., very dry, hot areas where st omates are primarily open at night) where a different window may better characterize ozon e exposure. It may be appropriate to give States discretion, in these instances , to shift or extend the 12-hour window for calculating exposure in these areas.”

Response: For the reasons discussed in the pr eamble, EPA has determined that it is appropriate to adopt an 8- hour average secondary standa rd instead of a cumulative

seasonal standard.

(2) Comment: Some commenters, however, incl uding NESCAUM, NYSDEQ, AMC, and ADEQ, contended that the appropriate diurna l window for vegetation exposure is longer than 12 hours and typically recommend a 24-hour window. Some of these commenters provided additional air quality analyses a nd cited both published and unpublished sources

of data that document the co -occurrence of sensitive spec ies and elevated nighttime exposures. NESCAUM stated th at it “...believes the lite rature on nighttime adverse ozone impacts is strong and can support an ozone secondary NAAQS that encompasses nighttime hours. This is important to th e NESCAUM states as elevated nighttime ozone concentrations occur in many [high elev ation] locations th roughout the region.” NESCAUM also noted that the number of daylight hours during EPA’s presumed 3- month growing season is greater than 12 hours at th e latitudes of the NESCAUM region.” The Appalachian Mountain Club stated that “...we strongly disagree with the Staff and Administrator’s opinion that more evidence is needed ‘about the extentto which this cooccurrence of sensitive species and elevated nocturnal O 3 exposure exists’ ...to warrant a 24-hour standard.” AMC also provided four examples of National Parks and other federal lands where both elevated nighttime O 3 exposure and sensitive species are present, some of which have been identifie d as showing nocturnal stomatal conductance in the review by Musselman and Minnick (2000). Arizona DEQ stated “...cacti and other desert succulents breathe at night when th ey lose less water. One of the impacts of ozone exposure identified in the literature is the inab ility of the guard cells to fully close stomata. If cacti and succulents cannot close stomata during the daytime, the resulting water loss may substantially weaken the plants or directly kill th em. In addition, ozone115 damage could make stomata stay open overnig ht for most vegetative species, which exchange gases diurnally. Therefore, ADEQ supports a 24-hour time horizon for the Secondary Standard.”

Response: For the reasons discussed in the preamble, EPA has determined that it is appropriate to adopt an 8- hour average secondary standa rd instead of a cumulative

seasonal standard.

iii. Annual vs. Three Year Average

With respect to comments concerning the a nnual versus three-year averaging period for the cumulative form, comments are fairly even ly divided between support for an annual and support for a three year average. However, many of those commenters who agreed that a threeyear average could be appropriate only did so w ith the condition that the level of the standard selected should be lower to protect against adverse levels in one year.

(1) Comment: Some commenters expr essed support only for the annual averaging time in order to provide the appropriate degree of pr otection from effects occurring to vegetation

on an annual basis.

Response: EPA disagrees that onl y an annual form of the secondary standard could provide the appropriate degr ee of protection for annual plants. EPA recognizes and agrees that the adverse impact of some O 3 -induced vegetation effect s are realized within

an annual timeframe and are based on the cumulative O 3 exposure that occurs in that same year. These effects can include growth and reproductive effects in annual species, crop yield loss, and foliar injury symptoms on both annuals and perennial species, including trees growing in pr otected national areas. EP A notes, however, that with regard to crop yield loss, foliar injury symptoms, and tree seedling biomass loss, determining what degree of vegetation impact is adverse, and, therefore, for which appropriate protection is require d in any given year, is more uncertain. As discussed in the preamble, EPA believes that appropriate protection for vegetation can be achieved using a 3-year average of the 8-hour average form.

(2) Comment: As stated above, many commenters, while preferring an annual standard, also gave conditional support to a three-year averag ing time, on the condition that the level of

the standard is lowered to achieve the same level of protection judged requisite on an annual basis. For example, NESCAUM stated that “...adverse vegetation damage occurs on an annual basis... If multi-year averaging is employed to promote a more ‘stable’ NAAQS (as opposed to more stab le ecological health), the le vel should be set lower than

what would otherwise have been set for an annual NAAQS. A reduction of the needed annual level by at least one-third can help a ssure that the intended threshold is not exceeded in individual years.”

Response: EPA agrees that the degree of protec tion provided by a standard is based on the combination of averaging time and level a nd thus should be considered together in establishing a standard that pr ovides the requisite degree of protection. For the reasons116 discussed in the preamble, EPA has determined that it is appropriate to adopt an 8-hour average secondary standard instead of a cumulative seasonal standard.

(3) Comment: In contrast, several other commenter s, including NC DFR, NC DAQ, MidOhio Regional Planning Comm ission, IDNR and IDPH, expr essed the view that the cumulative, seasonal standard should be based on a 3-year average, rather than a 1-year average, regardless of level, due to concer ns regarding the volatility of using a one-year averaging time with the W126 form. For example, Iowa DNR stated “...using only one year of monitoring data to compute the W126 ma kes it particularly volat ile, as infrequent high hourly ozone spikes make it through the sigmoid filter and cont ribute to the three month sum but frequently occurri ng low ozone values do not.”

Response: EPA agrees that stability in a standard is a desirable trait that confers benefit to the public welfare. Because EPA conclude d that the appropriate degree of protection for vegetation can be achieved using a 3-year average form, EPA further concludes that a three year average form is both desirable and appropriate.

c. Level

(1) Comment: One group of commenters, which included the National Park Service, Environmental Defense, NESCAUM, NACAA, St ate, Tribal and local environmental groups, stated support for the CASAC range of 7- 15 ppm-hours. Many of these same commenters further emphasized the lower end of the proposed range as necessary to provide adequate protection for sensitive species. For example, the NPS “...strongly supports CASAC’s recommendation that the upp er bound of the range for the standard should not exceed a W126 of 15 ppm-hours. Further, the NPS strongly recommends a value for the secondary standard that is representative of the low end of the range recommended by CASAC.” Similarly, NESC AUM states that it “...does not support a secondary NAAQS above 15 ppm-hrs...” and “...furthermore, based on observed ozone damage to forests in the NESCAUM region at current ozone levels, a secondary NAAQS

of the W126 form towards the lower e nd of the CASAC-recommended range would provide better protection in the NESCAUM region.” The Appalachian Mountain Club stated “...we urge the more protective 7 ppm- hours level, proposed by EPA, be adopted for areas with known sensitive species and ar eas under special federa l protection related to air quality. This protec tive approach should be used to ensure that Federal Land Managers are able, as directed by Congress, to protect the air quality related values in our

National Parks and Forests and Wilderne ss areas for future generations.”

These commenters who recommended a level at the mid- to lower end of the proposed range based their recommendation primarily on four sources of information: (a) fieldbased evidence of foliar injury occurring on se nsitive species at air quality levels well below that of the current standard; (b ) the 1996 consensus workshop recommendations for protective levels in terms of cumulative exposures fo r different vegetation types; (c) CASAC advice and recommendations; and (d) “n ew” studies published after the close of117 the 2006 CD that potentially point to a str onger link between species level impacts and

ecosystem response.

Response : EPA notes that in considering what standard is requisite to protect public welfare from known or anticipat ed adverse effects, judgment is required, based on an interpretation of the evidence and other info rmation, that neither overstates or understates the strength and limitations of the eviden ce and information nor the appropriate inferences to be drawn. In light of signifi cant remaining uncertainties, described by other commenters below, EPA disagrees that the a ppropriate level of pr otection for vegetation lies within the CASAC range. For the reas ons discussed in the preamble, EPA has determined that it is appropriate to adopt an 8-hour average secondary standard instead of

a cumulative seasonal standard.

The other group of commenters, including E xxon-Mobil, the Annapolis Center, AAM, and State and local organizations , did not support revising the curr ent secondary standard. While many of their comments regarding sources of uncertainties associated with the effects evidence and the exposure and risk assessments have been addressed in section IV.B.2 of the preamble

and in sections II.B.3 and II.B .4 below, some of their commen ts also identify uncertainties regarding the sources of information relied upon by the first group of commenters as support for a level within the range of leve ls recommended by CASAC.

(2) Comment: With regard to the usefulness of foliar injury evidence to inform selection of a level of protection, Exxon-Mobil stated “...EP A has not addressed potential confounders, such as soil moisture, or related the visibl e foliar injury symptoms to other vegetation effects.” Georgia DNR also identified uncerta inties associated with visible foliar injury including “...a lack of linkage between visibl e foliar injury and othe r vegetation effects, and the inability to quantitatively assess the degr ee of visible foliar inju ry that should be judged adverse in all settings and across all species.”

Response: In the proposal notice and preamble to the final rule, EPA concluded that foliar injury information available in this review provides compelli ng evidence that the current standard is inadequate to protect against this vege tation effect. However, EPA also concludes, given the many sources of un certainty that have been raised regarding using the foliar injury data as a basis fo r determining an appropriate level of public welfare protection, that the foliar injury data available at this tim e is insufficient to specifically inform quantitative judgments re garding the selection of an appropriate standard and should only be considered qualitatively.

(3) Comment: With regard to comments received stating concern with EPA’s and/or CASAC’s apparent reliance on the recomme ndations from the 1996 consensus workshop in selecting a range of leve ls, both the Annapolis Center and AAM state that “...[i]f the workshop recommendations are to be used for standard settin g, then the studies underlying their basis, as well as the me thod for reaching the recommended values,

should be stated in more detail than in the cited workshop summary. The basis for establishing a standard should be transpar ent and reproducible.” More specifically, Exxon-Mobil stated “...this workshop was by invitation only, and documentation is not118 available to the public. The reference [s ic] cited is short and provides consensus recommendations, but without deta ils as to their basis. In particular, the basis for the recommendation to consider a 2 percent effect le vel to be significant is not provided. It is not clear how this effect level could be expe rimentally determined, if it is discernable from biological variability, or what references suggest the potential compounding effect over multiple years, ....” If available, a more detailed report of the consensus workshop should be released. If studies to suppor t the recommendations ca nnot be provided, then

the recommendations should be used with great caution.”

Response: With regard to comments stating con cern with EPA’s apparent reliance on the

recommendations from the 1996 consensus work shop in selecting a ra nge of levels, EPA agrees that though the workshop participants we re asked to review, and thus were aware of, the scientific literature available at the time, as described in both the 1996 O 3 Criteria Document and Staff Paper, the workshop disc ussion of ranges of levels recommended as protective of different vegetation types for different effects falls short of providing a scientific basis for determining at what level these effects become adverse to the public welfare. In addition, EPA agrees that the sc ientific basis for esta blishing a 2% level of biomass loss in tree seedlings as a benchm ark of concern to take into account the possibility of compounding is unclear, though th ere was and continues to be, evidence of the potential for compounding effects to occur over multiple years. As the proposal states (72 FR 37885, 37886) with respect to potential compounding, there is important evidence that “...in perennial plant species , a reduction in carbohydrate storage in one year may result in the limitation of growth the following year (Andersen et al., 1997). Such ‘carry-over’ effects have been document ed in the growth of tree seedlings (Hogsett et al., 1989; Sasek et al., 1991; Temple et al., 1993; EPA, 1996a) and in roots (Andersen et al., 1991; EPA, 1996a)”. However, EPA concludes that significant uncertainty

remains as to what level of annual tr ee seedling biomass loss when compounded over multiple years should be judged adverse to the public welfare. Since tree seedling risk numbers were often compared to this level of biomass loss derived from expert judgment, EPA also notes that this issue adds additional uncertainty in judging the adversity of relative risks of tree seedling biomass loss pred icted under different alternative air quality

scenarios.

(4) Comment: With regard to the strength of the scientific basis for CASAC’s views, the Annapolis Center and AAM st ated that “...if ozone mon itoring is continued under the current guidelines, the ranges for a seasonal seco ndary standard must be adjusted upward. Based on the reduction in ozone exposure at plan t height of a factor of two compared to that at measurement height, the range shoul d be increased by roughl y a factor of two.

Neither CASAC nor EPA took this into account in making their recommendations concerning the level of the secondary standard.” AAM also stated “... [i]t is now widely accepted that ozone concentrations at the ‘sta ndard measurement height’ are not the same as the ozone exposures at plant height. When this factor was corrected in the vegetation risk assessment, the SUM06 and W126 exposures at plant height were approximately half those at measurement height.”119 Response: With regard to the uncertainty associ ated with monitor height gradients and its consideration by CASAC and EPA in ma king recommendations on an appropriate range of levels, EPA notes that the risk assessments conducted by EPA on both tree seedling biomass loss and crop yield loss included an exposure adjustment factor to better account for this issue. As a result, both EPA and the CASAC were fully aware of this issue when making recommendations on a range of levels for the Administrator’s consideration. However, the Staff Paper al so “...recognizes that a 10% adjustment to hourly monitoring data across the country is a very simple method to deal with a complicated issue.” Thus, because there stil l remains significant uncertainty associated with selecting an appropriate adjustment met hod and because the impact of this issue on establishing the appropriate re lationship between exposures m easured at monitor height and predicted adverse levels of plant res ponse for short vegetati on (e.g., crops and tree seedlings) has not been fully evaluated, EPA be lieves caution should be used in selecting a level of air quality that would not be more protective than necessa ry in areas where the height of vegetation canopies are significantly lower than that of the monitor probe height (e.g., grasslands, croplands).

EPA believes that this important uncertainty should be taken into ac count in establishing

a standard that is not more protective than necessary. In so doing, EPA recognizes that the degree of protection afforded by a standard is determined by the combination of the various elements of a standard, including fo rm, averaging time and level. Thus, EPA believes that this uncertainty can be addresse d in part by coupling a standard level in the proposed range with a three year average st andard, rather than an annual standard.

(5) Comment: The Annapolis Center stated an addi tional concern that the CASAC made its

recommendations based on the draft Staff Pa per that contained errors overstating the magnitude of vegetation effects. In partic ular, the Annapolis Cent er states “...[t]here were major errors in the translation of the results of the vegetation risk assessment into the second draft Staff Paper, overstating the magnitude of crop loss from ozone....While this was corrected in the final SP, CASA C made its recommendations concerning the secondary standard based on the draft text th at contained numerous errors overstating the magnitude of vegetation effects.”

Response: EPA disagrees that this error factored significantly into CASAC’s

recommendations. CASAC considered the entire body of information available during

the review to inform its recommendations. In addition, CASAC reviewed the final Staff Paper and submitted an additional letter (Henderson, 2007) restating and in some cases elaborating on their earlier a dvice to the Administrator on the second draft Staff Paper (Henderson, 2006). Had the change in risk results significantly factored into their reasons for recommending a revised secondary, they would have revised their advice to

the Administrator in their final letter followi ng their review of the final Staff Paper to reflect this change. As they did not do so, it can be concl uded that their final advice to the Administrator did not depend on the vegetation risk numbers.120 3. Specific Comments on the Interpretation of Scientific Evidence

Comments related to the interpretation of the vegetation and ecosystems effects evidence

for O 3 are addressed in this secti on. Incorporating responses cont ained in Section IV.B.2.a and IV.C.4 of the preamble to the final rule, EPA provi des the following responses to specific issues related to the interpretation of the vegetation and ecosystems effects evidence. Comments related to the overall weight pl aced on the vegetation and ecosyste m effects evidence in reaching

decisions on the need to revise the current standard and on an appropriate standard level are addressed in the preamble and in Sections II.B.1 and II.B.2.c above.

(1) Comment: A number of commenters referenc e information from “new” studies published after the close of th e 2006 Criteria Document in su pport of their positions, both for and against revision of the secondary standard.

Response: EPA notes that as in past NAAQS reviews, it is ba sing the final decisions in

this review on the studies and related information included in the O 3 air quality criteria that have undergone CASAC and public review and will consider newly published studies for purposes of decision making in the next O 3 NAAQS review. In evaluating commenters’ arguments, as discussed below in section II.B.3, EPA notes that its provisional consideratio n of “new” science found that su ch studies did not materially change the conclusions in the Cr iteria Document (See Appendix).

(2) Comment: Several commenters questioned EP A’s basis for concl uding that adverse effects on vegetation would be expected to oc cur under air quality that met or was below that of the current 8-hour secondary standar d. In particular, E xxon-Mobil stated that “EPA is incorrect in concluding vegetation im pacts at the current standard” and further

that the “...newer field-based evidence EP A cites for ozone impacts on seedlings, saplings and mature trees i ndicates ozone impacts but at exposures that are likely in exceedence of the current secondary standard.” This commenter also asserted that “...the analysis is not transparent because diffe rent indices are not di rectly correlated, but the mean or seasonal ozone exposures provided appear to be sufficiently high that they would include multiple days with an 8-hour daily maximum average exceeding 80 ppb. Therefore, while these studies demonstrate oz one impact, they do not appear to provide additional evidence for adverse vegetation im pacts under air quality scenarios meeting

the current standard”. Exxon-Mobil also provided specific comment on a number of studies cited by EPA in the proposal, includi ng: (a) King et al., 2005; (b) Gregg et al., 2003; (c) Karnosky et al., 1999; and (d) Iseb rand et al., 2001, and states that “...[w]hile these studies provide additional support for ozone impact on vegetation, including

observance of ozone effects in field settings without ch ambers, they do not provide support for the conclusion that ambient levels in compliance with the current standard would result in significant ozone impact .” The specific comments on each study are presented individually below. The comment regarding transparency is addressed in a separate comment below.

(a) The commenter stated that King et al . (2005) “...provided ozone concentrations as seasonal daily averages (49-55 ppb) and tota l seasonal sums (81-97 ppm-hrs for 4.5 to 5121 months. Given expected daily fluctuations, it is likely that the curr ent secondary standard was exceeded for the ozone levels specified, as would the W126 values. This study does not demonstrate impact from ozone levels at or below the current standard.”

(b) The commenter stated that “...the am bient areas where effects were reported had ozone concentrations that likely exceeded th e current secondary st andard....” However, “...[i]n Gregg et al. the ambient concentratio ns are NOT presented as exceedance of 8- hour daily average or even as a cumulative metric, but rather as an annual seasonal 12- hour mean ozone.... Whereas the data of Gregg et al. indicate that ambient levels of O 3 are sufficient to produce biomass loss, it does not address if these ambient levels fall

above or below the current standard.”

(c) The commenter stated that “Karnosky et al. (1999) reports foliar injury in two higher ozone ambient sites and no injury in one low ozone site. Symptoms were worse in FACE plots than in ambient gradie nt sites. Ozone exposure c oncentrations were: ambient higher ozone sites - seasonal sum over 12 hr/d ay = 47-70 ppm hr (5 -43% leaves show injury); FACE exposures with symptoms – seasonal sum over 12 hr/day = 57-61 ppm hr, 12 hr seasonal mean = 54-56 ppb, and 24 hr AOT40 = 27-31 ppm-hrs (11-55% leaves show injury); OTC exposures that produced symptoms – seasonal sum over 12 hr/day = 50-60 ppm hr (50 percent leaves show injury of sensitive clones). These exposures are likely to include exceedances of the current secondary standard.”

(d) The commenter stated that “Isebrand et al. (2001) reports resu lts for FACE plots of elevated ozone, although the levels in oz one addition treatments are indicated to be representative of current conditions in many areas surrounding midwestern [sic] cities. The exposures show episodic total seasonal exposures of 90 ppm-hr. The five clones studied showed significant variability in re sponse to ozone, with one showing increased growth under elevated ozone. Th e results of this study support the poten tial of ozone to impact vegetation, but again the ozone exposure level is sufficiently high to indicate that there were likely multiple exceedances of the current secondary standard.”

Response: The commenter is mistaken in its asse rtion that EPA is claiming that the above named studies, in and of themselves , demonstrate support for concluding that

adverse O 3 -induced impacts on vegetation would occur at air quality levels that meet or

are below the standard. Rather the conclusion reached by EPA regarding these field based studies, as the following excerpts from the proposal notice show, is that the new field based studies provided limite d qualitative support to the us e of the OTC derived C-R functions to describe plant response in the field. Specifically, the proposal notice states “One such study is of particular importance in that it documented growth effects from O 3 exposure in the field without th e use of chambers or other fumigation methods that were as great as those seen in OTC studies (G regg et al., 2003).... A nother recent set of studies employed a modified Free Air CO 2 Enrichment (FACE) methodology to expose vegetation to elevated O 3 without the use of chambers. Taking all of the above into account, results from the Wisconsin FACE s ite on quaking aspen appear to demonstrate

that the detrimental effects of O 3 exposure seen on tree growth and symptom expression in OTCs can be observed in the field using this exposure method (Karnosky et al., 1999;122 2005). The Staff Paper thus concluded that the combined evidence from the AspenFACE and Gregg et al. (2003) fiel d studies provide compelling and important support for the appropriateness of continued use of the C- R functions derived using OTC from the

NHEERL-WED studies to estimate risk to these tree seedlings under ambient field exposure conditions. These studies make a si gnificant contribution to the coherence in the weight of evidence available in this review and provide additional evidence that O 3 - induced effects observed in chambers also occu r in the field” (72 FR 37886). As a result of this primary conclusion, th e proposal then states “[o]n th e basis of such key studies, the Staff Paper concludes that the expanded body of field-based evidence, in combination

with the substantial corrobor ating evidence from OTC data , provides stronger evidence

than that available in the last review that ambient levels of O 3 are sufficient to produce visible foliar injury symptoms and biomass loss in sensitive vegetative species growing in natural environments” (72 FR 37897). In rega rd to comments on particular studies, EPA notes the following:

(a) EPA agrees that the findings of King et al., 2005 do not demonstrate effects below

the level of the current standard. Howe ver, the most important contribution of this study is not the level of exposures that produced the resp onse, but that the response occurring in the field was comparab le to that of previous OTC studies, thus strengthening the cohe rence across the available weight of evidence. (b) EPA agrees that Gregg et al., 2003 did not directly address whether the ambient concentrations experienced in the study fe ll above or below the current standard. However, EPA obtained the raw data from the authors in order to calculate the W126 values for those same ambient expos ures (Figure 7-17 on page 7-57 of the Staff Paper). From this raw data, EPA observed that significant biomass loss was

observed at O 3 air quality ranging from the level of the current standard to 4 th
highest daily maximum 8-hour averages well below (e.g., 0.072 ppm) the current

8-hr standard. (c) EPA agrees that while not demonstrati ng effects below the level of the current standard, Karnosky et al. (1999) demonstr ated that across FACE, gradient and OTC studies using the same tree species, the magnitude of O 3 -induced effects were similar, increasing EPA’s confid ence in using OTC C-R functions and strengthening the coherence across th e available weight of evidence. (d) EPA agrees that while not demonstrati ng effects below the level of the current standard Isebrand et al. (2001) further de monstrated that the response occurring in the field was comparable to that of prev ious OTC studies, thus strengthening the coherence across the available weight of evidence.

(3) Comment: Exxon-Mobil asserted that the “...FACE and grad ient studies show that ozone can impact tree species, but specifi c provision and/or comparison of the concentration-response functions from these studies with those fr om OTC studies is limited. Thus, these studies, while very info rmative, do not reduce the uncertainties in the OTC concentration-response functi ons.... EPA should develop concentrationresponse functions based upon the newer data in the same form as the existing ones, to allow direct comparison.”123 Response: Because the C-R functions devel oped in OTC included multiple exposure levels including charcoal filtered air repr esenting below ambient conditions, ambient and above ambient, it is not currently possible to create directly comp arable C-R functions based on the FACE or gradient study data , since they cannot exclude ambient O 3 concentrations. However, in these field studies (e.g., the FACE studies) the observed vegetation response from O 3 exposures at ambient or abov e was similar to that observed in OTC studies at similar levels of exposur e. Though these studies are still limited in scope, it is nevertheless EP A’s conclusion that such fiel d-based evidence reduces the

uncertainties associated with the C-R functions generated in OTC studies that were noted by the Administrator in the last review. Thus, the current body of evidence increases

EPA’s confidence in the results from the OTC studies which demonstrate O 3 -related effects at exposure levels below that of the current standard.

(4) Comment: Exxon-Mobil stated that “[s]everal tim es in the proposed rule, EPA indicates the potential for a compounding effect of ozone exposures on perennial species, including studies that document carryover effects. (72 Fed. Reg. at 37,898). EPA fails to provide documentation that supports this claim. Neither the proposal nor the CD and SP reference studies that provide evidence of carry-over effects. The multiple-year studies on tree species cited by EPA do not demonstrat e a carry-over or compounding effect, but rather that ozone resulted in a similar pe rcent change across st udy years (Figure 4 in Isebrand et al. 2001; Figure 2 in King et al. 2005; ...). EPA should conduct analyses on

other available data sets to determine if the results of th e two studies cited above are generally representative.

Response: The commenter is mistaken in a sserting that EPA has not provided documentation for its claim of the possibility of carry-over effects. EPA directs the commenter to pp. 9-6 and 9-9 of the Criteria Document, 7-6 of the Staff Paper and pp. 72 FR 37886, 37894, 37897, and 37898. For example, the proposal notice (72 FR 37886), in citing back to the Criteria Document states “Trees and other perenni als, in addition to cumulating the effects of O 3 exposures over the annual growing season, can also cumulate effects across multiple years. It has been reported that effects can “carry over” from one year to another (EPA, 2006a). Growth affected by a reduction in carbohydrate storage in one year may result in the lim itation of growth in the following year (Andersen, et al., 1997 ). Carry-over effects have been documented in the growth of some tree seedlings (Hogsett et al. 1989; Simini et al., 1992; Temp le et al., 1993) and in roots (Andersen et al., 1991; EPA, 1996a). On th e basis of past and recent OTC and field study data, ambient O 3 exposures that occur during the growing season in the United States are sufficient to potentially affect the annual growth of a number of sensitive seedling tree species. However, because mo st studies do not take into account the possibility of carry-over effect s on growth in subsequent years, the true implication of these annual biomass losses may be missed. It is likely that under ambient exposure conditions, some sensitive trees and pere nnial plants could experience compounded impacts that result from multiple year exposures.”

(5) Comment: Exxon-Mobil stated that “[w]hile EPA is correct in stating that the field data indicate some level of visible ozone injury at ambient levels that meet the current124 secondary standard (Jacobson, 1977), EPA has not addressed potential confounders, such

as soil moisture or related the visible foliar injury symptoms to other vegetation effects. EPA also indicates a major confounder for ozon e induced visible foli ar injury is soil moisture – with dry periods in local areas decreasing incidence and severity of visible foliar injury (p. 7-61). These same cond itions would favor higher ozone levels. Furthermore, the W126 values for these sites ar e not provided, so it cannot be assessed if the proposed W126 standard would provide additional protection. EPA should provide the comparable W126 values and compare folia r injury at ‘non-background’ sites with ‘background’ sites, to better understand the impact of ozone exposures above background

levels.”

Response: EPA disagrees with the commenter that it has not addressed potential

confounders such as soil moisture. EPA disc usses this issue pg. 7-61 of the Staff Paper and clearly takes this into acc ount in considering how much we ight to put on foliar injury data (see also discussion under Form above). EPA further notes that it assessed incidence of visible foliar injury across a f our year period (e.g., 2001-2004). Though not specifically evaluated, within th at four year period it is likely that a variety of soil moisture conditions existed, both temporally and spatially. Ev en so, at no point in that four year period, did incidence of foliar in jury drop below 21% for areas that met the level of 0.084 ppm (see Table 7-4, Staff Paper p. 7-64). At the time this analysis was conducted, EPA was still considering using the SUM06 form, so only SUM06 comparisons are included in the table. Howe ver, EPA notes that a SUM06 of 25 ppm-hrs is approximately equivalent to a W126 of 21 ppm-hrs so that an approximate comparison

could be made.

(6) Comment: Exxon-Mobil stated that “EPA also indicates that Morgan et al. 2003 show

consistent deleterious effects of ozone exposures on soybean from 1973-2001.” The commenter goes on to assert however that “... the Morgan et al. 2003 meta-analysis is not presented by year and provides results by tim e, so it cannot be us ed to support the

statement of consistent deleterious effects over time. Morgan et al. provide ranges of ozone impact for ozone concentrations in th ree average daily concentration categories: 30-59 pb [sic], 60-79 ppb, 90-120 ppb. For the highest two categories and the upper range of the lowest category, it is likely that there were multiple exceedences of the current 8-hour secondary st andard. EPA should follow its own recommendation included in footnote number 57 on page 37889 and develo p new concentration-response functions for new studies that are updated to meet recent air quality conditions.”

Response: The commenter is correct in that Morgan et al. ( 2003) does not list the studies by date. However, in Figure 2 of the paper O 3 is shown to have a negative effect on nearly all the variables measured on soyb ean. Most importantly, seed yield was consistently lower under elevated O 3 concentrations. This stu dy was not cited to address whether effects were still occurring at the curren t standard level. It was cited to point out that across many cultivars in studies conducte d over many years there is an apparent consistency of negative e ffects on soybean yield.125 (7) Comment: Several commenters argued that be cause the C-R functions used in this review were developed under the NCL AN program which used exposure regimes containing numerous hourly values greater than 100 pp m (Lefohn and Foley, 1992), a concentration response function should be de veloped that includes components for both the cumulative seasonal ozone exposure and fr equency of hourly peaks. For example,

Exxon-Mobil states that “Researchers have documented that the NCLAN studies contain numerous hourly values gr eater than 100 ppb (Lefohn and Foley, 1992). Failure to include these values known to be key dete rminants of plant effects in the exposureresponse function is a significant oversight for a proposed national standard. The number of hourly values greater than 100 ppb ...indi cates that many of the NCLAN exposures would have multiple exceedences of an 8-hour standard of 80 ppb. Therefore, reliance on NCLAN data to support the conclusion that exposures below an 8-hour standard would result in ozone impact has significant limitati ons if the response func tion fails to consider these peak concentrations.

Response: EPA agrees with these commenters th at a biologically rele vant concentration response function should take into account both cumulative and peak exposures. However, EPA does not agree with the commen ters that the W126 alone fails to do so. The W126 was designed to cumulate exposures while giving greater weight to peak

concentrations. The Criteria Docume nt and CASAC recommended a cumulative weighted metric (such as W126) as the mo st appropriate index and did not recommend the addition of N100 or any other modifications to W126.

(8) Comment : Exxon-Mobil stated “ Despite previous requests, EPA has not provided the concentration-response functi ons for the 8-hour form of the standard. Therefore, a comparative analysis of the relative protec tion afforded by an 8-hour form to that provided by the proposed W126 form cannot be completed... EPA has failed to show that the current 8-hour standard would provide less than requisite protection. EPA should develop concentration response relationships using the 8-hour form of the standard for

the same datasets that form the basis for th e proposed W126 standard. Frequency of peak

occurrence should also be included in the anal ysis. This is the only meaningful way to compare the level of protection afforded by the different standards.” This commenter further stated that without such a compar ison, EPA fails to show that the currently proposed W126 standard would result in addi tional protection than the current 8-hour secondary standard.

Response: For the reasons discussed in the preamble, EPA has determined that it is appropriate to adopt an 8- hour average secondary standa rd instead of a cumulative seasonal standard. In response to the comment that EPA has failed to produce C-R functions in terms of the 8-hour form, EPA poi nts the reader to Appendix 7E (Figure 7E1) of the Staff Paper that shows the NCLAN crop yield loss data recal culated in terms of the 8-hour form. This graph shows that a 4 th highest maximum daily 8-hour average level that corresponds to the pr otection level used in the last review (e.g., no more than 10% yield loss in 50% of the crop cases) woul d be close to 0.06 ppm. Therefore, the current 8-hour average secondary standard set at the current le vel (0.084 ppm) clearly does not provide the level of protection e xpected and judged to be requisite by the126 Administrator in the last re view as expressed in terms of a SUM06 of 25 ppm-hrs (approximately equivalent to W126 of 21 ppm-hr s evaluated in this re view). Field-based information that shows effects occurring in th e field at ambient air quality levels at and

below the level of the current 8-hour standa rd support this conc lusion. For example, EPA staff obtained the raw hourly data that pr oduced the results in Gregg, et al., 2003 in

order to calculate the W126 values associat ed with the cottonwood tree seedling biomass loss as graphed in Figure 7-17 on page 7-57 of the Staff Paper. Though the 4 th highest maximum daily 8-hour averages were not presen ted in the Staff Paper, the raw data to

calculate this are available in the docket. 7 From this raw data, EPA observed that significant biomass loss was observed at O 3 air quality ranging from the level of the

current 8-hour standard to 4 th highest daily maximum 8-hour averages well below (e.g., 0.072 ppm) the current 8-hour standard. Taken to gether with the foliar injury data which occurred at areas meeting and/or below the le vel of the current 8-hour standard (see Staff Paper p. 7-61 to 7-64; Table 7-4), EPA conc luded that significant vegetation effects can occur at air quality levels that meet or ar e below the level of the current 8-hour, 0.08 ppm secondary standard.

(9) Comment : Exxon-Mobil stated that “[t]he basi s for a regulatory standard should be transparent.” This commenter then identifi es three areas where it alleges a lack of transparency: (a) “Inconsisten t use and reporting of metrics and, in some cases, reference to unavailable information, result in a gene ral lack of transparency in the science supporting a revised secondary standard. The studies pres ented differ in metrics and some studies fail to present all metrics. EP A has failed to conduct a re-evaluation of the studies in order to report resu lts in a consistent format....E PA should provide re-analysis of data and reporting in common metrics as a ppropriate, particularly to support the key points of its rulemaking.” (b) “...EPA c ites the recommendations of a consensus workshop (Heck and Cowling, 1997) several times. However, this workshop was by invitation only, and documentation is not avai lable to the public. The reference [sic] cited is short and provides consensus recomm endations, but without details as to their basis. In particular, the basis for the recomm endation to consider a 2 percent effect level to be significant is not provided. It is not clear how this effect level could be experimentally determined, if it is discer nible from biological variability, or what references suggest the potential compounding e ffect over multiple years, given the results of Isebrand et al. (2001) and Ki ng et al (2005) cited above.... If available, a more detailed report of the consensus workshop should be released. If stud ies to support the recommendations cannot be provided, then the recommendations should be used with great caution.” (c) “An addi tional reference cited in the SP (section 7.5.1) as the source of key information on crop and seedling concen tration-response, Lee and Hogsett (1996),

is not available. This document is an EPA report, and its release was requested in previous comments to EPA. However, it could not be found on a search of the EPA

7 Data for Figure 7-17 on pg. 7-57 of the final ozone staff paper: The hourly ozone data in

this file was used to calcul ate the 12-hr W126 ozone exposures for the cottonwood trees grown in the New York City area. Docket N o. EPA-HQ-OAR-2005-0172-6753. November 29, 2007.127 website or a specific search of EPA public ations....EPA should also make the Lee and Hogsett (1996) report ava ilable to the public”

Response : (a) EPA agrees that different studies have used different metrics for reporting

results and that this has result ed in a lack of direct compar ability between these studies. However, in some of these studies, the authors have directly compared their results in the

field to those from OTC studi es and reported that result s are similar between plant response in OTCs and in the field. It is th is latter point of comp arison that EPA felt was

most informative in the context of this revi ew. Thus, EPA does not agree that converting all exposure metrics to a common metric for co mparability is a critical activity for the purpose of this review.

(b) EPA agrees that insufficient information is available to judge the scientific basis for the consensus statements from the Heck and Cowling, 1997 consensus workshop. The preamble to the final rule states “With rega rd to comments stating concern with EPA’s apparent reliance on the recommendations from the 1996 consensus workshop in selecting a range of levels, EPA agrees that though the workshop part icipants were asked to review, and thus were aware of, the scien tific literature available at the time, as

described in both the 1996 O 3 Criteria Document and Staff Paper, the workshop discussion of ranges of levels recommended as protective of different vegetation types for different effects falls short of providing a scie ntific basis for determining at what level these effects become adverse to the public welfare. In addition, EPA agrees that the scientific basis for establishing a 2% leve l of biomass loss in tree seedlings as a

benchmark of concern to take into account the possibility of compounding is unclear, though there was and continues to be eviden ce of the potential for compounding effects to occur over multiple years (72 FR 37885, 37886).

(c) EPA notes that the 1996 article by Lee a nd Hogsett is available in the docket (Docket No. EPA-HQ-OAR-2005-0172-0069. January 25, 2007.)

(10) Comment: A number of commenters expressed c oncern that the possible impact of O 3 - related reductions in plant pr oductivity could result in a redu ced capacity of vegetation to serve as a carbon sink to mitig ate the impacts of rising CO 2 in a changing climate, citing to a “new” study on that topic (Sitch et al., 2007). Many of these same commenters also

cited to “new” field-based studies in the Great Smoky Mountain National Park that find a relationship between O 3 exposure, tree stem growth loss, tree water use and stream flow

as evidence that current ambient O 3 levels can impact ecosystems and that ecosystems should be afforded protection from such potenti al effects. For example, some of these

commenters note that “new” studies in th e Great Smoky Mountain National Park (McLaughlin, et al., 2007a,b) ha ve found that (1) ambient O 3 caused substantial growth

reductions in mature trees in a mixed deciduous forest, which was due in part to increased

O 3 -induced water loss and led to seasonal loss es in stem growth of 30 - 50 percent for most species in a high-ozone year; (2) increasing ambient O 3 levels also resulted in depletion of soil moisture in the rooting zone and reduced late-season stream flow in the watershed; and (3) O 3 may amplify the adverse effect s of increasing temperature on forest growth and forest hydrology and may exacerbate the effects of drought on forest128 growth and stream health. Other “new” research noted by these commenters as supporting EPA’s findings that current O 3 exposures cause significant biomass losses in sensitive seedlings of various tree species in clude a study that predic ted up to 31 percent growth loss in aspen in certain areas of its North American range in 2001-2003 (Percy, et al., 2007).

Response : EPA agrees that O 3 exposure can decrease the poten tial for plants to sequester carbon. This topic is discussed in the Cr iteria Document, Staff Paper and proposal notice. The proposal states (72 FR 37888/9) “Temperate forests of the northern hemisphere have been estimated to be a net sink of C per year (Goodale et al. 2002). Ozone interferes with photosynthesis, causes some plants to senesce leaves prematurely and in some cases, reduces allocation to stem and root tissue. Thus, O 3 decreases the potential for C sequestration. In the presence of high O 3 levels, the stimulatory effect of rising CO 2 concentrations on forest productivity has been estimated to be reduced by more that 20 percent (Tingey et al. , 2001; Ollinger et al. 2002; Karnosky et al. , 2003). In summary, it would be anticipat ed that meeting lower O 3 standards would increase the

amount of CO 2 uptake by many ecosystems in the U.S. However, the amount of this improvement would be heavily dependen t on the species composition of those ecosystems. Many ecosystems in the U.S. do have O 3 sensitive plants. For, example forest ecosystems with dominant species su ch as aspen or ponde rosa pine would be expected to increase CO 2 uptake more with lower O 3 than forests with more O 3 tolerant species. With regard to the other effects de scribed in the “new” studies, EPA refers the reader to the Appendix.

4. Specific Comments on the Vegetati on Exposure and Risk Assessments

Comments related to the quantitative vege tation exposure and risk assessments conducted

for O 3 are addressed in this section. Incorporat ing responses contained in Section IV.B.2.b and IV.C.4 of the preamble to the final rule, EPA provi des the following responses to specific issues

related to these assessments. Most comments received on these assessments were from those commenters opposed to revising th e current secondary standard, including Exxon-Mobil, UARG, the Annapolis Center, AAM, and some State agenci es. Comments related to views regarding the appropriate weight to place on the vegetation exposure and risk assessments in reaching

decisions on the need to revise the current standard and on an appropriate standard level are addressed in the preamble a nd in section II.B.2.a above.

(1) Comment: In general, as stated by AAM, thes e commenters asserted that “there are problems, flaws and concerns with the St aff Paper analysis and vegetation risk assessment that precludes the establishment of a separate secondary standard to protect vegetation.

Response: EPA agrees that there are uncertainties and limita tions associated with the vegetation exposure and risk assessments. Co mments regarding specific concerns will be addressed individually below. However, EPA disagrees that such limitations would necessarily “preclude the esta blishment of a separate sec ondary to protect vegetation.”129 (2) Comment: A number of commenters asserted that EPA used unrealistically low levels of

PRB that resulted in an overestimate of risk s and benefits associat ed with just meeting alternative standards. In particular, the Annapolis Center states that “...[t]he same analyses, arguments, and data that apply to considerati on of background for the primary standard also apply to the secondary standard.”

Response: EPA strongly disagrees with the as sertion of these commenters that EPA used unrealistically low levels of PRB, for the reasons documented in section II.A.5 above, and in the preamble to the final rule in section II.B.2.b, which addresses this and other comments related to EPA’s approach to estimating PRB and its role in exposure

and risk assessments related to the primary standard.

(3) Comment: The Annapolis Center and AAM state that “...the global model EPA relied on is not capable of resolving the phenomena that contribute to attainment or nonattainment of secondary ozone standards throughout the country. In fact, even a more refined, higher resolution model, the Community Mu lti-Scale Air Quality (CMAQ) modeling system... performed poorly in predicting the observed 2001 SUM06 and W126 in the west.... This means that the sources and processe s that contribute to substantial levels of

both SUM06 and W126 in rural and remote areas in the Western U.S. are not wellcaptured in state-of-the-art chemical tran sport models....” These commenters further state that “...[t]he map of ‘as is’ W127 leve ls included as Figure 7-6 of the SP shows W126 levels exceeding 7 ppm-hrs throughout many areas of the country...The overall pattern of W126 suggests both a contribution from U.S. man-made emissions and a background component that could involve bi ogenic emissions, ag ricultural emissions, long-range transport from non-U.S. sources , and a stratospheric component. In particular, W126 levels great er than 7 ppm-hr exist in many locations throughout the country, including many rural and remote Western sites well-removed from anthropogenic emission source areas. AAM furt her elaborates that “...[t]hese levels could be explained in part by NOx emissions from soils due to microbial processes. Jaegle, et al. [(2005)], using satellite observations of NO 2 columns, found that soil NOx emissions were twice as high as assumed in the GEOSS-CHEM model. This will result

in a misallocation of ozone between man-made and natural sources. The presence of a large soil NOx source in the Great Plains also may help explain the discrepancy between

the locations of elevated SUM06 and W126 and the major populated areas of the country. Thus, “EPA and CASAC assume, incorrectl y, based on the Fiore et al. 2003 global modeling analysis, that SUM06 or W126 is not confounded by background ozone.

Response: EPA’s conclusions regarding the ap propriateness of using the GEOSS-CHEM model predictions of PRB are discussed in de tail in section II.A.5 above. Because PRB is defined as including those sour ces of ozone or ozone precu rsors that are uncontrollable by the U.S., the natural sources of O 3 precursors such as soil NOx concentrations and stratospheric intrusions, as well as long-range transport from non-U.S. sources have already been included in these estimates. Base d on the range of PRB values estimated in this review (e.g., 0.015 to 0.035 ppm), EPA calculated the maximum PRB background contribution that would be po ssible using the 3-month 12-hr W126 exposure index (see130 Staff Paper, p.7-22). Using a constant hourly O 3 concentration of 0.035 ppm (the upper end of the PRB range), multiplied by the very low weight assigned by the W126 weighting scheme and cumulated for 12 hours a day for 3 months (92 days), the PRB value is less than 1 ppm-hr. Thus, on this basis, EPA concludes th at areas experiencing W126 values of 7 ppm-hrs or greater, as depict ed in Figure 7-6 of the Staff Paper, likely have a very low contributi on from PRB and a substantia l contribution from non-PRB sources. It is unclear why the commenter views long-range transport of anthropogenic precursors of O 3 or O 3 itself from source regions within the U.S. improbable, since the possibility of long-range transport of th ese pollutants from non-U.S. sources in contributing to PRB has already been acknowle dged. On a final note, the study cited by the commenter (e.g., Jaegle et al., 2005) was not evaluated in the Cr iteria Document or Staff Paper and is considered a “new” study (see discussion under II.B.3, above).

The proposal notice further discusses considera tions regarding the pot ential influence of PRB on the W126 value at high elevation sites and states “[t]he Cr iteria Document (EPA, 2006a), discusses policy relevant background (P RB) levels for high elevation sites and makes the following observations: (1) PRB concentrations of 0.04 to 0.05 ppm occur occasionally at high-elevation sites ( e.g. , >1.5 km) in the spring due to the freetropospheric influence, including some limite d contribution from hemispheric pollution (O 3 produced from anthropogenic emissions outside North America); and (2) stratospheric intrusions mi ght occasionally elevate O 3 at high-altitude sites, however, these events are rare. Therefore, the Staff Pa per concludes that springtime PRB levels in the range identified above and rare stratospheric intrusions of O 3 are unlikely to influence

3 month cumulative seasonal W126 values...” that are calculated for the maximum 3 month period during the O 3 season.

(4) Comment: Another commenter disputed EP A’s calculation of the maximum PRB contribution to 3-month, 12-hour W126 values. Specifically, UARG a sserts that “...[i]f, however, one takes monitored air quality at the remote Trinidad Head, California monitoring site as indicativ e of PRB, the contribution to the 3-month, 12-hour W126 could be as much as 3.50 ppm-hour.” In a f ootnote to the comment, UARG explains that this value was arrived at by assuming that two-thirds of the 24-hour W126 value calculated for the 3-month period April to June 2003 would be equal to the 12 hour value.

Response: As EPA has already stated in II. A.5, above, both EPA’s experts and CASAC endorsed the use of the peer-reviewed, t horoughly evaluated mode ling approach (GEOSCHEM) described in the Criteria Document as the best approach for estimating PRB

levels. The Criteria Document reviewed de tailed evaluations of GEOS-CHEM with O 3 observations at U.S. surface sites (Fiore et al., 2002, 2003) and comparisons of GEOSCHEM predictions with observations at Trin idad Head, CA (Golds tein et al., 2004) and found no significant differences between the mo del predictions and observations for all conditions, including those reflecting those gi ven in the PRB definition. The Criteria Document (p. 3-49) states that the current m odel estimates indicate that PRB in the U.S. is generally 0.015 to 0.035 ppm th at declines from spring to summer and is generally < 0.025 ppm under conditions conducive to high O 3 episodes. The Criteria Document acknowledges that PRB can be higher, especial ly at elevated sites in the spring due to131 stratospheric exchange. Howeve r, unusually high springtime O 3 episodes tied to stratospheric intrusion are rare and generally occur at elevated locations and these can be readily identified and excluded under EPA’s exceptional events rule (72 FR 13560) to avoid any impact on attainment/non-attainment st atus of an area. Thus, EPA concludes that such a high PRB value would be extremel y rare, and highly unlikely to occur during the maximum 3-month daytime period evaluated against the level of the W126 standard. If due to stratospheric exch ange, this value would be excluded from consideration.

(5) Comment: Many commenters also asserted that there was a lack of new information

since the last review that w ould, in their judgment, materi ally reduce the uncertainties present in the assessments conducted for the last review. For example, the Annapolis Center asserted that “...[s]ome of the most important caveats and uncertainties concerning the exposure and risk assessments fo r crop yield that were listed in the [1996] proposal included (a) extrapola ting from exposure-response functions generated in opentop chambers to ambient conditions; (b) the lack of a performance evaluation of the national air quality extrapolat ion; (c) the methodology to adjust modeled air quality to

reflect attainment of various al ternative standard options; and (d) inherent uncertainties in

models to estimate economic values associated with attainment of a lternative standard. . .

. Because of the lack of new data or subs tantive improvements in the risk assessment, these same issues remain today, contributing a similar degree of un certainty, as was the case in the prior review.”

Response: While EPA recognizes that important uncertainties remain in estimates of vegetation exposure and O 3 -related risk to vegetation, especially with regard to O 3 -related effects on crop yields, EPA disagrees with commen ts that assert that the uncertainties in such assessments remain unchanged or generally have not been materially reduced since

the last review. EPA discusses each of the uncertainties from the 1997 review identified by the commenters in turn below.

(a) With regard to the uncertainties associ ated with using the OTC C-R functions, the Annapolis Center further stated that “C ASAC characterized the estimates as rough estimates because the open-t op chambers alter the ambi ent microclimate conditions introducing uncertainty. The concern was raised that in these studies, plant response to ozone has been optimized under conditions that do not reflec t real-life field conditions....The Panel concluded that ‘five year s from now, if we do not have the results of research coupling ozone air quality and plant biology under conditions more representative of ambient field conditions, th en we will continue to be hampered by our inability to come to consensus on the levels of air quality that are protective of vegetation and ecosystems...’ ”. In addition, the Annapo lis Center states that “...[t]en years have now elapsed, and the same concentration-res ponse functions from the OTC studies of the 1980’s are still the only viable data to us e to estimate crop loss .... The 1996 CASAC Panel agreed that the estimates of crop loss at that time were highly uncertain. It raised specific issues concerning the procedures and noted that the background estimate of 0.025 ppm was too low and would over-infla te the crop loss estimates.”132 While EPA agrees that important uncertainties continue to be associ ated with the use of the C-R functions generated many years ago us ing OTC studies for crop yield loss, EPA does not agree that the new information avai lable in this review has not reduced the

uncertainties identified above and in th e last review. EPA concludes that the

uncertainties associated with continued use of the C-R functions derived from the

NCLAN OTC studies have been materially reduced in three important ways by the recent information. First, and most importantly, as described above and in the Staff Paper and proposal, the results of signi ficant new field based studies (e.g., AspenFACE, SoyFACE and gradient) show that the levels of vegeta tion response that have been observed in the field are of similar magnitude as those obs erved in OTC experiments, thus providing qualitative evidence that use of C-R functions generated in OTC would not be expected to overestimate risk to vegetation in the fiel d. Second, the lower estimates of PRB in this review (e.g., 0.015 to 0.035 ppm) now bracket the 0.025 ppm level used as the lowest exposure level representing background in th e OTC studies. This further reduces the

concern that these C-R functions result in an overestimation of risks in the field. Third,

limited information available in this review on the O 3 sensitivities of some crop species (e.g., soybean, cotton) suggests that O 3 sensitivity has not cha nged significantly in the intervening years. Taking a ll the above into account, EPA’ s level of confidence in the applicability of the OTC gene rated C-R functions to repres ent ambient conditions in the field has materially increased.

(b) With regard to the lack of a perfor mance evaluation of the national air quality extrapolation, EPA disagrees a nd notes that there have been advancements in the tools and methods used for such extrapolations and the characterization of associated

uncertainties since the last review. With respect to the generation of interpolated O 3 exposure surfaces, EPA employed a different appro ach than that used in the last review and undertook a quantitative assessment of the uncertainties associat ed with the use of this method. This uncertainty assessment was accomplished by sequentially dropping out of the interpolation each m onitoring site and then reca lculating the exposure surface using the remaining monitoring sites. As di scussed in the Staff Paper, this method of evaluation may result in a slight overestimati on of error and bias for the exposure surface, since dropping out monitors loses information that the interpolation uses in that local area. As another point of comparison, EPA al so examined the subset of rural CASTNET sites to illustrate how the interpolation t echnique predicted air qua lity in that rural monitoring network. For this subset, the ev aluation indicated that in general, the interpolation technique sligh tly overestimated W126 exposures at relatively low levels and underestimated W126 exposure at relati vely high levels. This aspect of the estimation method potentially resulted in an und erestimation of the more important risks associated with higher cumulative exposures in some areas. Base d on this evaluation, EPA reiterates the conclusion in the Staff Pape r that “...the calculation of error and bias metrics for the interpolation represents a notable improvement over the 1996 assessment

which did not have such an evaluation.” EPA further concludes that in general, the sources and likely direction of uncertainties associated with th e exposure and risk

assessments have been better accounted for a nd characterized than in the last review.133 (c) With regard to criticisms of the met hodology used to adjust modeled air quality to

reflect attainment of various alternative standard options, the Annapolis Center further states that “EPA’s analysis to date does not evaluate the impact of the nation’s ozone control program on W126 in a scientifically sound manner.” EPA strongly disagrees and

notes that this issue has been raised in the context of both the primary and secondary

standards. As noted above in section II.B.2.b, based on information in the Staff Paper (section 4.5.6) and in more detail in a st aff memorandum (Rizzo, 2006), EPA concluded that the quadratic air quality adjustment approach used in this assessment generally best represented the pattern of reductions across the O 3 air quality distri bution observed over the last decade in areas implementing c ontrol programs designed to attain the O 3 NAAQS. While EPA recognizes that future ch anges in air quality distributions are areaspecific and will be affected by whatever spec ific control strategies are implemented in the future to attain a revised NAAQS, ther e is no empirical evid ence to suggest that

future reductions in ambient O 3 will be significantly different from past reductions with respect to impacting the overall shape of the O 3 distribution.

(d) With regard to comments that asserted that inherent uncertainties in models to estimate economic values of crop loss have not been reduced since the last review, EPA acknowledges that while an upda ted state of the art model, the AGSIM benefits model, was used in this review, substantial uncertain ties remain in these estimates of economic crop loss. Further, EPA notes that these estimates were not relied on as a basis for reaching a decision on the need to revise the current standard.

(6) Comment: Some commenters also asserted that the estimated exposures and risks associated with air quality just meeting the cu rrent standard have not appreciably changed

since the last review. These commenters used this conclusion as the basis for a claim that there is no reason to depart from the Ad ministrator’s 1997 decision that the current secondary standard is requisite to protect public welfare.

Response: EPA believes that this claim is f undamentally flawed for three reasons, discussed in turn below: (a) it is fact ually inappropriate to compare quantitative vegetation risks estimated in 1997 with those es timated in the current rulemaking; (b) it

fails to take into account that with similar risks, increased certainty in the risks presented by O 3 implies greater concern than in the last review; and (c) it fails to recognize that the

Administrator has used these estimates in a supportive role, in light of the significant uncertainties in the exposure and risk es timates, to inform the conclusions drawn primarily from the integrative assessment of the vegetation effects information on

whether adverse O 3 -induced effects to vegetation observed under ambient O 3 levels

allowed under the current stan dard are sufficiently advers e to the public welfare to

warrant a revision of the O 3 standard.

(a) The 1997 risk estimates, or any comparis on of the 1997 risks estimates to the current estimates, are irrelevant for the purpose of judging the adequacy of the current 8-hour standard, as the 1997 estimates reflect outdated analyses that have been updated in this

review to reflect the current sc ience. In particular, as disc ussed in section 7 of the Staff Paper, there have been significant improvement s to the exposure and risk methods used,134 incorporation of additional sources of inform ation, more sophisticati on in application of approach and methods evaluation/uncertainty characterization that make comparisons inappropriate between the pr ior and current review.

(b) It is important to take into account EPA’s increased level of confidence in use of OTC derived C-R functions to predict risks in the field based on impor tant new field data

and the lower estimates of PRB estimated in this review, since in judging the weight to place on quantitative risk estimates it is impor tant to examine not only the magnitude of the estimated risks but also the degree of confidence in those estimates.

(c) Quantitative vegetation risk estimates we re not the main basis for EPA’s decision in setting a level for the secondary standard in 1997, and they do not set any quantified “benchmark” for the Agency’s decision to revise the current standard at this time. The proposal notice made clear that decisions about the need to revise th e current standard are mainly based on an integrated evaluation of evidence available across a broad array of vegetation effects, while the more uncertain exposure, risk and bene fits estimates were used in a supportive role. Both the Staff Paper and proposal clea rly distinguished the roles that these different types of informa tion played in informing the Administrator’s proposed decision. The proposal states that “...due to multiple sources of uncertainty, both known and unknown, that continue to be as sociated with these analyses, the Staff Paper put less weight on this information in drawing conclusions on the adequacy of the current standard. However, the Staff Paper also recognizes that some progress has been

made since the last review in better characte rizing some of these associated uncertainties and, therefore, concluded that the results of the exposure and risk as sessments continue to provide information useful to informing judgm ents as to the relative changes in risks predicted to occur under expos ure scenarios associated w ith the different standard

alternatives considered.” In determining the requisite level of protection, the Staff Paper recognized that it is appropriate to weigh th e importance of the predicted risks of these

effects in the overall context of public welfare protection, al ong with a determination as to the appropriate weight to place on the a ssociated uncertainties and limitations of this information. Thus, while EPA is fully mindful of the uncertainties associated with the estimates of exposure, risk and benefits, as discussed above, it judges that these estimates are still useful in providing additional s upport for his judgment that the current 8-hour secondary standard does not adequa tely protect sensitive vegetation.

C. Specific Comments Related to Data Handling (Appendix P)

The primary and secondary ozone NAAQS are speci fied in terms of an indicator (i.e., the specific pollutant to be measured), a level that defines the highest ambient concentration for a monitoring site to be considered to be in attainment with the NAAQS, and a statistical form. To determine whether an ambient monitoring site vi olates the NAAQS, the relevant portion of the

historical record of ambient con centrations of the indicator polluta nt at the monitoring site must be selected, evaluated for suitab ility for making a determination, and if suitable summarized into135 a statistic appropriate for comparison to the adopted form and level of the NAAQS. An important aspect of the suitabili ty evaluation is to determine wh ether the ozone monitoring data set is complete enough to represent the actual air quality situation well enough to allow any

determination of current attainment or nonattai nment to be made. These steps collectively are referred to as data handling. Precisely how thes e steps are performed affe cts the stringency of the NAAQS, so the detailed requirements for thes e steps are generally proposed and adopted at the same time as the NAAQS. In this case, they were proposed in the form of a new Appendix P to 40 CFR 50, and were discusse d in the preamble to the no tice of proposed rulemaking.

Appendix P as proposed was a modification of the existing Appendix I which applies to the ozone NAAQS adopted in 1997. The major m odification consisted of conforming revisions to reflect that the proposed 3-decimal-places form of the proposed revised 8-hour primary standard simplifies the steps for comparing th e monitoring data to the level of the NAAQS (because rounding is no longer needed). This issue is not fully separable from the choice of the level of the NAAQS. Comments on the level is sue per se are addressed elsewhere in this

document. The second set of modifications were new provisions for all aspects of data handling for the proposed secondary NAAQS using the cu mulative peak weighted index (because the 1997 primary and secondary NAAQS were identical a nd so no special provisions were needed for the secondary NAAQS).

In the preamble, EPA also invited comment on one particular issue related to data completeness, on possible objective criteria for cons idering ozone levels to have been low during a period of hours or days when ozone mon itoring data was not successfully obtained.

Comments regarding data handling for th e 8-hour NAAQS were mostly about the issue of using 3 decimal places in the level of the NAA QS. A majority of the comments this issue supported EPA’s proposal. Some of the favorable commenters noted that monitor precision allowed rounding to the third d ecimal place; others argued that the proposal would close an existing “loophole” that allowed communities to clai m attainment at concentrations higher than

the standard. Other commenters wrote that the st andard should not be ex pressed to three decimal places. These commenters generally asserted, implic itly or explicitly, that ozone monitoring data has too much uncertainty to allow comparison to a pass/fail limit expressed with three decimal places. There were a few comments on othe r topics, which are included below.

Only a small number of comments were re ceived on the portions of Appendix P that are relevant to a secondary standa rd non-identical to the primar y standard. These generally concerned the proposed data completeness rules, including whether and how to compensate for an incomplete monitoring record.

1. Specific Comments on Data Handling Related to the 8-hour Standard

(1) Comment: Specifying the standard to the th ird decimal place implies a degree of precision in the underlying health effects data that does not exist. EPA recognized this when it adopted the current standard in 1997. It stated, at that time, that it was specifying the standard to two decimal places “in part to reflect uncertainties in the health effects evidence upon which the proposed standard is based,” including “the measurement136 uncertainty and representativene ss inherent in the reported O 3 concentrations used in field and epidemiological studies and the uncertain ty in the exposure estimates upon which the quantitative risk estimates have been base d” (62 FR 38886). Those uncertainties remain. EPA has not explained why those uncertainties should not lead to the same conclusion

reached in 1997.

Response: The body of scientific evidence supp orting EPA’s current revision of the primary O 3 NAAQS is different than the evid ence considered in 1997, so EPA’s statements in 1997 cannot be taken to necessarily apply to the newer body of evidence and the new level of the NAAQS. The interpreta tion of that evidence is discussed in the final rule preamble.

EPA notes that we are not asserting that mon itoring precision in the field has broadly and substantially improved since 1997, although impr ovements have been made. We do not believe that major improvement is a prec ondition for the adoption of a NAAQS specified with three digits.

EPA also notes that as a pract ical matter, given current O 3 concentration measuring equipment and reporting practices , it is inevitable that three di gits will be used in making comparisons to the NAAQS, effectively maki ng the NAAQS have three significant digits even if nominally expressed with only two. Almost all States report hourly O 3 concentrations with three digits. It is nece ssary, therefore, for th e NAAQS rule to specify how those reported digits will be treated thr ough all the steps leading up to and including the final comparison to the NAAQS. If the NAAQS were to be nominally expressed with only 2 digits, it would still be necessary to specify which fina l 3-year average values are considered to be in compliance. So, for example, a hypothetical NAAQS of 0.07 ppm functionally would be either 0.074 ppm (if the rule were to speci fy that the third digit of the final 3-year average value is rounded, as Appendix I specifies) or 0.079 ppm (if the third reported digit of the final 3-year average value were truncated) 8 . That is, the effective level of the NAAQS depends on th e combination of the number of digits specified and the data handling and final co mparison instructions. EPA believes that explicit use of three digits in the definition of the NAAQS is the more transparent approach, as well as the only approach that allows the NAAQS to be set so that 0.075 ppm is treated as complying and 0.0 76 ppm is treated as noncomplying.

(2) Comment: EPA’s ambient air monitoring referen ce methods specify a precision of two decimal places (0.01 ppm) for O 3 concentrations (40 C.F.R. § 53.20, Table B-1).

Response: The Table cited in CFR represents the minimum performa nce specifications and the 0.01 ppm precision is literally a pass/ fail test to determine whether it is appropriate to employ a method in the field. Ac tual monitor precision is much better than the pass/fail limit (about 3 percent precision and about 0 percent bias).

8 In 1997, we considered establishing a NAAQS level of 0. 08 ppm and data handling procedures that would result in any values above 0.080 ppm being considered a violation; in effect that would have been setting a NAAQS of 0.080

ppm.137 (3) Comment: In 1997, EPA also stated its belief that “...expressing the proposed standard to the second decimal place is also consistent with the quality assurance guidelines that indicate the precision for such O 3 measurements shall be within +15%....” Both of those concepts seem valid and appropriate.

Response: The precision limit stated by quality a ssurance guidelines reflects a maximum limit of tolerance and does not at all repres ent what is occurring in the field. As of 2006, the precision limit for O 3 has been lowered to 7% from the original 15% benchmark (40 CFR Part 58, p.61304, section 2.3.1.2).

(4) Comment: The Agency’s calculation of measurement uncertainty is at odds with research showing that instrument imprecision can repr esent 7-40% of the temporal variation in daily measurements for pollutants and that the population-weighted variation in daily ambient air pollutant levels can be as hi gh as 20% for both instrument imprecision and spatial variability.

Response: The statistics cited by the comm enters were taken from an AWMA publication (Wade et al) and were not confined to O 3 monitoring precision and variability but included many other pollutant gases and part iculate species. A close examination of the Wade publication (Table 3) shows th at the estimated “nugget” parameter for O 3 was approximately 0.10 which the authors define to be the ratio of the standard deviation of

the difference between two colloca ted monitors to the standard deviation of their mean.

Since the ratio of the standard de viation of daily maximum 8-hour O 3 to the mean concentration is approximately 0.3 in many urban areas, the nugget value reported by the authors (i.e. 0.10) translates in to a coefficient of variation of approximately 3 percent for

the mean difference between two collocated O 3 monitors (0.10 X 0.30 about 0.03). The value of 3 percent is very cl ose to the median precision associated with EPA’s assessment of the precision of O 3 monitors nationally. The statistics cited that relate to the spatial variability of pollutant concentrations are not relevant to this issue.

(5) Comment: The analysis cited by EPA in 1997 (Sys tems Analysis, International –SAI)

concluded that “a conservative estimate for the typical er ror associated with an O 3 concentration measurement in th e real world is on the order of 4 ppb." It is unclear what has changed with respect to O 3 monitor performance since the 1997 assessment. Moreover, questions have been raised about the recent analysis done by EPA staff and its applicability to the older monitors that ma ke up much of the ambient monitoring network. The recent analysis should not, therefore, be taken as resolving the issue of whether to express the 8-hour NAAQS to the thousandth ppm.

Response: EPA is not asserting that the nati onal monitoring network is necessarily producing more accurate data now than in 1997. In fact, subsequent analysis (see comment below) confirms that theoretically derived O 3 measurement error is still approximately 4 ppb, based on the analysis by Mikel (2006).

(6) Comment: A number of commenters made refere nce to the analysis performed by SAI (1997) and a subsequent reanal ysis (Mikel 2006) to estima te the “systematic error”138 involved in the collection of O 3 data. Since each analysis concluded that “systematic error” for hourly O 3 measurements is approximately 4 ppb, these commenters assumed the term “systematic error” meant that O 3 measurements have an inherent error of 4 ppb for each hour measured during the O 3 season.

Response: The SAI (1997) and Dennis Mikel analys is (used in Cox and Camalier, 2006) independently assessed the potential for meas urement uncertainty in the total monitoring system, which consists of combinations of error due to drift, detector non-linearity, precision and instrument calibration, and NIST standard calibration. The term “systematic error” is used in these documents to emphasize that the error estimate reflects all the components of the overall O 3 monitoring system. It wa s not intended and does not

mean that the O 3 monitoring system always produces er rors of 4 ppb (or larger). Rather, random errors are centered on zero, thus producing equally probable positive and negative errors, with most er rors being less than 4 ppb.

(7) Comment: Several commenters argued that EPA should not base its proposal on the Cox and Camalier (2006) analysis. The instrument bias shown has not been proved to be

random.

Response: With regard to the Cox and Camalier (2006) simulation analysis, the reference to “random bias”, was perhaps misleading and should have been referred to as “random

error”. Bias connotes a cons tant deviation between truth and observation which certainly does not apply to O 3 ambient monitors operating in the field. An assessment of the precision and bias of the reported data from the national network of O 3 monitors has shown a median precision to be about 3 to 4% and bias to be about 0%. Since these statistics are based on individual hourly m easurements, the precision and bias of an individual 8-hour daily maximu m can be no larger and almost certainly smaller due to averaging of errors. Based on the national O 3 performance statistics and additional information regarding the performance of individual O 3 monitors, the simulation study assumed a “random error” of 0.004 ppm to be conservative (larger than necessary) but reasonably representative of an upper bound for a single individual daily maximum 8-

hour concentration. As demonstrated in the simulation study, this level of concentration uncertainty has a minimal impact (about 0.001 ppm) on the accuracy of the O 3 design

(8) Comment: EPA has access to considerable data on the site-specific precision and bias estimates, such as Langstaff, who reports bi as estimates for individual Boston monitors varying between -7 and + 11 % in 2003

Response: The values of precision and bias used in John Langstaff’s report were taken from a Quality Assurance assessment repor t which uses one-sided, upper confidence bound precision and bias indicators intended to trigger a quality assurance response by protecting against calibration issues a nd instrument malfunctions. While this conservatism may be useful to feed into th e exposure models employed by Langstaff, the precision and bias results are overestimated and do not reflect the true uncertainty that is occurring at the particular monitor. Furt hermore, the bias noted above by Langstaff represents the very high end of the bias values at individual sites across the country. Most139 sites have bias values close to zero. Therefore, the Boston monitor example is unrepresentative of the perfor mance of the network overall.

(9) Comment: Regarding quality assurance pro cedures, one commenter wrote that,

“Determination of O 3 NAAQS attainment requires three years of data but of the more than 13,000 hourly observations taken over three years at a typical O 3 monitoring site,

less than 0.75% of the data receives significant scruti ny during the attainment determination process. Although statistical ap proaches utilizing all available precision and audit data are valuable for assessing overall O 3 data quality EPA should seek and investigate concepts that focus on QA measur es taken shortly before and after (e.g., 3-7 days) peak 8-hour O 3 concentrations are recorded. This approach would better assess the quality of O 3 data in the higher concentration range which, ultimately, drives the attainment process.”

Response: EPA appreciates the comment; however it is outside the scope of this rulemaking.

(10) Comment: One commenter suggested that EPA add a site-specific “method detection level” (MDL) requirement to O 3 measurement QA procedures: “this could be similar to the currently proposed MDL test for precursor trace gases11 in which SLT organizations challenge field-based monitors repeatedly with low concentration gases. The instrument’s

MDL is calculated as the standard deviat ion of the average response multiplied by the

Student’s t-test value for the number of test values. By performing this test under “as

installed” conditions a more re liable gauge of an instrument ’s sensitivity is generated. Additionally, monitoring organi zations may discover and correctsiting- or installationrelated problems while performing such tests and thus generate hi gher quality data.”

Response: Although it is not a requirement, monito ring organizations do have the option to report their derived MDL or the vendor MD L to the Air Quality System (AQS). EPA appreciates the comment; however it is outside the scope of this rulemaking.

(11) Comment: Regarding data completeness, one commenter generally supported EPA’s proposal and also urged EPA to allow State or local air pollution control agencies the flexibility to determine that certai n days were not conducive to high O 3 levels, should a monitor not be operational. They stated th at the decisions may need to be made on a case-by-case basis, but listed the types of meteorol ogical conditions that are generally not associated with high O 3 levels: days with significant rain between 10 a.m. to 6 p.m.; days with cooler temperatures (< 60°F); days with north winds and frontal passages.

Response: EPA recognizes the comment, howev er, EPA believes there are too many meteorological conditions to list; therefore, EPA will continue to handle this issue on a case-by-case basis as expl ained in Appendix P.

(12) Comment: One commenter suggested that the ru le allow for averaging the monitoring results among O 3 monitors that are located in close proximity to each other in order to determine compliance. The commenter suggests th at States have the option to average the140 O 3 measurements between monitors that are located within 20 miles of each other [suggested regulatory text included in comment].

Response: EPA disagrees with this comment since local O 3 concentrations may be impacted by local NO

x emissions from sources such as motor vehicles. Thus, local concentrations averaged together may not ad equately characterize the true exposure to the local population.

(13) Comment: One commenter wrote that the po tential impact of stratospheric O 3 intrusion needs to be thoroughly evaluated.

Response: EPA’s Exceptional Event Rule handles the impact of stratospheric O 3 intrusion.

(14) Comment: In calculation of using raw data (suc h as computation of eight hour averages or design values) we recommend rounding the results of these calcu lations instead of truncating them, as truncation may result in low bias in the final design value.

Response: EPA appreciates the comment. However, it has been standard practice since the 1997 NAAQS to report and handle O 3 data by truncating. Consequently, our interpretation of the rela tionship between reported O 3 concentrations and health effects in epidemiology studies inherently corrects fo r the small downward bias in multi-hour and multi-day average concentrations. In all or nearly all cases, data available to health

effects researchers were truncated to thr ee decimal places when submitted to AQS or stored in state monitoring agency or other da ta bases. Reports of prevailing multi-hour

O 3 concentrations in study areas were also made on the basis of truncated averages of hourly concentrations. Hence, the small downward bias in O 3 statistics that will be compared to the NAAQS is the same as the small bias in nominal O 3 concentrations

examined in the assessment of the health studies and in the O 3 risk assessment. The net effect should be nearly the same as if all O 3 concentration averaging were done with rounding.

2. Specific Comments Related to Non-identical Secondary Standard Provisions of Appendix P

(1) Comment: Since the proposed W126 method "weight s" certain hours more than others, not all missing hours would be of equal impact. The usual standard of 75% data completeness may therefore not be appropriate in this case. EPA should consider this further and address data completeness re quirements in a conservative manner.

Response: EPA appreciates the comment. Given the Administrator’s final decision to set the secondary standard identical to the primary standard, the comment is moot.

(2) Comment: One commenter presented specific recommendations about missing data adjustment and data handling conventions:141 In place of Equation 2, the commenter sugge sts the following missi ng data substitution

scheme for all months with le ss than 100 percent completeness:

1. For one or two hour missing data gaps , use a simple interpolation scheme.

2. For three or more hour missing data gaps: -- Fill in using data from the clos est representative monitoring site. “Representative” means that both sites measure O 3 plumes from identical source regions; -- If data from a representative monitoring site are not available, then fill in using a technique approved by the administrator.

Response: EPA appreciates the comment. Given th e Administrator’s final decision to set the secondary standard identical to the primary standard, the comment is moot.

(3) Comment: To be consistent with data ha ndling conventions for the primary O 3 NAAQS, NESCAUM recommends the following revisions to section 4.3 of Appe ndix P to Part 50:

1. The secondary ambient O 3 air quality standard is met when the annual maximum W126 value based on a consecutive 3-month period at an O 3 air quality monitoring site is less than or equal to [7 to 15] ppm-hours. The number of significant figures in

the level of the standard dictates the rounding convention for comparing the computed W126 value with the level of th e standard. The first decimal place of the computed W126 value is rounded, with valu es equal to or greater than of 0.5 rounding up.

2. This requirement is met for the three month period at a monitoring site if O 3 concentrations are available (before substituting for missing data) for at least 90% of the possible index hours with a minimum data completeness in any one month of at least 75% of the possible index hours.

3. Months with W126 values greater than the le vel of the standard shall not be ignored on the ground that they have less than comp lete data. Thus, in computing the 3-month W126 value, months with less than 75% da ta completeness (before substituting for missing data) shall be include d in the computation if th e 3-month W126 value is greater than the level of the standard.”

Response: EPA appreciates the comment. Given the Administrator’s final decision to set the secondary standard identical to the primary standard, the comment is moot.

D. Comments Related to Monitoring142 1. Specific Comments Related to Monitoring and the Primary Standard

(1) Comment: Several commenters stated that EP A’s revision of the primary ozone NAAQS will be “seriously compromised” unless it is supported by accurate data establishing

current ambient levels of ozone. For exam ple, NACAA stated: “The proposed rule, however, ignores the needs that states and loca lities will have for additional monitors to

measure ozone levels in cu rrently under-monitored areas and, in particular, in

unmonitored areas that have populations under 350,000. Unless th is latter deficiency is corrected in the final rule, the health be nefits of EPA’s ozone NAAQS revision will likely be limited to those living in MSAs with populations greater than 350,000.”(NACAA, p. 9)

Response: EPA recognizes that the issues raised by the commenters are important and will likely require changes in the monitoring requirements to address MSAs with a population lower than 350,000. As noted in sect ion VI of the preamble to the final rule, EPA intends to address these issues as part of its proposed monitoring rule. EPA will likely consider proposed revisions to the mi nimum monitoring requirements that apply to smaller MSAs, as well as options for EPA Re gional Administrators to consider in deviating from such revised minimum monitoring requirements, as is now permitted in certain sections of 40 CFR part 58, Appendix D.

(2) Comment: Several commenters raised simila r concerns, adding that the current breakpoint of 85 percent of the standard to de termine if an ozone monitor is required in an MSA is “sorely inadequate.” They also questioned how EPA determines if an area is below the 85 percent threshold without m onitoring. While one commenter supports the current breakpoint, they also co ntend that all areas, includi ng rural areas that have the potential to exceed this breakpoint at least f our times per year will need to have a large

number of additional ozone monitors in order to demonstrate attainment with a new

lower standard.

Response: EPA notes that the curren t breakpoint of 85 percent of the standard (to require additional monitors in an MSA) provides a margin of safety by increasing minimum monitoring requirements as the design va lue for an MSA approaches any of the applicable NAAQS. This approach was adopted for O 3 and PM 2.5 minimum monitoring requirements on October 17, 2006 as part of a comprehensive review of ambient monitoring requirements for all criteria pol lutants. (See 71 FR 61236). Specifically for

O 3 , an 8-hour O 3 design value of 0.068 ppm triggere d increased minimum monitoring requirements for an MSA based on the pre-ex isting primary standard level of 0.08 ppm. With the decision to revise the 8-hour prim ary standard to a level of 0.075 ppm, the 8-

hour O 3 design value that will trigger increased minimum monitoring requirements for an MSA has decreased from 0.068 ppm to 0.064 pp m. Therefore, MSAs with 8-hour design values between 0.064 ppm and 0.067 pp m are now required to increase the

number of monitors operating to meet minimum requirements. EPA notes that in practice, however, virtually all of these areas already ar e operating at least as many monitors as the new requirements based on the revised primary st andard, so the number143 of monitors which would need to be init iated (or moved from a location of excess monitors) would be negligible. With rega rd to the specific co mment about how EPA

could determine if an area is below the 85 percent threshold w ithout monitoring, EPA recognizes that current monitori ng requirements do not require O 3 monitors to be added

in smaller MSAs in the absence of a O 3 design value, and that this issue has become more important with the decision to revise the leve l of the primary standard to 0.075 ppm. As a result, EPA intends to issue a proposed m onitoring rule in June 2008 and a final rule by March 2009, as stated in the preamble to the final rule, to deal with monitoring issues

related to revisions of the primary and secondary standards.

(3) Comment: Several commenters advocated for an expanded ozone monitoring network. They wrote that EPA needs to provide adequate funding for monitoring and the development of more appropriate ways to info rm and display that da ta to the public and natural resource managers. One commenter c ontends that EPA must expand the national ozone monitoring network in areas with populations of less than 150,000 to identify natural background levels and the nature and pa tterns of domestic and international ozone

transport.

Response: As noted elsewhere in this Response to Comments document, EPA intends to issue a proposed monitoring rule in June 2008 and a final rule by March 2009 to deal with monitoring issues related to revisions of the primary and secondary standards. EPA notes that about 400 monitors are presently required in MSAs, but about 1100 are actually operating in MSAs because most States operate more than the minimum required number of monitors. Of these approximately 700 monitors that are operating in excess of minimum requirements, EPA expects that oppo rtunities will exist for relocations of monitors to smaller MSAs that are presentl y unmonitored, allowing for more efficient use of existing O 3 -related resources without increasing th e overall size of an already robust

O 3 network. EPA also expects to work with the Office of Atmospheric Programs (OAP) to finalize quality assurance upgrades to CA STNET monitors operati ng primarily in rural areas, to meet some of the objectives (monito ring background levels, transport patterns) noted by the commenter.

(4) Comment: The New York State Department of Environmental Conservation noted that the proposed monitoring regulations essentially overlook the issue of the adequacy of the existing ozone monitoring network for dete rmining compliance with the alternate proposed levels. They noted that in the sect ion of the proposed regulations related to ambient monitoring, the EPA states that “The EPA does not intend to propose any changes to these requirements, because we be lieve these requirements would continue to be appropriate to support implementation of a revised O 3 NAAQS.” This commenter noted that this statement is accurate only if the new primary standard remains at or near

the current effective standard of 0.084 ppm or if the standard is dropped to as low as 0.060 ppm. At levels in the range that the EPA is proposing, 0.070 - 0.075 ppm, the monitoring network become s less than adequate.....”144 Response: As noted elsewhere in this Response to Comments document, EPA intends to issue a proposed monitoring rule in June 2008 and a final rule by March 2009 to deal with monitoring issues related to the revisi on of the primary and secondary standards, including the specific issue noted by this commenter.

(5) Comment: Several comments were received on possible changes to the required O 3 monitoring season if the primar y standard is revised downw ard. For example, The New York State Department of Environmental Cons ervation stated: “The season for measuring Ozone is selected on a State by State basis on historical data and th e standards that the data will be compared to. The season in Ne w York (April through October) is appropriate if the proposed standard is set at a level at or near the current sta ndard. If the standards are dropped to the low end of the proposed standards, it is likely that Ozone

concentrations could be elevat ed in relation to the standard s during periods prior to and following the currently designated Ozone s eason.” NESCAUM commented: “Moving to a primary ozone NAAQS of 0.070 ppm or lower may result in the need for additional sites to properly reflect n on-urban population exposures. In addition, depending on the final NAAQS level, the ozone (and possibl y the PAMS (photochemical assessment monitoring stations)) season may need to be extended. NESCAUM supports efforts that would better characterize public exposure to ozone, and urges that EPA be prepared to provide funding support for states to carry out such efforts.”

Response: EPA agrees that the length of the required O 3 monitoring should be reviewed in light of the Administrator’s decision to re vise the level of the primary and secondary standard. EPA does not agree that the O 3 season issue is linked to a primary standard level of 0.070 ppm or lower, and notes that the revision to a level of 0.075 ppm necessitates such a review as part of the pr oposed monitoring rule discussed elsewhere in this Response to Comments document. EPA has done a preliminary analysis of 2004-

2006 ambient data to address the issue of wh ether extensions of currently required O 3 monitoring seasons are appropr iate in light of the revi sed primary and secondary O 3 standard level and the revise d breakpoints for the AQI. Th e results of the analysis

demonstrated that out-of-season exceedances of the revised primary standard level occurred in eight states during the study peri od. Additionally, the frequency of days with

O 3 concentrations that reached the revised Moderate AQI category (based on a breakpoint of 0.060 ppm) was much greater compared with the frequency of days with concentrations that reached the pre-ex isting Moderate AQI category (based on a breakpoint of 0.065 ppm). This increased frequency of days with Moderate AQI levels was noted to occur during periods before and after the currently required O 3 seasons. Based on these preliminary analyses, EPA intends to consider change s to the length of the required O 3 season for the coming monitoring rulemaking. Such changes could be based solely on the frequency of exceedan ces of the revised primary and secondary standards, or could also consider the fre quency of concentrations in the Moderate category of the AQI.

2. Specific Comments Related to Monitoring and the Secondary Standard145 (1) Comment: Several commenters questioned whether the current monitoring system will be sufficient for monitoring a new standard, such as W126, particularly in rural areas. For example, the ACC noted that “there is also the very practical problem of the lack of a rural monitor network to suppor t a W126 standard. Thus, even if evidence is directionally pointing to establishing a cumulative standar d, it is premature to do so now.” With regard to how to address the lack of a ru ral monitoring network, Alan Leston noted that “EPA should more fully address the coverage and quality of non-urban ozone monitoring by regulation. As a starting point EPA might require that 10% of a State’s ozone monitoring sites (or at least 2 sites, whichever is greater) be located in non-urban areas.” The Iowa Department of Natural Resources urged EPA to include monitoring requirements regarding the secondary standard – in particular requiring monitoring in areas that contain ozone-sensitive crops or ecosystems.

Response: In light of the Administrator’s decision to revise the 8-hour secondary standard by setting it identical in all respects to the 8-hour primary standard, EPA believes that it is appropriate to consider whether the existing urban-based monitoring requirements are adequate and appropriate to characterize th e exposure in more rural areas where O 3 - sensitive plant species and more sensitiv e ecosystems exist, and where resulting vegetation damage would adversely affect la nd usage. Such areas would likely include public lands that are protected areas of national interest (e .g., national parks, wilderness areas). In consideration of the spatial gaps that currently exist in the rural ozone monitoring network, and to the ex tent that the existence of su ch gaps has contributed to the overall uncertainty that exists in the understanding of ambient O 3 levels that occur throughout rural areas, EPA believes that there is merit in considering whether additional monitoring requirements in certain rural ar eas would help support ongoing ecosystem

research studies as well as future reviews of the O 3 NAAQS by providing a more robust

data set with which to assess the re lationship of vegetation damage to O 3 concentrations. Accordingly, as part of its separate m onitoring rulemaking, EPA intends to consider specific requirements for a minimum number of rural monitors per State, with detailed rule language to ensure that States locate such monitors in appr opriate areas. For example, these areas could include Federal, St ate, or Tribal lands characterized by areas of sensitive vegetation species subject to visible foliar injury, seedling and mature tree biomass loss, and other adverse impacts to a degree that could be considered adverse depending on the intended use of the plant a nd its significance to th e public welfare.

(2) Comment: NESCAUM recommended that EPA and th e states explore together how the CASTNET (Clean Air Status and Trends Ne twork) program might be augmented and

made more efficient and cost-effective to e nhance the monitoring ne twork, especially in

rural areas. Some commenters expressed concern about the qua lity assurance practices at CASTNET sites with regard to certain aspects of O 3 monitoring. They recommended that EPA upgrade such practices to meet the 40 CFR Part 58 Appendix A quality assurance requirements already followed by the St ates so that the resulting data could be used in assessing compliance with th e revised secondary standard.

Response: EPA agrees that CASTNET sites repr esent a valuable resource to help provide rural monitoring cove rage in support of the revise d level of the secondary O 3146 NAAQS. EPA notes that O 3 monitoring technology and proc edural upgrades have been completed at some of the CASTNET sites, a nd that such upgrades will be completed at all CASTNET sites by 2009. The resulting O 3 ambient data from the upgraded sites will meet Appendix A requirements as is presently the case for O 3 data from State operated

monitors and NPS monitors. These data will be deemed acceptable for NAAQScomparison objectives and available in the AQS database beginning in 2008.

(3) Comment: The National Park Service noted that th e level of monitoring in non-urban and natural areas, such as Class I areas in national parks and w ilderness areas, is inadequate to identify all areas that might violate a secondary standard. NPS urged EPA to consider alternative monitoring approaches since typi cal monitoring may not be possible in some

areas due to lack of electr icity and other restrictions.

Response: While EPA notes the value of non-tradit ional monitoring approaches to meet certain research oriented objectives, we belie ve that monitors intended for demonstrating compliance with the primary and seconda ry NAAQS must employ federally approved reference or equivalent methods to insure that data of known and acceptable quality are used in the designation of areas as attainme nt or non-attainment. EPA is aware of the potential logistical difficulty of locating monitors in remote areas and that the lack of monitoring data may complicate the assessment of areas with the regard to compliance

with the revised level of the secondary NAAQS. Future guidance or rulemaking on O 3 implementation issues may deal with this issue.

III. RESPONSES TO LEGAL, ADMINISTRATIV E, AND PROCEDURAL ISSUES AND

MISPLACED COMMENTS

A number of comments were received that addressed a wide range of issues including legal, administrative, and procedural issues . Many legal issues ar e addressed generally throughout the preamble to the final rule. Specific legal issues ar e more fully addressed below in section III.A. In addition, a number of comments were submitted related to issues that are not germane to the review of the NAAQS, including implementation issues. Implementation issues are addressed generally in section I.C of th e preamble to the final rule. Comments on implementation and other issues that have b een categorized as “misplaced” comments are

included in section III.B below.

A. Legal, Administrative and Procedural Issues

(1) Comment: By law, the Clean Air Scientific Advisory Committee (CASAC) is charged with performing both a scien tific review and policy advi ce function (Clean Air Act, section 109(d)(2)). This means that EPA must be extraordinarily caref ul in how it listens to CASAC to ensure that it clearly dis tinguishes scientific insight from policy prescription (NAM, pp. 53-54).147 CASAC’s primary scientific res ponsibility is to perform a scie ntific peer review of EPA’s various risk assessment documents, including Criteria Documents and Staff Papers. CASAC is directed to “complete a review of the criteria publis hed under section 108,” which requires that air pollution criteria “accurately reflect the latest scientific knowledge.” CASAC’s primary duty is to ensure that EPA’s risk assessment is accurate, clear and unbiased. CASAC is not charged with performing a de novo synthesis of the science, which is EPA’s job through prepara tion of the Criteria Document. Since the Criteria Document should be completely free of policy considerations, there is no reason why CASAC should ever stray in to policy matters (NAM, p. 55).

CASAC’s review of the EPA Staff Paper is n ecessarily different, for the Staff Paper is by design a complex mix of scien ce and policy recommendations from Agency staff. In principle, the design of the Staff Paper s hould make it relatively easy for CASAC to

maintain a clear distinction between its scie ntific review and policy advocacy roles. CASAC does not seem to have adhered to that pr inciple. It is difficult to discern where it is commenting on science and opining about policy (NAM, p. 55).

CASAC’s members also are invited to provi de the Administrator with their opinions regarding how he ought to exercise his stat utory discretion in re vising or retaining NAAQS. Because their principal charge is sc ientific, the public might reasonably expect

CASAC members to limit their advice to matte rs of a strictly scientific nature, as befitting their technical expertise. Howeve r, the law does not limit CASAC to advising on matters of science, nor does it cons train them from providing pure policy advice reflecting their persona l values and preferences (NAM, p. 56).

The law invites CASAC to provide policy advice several ways. First, it specifies that one member of the committee must represent State air pollution agencies. Like EPA, these agencies are regulatory rather th an scientific in nature, func tion, or organization, and they are populated with personnel who quite reasona bly share their agency’s (and EPA’s) air pollution control mission. Furthermore the act of representation is inherently a stakeholder role (NAM, p. 56).

CASAC members are asked to “recommend to the Administrator any new national ambient air quality standards and revisions of existing criteria and standards as may be appropriate” (section 109(d)(2)(B)). In short, they are invited to speculate as to how they think they would exercise the Administrator’s st atutory discretion if th ey were standing in his shoes. Despite the fact that CASAC me mbers all have scientific training and have distinguished themselves in one or more scient ific fields, there is no thing scientific about this assignment (NAM, p. 57).

Response: Under section 109(d)(2)( B) of the Clean Air Act, CASAC “shall complete a review of the [air quality criteria] and [the NAAQS] and shall recommend to the Administrator any new national ambient air quality standards and revisions of existing criteria and standards as may be appropriate under section 108 and s ubsection (b) of this section.” Thus CASAC has two primary res ponsibilities: to re view the air quality

criteria and advise EPA on a ppropriate revisions to the cr iteria, and to review the148 NAAQS and advise EPA on appropriate ne w or revised NAAQS. The Act does not distinguish between these oblig ations and does not establish different ranking or priority between them; instead they are of equal statutory status.

The Act does not specify how CASAC is to pe rform its statutory function. For example, it neither requires nor prohibits CASC from conducting a “de novo synthesis” of the science. For many years, as in this review, the method employed by CASAC in discharging its advisory role has be en to provide comments, advice, and recommendations to EPA on draft and final versions of the air quality criteria document, Staff Paper, and related exposure and/or risk as sessments. In certain cases, as it has here, CASAC has also provided advice and recommendations on a range of potential

alternative standards. EPA has found this ove rall approach to be a very constructive and useful method for CASAC to provide its advi ce. Since passage of the CAA Amendments in 1977, EPA has carefully considered all such advice and recommendations provided by

CASAC.

EPA recognizes that CASAC serves in an advisory capacity and that the judgments required under section 109(b) are made by the Administrator and not CASAC. Advice of

the CASAC is available to the Administrato r to use as deemed appropriate in making decisions on the proposal and final rulema king. The Administrator has followed that approach in this rulemaking.

In providing advice and recommendations to EPA on these various documents, CASAC has properly provided both their views on the science as well as their views on appropriate new or re vised NAAQS. It is the latter a dvice, on new or revised NAAQS, that EPA understands NAM to mean by the te rm “policy advice.” Providing advice and recommendations on new or revised NAAQS ca lls for CASAC to apply its understanding

of the science to the criteria in section 109(b) for setting the NAAQS. This by definition means providing advice and recommendations on the public health and welfare policy judgments inherent in judging, for example, wh at primary standard would be requisite to protect public health with an adequate margin of safety. This is fully appropriate based on the charge to CASAC in the CAA. In ge neral, as in this case, CASAC has provided such advice by recommending a range of possibl e new or revised standards, as compared to recommending a single standard, r ecognizing that section 109 calls for the Administrator to exercise his own public health and welfare policy judgment.

In considering CASAC’s advice and recommenda tions EPA fully agrees that it is very important to pay close attent ion to the content of the advice and weigh it carefully,

whether it be advice on the scie nce or advice on policy matters related to new or revised NAAQS. EPA in fact does this, as seen in the many and varied revisions made to the

draft documents CASAC has reviewed and comme nted on, such as the air quality criteria document, the Staff Paper, and the related expos ure and risk assessments . It can also be seen in the careful attention paid by the Ad ministrator to CASAC’ s advice in both the proposed rule and in this final rule. The Ad ministrator has carefully explained where he has accepted CASAC’s advice and where he has not, and explained in detail his reasoning.149 In general, EPA has found CA SAC’s science and policy advice to be very important and helpful. The result has been a robust and comprehensive peer review of the various documents noted above, all of which have info rmed EPA’s proposed and final rule in this review. EPA recognizes that the nature of the advice and recommendations from CASAC, whether on the science or on the polic y judgments in applying the science to the criteria for the NAAQS, does vary depending wh ether the focus of the document at issue is on the science, as in the Criteria Document , or on applying the scie nce to the standardsetting criteria of section 109(b), as in the St aff Paper or the proposal . EPA also agrees

that advice and recommendations from CASAC are most useful when the science and/or policy basis of the advice are clea rly expressed and identified.

In this rulemaking, EPA is confident that it has been able to clearly differentiate CASAC’s science advice from the policy advi ce on the appropriateness of new or revised NAAQS. NAM has not identified examples where it believes EPA has failed to so differentiate, nor examples where CASAC ha s improperly mixed science and policy in providing its advice. For example NAM ha s not identified where CASAC’s science advice on the air quality criteria was imprope r because it was based on policy instead of

science considerations. Nor has NAM identi fied any area where it believes CASAC is speculating about new or revised NAAQS, as compared to exercising their judgment. EPA fully agrees that it needs to pay clos e attention when evaluating the advice of CASAC to properly understand its scientific basis as well as its policy basis; however, NAM has provided no example where EPA ha s failed to do so or where EPA has

confused or misunderstood the basis for CASAC's advice. In fact, this rule indicates that EPA is fully capable of disagreeing w ith CASAC on its advice and recommendations, and explaining why EPA either was not pe rsuaded or did not agree with CASAC’s reasoning or conclusions.

(2) Comment: Because it is an independent body outsi de of the Agency’s control, CASAC is exempt from federal information quality guide lines. However, EPA is not exempt when it disseminates or uses information provi ded by CASAC. EPA cannot simply cite CASAC as a scientific authority without re gard for whether their content adheres to applicable information quality standards. Where EPA disseminates covered information

obtained from CASAC in a manner that a reas onable person would construe as Agency agreement, EPA must ensure that the information satisfies applicable information quality standards as if the Agency itself ha d produced the information (NAM, p. 54).

EPA’s Notice of Proposed Rulemaking contains numerous subsections in which the input

it received from CASAC is summarized. In so me places, this input is clearly described as scientific information, subj ect to applicable information quality guidelines. But in most instances, EPA does not carefully disti nguish CASAC’s scientific review from its policy advice. This is en tirely understandable insofar as CASAC itself did not make these distinctions clear. However, adheren ce to information quality guidelines is EPA’s responsibility and not that of CASAC. Moreover, in its ch arge to CASAC, EPA did not ask the committee to clearly distinguish betw een its scientific re view and its policy recommendations. For example, EPA did not ask CASAC to apply the Agency’s150 information quality guidelines, and CASAC di dn’t do so. Nor did EPA disclose any predissemination review of the input it received from CASAC (or any other third party) to ensure that applicable information quali ty requirements were met (NAM, p. 57).

To minimize the number of e rror correction requests they receive, agencies are required by OMB’s government-wide information quali ty guidelines to establish effective procedures for dissemination review. In EPA’ s own guidelines the Agency states that it has in place sufficient pre-dissemination review procedures to ensure that information quality error is rare. The problem, though, is that none of the documents subject to this RFC contain any text sugges ting that pre-dissemination re view actually occurred. Information quality and its associated con cepts and definitions simply don’t appear (NAM, pp. 57-58).

Response: CASAC is a separate entity from EP A and, as such, assess es scientific and other documents produced by EPA independent ly of Agency oversight. While EPA gives careful consideration to the advi ce provided by CASAC members, EPA cannot subject CASAC recommendations to informati on quality standards. In using CASAC panel advice, however, EPA agrees that it is subject to following information quality guidelines.

EPA’s Guidelines for Ensuring and Maximizi ng the Quality, Objectivity, Utility, and Integrity of Information Disseminated does not require the Agency to discuss, separately, whether the pre-dissemination review actually occurred. The Guidelines, rather, provide a process for developing quality actions, of which the pre-diss emination review procedures are a part. This process is also a part of EPA’s Action Development Process (ADP). EPA’s ADP is a mechanism that assists the Agency in achieving the objectivity and transparency of information used in devel oping regulations. The st akeholder involvement and consultation that is a partof the ADP are a valuable co mponent of pre-dissemination review. In fact, NAM’s comments are also a part of this process to ensure that the information EPA disseminates is of appropriate quality.

Throughout this O 3 NAAQS review there has been public review and comment of drafts of the Criteria Document, the Staff Paper, the risk and exposure assessments, and comment on the proposal notice. In additi on, the CASAC meetings were open to the public, and interested parties had the opportunity to submit comments and/or present oral testimony. In EPA’s view, this process has en sured a robust review of the science. EPA believes that this lengthy and transparen t process is an effective procedure for

dissemination review.

The discussions in both the proposed and final rule of the science, the risk and exposure assessment, and the public health and welf are judgments supporting the proposed and final standards make clear not only the basi s for the Administrator’s decision but also what advice was received form CASAC, and how EPA differentiated between advice on

the science and advice on the policy matters relevant to se tting the NAAQS. It also shows where EPA disagreed with CASAC and the basis for any such disagreement.151 NAM has not identified any example where EPA failed to properly differentiate between science and policy advice from CASAC.

(3) Comment: NAM contends that EPA demonstrates presentational bias through selective citation of statements made by the CASAC for the purpose of conveying the impression

that CASAC endorsed all or virt ually all of the EPA staff anal yses. In the first set of examples, NAM contends that EPA demonstrates this presentational bias by citing text from a paragraph that supports its analyses, but does not cite othe r text in the same paragraph that does not. In the second set of examples that allegedly demonstrate presentational bias, NAM finds important scientific comments from the CASAC O 3 Panel that it contends do not support EPA’s interpretation of the da ta and also contends that these comments do not appear in the NPRM. (NAM, pp. 23-27)

First set of examples:

1. NAM contends that EPA di d not fully present the CASAC O 3 Panel’s concerns about the utility of time-series mortality studies a nd whether use of such studies allows us to confidently attribute obser ved effects specifically to individual pollutants.

2. NAM contends that EPA did not fully present the CASAC O 3 Panel’s concerns about the limited information on the specific ch emical composition, toxicity and, equally importantly, the population exposure of oxidant pollutants other than O 3

.

3. NAM contends that EPA did not fully present the CASAC O 3 Panel’s comments concerning inclusion of health endpoints in the risk assessm ent and the CASAC advice to qualitatively discuss ot her health endpoints.

Second set of examples: 4. NAM contends that EPA did not fully include in the prop osal notice CASAC’s comments concerning exposure measurement er ror which were expressed in CASAC’s

letter on the final Criteria Document (Henderson, 2006b, pp.3-4) and that in NAM’s view these CASAC comments support the view that 1) data from ambient monitors yield upwardly biased estimates of risk, 2) pe rsonal exposure cannot be correlated with ambient exposures and thus associations between data from ambient monitors and mortality are spurious, and 3) that short-term studies do not provide supportive evidence that positive associations in time series results are true.

5. NAM contends that EPA did not present the CASAC O 3 Panel’s comment that O 3 measurement error would be expected to upw ardly bias estimates of risk and have a substantial impact on the ability to detect a threshold of the c oncentration-response relationship below which no ozone effects are di scernible. NAM also contends that this aspect of O 3 measurement error would underm ine EPA’s risk assessment.

6. NAM contends that EPA did not presen t in the proposal no tice CASAC’s comments recommending an alternative approach to calcul ate risks relative to the current standard which would avoid the problem of estimating PRB.152 7. NAM contends that EPA did not presen t in the proposal no tice CASAC’s comments on the final Criteria Document (Henders on, 2006b, p. 4) that NAM states support conclusions that “attributing the observed associations betw een ozone and mortality in time-series studies masks the underlying fact or(s) actually respons ible” (NAM, p.27) and “If ozone is not the relevant factor, and its control will not serendipitously reduce the relevant factor(s) then the risk reductions predicted by EPA will not be realized” (NAM, p. 27).

Response: EPA strongly denies NAM’s contention that it demonstrated presentational bias. As an initial matter, EPA is not requ ired to quote verbatim all of an important comment made by the CASAC O 3 Panel. Doing so in the Staff Paper or NPRM could have the effect of obstructing clear communicat ion of the concepts involved rather than facilitating communication. Most of the exam ples listed above were comments made by

the CASAC O 3 Panel to point out issues that were not fully addr essed in the final Criteria

Document that it wanted to ha ve addressed in the final Staff Paper. The issues were fully addressed in the final Staff Paper and thoroughl y discussed in the NPRM . If these issues had not been fully addressed, the CASAC O 3 Panel would have noted that in its final review of the Staff Paper, but it did not. Instead it praise d the final Staff Paper in its March 26, 2007 letter:

Members of the CASAC Ozone Review Pa nel were pleased to review EPA’s Final Ozone Staff Paper. The members of CASAC and the Ozone Panel were unanimous in their praise of both the responsiveness of the Agency to our previous recommendations and of the clarity of this document. (Henderson, 2007) (emphasis added)

With respect to the specific examples cite d by NAM, EPA’s responses are given below.

First set of examples: 1. Contrary to NAM’s contention, EPA fully presented the CASAC O 3 Panel’s views on the utility of time-series studies, and addresse d this issue in both the Staff Paper and the NPRM. In section 3.4 of the Staff Paper, EPA described importan t issues related to assessment of epidemiological studies and th is included discussion of NAM’s examples 1, 5 and 2 above, respectively: the genera l issue of the util ity of time-series epidemiological studies in assess ing the risks from exposure to O 3 and other criteria pollutants, as well as related issues about exposure measurement error in O 3 mortality

time-series studies and O 3 as a surrogate for the broader mix of photochemical oxidant pollution in time-series studies. EPA furthe r goes on to note that the implications of

these three issues for staff conclusions about the adequacy of the current O 3 NAAQS and the identification of options for consid eration are considered in Chapter 6.

With regard to whether use of time-series studies allows us to confidently attribute observed effects specifically to individual pol lutants, in section 6.3.4.1 of the Staff Paper,

on the evidence-based considerations in selectin g the level of the standard, staff generally

concludes that:153 Toward the lower end of the range of O 3 concentrations observed in such studies, ranging down to background levels, however, we conclude that there is increasing uncertainty as

to whether the observed associations remain plausibly related to exposures to ambient O 3 , rather than to the broader mix of air polluta nts present in the ambient atmosphere. (EPA 2007a, p.6-61)

This conclusion is carried over to section II .D.4.a, the discussion of the evidence based considerations from the Staff Paper the le vel section in the NPRM (72 FR 37875). The uncertainty about whether observe d associations remain plausi bly related to exposures to

ambient O 3 at the lower end of the range was among the uncertainties that were included

in the rationale for concl uding that a standard level below 0.070 ppm would not be appropriate. In this ratio nale the Administrator judge d that evidence of a causal relationship between adverse health outcom es and O3 exposures becomes increasingly

uncertain at lower levels of exposure. (72 FR 37880)

Moreover, EPA highlights this issue in section 6.4 of the Staff Paper as a key uncertainty

that merits more research in the future. In this section staff notes:

Most epidemiological studies of short-term e xposure effects have been time-series studies in large populations. Time-series studies rema in subject to uncertainty due to use of

ambient fixed-site data servi ng as a surrogate for ambient e xposures, to the difficulty of determining the impact of any single pollutant among the mix of pollutants in the ambient air, to limitations in existing statistical models, or to a combination of all of these factors. Independent variables for ai r pollution have generally be en measurements made at stationary outdoor monitors, but the accuracy with which these measurements actually reflect subjects’ exposure is not yet fully understood. Also, additional research is needed to improve the characterization of the degr ee to which discrepanc y between stationary monitor measurements and actual pollutant exposures introduces error into statistical estimates of pollutant effects in tim e-series studies. (EPA 2007a, p. 6-89)

2. Contrary to NAM’s contention, EPA fully presented the CASAC O 3 Panel’s views on the limited information on the specific chem ical composition, toxicity and the population exposure of oxidant pollutants other than O 3 , and addressed this i ssue in both the Staff Paper and the NPRM. As noted above, EPA firs t described this issue in section 3.4 of the Staff Paper. In section 6.3.2 of the Staff Pape r, in the discussion of the most appropriate surrogate for ambient photochemical oxidants, EP A again discusses this issue. In section 6.3.6 of the Staff Paper, summary of staff conclusions and recommendations on the primary O 3 NAAQS, staff concludes:

It is appropriate to continue to use O 3 as the indicator for a standard that is

intended to address effects a ssociated with exposure to O 3 , alone or in combination with related photochemical oxidants. Based on the available information, and consistent with the view s of CASAC and public commenters, we

concluded that there is no ba sis for considering any alte rnative indicator at this time. Staff notes that while the new body of time-series epidemiological evidence cannot resolve questions about the relati ve contribution of other photochemical154 oxidant species to the range of morbidity and mortality effects associated with O 3 in these types of studies , control of ambient O 3 levels is generally understood to provide the best means of controlling phot ochemical oxidants in general, and thus of protecting against effects that may be associated with individual species and/or the broader mix of photochemical oxidants, independent of effects specifically

related to O 3 . (Staff Paper, p. 6-85)

The CASAC O 3 Panel obviously endorsed this assessm ent because in its letter on the final Staff Paper it notes that the panel, “agreed with the choice of indicator, statistical form and averaging time for the primary Ozone NAAQS suggested by Agency staff.” (Henderson, 2007)

However, the CASAC O 3 Panel further noted that “There is an urgent need to fund more research on the effects on sensitive subpopulatio ns of low levels of the photochemical oxidant mixture for which ozone is used as a surrogate. More information on the effects of low levels of oxidant mixtures on public health is essential to inform the future decision-making process.” (Henderson, 2007) This view about the need for additional research mirrored the view expressed by EPA Staff in Section 6.4 of the Staff Paper, summary of key uncertainties a nd research recommendations re lated to setting a primary

O 3 standard, which noted:

The extent to which the broad mix of phot ochemical oxidants and more generally other copollutants in the ambient air (e.g., PM, NO 2 , SO 2 , etc.) may play a role in modifying or contributing to the obser ved associations between ambient O 3 and various morbidity effects and mortality continues to be an important research question. Ozone has long been known as an indicator of heal th effects of the entire photochemical oxidant mix in the am bient air and has served as a surrogate for control purposes. A better understanding of sources of the broader pollutant mix, of human exposures, and of how othe r pollutants may modify or contribute

to the health effects of O 3 in the ambient air, and vice versa, is needed to better inform future NAAQS review s. (Staff Paper, p. 6-88)

In the NPRM, the issue of the limited inform ation on the specific chemical composition, toxicity and the population exposure of oxidant pollutants other than O 3 was discussed in

section II.D.1 on the indicator for the primary standard. (72 FR 37872)

3. EPA rejects NAM’s contention that EPA did not present the CASAC O 3 Panel’s comments in the proposal notice regarding CA SAC’s advice on health effects which it should discuss qualitatively. In the proposal notice EPA states,

However as noted by CASAC (Henderson, 2007) and in the Staff Paper, there are a number of health endpoint s (e.g., increased lung infla mmation, ...and increased school absences) for which there currently is insuffici ent information to develop quantitative risk estimates, but which are important to consid er in assessing the overall public health impacts associated with exposure to O 3 . (72 FR 37856)155 With respect to the first part of the CASAC letter quote that EPA omitted, CASAC was simply agreeing that the health endpoints based on epidemiological evidence that EPA included in its risk assessment were appropria te. EPA stated in the proposal notice that

“the CASAC O3 Panel concluded “... that the selection of health endpoints for inclusion in the quantitative risk assessment was appropriate” (72 FR 37856)

Second set of examples: 4. EPA rejects NAM’s contention that EPA di d not fully discuss the issues raised by CASAC with respect to the role of exposur e measurement error in O3 mortality timeseries studies. EPA does not agree with the set of conclusi ons that NAM draws from the CASAC comments with regard to whether this issu e undermines the use of epidemiological studies in risk assessment. Rather, EPA concludes that until more data on personal O 3 exposure becomes available, the us e of routinely monitored ambient O 3 concentrations as a surrogate for personal expos ures is not generally expected to change the principal conclusions from O 3 epidemiologic studies. Th erefore, population health risk estimates derived using ambient O 3 levels from currently available observational studies, with appropriate caveats about persona l exposure considerations, remain useful. As noted in the general response to this comment, evidently the CASAC O 3 Panel agreed with this assessment in the final Staff Pape r. Far from downplaying this issue, EPA highlights it again in section 6.4 of the Staff Paper as a key uncertainty that merits more research in the future. (EPA 2007a, p. 6-88) The discussion of measurement error and

the overall conclusion about th e usefulness of epidemiologi cal studies in estimating population risk can be found in sectio n II.A.3.a, assessment of evidence from epidemiological studies, in th e proposal notice (72 FR 37838).

5 and 7. EPA rejects NAM’s contentions that EPA did not present the CASAC O 3 Panel’s comments that O 3 measurement error would be expected to have a substantial impact on the ability to detect a threshol d of the concentratio n-response relationship

below which no ozone effects are discerni ble and that attributing the observed associations between O3 and mortality in time-series studies masks the underlying factor(s) actually responsible. EPA also disagrees with NAM ’s contention that this issue

undermines EPA’s risk assessment.

EPA has thoroughly discussed the issue of measurement error and the impact on the ability to detect a threshold in section 3.4 of the Staff Paper. In this section, EPA notes

that:

...the use of ambient O3 concentrations ma y obscure the presence of thresholds in epidemiologic studies (CD p. 7-9). Brauer et al. (2002) concl uded that surrogate measures of exposure, such as those from centrally located ambient monitors, that were not highly correlated with person al exposures obscured the presence of thresholds in epidemiologic studies at the population level, even if a common

threshold exists for individuals with in the population. (Staff Paper, p. 3-41)

With regard to whether the issue of exposure measurement error undermines the use of epidemiological studies in risk assessment , EPA reaches a different conclusion than156 NAM. EPA concludes that until more data on personal O 3 exposure becomes available, the use of routinely monitored ambient O 3 concentrations as a surrogate for personal exposures is not generally expected to change the principal conclusions from O 3 epidemiologic studies. Therefor e, population health risk es timates derived using ambient

O 3 levels from currently available observati onal studies, with appr opriate caveats about personal exposure considerations , remain useful. As noted in the general response to this comment, evidently the CASAC O 3 Panel agreed with this assessment in the final Staff Paper. Far from downplaying this issue, EPA highlights it again in section 6.4 of the Staff Paper as a key uncertainty that merits more research in the future. (EPA 2007a, p. 6-88) The discussion of measurement e rror obscuring population thresholds and the

overall conclusion about the usefulness of epidemiological studies in estimating population risk can be found in sectio n II.A.3.a, assessment of evidence from epidemiological studies, in the proposal notice. (72 FR 37838)

6. EPA has included CASAC’s comments rela ted to PRB and its suggested alternative approach and EPA’s response to this comme nt above in section II.A.5 (see comment number (20)).

(4) Comment: NAM claims that it is a violation of the informa tion quality standard of objectivity to use terms such as "likely" in ways that conflict with their actual use in appropriate context or without clear definiti on. NAM contends that EPA must establish clear rules and procedures for how such terms will be used based on the following principals: (1) where possible a ssign quantitative values to st atements about likelihood to reduce interpretative heterogeneity, (2) th e values assigned by EPA to likelihood statements and probability descriptors must be consistent with both intuition and scientific research about such terms, (3) to adhere to applicable information quality

standards EPA must at a minimum make tr ansparent what it means when it uses likelihood statements and probability descri ptors, and (4) EPA must have full and complete documentation of what it proposes and subject its work to pre-dissemination review (such as peer review by qualified psychologists).

Response: EPA agrees that where available in formation provides a basis for assigning quantitative values to probabilistic statements that it is generally appropriate to do so. On the other hand, EPA does not agree that it is appropriate to interpret information in quantitative terms if available information doe s not provide a basis to do so, which would

have the effect of communicati ng a higher degree of precision than is warranted, or that the Information Quality Guidelines either require such an interpretation or that EPA establish clear rules and procedures for how commonly used probabilistic terms will be

used in a NAAQS review. The commenter specifically refers to EPA’s use of the term “likely” as an example of a probabilistic st atement that should be assigned quantitative values. EPA disagrees. EPA has used this and other similar types of words throughout

the relevant documents based on their comm on definitions when appropriate, in the absence of information that would support a more quantitative statement. In so doing, EPA has been consistent in using such words and has explained the scientific and logical

basis for the statements in which such words appear. For example, the word “likely” is intended to convey its common meaning, i.e., having the qualities or characteristics that157 make something probable. This meaning re flects a judgment, for which EPA provides a

reasoned basis in these documents. NAM has not identified any specific instance in which the Agency’s use of terms such as “likel y” or “unlikely” is not consistent with the common meaning of these terms. EPA doe s not agree that the process that NAM suggests would add to the accuracy, clarity, completeness, or unbiased dissemination of information in NAAQS reviews or would be an appropriate use of Agency resources.

(5) Comment: One commenter (NAM, pp. 47-49) contends that EPA used default values in its assessments and that this violates information quality principles.

Response: EPA rejects NAM’s contenti on that it used default va lues in its assessments. More specifically, EPA used the best avai lable scientific information and included

distributions based on available scientific and tec hnical data in its exposure and health risk assessments to characterize variability. Further, the commenter offered no specific examples of where EPA used default values.

(6) Comment: One commenter (NAM, pp. 20-21, 56 fn. 31) states that EPA needs to draw a

distinction between studies included in the la st review (“old” st udies) and subsequent studies (“new” studies). EP A should discuss old studies on ly to set the stage for the review of new studies, since the Administra tor's charge under section 108 and 109 is to

utilize the best available new scientific inform ation. None of the old studies has utility in deciding in this review whether to change th e standard, absent some finding of error or other reason to change the pr ior evaluation of the old study. CASAC’s advice includes reference to various studies published betw een 1988 and 1993, noting that the relevance of these studies is unclear given CASAC’ s charge to focus on new research.

Response: EPA disagrees with th e construct suggested by th e commenter, on both legal and scientific grounds. Section 108 calls for th e air quality cr iteria to “accurately reflect the latest scientific knowledge useful in indi cating the kinds and exte nt of all identifiable effects on public health or welfare.” EPA implements this charge by reviewing the newest scientific information, and conducti ng this review not in isolation but by synthesizing and integrating the newest info rmation with the prior scientific knowledge. An integrated synthesis of the entire body of evidence allows all of the evidence to be evaluated in context, without artificially segr egating new from old information. It allows EPA to draw the most appropriate implications and conclusions from the evidence when seen as a whole. The commenter’s appr oach would instead call for freezing our understanding of the information gained from the “old” studies, and would not allow EPA to fully evaluate what the old studies teach us in drawing proper implications from the entire body of evidence. The commente r’s approach is not grounded in scientific principles, and would interfere with developing the most useful analysis of the evidence. The commenter’s approach is neither required nor appropriate.

(7) Comment: One commenter (NAM, pp. 45, 65) stated that the overall result of various

errors in the risk assessment is that the Admi nistrator has been misled to believe that the risk estimates are much more certain than they actually are. For these and various other errors, the risk assessment should only be used for purposes of a screening level158 assessment, and should not be used for maki ng the important public health decision in

this review.

Response: In both the preamble and this Response to Comments document EPA has responded to a wide variety of comments on th e risk assessment, as well as comments on the Staff Paper and Criteria Document. Th e exposure and risk assessment, the Staff paper and the Criteria Document have all carefully identified the many sources of uncertainty in the science or the analysis reported. Thr oughout the development of these documents EPA received comments on many of these same issues, and addressed them appropriately in many cases by recognizing a nd describing or othe rwise characterizing

the uncertainties.

As in prior NAAQS reviews, the degree of unc ertainty in the science and the analyses developed using the science is a criti cal component of decision making by the

Administrator. In this review the Administ rator has been fully aware of all of these sources of uncertainty. He has taken them into account in maki ng provisional decisions in the proposal, as well as in making d ecisions in the final rule. For example, uncertainties associated with the exposure and risk assessment results was discussed extensively in the proposal ( See e.g . 72 FR 37851, 37852, 37856, and 37862). The Administrator explained that he took these uncertainties into consideration when evaluating the adequacy of the current stan dard, and when evaluating what range of standards would be appropriate (72 FR 37871, 37880). As desc ribed in the preamble to the final rule, the Administrator has fully considered the uncertainties in the science and in the exposure and risk assessment. Based on this consideration, he has placed primary emphasis on the scientific evidence and impli cations drawn from it. He has also placed more emphasis on the exposure assessment than the risk assessment. This reflects a reasoned approach that considers and evaluate s the uncertainties, and places more weight where there is more certainty and less weight where there is less certainty. The lengthy public process leading to this final rule has provided a full and comprehensive review of both the science and the various analyses base d on the science, as well as the type and degree of uncertainties in each of these areas.

(8) Comment: One commenter, NAM, submitted a Request for Correction (RFC) concerning

certain information it claims was disseminated by EPA in its proposal notice. In its RFC, NAM describes numerous alleged information qua lity errors in the description, analysis, and presentation of scientific informati on and information quality errors in the

assessment of human health risks. NAM also claims the existence of information quality

errors in the consider ation of reports from CASAC, in the rollback assumption, and in the description of PRB.

Response: The RFC has been treated as a comment on our proposal notice. EPA has

reviewed NAM’s RFC and finds th at there is no merit to their objections. EPA disagrees with NAM’s allegations that EPA has not complied with the requirements of the Information Quality Act or the Agency's policies for ensuring information quality. EPA has responded to NAM’s significa nt comments in the preamble to the final rule or in this

document.159 (9) Comment: Some commenters argued th at EPA has not provided any rational justification for disagreeing with CASAC’s recommendations , in violation of th e requirements of section 307 (d) (ALA et al.).

Response: The EPA disagrees with this character ization of its explanation at proposal, and refers also to its detailed response in se ctions II.A regarding d ecisions not to accept CASAC’s recommendations regarding the level of the 8-hour standard for O 3.

(10) Comment: The standards must protect these vulne rable populations – including persons with heart disease, hypertension, diabetes, a nd chronic bronchitis or asthma -- with an adequate margin of safety, the same standard s that apply to the ge neral population (ALA et al.).

Response: The EPA agrees with this comment, and has carefully considered effects on vulnerable subpopulations in consideri ng whether and how to revise the O 3 NAAQS (See e.g. section II.A.2).

(11) Comment: Some commenters (e.g., ALA et al.) argued th at EPA must adopt a precautionary approach to the standard setting process, and set standards in a manner that deals with uncertainty not by ignoring uncerta in effects but rather by protecting against

adverse health effects even where those e ffects may be uncertai n. In support of it s argument, the ALA et al. specifically cited ATA III , 283 F. 3d at 369 (EPA must promulgate protective NAAQS even where risks cannot be qua lified or precisely identified) and Lead Industries , 647 F. 2d at 1155 (requiring EPA to wait until it can conclusively demonstrate that a particular effect is adverse to human health is inconsistent with the statute’s preven tative and precautionary orientation).

Response: The EPA agrees generally with this comm ent, but notes further that a general invocation of precautionary principles doe s not determine where in the range of

reasonable values EPA could establish the leve l of a standard --in this case, the 8-hour average O 3 standard. Section II.C.4 to the preamble to the final rule explains in detail why it is appropriate to set th e level of the 8-hour standard at 0.075 ppm. The EPA notes

further that this choice is consistent with case law in the D.C. Circuit (not cited by the commenter) that the Administrator is to careful ly examine all of the relevant studies in the record, but need not base the level of th e standard on either the highest or lowest value in these studies. Rather, an informed judgment is called for. API , 665 F. 2d at 1187; NRDC v. EPA , 902 F. 2d 962, 970. Section II.C.4 to the preamble to the final rule

states the basis for the Administrator’s exercise of informed judgment here, in particular, setting the level of the 8-hour standard below the level at wh ich health eff ects related to O3 have been clearly demonstrated to occu r (i.e. at and above 0.080 ppm) in controlled human exposure studies.

Far from “ignoring uncertain effects,” the Ad ministrator has focused closely on the issue of “uncertain effects” in determining wher e the 8-hour level should be set, recognizing the significant uncertainty ove r whether adverse effects occu r from exposure at various160 ambient levels of O 3. As discussed above, Lead Industrie s is not on point as the issue in

that case concerned when an effect should be considered adverse, and the authority to

determine that an effect was adverse before there was clear evidence that the effect was

harmful. Here there is no issue that mo rtality and serious morbidity are adverse.

(12) Comment: Environmental Defense commented th at EPA’s proposed alternative to set the secondary standards at the same le vel as the primary standard flouts the recommendations of both CASAC and Staff, an d is scientifically unsupportable. The commenter stated that EPA provides no reasoned basis for rejecting CASAC’s recommendation on this score, and that EP A concedes that the cumulative seasonal

W126 standard is the most biol ogically relevant way to pr otect against adverse welfare effects on vegetation. Environmental Defense cl aims that EPA cites no scientific or other rational relationship between the proposed prim ary standards and protection of vegetation against adverse welfar e effects. Because there is no rational connection between the proposed primary standard and the level of protection needed to protect vegetation against adverse O 3 -induced welfare effects, any EPA finding that the primary standards would be sufficient for secondary standards pur poses would be arbitrary. The most that

EPA asserts is that there coul d be significant overlap in th e areas protected by the 8-hour and W126 forms, and that the proposed primary standards.

Response: EPA agrees that the W126 form is cu rrently the most bi ologically relevant form available for reflecting vegetation response to O 3 exposures. However, EPA does not agree that a biologically relevant form is a mandatory requirement in setting a secondary standard, under all circumstances. Indeed, EPA has a long history of judging that a secondary standard set identical to the primary standard form and level will be requisite to protect public we lfare, based on the entire body of information available at that time. This judgment has often been made , in large part, as a result of the often significant uncertainties that remain regardi ng what combination of form and level are most appropriate for a secondary standard, as was the case at the conc lusion of the last O 3 NAAQS review in 1997. EPA’s reasons for adopting an 8-hour average standard are discussed in the preamble.

(13) Comment: Environmental Defense commented that EPA’s proposal to set a W126 secondary standard in the range of 7-21 ppm- hrs unlawfully and arbitrarily departs from CASAC’s recommendation and the supporting scie nce. The commenter stated that the Act and settled principles of administra tive law require EPA to provide a reasoned justification for departing from CASAC’s recommendation with respect to the upper bound of the proposed W126 standard and EPA ha s failed to provide such a justification here. The Agency merely asserts that “[g]iven the uncertainty in determining the risk

attributable to various levels of exposure to O 3 , the Administrator believes as a public welfare policy judgment that this is a r easonable range to propose” 72 Fed. Reg. 37,903.

The commenter claimed that this bare asse rtion is grossly deficient as a basis for departing from CASAC’s recommendation, as described in paragraphs (a) through (c)

below.161 (a) The commenter asserted that EPA fails to identify its basis for claiming uncertainty in determining the risk attributable to various O 3 levels or explain why the degree of alleged uncertainty is so great as to render the findings of a dverse effects at those levels improbable. The agency cites no facts suppor ting the claim of uncertainty and does not explain any rational connection between the de gree of alleged uncertainty and specified levels of the standard. The agency does not show, nor does the record support a finding that uncertainty of the eviden ce of adverse effects at 15 ppm -hours is materially greater than at 21 ppm-hours, or that any alleged un certainty of adverse effects at 15 ppm-hours is so great as to render adverse effects at that level improbable. To the contrary, the

record shows that conclusions of a consensu s workshop of independent scientists that limits below 15 ppm-hours are requisite to prot ect against adverse effects to vegetation. 72 Fed. Reg. 37902/2. Evidence in the Criteria Do cument and analysis in the Staff paper provides further support for these consen sus recommendations, and indeed the Staff found nothing in more recent information to call these recommendations into question.

(b) EPA does not meet its burden of rationall y justifying its choice of standards and its rejection of CASAC’s recommenda tion merely by asserting that its decision is a “policy judgment.” The Criteria Document and other ev idence in the record support a finding of adverse welfare effects on vegetation at W 126 levels at and below 15 ppm-hours. To justify setting the secondary standard at a higher level than that, EPA must provide a reasoned justification for disr egarding or giving limited weight to the studies and scientific findings of adverse effects at and below 15, and for rejecting CASAC’s

recommendation.

(c) Based on the evidence of advers e welfare effects on vegetation from O 3 levels as low as 7 ppm-hours, EPA must set the secondary st andard at the lowest end of the range. Section 109 (b) (2) of the Act requires EPA to set the sec ondary standard at a level “requisite to protect the public welfare fr om any known or anticipated adverse effects associated with the presence of such air polluta nt in the ambient air.” Because the record documents known or anticipated adverse O 3 welfare effects on vege tation at levels of 7 ppm-hours (and even below), EPA must set th e standard at or below that level.

Response: Congress explicitly recognized that in making judgments about how to use uncertain evidence to set standards, the Ad ministrator may not always agree with his scientific advisors, s ee CAA 307(d)(3), but EPA agrees th at where the NAAQS differs in any important respect from the advice of CASA C, it must provide an explanation of the reasons for such differences. EPA fully cons idered CASAC’s advice with regard to the range of W126 levels proposed, as is clear from the expansion of the original range identified in the second draft Staff Paper (ra nge 13 to 21 ppm-hours) to include the lower end of the CASAC recommended range (7 ppm -hours), and explained that the level selected within the range of 7 to 21 ppm- hrs is largely a policy judgment as to the requisite level of protection n eeded. Specifically, the Staff Paper states “In the absence of any information regarding a threshold of O 3 exposures for vegeta tion, staff recognizes

that the level selected is la rgely a policy judgment as to th e requisite level of protection needed. In determining the requisite leve l of protection for crops and trees, the Administrator will need to weigh the importance of the predicted risks of these effects in162 the overall context of public welfare protection, along with a determination as to the appropriate weight to place on the associat ed uncertainties and limitations of this information.” (EPA, 2007a)

(a) With regard to the Commenter’s asserti on that EPA fails to identify its basis for claiming uncertainty in determining the risks attributable to various O 3 levels, EPA refers the Commenter to the Staff Paper discussi ons regarding the nature and scope of uncertainties associated with the exposure (Staff Paper, pp.7-34 to 7-37), risks (Staff Paper pp. 7-43 to 7-47 for crops; 7-69 to 7-70 fo r trees,) and benefits (Staff Paper, pp. 7- 52 to 7-53) assessments as well as similar disc ussions in parallel sec tions of the proposal notice (e.g., 72 FR 37897). The uncertainties as sociated with each of these assessments

translate into uncertain levels of risks to vegetation for each of the different air quality scenarios evaluated. EPA, in being careful to discharge its mandate to provide the requisite level of public welfar e protection, i.e. sufficient but not more than necessary,

took into account to the best of its ability, all th e information it had available to help inform its judgments on requisite protecti on. EPA’s intention to do so is clearly articulated throughout the proposal notice (e .g., 72 FR 37904/5). EPA notes that the uncertainties associated with the exposure a nd risk assessments affect the predictions of risk to vegetation at different levels equally, so they do not, by themselves, make the risks at one level of exposure any more or less pr obable than another. What they do show, however, is that at lower and lower levels of O 3 air quality, remaining risks to vegetation appear to decline so that the relative risks among the different air quality scenarios can be compared to each other.

However, in addition to comparing the relativ e risks of effects occurring at any given level, EPA must make a further determinati on as to the significance of those remaining risks to the public welfare and at what leve l those risks could reas onably be considered adverse to the public welfare. Thus, it is not only the uncertainty associated with reductions in the presence of effects but the unc ertainties associated with the degree of public welfare impact of those reduced leve ls of effect that must be weighed.

(b) Based on the statutory language in the s ection 109(b) (2) of the CAA, EPA notes that Congress clearly envisioned a role for “the j udgment of the Administrator” in identifying the “requisite level of protection” for the public welfare. As stated in the proposal notice, “the level selected is largel y a policy judgment as to the requisite level of protection needed. In determining the requisite level of protection for crops and trees, the Staff Paper recognizes that it is appropriate to we igh the importance of th e predicted risks of

these effects in the overall context of public welfare protection, along with a determination as to the appropriate weight to place on the associated uncertainties and limitations of this information.” (72 FR 37903). Comments received following proposal further helped inform EPA’s judgments bot h as to the likelihood of predicted risks occurring and potential adversity in the c ontext of public welfare. In particular, comments regarding the significance of the un certainties and limitations associated with the exposure and risk assessments, as well as the field based data, helped inform EPA’s judgments regarding how much weight to place on these uncertainties, in reaching a decision regarding what standa rd is requisite to protect the public welfare.163 EPA disagrees that it has not provided a reas oned justification for departing from the CASAC recommended form and range. This ju stification is described in the proposal notice and further refined in the preamble to the final rule to take into account comments received on the proposal notice. The Administra tor notes that he is in general agreement

with the CASAC Panel’s views concerning the interpretation of the scientific evidence.

The Administrator also notes that there is no bright line clearly directing the choice of standard for any of the effects of concern, a nd the choice of what st andard is appropriate is clearly a public welfare policy judgment entr usted to the Administrator. This judgment must include consideration of the strengths and limitations of the evidence and the appropriate inferences to be drawn from the evidence and the exposure and risk assessments. In reviewing the basis for the CASAC Panel’s recommendations for the form and range of the secondary O 3 standard, the Administ rator observes that the CASAC Panel apparently placed appreciable weight on the combined science and policy views contained in a report from a 1996 c onsensus building workshop held by a group of independent scientists to inform its policy judgments on standard levels that would be protective against various types of O 3 -related effects. While the Administrator finds the views expressed in that report to be relevant and of interest, he does not see in that report clear linkages between the underlying scie ntific information and the recommended standard levels. Lacking such linkages, the Administrator can find no appropriate scientific basis for deferring to the policy judgments reflected in that report. Similarly, in presenting their recommendations, the CASA C Panel did not provide clear linkages between their interpretation of the scientific evidence, the substantial uncertainties associated with that evidence, and their reco mmended range of levels. The Administrator more heavily weighs the implications of the uncertainties associated with the scientific evidence and with the Agency’s vegetation exposure and risk assessments than the CASAC Panel apparently does, and disagr ees with CASAC that the evidence and assessment results appropriately serve as a ba sis for concluding that a seasonal standard with a level no higher than 15 ppm-hours is re quired for an annual standard, or that an even lower level is required for a standard averaged over three years.

After carefully taking the above comments a nd considerations into account, and fully considering the scientific and policy views of the CASAC, the Administrator has decided to set the secondary standard e qual to the primary standard, as discussed in the preamble.

(c) EPA disagrees that it must set the standa rd at the lowest leve l for which there are

known adverse effects. As stated above in (b), the CAA does not require that secondary

standards be set at a zero-risk level, but rather at a level that reduces risk sufficiently but not more than what is necessary to prot ect public welfare from known or anticipated

adverse effects. EPA further notes that the same effect ma y have different degrees of adversity to the public welfare, depending on th e intended use of the plant and where it is growing. In addition, in conc luding that the appropriate ra nge for EPA to consider was between 7-15 ppm-hours, the CASAC Panel, as stated in (b) above, apparently placed appreciable weight on the combined science and policy views contai ned in a report from a 1996 consensus building workshop held by a gr oup of independent scientists to inform its policy judgments on standard levels that would be protecti ve against various types of164 O 3 -related effects. However, though EPA found the views expre ssed in that report to be relevant and of interest, as st ated in section II.B.2.c above, it concludes that these views fall far short of providing a scientific basis for determining at what level these effects become adverse to the public welfare.

(14) Comment: EPA also asks for comment on setting differing levels of protection for different types of vegetation. Because EPA ha s not proposed the specific levels for such a proposal, or methods for implementing it, the agency cannot pursu e it further without

additional notice and comment.

Response: EPA agrees that should such an alte rnative approach have been chosen, EPA may have needed to issue a supplemental pr oposal providing more detail on a proposed approach. EPA notes that since the Agency did not choose this alternative path, such a supplemental proposal is not necessary.

(15) Comment: UARG states in a footnote that “EPA has previously noted that ‘striking anomalies arise in attempting to set welfare- based air quality standards according to some

welfare effects but not others.’ 49 Fed. Reg. 10,408, 10,417 (March 20, 1984). The Agency did not then resolve how such a nomalies should be addressed. Nor has the Agency ever considered whether and how the beneficient [sic] effect s of a pollutant (e.g., protection provided by tropospheric O 3 against UV-B radiation-related health effects such as cataracts and melanoma) should be consid ered in selecting a secondary NAAQS that differs from the primary one. Should the Admini strator decide in this rulemaking to set a secondary standard different from the primar y one, these are issues that he would be compelled to address.

Response: In the 1984 notice of proposed rulemaking cited by UARG, the question as to

whether EPA could consider the costs of implementation in setting the secondary standard had not been resolved by a court. Although EPA explained th at the better view

of the CAA was that EPA could not consider costs in setting the standard, it noted that it

was uncertain whether a court would reach the same conclusion. The “striking anomalies” noted by EPA arose from the possib ility that EPA could consider the costs of implementation in setting a secondary NAA QS. As the Supreme Court has now resolved the issue of whether EPA may consid er the costs of implementation in setting a secondary standard, the Agency need not reso lve how such “anomalies” described in the

1984 NPRM should be addressed.

B. Misplaced Comments

Some comments received on the proposed O 3 NAAQS addressed issues that are not

relevant for consideration in th e review of the NAAQS. These include several comments that address implementation issues. In addition to comments related to implementation of the O 3 NAAQS that are generally addressed in section I.C of the preamble to the final rule, these comments and other “misplaced” comments are discussed more fully below.165 (1) Comment: Many commenters noted that the curre nt standard has not yet been fully implemented and felt that EPA should allow time for existing regulations to work before revising the ozone standard. State agencies and industry have sp ent years planning and implementing strategies for how best to implement reductions mandated by current regulatory programs, and a revised standa rd could undo much of that planning. Numerous commenters expresse d concern over the substantia l burden placed on states to adopt a new set of implementation plans. Further, state plans to achieve a revised standard would probably be due in 2013, which is in the middle of th e current attainment

effort and before the results of current activities will be known. Several commenters believed that more significant public hea lth gains can be achieved by focusing all resources on meeting the current 8-hour st andard versus starting the SIP process over again. One commenter felt that EPA shoul d not propose to lower the current 8-hour

ozone standard until such time as NOx reductio ns from federal programs are realized. One commenter stated that a tighter ozone standard could discourage the use and development of greenhouse-gas-friendly ener gy and biofuels. The commenter believes that reducing reliance on imported fossil fu els and developing technologies to reduce greenhouse gas emissions is more important th an a “marginal change in ozone levels.”

(2) Comment: Numerous commenters from state en vironmental organizations, industry, and private citizens stated that they did not beli eve that the proposed sta ndard was attainable. Several commenters expressed concern over the impact of additional nonattainment areas on regulatory agencies charged with planning for attainment of the new standards. Several commenters expressed concern that ne ither state agencies nor industry will be able to devise a successful compliance stra tegy for the proposed standard because the control technology does not exis t. Others commented that as nonattainment counties become more rural, the choice of sources that can be controlled becomes very limited and

offsets would not be as availabl e, which would hi nder the economy.

(3) Comment: Several commenters representing industry and economic development

associations felt that if the lower standard is not achievable, that it calls into question the validity of the asserted health benefits of such a standard. The Gulf Coast Lignite Coalition stated that the proposed standard was overly conservative and would not benefit the health of residents in many newly desi gnated nonattainment area s that are relatively rural, large in size, and have a low populati on density. The Coalition did not believe that monitoring data was appropria te for estimating exposure.

(4) Comment: Several organizations believed that in ternational and interstate impacts on ambient ozone levels will likely result in mo re stringent requirement s placed on facilities that are not significant contribu tors to local air quality. Other commenters stressed that improving air quality in areas affected by transport of ozone and ozone precursors depends largely on reducing ozone levels in areas currently in nona ttainment. In some cases, reducing local production of ozone w ould not attain a lower standard. For example, the Associated Industries of Massac husetts indicated that Massachusetts will be

in nonattainment for the foreseeable future if the standard was lowered to 0.070 ppm. The issue is a result of upwind pollution tran sported into Massachusetts and there are no166 further reductions that can be made. Similarly, the Gila River Indian Community asked that EPA acknowledge and address in the fi nal rule the problem of identifying the Community as a nonattainment area when the la rgest source of ozone precursors is one over which the Community doe s not have jurisdiction.

(5) Comment: Several commenters questioned EPA’s focus on mean background rather than the extremes of the background, believing that it resulted in EPA’s failure to propose an attainable standard. Further, others men tioned that when EPA established the current primary standard for ozone, the EPA Administ rator specifically rejected a standard of 0.070 ppm as being too close to background levels. The AAM st ated that reliance on one particular global model is not a scientifica lly sound way to estimat e the contribution of

uncontrollable ozone to an extreme value sta ndard. Some industry groups believed that the proposed welfare standard should be dropped until the issue of background ozone

levels and achievable ozone limits is better understood and assessed.

Response to Comments 1-5 : Questions of implementation or attainability consequences of a NAAQS are legally irrelevant in determining which standards are requisite to protect public health with an adequate margin of safety. API v. Costle , 665 F. 2d at 1185-86. In addition, section 109(d) requires EPA to reev aluate the NAAQS no later than five years after completion of the last review, and de termine whether new or revised NAAQS are appropriate in light of current science, as reflected in th e updated air quality criteria. Issues of implementation or at tainability are not a basis to delay conducting and finishing the review and making the decisions require d under section 109(d). The EPA therefore

did not consider these comments in its decision-making process.

(6) Comment: Several organizations, including the American Asso ciation of State Highway and Transportation Officials and the Associat ion of Metropolitan Pl anning Organizations,

recommend that EPA initiate research to identify innovative new strategies and technologies including new federa l emission control programs th at will assist regional or multi-state nonattainment areas in meeting the existing standard or any new standard that is adopted. They also suggest that EPA address regional pollut ant transport issues, including research, guidance on offsets, and a ttainment dates. The Fertilizer Institute

recommended that chemical interactions that lead to ground-level ozone formation clearly need to be further studied prio r to mandating further source reductions in precursor compounds.

(7) Comment: The Texas Department of Trans portation commented that EPA should

evaluate the effects and addr ess the applicability of W126 on transpor tation and general conformity. If conformity does not a pply, the commenter recommended that EPA provide a mechanism to exempt transporta tion programs from the conformity provision

in areas where on-road mobile sources are not a significant contributor to the nonattainment problems, and also in areas where nonattainment is largely caused by ozone transport. The Washington Departme nt of Ecology also commented about the implementation of the secondary standard, and stated that EPA needs to consult with and assist states that are inexperienced with de aling with a secondary standard. The National Association of Regional Councils also noted that creating two sta ndards of evaluation167 would make planning infrastr ucture complicated; the same primary and secondary standard would be a simpler approach.

(8) Comment: Several organizations expressed con cerns about how the implementation of a

revised standard would be c oordinated with other policies and programs. The U.S.

Chamber of Commerce and several other or ganizations commented that the proposed NAAQS standard would be in force at the “Twenty in Ten” target date set for a 35- billion-gallon renewable fuel standard and w ill last eight years past that date. The commenter believes that ozone precursors will ri se significantly with the renewable fuels standard, which will impact co mpliance with the ozone NAAQS.

(9) Comment: Several commenters, including the In dian Nations Council of Governments and others, recommended that EPA provide for better synchronization of various programs and policies at the federal level, including the Regional Haze Program, HeavyDuty Highway Rule, and Regional Trans port from Ground-Level Ozone Program.

Several commenters were concerned about th e impacts that a revised standard would

have on current NOx emission control activ ities under EPA’s NOx SIP call, CAIR, and Regional Haze Program (e.g., Best Availa ble Retrofit Technology and reasonable progress). One commenter reque sted that EPA provide funding commensurate with that provided to these other air quality programs.

(10) Comment: Several commenters stated that designation of additional nonattainment areas would significantly impact the Congestion Mi tigation and Air Quality Program. One commenter predicted that th e revision could possibly crea te unfunded mandates for many regions. Local governments do not have the resources or contro ls to address the changing requirements. Another commenter suggested that program funding be increased and protected from budget cuts.

(11) Comment: With respect to implementing a revised standard, many commenters expressed that EPA needs to issue tim ely implementation guidance, identifying reasonable practical measures that can aid st akeholders, and work with state and local governments to develop national strategies to address ozone. They also noted that EPA should provide the maximum time allowed under the CAA to set the standards and implement and attain such standards. Th e South Carolina Department of Health and Environmental Control felt that the impleme ntation process should reward and provide flexibility to programs that attain the standards on an accelerated basis.

(12) Comment: Numerous commenters asked that EP A consider simultaneous strengthening of other national policies/measur es that affect ozone nationwid e. Several felt that more stringent controls on mobile sources would be appropriate to help achieve the standard and avoid undue burden on stationary sources . One commenter stated that because mobile source emission controls rest solely with the federal gove rnment, the reductions

needed to meet attainment under the current standard are greate r than the amount of emissions that the State of Texas currently regulates. One commenter suggested that EPA further tighten standards for on-road he avy-duty and off-road new diesel engines to

further reduce ozone levels.168 (13) Comment: One commenter recommended that if EP A revises the current standard that it should adopt SIP criteria to allow states to factor out background ozone and transported ozone from emission rollback requirements in their nonattainment SIPs. The commenter further suggested that EPA adopt an optiona l form of identifying reasonable progress

toward attainment based on making reductions in the population and magnitude-weighted exposure to ozone levels remaining above the standard.

(14) Comment: One commenter recommended that if EP A revises the current standard that it should adopt SIP criteria to allow states to factor out background ozone and transported ozone from emission rollback requirements in their nonattainment SIPs. The commenter further suggested that EPA adopt an optiona l form of identifying reasonable progress

toward attainment based on making reductions in the population and magnitude-weighted exposure to ozone levels remaining above the standard.

(15) Comment: Several commenters, including public citizens and industry organizations, suggested technologies and pr actices to help reduce ozone : hybrid cars, low emission engines, solar energy, low-carbon fuel, and a carbon tax. Other commenters called on EPA to make educational, modeling or policy changes to promote the integration of landuse and transportation planning and implement ation. Another commenter was concerned about the potential consequences of expande d use of reformulated gasoline on refiners

and consumers.

Response to Comments 6-15 : As noted above, comments concerning implementation of a NAAQS are legally irrelevant in determini ng which standards are requisite to protect public health with an adequate margin of safety. API v. Costle , 665 F. 2d at 1185-86.

The EPA therefore did not consider this comm ent in its decision making process. For the purpose of informing the public, a variety of information on control strategies is

discussed in the RIA.

(16) Comment: Numerous comments were received regarding signif icant issues associated with the Regulatory Impact Analysis (R IA), including the scope, assumptions and methodology, and additional analyses suggested.

Response: Because the costs of implementation cannot be considered in setting or revising the NAAQS (see section I.B of the preamb le to the final rule), the results of the

RIA were not considered in EPA’s decisions on the O 3 standards. For the same reason,

comments on the RIA were not considered in the decisions. Comments on the Interim RIA were considered, as a ppropriate, in developing the RIA for the final rule.169 References
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## Appendix

Provisional Consideration of Recent Studies

EPA has provisionally considered th e recent literature related to th e health and ecological effects of ozone (O 3 ) to identify pertinent “new” studies that were not included in the O 3 Criteria

Document. The O 3 Criteria Document included a rigorous and thorough review of the pertinent literature that included studies accepted for publication through December 2004. More recent studies accepted for publication in 2005 and 2006 were also included in the 2006 Criteria Document. These papers were identified by EP A staff, or by public comments and the Clean Air Scientific Advisory Committee (C ASAC) as adding significantly to the existing body of data on critically important topics. T ypically, these studies examined effects at lower O3 levels than previously reported or discussed epidemiologic methodological issues. The Criteria Document

forms the scientific basis for this review of the national ambient air qua lity standards (NAAQS)

for O 3

.

A number of commenters submitted more recentl y published studies along with their public comments on the proposed revisions to the NAAQS. In addition, EPA has screened and surveyed the recent literature and provisionally considered those “new ” studies of potentially greatest relevance to place them in th e context of the findings of the 2006 O 3 Criteria Document.

The intent of this effort is to determine if th e new studies published sinc e the Criteria Document materially change the conclusions of that documen t. Overall, EPA’s provi sional consideration of “new” studies, as discussed below, concludes that , taken in context, the “new” information and findings do not materially change any of the broa d scientific conclusions regarding the health and ecological effects of ozone exposure made in the O 3 Criteria Document.

This effort cannot be considered a complete l iterature review. While the papers have been individually peer-reviewed, this provisional consideration has not been subjected to peer review or the public comment process, and it has not be en reviewed by the CASAC, as is done in the development of the Criteria Document and Staff Paper.

The following sections highlight find ings of recent studies from th ree scientific disciplines that were the major focus for the relevant recent studies submitted by public commenters: (1) epidemiology, (2) human exposure, and (3) ecology.



### 1. Epidemiologic Studies of Oz one-Related Health Effects

EPA has screened and surveyed the recent epidem iologic literature and identified a number of

“new” studies on the health effects associated with O 3 exposure. This pr ocess has identified approximately 90 epidemiologic studies that encompass the majority of health outcomes

addressed in the O 3 Criteria Document. The following s ections summarize the results of EPA’s provisional consideratio n of these epidemiologic studies fo r a range of health outcomes; theA-2 overall conclusions from the O 3 Criteria Document are presen ted at the beginning of each

section.



### 1.1. Human Health Effects Associated with Short-Term Exposures to Ozone

1.1.1 Mortality

The analysis of several large multi-city studies, single-city studies, and additional meta-analyses

of these studies in the O 3 Criteria Document found a “posi tive association between increasing

ambient O 3 concentrations and excess risk for non- accidental and cardio-pulmonary-related daily mortality (EPA, 2006).” The O 3 Criteria Document, therefore, c oncluded that the literature is “highly suggestive that O 3 directly or indirectly c ontributes to non-accidental and cardiopulmonary-related mortality,” but the underl ying mechanisms by which such effects occur are not entirely clear (EPA, 2006).

This provisional consideration identifi ed a number of “new” short-term O 3 exposure mortality studies; however, not all of them focused solely on O 3 -related health effects. 9 These are

summarized below.

One of the studies examined potential confounding in the O 3 -mortality relationship using the multicity data from the National Morbidity, Mo rtality, and Air Pollution Study (NMMAPS). In Bell et al. (2007), confounding was in vestigated by analyzing the e ffect of PM on the association between short-term exposure to O 3 and mortality using data fr om 98 U.S. communities. By estimating the correlation between daily PM and O 3 concentrations, along with including PM as a covariate in various models, Bell et al. (2007) concluded that neither PM 10 nor PM 2.5 is a likely

confounder of the observed O 3 and mortality relationship.

The additional short-term exposur e mortality studies identified c onsisted of studies that were conducted in: Italy (Forastiere et al. (2005), Parodi et al. (2005 )), China (Qian et al. (2007)), South America (Cakmak et al. (2007), Australi a (Simpson et al. (2005)), and one that was conducted in the U.S. (Zanobetti and Schwartz (2007 )). Forastiere et al. (2005) and Qian et al. (2007) did not find an association between short-term O 3 exposure and out-of hospital coronary deaths in Rome, and non-acciden tal mortality in Wuhan, China, respectively. The lack of an

association in these two studies may be attributed to the fact neither study focused specifically on

the “O 3 season.” Several studies reported associations between O 3 and mortality:

• Zanobetti and Schwartz (2007) examined morta lity displacement, which postulates that deaths associated with exposure to air pollu tants are occurring in frail individuals, by studying an unconstrained and sm ooth distributed lag of O 3 with 21 lags. The authors

found that the effect size estim ate was greatest when observing 21 days of ozone instead of a single day, which indicates that the effect observed is not due to mortality

9 Two of studies identified did not focus on O 3 -related mortality: Kan et al. (2007 ) studied the effect of short-term exposures to PM on mortality; whereas, Medina-Ramon et al. (2007) focused solely on the temperature-mortality relationship.A-3 displacement. As a result, the authors conc luded that single day lags may underestimate

the true effect of short-term O 3 exposure on mortality.

• Parodi et al. (2005) and Cakmak et al. (2007) both investig ated the association between

O 3 and mortality in populations consisting prim arily of elderly inhabitants. In Genoa, Italy, Parodi et al. found an association be tween both total and cardiovascular mortality throughout the whole year, but the effects were more pronounced during the warm season (May-October). Similarly, Cakmak et al. in their study in Chile conc luded that the very elderly, >85, had the largest percent increase in mortality due to O 3 exposure compared to rest of the population.

• Simpson et al. (2005) assessed th e effect of air pollution on mo rtality in four Australian cities (Brisbane, Melbourn e, Perth, and Sydney). The authors found an association between short-term exposure to O 3 and respiratory-related mortality.

The remaining short-term exposure mortality stud ies identified (Ren et al. (2007a), Ren et al. (2007b), Rainham et al. (2005), Gon çalves et al. (2007)), analyzed the potential modification of

the effect of O 3 on mortality due to various weather variables, including temperature. 10 In two separate studies, Ren et al . (2007a, 2007b) analyzed whethe r temperature modified the O 3 - mortality effect and whether O 3 modified the temperature-mortality effect, respectively. Ren et al. (2007a) found in a study of 60 large easte rn U.S. communities that temperature synergistically modifies the O 3 -mortality effect, but the modification varies depending on the geographic location. On the other hand, Ren et al. (2007b) found in a study of 95 large U.S. communities, using the NMMAPS data, that O 3 modified the temperature effect on cardiovascular mortality across all regions of the U.S. Unlike the two Ren et al. studies, Rainham et al. (2005) and Gonçal ves et al. (2007) analyzed the overall effect of weather on the air pollution-mortality association. Rainham et al. (2005), in a study in Toronto, Canada, did not find a systematic pattern of modification, but a modification effect seem s dependent on the type of synoptic climatology category 11 analyzed. Similarly, Gonçalves et al. (2007), in a study of cardiovascular mortality in Sao Paulo, Brazil, did not find an association between weather

variables and O 3 concentrations on cardiovascular mortality.

1.1.2 Respiratory Morbidity

Results from controlled human exposure studie s and animal toxicological studies analyzed during the completion of the O 3 Criteria Document “provide clear evidence of causality for the associations observed between acute ( ≤ 24 h) O 3 exposure and relatively sm all, but statistically

10 In addition to the studies that focu sed on the potential m odification of the O 3 effect, the

literature search identified three studies th at investigated the effect of ambient O 3 concentrations and temperature on mortality in response to the Eur opean heat wave that occurred in the summer of 2003 (Dear et al. (2003), Filleul et al. (2006), Keati nge et al. (2006)).

11 Synoptic categories, which are also referred to as air mass ca tegories were devised through a complex statistical approach that classifies various meteorological components (i.e., temperature, dew point, components of wind, cloud cover, and sea level pressure) into six categories.A-4 significant declines in lung f unction observed in numerous re cent epidemiologic studies. Declines in lung function were par ticularly noted in children, asth matics, and adults who work or exercise outdoors (EPA, 2006).”

Respiratory morbidity studies analyzed in the O 3 Criteria Document pr ovide evidence of associations between acute exposure to ambient O 3 and an increase in respiratory symptoms in

asthmatic children. This consideration identified f our studies that analyzed the effect of ambient

O 3 concentrations on asthma symptoms (Feo Brito et al. (2007), Ho et al. (2007), Kim et al. (2007), Schildcrout et al. (2006)). The first three report an association, which is consistent with the 2006 Criteria Document; however, one - Schi ldcrout et al. (2006) - did not observe an

association between O 3 and respiratory symptoms.

The following observations were made from t hose studies that reported an association:

• Ho et al. (2007) investig ated the relationship between air pollution, including O 3 , and weather on asthma prevalence and asthma att ack rate in a study of junior high school

students in Taiwan. The authors found in models examining only the effect of air pollution on each outcome, that air pollution, including O 3 , is associated with asthma

attack rate.

• Kim et al. (2007) examined the effect of ambient O 3 on pulmonary function and asthmatic symptoms in 17 moderate to severe asthmatics in Korea. The authors observed

an association between O 3 and asthma symptoms even at O 3 concentrations below 80 ppb.

• Feo Brito et al. (2007), in a cohort of asthma tic patients in two Spanish towns, found an

association between O 3 concentrations and asthma sy mptoms. However, the study focused on the development of asthma symp toms during the pollen season, which also influences the presentation of asthma symptoms.

Schildcrout et al. (2006) investigated the relation between ambien t criteria pollutant

concentrations and asthma exacerbations in a cohort of children in 8 U.S. cities. Schildcrout et al. included a population of children in which th e severity of their asthma was not clearly

identified. Other studies descri bed in the 2006 Criteria Document, sp ecifically Gent et al. (2003) and Mortimer et al. (2002), obser ved associations in children cl early defined as having severe asthma. Although the study population in Schildcr out et al. encompasses children that do not have severe asthma, the study resu lts are generally consistent with the pattern of results observed in the larger body of eviden ce on the relation between O 3 exposure and respiratory symptoms as

reviewed in the O 3 Criteria Document. The following issu es were brought to the forefront by the primary author of the study, which further indica te that the lack of an association found in

Schildcrout et al. is not in consistent with the conclusi ons of the Criteria Document 12 :

12 Jonathan Schildcrout provided an email to EPA discussing the results of the 2007 study in which he was the lead author on January 4, 2008.A-5 • Shildcrout et al. included a study populat ion of 990 children with, on average, 12 children being examined every day. The O 3 analysis included the months May through September, which resulted in the study population being less th an the 990 children observed during the course of the full study. As a result, the total number of children observed by Schildcrout et al. is not comparab le to other large multi-city studies that

examined the effect of O 3 concentrations on asthma exacerbation, such as Mortimer et al. (2002).

• Although Schildcrout et al. did no t find an association between O 3 concentrations and asthma exacerbation, Shildcrout does not imply the results are inconsistent with those previously found because a thorough evalua tion of study populations , uncertainty in parameter estimates, precise scientific que stions, and additional comparisons between

studies that examined the effect of O 3 exposure on asthma exacerbations has not been

conducted.

A few “new” studies were identif ied during the provisional cons ideration that addressed the

effect of short-term O 3 exposure on lung function. In two U. S. studies, Lagorio et al. (2006) a small panel study of individuals with co-mor bid conditions (Chronic Obstructive Pulmonary Disease (COPD), asthma, or Ischemic Heart Di sease (IHD)), and Girard ot et al. (2006) an observational study of healthy hi kers, no association was found between exposure to ambient O 3 concentrations and a decrease in lung function (i.e., FEV 1 or FVC). However, in the Girardot et al. study all measured O 3 concentrations were below the current O 3 NAAQS, which is below the concentration in which lung decrements have been consistently observed in exercising individuals. The final lung f unction study identified, Lewis et al . (2005), did find an association between increasing ambient O 3 concentrations and redu ced lung function (i.e., FEV 1 ) in a study of 86 school age children in Detroit, but greate r than 75% of the children included in the study were classified as having persistent asthma.

1.1.2 Cardiovascular Morbidity

The “generally limited body of evidence is highly suggestive that O 3 directly and/or indirectly

contributes to cardiovascular-rela ted morbidity,” including physio logic effects (i.e., release of platelet activating factor (PAF)), heart rate variability (HRV), arrhythmias, and myocardial infarctions (EPA, 2006). However, the avai lable body of evidence reviewed during the O 3 Criteria Document does not “fully su bstantiate links between ambient O 3 exposure and adverse cardiovascular outcomes (EPA, 2006).”

Four “new” studies were identified (Sarnat et al . (2006), Rich et al. (2006 a), Rich et al. (2006b), Metzger et al. (2007)) that i nvestigated the effect of O 3 on arrhythmias. Each study used different cardiac episodes to id entify an arrhythmia event: Sarnat et al. (2006) used supraventricular and ventricular ectopy, Rich et al. (2006a) used paroxysmal atrial fibrillation episodes (PAF), Rich et al. (2006b) used ventricular arrhythmias, and Metzger et al. (2007) used tachyarrhythmic events. Of these studies, Sarn at et al. (2006) and Rich et al. (2006a) found an

association between O 3 concentrations and the onset of arrhythmias in a study of 32 nonsmoking older adults, and in a st udy of 203 patients with implanta ble cardiac devices (ICDs) in Boston, respectively. However, Rich et al. (200 6b) in a study of 56 patients with ICD in St.A-6 Louis observed a weak association between O 3 concentrations and arrhythmias, while Metzger et al. (2007) did not find any association in a st udy 518 patients with tach yarrhythmia that had

ICDs in Atlanta.

In addition, two studies were iden tified that examined physiologic e ffects, the rel ease of PAF - a potential stroke precursor, and B- type natriuretic pep tide (BNP) - a marker of congestive heart failure (HF) severity, in response to O 3 exposure (Chuang et al. (2007), Wellenius et al. (2007)). Chuang at al. (2007) found an increase in PAF along with other cellula r proteins (i.e., highsensitivity C-reactive protein (hs-CRP), 8-hydr oxy-2'-deoxyguanosine (8-OHdG)) and HRV, in response to an increase in O 3 concentrations. Two additional st udies, one assessi ng the effect of

O 3 concentrations on HRV in a cohort of men in Boston (Park et al. (2007)) 13 , and another observing the impact of O3 on stroke in France (Henrotin et al. (2007)) along with Chuang et al. (2007) contribute to the body of evidence suggesting a potential effect of O 3 on HRV and stroke. In the Wellenius et al. (2007) study the authors did not observe any fluctuati ons in BNP, but this could be due to within-person variability in BNP levels.

1.1.3 Respiratory/Cardiovascular Hospital Admi ssions and Emergency Department Visits

Numerous population time-series studies have “observed that ambient O 3 concentrations are positively and robustly associated with respirator y-related hospitalization and asthma emergency department (ED) visits during the warm seas on. These observations are strongly supported by the human clinical, animal toxicologic, and epidemiologic evidence for lung function decrements, increased respiratory symptoms, ai rway inflammation, and airway hyperreactivity. Taken together, the overall ev idence supports a causal relatio nship between acute ambient O 3 exposures and increased respiratory morbid ity resulting in increased ED visits and hospitalizations during the warm season (EPA, 2006).”

This provisional consideration identified numerous studies that focus on respiratory hospitalization and emergency department visits, of which one (Chen et al. (2007)) did not assess the effect of ozone, and, as a resu lt, was excluded from this consid eration. The remaining studies were conducted in the U.S. (Medina-Ramón et al . (2006), Babin et al. ( 2007)), Canada (Cakmak et al. (2006)), Australia (Erbas et al. (2005), Barnett et al. (20 05)), Hong Kong (Ko et al. (2007), Lee et al. (2006)), Korea (Kim et al. (2007)), an d Taiwan (Bell et al. ( 2007), Yang et al. (2007), Tsai et al. (2006)). All of these studies, except Barnett et al. (2005) found an association

between ambient O 3 concentrations and respiratory hospita l admissions. A brief description of each of the multi-city analyses is outlined below:

• Medina-Ramón et al. (2006) evaluated the effect of ambient O 3 on respiratory hospital

admissions in 36 U.S. cities. The authors found an association between O 3 exposure and chronic obstructive pulmonary disease (COPD) and pneumonia hospital admissions during the warm season.

13 Park et al. (2007) examined the effect of O 3 on HRV, and the originating location of the ambient air. An association was only found when the air originated in the west.A-7 • Cakmak et al. (2006) examined whether comm unity income and education modified the effect of gaseous pollutants, including O 3 , on respiratory hospita lizations in 10 large Canadian cities. Although the analysis focu sed on income and educ ation variables, the study did find an association between O 3 exposure and respiratory hospital admissions in a single pollutant model, which excluded both variables.

“Highly suggestive evidence for O 3 -induced cardiovascular effect s [has been] provided by a few population studies of cardiovascular hosp ital admissions, which reported positive O 3 associations during the warm season between ambient O 3 concentrations and cardiovascular hospitalizations [and ED visits] (EPA, 2006).” The O 3 Criteria Document, theref ore, concluded, that the “generally limited body of eviden ce is highly suggestive that O3 directly and/or indirectly contributes to cardiovascular morbidity, but more re search is needed to further substantiate the

links between ambient O 3 exposure and adverse cardiovasc ular outcomes (EPA, 2006).”

Five “new” cardiovascular hospita l admission and ED visit studies were identified (Peel et al. (2007), Ballester et al. (2006), Chan et al. (2006), von Klot et al. (2005), Barnett et al. (2006)),

all of which found an association between ambient O 3 concentrations and either hospital admissions or ER visits except Barnett et al. (2 006). Individual observations for two of these studies are presented below:

• Peel et al. (2007) examined the effect of ambient O 3 concentrations on cardiovascular ED visits from 31 hospitals in Atlanta for individuals inflicted with co-morbid conditions (e.g., hypertension, diabetes, COPD, et c.). The authors observed an increase

in cardiovascular ED visits due to effect modification in individuals co-morbid with COPD in response to ambient O 3 levels. These results add to the evidence that

individuals co-morbid with various conditions, including COPD, have an increased susceptibility to ambient air pollution.

• Ballester et al. ( 2006) evaluated the e ffect of ambient O 3 concentrations on cardiovascular ED visits in 14 Spanish ci ties. Focusing specifically on the warm season when analyzing O3, the auth ors found an association between O 3 concentrations

and ED visits for both cardiovascular disease (CVD) and he art disease (HD).

In addition to the respiratory and cardiovascular specific hospital admissi on and ED visit studies already presented, four studies ex amined the effect of ambient O 3 concentrations on both respiratory and cardiovascular hospital admissi ons and ED visits (Zanobetti and Schwartz (2006), Hinwood et al. (2006), Chan et al. (2006), Simpson et al. (2005)). Hinwood et al. (2006)

and Zanobetti and Schwartz (2006) both found that O 3 was not associated with an increase in cardiovascular and respiratory, or myocardial and pneumonia hospital admissions, respectively. In contrast, Simpson et al. ( 2005) in a study conducted in fo ur Australian cities found an

association between O 3 concentrations and hospital admission s for both asthma and COPD in the elderly for three of the four cities; whereas, Ch an et al. (2006) found an association between O 3 concentrations and cerebrovascular disease in Taiwan.A-8 

### 1.2 Health Effects Associated wi th Long-Term Exposures to Ozone 14

1.2.1 Mortality

Few epidemiologic studies have assessed the relationship between long-term exposure to O 3 and mortality. As a result, the O 3 Criteria Document concluded that an insufficient amount of evidence exists “to suggest a causa l relationship between chronic O 3 exposure and increased risk for mortality in humans (EPA, 2006).”

This provisional consideration identified a few studies that examined the association between long-term exposure to O 3 and mortality. Two of these studies focused specifically on traffic density (Lipfert et al. (2006a), Li pfert et al. (2006b)), and therefor e, were not addressed in this analysis. The remaining studies (K rewski et al. (2005), Jerret et al. (2005)) did analyze the effect of long-term exposure to O 3 on mortality, but consistent with the conclusions of previous longterm O 3 exposure studies, did not find a clear association with mortality.

1.2.2 Lung Function

“The epidemiologic data, collectively, indicate s that the current evid ence is suggestive, but inconclusive for respiratory h ealth effects from long-term O 3 exposure (EPA, 2006).” This provisional review identified two 15 well conducted cohort studies thatassessed the effect of longterm exposure to O 3 on lung function development (Islam et al. (2007), Rojas-Martinez et al. (2007)). A description of each of the aforemen tioned studies and their findings are presented

below:

• Islam et al. (2007) investigated the relationship between air pollution, lung function, and the subsequent development of asthma in a cohort of 9 and 10 year

old children without asthma or wheeze from the Children’s Health Study. The authors found that long-term O 3 exposure did not have any observable effect on forced expiratory flow (FEF), and, ther efore, was not associated with lung damage or asthma development.

• Rojas-Martinez et al. (2007) evaluate d the association between long-term exposure to O 3 and lung function development in Mexico City schoolchildren. In this study, the authors found that deficits in FVC and FEV 1 were associated with

O 3 exposure.

14 In addition to the studies presente d in this section, three long-term O 3 exposure studies were identified that did not warrant analysis because they either focused specifically on proximity to traffic (Meng et al. (2007), McC onnell et al. (2006a)), or the impa ct of cat and/or dog ownership along with air pollution levels on asthmatic occurrences (McConnell et al. (2006b)).

15 Morgan et al. (2005) also st udied lung function and the devel opment of wheeze; however, the study does not take into consider ation the role of ai r pollution on both. As a result, it was excluded from this analysis.A-9 1.2.3 Lung Cancer

“The weight of evidence from recent animal toxi cological studies and a very limited number of epidemiologic studies do not support ambient O 3 as a pulmonary carcinogen (EPA, 2006).” This provisional consideration identifi ed two studies (Chen et al. ( 2006), Huen et al. (2006)), which both observed cytogenic damage (i.e., micronuclei formation and degenerated cells) in response

to an increase in O 3 exposure. Although cytogenic damage could potentially lead to cancer development, neither study concluded that O 3 is a pulmonary carcinogen.

1.2.4 Prenatal and Neonatal Outcomes

A limited number of studies have examined the relationship between O 3 exposure and birthrelated outcomes, including mortality, premature bi rths, low birth weights, and birth defects.

The O 3 Criteria Document concluded that “O 3 [is] not an important pr edictor of several birthrelated outcomes including intrauterine and infa nt mortality, premature births, and low birth weight (EPA, 2006).”

This provisional consideration identified “new ” studies that analyzed the effect of O 3 exposure on various birth outcomes, including pre-term bi rth (Hansen et al. (2007)); low birth weight (LBW) (Salam et al. (2005), Dugandzic et al. (2006), Hansen et al . (2007)); respiratory effects/hospitalizations (Triche et al. (2006), Dales et al. (2006 )); and mortality (Tsai et al. (2006a), Tsai et al. (2006b), Ha jat et al. (2007)). A synopsis of the findings for each birth outcome is presented below:

• Pre-Term Birth : Hansen et al. (2007) analy zed the association between O 3 exposure during pregnancy and pre-term birth in 28,000 singleton births in Brisbane, Australia. The author s found that an increase in O 3 exposure during the

1 st

trimester was associated with pre-term birth.

• Low Birth Weight (LBW) : Salam et al. (2005) assesse d the effect of increasing

O 3 concentrations on LBW in a population of infants born in California from 1975 – 1987. The authors concluded that a po sitive association exists between an

increase in O 3 concentrations and LBW over th e entire pregnancy with the association being the strongest in the 2 nd and 3 rd trimesters. Dugandzic et al (2006) and Hansen et al. (2007) 16 also analyzed the effect of O 3 on LBW in Canada and Australia, respectively. In both instances, neither study observed an

association between O 3 exposure and LBW during any trimester.

• Respiratory : Triche et al. (2006) examin ed respiratory effects of O 3 in infants of

asthmatic mothers. The authors found th at infants of asthmatic mothers had a greater likelihood of wheeze and difficulty breathing compared to infants whose mother did not have asthma for every interquartile-range increase in 24-hr

16 Hansen et al. (2007) also observed the effect of O 3 on Head Circumference and Crown-Heel Length. The authors also found no association between O 3 exposure and these health effects.A-10 average ozone. 17 In addition, Dales et al. (2006) tested the association between daily neonatal respiratory hos pitalizations and ambient O 3 concentrations in 11 large Canadian cities. The au thors concluded that current O 3 levels are responsible for a significant proporti on of hospitalizations in neonates.

• Mortality : Tsai et al. (2006a), Tsai et al. (2006b), and Hajat et al. (2007) in studies conducted in Taiwan, Taiwan, and the United Kingdom, respectively, all

found a weak association between O 3 exposure and infant mortality.



### 1.3 Vulnerability/Susceptibility

1.3.1 Heightened Vulnerability

Epidemiologic studies reviewed in the O 3 Criteria Document suggest that “exercising (moderate to high physical exertion) children and adol escents appear to demonstrate increased responsiveness to ambien t concentrations of O 3 and may be more likely to experience O 3 - induced health effects (EPA, 2006).” During this provisional cons ideration, a study was

identified that examined the effect of exercise on O 3 -related health effects (Wong et al. (2007)), however, the study focused on mortality in indi viduals > 30, instead of more benign health

effects in children and adolescents . In this study, Wong et al. (2007) examined the relationship

between habitual exercise and air pollution associated mortal ity in Hong Kong. The authors

found an association between O 3 exposure and mortality in people ≥ 65 who never exercised. As a result, the authors concluded that habitual ex ercise may reduce the risk of premature death attributed to air pollution.

1.3.2. Genetic Susceptibility

Human clinical and epidemiologic studies analyzed in the O 3 Criteria Document demonstrated that “genetic polymorphisms fo r antioxidant enzymes and inflammatory genes (GSTM1, NQO1,

and Tnf- α ) may modulate the effect of O 3 exposure on pulmonary function and airway inflammation (EPA, 2006).” This provisional considerati on identified three st udies (Islam et al. (2007), Chen et al. (2007), Romi eu et al. (2006)) along with tw o review papers (London (2007), McCunney (2005)), which found that genetic polymorphisms in antioxidant genes can lead to a decrease in lung function upon exposure to O 3

.

17 An association was not observed for wheeze fo r an interquartile-range increase in 8-hr

maximum or 1-hr maximum.A-11 

### 1.4 Provisional Consideration of Epidemiologic Studies Summary

EPA emphasizes that this is a provisional consid eration of the recent li terature, and it is not intended to serve as a supplement to the Criteria Document. This summary of “new” studies has not undergone the detailed and extensive review pr ocess entailed in the development of a Criteria Document, and it has not been discussed by CASA C. Overall, the “new” study results support and expand upon findings in the 2006 O 3 Criteria Document. The esse ntial conclusions of this provisional consideratio n are that the science supporting evaluation of the potential health impacts of O 3 on human health continues to expand and hence provides a larger knowledge base for better characterizing th e relationships between O 3 and health effects. The “new” studies provide additional insights on the health effects of O 3 exposure, but the results do not materially change any of the broad scie ntific conclusions regardi ng the health effects of O 3 exposure made

in the 2006 O 3 Criteria Document.



### 2. Human Exposure Studies

Three “new” studies were identified that addres sed the relationship of personal exposures to

ambient O 3 concentrations: Koutrakis et al. (2005), Sarnat et al. (2006), and McConnell et al. (2006c). The Koutrakis et al. ( 2005) study is a research report su mmarizing results presented in peer-reviewed publications that were reviewed in the O 3 Criteria Document (Sarnat et al., 2000, 2001, 2005). As described in these publica tions, the report found that ambient O 3 concentrations were significantly associated with personal O 3 exposures in a study in Boston during the summer, although a similar study conducted in Baltimore found that ambient O 3 concentrations showed stronger associations with personal exposures to PM 2.5 than to O 3 . The poor correlations observed during the winter between ambient concentra tions and personal exposure measurements may be due to the inability of personal monitors to detect low O 3 concentrations (below 5 ppb), along with differences in activit y patterns and building ve ntilation compared to the summer. The study conducted in Steubenv ille, OH by Sarnat et al. (2006) observed significant associations between ambient O 3 concentrations and personal O 3 exposures in both summer and fall seasons, with higher associatio ns observed for subjects spending time under high building ventilation conditions . A modeling study to quantitati vely estimate the effect of

NO

x emissions on O 3 concentrations near roadways (McConnell et al. (2006c)) predicted

decreased O 3 concentrations near roadways, contributi ng to increased spatia l variability and poor

associations between residentia l outdoor concentrations and m easured at ambient monitors; however, mean O 3 concentrations measured outside hom es were within 3 ppb of fixed-site monitor values (33 ppb vs. 36 ppb).

The results of these studies are generally consiste nt with, and do not materially change, the broad

scientific conclusions reached in the 2006 O 3 Criteria Document regarding the spatial variability

of ambient O 3 concentrations and relationships be tween personal exposures and ambient

concentrations of O 3 . In one case (Koutrakis et al. ( 2005)), data from the study had been presented in peer-reviewed publications that were considered during prep aration of the Criteria

Document.A-12 

### 3. Ecological Studies

EPA has screened and surveyed the recent vegeta tion and ecological litera ture and identified a

number of “new” studies on effects associated with O 3 exposure. The following discussion summarizes the results of EPA’s provisional consider ation of these studies for a range of issues

related to the effects of O 3 on vegetation and ecosystems.

Two recently published companion papers (McL aughlin et al 2007a, McLaughlin et al 2007b) investigated the effects of ambient O 3 on tree growth and hydrology at fo rest sites in the southern Appalachian Mountains. The aut hors reported that the cumulative effects of ambient levels of

O 3 decreased seasonal stem growth by 30-50% for most trees species in a high ozone year in comparison to a low O 3 year (McLaughlin et al 2007a). The authors also report that high

ambient O 3 concentrations can disrupt whole tree water use and in tu rn, reduce late-season stream-flow (McLaughlin et al 2007b).

Several new studies were published since the O 3 Criteria Document from the Aspen FACE “free

air” O 3 and carbon dioxide exposure experiment in a forest in Wisconsin (Kubiske et al. 2006a, Kubiske et al. 2006b, Liu et al. 2007, Percy et al . 2007, Darbah et al. 2007). Kubiske et al. (2006b) reported that elevated O 3 may change the intra- and inter-species competition. For example, O 3 treatments increased the rate of conver sion from a mixed aspen-birch community to a birch dominated community. In another study at this site, Percy et al. (2007) showed that negative growth effects were seen below the current 8-hour O 3 standard level (0.084 ppm). The authors also attempted to compare different O 3 metrics to predict effect s on tree growth by using trees repeatedly measured over 5 year s. The authors suggested that 4 th highest maximum metric performed the best, but they did not include the 3-month 12-hr W126 in their analysis.

Several new studies have been published on the in cidence of foliar injury in the field due to

ambient O 3 concentrations (Kohut 2007, Chappelk a et al. 2007, Davis 2007a, Davis 2007b, Davis & Orendovici 2006). Kohut (2007) presente d a foliar injury assessment for 244 National parks over 5 years. The author reported that risk of foliar injury was hi gh in 65 parks, moderate in 46 parks, and low in 131 parks. Chappelka et al. (2007) reported that the average incidence of

O 3 -induced foliar injury of was 73% on milkweed in the Great Smokey Mountain National Park in the years 1992-1996. Three papers (Davis 2007a, Davis 2007b, Davis & Orendovici 2006) reported O 3 -induced foliar injury in several plants sp ecies in National Wildlife Refuges in Maine, Michigan and New Jersey.

In a large-scale modeling analysis, Sitch et al. (2007) suggested that increasing ambient O 3 concentrations across the globe suppresses the land carbon sink because O 3 decreases plant productivity. As a consequence, more CO 2 is accumulating in the atmosphere. The authors suggest that the radiative forcing of this extra CO 2 is greater than the direct radiative forcing of

O 3 as a greenhouse gas alone.A-13 Overall, EPA’s provisional consideration of these “new” studies concludes that, taken in context, the new information and findings do not materi ally change any of the broad scientific conclusions regarding the effects of O 3 exposure on vegetation and ecosystems made in the O 3 Criteria Document.A-14 

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