Comments Regarding CASAC Advice on Reconsideration of the 2008 

Primary Ozone National Ambient Air Quality Standard

Prepared for the Alliance of Automobile Manufacturers

Jon M. Heuss

Air Improvement Resource, Inc.

February 7, 2011 

Introduction

As indicated in Lydia Wegman’s January 25, 2011 Memo to Holly Stallworth of the EPA 

Science Advisory Board Staff, EPA is requesting additional advice from the Clean Air 

Scientific Advisory Committee (CASAC) on the strengths and limitations of the 

scientific evidence at issue in the Administrator’s proposal for reconsideration. 

Although EPA is asking CASAC to focus on nine specific charge questions, the memo 

also indicates “...we would appreciate any further advice that CASAC wishes to provide.” 

In addition, the memo cautions that Panel members should be mindful that they should 

consider only information that was in the record of the 2008 NAAQS review. Finally, 

the memo indicates that the Administrator looks forward to CASAC’s consensus advice 

on the charge questions as she considers a standard in the range of 0.060 to 0.070 ppm. 

The Alliance of Automobile Manufactures participated in the 2008 NAAQS review and 

the re-consideration, providing detailed comments to the Agency.1 Based on a review of 

the EPA request, we offer comments below on the specific charge questions. Our 

comments also refer to the locations in earlier submissions of the Alliance and other 

interested parties where further detail can be found. However, we respectfully begin 

with comments to CASAC on the framework and process being followed in the 

teleconference. 

First, because of the importance of the choice of an ozone NAAQS that is sufficient to 

protect the public health but not more stringent than necessary, we encourage CASAC to 

go beyond the charge questions and provide additional advice. For example, we raise 

additional important questions in these comments that CASAC should address. Second, 

we urge the CASAC Panelists to provide their advice without artificially enforcing a 

consensus view. If there is consensus, or a range of opinion, that information should be 

provided to the Administrator. 

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

1

 Comments of The Alliance of Automobile Manufacturers on EPA’s Proposal for 

Reconsideration of the Primary and Secondary National Ambient Air Quality Standards for 

Ozone, March 22, 2010, Docket ID No. EPA–HQ–OAR–2005–0172- 12133.1. “Alliance 

Comments,”
"

Third, we ask CASAC to consider whether the limited time for discussion of each 

question, less than 18 minutes per question in the draft Agenda for the February 18, 2011 

call, is sufficient to allow the Panel time to fully explore the issue and respond to the 

charge. In addition, there is no time on the Agenda to address other issues that Panelists 

may want to bring up. We would encourage the Panel to take the necessary time in a 

public format to discuss and develop its answers.

Fourth, we ask CASAC to address the difficulties the Panel faces because it is being 

asked to develop its views based only on the information available in the record of the 

2008 review. The 2008 review was based primarily on the February 2006 Criteria 

Document that assessed literature through 2004 along with selected studies published in 

2005 and 2006. It thus represents the state of science as of six years ago. Since the Clean 

Air Act requires EPA to update the “criteria” every five years, it follows that the “reconsideration” is not based on the accurate and latest science envisioned by the Clean Air 

Act requirement. In addition, since the Panelists are aware of the recent literature (and 

older studies that may be important but not included in the 2006 CD), it puts them in an 

awkward position to ask them to ignore new thinking about ozone health-related science. 

Fifth, with regard to the newest science, there is substantial new information that calls 

into question a number of key assumptions EPA made in the re-consideration proposal. 

EPA carried out a 38-page Provisional Assessment (PA) of the post-2006 CD literature at 

the time of the re-consideration and reported that the newest literature does not materially 

change the conclusions of the Agency’s science assessment. However, a detailed 

analysis of the PA and the relevant literature by the Alliance indicates that the PA does 

not reflect the latest science because it completely overlooks several significant new 

scientific studies, is not a thorough assessment of the studies it does summarize, and 

omits consideration of new information concerning a key issue in the review, the 

background of ozone. We urge the CASAC panel to read the critiques of the PA 

submitted to the Agency by the Alliance2 and by the National Association of 

Manufacturers3 (NAM) prior to the February 18, 2011 teleconference. 

Sixth, we believe that CASAC needs to provide the Administrator with additional advice 

concerning the limitations of the method used to estimate background ozone. In the 1997 

Review, the Administrator found that a standard set at a level of 0.07 ppm was not 

requisite to protect public health in part because, based on the 1996 CD, an 8–hour 

standard set at 0.07 ppm would be closer to peak background levels that infrequently 

occur in some areas due to non-anthropogenic sources of ozone. In the 2008 Review, 

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2

 Alliance Comments, supra note 1, Appendix A, Review of More Recent Relevant Studies to the 

Choice of Ozone NAAQS. 

3

 NAM, Attachment 1, A Detailed Review of the New Data in EPA’s Provisional Assessment and 

the New Data Excluded from the Assessment Does Not Support a Reduction in the Ozone 

Standard, Docket ID No. EPA–HQ–OAR–2005–0172-12439.3. 
#

EPA changed the way background was evaluated, relying solely on the use of a global 

atmospheric model to calculate mean background. EPA also neglected to estimate the 

extreme values of background even though the statistical form of the ozone NAAQS is an 

extreme value. This is an important omission that led the Agency and CASAC to assume, 

incorrectly, that a standard in the range of 0.06 to 0.07 ppm was substantially higher than 

background and achievable throughout the country. 

Comments on the charge questions

In the following, the eight charge questions are repeated and Alliance comments are 

provided, along with references to sections of earlier public submissions that provide 

additional detail. 

1. What is your advice on the overall strengths and limitations of the evidence from 

controlled human exposure and epidemiological studies and the results of the 

exposure and risk assessments, in the context of EPA's selection of a standard level 

within the proposed range that would be requisite to protect public health with an 

adequate margin of safety, including the need to protect susceptible populations, 

such as children and people with asthma? 

The controlled human exposure studies provide a strong and consistent body of 

information on the effects of 1-to-3 hour and 8-hour exposures to ozone. The first 

effects - transient, reversible FEV1 decrements - are the body’s reflexive reaction to the 

presence of an irritant gas unrelated to sensations of discomfort. Such effects occur after 

exposures to 0.08 ppm for 6 to 8 hours when the subjects are exercising at a rate that 

would be considered strenuous when carried out intermittently for an eight-hour period. 

Whether such effects occur at 0.06 or 0.07 ppm is highly controversial since the answer 

depends on how the baseline is evaluated, how the precision of the test is considered, 

how the day-to-day variability of a subject is evaluated, and how the data is statistically 

analyzed. In either case, single incidences of the effects at 0.08 ppm (for either healthy 

or asthmatic subjects) were not considered to be adverse by CASAC and EPA staff in the 

1997 review. Nothing in the body of controlled studies has changed to alter that view. 

Since the first effects on the performance of lung function tests occur at 0.50 ppm in 

sedentary individuals, the vast bulk of personal exposures of either the general population 

or the susceptible population are far below the thresholds for the first effects identified in 

controlled studies. This provides a large margin of safety for the population as they go 

about their daily activities. 

Other effects on the respiratory system, as discussed in the response to question #2, occur 

at higher concentrations as ozone triggers responses in the body’s defense mechanisms. 

Since the threshold for even the first indications of an inflammatory response is higher 

than that for the reflexive FEV1 response, no adverse health effects are to be expected at 

either the current 0.075 ppm standard or a more stringent standard. 

In contrast to the controlled studies, the epidemiological studies have severe limitations 
$

beyond those already acknowledged by the Agency. These limitations are discussed in 

the answer to questions #6 and #8 and in detail in the Alliance Comments Appendix B at 

pages 17 to 35.4 Basically, the full pattern of results in comprehensive studies 

demonstrates a biologically implausible wide range of results from positive to negative 

and spatial and temporal variability that is not consistent with the spatial and temporal 

distribution of ozone. Therefore, it is inappropriate to assume that ozone is causing 

premature mortality or hospital admissions. The full pattern of results demonstrates a 

heretofore underestimated stochastic variability in the data. Although there may be 

somewhat more positive associations than negative associations in comprehensive 

studies, 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. Based on the body of controlled studies, a standard at the upper end of 

the range or the current 0.075 standard would adequately protect the public health.

2. Recognizing that controlled human exposure studies at 0.080 ppm O3 and above 

have provided evidence of other health effects, including inflammation and 

increased airway responsiveness which may occur through different physiological 

mechanisms than the reduction in FEV1, how should the results of these studies 

inform our understanding the health effects to healthy adults at exposures levels 

from 0.060 to 0.070 ppm? 

As noted in the answer to question #1, other effects on the respiratory system occur at 

higher concentrations than those that cause FEV1 decrements as ozone triggers responses 

in the body’s defense mechanisms. For example, the immune system responses noted by 

EPA as the first indications of “inflammation” are physiological processes that occur in 

all living organisms under the stimuli of daily life. The first reported changes (that occur 

in humans with heavy exercise after 1- to 3-hours above a threshold of 0.18 to 0.20 ppm) 

are small and reversible and well within the range of physiological variability. They fall 

into the category of biochemical markers that the American Thoracic Society indicates do 

not necessarily imply adversity. The review by Mudway and Kelly5 notes that for 

neutrophils transiting into the lung -- one of the earliest of these responses -- it is not 

clear if the response should be considered beneficial (functioning to clear necrotic cells) 

or detrimental (leading to an active inflammation with tissue injury). The 2006 CD notes 

that generally, “the initiation of inflammation is an important component of the defense 

process; however, its persistence and/or its repeated occurrence can result in adverse 

health effects.” Since the threshold for even the first indications of an inflammatory 

response are higher than that for the reflexive FEV1 response, no adverse health effects 

are to be expected at either the current 0.075 ppm standard or a more stringent standard.

Another effect that occurs at somewhat higher exposures than the FEV1 decrements 

are mild symptoms and sensations of discomfort. These are also transient and reversible. 

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

4

 Alliance Comments, supra note 1, Appendix B, Comments of the Alliance of Automobile 

Manufacturers on EPA’s Proposal to Revise Ozone NAAQS, filed October 9, 2007. 

5

 I. Mudway and F. Kelly, Ozone and the Lung: A Sensitive Issue, Mol. Aspect. Med., 21, 1-48 

(2000).
%

Thus, the inflammatory and other responses at 0.08 and higher ozone exposures when 

exercising do not inform the understanding of effects in the 0.06 to 0.07 ppm range. 

Additional relevant discussion can be found at pages 9-11 and 35-36 of Appendix B of 

Alliance Comments.

3. How should the results of the controlled human exposure studies at 0.060 ppm 

O3, showing effects on FEV1 and respiratory symptoms, in the context of the larger 

body of evidence from controlled human exposure studies, mentioned above, inform 

our understanding of the health effects to healthy adults at exposure levels from 

0.060 to 0.070 ppm? 

The controlled human exposure studies provide a strong and consistent body of 

information on the effects of 1-to-3 hour and 8-hour exposures to ozone. The first 

effects - transient, reversible FEV1 decrements - are the body’s reflexive reaction to the 

presence of an irritant gas unrelated to sensations of discomfort. Such effects occur after 

exposures to 0.08 to 0.12 ppm for 6 to 8 hours when the subjects are exercising at a rate 

that would be considered strenuous when carried out intermittently for an eight-hour 

period. 

Whether such effects occur at 0.06 or 0.07 ppm is highly controversial since the answer 

depends on how the baseline is evaluated, how the precision of the test is considered, 

how the day-to-day variability of a subject is evaluated, and how the data is statistically 

analyzed. Public comments by the National Association of Manufacturers6 and the 

Alliance7 provide more detailed discussions of this issue.

The Alliance points out that the small group mean changes that are at issue are well 

within the range of normal measurement variability and well below the 10 to 20% 

changes which are considered moderate and potentially of health concern in the Staff 

Paper. Thus, the appropriate question in interpreting these studies is not whether there 

are small changes in the performance of lung function tests, but what these small changes 

mean for public health given the involuntary reflex mechanism causing the changes. 

NAM documents that a variety of environmental exposures and stresses to which many 

people, including children, are routinely exposed produce changes in pulmonary function 

tests of the same magnitude as proposed as “exposures of concern” for the ozone 

NAAQS. Many children experience minor exposures and stresses that result in transient 

FEV1 decreases of 10-15%. Further, in some cases, these routine changes or effects occur 

consistently rather than infrequently, i.e. once per year.

In the 1997 review, single incidences of the FEV1 effects at 0.08 ppm (for either healthy 

or asthmatic subjects) were not considered to be adverse by CASAC and EPA staff. 

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

6

 NAM, Attachment 2, Critical Review of the Health Data in EPA’s 2008 Proposed NAAQS for 

Ozone Cited in the Current 2010 Proposed Rulemaking, Docket ID No. EPA–HQ–OAR–2005–

0172-12439.4, at pages 1 to 7.

7

 Alliance Comments, Appendix B, at pages 9-11. 
&

There was considerable discussion of this in the Staff Paper at that time. Nothing in the 

body of controlled studies has changed to alter that view. The acute decrements are 

transient, reversible decrements in the performance of the lung function test (that requires 

maximal inspiratory effort) due to a protective reflex and not a change in long-term lung 

function of any clinical or pathological significance. 

The threshold for these first effects varies depending on ozone concentration, time of 

exposure and breathing rate. Since the first effects on the performance of lung function 

tests occur at 0.50 ppm in sedentary individuals, the vast bulk of personal exposures of 

either the general population or the susceptible population are far below the thresholds 

for the first effects identified in controlled studies. This provides a large margin of safety 

for the population as it goes about its daily routine. 

The new data extending lung function effects to lower concentrations establishes that the 

response is non-linear in contrast to the linear assumption made in the 1997 review. This 

means that, for a given ozone exposure below the current standard, the risk of lung 

function decrements is now lower than thought in the 1997 review, when the standard 

was lowered to 0.08 ppm. The Second Draft Staff Paper in the 2008 review included a 

statement that the risk estimates “are now appreciably lower than in the last review.”8

The final Staff Paper removed the statement but the risk estimates remained. 

 

Given these facts, making the ambient ozone standard more stringent with the aim of 

reducing the number of transient pulmonary function events and the number of 

“exposures of concern” will not likely have any effect on children’s or adult’s health. 

4. With respect to the information from controlled human exposure studies at 0.060 

ppm O3, what is the scientific importance of the small, group mean FEV1

decrements relative to the findings that 7 to 20% of the subjects experienced FEV1

decrements > 10%? Please consider this question from both a public health and a 

clinical perspective. 

As discussed in the answer to question #2, small group mean FEV1 decrements, whether 

or not statistically significant, are not medically significant. The EPA focus on a subset 

of responses in the 7 to 20 % range is also problematic since the Adams 2006 study was 

not designed to test for the presence or absence of high responders. EPA focuses on socalled responders but to have a very small mean difference in the presence of some larger 

decrements means that there are also subjects whose FEV1 increased during the exposure. 

Thus, there is substantial variability in the subject’s responses. For example, the range of 

individual FEV1 changes in the filtered air group in these studies was -6.0 to 12.4 %. 

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

8 U.S. Environmental Protection Agency, Review of the National Ambient Air Quality Standards 

for Ozone: Policy Assessment of Scientific and Technical Information, OAQPS Staff Paper -

Second Draft, EPA-452/D-05-002, July 2006, at pages 5-71 and 6-27.
'

Dr. Roger McClellan, a former member and chair of CASAC, who has followed the 

human health effects literature for many years and Dr. Regis McFadden, a Professor of 

Medicine and a pulmonary physician with much research and clinical experience with 

asthmatics, have questioned EPA’s interpretation of the data.9 Dr. McClellan has 

indicated that the validity of EPA’s reinterpretation of the data and the significance of the 

functional changes are debatable. Dr. McFadden describes the reported FEV1 decrements 

in Adams’ subjects when exposed to an ozone concentration of 0.08 ppm or less as “quite 

minimal and likely nondetectable by the subjects.” Dr. McFadden does not regard such 

events as medically significant. He notes that the symptoms reported were barely 

discerned and the maximum effect (at 0.08 ppm) represented only a 6% increase over 

control. For example, the total mean symptom scores on the scale reported by Adams 

(2006) were only 2-4 units at 0.04 and 0.06 ppm out of a possible total score of 160. 

Adams had indicated that the differences in the symptoms between the 0.04 and 0.06 ppm 

exposures and the filtered air control were not significant. As the NAM Attachment 2 

comments point out, EPA’s conclusions concerning the variability in individual response 

and a higher level of response in a small subset of individuals are speculative and should 

not be used as a basis for a revised NAAQS. 

5. The evidence, including that summarized above, indicates that susceptible 

populations may have greater responses than healthy people. In light of this 

evidence, how can we appropriately use the results of controlled human exposure 

studies conducted on healthy adults, as well as the epidemiological studies of 

susceptible groups, to inform a judgment on the effects of ozone exposure on 

susceptible populations? 

With regard to the controlled studies, Dr. McFadden also reviewed the clinical data on 

whether asthmatics or other susceptible populations may have greater responses than 

healthy people as well as EPA’s arguments as to why this might be the case. He 

concluded that the data at 0.12 ppm and higher do not show any major effects on 

asthmatics. He described EPA’s arguments as to why there might be greater concern as a 

series of unproven assumptions. He concludes the assumptions remain an unproven 

theory regarding whether the responses seen in controlled studies would lead to clinical 

manifestations in terms of exacerbations of asthma or other adverse health effects.

Dr. McFadden provides a number of reasons for his conclusion that transient decreases in

FEV, of 10-20% are not by themselves significant or meaningful to asthmatics. He 

points out that based on his experience from examining and studying thousands of 

patients for both clinical and research purposes that asthmatics typically will not begin to 

sense bronchoconstriction until their FEV1 falls about 50% from normal. By way of 

comparison, he notes that asthmatic patients presenting to a physician or emergency room 

for treatment of acute exacerbations of their illness often have decreases in FEV1 of 65-

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

9 Comments of E. R. McFadden, Jr., M.D. on Health Significance of Asthmatics' Responses

Reported in Clinical Studies of Short-Term Ozone Exposure, September 14, 2007, Docket ID No. 

EPA–HQ–OAR–2005–0172-4054. 

(
)

70% from normal. In addition to Dr. McFadden’s statement in the record, there are 

statements in the record by eight other Medical Doctors concerning the lack of clinical 

significance of transient, reversible FEV1 decrements of 10 to 20 % for asthmatics.10

With regard to the epidemiological data, the Alliance Appendix B comments at pages 22 

and 23 point out while there are some positive associations that implicate ozone as a 

responsible pollutant, taken as a whole the studies are mixed and inconsistent with regard 

to ozone and often implicate other pollutants. Overall, the data on susceptible 

populations is not any stronger than understood or assumed in the 1997 review. The 

mixed and inconsistent pattern is not surprising given the substantial stochastic variability 

in the data that is not acknowledged by the Agency. A large component of stochastic 

variability that goes well beyond just heterogeneity of response is apparent in the data 

from multi-city studies or comprehensive studies. The kinds of respiratory responses that 

EPA hypothesizes may occur in human populations from current ozone levels are not 

consistently seen in observational studies and, to the extent they are, the associations 

often implicate pollutants other than ozone. Therefore, there is little support for 

assuming that susceptible individuals are experiencing greater ozone effects than healthy 

individuals. 

6. To what extent does your confidence that the effects observed in epidemiological 

studies are attributable specifically to O3 lessen or otherwise change, if at all, at the 

lower levels in the proposed range as compared to the higher levels? 

This question is quite specific. Instead, EPA should be asking CASAC more generally 

about the interpretation of epidemiological studies as it informs the Administrator’s 

decision. For example, the American Petroleum Institute offered additional questions 

regarding epidemiology that address key issues in the interpretation of the epidemiology -

geographic heterogeneity, confounding by other pollutants and possible “doublecounting” of effects, and the implications of the no-threshold assumption.11 We urge 

CASAC to address all these issues.

The “effects” observed in epidemiological studies are associations not necessarily effects 

caused by or exacerbated by ozone. The overall pattern of associations in multi-city 

studies and in comprehensive studies in single cities is not biologically plausible. 

Analysis of time-series single-city associations in large multi-city studies such as the 

National Morbidity and Mortality Air Pollution Study (NMMAPS), shows significant 

variability of positive and “negative” associations unaccounted for in the published 

literature or EPA’s analysis. Such a wide range that includes both strong positive and 

strong negative associations goes well beyond heterogeneity of response and is not 

biologically plausible. 

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10 A list of the statements is provided in Docket ID No. EPA–HQ–OAR–2005–0172-0052.3. 

11 January 25, 2011 letter from Howard Feldman to Assistant Administrator Regina McCarthy, 

Docket ID No. EPA–HQ–OAR–2005–0172-13001.1. 
*

Air pollution time-series epidemiology studies suffer from problems associated with 

publication bias, model uncertainty, model selection issues, lack of adequate control for 

confounding variables such as other pollutants and weather, and exposure 

misclassification arising out of the poor correlation between ambient monitors and 

personal exposure. In its June 2006 letter to the Administrator, CASAC confirmed this 

view in evaluating mortality time-series studies, noting that “[b]ecause results of timeseries studies implicate all of the criteria pollutants, findings of mortality time-series 

studies do not seem to allow us to confidently attribute observed effects specifically to 

individual pollutants.”12 

With regard to assuming that ozone associations are causal, there are a number of 

additional problems. Because of the wide range in individual city associations, shown for 

example in Figure 7-17 of the 2006 CD, combined results are usually presented. 

However, the combined association in winter is actually negative, so the emphasis in the 

literature has been on evaluating summer-only or all-year associations. It is 

incomprehensible that ozone would be causing mortality in the summer but protecting 

against mortality in the winter. The Agency has not fully evaluated all the possible 

reasons for this discrepancy and their policy implications. In multi-pollutant models for 

the summer case, the combined positive ozone association was reduced and became nonsignificant at all three lags evaluated as shown in Figure 7-31 of the CD.

In addition to the literature considered in the 2008 review, there is now a larger data base 

of multi-city studies which can inform the Administrator’s decision. A full consideration 

of the ramifications of these studies would change the Administrator and CASAC 

judgments regarding an independent ozone mortality effect. Alliance and NAM 

comments summarize these studies.13 In October, 2009, the Health Effects Institute (HEI) 

published Air Pollution and Health: A European and North American Approach 

(APHENA).14 The APHENA project was designed to take advantage of the largest 

databases available, in the U. S. Europe, and Canada. As documented in the Alliance and 

NAM submissions, the pattern of combined associations reported in the APHENA study 

does not support EPA’s claims of causal relationships between ozone and mortality or 

between ozone and hospital admissions. 

There are at least six new multi-city studies that have evaluated ozone associations with 

mortality or hospital admissions since the 2006 CD. All the studies that report or plot 

the individual-city associations show a biologically impossible wide range of associations 

from positive to negative for mortality and hospital admissions. We note two relevant 

findings. 

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

12 R. Henderson, CASAC Letter, EPA-CASAC-06-07, June 5, 2006 at page 3.

13 Alliance Comments Appendix A and NAM Comments Attachment 1. 

14 Katsouyanni K. and Samet, J. (2009). Air Pollution and Health: A European and North 

American Approach (APHENA), Health Effects Institute Report 142, October, 2009. 
+,

When Bell et al., 200715 restricted the analysis to days with low ozone, in order to see if 

the small combined association persisted, the range in individual-community associations 

widened. For example, when the data was restricted to days with ozone less than 20 ppb, 

the range in individual city mortality associations for a 10 ppb increase in ozone was 

from – 20 % to + 30 %. It is inconceivable that such low ozone exposures would be 

causing a dramatic increase in mortality in one city and protecting against mortality in 

another. With such wide variation, the interpretation of a small combined association as 

a health effect is highly questionable.

There also is strong evidence of regional differences in ozone associations that are not 

consistent with ozone causing mortality. Bell and Dominici, 200816 and Smith, Xu, and 

Switzer, 200917 present results of combined associations broken down into the seven 

regions of the U.S. that were used in the NMMAPS PM studies. The combined ozone 

associations are significant and positive in some regions and negative or null in other 

regions. The spatial pattern is not consistent with ozone causing mortality. The spatial 

pattern, however, is similar to that for PM suggesting that ozone may be acting as an 

indicator of toxic PM constituents that are prevalent in some parts of the U. S. Other 

possible explanations also need to be considered.

Since the spatial and temporal pattern of associations in multi-city studies is not 

consistent with ozone causing premature mortality, the Agency should not assume that 

ozone has an effect on mortality at the levels under consideration.

7. EPA’s exposure assessment quantified the number of all children and asthmatic 

children likely to be exposed to specific benchmark levels of ozone, including in 

particular 0.060 and 0.070 ppm. Considering the patterns of change in the estimates 

of exposures of concern at and above the 0.060 and 0.070 ppm benchmark levels, 

and the uncertainties and limitations in the estimates, what is the relative 

importance from a public health perspective of the estimated reductions in 

exposures of concern, as well as the exposures remaining, for alternative standards 

across the proposed range? 

The exposure/exertion protocols used in the human clinical studies do not mimic typical 

human behavior so the results must be mapped onto realistic exposure/activity scenarios 

to determine the risk. The chance of experiencing an exposure of concern requires that a 

person be outside, at the location of the high ozone, at the time of peak ozone, and 

exercising heavily. During the 1996/1997 review, EPA staff undertook an extensive 

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15 Bell ML, Kim JY, Dominici F. Potential confounding of particulate matter on the short-term 

association between ozone and mortality in multisite time-series studies. Environ Health Perspect 

2007;115:1591-5. 

16 Bell ML, Dominici F. Effect modification by community characteristics on the short-term 

effects of ozone exposure and mortality in 98 U.S. communities. Am J Epidemiol 2008;167:986-

97. 

17 R. L. Smith, B. Xu, and P. Switzer, Reassessing the Relationship Between Ozone and Shortterm Mortality in U.S. Urban Communities, Inhalation Toxicology, 29(S2), 37-61, 2009. 
++

exposure and risk assessment with input from CASAC. To estimate the risk, staff made a 

series of conservative assumptions. For example, the analysis used an algorithm to 

assign ventilation rates based on individuals who exercised regularly and were motivated 

to reach a high ventilation rate. As a result, the 1996 Staff Paper acknowledged that the 

analysis allowed more high ventilation rates (hence greater risk) than would actually 

occur in the populations of interest -- outdoor workers, outdoor children, etc. 

The 2008 review included an update to the exposure and risk assessment. The APEX 

model developed estimates of the number of all school age children and asthmatic school 

age children exposed one or more times a year to various 8-hour ozone concentrations 

(0.06 ppm, 0.07 ppm, and 0.08 ppm) while undergoing moderate exertion in a number of 

urban areas. These exposure metrics are discussed as benchmark “exposures of concern.” 

The Agency noted that only a subset of the individuals in these groups would actually be 

expected to experience effects. To the extent that there are significant biases in the 

exposure and risk assessment, the interpretation of the public health protection afforded 

by either the current standard or various alternatives would change.

The Alliance Comments document at least five ways in which the clinical exposure and 

risk assessment is biased, overstating the exposures and risks that would accompany any 

of the alternative standards under consideration. Specifically, there are three ways that 

the APEX model used in the current risk assessment overestimates the number of 

occurrences of elevated 8-hour ozone exposures during strenuous work or play18 and two 

ways in which the Risk Assessment (RA) overestimates the benefits of alternative 

standards.19 Details can be found at pages 13 to 17 of Appendix B to the Alliance 

Comments. The American Petroleum Institute has also provided a detailed analysis that 

indicates that the exposure analysis overestimates the exposures of concern by at least a 

factor of three.20

Since there is substantial evidence that the exposures assessment overestimates the 

number of exposures of concern at any given ozone level, the estimated reductions from a 

more stringent standard shown in Table 3 of the January 19, 2010 proposal are also 

overestimated. Thus, the results of the exposure assessment overstate the impacts of a 

more stringent standard and should not be used until the biases are removed.

8. EPA’s quantitative risk assessment estimated the numbers of occurrences of 

various ozone-related health effects associated with just meeting alternative 

standard levels down to a standard level of 0.064 ppm. Considering the patterns of 

change in the estimates of health effects in the risk assessment at the alternative 

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18 The model does not correct for ozone at person height compared to ozone at measurement 

height; the model treats the upper tail of the distribution of breathing rates incorrectly; the model 

predicts substantially more elevated ventilation rate occurrences than observed in real world data.

19 The way the model rolls back ambient concentrations does not mimic the changes that will 

occur as emissions are reduced and man-made ozone is reduced; the background ozone assumed 

in the risk assessment is too low. 20 Docket ID No. EPA–HQ–OAR–2005–0172-4141.2 at pages 27 to 29.
+"

standard levels, and the uncertainties and limitations in the estimates, what is the 

relative importance from a public health perspective of the estimated reductions in 

risk, as well as the risk remaining, for alternative standards across the proposed 

range? Please consider this question in light of the scientific evidence as a whole. 

The risk assessment included estimates of the lung function responses for various 

alternative standards as well as effects estimated from selected epidemiological 

associations. Each will be discussed in turn.

For the lung function responses, the exposures from the APEX model were used with 

dose-response functions for FEV1 changes to estimate the number of moderate or greater 

lung function responses for all and asthmatic school age children. It is important to 

recognize, as noted above, that the lung function risk estimates are now appreciably 

lower than in the 1997 review when the 0.08 ppm standard was established. It is also 

important to recognize that the risk estimates are biased high because of the five factors 

referred to above that are discussed in the Alliance comments. Thus, the estimated 

number of lung function decrements reported in Table 2 of the January 19, 2010 proposal 

are substantial overestimates. In addition, incidences of exposure that might be expected 

to lead to decrements in the performance of lung function tests would not be discernable 

to the adult or child. In previous reviews of the ozone NAAQS, single incidences have 

not been deemed as adverse. The extreme value form of the current 8-hour standard, in 

itself, drastically limits the number of potential repeat exposures, providing a substantial 

margin of safety. Thus, for respiratory effects that we know are caused by ozone, the 

current standard is highly protective. 

With regard to the risk estimates from epidemiology, there is substantial controversy over 

whether ozone is causing effects below the current standard. As noted above, the overall 

patterns in the ozone associations in comprehensive or multi-city studies are not 

biologically plausible. The Agency asserts plausibility by selecting positive associations 

from the literature. However, the mean personal exposures of the population are at or 

below the mean background, when considering the fact that people spend 90 percent of 

their time indoors where ozone concentrations are significantly lower than ambient. Such 

personal exposures do not trigger FEV1 responses through the vagal mechanism and have 

not been shown to trigger inflammation. It is not clear how such low personal exposures 

could cause or contribute to the premature mortality or hospital admissions estimated in 

the risk assessment. Alliance Comments Appendix B at pages 17 to 35 and NAM 

comments Attachment 2 at pages 30 to 43 provide additional detail concerning the 

interpretation of the epidemiological results. As noted above, studies published since the 

2006 CD confirm spatial and temporal patterns in the ozone mortality associations that 

are not consistent with causality. 

Because of all the issues with the epidemiology, the Administrator should heavily 

discount the quantitative risk assessment using epidemiological associations. Instead, as 

EPA has reviewed the five criteria pollutants for which time-series epidemiology is 

available, by focusing on selected single-pollutant model results the Agency has claimed 

independent effects from four of the five pollutants. This is not scientifically defensible.
Before the 

ENVIRONMENTAL PROTECTION AGENCY 

Docket No. EPA–HQ–OAR–2005–0172 

National Ambient Air Quality Standard for Ozone; Proposed Rule 

 

75 Fed. Reg. 2938 (January 19, 2010) 

Comments of 

THE ALLIANCE OF AUTOMOBILE MANUFACTURERS 

March 22, 2010 

For more information, please contact 

Giedrius Ambrozaitis (gambrozaitis@autoalliance.org) 

or Susan Conti (sconti@autoalliance.org) 

Alliance of Automobile Manufacturers 

1401 Eye Street N.W., Suite 900 

Washington, D.C. 20005-6562 

Telephone: (202) 326-5512 
! !

"!

THE ALLIANCE OF AUTOMOBILE MANUFACTURERS 

COMMENTS ON EPA’S PROPOSAL FOR RECONSIDERATION OF THE 

PRIMARY AND SECONDARY NATIONAL AMBIENT AIR QUALITY 

STANDARDS (NAAQS) FOR OZONE. 75 Fed. Reg. 2938 (January 19, 2010) 

Docket ID No. EPA–HQ–OAR–2005–0172 

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INTRODUCTION 

!!!

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!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

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84@c>D49M!Health Effects Institute Report![V"M!F'+(.%-M!"YYe<!
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DETAILED COMMENTS 

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CONCLUSION 

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APPENDIX A 

REVIEW OF MORE RECENT STUDIES 

RELEVANT TO THE CHOICE OF OZONE NAAQS

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The APHENA study was not included in the Provisional Assessment and does not support 

EPA’s claims of causal relationships between ozone and mortality or between ozone and 

hospital admissions. 

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["!

&/0*/6/',*+!-%5,+/(*&$/:&!,-%!6(1*2!/*!%/+$%-!+$%!;<=<!(-!/*!>1-(:%<!N(*&%]1%*+53M!+$%!T%/0$+!(6!

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,2)/&&/(*&<!!

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,*2!/*!#,.5%!"!6(-!$(&:/+,5!,2)/&&/(*&<!!

Table 1: APHENA modeling results for mortality

Cause of Death Canada Europe United States 

455!N,1&%!g!,55!,0%&! "Vl"V! [\l"V! ["l"V!

!!!!!!!!!!!!!!!!!!!!!!U\!3-&! "bl"V! "l"V! Zl"V!

!!!!!!!!!!!!!!!!!!!!m!U\!3-&! [Xl"V! ""l"V! [Yl"V!

455!N,1&%!@7!'(*+-(55%2!g!,55!,0%&! VlX! Xl[Z! Yl[Z!

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!U\!3-&! YlX! bl[Z! Yl[Z!

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!m!U\!3-&! \lX! [Vl[Z! Yl[Z!

455!N,1&%!g!&1))%-!(*53! ele! [Xl[X!8Vl["9n [Xl[X8Yl["9n!

N,-2/(?,&'15,-!g!!!U\!3-&! "Vl"V! bl"V! "l"V!

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!m!U\!3-&! Yl"V! Xl"V! "l"V!

N,-2/(?,&'15,-!g@7!'(*+-(55%2!!!U\3-&! YlX! Yl[Z! Yl[Z!

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!m!U\!3-& YlX! \l[Z! "l[Z!

N,-2/(?,&'15,-!g!&1))%-!(*53! YlZ! Xl["8YlX9n! [[l["8YlX9n!

B%&:/-,+(-3!g!,55!,0%&! Yl"V! Yl"V! Yl"V!

!!!!!!!!!!!!!!!!!!!!!!!!!U\!3-&! Yl"V! Yl"V! Yl"V!

B%&:/-,+(-3!g!@7!'(*+-(55%2!g!,55!,0%&! YlX! Yl[Z! Yl[Z!

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!U\!3-&! YlX! Yl[Z! Yl[Z!

B%&:/-,+(-3!g!&1))%-!(*53! ZlZ! Vl["8YlX9n! "l["8YlX9n!

n_%*(+%&!+$%!@7!'(*+-(55%2!-,+/(!

#$%!*1)%-,+(-&!-%:-%&%*+!+$%!*1).%-!(6!)(2%5&!+$,+!&$(T%2!,!:(&/+/?%!,*2!&+,+/&+/',553!

&/0*/6/',*+!-%5,+/(*&$/:!.%+T%%*!Fb!,*2!)(-+,5/+3M!T$/5%!+$%!2%*()/*,+(-!/&!+$%!+(+,5!*1).%-!(6!

)(2%5&!-1*<!
! !

[b!

Table 2: APHENA Modeling Results for Hospital Admissions for Patients 65 Years and 

Older 

Type of Admission Canada Europe United States

B%&:/-,+(-3! [Xl"V! Xl"V! Ul"b!

B%&:/-,+(-3!g!@7!'(*+-(55%2! YlX! Ul[Z! \l[Z!

B%&:/-,+(-3!g!&1))%-!(*53! blb! YlV! YlV!

N,-2/(?,&'15,-! \l"V! Yl"V! bl"V!

N,-2/(?,&'15,-!g!@7!'(*+-(55%2! blX! [Zl[Z! Yl[Z!

N,-2/(?,&'15,-!g!&1))%-!(*53! YlV! YlV! YlV!

#$%!*1)%-,+(-&!-%:-%&%*+!+$%!*1).%-!(6!)(2%5&!+$,+!&$(T%2!,!:(&/+/?%!,*2!&+,+/&+/',553!

&/0*/6/',*+!-%5,+/(*&$/:!.%+T%%*!Fb!,*2!,2)/&&/(*&!T$/5%!+$%!2%*()/*,+(-!/&!+$%!+(+,5!*1).%-!(6!

)(2%5&!-1*<!

Based on new studies subsequent to the 2006 CD,!+he pattern of results in new multi-city 

studies of mortality and hospital admissions is not consistent with ozone having a causal 

role in mortality or morbidity below the current standard. 

 

! #$%-%!,-%!*(T!,!*1).%-!(6!*%T!)15+/R'/+3!&+12/%&!+$,+!$,?%!%?,51,+%2!(G(*%!,&&('/,+/(*&!

T/+$!)(-+,5/+3!(-!$(&:/+,5!,2)/&&/(*&!&/*'%!+$%!"YYZ!N_<!#$%!5,-0%&+!(6!+$%&%!/&!+$%!4@c>D4!

&+123!2/&'1&&%2!,.(?%<!!455!+$%!&+12/%&!+$,+!-%:(-+!(-!:5(+!+$%!/*2/?/21,5R'/+3!,&&('/,+/(*&!&$(T!,!

./(5(0/',553!/):(&&/.5%!T/2%!-,*0%!(6!,&&('/,+/(*&!6-()!:(&/+/?%!+(!*%0,+/?%!6(-!)(-+,5/+3!8J%55!

%+!,5<M!"YYU[[f!P-,*C5/*!,*2!='$T,-+G!"YYX["f!N,C),C!et al<M!"YYZ[bf!J%55!,*2!_()/*/'/M!"YYX[V9!

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'/+3!,&&('/,+/(*&!/*!J%55!,*2!_()/*/'/M!"YYX!/&!6-()!R!b!o!+(!p!V!o!:%-![Y!::.!/*'-%,&%!/*!+$%!

2,/53!,?%-,0%!(G(*%!(?%-!+$%!:-%?/(1&!T%%C<!!`*!+$%!J%55!et al<M!"YYU!&+123!+$%!-,*0%!/*!/*2/?/21,5!

'/+3!-%&15+&!/&!6-()!g!\!o!+(!p![Y!o!:%-![Y!::.!/*'-%,&%!/*!+$%!,?%-,0%!(6!+$%!'1--%*+!,*2!

:-%?/(1&!2,3A&!(G(*%<!!`*!+$%!P-,*C5/*!,*2!='$T,-+GM!"YYX!&+123!+$%!-,*0%!/&!6-()!g![!o!+(!p!b!

o!6(-!,![Y!::.!/*'-%,&%!/*!&1))%-+/)%!'1--%*+!2,3!(G(*%<!!!K$%*!J%55!et al<M!"YYU!-%&+-/'+%2!+$%!

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

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(G(*%!,*2!)(-+,5/+3!/*!)15+/&/+%!+/)%R&%-/%&!&+12/%&<!>*?/-(*!c%,5+$!@%-&:%'+!"YYUf[[\a[\e[R\<!!

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"Y!

APPENDIX B 

COMMENTS OF THE ALLIANCE OF AUTOMOBILE 

MANUFACTURERS ON EPA’S PROPOSAL TO REVISE OZONE NAAQS 

72 FED. REG. 37,818 (JULY 11, 2007) 

OCTOBER 9, 2007 
BEFORE THE

ENVIRONMENTAL PROTECTION AGENCY 

Docket NO. EPA-HQ-OAR-2005-0172 

National Ambient Air Quality Standards for 

Ozone; Proposed Rule 

Comments of 

THE ALLIANCE OF AUTOMOBILE MANUFACTURERS 

October 9, 2007 

Gregory J. Dana 

Vice President - Environmental Affairs 

Alliance of Automobile Manufacturers 

1401 Eye Street NW, Suite 900 

Washington, DC 20005-6562 

(202) 326-5518 (tel) 

(202) 326-5568 (fax) 

email: gdana@autoalliance.org 

 
ii 

TABLE OF CONTENTS

 Page

 

EXECUTIVE SUMMARY ............................................................................................... 2 

DETAILED COMMENTS ............................................................................................... 7

 Introduction.................................................................................................................. 7 

 I. Comments on EPA’s Proposal to Revise the Primary Standard 

 for Ozone ........................................................................................................... 8 

 

 A. The Clinical and Epidemiology Evidence Indicate Less Risk 

 from Ozone Exposure than in 1997 .......................................................... 8 

 1. The risk of respiratory effects is substantially reduced from 

 what was estimated in the 1997 Review............................................. 8 

 2. The clinical data do not support the reversal of EPA’s 1997 

 determination that the current standard is requisite to protect 

 the public health with an adequate margin of safety .......................... 9

3. EPA’s risk assessment based on the clinical studies does not 

 support the conclusion that a tightening of the standard is 

 requisite to protect the public health................................................... 12 

 B. Time-Series Studies Do Not Provide Support for Causality of Effects 

 But Instead Confirm Significant Uncertainties Present in the 

 1997 Review ............................................................................................. 17 

 1. In interpreting the epidemiological evidence, EPA downplays 

 the major new findings concerning uncertainty due to model 

 selection issues ................................................................................... 17 

 2. In interpreting the epidemiological studies, EPA relies on 

 single estimate and single-site analyses and fails to address 

 the effect of publication bias............................................................... 19 

3. Analysis of more complete data sets, such as NMMAPS, 

 suggests significant variability of positive and “negative” 

 responses unaccounted for in the published literature or 

 in EPA’s analysis ............................................................................. 20 
iii 

4. EPA has a duty under the Data Quality Act to consider all 

 the results, including both positive and non-positive 

 results ................................................................................................ 21 

 5. The new data on asthmatics and symptoms/medication use 

 does not provide clear and convincing evidence of an 

 increase in risk due to ozone exposure that was not present 

 in the 1997 Review ............................................................................. 22 

 6. The claim that a more stringent ozone standard will address 

 the growing asthma problem in the U.S. is without scientific 

 merit ................................................................................................... 23 

 a. There is no evidence that ozone levels at or below the 

 current standard cause asthma ................................................. 23

 b. The epidemiology data do not show that ozone levels at or 

 below the current standard cause asthma ............................... 24

C. The Evidence on Premature Mortality is too Limited in Nature and 

 Should Not Be Relied Upon in Basing Conclusions on the Health 

 Effects from Exposure to Ozone................................................................ 24 

 

 1. CASAC itself had reservations on the use of the data........................ 25 

 2. A new NMMAPS analysis that extends the previous analyses, 

 and the Huang et al. (2005) analysis of a subset of 19 large U.S. 

 cities is limited, and does not support a finding of 

 causality .............................................................................................. 25 

 a. There are major deficiencies in the Bell et al. 2004 paper, 

 including the omission of the winter ozone results and 

 limited analyses regarding other pollutants.............................. 25 

 b. The pattern of individual-city associations in the Huang et al. 

 study is not consistent with a causal association, and may 

 reflect the confounding role of another pollutant .................... 26 

3. While the SP downplays confounding by co-pollutants, a more 

 comprehensive review of the data implicates other pollutants 

 as potential causes of the reported mortality associations 

 in time-series studies .......................................................................... 27 

 

 
iv 

4. Weather factors remain a key confounder in the mortality 

 analysis relied on by EPA................................................................... 28 

D. EPA’s Risk Estimate for Mortality and Certain Respiratory 

 Endpoints Fail to Confirm an Increase in Risk ......................................... 29 

 

 1. New studies on emergency room visits and hospital admissions 

 do not provide supporting evidence of a causal 

 relationship ....................................................................................... 33 

 2. Overall the school absence data are weaker than noted in the 

 proposed rule and do not confirm causality or effects below 

 the current standard .......................................................................... 35 

E. EPA Improperly Characterizes the Impact of New Information Since 

 the Last Review, Particularly as it Relates to Mechanisms of Ozone 

 Action and Support for Causality of Mortality and Other 

 Important Epidemiological Health Endpoints .......................................... 35 

F. The Clean Air Act Does Not Require EPA to Set Standards That 

 Eliminate All Risk .................................................................................. 39 

G. Since EPA Has Not Provided a Reasonable Analysis Supporting 

 its New Judgment on What is Requisite to Protect Public Health or 

 Welfare, its Actions Could Be Found to Be “Arbitrary and 

 Capricious” ................................................................................................ 40 

H. EPA Has Not Correctly Evaluated the Potential Risk Reduction as 

 a Result of its Proposed Change to the Current Ozone 

 Standard ..................................................................................................... 40 

 1. In contrast to the 1997 Review, EPA failed to evaluate the 

 extreme values of ozone background levels ...................................... 41 

 2. EPA’s definition of PRB incorrectly excludes man-made 

 emissions from Canada and Mexico........................................... 42 

3. EPA does not provide sufficient rationale for relying on 

 modeled results over monitoring data for assessing 

 background ambient ozone levels ...................................................... 42 
v 

4. The proposed rule ignores the conclusions of several 

 researchers and previous conclusions of EPA regarding 

 maximum background levels ............................................................ 43 

 

 5. Because the PRB varies substantially there will be times 

 and places where the background approaches or exceeds the 

 levels recommended by CASAC for both the primary 

 and secondary standards .................................................................... 45 

 

6. The lack of consideration of the extremes of ozone background 

 levels is an omission that led both the Agency and CASAC 

 to assume that the recommended standards are 

 attainable............................................................................................. 45 

I. EPA Has Not Adequately Considered That in Many Areas of the 

 U.S. Additional Reductions, Beyond Those Needed to Meet the 

 Current Standard, May Not Be Achievable With Known Control 

 Technology and Could Impose Ruinous Economic 

 Consequences ............................................................................................ 47 

J. The Agency’s Estimates of Health Benefits Are Highly Sensitive 

 to Assumptions Regarding Background Levels......................................... 49 

K. CASAC’s Conclusion That the Current Standard is Unjustified 

 is Based on Unsupportable Assumptions................................................... 49 

L. Tropospheric Ozone Protects Against UV-Induced Health 

 Effects ........................................................................................................ 51 

 

M. The Scientific Data and Precision of Ozone Measurement Monitors 

 Does Not Support Specifying the Standard to the Third Decimal 

 Place ........................................................................................................... 52 

 

N. While EPA Should Retain the Current Standard, the Form of the 

 Standard Should Be Changed to the Fifth Highest Daily Maximum 

 8-Hour Average Concentration.................................................................. 53 

 

II. Comments on EPA’s Proposed Secondary Standard ........................................... 54 

 

 A. A Careful Review of the Existing Scientific Evidence Demonstrates 

 That the Existing Secondary Standard is Requisite to Protect 

 Public Welfare .......................................................................................... 54 

 
vi 

 

 1. All the issues and problems that led the Administrator in 

 1997 to reject the option of a seasonal ozone metric 

 are still relevant ................................................................................ 54 

 2. There are problems, flaws and concerns with the SP 

 analysis and vegetation risk assessment that preclude the 

 establishment of a separate secondary standard to 

 protect vegetation ............................................................................. 56 

 a. Extremes of background ozone concentrations were 

 not considered .......................................................................... 56

 b. The pattern of current W126 levels suggests contributions 

 from both man-made emissions and uncontrollable 

 background ............................................................................. 56 

 

 c. EPA and CASAC relied on an inadequate model in 

 recommending secondary standards that fall within the 

 range of uncontrollable background......................................... 57

 d. There is no new data on vegetation effects suitable for 

 establishing secondary standards ............................................ 58

 e. The choice of an appropriate ozone metric to protect 

 vegetation is difficult .............................................................. 58

f. The European experience with cumulative standards 

 has been disappointing .............................................................. 59 

 

g. The analysis used to discriminate between cumulative 

 standards and the current 8-hour standard is 

 flawed ....................................................................................... 59 

 h. The estimates of crop loss are substantially lower than 

 those of the previous review ...................................................... 60 

 

i. Studies of foliar injury do not support a cumulative 

 metric ....................................................................................... 60 

 j. CASAC made its recommendations based on the draft 

 SP that contained errors overstating the magnitude of 

 vegetation effects .................................................................... 61 
vii 

 k. The recommended range for a cumulative standard 

 needs to be adjusted upward .................................................... 61

l. The tools needed to implement a seasonal ozone standard 

 are not in place .......................................................................... 62

III. Comments on EPA’s Regulatory Impact Analysis for the Agency’s 

 Proposal to Revise the National Ambient Air Quality Standards 

 for Ozone ..................................................................................................... 63 

A. EPA’s Alleged Benefits from Lowering the Ozone NAAQS Are 

 Not Likely to Occur ............................................................................. 63 

 

 1. EPA’s estimates of acute mortality rely on weak epidemiology 

 evidence and incorrectly assume causality ................................. 64 

 2. The RIA incorrectly bases benefit estimates from reduced 

 hospital admissions for respiratory disease on selective 

 studies .......................................................................................... 66 

 3. The data on school absences are weaker than noted in the 

 proposed rule and are not reliable for purposes of 

 estimating benefits ....................................................................... 67 

 

 4. EPA should include a lower bound of zero for the benefits 

 of minor restricted activity days ................................................... 68 

 

 5. Given questions of PM speciation and other uncertainties, 

 the lower bound of the ancillary PM2.5 benefits should 

 also be zero ................................................................................... 68 

B. Even Though the Benefits Are Uncertain, the Costs of Meeting a 

 More Stringent Ozone Standard Will Occur and the EPA 

 Analysis Likely Underestimates Those Costs...................................... 71 

 

 1. The RIA shows many existing nonattainment areas will 

 not attain the current standard with all known control 

 technologies, even when applied to regions outside 

 the nonattainment area .............................................................. 71 
viii 

 

 2. The RIA relies on unknown control technology to 

 demonstrate attainment .............................................................. 72 

 3. The RIA correctly characterizes this extrapolation of 

 costs from known to unknown technologies as a highly 

 speculative exercise. Actual costs are likely to be 

 significantly higher .................................................................... 72 

 
1 

Comments of the Alliance of Automobile Manufacturers 

Docket No. EPA-HQ-OAR-2005-0172 

THE ALLIANCE OF AUTOMOBILE MANUFACTURERS 

COMMENTS ON EPA’S PROPOSAL TO REVISE NATIONAL 

AMBIENT AIR QUALITY STANDARDS FOR OZONE 

72 Fed. Reg. 37, 818 (July 11, 2007) 

These comments are being submitted by the Alliance of Automobile Manufacturers 

(Alliance) on behalf of its member companies in response to the U.S. Environmental Protection 

Agency’s (EPA or the Agency) Proposed Rulemaking for National Ambient Air Quality 

Standards for Ozone (Proposed Rule). The Alliance is a trade association of nine car and light 

truck manufacturers including BMW Group, Chrysler LLC, Ford Motor Company, General 

Motors, Mazda, Mitsubishi Motors, Porsche, Toyota and Volkswagen. One out of every ten jobs 

in the United States is dependent on the automotive industry. 

 The Alliance members share the concerns of our customers and the American public 

about this nation’s air quality and recognize the importance of assuring clean air that protects 

public health. While GDP, vehicle miles traveled, and energy consumptions have all increased, 

our air is cleaner today than it was a generation ago and air quality is continuing to improve. 

According to EPA’s most recent air trends analysis, between 1970 and 2006, when gross 

domestic product increased 203 percent, vehicle miles traveled increased 177 percent and energy 

consumption increased 49 percent, total emissions of the six principal air pollutants dropped by 

54 percent.1

 Investments and improvements in vehicle technology and manufacturing processes 

are a major part of this success story. Today’s vehicles are 99 percent cleaner than vehicles of 

the 1970s, which has resulted in dramatic reductions in smog-forming emissions.2 

Further, significant and additional emission reductions will occur over the next 20 years 

as a result of already promulgated regulations for mobile sources. According to EPA’s own 

statistics, nitrogen oxide emissions from light duty vehicles will be reduced by over 70 percent 

by 2030 as the result of the Tier II Vehicle and Gasoline Sulfur Program.3

 These reductions will 

help to reduce ozone concentrations across the country, and the improvements to air quality as a 

result of these reductions will occur regardless of whether the existing ozone standard is revised. 

 

1

 U.S. Environmental Protection Agency, Comparison of Growth and Emissions, 1970-2006, available at

http://www.epa.gov/airtrends/images/comparison70.jpg (last visited Oct. 2, 2007). 2

 Alliance of Automobile Manufacturers, Environment, available at http://www.autoalliance.org/environment/ (last 

visited Oct. 5, 2007). 

3

 http://www.epa.gov/tier2/faqs.htm. 
2 

Comments of the Alliance of Automobile Manufacturers 

Docket No. EPA-HQ-OAR-2005-0172 

EXECUTIVE SUMMARY

Under Section 109(a) of the Clean Air Act (CAA), 42 U.S.C. § 7409(a), EPA is required 

to set national ambient air quality standards (NAAQS) for criteria pollutants. NAAQS include 

(a) a primary standard, which in the judgment of the Administrator, based on air quality criteria 

and allowing for an “adequate margin of safety,” is “requisite” to protect the public health and 

(b) a secondary standard, which in the judgment of the Administrator, based on air quality 

criteria, is requisite to protect the public welfare from any known or anticipated adverse effects 

associated with the air pollutant.4 EPA last reviewed and revised the ozone standard in 1997, 

when it promulgated the current 8-hour standard (0.08 ppm) to replace the previous, less 

stringent 1-hour standard (0.12 ppm) (referred to as the “1997 Review”).5

The Alliance has carefully examined the evidence in the Ozone Criteria Document (CD), 

EPA’s Staff Paper (SP) and in this proposed rule. The current ozone standard is protective of 

public health with an adequate margin of safety and protective of public welfare in accordance 

with Section 109. There is no basis for EPA to revise the standard at this time. 

These comments focus on the reasons why EPA’s scientific justification and legal grounds 

for lowering the existing ozone standard are unfounded and not supported by the relevant 

scientific body of literature and evidence produced since the Agency’s 1997 Review. 

 

1. The clinical and epidemiology evidence indicate less risk from ozone exposure than 

in 1997. 

Although new clinical studies since 1996 have added to the available data, the 

fundamental understanding of effects at 0.08 ppm and above has not changed since the 

last review. In fact, the latest controlled human exposure studies shows there is less risk 

of lung function decrements and symptoms now than assumed in the 1997 Review. The 

data, that EPA has used to extend lung function effects to lower concentrations, 

establishes that the response is non-linear in contrast to the linear assumption made 

previously. The public health significance of these potential risks has also declined. The 

percent of the population undergoing exposures of concern is significantly smaller in the 

current modeling than originally thought in 1996/1997.6

 The Second Draft SP relied 

upon this evidence in concluding that the estimates of lung function effects “are now 

appreciably lower than in the last review”7 to support the view that the current standard 

protects the public health with an adequate margin of safety. Nothing in the final SP or 

proposed rule contradicts this evidence. Therefore, the new clinical studies do not 

provide a basis for lowering the NAAQs. 

 

4

 42 U.S.C. § 7409(b). 

5

 62 Fed. Reg. 38,855 (July 18, 1997). 

6

 U.S. Environmental Protection Agency, Review of the National Ambient Air Quality Standards for Ozone: Policy 

Assessment of Scientific and Technical Information, OAQPS Staff Paper - Second Draft, EPA-452/D-05-002, July 

2006, at 5-71 (“Second Draft SP”). 

7

 Second Draft SP at 6-27. 
3 

Comments of the Alliance of Automobile Manufacturers 

Docket No. EPA-HQ-OAR-2005-0172 

2. Time-series studies do not provide support for causality of effects but instead 

confirm significant uncertainties present in the 1997 Review. 

Time-series epidemiology studies suffer from problems associated with publication bias, 

model uncertainty, model selection issues, lack of adequate control for confounding 

variables, such as other pollutants and weather, and exposure misclassification arising out 

of the poor correlation between ambient monitors and personal exposure. In its June 2006 

letter to the Administrator, EPA’s Clean Air Scientific Advisory Committee (CASAC) 

confirmed this view in evaluating mortality time-series studies, noting that “[b]ecause 

results of time-series studies implicate all of the criteria pollutants, findings of mortality 

time-series studies do not seem to allow us to confidently attribute observed effects 

specifically to individual pollutants.”8

 

Analysis of time-series single-estimate results and more complete data sets, such as the 

National Morbidity and Mortality Air Pollution Study (NMMAPS), shows significant 

variability of positive and “negative” responses unaccounted for in the published 

literature or EPA’s analysis. 

3. The evidence on premature mortality is too limited in nature and should not be 

relied upon in basing conclusions or estimating health effects from exposure to 

ozone. 

In its June 2006 letter to the Administrator, CASAC questioned whether the effect of 

individual pollutants, such as ozone, can be determined from time-series mortality studies 

because these studies implicate all of the criteria pollutants.9

 Furthermore, due to the 

significant potential for exposure misclassification, the overall utility of the time-series 

mortality estimates is severely limited. The results from time-series studies of 95 

individual cities, shown in Figure 7-17 of the CD, are inconsistent at best, ranging from 

strongly negative to strongly positive.10 Such a wide range is not biologically plausible. 

4. EPA’s risk estimate for mortality and certain respiratory endpoints fails to confirm 

an increase risk from 1997. 

EPA’s risk assessment fails to account for several major uncertainties, the correction of 

which would result in a significant reduction in the estimated risk. In estimating risk, 

EPA assumes causality. As discussed above, time-series studies have produced an 

implausibly wide range of associations from strongly positive in some cities, to no effect 

in some cities to strongly negative (implying protective effects) in some cities. In 

accordance with the recommendations of the National Academy of Sciences (NAS), the 

risk assessment should address this pivotal uncertainty by including a probabilistic 

 

8

 R. Henderson, CASAC Letter, EPA-CASAC-06-07, June 5, 2006 at 3 (“June 2006 CASAC Letter”). 

9

 June 2006 CASAC Letter at 3. 

10 See U.S. Environmental Protection Agency, Air Quality Criteria for Ozone and Related Photochemical 

Oxidants, Vol. I of III, EPA 600/R-05/004aF, Feb. 2006, Figure 7-17 at 7-90 (“CD”). 
4 

Comments of the Alliance of Automobile Manufacturers 

Docket No. EPA-HQ-OAR-2005-0172 

analysis of the major uncertainties, including the possibility the associations may not be 

causal.11 Given the magnitude of the uncertainties and EPA’s failure to conduct an 

integrated uncertainty analysis, the current state of the scientific evidence supports 

retention of the current 8-hour standard. 

5. The CAA does not require EPA to set standards that eliminate all risk. 

EPA’s obligation under the CAA is to establish standards that are “neither more nor less 

stringent than necessary” to protect public health.12 This means establishing standards at 

a level that reduces risk sufficiently to protect public health with an adequate margin of 

safety. A careful review of the scientific evidence shows that lowering the current ozone 

standard would result in controls unnecessary to protect public health. 

6. Since EPA has not provided a reasonable analysis supporting its new judgment on 

what is requisite to protect public health or welfare, its actions could be found to be 

“arbitrary and capricious.” 

In exercising his judgment to revise the existing NAAQS, the Administrator must provide 

a reasonable, scientific analysis for the change. Specifically, EPA must explain why its 

earlier judgment regarding what is requisite to protect public health or welfare no longer 

governs. To reverse its position in the face of precedent that is not persuasively 

distinguished is arbitrary and capricious.13 Given that EPA’s estimate of health risks has 

declined and new information on the public health significance of these effects suggests 

less cause for concern, EPA cannot persuasively say why it must depart from its 1997 

decision that the current standard is requisite to protect public health. 

7. EPA has not correctly evaluated the potential for further risk reduction as a result 

of its proposed change to the current primary standard for ozone. 

EPA has taken the largely unsupportable step of substituting modeled ozone background 

concentrations for ambient monitoring based background. The new modeled 

concentrations, which suggest significantly lower concentrations of ozone background 

levels, suffer from several flaws, including a significant under-estimation (by a factor of 

2) of NOx emissions from soils. An independent analysis shows that employing the 

more realistic ozone background levels used in the 1997 Review would eliminate over 95 

percent of EPA’s estimated risk from exposure to ozone without correcting for additional 

biases in EPA’s risk assessment. 

 

11 National Research Council, Estimating the Public Health Benefits of Proposed Air Pollution Regulations, The 

National Academies Press, Washington, DC, September 2002. 

12 Whitman v. American Trucking Ass’ns, Inc., 531 U.S. 457, 473 (2001) (citation omitted). 13 Motor Vehicle Mfr.’s Ass’n v. State Farm Mut. Auto. Ins. Co., 463 U.S. 29, 42 (1983) (presumption “against 

changes in current policy that are not justified by the rulemaking record”). 
5 

Comments of the Alliance of Automobile Manufacturers 

Docket No. EPA-HQ-OAR-2005-0172 

8. EPA has not adequately considered that in many areas of the U.S., additional 

reductions beyond those needed to meet the current primary standard for ozone, 

may not be achievable with known control technology and could impose ruinous 

economic consequences. 

The situation in several nonattainment areas is direr than implied by EPA in its proposed 

rule. Several nonattainment areas have recently submitted State Implementation Plans 

(SIPs) that fail to demonstrate attainment with the current standard, even when 

considering all currently known control technologies. Although the Administrator is not 

allowed to consider the costs of attaining the standard, it is clear that the CAA was not 

intended to impose ruinous conditions on industry or the American public. In some 

areas, the near elimination of all stationary and mobile source emissions would be 

required to meet the current standard. Moreover, in making a policy judgment on what is 

requisite to protect public health, the Administrator should consider the adverse impacts 

on health and quality of life from such stringent measures, particularly on the low income 

populations. 

9. CASAC’s conclusion that the current primary standard for ozone is unjustified and 

is based on unsupportable assumptions. 

Based on the information presented to CASAC from the GEOS-CHEM model, CASAC 

was led to believe that ozone background levels never exceed 0.040 ppm. As a result, 

CASAC incorrectly assumed that a standard as low as 0.060 ppm is attainable and that, 

therefore, exposures of concern could be essentially eliminated. CASAC also erred in 

evaluating the risk of clinical effects. Although the Second Draft SP showed that the risk 

of lung function effects is lower than thought in 1997, the current CASAC panel 

appeared to believe that the APEX model used in the risk assessment for the clinical 

effects systematically under-predicted measured values.14 In actuality, the model 

significantly overestimated the number of exposures of concern as detailed elsewhere in 

these comments. 

10. EPA’s estimate of non-mortality health benefits, while small, still overestimates the 

potential benefit of meeting a lower primary standard 

The benefits of a 0.070 ppm standard (or any of the alternatives proposed by EPA) 

depend on highly questionable assumptions concerning mortality causality. EPA’s 

Regulatory Impact Analysis (RIA) acknowledges that the direct benefits from ozone 

reduction itself are $190 million per year for the 0.070 ppm alternative if it is assumed 

that ozone does not cause premature mortality.15 Given EPA’s estimate of the morbidity 

effects of ozone in the RIA are highly exaggerated due to model selection issues and 

other factors discussed in these comments, all the alternative standards below the current 

 

14 See, e.g., R. Henderson, CASAC Letter, EPA-CASAC-07-001, October 26, 2006, at 11. 15 U.S. Environmental Protection Agency, Regulatory Impact Analysis of the Proposed Revisions to the National 

Ambient Air Quality Standards for Ground-Level Ozone, EPA-452/R-07-008, July 2007, at 6-2 (“RIA”). 
6 

Comments of the Alliance of Automobile Manufacturers 

Docket No. EPA-HQ-OAR-2005-0172 

standard are likely to achieve very little if any additional health benefits, even though 

achievement of such standards will require a massive investment and dramatic change in 

the quality of life for Americans. 

11. A careful review of the existing scientific evidence demonstrates that the existing 

secondary standard for ozone is requisite to protect public welfare. 

EPA’s recommendation to use a new seasonal secondary ozone standard does not address 

the uncertainties and limitations associated with the use of such a standard. Limitations 

include: (1) the lack of ozone monitoring data at vegetation height in rural areas; (2) the 

likelihood that extreme ozone background levels overlap with the ranges recommended 

for the secondary standard; and (3) the inability of the seasonal metric to account for the 

variable uptake of ozone by plants. The new data developed since 1997 does little to 

address these important uncertainties. 

A new secondary standard also raises significant implementation issues. For instance, 

emission inventories (particularly for agricultural emissions) and modeling tools needed 

to implement a seasonal standard, particularly in the Western United States, are not 

currently available. Establishing a secondary standard without these tools would impose 

an unreasonable implementation burden on states and local communities. 
7 

Comments of the Alliance of Automobile Manufacturers 

Docket No. EPA-HQ-OAR-2005-0172 

DETAILED COMMENTS

Introduction 

Section 109 of the Clean Air Act requires the Administrator to set a primary national 

ambient air quality standard (NAAQS), the attainment and maintenance of which in the 

judgment of the Administrator are requisite to protect the public health with an adequate margin 

of safety. EPA’s obligation under the CAA is to establish standards that are “neither more nor 

less stringent than necessary” to protect public health. This means establishing standards at a 

level that reduces risk sufficiently to protect public health with an adequate margin of safety. 

Lowering the current ozone standard would result in controls unnecessary to protect public 

health. 

A careful review of the scientific evidence shows that EPA’s understanding of the potential 

risks from exposure to ozone at the current standard remains largely the same as in 1997, and 

that the actual risk from exposure to levels below the standard, based on clinical evidence, may 

now be lower than what was assessed in 1997. In addition, it is clear from the Second Draft of 

EPA’s Staff Paper that the percent of the population undergoing exposures of concern is 

significantly smaller in the current modeling than originally thought in 1997. As EPA states in 

the preamble, its task under Section 109 is to “establish standards that are neither more nor less 

stringent than necessary for these purposes.”16 Lowering the standard in light of the 1997 

determination would result in controls that would be unnecessary to protect public health. 

Since EPA has not provided a reasonable scientific analysis supporting its new judgment 

on what is requisite to protect public health or welfare, its actions could be found to be “arbitrary 

and capricious.” In exercising his judgment to revise the existing NAAQS, the Administrator 

must provide a reasonable, scientific analysis for the change. Specifically, EPA must explain 

why its earlier judgment regarding what is requisite to protect public health or welfare no longer 

governs. To reverse its position in the face of precedent that is not persuasively distinguished is 

arbitrary and capricious. 

The weight of the science supports retention of the current ozone standard as requisite to 

protect public health and welfare. There is nothing in the science that deviates from EPA’s 1997 

analysis, and EPA failed to adequately explain its change of position. A careful review of the 

scientific studies EPA relies on to justify a lower standard illustrates that EPA’s current estimates 

of risk are inflated and unreliable. EPA’s own Regulatory Impact Analysis (RIA) shows that 

many areas of the country today are struggling to meet the current standard and that many more 

areas will be unable to attain a tighter standard with known technology. Requiring areas to meet 

a more stringent standard would impose “ruinous” conditions on the American public contrary to 

the intentions of the CAA. 

 

16 72 Fed. Reg. 37,818, 37,820 (July 11, 2007). 
8 

Comments of the Alliance of Automobile Manufacturers 

Docket No. EPA-HQ-OAR-2005-0172 

As these comments will show, the state of the science indicates that the current standard 

is requisite to protect public health and welfare, and that EPA has not provided a reasonable 

explanation to deviate from its finding in 1997. 

I. Comments on EPA’s Proposal to Revise the Primary Standard for Ozone. 

 EPA proposes to revise the primary NAAQS for ozone by reducing the current 8-hour 

standard of 0.08 ppm to a level within the range of 0.070 to 0.075 ppm. In addition, EPA seeks 

comments on alternative levels, down to 0.060 ppm, and up to retaining the current standard.17 

 An exhaustive review of the administrative record and the underlying studies on which 

the proposed revisions are based shows that a revision of the current 8-hour ozone NAAQS 

cannot be justified. Any tightening of the current standard would not meet the statutory test -- 

that the “attainment and maintenance of [such standard], ... allowing an adequate margin of 

safety, are requisite to protect the public health.” CAA at §109(b)(1). To be “requisite to protect 

the public health,” the standard must be “not lower or higher than is necessary.” Whitman v. 

American Trucking Associations, 531 U.S. 457, 476 (2001). As the Administrator found in 

1997, the current standard meets that test. While there have been many additional studies since 

that time, as demonstrated in the detailed comments below, those studies do not show that the 

risk from ozone is any greater than was recognized in the previous rulemaking, and the level of 

uncertainty over the existence of those risks has increased. EPA should retain the existing 

primary ambient NAAQS for ozone. 

A. The Clinical and Epidemiology Evidence Indicate Less Risk from Ozone 

Exposure than in 1997. 

1. The risk of respiratory effects is substantially reduced from what was 

estimated in the 1997 Review. 

 EPA is correct in concluding that controlled human exposure studies offer the best 

information on ozone effects. Although there are a wide range of epidemiological studies that 

report associations of ozone with health endpoints, the proposed rule notes that the 

epidemiological studies are not themselves direct evidence of a causal link between exposure to 

ozone and the occurrence of the effects.18

 A careful examination of the clinical data (including the new data) shows that there is 

less risk of lung function decrements and symptoms than was assumed in the 1997 review. Key 

findings from the clinical data include the following: 

The data extending lung function effects to lower concentrations establishes that the 

response is non-linear in contrast to the linear assumption made in the previous review. The 

preamble notes that the logistic form provides a very good fit to the combined data set used in 

 

17 72 Fed.Reg. at 37,818 (July 11, 2007). 

18 72 Fed. Reg. at 37,879. 
9 

Comments of the Alliance of Automobile Manufacturers 

Docket No. EPA-HQ-OAR-2005-0172 

the current Risk Assessment.19 Although the final Staff Paper (SP) does not show a direct 

comparison between the dose-response assumed in 1996 and the current dose-response, the 

Second Draft SP did include such a comparison in Figure 5-2 a., b., and c. The Figure clearly 

shows that the response rates for FEV1 decrements >10%, >15%, and >20% are lower at all 

concentrations below the current standard with the logistic form.20 This means that, for a given 

ozone exposure below the current standard, the risk of lung function decrements is now lower 

than thought in the previous review. 

Although there are many differences between the 1996 and 2007 clinical risk assessment 

methodologies, it is clear from the Second Draft SP that the percent of the population undergoing 

exposures of concern is significantly smaller in the current modeling than originally thought in 

1996/97. The Second Draft SP, which was the first draft that included staff’s recommendations 

for the level of the standard, used the fact that the estimates of lung function effects “are now 

appreciably lower than in the last review” to support the view that the current standard protects 

the public health with an adequate margin of safety. 

Finally, although respiratory symptoms in healthy children were estimated in the 1996 

review, that endpoint was not included in the current review since a number of field studies 

failed to find such effects. 

2. The clinical data do not support the reversal of EPA’s 1997 

determination that the current standard is requisite to protect the 

public health with an adequate margin of safety. 

 EPA’s conclusions from the 1997 Review are unaltered by more recent clinical studies 

and, thus, do not support a revised determination that the current 8-hour standard is no longer 

sufficient to protect public health with an adequate margin of safety. 

 The proposed rule notes that, in controlled human exposures, the first effects on the 

performance of lung function tests occur at 0.50 ppm in sedentary individuals. EPA focuses on 

FEV1, the volume of air expired in the first second during maximal expiratory effort. With 

increased levels of physical activity and breathing rate, the threshold for the first effects 

decreases. However, the thresholds for the first effects in controlled studies are still considerably 

above the vast bulk of personal exposures of the general population. During the 1997 Review, 

EPA staff concluded that the lowest range within which 1- to 3-hour exposures to ozone at heavy 

exertion produce group mean statistically significant lung function decrements is 0.12 to 0.16 

ppm.

21 They concluded that the lowest range for 6- to 8-hour exposures at moderate exertion is 

0.08 to 0.12 ppm.22 The exercise utilized in the 6- to 8-hour controlled exposure studies was 

intended to simulate work performed during a day of heavy to severe manual labor by outdoor 

 

19 72 Fed. Reg. at 37,858. 

20 Second Draft SP, Figure 5-2 a., b., c. at 5-17. col. 2. 

21 U.S. Environmental Protection Agency, Review of National Ambient Air Quality Standards for Ozone Assessment 

of Scientific and Technical Information, OAQPS Staff Paper, EPA-452/R-96-007, June 1996, at 49-150. (“1996 

Staff Paper”) 

22 1996 Staff Paper at 150. 
10 

Comments of the Alliance of Automobile Manufacturers 

Docket No. EPA-HQ-OAR-2005-0172 

laborers.23 Although the ventilation rate (40 L/min) is described by EPA as “moderate exercise,” 

activity maintained at this level for 6 to 8 hours has to be considered “heavy” or “strenuous work 

or play.” The staff conclusions regarding lowest effect levels for various respiratory endpoints in 

the current review are unchanged from the previous review with one exception, which is 

discussed below. 

 More importantly, in addition to establishing the presence or absence of physiological 

changes, the question of the public health significance of any measured changes needs to be 

addressed. In the previous review, there was considerable discussion of this question and a 

framework for evaluating the adversity of reported changes was developed with one set of 

criteria for healthy individuals and another for individuals with compromised respiratory 

systems. The two frameworks for evaluating adversity in the previous review are included, 

unchanged, in the current SP. 

 The Criteria Document (CD) acknowledges that there is a neurally-mediated mechanism 

that is responsible for the lung function decrements and symptoms seen in the clinical studies. A 

body of studies now shows that the first effects of ozone are caused by reflex responses of vagal 

nerve receptors. This response is the body’s reflexive reaction to the presence of an irritant gas 

and is unrelated to sensations of discomfort. Such a risk would be considered both safe and 

tolerable. The CD acknowledges that these effects are transient, of a reflex nature, and 

reversible.24 

 In the previous review, CASAC and staff determined that single, acute moderate lung 

function responses in healthy individuals should not be considered adverse. For asthmatics, staff 

previously concluded, based on discussions with medical experts, that single ozone exposures 

that resulted in moderate responses were not likely to interfere with normal activity nor would it 

result in increased frequency of medication or the use of additional medications. There is no 

scientific basis for changing these conclusions in the current review. In fact, in the proposed 

rule, the Administrator concurs noting that “[w]hile some experts would judge single 

occurrences of moderate responses to be a ‘nuisance,’ especially for healthy individuals, a more 

general consensus view of the adversity of such moderate responses emerges as the frequency of 

occurrence increases.”25 The concern over multiple occurrences arises not because of 

established effects but because of the potential for it leading to adverse consequences. However, 

there has been little or no discussion in the current review of the number of occurrences that 

should be considered adverse or of the public health significance of multiple occurrences, given 

the reflex mechanism that is responsible for the transient FEV1 changes. 

Although new clinical studies since 1996 have added to the available data, the 

fundamental understanding of effects at 0.08 ppm and above has not changed since the last 

review. In 1996, EPA concluded that a wide array of health effects were attributed to short-term 

 

23 W. McDonnell, H. Kehrl, S. Abdul-Salaam, P. Ives, L. Folinsbee, R. Devlin, J. O’Neil and D. Horstman, 

Respiratory response of humans exposed to low levels of ozone for 6.6 hours, Arch. Environ. Health, 46, 145-150 

(1991). 

24 CD at 6-44 to 6-45. 

25 72 Fed. Reg. at 37,850. 
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(1 to 3 hrs.), prolonged (6 to 8 hrs.) and long-term exposure to ozone at levels as low as 0.08 

ppm. The 1997 Review found acute health effects induced by short-term exposures to ozone 

concentrations as low as 0.12 ppm, occur generally while subjects are engaged in heavy exercise. 

These effects include pulmonary function responses, transient respiratory symptoms, effects on 

exercise performance, increased airway responsiveness, increased susceptibility to respiratory 

infection and transient pulmonary inflammation. Similar health effects in the 1997 Review were 

observed following prolonged exposures to ozone at concentrations as low as 0.08 ppm and at 

lower levels of exercise.26 EPA noted that some of the studies reporting effects at 0.08 ppm 

included Follinsbee et al. (1991), 1994, Gong et al. (1986), Hazucha et al. (1992), Horstman et 

al. (1990, 1995), Horvath et al. (1991), Koren et al. (1988,1989 and 1991), Lin et al. (1994) and 

McDonnell et al. (1991). 

However, new data (Adams 2006) extended the database on lung function effects down 

to 0.06 ppm and 0.04 ppm for 6 to 8 hours with moderate exercise.27 The interpretation of the 

latest data is controversial. In the Second Draft SP, EPA indicated that the lowest ozone effect 

level for pulmonary function decrements and increased respiratory symptoms was 0.08 ppm for 

6.6 hours,28 but in the final SP, this was lowered to 0.06 ppm for group comparisons29 and 

0.04 ppm for individuals.30 The change occurred for several reasons. First, EPA adjusted the 

Adams 2006 study’s results based on the assumption that the performance on lung function tests 

generally improves after exposure to the filtered air control. In addition, EPA also re-analyzed 

the data with a different statistical test. With these changes EPA drew completely different 

conclusions from those of the study’s author, with regard to possible statistical significance of 

group mean results. The author of the original study has subsequently objected to the 

conclusions of this re-analysis. EPA also inappropriately relied on the results in individual 

subjects in drawing their conclusions. 

It is important to note that the group mean decrement, even with the adjustment for the 

filtered air response was less than 3 percent, which is within the 3 to 5 percent range of normal 

measurement variability for an individual and substantially less than the 10 to 20 percent range 

discussed as adverse lung function decrements. For example, the range of individual FEV1

changes in the filtered air group in these studies was -6.0 to 12.4 percent. In fact, decrements of 

3 percent or less are noted in the SP as having no interference with normal activity for either 

healthy persons or persons with impaired respiratory systems. Given that the observed effects 

from the Adams 2006 study are not medically significant, the debate over whether the study 

demonstrates a statistically significant effect at specific ozone exposure levels is not meaningful. 

For this reason, the Administrator cannot rely on the Adams 2006 study as evidence to support a 

 

26 1996 Staff Paper at 24; 62 Fed. Reg. at 38,859. 

27 W. Adams, Comparison of chamber 6.6 h exposures to 0.04-0.08 ppm ozone via square-wave and triangular 

profiles on pulmonary responses, Inhalation Toxicology, 18, 127-136 (2006). 28 Second Draft SP, Table 3-4, at 3-78. 

29 U.S. Environmental Protection Agency, Review of National Ambient Air Quality Standards for Ozone: Policy 

Assessment of Scientific and Technical Information, OAQPS Staff Paper, EPA-452/R-07-007, July 2007, Table 3-4, 

at 3-84 (“SP”). 

30 SP at 3-1. 
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conclusion of significant public health effects below the current standard when the effects 

observed are not considered medically significant. 

3. EPA’s risk assessment based on the clinical studies does not support 

the conclusion that a tightening of the standard is requisite to protect 

the public health. 

 EPA’s interpretation of the risks based on clinical studies is flawed and does not support 

the conclusion that a more stringent standard is needed. 

 The exposure/exertion protocols used in the human clinical studies do not mimic typical 

human behavior so the results must be mapped onto realistic exposure/activity scenarios to 

determine the risk. The chance of experiencing an exposure of concern requires that a person be 

outside at the location of the high ozone, at the time of peak ozone and exercising heavily. 

During the 1996/1997 review, EPA staff undertook an extensive exposure and risk assessment 

with input from CASAC. To estimate the risk, staff used the output of a probabilistic exposure 

model together with concentration-response functions derived from the clinical studies. The 

conservative analysis, documented in the 1996 Staff Paper, assumed lung function decrements 

started at 0.04 ppm, assumed no attenuation of effects, assumed that children experienced the 

same level of symptoms as adults (available data suggests otherwise), ignored smoking status 

that would attenuate responses in outdoor workers, and used human time/activity and exertion 

data from California as well as other locations. The EPA analysis also used an algorithm to 

assign ventilation rates based on individuals who exercised regularly and were motivated to 

reach a high ventilation rate. As a result, the 1996 Staff Paper acknowledged31 that the analysis 

allowed more high ventilation rates (hence greater risk) than would actually occur in the 

populations of interest -- outdoor workers, outdoor children, etc. 

 The 1996 exposure and risk assessment demonstrated that there will be a minimal 

number of days of ozone-related respiratory effects with 8-hour concentrations up to 0.09 ppm 

and employing statistical forms allowing up to five exceedances per year. The risk analysis 

based on human clinical studies was one of the major factors in the Administrator’s choice of the 

current ozone standard. While the primary standard is required to allow for an adequate margin 

of safety, the extreme value form of the current 8-hour standard, in itself, adds a substantial 

margin of safety in that it drastically limits the number of potential repeat exposures. 

 The current review includes an update to the exposure and risk assessment. The APEX 

model developed estimates of the number of all school age children and asthmatic school age 

children exposed one or more times a year to various 8-hour ozone concentrations (0.06 ppm, 

0.07 ppm, and 0.08 ppm) while undergoing moderate exertion in a number of urban areas. These 

exposure metrics are discussed as benchmark “exposures of concern.” The proposal notes that 

only a subset of the individuals in these groups would actually be expected to experience 

effects.32 The benchmark metrics were evaluated for both “as-is” ozone concentrations for the 

 

31 1996 Staff Paper at 102. 

32 72 Fed. Reg. at 37,855. 
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years 2002 to 2004 and then for the ozone concentrations estimated to occur upon meeting 

alternative standards. The exposures from the APEX model were then used with the doseresponse functions for FEV1 changes to estimate the number of moderate or greater lung function 

responses in the same groups for both the “as-is” air quality and that estimated upon attainment 

of various alternative standards. 

 The proposed rule notes that the Administrator considered the number of persons exposed 

at or above the 0.07 ppm benchmark and the clinical risk estimates along with other factors in 

evaluating the adequacy of the current standard.33 In fact, the proposed rule notes specifically 

that the Administrator focused on the risks remaining upon just meeting the current standard in 

considering the adequacy of that standard.34 In addition, the Administrator relied significantly 

on the exposure and risk assessment results in choosing the range of 0.070 to 0.075 ppm for the 

proposed revised primary standard. To the extent that there are significant biases in the exposure 

and risk assessment, the interpretation of the public health protection afforded by either the 

current standard or various alternatives would change. 

 There are at least five ways in which the clinical exposure and risk assessment is biased, 

overstating the exposures and risks that would accompany any of the alternative standards under 

consideration. Specifically, there are three ways that the APEX model used in the current risk 

assessment overestimates the number of occurrences of elevated 8-hour ozone exposures during 

strenuous work or play and two ways in which the Risk Assessment (RA) overestimates the 

benefits of alternative standards. The five areas are: 

1. The CD acknowledges that ozone exposure is lower at “person” height compared to 

“measurement” height (3-15 meters).35 For example, Wisbeth et al.36 measured the 

increment between ozone at 2 and 10 meters and reported an average 13 percent 

difference. In addition to the height differential, ozone monitors are also sited in open 

areas removed from sources so as to capture the highest ozone concentrations expected in 

an area. Since downwind sites are usually the design value sites, they will dominate the 

upper tail of the ozone distribution and yet may not reflect the overall outdoor exposures 

in the vicinity of the site. If people spend time outdoors in closer proximity to streets or 

in areas with more surface area (buildings, etc.) to quench ozone, their exposures will be 

below that measured at the monitor. The APEX model assumes that whatever ozone is 

interpolated from the monitor measurement is the actual ozone exposure in the outdoorsother microenvironment. The Langstaff Memorandum acknowledges the issue of vertical 

variation in ozone but indicates that the Agency does not plan to address it due to a lack 

of data.37 This difference was corrected in the vegetation risk assessment but not in the 

 

33 72 Fed. Reg. at 37,871. 

34 72 Fed. Reg. at 37,871. 

35 See CD at 3-15, AX3-190-91. 36 A. Wisbeth, G. Meiners, T. Johnson, and W. Ollison, Effect of monitor probe height on measured ozone 

concentration, Paper No. 96-RA111.02, presented at the 89th Annual Meeting of the Air & Waste Management 

Association, Nashville, TN, June 1996. 

37 J. Langstaff, Technical Memorandum, Analysis of Uncertainty in Ozone Population Exposure Modeling, Jan. 

2007, at 21-22 (“Langstaff Memorandum”) . 
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human risk assessment. In the vegetation risk, the metric summing concentrations of 

0.06 ppm and higher was halved with a 10 percent vertical correction. By analogy, a 

vertical correction in the human risk assessment would likely halve the number of human 

exposures of concern at ground level. Because this effect would correct a bias in the 

exposure calculations, it is particularly important to evaluate and include it in the risk 

assessment before the final rule. 

2. The upper tail of the distribution of breathing rates -- equivalent ventilation rates (EVR) 

-- is particularly important because it is a critical factor in determining the number of 

exposures of concern. EPA assumes that all exposures between 13 and 27 EVR respond 

as though they were at 20 EVR, substantially overestimating 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 number of exposures of concern. The 

1996 CD showed that 1- to 2-hour ozone responses vary with EVR and Ollison has 

shown that the 8-hour responses in the Folinsbee/Horstman data do too.38 Thus, the doseresponse curve varies with EVR. The distribution of exposures also varies with EVR. 

We expect many more 8-hour occurrences of ozone exposures at 13 EVR than at 20 and 

many more at 20 EVR than at 27. Thus, the approximation that all exposures between 13 

and 27 EVR respond as though they were at 20 EVR substantially overestimates the risk. 

Since the model calculates EVR to a much finer scale, the distribution of EVR should be 

presented in the risk assessment and dose-response curves should be developed as a 

function of EVR to avoid the overestimation of risk. At a minimum, this issue should be 

evaluated in a sensitivity analysis. The Langstaff Memorandum indicates that the EVR 

cutpoints input to APEX are selected for the risk calculations and are not considered as 

uncertain for the purposes of the uncertainty analysis.39 However, it would be simple to 

break the wide EVR range used for the risk calculations into a number of smaller bins to 

test the hypothesis that the use of such a wide EVR range biases the overall result. In 

addition, the American Petroleum Institute (API) has provided EPA with a dynamic 

statistical model that can be implemented in APEX and provide more highly refined 

FEV1 decrements.40 The sensitivity of APEX predictions to the use of the API model 

should be evaluated prior to the issuance of the final rule. 

3. The model predicts more elevated ventilation rate occurrences than observed in real 

world data. Langstaff acknowledged that the “values produced by the ventilation rate 

algorithm may exhibit an excessive degree of variability.”41 The final sensitivity analysis 

for APEX includes a comparison of predicted ventilation rates with mean values in the 

literature, but the upper tails of the distribution which impact the risk estimates were not 

 

38 American Petroleum Institute Comments on EPA’s Dec. 13, 1996 Proposed Ozone Rule, Appendix A. 

39 Draft Langstaff Memorandum at 43. 

40 Memorandum from Ted Johnson, TRJ Environmental, to John Langstaff and Harvey Richmond, U.S. EPA, An 

algorithm for APEX that estimates one-minute ozone-induced FEV1 decrements, (July 31, 2006) (included as 

attachment to Memorandum from Will Ollison, API Energy, to Karen Martin, U.S. EPA (Aug. 29, 2006) (EPA-HQOAR-2005-0172-0037.1)). 

41 Draft Langstaff Memorandum at 42. 
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compared.42 This is an important oversight because the upper percentiles of ventilation 

rate are responsible for the exposures that cause the perceived risk. In the comparison of 

the APEX modeled values with the measured ventilation rates from Brochu et al. 2006,43

the model over-predicted mean daily ventilation rates for persons below age 11 and over 

age 40. More importantly, the model had a much higher standard deviation at all ages. 

This suggests that the upper percentiles of ventilation rates in the model are substantially 

above those measured in a database of over 30,000 person-days from a cohort of over 

2200 free-living individuals between the ages of 3 and 96. This is particularly important 

since the comparison was not available to CASAC before the panel provided its 

recommendations. A detailed analysis of the upper tails of the distribution of predicted 

and measured ventilation rates must be carried out before the final rule is issued. 

The following Figure 1 shows that the APEX model EPA uses in the risk assessment 

significantly overestimates the breathing rates of male children, particularly for the upper 

tails of the distribution that are responsible for the exposures of concern discussed in the 

proposed rule. The data underlying these distributions (means and standard deviations) 

come from Table 25 in the 2007 Langstaff Memorandum on uncertainty in the exposure 

model. In fact, of the 16 comparisons in Table 25, for eight age groupings each of males 

and females, 15 had substantially higher modeled ventilation rates compared to the data 

reported by Brochu, et al. 2006 at the upper end of the distribution. 

 

42 J. Langstaff, Technical Memorandum, Analysis of Uncertainty in Ozone Population Exposure Modeling, Jan. 31, 

2007 at 52 (“2007 Langstaff Memorandum”) (EPA-HQ-OAR-2005-0172-0174). 

43 See P. Brochu, J. Ducre-Robitaille, and J. Brodeur, Physiological daily inhalation rates for free-living individuals 

aged 2.6 months to 96 years based on doubly labeled water measurements: comparison with time-activityventilation and metabolic energy conversion estimates, Int. J. Hum. Ecol. Risk. Asses., 12, 736-761 (2006). 
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Figure 1: Comparison of Measured vs. Modeled Daily Ventilation 

Rates for 7- to 10-Year Old Boys 

4. The EPA risk assessment uses the current distribution of ozone concentrations as a 

baseline input. To estimate risk associated with a given standard, the model “rolls back” 

ozone levels to the given standard. There are several problems with the rollback 

methodology EPA used. It is arbitrary and does not mimic the changes that will occur as 

emissions are reduced and man-made ozone is reduced. Importantly, EPA ignores 

background when rolling back the distribution of ozone concentrations at individual sites. 

Currently, NOx emissions suppress ozone a significant portion of the time via the NO + 

O3 reaction. As ozone precursor emissions are reduced, there is a reduction in the highest 

daily 8-hour ozone concentrations but lower ozone concentrations actually increase. The 

CD notes this behavior (see CD at 3-32 to 3-35) referring to Figures 3-17 and 3-18 which 

show the year-to-year trends in the distribution of mean daily 8-hour averages and the 

95th percentile of daily 8-hour averages across the country. The text indicates that the 

highest ozone concentrations decreased over the past 15 years, but there has been little 

change in the middle of the distribution and a slight increase in ozone concentrations near 

the bottom of the distribution because of reduced titration of ozone with NO in response 

to reductions of NOx emissions. EPA’s rollback misses the increase in ozone 

concentrations near the bottom of the distribution as the man-made influence on ozone is 

decreased. EPA’s rollback overestimates the change in ozone at mid- and low 

0%

2%

4%

6%

8%

10%

12%

14%

16%

18%

20%

0 5 10 15 20 25

Ventilation Rate (m3/day)

Measured

Modeled

Male Ventilation Rate Distributions, 7 to < 11 Years Old

Air Improvement Resource, Inc.
17 

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concentrations and, thereby, overestimates the benefits of alternative standards. The 

rollback should be applied to the man-made portion of ozone not the entire distribution. 

5. The background ozone assumed in the risk assessment is too low. Since the risk 

assessment subtracts the risk from background, a higher background will result in a lower 

risk from attaining the current standard. As demonstrated elsewhere in these comments, 

the Agency’s approach to estimating background is flawed. As in previous ozone 

reviews, both the mean and extremes of background need to be evaluated in order to 

properly account for the ozone that is not controllable through control of U.S. man-made 

emissions. 

 Corrections to the exposure and risk assessment for these five major biases should 

substantially increase the health benefits and reduce the potential risk associated with attaining 

the current standard. The corrected risk assessment would confirm that the current standard is 

protective of public health in accordance with the requirements of Section 109 of the CAA. 

Even with significant overestimates of the number of exposures associated with exercise, 

the APEX results presented in the SP demonstrate that the current standard limits the number of 

persons and person-occurrences of ozone exposures to 0.08, 0.07, and 0.06 ppm for 8-hours with 

moderate exertion (strenuous work or play). Correcting major biases would significantly reduce 

the estimates further and confirm the protectiveness of the current standard and the unlikelihood 

of achieving additional public health benefits from lowering the standard. 

B. Time-Series Studies Do Not Provide Support for Causality of Effects But 

Instead Confirm Significant Uncertainties Present in the 1997 Review. 

1. In interpreting the epidemiological evidence, EPA downplays the 

major new findings concerning uncertainty due to model selection 

issues. 

Model selection uncertainty relates to confounding of air pollutant associations by 

temporal trends, weather and co-pollutants. EPA acknowledges that the uncertainties in the 

estimates of ozone effects (or those of any other pollutant) are understated by consideration of 

the statistical uncertainty of the fitted model alone. Much more uncertainty arises from the lack 

of information regarding the choice of appropriate models for adjusting confounding by other covariates, and the choice of appropriate lag structures. As Lumley and Sheppard (2003) point out: 

Estimation of very weak associations in the presence of measurement error and 

strong confounding is inherently challenging. In this situation, prudent 

epidemiologists should recognize that residual bias can dominate their results. 

Because the possible mechanisms of action and their latencies are uncertain, the 

biologically correct models are unknown. This model selection problem is 
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exacerbated by the common practice of screening multiple analyses and then 

selectively reporting only a few important results.44

Others have also pointed out the critical importance of model choice, particularly when effect 

estimates are small. For example, Smith et al. caution: 

From a statistical point of view, the common epidemiological practice of choosing 

variables (including lagged variables, co-pollutants, etc.) that maximize the 

resulting effect estimates is a dangerous approach to model selection, particularly 

when the effect estimates are close to 0 (i.e., RR close to 1).45

Smith et al. note that Lumley and Sheppard (2000)46 showed that the effect of choosing lags in 

this fashion has a bias which is of the same order of magnitude as the relative risk being 

estimated. 

The revised analyses necessitated by the problems with the commonly used software for 

time-series analyses clearly show that methods used for controlling temporal trends and weather 

can profoundly affect the results. To make matters worse, there appears to be no objective 

statistical test to determine whether these factors have been adequately controlled. The Health 

Effects Institute Expert Panel47 for the re-analysis states, “Ritov and Bickel (1990)48 have shown, 

however, that for any continuous variable, no strictly data-based (i.e., statistical) method can 

exist by which to choose a sufficient number of degrees of freedom to insure that the amount of 

residual confounding due to that variable is small. This means that no matter what statistical 

method one uses to select the degrees of freedom, it is always logically possible that even if the 

true effect of pollution is null, the estimated effect is far from null due to confounding bias.” The 

expert panel concluded further, “Neither the appropriate degree of control for time, nor the 

appropriate specification of the effects of weather, has been determined for time-series analyses”. 

In other words, it is impossible to adjust temporal trends without accurate information from 

external sources regarding the appropriate degrees of freedom to use. Such information simply 

does not exist. 

 

44 T. Lumley and L. Sheppard, Time-series analyses of air pollution and health: straining at gnats and swallowing 

camels? Epidemiology, 14, 13-14, 2003. 45 R. Smith, P. Guttorp, L. Sheppard, T. Lumley and N. Ishikawa, Comments on the Criteria Document for 

Particulate Matter Air Pollution, Northwest Research Center for Statistics and the Environment Technical Report 

Series No. 66, July 2001. 

46 T. Lumley and L. Sheppard, Assessing seasonal confounding and model selection bias in air pollution 

epidemiology using positive and negative control analyses, Environmetrics, 11, 705-717 (2000). 47 Health Effects Institute, Special Report: Revised Analyses of Time-Series Studies of Air Pollution and Health, 

Health Effects Institute, Cambridge, Massachusetts, at 267, 269 (2003). 

48 Y. Ritov and P. Bickel, Achieving information bounds in non- and semi-parametric models, Ann. Stat., 18, 925-

938 (1990). 
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With regard to uncertainty due to model selection, the Koop and Tole 200449 conclude: 

Point estimates of the effect of numerous air pollutants all tend to be positive, 

albeit small. However, when model uncertainty is accounted for in the analysis, 

measures of uncertainty associated with these point estimates became very large. 

Indeed they became so large that the hypothesis that air pollution has no effect on 

mortality is not implausible. On the basis of these results, we recommend against 

the use of point estimates from time-series data to set regulatory standards for air 

pollution exposure. 

 EPA has failed to adequately account for the significance of model uncertainty in either 

its qualitative or quantitative assessment of the health effects from exposure to ozone. Given that 

the small positive results from time-series studies may reflect residual bias of the models due to 

weather, temporal or other unaccounted confounding factors, EPA cannot and should not draw 

conclusions on causality from these studies. 

2. In interpreting the epidemiological studies, EPA relies on single 

estimate and single-site analyses, and fails to address the effect of 

publication bias. 

 The SP and proposed rule discuss three new meta-analyses of ozone mortality 

associations and point out that they come to similar conclusions. When these studies were 

published, they were accompanied by two commentaries referenced in the CD but not the SP or 

proposed rule. The commentary by Goodman is particularly insightful.50 It notes that the 

implications of the EPA-sponsored exercise of funding three separate meta-analyses “go far 

beyond the question of the ozone mortality effect.” He cautions that “depending on published 

single-estimate, single-site analyses are an invitation to bias.” He notes that “the most plausible 

explanation is the one suggested by the authors, that investigators tend to report, if not believe, 

the analysis that produces the strongest signal; and in each single-site analysis, there are 

innumerable model choices that affect the estimated strength of that signal.” Although the 

proposed rule mentions the issue of publication bias, it is discounted by asserting that ozonemortality associations remained after accounting for the bias. However, the current methods for 

estimating and correcting publication bias are only partial and incomplete. For example, the 

current method of plotting the effect size versus the standard error (referred to as a funnel plot) 

and using the trim and fill method to provide a symmetrical plot, resulted in the order of a 10 

percent reduction in effect size in the Ito et al.

51 meta-analysis, but Bell et al.52 and Goodman 

noted factors of three or more reduction in effect size comparing the published single-city studies 

with the comprehensive NMMAPS data set. The reasons for the discrepancy is likely the result 

 

49 G. Koop and L. Tole, Measuring the Health Effects of Air Pollution: to What Extent Can We Really Say that 

People are Dying from Bad Air, J. of Environmental Economics and Management, 47, 30-54. (2004). 50 S. Goodman, The Methodologic Ozone Effect, Epidemiology, 16: 430-435 (2005). 51 K. Ito, S. de Leon, and M. Lippmann, Associations between ozone and daily mortality, Epidemiology, 16: 446-

457 (2005). 

52 M. Bell, F. Dominici, and J. Samet, A meta-analysis of time series of ozone and mortality with comparison to the 

National Morbidity, Mortality, and Air Pollution Study, Epidemiology, 16: 434-445 (2005). 
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of many non-random model selection choices in the conduct of the study in addition to the nonrandom choice of whether to publish. 

3. Analysis of more complete data sets, such as NMMAPS, suggests 

significant variability of positive and “negative” responses 

unaccounted for in the published literature or in EPA’s analysis. 

 While there are some inverse or negative air pollution associations reported in the 

literature (implying an unlikely protective effect from exposure to ozone), the NMMAPS study 

shows that there are many more “negative” associations in the data than in the literature. When 

the statistical issues with the General Additive Model (GAM) were raised, Ito53 systematically 

re-analyzed the 1220 separate air pollution mortality and morbidity associations that were 

included in the original Lippmann et al. 2000 study of Detroit, comparing the results using the 

General Linear Model (GLM) to those with the suspect GAM. As shown in Figure 2, there was 

a wide range of negative and positive excess risks (associations) in Detroit when a large number 

of pollutants, lags and morbidity and mortality endpoints were considered. All the combinations 

of pollutant, lag and health outcome evaluated in the original Lippmann study were considered 

plausible candidates for air pollution health effects. Ito showed in separate figures that the wide 

range of associations occurred for each pollutant, including ozone. Although the focus in the 

original Lippmann study, as it is in almost all the published literature, was on the positive 

associations, Ito’s plot shows that there are many negative associations in the data. 

 Figure 2: Comparison of Generalized Additive Model With 

Generalized Linear Model54

 

53 K. Ito, Associations of Particulate Matter Components with Daily Mortality and Morbidity in Detroit, Michigan, 

in Health Effects Institute, Special Report: Revised Analyses of Time-Series Studies of Air Pollution and Health, 

May 5, 2003, at 143-156. 

54 Id. 
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Although there may be somewhat more 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. Thus, timeseries epidemiology of air pollution associations is a very blunt tool. CASAC raised this issue in 

a June 2006 letter to the Administrator, noting that “because results of time-series studies 

implicate all of the criteria pollutants, findings of mortality time-series studies do not seem to 

allow us to confidently attribute observed effects specifically to individual pollutants.”55 Further, 

due mainly to exposure misclassification concerns, they questioned the utility of the time-series 

mortality estimates. 

If all positive associations (or excess risks) are assumed or concluded to be health effects 

then all negative associations should be considered health benefits due to ozone or other air 

pollutants. Since no one believes the observed negative associations are proof that air pollutants 

actually provide health benefits on a day-to-day basis, the assumption that all positive 

associations are health effects is also not plausible. For example, the various ozone/mortality 

associations in 95 U.S. cities shown in Figure 7-17 of the CD at 7-90 (ranging from - 6 to + 10% 

per 0.02 ppm increase in 24-hr. average ozone in the previous week) would imply that ozone is 

dangerous in about a third of the cities, but is harmless or even beneficial in about half the cities. 

This is not biologically possible, if it is assumed that these associations represent causal 

relationships. 

 Instead of focusing only on and relying on the studies in the literature reporting positive 

associations, the Agency should address questions such as how there can be such a wide 

variation of ozone associations both positive and negative in the data. It is not biologically 

plausible that ozone would be causing mortality in some cities in the summer and protecting 

against mortality in others. Similarly, it is not plausible that ozone is, on balance, dangerous in 

the summer and protective in the winter. 

4. EPA has a duty under the Data Quality Act to consider all the results, 

including both positive and non-positive results. 

The 2000 Data Quality Act requires federal agencies to issue information quality 

guidelines ensuring the quality, utility, objectivity and integrity of information that they 

disseminate and provide mechanisms for affected persons to correct such information.56 

According to federal guidelines objectivity involves both the presentation and substance of 

information. In order for information to be considered objective, however, it must be presented 

in an accurate, clear, complete and unbiased manner, although data subjected to formal, 

independent, external peer review is presumed to be of acceptable objectivity, the presumption is 

rebuttable.57 EPA’s analysis of the epidemiology does not meet the standard of objectivity 

required under the 2000 Data Quality Act because it ignores the inherent variability of the data 

by focusing on only the positive results. 

 

55 June 2006 CASAC Letter at 3. 

56 44 U.S.C. § 3501 et seq. 57 See Guidelines for Ensuring and Maximizing the Quality, Objectivity, Utility, and Integrity of Information 

Disseminated by Federal Agencies; Republication, 67 Fed. Reg. 8452, 8459 (Feb. 22, 2002). 
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5. The new data on asthmatics and symptoms/medication use does not 

provide clear and convincing evidence of an increase in risk due to 

ozone exposure that was not present in the 1997 Review. 

 EPA incorrectly concludes that the new evidence on asthmatics suggests an increased risk 

compared to that assumed in the previous review: 

The Administrator also notes that clinical studies, supported by epidemiological 

studies, provide important new evidence that people with asthma are likely to 

experience larger and more serious effects than healthier people from exposure to 

O3.

58 

The discussion of clinical studies in Section 6.3.2 of the CD indicates that there are some studies 

that report slightly higher functional responses in asthmatics compared to normal subjects, some 

studies that report similar responses, and one new study that reports lesser responses in 

asthmatics. In the 1996 review, the Agency considered this issue and developed separate 

guidelines for evaluating the adversity of respiratory effects for healthy individuals and those 

with impaired respiratory systems. The same guidelines are included in the SP. Therefore, there 

is no important new information from clinical studies that changes the interpretation of risk for 

asthmatics relative to healthy individuals compared to that in the previous review. However, the 

overall risk for both groups is lower than thought in 1996 due to the non-linear nature of the 

pulmonary function responses noted above. 

 The SP refers to a number of panel studies that report associations of ozone with daily 

symptoms/asthma medication use. The SP and CD stress the multi-city study of Mortimer et al.

2002 as providing a sample of asthmatics that is most representative of the U.S. The SP cites the 

CD as indicating that the panel studies as a group indicate a positive association between 

ambient concentrations and respiratory symptoms, and increased medication use in asthmatics.59 

The evidence is characterized as much stronger than in the previous review. 

 The reliance on single-pollutant results from Mortimer et al. 2002, however, is highly 

misleading. The Mortimer study presents the results of single- and multi-pollutant models. 

Because the various possible confounders were not all measured in the eight cities, the results are 

shown for various subsets of the data. Only SO2 was measured in all eight cities, and when SO2

was included in two pollutant models, the ozone coefficient was reduced from 1.16 to 1.11 and 

became non-significant. For seven areas both SO2 and NO2 were available. In multi-pollutant 

models the ozone coefficient was reduced to 1.06 and again was non-significant. In three cities 

PM10 was also available, and in those areas the ozone coefficient was reduced to 1.04 in a 2-

pollutant model with PM10 and to 1.00 in a multi-pollutant model with all four pollutants. As the 

authors indicate, only SO2 remained significant in the seven urban areas with complete data for 

the three gases. Overall, each of the four pollutants was associated with symptoms in singlepollutant models and the strongest association was with NO2 in single-pollutant models and with 

 

58 72 Fed. Reg. at 37,878. 

59 SP at 3-10. 
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SO2 in multi-pollutant models. In fact, the authors of the study specifically mention that they 

focus on ozone as a good marker of summer air pollution and refer to the study’s finding as 

effects of summertime air pollution rather than ozone, per se. 

 A new study by Schildcrout et al.60 evaluated the relation between various pollutants and 

asthma exacerbations (daily symptoms and use of rescue inhalers) among 990 children in eight 

U.S. cities (including Boston) and reported associations with several pollutants, but ozone was 

unrelated to exacerbations. When the new Schildcrout et al. study is considered along with the 

nine other studies that are described in the CD as having limited or a lack of evidence for ozone 

effects, the overall findings relative to effects of ozone on asthmatics on symptoms and 

medication use should be described as mixed and inconsistent rather than clear and very strong 

evidence of an ozone effect. 

 In addition to man-made air pollutants, confounding by bioaerosols may also be a 

possible explanation for some of the variation in results for asthmatics. Some bioaerosols are 

known to exacerbate asthma but are generally not considered or included in air pollution studies. 

During the 1996 review, EPA staff included moderate or severe pain on deep inspiration in the 

exposure and risk assessment. However, the current CD correctly notes that there is no 

consistent evidence of an association between ozone and respiratory symptoms in healthy 

children. Therefore, the Agency does not include this health outcome in the current risk 

assessment. For asthmatics, however, the current risk assessment does include an estimate of 

respiratory symptoms in Boston using associations reported by Gent et al. 2003. 

 Given the Schildcrout et al. study, the lack of adequate control for other pollutants (manmade or biogenic), and the overall inconsistent results in the epidemiology data, EPA cannot 

conclude that the health risk to asthmatics from exposure to ozone is greater than the risk 

observed in 1997. 

6. The claim that a more stringent ozone standard will address the 

growing asthma problem in the U.S. is without scientific merit. 

a. There is no evidence that ozone levels at or below the current 

standard cause asthma. 

Although there has been an increase in asthma in both developed and developing nations 

in the past 20 or 30 years, outdoor air pollution, in general (and ozone, in particular), has been 

decreasing. Outdoor air pollution cannot be the cause of the increase in asthma. Changes in 

living conditions in the indoor environment due to energy conservation may play a role by 

increasing exposure to common household allergens such as mold, dust mites and animal dander. 

A recent Annapolis Center Report61 concludes that certain allergens and irritating chemicals, as 

 

60 J. Schildcrout, L. Sheppard, T. Lumley, J. Slaughter, J. Koenig and G. Shapiro, Ambient air pollution and asthma 

exacerbations in children: An eight-city analysis, Am. J. Epidemiology, advance access published June 23, 2006. 61 Asthma and Air Quality, A Report of the Annapolis Center for Science-Based Public Policy, Annapolis, MD, 

2004. 
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well as passive smoking can cause asthma, but that there is insufficient evidence to determine 

whether many common indoor or outdoor air pollutants cause asthma. 

 

b. The epidemiology data do not show that ozone levels at or below 

the current standard cause asthma. 

 Dockery et al.62 evaluated asthma prevalence and respiratory symptoms in a group of 

13,369 8 to 12 year old children in 24 communities and reported that the prevalence of asthma or 

asthmatic symptoms was not associated with chronic exposure to ozone. McConnell et al.63

followed 3,535 children with no history of asthma from 12 communities in Southern California. 

The risk for developing asthma was not greater in high ozone communities compared to low 

ozone communities. However, in a subset of children, those playing three or more sports, there 

was an increased risk of developing asthma in the high ozone communities but not in the low 

ozone communities. Because the number of children in the subset was very low, it is not clear if 

this is a true effect of ozone combined with high exercise levels. If it is true, the effect is limited 

to a subset of the population and associated with ozone levels in Southern California in the mid1990s – levels that were substantially above the current standard. 

There are many different environmental stimuli that can trigger or aggravate an asthma 

attack, including weather, changes in weather, bioaerosols and indoor allergens. The Institute of 

Medicine has concluded that various indoor pollutants, primarily biologic agents, and some 

chemical agents cause exacerbation of asthma.64 For traditional outdoor air pollutants, the 

Annapolis Center concludes the situation is not as clear because the data are not as consistent as 

for the major indoor triggers. Although ozone is a candidate for exacerbating asthma, the 

epidemiologic literature is not consistent and implicates all the major outdoor pollutants to some 

degree or another. 

C. The Evidence on Premature Mortality is too Limited in Nature and Should 

Not Be Relied Upon in Basing Conclusions on the Health Effects from 

Exposure to Ozone. 

 In the 1996 review, there was limited evidence of an ozone association with daily 

mortality. The 1996 CD concluded that an association has been suggested, but that the strength 

of any such association remained unclear at that time. Since then, there has been considerable 

study of the association of daily mortality with ozone and several other major pollutants. The 

current SP and the proposed rule place significant emphasis on the question of ozone mortality 

effects, especially from the results of multi-city analyses. 

 

62 D. Dockery, J. Cunningham, A. Damokosh, L. Neas, J. Spengler, P. Koutrakis, J. Ware, M. Raizenne and F. 

Speizer, Health Effects of Acid Aerosols on North American Children: Respiratory Symptoms, Environmental Health 

Perspectives, 104: 500-505, 1996. 

63 R. McConnell, K. Berhane, F. Gilliland, S. London, T. Islam, W. Gauderman, E. Avol, H. Margolis and J. Peters, 

Asthma in exercising children exposed to ozone: a cohort study, The Lancet, 359: 386-391, 2002. 64 Institute of Medicine, Clearing the Air: Asthma and Indoor Air Exposures, 2000. 
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1. CASAC itself had reservations on the use of the data. 

 Because of all the issues with the publication bias, model uncertainty, confounding, etc.

discussed above, time-series epidemiology of air pollution associations is a very blunt tool. 

CASAC raised this issue in a June 2006 letter to the Administrator noting that “[b]ecause results 

of time-series studies implicate all of the criteria pollutants, findings of mortality time-series 

studies do not seem to allow us to confidently attribute observed effects specifically to individual 

pollutants.”65 Further, due mainly to measurement error issues, they questioned the likelihood 

of ozone itself causing mortality and noted the limitation that measurement error obscures 

thresholds in time-series studies, adding additional concerns about the utility of the time-series 

mortality estimates.66 

2. A new NMMAPS analysis that extends the previous analyses, and the 

Huang et al. (2005) analysis of a subset of 19 large U.S. cities is 

limited, and does not support a finding of causality. 

a. There are major deficiencies in the Bell et al. 2004 paper, 

including the omission of the winter ozone results and limited 

analyses regarding other pollutants. 

 There are major deficiencies in the new NMMAPS analysis, Bell et al. 2004, that omitted 

winter ozone results and limited the analyses regarding other pollutants. If the positive 

combined association of ozone with mortality in the summer is causal, it implies that ozone 

levels well within background are linked to premature mortality. Since the ozone exposures of 

the frail population (since they spend their time indoors) will be roughly half or less than that 

measured at central monitors, the paper implies that levels well below background (average 

exposures of 0.01 to 0.015 ppm) are causing significant mortality. This is not biologically 

plausible. Bell et al. argue that the pattern of association they observe would be anticipated for 

ozone since ozone produces acute inflammatory responses in the lung. However, the doses of 

ozone that result in initial inflammatory changes are considerably elevated compared to the doses 

the frail population experiences on a day-to-day basis. 

 In addition, while Bell et al. focus on the combined associations, the results from the 95 

individual cities, shown in Figure 7-17 at 7-90 of the CD, range from strongly negative to 

strongly positive (-6 to + 10% increase in mortality per 0.02 ppm increase in 24-hr. average 

ozone in the previous week). Such a wide range is not biologically plausible. 

 Finally, Bell et al. (2004) provided adjustment for the potential confounding by PM10.

However, Bell et al. did not have the necessary air quality data to provide similar and adequate 

adjustment for the potential confounding effects of fine PM, which EPA has concluded also 

causes mortality. Rather, Bell et al. only provided adjustment for the long-term average of 

PM2.5. It is well known that ozone is not highly correlated with PM10. Rather, ozone levels, 

 

65 June 2006 CASAC Letter at 3. 

66 CASAC Letter, EPA-CASAC-06-07, June 5, 2006, at 3 and 4. 
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particularly in summer, are highly correlated with PM2.5. Thus, it was not possible for Bell et al.

to conclude that the acute ozone mortality signal they observed was due to ozone exposure alone. 

b. The pattern of individual-city associations in the Huang et al. 

study is not consistent with a causal association, and may reflect 

the confounding role of another pollutant.

The largest multi-city study, the National Morbidity and Mortality Air Pollution Study 

(NMMAPS), evaluated air pollutant-mortality relations in the 90 largest U.S. cities. In 2002, 

statistical issues with the GAM commonly used in such time-series studies were raised and many 

time series studies (particularly particulate matter studies) were re-analyzed. The SP thus refers 

to the original NMMAPS analysis and the NMMAPS re-analysis, but focuses on a new 

NMMAPS analysis67 that extends the previous analyses and the Huang et al. 2005 analysis of a 

subset of 19 large U.S. cities. 

 In the original NMMAPS analysis and in the re-analysis in single-pollutant models, 

ozone had a small positive combined association in summer, but also a small negative combined 

association in winter.68 In multi-pollutant models for the summer case, the combined positive 

ozone association was reduced and became non-significant at all three lags evaluated as shown in 

Figure 7-31 of the CD. Ozone is not the only pollutant for which NMMAPS seasonal results 

have been published to date; a seasonal PM10 analysis has also been carried out.69 Peng et al.

used updated mortality data from 1987-2000 in 100 cities and found that summer was the only 

season for which the combined PM10 effect was statistically significant. 

 In the Huang et al. study of 19 cities, the pattern of individual-city associations is not 

consistent with a causal association. For example, the range in individual-city associations is 

from –6 to + 16% per 0.02 ppm increase in 24-hour ozone and lower ozone levels in the cities 

were associated with higher mortality associations.70 Also, Huang et al. actually reported that 

inclusion of PM10 markedly reduced the ozone mortality coefficients, in many cases to nonstatistically significant levels. The SP also discusses the Gryparis et al. 2004 23-city study and 

the Schwartz 2005 14-city study. Both studies also reported a very wide range of individual city 

associations ranging from negative to positive. Schwartz notes the negative association in winter 

and suggests that it may reflect the negative association between wintertime ozone and primary 

air pollutants. Schwartz goes on then to ask “might not the positive association in the summer 

likewise reflect confounding with some other pollutant?” These and other possible explanations 

need to be rigorously considered by EPA. 

 

67 M. Bell, et al.(2004), at 2372-2378. 68 F. Dominici, et al. (2005), at 1071-1092. 69 R. Peng et al. (2005), at 585-594. 70 CD at 7-104. 
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3. While the SP downplays confounding by co-pollutants, a more 

comprehensive review of the data implicates other pollutants as 

potential causes of the reported mortality associations in time-series 

studies. 

 The SP continues to downplay confounding by co-pollutants resulting in the conclusion 

that single-pollutant model results should be the baseline for the quantitative risk assessment. 

However, several major findings from the Stieb et al. 2002, 2003 meta-analyses (cited in the CD) 

show that confounding by co-pollutants remains a major problem. Stieb et al. evaluated 

mortality associations for each of the major pollutants and found a very similar distribution of 

associations for each in their analysis of 109 separate mortality/time-series studies. For example, 

the patterns in Figures 1 to 5 of Stieb et al. 2002 are remarkably similar to one another. They 

also reported a similar pattern of associations with various categories of death and stronger 

associations in the warm season than in the cold season for all the pollutants. When multipollutant models were compared to single-pollutant models, the associations were reduced in the 

case of each pollutant. In the case of ozone, the combined association became non-significant in 

multi-pollutant models. Since various investigators included different pollutants as potential 

confounders and different modeling strategies, the multi-pollutant analyses available in the 

literature are not a systematic evaluation of the issue. Nevertheless, the relative risk reported in 

single-pollutant model results was reduced substantially for each pollutant when multiplepollutant models were used. This suggests that the effect observed may not be due to ozone but 

rather from exposure to other pollutants, such as PM2.5, that are highly associated with ozone 

exposures. 

 The analysis of the NMMAPS data and findings of the Stieb et al. studies, and the 

results of the HEI re-analysis, implicate all the pollutants as potential causes and/or confounders 

of excess mortality in time-series studies, and show that stronger associations in the summer are 

not restricted to ozone. Since the Stieb et al. meta-analyses like the other meta-analyses are 

subject to publication bias; the associations reported are likely to overstate the true associations. 

Nevertheless, the pattern of results should not be affected by publication bias the way the 

magnitude is. 

 The NMMAPS database is valuable because, by including all the largest U.S. cities with 

data, it avoids the issue of publication bias. On the other hand, it is questionable to use the same 

approach to adjust for meteorological factors in cities with widely differing weather conditions 

(e.g., Los Angeles versus Chicago). The wide range of ozone associations in the data, using the 

same methodology, demonstrates the inherent noise or variability in the data. The same wide 

pattern of mortality associations ranging from strongly positive to strongly negative is observed 

in the individual NMMAPS data for all the pollutants studied (PM10, ozone, CO, NO2, and SO2) 

at all the lags studied.71 

 

71 J. M. Heuss and J. J. Vostal, Comments on the Fourth External Review Draft of Air Quality Criteria for 

Particulate Matter, EPA 600/P-99/002aD, June 2003, prepared for General Motors Corporation, Aug. 28, 2003. 
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In the HEI re-analysis, in single-pollutant models, ozone had a small positive combined 

association in summer, but also a small negative combined association in winter. In multipollutant models for the summer case, the combined positive ozone association was reduced and 

was not significant at all three lags evaluated. 

 The SP and CD dismiss concern over confounding by gases since the peaks of the various 

pollutants occur in different seasons and because ozone is generally not highly correlated with 

other pollutants. This is unwarranted since the Stieb et al. meta-analysis shows that the mortality 

associations for these potential confounders are strongest in the warm period. The cause or 

causes of these seasonal patterns are not clear. It could be a seasonally varying bias that is yet 

unidentified. It could be related to toxic constituents (gases or particles) that have a summer 

maximum. Since it occurs for each pollutant, confounding by as yet not understood weather 

effects is a likely candidate. As discussed in the next section, many air pollution analysts dismiss 

weather effects but the substantial seasonal trends in the health data are caused by subtle effects 

related to changes in weather and human behavior. Therefore, confounding by weather is a 

candidate. 

4. Weather factors remain a key confounder in the mortality analysis 

 relied on by EPA. 

 A recent paper by Keatinge and Donaldson72 provides important new insights into the 

issue of modeling weather effects in ozone studies. They evaluated whether mortality that is 

often attributed to ozone and other pollutants in hot weather results from confounding by 

neglected weather factors. Their analysis was restricted to days when the mean daily air 

temperatures exceeded 18 degrees!C in Greater London from 1991 to 2002, and evaluated 

mortality counts at an age greater or equal to 65. The adjustment for acclimatization was based 

on the characteristic pattern that has been reported by various investigators that the rise in 

mortality on hot days is followed by a prolonged reduction in mortality lasting at least 14 days. 

When only current temperature (average of days 0 to –2) was considered in the model, 

significant mortality was attributed to ozone. When they allowed for cumulative exposure to 

heat throughout the summer and for sunshine (which contributes to heat stress at any given 

temperature), the ozone association was reduced by a factor of 10 and was no longer statistically 

significant. This study indicates that previously neglected weather factors may be confounding 

the mortality analyses relied on in the SP. It is noted in the CD that variations in treatment of 

weather can change the results by a factor of 2 and that publication bias can inflate the perceived 

association by a factor of 3.73 The Keatinge and Donaldson analysis suggests that previously 

overlooked weather factors can reduce the association by a factor of 10. Thus, the fact that the 

uncertainty due to model selection is much larger than the typical confidence limits on any given 

statistical association should be highlighted by EPA and considered in the interpretation of the 

risk assessment. 

 

72 W. Keatinge and G. Donaldson, Heat acclimatization and sunshine cause false indications of mortality due to 

ozone, Environmental Research, 100, 387-393 (2006). 73 CD at 7-96. 
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D. EPA’s Risk Estimate for Mortality and Certain Respiratory Endpoints Fail 

to Confirm an Increase in Risk. 

There are five significant sources of uncertainty in EPA’s risk assessments for mortality and 

respiratory health effects: 

" EPA failed to show that the associations between ozone and health 

endpoints are causal. The risk assessment, therefore, should include a 

probabilistic consideration that the associations may not be causal. 

 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 first and main issue in 

interpreting the epidemiologic associations is determining the cause of the observed effects. 

Chapter 5 of the Second Draft SP acknowledged such noting “the most important uncertainty is 

the extent to which the associations between O3 and the health endpoints included in the 

assessment actually reflect causal relationships.”74 (The final SP acknowledges the five sources 

of uncertainty as “major” at pages 5-42 and 5-43) Although there clearly are positive 

associations in the literature for these health endpoints, the overall pattern of associations is not 

biologically plausible. In multi-city studies, there is an implausibly wide range of associations 

for mortality from strongly positive in some cities, to no effect in some cities to strongly negative 

(implying protective effects) in some cities. The full range for several multi-city studies is 

shown below in Table 1. 

Table 1 

Range of Ozone Individual-City Single-Pollutant Mortality Associations 

in Multi-City Studies Per Standard Ozone Increment as Defined in the CD 

(subject to model selection uncertainty, but not publication bias) 

NMMAPS II (warm season) -6% to + 6% 

Gryparis et al. (warm season) -8% to + 8% 

Gryparis et al. (year-round) -12% to + 6% 

Bell et al. 2004 (warm season) not reported, but large as shown in CD 

Figure 7-17 

Huang et al. 2005 (warm season) -3% to + 8% 

 With this range of heterogeneity, the practice of using Bayesian techniques to shrink the 

city-specific estimates towards the overall mean is highly questionable. The individual-city 

estimates are dramatically pulled towards the mean and this masks the heterogeneity, especially 

when the heterogeneity includes both no effect and protective effects. 

 As noted above, the SP fails to fully acknowledge that the body of studies since 1996 

demonstrates major uncertainties and issues related to model selection and publication bias. 

 

74 Second Draft SP at 5-76. 
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When the full range of studies in the CD is viewed, the range is also very wide but shifted to 

more positive findings. This is shown below in Table 2. The heterogeneity implied by these 

ranges is biologically implausible. While the input from the panelists in the December 2005 

CASAC consultation varied regarding the use of these data, there was much more skepticism 

regarding causality than was the case in the PM review. This is reflected in CASAC’s June 5, 

2006 letter to the Administrator that raises serious issues regarding the use of time-series 

studies.75 The risk assessment, therefore, should include a probabilistic consideration that the 

associations may not be causal. In fact, the Regulatory Impact Analysis (RIA) does evaluate the 

case assuming that ozone mortality associations are not causal. 

Table 2 

Range of Ozone Individual-City Single-Pollutant Associations in Studies 

Included in CD Figures per Standard Ozone Increment as Defined in the CD 

(subject to model selection uncertainty and publication bias) 

Figure 7-8 Emergency visits for asthma - 20% to + 90% 

Figure 7-9 Respiratory hospitalizations - 17 % to + 17 % 

Figure 7-13 Cardiovascular hospitalizations - 12 % to + 35 % 

Figure 7-14 All-cause mortality year-round - 8 % to + 7 % 

Figure 7-19 All-cause mortality by season - 4 % to + 17 % 

 While staff indicate that there is clear and very strong evidence supporting the judgment 

that the relationships are causal for respiratory symptoms in asthmatic children and respiratory 

hospital admissions, staff acknowledges that there is greater uncertainty regarding mortality, 

describing the overall body of evidence only as highly suggestive.76 However, as noted above, 

the latest multi-city study of asthmatic children in eight cities, including Boston, found 

associations with other air pollutants but not with ozone. In addition, the Mortimer study 

implicates air pollution in general, not ozone in particular. Therefore, the data for asthmatic 

effects in children is best described as mixed and inconsistent rather than clear and very strong 

evidence of an ozone effect. The results for respiratory hospital admissions, similarly, are more 

inconsistent than staff acknowledges. 

" Ambient monitors do not provide an adequate estimate of personal 

 exposure. 

 A second major uncertainty staff discusses is related to the adequacy of ambient monitors 

as surrogates for population exposure.77 CASAC’s June 5, 2006 letter points out that “personal 

exposure to ozone is not reflected adequately, and sometimes not at all, by ozone concentrations 

measured at central outdoor monitoring sites.”78 CASAC also pointed out that personal 

 

75 June 2006 CASAC Letter at 3. 

76 Second Draft SP at 5-76. 

77 Second Draft SP at 5-35; SP at 5-43. 

78 June 2006 CASAC Letter at 3. 
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exposures are much lower than ambient and that the susceptible population would be exposed to 

very low concentrations of ozone indeed.79 Finally, CASAC pointed out that ozone 

measurement error obscures true thresholds in the concentration-response relationship and that 

this effect worsens with increasing degrees of measurement error.80 

 Since the true underlying personal exposure-response relationships implied by the 

disputed ozone/mortality associations are stronger by a factor of 2 to 4 than the concentrationresponse relationships suggest (due to the fact that indoor exposures are 2 to 4 times lower than 

outdoor exposures), the range of results in multi-city studies is actually 2 to 4 times larger (both 

positive and negative) than that indicated in Table 1. Such a wide range is biologically 

impossible. 

 In addition, the fact that the underlying personal exposure-response relationships implied 

by these associations are stronger by a factor of 2 to 4 than the ambient concentration-response 

relationships provides an even greater challenge to explain how low ozone concentrations, within 

the range of background, can be causing the premature mortality estimated in the risk 

assessment. If one takes the ozone associations at face value as evidence of effects, then one 

also has to explain how ozone can be both damaging in some cities and protective in others as 

well as damaging, on balance, in the summer and protective, on balance, in the winter. This 

pattern is not plausible and is not adequately acknowledged or discussed in the SP or proposed 

rule. The wide pattern is shown in Figure 7-17 at 7-90 of the CD, but downplayed as just 

heterogeneity due to differences in the cities. 

" The shape of the empirically-estimated concentration-response function is 

uncertain due to uncertainties in model selection, shape of the response 

and confounders. 

A third major area of uncertainty noted by staff is a set of issues related to the 

empirically-estimated concentration-response relationships.81 These include uncertainty related 

to model selection, shape of the response and confounding. As we document above, the 

uncertainty in the “true” relation is much larger than the statistical uncertainty in any given 

association. While staff concludes that a linear response down to background should be applied, 

there are many reasons why this should not be the baseline estimate. CASAC rejected this 

approach for PM even though the PM database was viewed as more consistent. From the 

controlled human studies, we know that the body has mechanisms to deal with oxidative stress 

and the first responses are non-linear, transient and reversible. Without strenuous work or play 

for several hours or more, these responses are not found. Respiratory symptoms in healthy 

children were not included as an endpoint in this review because the CD concluded that there 

was no consistent evidence of an association between ozone and respiratory symptoms in 

children. Earlier drafts of the CD and SP concluded that the evidence for respiratory emergency 

room visits is inconsistent and inconclusive, as is the evidence for cardiovascular hospital 

 

79 June 2006 CASAC Letter at 3. 

80 June 2006 CASAC Letter at 4. 

81 Second Draft SP at 5-34, 5-76; SP at 5-42. 
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admissions. Assuming that there are mortality effects at background levels violates the 

coherence guideline from toxicology whereby lesser effects are seen at lesser doses and greater 

effects at greater doses. For all these reasons, mortality effects and any effects down to 

background levels of ozone should be severely discounted. 

" EPA’s reliance on GEOS-CHEM for estimates of background 

concentrations significantly underestimates ozone background levels. 

 The fourth major uncertainty relates to the use of the GEOS-CHEM model results for 

policy-relevant background.82 As documented in comments submitted to EPA by Air 

Improvement Resources Inc. on behalf of the Alliance [EPA=HQ-OAR-2005-0172-0019] (dated 

January 17, 2006), the model will systematically underestimate the peak background levels. 

Therefore, several alternative higher background assumptions should be used. They could 

include a constant 0.040 ppm background, scaling the seasonal pattern from the Trinidad Head 

data, and a probabilistic formulation that provides yearly peak 8-hour values in the range of 

0.060 to 0.075 ppm. 

" EPA fails to adequately consider the air quality benefits of meeting the 

current standard and overestimates the benefits of alternative standards. 

 The fifth source of uncertainty relates to the adjustment to the air quality data to simulate 

just meeting alternative standards. The SP indicates that the shape of the distribution upon just 

meeting the current standard or an alternative standard is not known.83 Importantly, EPA ignores 

background when rolling back the distribution of ozone concentrations at individual sites. EPA’s 

rollback misses the increase in ozone concentrations near the bottom of the distribution as the 

man-made influence on ozone is decreased. The rollback overestimates the change in ozone at 

mid- and low concentrations and, thereby, overestimates the benefits of alternative standards. 

The rollback should be applied to the man-made portion of ozone not the entire distribution. The 

Agency is in a position to estimate the magnitude of this bias before the final rule using the 

ozone modeling carried out for the RIA, and correct the risk assessment before a final decision is 

reached. 

 As a result of all these uncertainties, the risk results presented in Chapter 5 of the SP and 

summarized in the proposed rule severely mischaracterize the magnitude of the risk and the 

certainty with which the risk is known. Since there are now more issues and inconsistencies 

related to the interpretation of the time-series studies than there were in 1996, when the decision 

was made not to rely on ozone/mortality associations, a similar decision is warranted for this 

review. EPA should acknowledge and discuss the full range of mortality associations in the 

literature, and the public should be informed that this range is not biologically plausible. 

Comparisons of multi-city results with meta-analyses have demonstrated a major issue with 

publication bias as noted by Goodman. Goodman’s caution about publication bias and the 

 

82 Second Draft SP at 5-35, 5-77; SP at 5-43. 

83 SP at 5-43. 
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current weaknesses of single-site reports, along with Koop and Tole’s caution84 about the use of 

point estimates from time-series to set regulatory standards, need to be carefully considered by 

the Administrator before the final rule. 

1. New studies on emergency room visits and hospital admissions do not 

provide supporting evidence of a causal relationship. 

 Although EPA’s interpretation of the data on emergency room visits has changed, the 

evidence remains weak with inconsistent results. The literature on emergency room visits shows 

a very wide range of single-pollutant ozone associations. For asthma–related emergency room 

visits, the range is from –20 to + 80% per standard ozone increment (0.02 ppm change in 24-hr. 

ozone or 0.03 ppm change in 8-hr. ozone) as shown in Figure 7-8 at 7-68 of the CD. For total 

respiratory hospital admissions, the range is from –15 to +15% per standard ozone increment as 

shown in Figure 7-9 at 7-73 of the CD. 

 Although the data remained the same, EPA’s interpretation changed during the ozone 

review process. In the Second Draft CD and the First Draft SP, the conclusion was drawn that 

the body of evidence remains inconclusive regarding effects of ozone on the risk of emergency 

department (ED) visits.85 However, that conclusion was removed from the final CD and SP and 

replaced with a statement indicating that there are generally positive associations in summer 

analyses for asthma ED visits. 

 The proposal incorrectly notes that the studies concluded that co-pollutants are not 

significant confounders: 

Most studies in the United States and Canada indicated positive, statistically 

significant associations between ambient O3 concentrations and respiratory 

hospital admissions in the warm season. However, not all studies found a 

statistically significant relationship with O3, possibly because of very low ambient 

O3 levels. Analyses for confounding using multipollutant regression models 

suggest that copollutants generally do not confound the association between O3

and respiratory hospitalizations. Ozone effect estimates were robust to PM 

adjustment in all-year and warm-season only data.86 

A number of rigorous evaluations of this literature come to different conclusions regarding 

consistency and possible confounding. Anderson, et al. 199887 reported that ozone, SO2, NO2, 

and particles all had positive associations with emergency asthma admissions in London, but that 

 

84 G. Koop and L. Tole, Measuring the Health Effects of Air Pollution: to What Extent Can We Really Say that 

People are Dying from Bad Air, J. of Environmental Economics and Management, 47, 30-54. (2004). 85 See U.S. Environmental Protection Agency, Review of the National Ambient Air Quality Standards for Ozone: 

Policy Assessment of Scientific and Technical Information: OAQPS Staff Paper – First Draft, EPA-452/D-05-002, 

Nov. 2005 at 3-8 (referring to the second draft CD at 7-62 as concluding that “the body of evidence remains 

inconclusive regarding the effects of O3 on the risk of emergency department visits.”) 86 72 Fed. Reg. at 37,832. 

87 H. Anderson, A. Ponce de Leon, J. Bland, J. Bower, J. Emberlin and D. Strachen, Air pollution, pollens, and 

daily admissions for asthma in London 1987-92, Thorax, 53, 842-848 (1998). 
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there was a lack of consistency across age groups and seasons. Anderson et al. also evaluated 

15 other studies of air pollution and daily asthma emergency visits and admissions in the 

literature and concluded “Taken overall, it is apparent that the evidence is not coherent as to 

whether there is an effect of pollution or the responsible pollutant.” They list a number of 

possible reasons for the lack of consistency, including false negatives due to lack of statistical 

power and false positives due to chance, multiple significance testing, post hoc hypothesis 

testing and publication bias. They also note differences in pollution levels and mix between 

cities, the presence of highly correlated pollutants, and that pollutants acting as surrogates for 

unmeasured pollutants or ambient aeroallergens may be involved. They conclude that, while 

there is evidence that all of the pollutants may have an effect on asthma, there is a lack of 

consistency in the specific pollutant responsible. 

 The review of ED studies during the 2004 ozone standard review in California indicated 

that if hospital admissions are affected by ozone, then it is likely that ED visits would also be 

affected, and to a greater degree. However, the ED results are less consistent and summarized as 

being inconclusive, as noted in the first draft SP. The California review88 noted that of 20 

studies they evaluated, 16 reported at least one significant association involving ozone. Given 

that studies without effects are difficult to publish and that these studies often include multiple 

comparisons, it is not surprising that there would be a number of positive associations in the 

literature. However, the California review also acknowledged that there is no clear pattern of 

association with specific respiratory disease outcomes.89 For asthma ED visits, the results are 

described as variable. In the 27 studies of daily ED visits included in Table AX7-3 at AX7-40 of 

the CD, there is a very wide range of results with some multi-year studies reporting positive 

associations in only some years, with some ozone associations not robust to inclusion of other 

pollutants, with many single-pollutant associations being positive for only one of many lags or 

age groups. Therefore, it is hard to accept this data as strong evidence of consistent effects. 

 For hospital admissions, the 1996 risk assessment and the current risk assessment both 

use results from the Thurston et al. 1992 study of New York City. As such, this adds no new 

information. Also, the current risk assessment for hospital admissions uses the results from a 

study reporting no consistent increase in respiratory hospital admissions attributed to ozone in 

Los Angeles, an area with very high ozone levels. EPA uses one isolated result from the Linn et 

al. 200090 study of hospital admissions disregarding the totality of the results of the study, and 

the author’s conclusions regarding a lack of ozone association with hospital admissions. Overall, 

the risk coefficients for the studies EPA used for their 2006 risk assessment are similar to those 

they used in 1996. The slight increase in projected rates of hospital admissions is attributed 

entirely to EPA’s use of a lower background ozone level in the current risk assessment. See the 

general discussion of ozone background levels in Section H. 

 

88 California Air Resources Board, Review of the California Ambient Air Quality Standard for Ozone, Staff Report,

Vol III, Mar. 11, 2005, at 10-39. 

89 California Air Resources Board, Review of the California Ambient Air Quality Standard for Ozone, Public 

Review Draft, Vol. II, June 21, 2004, at 12-37. 90 W. Linn, Y. Szlacheis, H. Gong, P. Kinney and K. Berhane, Air pollution and daily hospital admissions in 

metropolitan Los Angeles, Environmental Health Perspectives, 108, 427-434 (2000). 
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2. Overall, the school absence data are weaker than noted in the 

proposed rule and do not confirm causality or effects below the 

current standard. 

 A review of the literature shows that the results of school absence studies are highly 

dependent on the statistical approach employed. The SP notes that the association between 

school absences and ozone was assessed in two relatively large field studies.91 The SP discusses 

the Chen et al. 2000 and Gilliland et al. 2001 studies of school absences, but quotes the CD that 

further replication is needed before firm conclusions can be drawn. The final CD discusses 

three analyses of the school absence data from the Southern California Children’s Health Study 

(Gilliland et al. 2001, Berhane and Thomas 2002, and Rondeau et al. 2005) that used different 

statistical approaches and assumptions, and came to very different conclusions concerning the 

presence and magnitude of an ozone effect using the same data set.

92 This is an indication that 

the choice of the statistical approach used to analyze the data can change the findings 

dramatically. Overall, the evidence for school absence associations with ozone is weaker than 

noted in the SP or the proposed rule. 

E. EPA Improperly Characterizes the Impact of New Information Since the 

Last Review, Particularly as it Relates to Mechanisms of Ozone Action and 

Support for Causality of Mortality and Other Important Epidemiological 

Health Endpoints. 

 Controlled studies with animals and cell systems fail to provide evidence for either 

systemic effects or cardiovascular effects except at very high dose levels. There is now a large 

body of controlled studies with animals and cell systems that provide information on ozone 

effects and the mechanisms that cause those effects. The determination of the medical 

significance of single or repeated exposures to ozone at various levels and the plausibility of 

various health effects needs to be evaluated with consideration of the body’s defense 

mechanisms against pollutants in general and an irritating gas such as ozone, in particular. These 

defenses include the presence of antioxidants in the epithelial lining fluid, the mucociliary 

clearance system, alveolar macrophages and aspects of the immune system that protect the lung 

from physical injury, infectious disease and inhaled particles. The CD notes that ozone reacts 

preferentially with ascorbate, reduced glutathione, and urate (all antioxidants) in the epithelial 

lining fluid in a protective response.93 Ozone also reacts with the carbon-carbon double-bond in 

polyunsaturated fatty acids. The products of these reactions can signal cellular responses such as 

inflammation. The CD notes that various models of these reactions do not agree as to whether 

ozone can penetrate the lining fluid and reach the epithelial cells.94 

 The review by Mudway and Kelly95 indicates that ozone is a highly reactive gas that is 

consumed by reactive processes on reaching the first interface in the lung and the lung lining 

 

91 SP at 3-12. 

92 CD at 7-57 to 7-60. 

93 CD at 5-5. 

94 CD at 5-2. 

95 I. Mudway and F. Kelly, Ozone and the Lung: A Sensitive Issue, Mol. Aspect. Med., 21, 1-48 (2000). 
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fluid compartment. They note that reactions between ozone and antioxidants tend to dominate in 

this compartment and these are generally thought of as beneficial or protective interactions. In 

their review, Mudway and Kelly discuss a range of antioxidant defenses. Mudway and Kelly 

further conclude that when ozone is relatively low-- probably less than 0.08 ppm -- the majority 

of ozone will be neutralized by reactions with uric acid in the nasal passages and upper airways. 

 As the ozone dose increases, the first effects of ozone are transient, reversible lung 

function decrements that are a reflex response due to vagal nerve receptors that involuntarily 

inhibit maximal inspiratory effort. This response is the body’s reflexive reaction to the presence 

of an irritant gas and is unrelated to sensations of discomfort. Although it is well-established that 

ozone causes transient, reversible lung function decrements, the observational evidence argues 

against the presence of chronic lung function decrements related to ozone which, if present, 

would be a public health concern.96 The acute decrements are decrements in the performance of 

the lung function test (that requires maximal inspiratory effort) and not a change in lung function 

of any clinical or pathological significance. The threshold for these first effects varies depending 

on ozone concentration, time of exposure and breathing rate. At somewhat higher exposures, 

there are mild symptoms and sensations of discomfort that also occur. These are also transient 

and reversible. 

 As the dose is increased, the reflex response noted above and then immune system 

responses begin to come into play. Even the immune system responses which are noted as the 

first indications of “inflammation” are physiological processes that occur in all living organisms 

under the stimuli of daily life. The first reported changes (that occur in humans with heavy 

exercise after 1- to 3-hours above a threshold of 0.18 to 0.20 ppm) are small and reversible and 

well within the range of physiological variability. They fall into the category of biochemical 

markers that the American Thoracic Society indicates do not necessarily imply adversity. For 

example, Mudway and Kelly note that for neutrophils transiting into the lung -- one of the 

earliest of these responses -- it is not clear if the response should be considered beneficial 

(functioning to clear necrotic cells) or detrimental (leading to an active inflammation with tissue 

injury). The CD notes that generally, “the initiation of inflammation is an important component 

of the defense process; however, its persistence and/or its repeated occurrence can result in 

adverse health effects.”97

 Based primarily on animal studies, after repeated doses that induce inflammation or acute 

high concentration doses, the acute inflammation can develop into chronic inflammation, 

continued inflammation can alter the structure and function of pulmonary tissue, and tissue 

injury and/or inflammation can interfere with the lungs response to other challenges such as 

other pollutants, viruses, bacteria, and allergens. In general, lesser effects are seen at lesser doses 

and greater effects at greater doses. There is little evidence for either systemic effects or 

cardiovascular effects from the literature on controlled studies unless the doses are such that 

there are strong respiratory effects. 

 

96 72 Fed. Reg. at 37,833. 

97 CD at 5-32. 
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 In controlled studies, there are many instances of attenuation of some ozone responses 

with repeated exposures. In a general sense, these are manifestations of the body’s defense 

mechanisms dealing with and adjusting to the presence of an irritant gas. 

 There is also now a large body of information related to ozone health effects from 

observational (statistical correlation) studies that can lead to a hypothesis of exposure cause and 

health effects but cannot confirm cause and effect. Since observational (statistical correlation) 

studies cannot by themselves establish cause and effect, a number of factors need to be evaluated 

before any given association of ozone with a health outcome can be viewed as causal or a real 

health effect. These factors include the strength, consistency, coherence and biologic 

plausibility. Biologic plausibility involves both the kinds of effects seen and the doses that cause 

the effects. 

 Based on the kinds of effects seen in well-designed controlled human exposure studies, 

one might predict finding acute lung function decrements, respiratory symptoms, and respiratory 

inflammation in susceptible subjects or in the healthy population in observational studies. One 

might also consider evidence of chronic respiratory problems associated with ozone plausible. 

One would not expect to see associations with cardiovascular hospital admissions or 

cardiovascular mortality, but one might not be surprised to see associations with respiratory 

hospital admissions or emergency room visits or possibly respiratory mortality. With regard to 

dose plausibility, one would expect to see thresholds in the data with effects at higher ozone 

concentrations or in subjects who exercise outdoors in the afternoon. 

 When the epidemiological literature of statistical correlation studies is compared to this 

expectation, there are areas of agreement and areas of disagreement. The small lung function 

decrements reported in field studies of children at summer camps and in other populations 

spending time outdoors may be real but, based on EPA’s guidelines are not medically of 

concern.98 Moreover, EPA indicates there is no consistent association with symptoms in healthy 

children or adults. In addition, there is less consistency in the association with symptoms or 

medication use in asthmatics than EPA claims. The data on respiratory hospital admissions or 

emergency room visits is also less consistent than EPA claims. Whether the positive ozone 

associations in the literature for respiratory morbidity are real health effects is not clear at 

present. 

 The fact that there is no consistent chronic ozone signal in the data is probably a result of 

the very low day-to-day exposures of either the general population or the susceptible population. 

For example, in cities where the day-to-day monitored ozone concentrations range from 0.01 to 

0.08 ppm, the personal ozone exposures of the population are on the order of 0.01 to 0.04 ppm 

 

98 In the 1996 review, the results of six summer camp studies were analyzed to estimate a 2 to 3% decrease in FEV1

at 0.12 ppm ozone, which is well within the range of normal measurement variability and well below the 10 to 20% 

changes which are considered moderate and potentially of health concern in the SP. Additional studies published 

since the 1996 review, for the most part, confirm the earlier results. The issue in interpreting these studies is not 

whether there are small changes in the performance of lung function tests, but what these small changes mean for 

public health given the involuntary reflex mechanism causing the changes. 
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during normal activity.99 The mean personal exposures of the population are at or below the 

mean background, when considering the fact that people spend 90 percent of their time indoors 

where ozone concentrations are significantly lower. Such personal exposures do not trigger 

moderate FEV1 responses through the vagal mechanism and have not been shown to trigger 

inflammation. 

 It is not clear how such low personal exposures could cause or contribute to the 

premature mortality estimated in the risk assessment. The lack of a cardiovascular hospital 

admissions signal in the data is not consistent with the mainly cardiovascular mortality 

associations with ozone. The likelihood that systemic effects or cardiovascular effects are 

causing mortality at the low day-to-day personal exposures of the population is also extremely 

low. As noted in the CD, by protecting against respiratory effects, systemic effects will likely be 

protected against also.100 While the possibility of acute cardiovascular effects is raised in the CD 

based on limited epidemiologic findings, the controlled study of Gong et al.101 which exposed 

subjects to 0.3 ppm ozone for three hours with exercise found little direct effect of ozone on the 

heart or vasculature for hypertensive or healthy subjects even though many pertinent variables 

were evaluated. Gong concluded that they did not find convincing evidence of significant direct 

cardiovascular effects from ozone exposure, analogous to effects reported in laboratory animals. 

The indirect effect they report, impaired gas exchange, can be explained as an effect secondary 

to the respiratory effects of the high ozone exposures. 

 Another possibility that is discussed in the CD and SP to explain a small positive warm 

season ozone association with mortality is that ozone is acting as a surrogate for other 

photochemical products. However, as noted above, greater warm season associations have been 

shown for all pollutants and the CD indicates that most widely present non-ozone oxidants have 

not been shown to have adverse effects in toxicological studies.102

 Assuming that there are mortality effects down to background violates the coherence 

guideline from toxicology, whereby lesser effects are seen at lesser doses and greater effects at 

greater doses. For example, Figure 5-15 at 5-79 of the SP shows that the vast bulk of the 

estimated mortality is attributable to days on which the 24-hour ozone is 0.040 ppm or less. This 

ozone level was assumed as mean background in the prior review. Since people spend 90 

percent of their time indoors where the ozone exposure is ! to " of the outdoor level, the 

personal exposures implicated as potentially causing mortality are well below background and 

there are no medically significant physiological ozone responses at such levels. 

 As discussed above, the single-pollutant time-series studies that are the basis for the 

respiratory admissions and mortality estimates are subject to a number of criticisms, regarding 

 

99 CD, Table 3-3, at 3-64. 

100 CD at 5-57. 101 H. Gong, R. Wong, R. Sarma, W. Linn, E. Sullivan, D. Shamoo, K. Anderson and S. Prasad, Cardiovascular 

effects of ozone exposure in human volunteers, Am. J. Respir. Crit. Care Med., 158, 538-546 (1998); A full report of 

the Gong et al. 1998 study is available as a report to the California Air Resources Board, Final Report, Contract No. 

93-327, May 2000. 

102 CD at 7-2. 
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publication bias, model selection uncertainty, and an unrealistic range of positive and negative 

associations in systematic analyses. For all these reasons, EPA should assign significantly less 

weight to mortality effects and any other respiratory effects extrapolated down to background 

levels based on these studies. 

 Similarly, in both the prior review and the current review, the possibility that there is no 

threshold for ozone effects was considered, primarily based on the observational results. The 

proposed rule now admits uncertainty with regard to threshold effects: 

In summary, the Criteria Document finds that, taken together, the available 

evidence from clinical and epidemiological studies suggests that no clear 

conclusion can now be reached with regard to possible threshold levels for O3-

related effects (EPA, 2006a, p. 8-44). Thus, the available epidemiological 

evidence neither supports nor refutes the existence of thresholds at the population 

level for effects such as increased hospital admissions and premature mortality.103

The likelihood of a threshold should also be considered in drawing any conclusions 

regarding potential mortality risks from exposure to ozone levels at or below the current 

standard. 

F. The Clean Air Act Does Not Require EPA to Set Standards That Eliminate 

All Risk. 

 Section 109 of the CAA requires the Administrator to set a primary standard, the 

attainment and maintenance of which in the judgment of the Administrator, are requisite to 

protect the public health with an adequate margin of safety. EPA’s task is to establish standards 

that are “neither more nor less stringent than necessary” to protect public health. This does not 

mean zero risk, but rather at a level that reduces risk sufficiently so as to protect public health 

with an adequate margin of safety. As Justice Breyer noted: 

Section 109(b) (1) directs the Administrator to set standards that are “requisite to 

protect the public health” with “an adequate margin of safety.” But these words 

do not describe a world that is free of all risk -- an impossible and undesirable 

objective. . . . Nor are the words “requisite” and “public health” to be understood 

independent of context. We consider football equipment “safe” even if its use 

entails a level of risk that would make drinking water “unsafe” for consumption. 

And what counts as “requisite” to protecting the public health will similarly vary 

with background circumstances, such as the public’s ordinary tolerance of the 

particular health risk in the particular context at issue. The Administrator can 

consider such background circumstances when “decid[ing] what risks are 

acceptable in the world in which we live.”104 

 

103 72 Fed. Reg. at 37,840. 104 Whitman, 531 U.S. at 494-95 (Breyer, J., concurring in part and concurring in judgment) (citation omitted). 
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EPA states in the preamble that its task under Section 109 is to establish standards that 

are neither more nor less stringent than necessary for these purposes. Lowering the standard in 

light of the 1997 determination would result in controls that would be more than necessary to 

protect public health. 

The Supreme Court has agreed with EPA that “requisite” under Section 109 means 

“sufficient, but not more than necessary.”105 The material presented in the CD and SP do not 

support EPA’s proposal to lower the standard. As discussed further in these comments above, 

EPA’s own assessment of the risks fails to show an increase in risk from exposure to ozone. In 

fact, as stated above, much of the evidence supports a reduction in risk. Given EPA’s data 

showing limited risks from exposure to the current standard and EPA’s analysis of the studies 

which shows greater, not less uncertainty, in the likelihood that the observed effects are caused 

by ozone, EPA should retain the current standard. As EPA states in the preamble, its task under 

Section 109 is “to establish standards that are neither more nor less stringent than necessary.”106 

G. Since EPA Has Not Provided a Reasonable Analysis Supporting its New 

Judgment on What is Requisite to Protect Public Health or Welfare, its 

Actions Could Be Found to Be “Arbitrary and Capricious.” 

In exercising his judgment to revise the existing NAAQS, the Administrator must provide 

a reasonable analysis for the change. Specifically, EPA must explain why its earlier judgment 

regarding what is requisite to protect public health or welfare no longer governs. To reverse its 

position in the face of precedent that is not persuasively distinguished is arbitrary and 

capricious.107 Given that EPA’s estimate of health risks has declined and our understanding of 

the uncertainty surrounding the results of the health studies has increased, EPA cannot 

persuasively say why it must depart from its 1997 decision that the current standard is requisite 

to protect public health. 

H. EPA Has Not Correctly Evaluated the Potential Risk Reduction as a Result 

of its Proposed Change to the Current Ozone Standard. 

 In the 1997 final ozone rule, EPA estimated, based on monitoring data, that background 

levels from natural sources could be as high as .07 ppm. This fact was important to EPA’s 

decision regarding the level of ozone deemed requisite to protect public health with an ample 

margin of safety: 

As many commenters have noted, based on information in the Criteria Document 

with regard to ambient concentrations of O3 from background sources, an 8–hour 

standard set at a 0.07 ppm level would be closer to peak background levels that 

infrequently occur in some areas due to non-anthropogenic sources of O3

 

105 Whitman, 531 U.S. at 473 (citation omitted). 106 72 Fed. Reg. at 37,820. 107 Motor Vehicle Mfr.’s Ass’n, 463 U.S. at 42 (presumption “against changes in current policy that are not justified 

by the rulemaking record”). 
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precursors, and thus more likely to be inappropriately targeted in some areas on 

such sources. After taking into account the public comments, and for the reasons 

outlined above, the Administrator finds that a standard set at a level of 0.07 ppm 

is not requisite to protect public health with an adequate margin of safety.108

EPA’s analysis of background levels in the current review is wholly deficient and does not 

support a lowering of the standard. 

1. In contrast to the 1997 Review, EPA failed to evaluate the extreme 

values of ozone background levels. 

 Uncontrollable ozone background levels due to transport of stratospheric air (high in 

ozone) into the troposphere, transport of man-made polluted air from locations outside the U.S., 

and photochemical formation from natural NOx and VOC emissions can significantly constrain 

an area’s ability to reduce ozone concentrations. As discussed in the next section, the 

uncontrollable background also plays a pivotal role in EPA’s estimate of the potential health 

benefits of further reductions in the ozone standard. In previous ozone reviews, EPA evaluated 

this background primarily based on measured observations of ozone and other compounds in 

remote locations. In the current review, the CD discusses estimates of background from both 

observations and models, but the SP relies entirely on one global chemical transport modeling 

study to model an estimated mean background. 

Because of the form of the standard, the background related to the extremes of the 

distribution of the daily maxima, as well as the means, must be evaluated as was done in the 

1997 Review. Ozone background levels must be evaluated for each ozone metric being 

considered for the primary and secondary standards. Since extreme value forms of the ozone 

standard are being proposed, then measured ozone values or modeled estimates of the extremes 

of policy-relevant background (PRB) must be considered. In previous ozone reviews, both the 

means and extremes of background were evaluated. For example, the Agency’s Staff Paper in 

the previous review concluded: 

...a reasonable estimate of the background O3 concentrations near sea level in the 

U.S. for a 1-hour daily maximum during the summer is usually in the range of 

0.03 to 0.05 ppm. At clean sites in the western U. S., the maximum annual hourly 

values are in the range of 0.06 to 0.075 ppm.109 

In the current review, the SP relies solely on the Fiore et al. 2003110 global modeling study to 

estimate mean background. However, the CD notes several important limitations of that study 

and the need for additional work to evaluate PRB with an ensemble of models comparing the 

 

108 62 Fed. Reg. at 38,868. 109 U.S. Environmental Protection Agency, Review of the National Ambient Air Quality Standards for Ozone: 

Policy Assessment of Scientific and Technical Information: OAQPS Staff Paper, EPA-452/R-96-007, June 1996 at 

20.

110 References denoted by author and year in the text can be found in the CD and SP . 
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model results with observations.111 The large grids in the global model mix air parcels of 

different composition and origin in an unrealistic way, severely limiting its ability to accurately 

simulate local photochemical activity, intercontinental transport, and the impact of stratospheric 

air inserted into the troposphere. The CD notes the need to include models with greater 

resolution to understand variability on shorter time scales and variability due to processes that 

are not captured in the global models. Until this is done, a range of background estimates from 

observations only should be used by the Agency. Because of the acknowledged limitations of 

global models, observations should be the primary source for estimates of extreme values of 

background at specific locations. 

The failure of the current final SP to provide information on the extremes of background is a 

serious omission. As a result, the ranges recommended by CASAC and EPA staff overlap with 

the extremes of background and are unlikely to be achievable in some areas of the country. 

2. EPA’s definition of PRB incorrectly excludes man-made emissions 

from Canada and Mexico. 

 The Agency defines a PRB as those concentrations that would result in the U.S. in the 

absence of anthropogenic emissions in North America; i.e. leaving no room for ozone caused 

from human activities. However, EPA’s definition of PRB is flawed for several reasons. The 

model exercise EPA relied on omits the contribution from the emissions from agricultural 

activities and it omits consideration of the contribution to ozone from anthropogenic emissions in 

Mexico and Canada. While there can be reductions in emissions from agricultural activities, as 

with other human activities, it would be impossible to drive them to zero. No one contemplates 

the cessation of human activities including the practice of growing crops and raising animals in 

the U.S. Omitting the impact of Canadian and Mexican emissions is also problematic because, 

even though the U.S. may have treaties with these countries, zero anthropogenic emissions and 

ceasing human activities in these countries is not a possible future outcome that can be controlled 

by U.S. regulations. 

3. EPA does not provide sufficient rationale for relying on modeled 

results over monitoring data for assessing background ambient ozone 

levels. 

 The SP notes that because of long-range transport from anthropogenic source regions 

within North America, estimates of PRB cannot be derived solely from measurements of 

ozone.112 However, it goes on to state that PRB estimates must be based on modeling. This is 

not true.113 While the transport of plumes from urban areas is well documented in the literature, 

the CD offers no observation-based analyses to demonstrate that the many instances of ozone 

greater than 0.06 ppm that are measured at remote monitoring sites are all caused by transport 

from urban areas. As documented in Volume II (Annexes 2 and 3) of the CD, there are still 

major uncertainties and limitations involved in using atmospheric models. The question is not 

 

111 CD at 3-55. 112 SP at 2-54. 113 SP at 2-54. 
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whether to use observations or models, both observations and models should be used to estimate 

PRB. 

For example, a recent paper by Jaegle, et al.114 used satellite observations of NO2

columns to derive estimates of NOx emissions from fuel combustion, biomass burning and soils. 

They conclude that there is a significant role for soil NOx emissions at northern mid-latitudes 

during summer, where they account for nearly half that of the fuel combustion source and a 

doubling of the inventory used in the GEOS-CHEM model. They further conclude that the 

contribution of soil emissions to background ozone is likely to be underestimated by the current 

generation of chemical transport models. 

There are NOx emissions from soils due to microbial processes. Fertilized agriculture 

produces the highest soil NOx emissions. By turning off the agriculture source in their PRB 

analyses, Fiore et al. systematically underestimated uncontrollable background. Since the total 

soil source is twice as high as used in the GEOS-CHEM model, Fiore et al. also misallocates the 

NOx between fuel combustion and natural sources. 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 may also help explain the discrepancy between the locations of elevated SUM06 and 

W126 and the major populated areas of the country. 

4. The proposed rule ignores the conclusions of several researchers and 

previous conclusions of EPA regarding maximum background levels. 

 Recently, Vingarzan115 reported the range of annual maxima at background stations in the 

U.S. and Canada. The annual maxima (1-hour) at Western U.S. and Canadian background sites 

approached or exceeded 0.08 ppm. 

 The level of background ozone first became a policy issue in 1971 when EPA set the 

NAAQS for Photochemical Oxidants at a concentration of 0.08 ppm for 1-hour, not to be 

exceeded more than once per year. In 1978, Singh et al.116 reported an analysis of long-term 

ozone data from remote sites that indicated summertime average daily 1-hour maxima in the 0.04 

to 0.05 ppm range but maximum 1-hour concentrations that can approach or exceed 0.08 ppm in 

the spring. Singh et al. concluded that achievement of a yearly 1-hour ozone standard of 0.08 

ppm may be impossible. 

 

114 L. Jaegle, L. Steinberger, R. Martin and K. Chance, Global partitioning of NOx sources using satellite 

observations: Relative roles of fossil fuel combustion, biomass burning, and soil emissions, Faraday Discussions, 

130: 407-423 (2005). 

115 R. Vingarzan, A review of surface ozone background levels and trends, Atmospheric Environment, 38, 3431-

3442 (2004).

116 H. Singh, F. Ludwig and W. Johnson, Tropospheric ozone concentrations and variabilities in clean remote 

atmospheres, Atmos. Environ., 12, 2185-2196 (1978). 
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 When EPA revised the federal 1-hour ozone standard in 1979 to 0.12 ppm, the Agency 

acknowledged that: 

Field measurements at some remote sites, where man-caused ozone is likely to be 

negligible, have shown low-but not insignificant- rates of exceedances of the 0.08 

ppm level originally proposed for the secondary standard.117 

In 1989, Logan118 reported the results of an analysis of ozone data from rural locations in 

the U.S. Logan reported that ozone concentrations above 0.080 ppm were common in rural areas 

of the Eastern U.S. in spring and summer (occurring between about 2 and 8% of the time) but 

were unusual at remote western sites, occurring less than 0.5% of the time. Logan also pointed 

out that concentrations of NOx in rural areas of the east are frequently high enough to permit 

significant photochemical formation of ozone during favorable weather conditions, but that NOx 

concentrations are much lower in remote regions of the west. The low NOx concentrations in 

the west are expected due to the low population and emissions density, and effectively limit the 

local formation of ozone in these air masses. Logan also reported that the median ozone 

concentrations of 0.03 to 0.04 ppm were similar at rural sites across the country even though 

there is a much greater population and emission density in the Eastern U.S. than in the Western 

U.S. 

 Lefohn and Foley119 reported in 1991 on an analysis of ozone data from 26 Class I 

national parks and wilderness areas. For the seven cleanest sites, the yearly maximum 1-hour 

average concentrations were in the range of 0.06 to 0.075 ppm. 

 In 1996, Altshuller and Lefohn120 published an analysis of background ozone in the 

planetary boundary layer of the U.S. They selected 11 sites for analysis. The criteria they used 

included using sites receiving the cleanest air masses from the upwind flow off a continent or 

ocean, and sites isolated from the influence of urban plumes or regional ozone formation from 

anthropogenic emissions. They reported that the maximum 1-hour concentrations in the Western 

U.S. in the April through October period ranged from 0.050 to 0.098 ppm and the maximum 1-

hour concentrations at coastal sites ranged from 0.044 to 0.080 ppm. For comparison, daily 

maximum 1-hour concentrations are typically 1.3 times higher than daily maximum 8-hour 

concentrations. 

 In 2001, Lefohn et al.121 reported an analysis that concluded that hourly levels of 0.05 

and 0.06 ppm are often exceeded at Northern U.S. and Canadian sites specifically selected to 

minimize anthropogenic influences. Most occurrences were in April and May but sometimes as 

 

117 44 Fed. Reg. 8202, 8212 (Feb. 8, 1979). 118 J. Logan, “Ozone in Rural Areas of the United States,” J. Geophys. Res., 94, D6, 8511-8532 (1989). 119 A. Lefohn and J. Foley, Estimated Surface-level Ozone Exposures in Selected Class I Areas of the United States, 

paper 91-144.2, presented at the 84th Annual Meeting of the Air & Waste Management Association, Vancouver, 

British Columbia, June 1991. 

120 A. Altshuller and A. Lefohn, Background Ozone in the Planetary Boundary Layer Over the United States, J. Air 

& Waste Management Association, 46, 134-141 (1996). 

121 A. Lefohn, S. Oltmans, T. Dann, and H. Singh, Present-day variability of background ozone in the lower 

troposphere, J. Geophys. Res., 106, D9, 9945-9958 (2001). 
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late as June. They concluded that many of these occurrences were associated with natural ozone 

sources, particularly upper tropospheric and stratospheric air. 

5. Because the PRB varies substantially, there will be times and places 

where the background approaches or exceeds the levels recommended 

by CASAC for both the primary and secondary standards. 

 The SP attempts to limit the discussion of policy relevant background to the 

meteorological conditions generally conducive to peak urban ozone formation. While this is 

often the limiting case for development of control plans, it would not be under the standards 

recommended by CASAC. The issue is not only what the background is on days of maximum 

photochemical potential, but also what the background is on days with the highest background. 

 To illustrate, if the background is 0.04 ppm and the standard is 0.07 ppm, the amount of 

ozone that can be allowed to be formed from man-made emissions is only 0.03 ppm. So even 

with a 0.04 ppm background, a 0.07 ppm standard would allow little room for human activities. 

On a day when the background is 0.06 ppm, there would be even less margin for human 

activities. While this illustration over-simplifies the complex chemical and meteorological 

processes involved in ozone formation and transport, it demonstrates that the variability of 

background due to transport of ozone from upwind natural and non-U.S. man-made sources can 

make some of the standards under consideration unattainable. 

 A practical example of this issue is found in Winner and Cass.122 Winner and Cass 

modeled the Los Angeles Basin over an entire year and evaluated VOC and NOx controls from 0 

to 95 percent. They concluded that the current 8-hour standard may be unattainable in the basin 

even with complete elimination of man-made emissions and, importantly, they found that the 

days with lower than peak ozone were less responsive to VOC and NOx reductions than the peak 

ozone days. This means that the days that are most difficult to control are not necessarily the 

days that produced the peak concentrations in the historical base year. 

6. The lack of consideration of the extremes of ozone background levels 

is an omission that led both the Agency and CASAC to assume that 

the recommended standards are attainable. 

 Ozone background concentrations are an important factor in setting and achieving ozone 

air quality standards and in estimating risk. Background concentrations also play a role in the 

designation of attainment or nonattainment, in the development of State Implementation Plans 

(SIPs), and in the ultimate achievability of any specific standard. EPA’s failure to accurately 

assess ozone background extremes resulted in recommendations for new standards that are 

unachievable. 

 It is clear from the structure of the CAA that Congress assumed that air quality standards 

would focus controls on man-made pollution and would be achievable in reasonable timeframes. 

 

122 D. Winner and G. Cass, Effect of Emissions Control on the Long-Term Frequency Distribution of Regional 

Ozone Concentrations, Environ. Sci. Technol., 34, 2612-2617 (2000). 
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Once a standard is set and designations of attainment/nonattainment are made, the CAA requires 

states to prepare SIPs to achieve the standard. Under Subpart 1, Section 172(a)(2)(A) of the 

CAA, non-attainment areas must attain the primary standard “as expeditiously as practicable, but 

no later than 5 years from the date such area was designated nonattainment.”123 The 

Administrator may extend the attainment date for a period of no greater than ten years based on 

the severity of nonattainment and the feasibility of pollution control measures.124 Under the 

ozone-specific provisions of Subpart 2, the Act assigns ozone nonattainment areas with a series 

of separate deadlines and control requirements based on the degree of nonattainment of the 

former 0.12 ppm 1-hour standard. In both frameworks, the underlying assumption is that the 

standard can be met with man-made controls. 

 The penalty for failure to meet by the designated deadline is a bump-up to a higher 

category with a longer deadline but also more prescriptive control requirements in the control 

region. The penalty for failure to plan properly is federal sanctions. 

 In recommending a range of 0.060 to 0.070 ppm, CASAC apparently assumed that an 8-

hour standard in this range was ultimately achievable from control of U.S. man-made emissions. 

As documented above, it is not at all clear that this is the case. One of the specific charges for 

CASAC under the CAA (Section 109(d)(2)(c)(iii)) is to “advise the Administrator on the relative 

contribution to air pollution concentrations of natural as well as anthropogenic activity.”125 A 

complete reading of the CD indicates that reliance on one particular global model is not a 

scientifically sound way to estimate the contribution of uncontrollable ozone to an extreme value 

standard. 

 The CAA also requires CASAC (Section 109(d)(2)(c)(iv)) to “advise the Administrator 

of any adverse public health, welfare, social, economic, or energy effects which may result from 

various strategies for attainment and maintenance of such national ambient air quality 

standards.”126 Accurate assessment of ozone background levels is key to the photochemical 

modeling used in the SIP development. Photochemical grid modeling has moved from the 

modeling of multi-day episodes in specific urban areas to modeling ozone concentrations 

throughout a season over large regions. For the latter situation, an accurate depiction of 

stratospheric/tropospheric exchange and subsequent transport is necessary. However, the 

simulation of stratospheric intrusions is notoriously difficult in global models because 

stratospheric-tropospheric exchange is an intermittent process—a series of strong exchange 

events separated by more quiescent periods. These events insert stratospheric air high in ozone 

into layers or filaments in the troposphere. Only rarely do these intrusions penetrate to ground 

level intact, but they intermittently insert high concentrations of ozone into the troposphere much 

more often. The layers or filaments of stratospheric ozone eventually mix with surrounding air 

in ways which are not yet fully understood, influencing ozone levels, photochemical activity and 

lifetimes of various species. Because of the complexity of these phenomena, an exceptional 

 

123 42 U.S.C. § 7502(a)(2)(A). 124 42 U.S.C. § 7502(a)(2)(A). 125 42 U.S.C. § 7409(d)(2)(c)(iii). 126 42 U.S.C. § 7409(d)(2)(c)(iv). 
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events policy would not be able to identify the contribution of stratospheric intrusions to groundlevel ozone. 

 When the EPA Administrator set the current federal 8-hour standard, she considered how 

close an 0.07 ppm standard would be to background, noting that “As many commenters have 

noted, based on information in the [CD] with regard to ambient concentrations of O3 from 

background sources, an 8-hour standard set at a 0.07 ppm level would be closer to peak 

background levels that infrequently occur in some areas due to non-anthropogenic sources of O3

precursors, and thus more likely to be inappropriately targeted in some areas on such sources.”127

 The lack of consideration of the extremes of background is an omission that led both the 

Agency and CASAC in the current review to assume that the standards recommended are 

attainable. If an 8-hour ozone standard were established at the lower end of the range 

recommended by CASAC, virtually the entire country would be designated nonattainment, even 

areas that are far removed from significant man-made emissions. It would be impossible to 

develop rational implementation plans for some areas and, for other areas, complete elimination 

of man-made emissions might be required to demonstrate attainment. 

I. EPA Has Not Adequately Considered That in Many Areas of the U.S. 

Additional Reductions, Beyond Those Needed to Meet the Current Standard, 

May Not Be Achievable With Known Control Technology and Could Impose 

Ruinous Economic Consequences. 

 EPA correctly notes that some cities will have difficulty in complying with the current 

standard within the next decade and invites comment on whether EPA can count the health 

benefits from these reductions: 

As a related concern, 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 decade. As a result, the full public health gains in these 

areas from a more stringent 8-hour standard are unlikely to be realized for a 

number of years. In light of the fact that these public health gains may not fully 

materialize within the attainment date structure set forth in the Clean Air Act, 

some commenters question whether the Agency can or should consider these 

projected gains as a health based criterion for its decision making. EPA requests 

comment on this view.128

The situation in several areas is direr than implied in the preceding paragraph. The SIPs 

prepared for the South Coast Air Basin and San Joaquin Valley of California that were due to 

EPA in June 2007 lay out the emission reductions required to attain the current 8-hour ozone 

standard in these air basins. In both cases, the emission reductions required for attainment that 

were determined using photochemical modeling are massive. Both these areas have been 

reducing emissions of ozone precursors for many decades, yet they still require an additional 75 

 

127 62 Fed. Reg. at 38,868. 128 72 Fed. Reg. at 37,881. 
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percent reduction in NOx emissions from current levels to demonstrate attainment.129 The 

overall reduction from uncontrolled levels is well in excess of 90 percent and the required 

reduction in emissions per capita or per unit of economic activity compared to uncontrolled 

levels is even greater. Neither District can identify the control strategies that will provide such 

additional massive reductions so the Districts are each asking to be reclassified to the ‘extreme’ 

category so they can take advantage of Section 185(e)(5) of the CAA, which allows extreme 

areas to submit approvable plans that rely on future advancements in technology, the so-called 

“black-box” emission reductions. 

 The San Joaquin Valley District concludes that currently available technology and known 

technology scheduled for future availability cannot provide sufficient emission reductions to fill 

the attainment gap. It is noted that this would be the case even if money was no object. In fact, 

the District concludes that shutting down all businesses, or shutting down agriculture, or 

removing all truck traffic, or removing all passenger cars, or replacing all motor vehicles with 

the newest and cleanest vehicles at the cost of $60 billion would not fill the attainment gap. The 

District notes that these extreme and unrealistic measures were evaluated only to illustrate the 

magnitude of the problem. 

 The use of the black box allows EPA to approve a SIP without having specific identified 

controls, but the experience with the black box in the South Coast District has not been 

favorable. After decades of research and development, the technologies for pollution control are 

mature and the improvements available now are small and incremental. There are no more lowhanging fruit that are available to provide major reductions in emissions in California. 

Therefore, it is unlikely that either District will be able to identify measures (short of drastic 

measures such as those noted above that would cause economic havoc and be a direct 

contradiction of the Supreme Court decision) to attain the current ozone standard within the 

timeframes required by law, even given the extreme classifications. 

 In addition, the Winner and Cass modeling study, noted above, raises the possibility that 

the modeling of current ozone episodes may not be the limiting case for ozone attainment and 

even more emission reductions may be required than in the 2007 District air quality plans. 

 EPA’s estimate of health benefits from lowering the ozone standard is based on a 

definition of policy relevant background that assumes man-made emissions can be eliminated. 

This, however, goes beyond the reach of the Act and is in direct contradiction with the Supreme 

Court decision. As the proposal notes: 

As discussed by Justice Breyer in Whitman v. American Trucking Associations, 

however, this interpretation of § 109 does not require the EPA to eliminate every 

health risk, however slight, at any economic cost, however great, to the point of 

 

129 See San Joaquin Unified Air Pollution Control District, 2007 Ozone Plan, Apr. 30, 2007; South Coast Air 

Quality Management District, Final 2007 Air Quality Management Plan, June 2007. 
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“hurtling” industry over “the brink of ruin,” or even forcing 

“deindustrialization.”130 

J. The Agency’s Estimates of Health Benefits Are Highly Sensitive to 

Assumptions Regarding Background Levels. 

 The proposed rule notes that changes in the assumed background can either double or 

halve the estimated mortality effects.131 This sensitivity to 0.005 ppm changes in background is 

a demonstration that the bulk of estimated mortality comes from days with ozone concentrations 

that are very low. This is not biologically plausible. 

 The sensitivity of clinical respiratory effects to background assumptions is not as large, 

but is still very important. For example, the Risk Assessment Technical Support Document 

(TSD)132 shows that the number of exposures of lung function responses of healthy and 

asthmatic children (Tables 3-28 and 3-31, respectively) is 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.133 Thus, the choice 

of background is extremely important in evaluating the adequacy of the current standard and in 

estimating the public health impact of a more stringent standard. 

Given all the issues with EPA’s assumed background noted above, the Agency should reevaluate its assumed background and then re-evaluate the clinical risks. Only then can the 

adequacy of the current standard be evaluated on a sound basis. The proposed rule recognizes 

the importance of this issue and indicates additional sensitivity analyses to background will be 

carried out.134 

K. CASAC’s Conclusion That the Current Standard is Unjustified is Based on 

 Unsupportable Assumptions. 

CASAC’s recommendation to tighten the ozone standard was not based on fundamental 

changes in the science from the 1996 review, but rather on EPA’s decision to lower its estimate 

of mean ozone background concentrations and ignore the extremes of background. In 1996, 

EPA staff and CASAC agreed on a range for the 8-hour standard between 0.07 and 0.09 ppm.135 

When queried individually, no one on the 1996 panel recommended a standard below 0.08 ppm. 

Currently, CASAC recommends a standard between 0.060 and 0.070 ppm. 

The major reason for the difference between the two panel’s recommendations is that the 

current panel assumed that mean background was substantially lower than previously thought in 

1997. The current CASAC panel did not carefully consider the extremes of background and so 

 

130 72 Fed. Reg. at 37,820 (quoting Whitman, 531 U.S. at 494). 131 72 Fed. Reg. at 37,862, n.45. 132 E. Post et al., Ozone Health Risk Assessment for Selected Urban Areas, EPA 452/R-07-009, July 2007. 133 U.S. Environmental Protection Agency, Ozone Health Risk Assessment for Selected Urban Areas, EPA-452/R07-001, Jan. 2007, Tables 3-28, 3-31, at 3-70, 3-73 (“RA TSD”). 

134 72 Fed. Reg. at 37,857, n.40. 135 G. Wolff, CASAC Letter, EPA-SAB-CASAC-LTR-96-002, Nov. 30, 1995 (“1995 CASAC Letter”). 
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incorrectly assumed that uncontrollable background was substantially lower than thought in the 

previous review. Based on the information presented to CASAC from the GEOS-CHEM model, 

CASAC was led to believe that ozone background levels never exceed 0.040 ppm. As a result, 

CASAC incorrectly assumed that a standard as low as 0.060 ppm is attainable and that, therefore, 

exposures of concern could be essentially eliminated. 

In the previous review, CASAC concluded that the estimates of risk for various 

alternative standards were very similar after reviewing the risk assessments for both clinical and 

epidemiological endpoints. Specifically, the 1996 panel concluded that there was no “bright 

line” that distinguished any of the proposed standards as being significantly more protective of 

public health.136 In making this judgment, the 1996 panel focused on the overlap and uncertainty 

between the estimates of the percent responding rather than on the absolute number of 

incidences.137 In contrast, the current CASAC Panel focused on the absolute number of 

incidences, even though they are only a very small fraction of the potential number of 

incidences, and again, the differences in incidences at alternate standards are minimal. 

Beyond the error in evaluating background, there are several other ways in which 

CASAC erred in evaluating the scientific information. Although the Second Draft SP showed 

that the risk of lung function effects is lower than thought in 1997, the current CASAC panel 

appeared to believe that the APEX model used in the risk assessment for the clinical effects 

systematically under-predicted measured values.138 In actuality, the model significantly 

overestimated the number of exposures of concern as detailed elsewhere in these comments. 

Although CASAC raised serious questions regarding the use of time-series studies to set 

regulatory standards in its June 2006 letter, those concerns were ignored in the October 2006 

letter which uncritically accepted single-pollutant positive associations as evidence of health 

effects. CASAC failed to provide a reason why the issues raised in the June 2006 letter no 

longer applies. Since the science did not change, the more logical conclusion is that the concerns 

raised in CASAC’s June 2006 letter still apply and should be considered by EPA in its review. 

For example, the June 2006 letter highlights the issue of exposure measurement error in 

time-series studies. In addition, the October 2006 letter acknowledges that “Panel members have 

little insight as to what we would find if we had actual exposure measurements.”139 

Nevertheless, in the October 2006 letter, CASAC claims that ED visits for respiratory disease, 

especially asthma, are relatively strong and relatively consistent, citing Figure 3-4 of the SP as 

evidence.140 However, the apparent consistency in the figure reflects only that there are a 

number of reports of positive associations with various health endpoints in single-pollutant 

models in the literature. 

 

136 See the October 2006 CASAC Letter at 11. 137 1995 CASAC Letter at 2-3. 138 See R. Henderson, CASAC Letter, EPA-CASAC-07-001, Oct. 24, 2006 at 11 (“Oct. 2006 CASAC Letter”). 139 October 2006 CASAC Letter at 10. 140 October 2006 CASAC Letter at 10. 
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In making a judgment with regard to consistency, CASAC did not consider the way EPA 

chose to present the data to establish consistency. If these were controlled studies, we would 

ask how many total experiments were conducted and how many were positive. We should know 

both the numerator (the number of positive associations) and the denominator (the total number 

of studies) before we make a judgment about consistency. For much of the epidemiology, we 

have only the numerator. For a given health endpoint, we do not know how many different 

models, cities, lags, etc. were evaluated. For purposes of drawing conclusions, there is a major 

difference between 6 out of 6 positive associations of ozone versus 6 out of 60 or 6 out of 600. 

CASAC did not evaluate the way EPA chose to present the data to establish consistency. In fact, 

the more rigorous analysis of the full body of data by Anderson et al. 1998 establishes that there 

is little consistency regarding ozone association with ED visits. 

L. Tropospheric Ozone Protects Against UV-Induced Health Effects. 

It is well-established that tropospheric ozone has a beneficial effect along with 

stratospheric ozone in protecting public health from solar UV radiation. A reduction in 

tropospheric ozone would act to increase UV exposures and UV-induced health effects. This 

topic is discussed in Section 10.2 of the CD and the conclusion is drawn that the beneficial 

effects of tropospheric ozone cannot be assessed quantitatively at this time. This conclusion is 

troubling and inconsistent with the science. The health effects from exposure to UV radiation 

are substantial and ozone’s causal link to UV radiation is better established than is the case for 

ozone and daily mortality. For example, the CD concludes that “[t]he current evidence strongly 

suggests a causal link between exposure to UV radiation and the incidence of both nonmelanoma 

and melanoma skin cancer.”141 The CD stresses the uncertainties and limitations in estimating 

beneficial effects and generally characterizes the impacts as small and uncertain. While this may 

be true, it is also true of the adverse health effects from exposure to ozone implied by many of 

the epidemiological associations discussed above. When EPA responded to a court’s remand to 

consider UV-related effects of ground level ozone, various estimates of these effects (made by 

EPA staff, EPA consultants and staff at other government agencies) were discussed at some 

length.142 In all cases, there was no disagreement with the fact that ground-level ozone has 

beneficial effects. The only disagreements centered on the magnitude of the effect or the 

certainty with which it can be estimated. 

EPA now argues that one needs to do a detailed analysis similar to the APEX exposure 

model to estimate the beneficial UV-related effects, and that all the necessary inputs for such a 

calculation are not available. EPA, however, does not adhere to this same view when estimating 

detrimental effects of ground-level ozone on mortality. Instead, a much cruder observational 

approach is tolerated that has enormous uncertainty associated with it. This created a clear 

double standard. 

The proposed rule asks for available studies or data that would be relevant to conducting 

a critical assessment with reasonable certainty of UV-induced health outcomes and how evidence 

 

141 CD at 10-29. 142 68 Fed. Reg. 614 (Jan. 6, 2003). 
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of UV-induced health outcomes might inform the Agency’s review of the primary ozone 

standard.143

Even though EPA indicates it cannot make reliable quantitative estimates of beneficial 

ozone impacts for this rulemaking, quantitative estimates of UV-related health effects have been 

made by EPA and others for various reasons. For example, as part of the estimate of the global 

burden of disease, the World Health Organization (WHO) has estimated that excessive UV 

exposure is responsible for about 1.5 million disability-adjusted life years and over 60,000 

premature deaths per year world-wide primarily due to cataracts and skin cancer.144 The 

situation is complex because people need some UV to maintain adequate Vitamin D levels. In 

the current review, the potential benefits of ground-level ozone should be weighed along with the 

potential harm, using similar approaches for each type of effect. 

The Alliance recommends that EPA use the same methods the WHO and the Agency did 

when estimating UV effects and allocate a reasonable portion of those effects to ground-level 

U.S. man-made ozone. If EPA does not accept such an approach, at a minimum, the Agency 

should acknowledge that its risk assessment estimates of ozone-mortality effects do not provide 

sufficient certainty. 

M. The Scientific Data and Precision of Ozone Measurement Monitors Does Not 

Support Specifying the Standard to the Third Decimal Place. 

In recommending the ozone standard be specified to the third decimal place, CASAC 

overstates the precision and accuracy of current ozone measurements. CASAC recommended 

that the ozone standard be specified to the third decimal place in ppm because current 

measurement technology “allows accurate measurements of ozone concentrations with a 

precision of parts per billion.”145 Although California recently specified an 8-hour ozone 

standard to the third decimal place in ppm, the California Air Resources Board (CARB) staff 

acknowledges that the third decimal place is an uncertain digit.146 At the 0.070 ppm level, CARB 

staff indicated that ozone measurements are uncertain in the third decimal place to the degree of 

plus or minus 0.003 ppm. Another way of expressing this uncertainty is that 95 percent of the 

true values will be within two standard deviations, or plus or minus 0.006 ppm. The EPA 

estimate of precision noted in the SP of plus or minus several percent is consistent as is the 

precision reported for the CASTNET sites where 98 percent of the audits were within plus or 

minus 10 percent. In discussing the uncertainty due to measurement error, Langstaff notes that 

federal reference and equivalent methods are required to have a precision of 0.01 ppm for 1-hour 

average concentrations (40 CFR Ch.1, Section 53.21) and that interference with other pollutants 

 

143 72 Fed. Reg. at 37,837. 144 R. Lucas, T. McMichael, W. Smith, and B. Armstrong, Global Burden of Disease from Solar Ultraviolet 

Radiation, Environmental Burden of Disease, Series No. 13, World Health Organization, Geneva, 2006. 145 Oct. 2006 CASAC Letter at 5. 146 California Air Resources Board, Staff Report, Review of the California Ambient Air Quality Standard for Ozone, 

Staff Report, Vol II, Mar. 11, 2005, at 6-3. 
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and humidity can lead to errors in measurements.147 Given this level of precision, the current 

round-off procedure is appropriate. 

The proposed rule refers to an analysis by Cox and Camalier (2006) that purports to show 

the impact of measurement error on the design value is small -- the order of 1 ppb for precision 

and 1 ppb for randomly occurring instrument bias.148 However, there is no reason to assume that 

the bias is random. EPA has considerable data on the site-specific precision and bias estimates. 

For example, Langstaff reports bias estimates for individual Boston monitors varying between -7 

and + 11 % in 2003 taken from the larger EPA database.149 

Given that the current requirement for the precision of monitors is specified to only two 

decimal places, the staff analysis is not sufficient to support a change to the round-off procedure. 

Making attainment determinations on the basis of the implied precision of the third decimal place 

would be inappropriate. 

N. While EPA Should Retain the Current Standard, the Form of the Standard 

Should Be Changed to the Fifth Highest Daily Maximum 8-Hour Average 

Concentration. 

While the evidence suggests that the current standard should be retained, EPA should 

revise the form of the standard to the fifth highest daily maximum 8-hour average concentration. 

If, as expected, ozone levels attributed to U.S. anthropogenic emissions continue to fall while 

background levels of ozone from biogenic sources and international sources continue to rise, 

more areas will be classified as nonattainment due to meteorological variations. A more stable 

statistic would aid states in their planning efforts and provide regulated entities greater certainty 

as to the control requirements they must meet. Changing the form of the standard to the fifth 

highest daily maximum 8-hour average concentration better comports with the health risks, 

which increase with significance with frequency of exposure. The likelihood of any adverse 

effect warranting protection under the Act with only two exceedances per year of the current 

standard is minimal. 

 

147 2007 Langstaff Memorandum at 11 (citing CD at 2-25 to 2-26). 148 72 Fed. Reg. at 37,874. 149 2007 Langstaff Memorandum, Table 2 at 11-12. 
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II. Comments on EPA’s Proposed Secondary Standard.

 The EPA proposal150 indicates that the Administrator would revise the current 8-hour 

secondary standard with one of two options. The first would be to promulgate a cumulative, 

seasonal standard expressed as an index of the annual sum of weighted hourly concentrations 

cumulated over the 12-hour period from 8:00 a.m. to 8:00 p.m, during the 3-month period in the 

ozone season with the highest index values. This index is referred to as W126, and it would be 

set within the range of 7 to 21 ppm-hours. The second option would be to make the secondary 

standard identical to the proposed primary 8-hour standard. EPA is also soliciting comments on 

an alternative approach that would establish a suite of secondary standards that would contain 

different ambient levels, with each standard set at a level requisite to protect public welfare based 

on the variation in plant effect, use and/or location. Under this approach, the specific standard 

applicable would depend on the classification of areas according to intended use and on the 

nature and sensitivity of the plant species in that area. 

 The Alliance believes that there is no evidence suggesting that the current secondary 

standard should be revised. The existing standard is requisite to protect the public welfare, and 

should not be altered. 

A. A Careful Review of the Existing Scientific Evidence Demonstrates That the 

Existing Secondary Standard is Requisite to Protect Public Welfare.

 

1. All the issues and problems that led the Administrator in 1997 to 

reject the option of a seasonal ozone metric are still relevant. 

 In the 1996 Federal Register notice proposing revised ozone standards, the Administrator 

recognized many limitations and uncertainties in the available data and analyses regarding 

secondary standards. The proposal acknowledged that “the selection of a single averaging time 

for a national standard will of necessity be a compromise...” and “specifying the form of a 

seasonal exposure index to correspond to the relationship between vegetation response and O3

exposure is complicated by the many biological variables that influence the uptake of O3 by the 

plant and plant responses to such uptake.”151 

 The 1996 proposal also acknowledged that “[b]ecause of a lack of monitoring data, 

national air quality typical of agricultural crop growing areas has not been characterized.”152 

Some of the most important caveats and uncertainties concerning the exposure and risk 

assessments for crop yield that were listed in the proposal included “[e]xtrapolating from 

exposure-response functions generated in open-top chambers to ambient conditions,...the lack of 

a performance evaluation of the national air quality extrapolation,...the methodology to adjust 

modeled air quality to reflect attainment of various alternative standard options,... and inherent 

 

150 72 Fed. Reg. at 37,818. 151 61 Fed. Reg. 65,716, 65,738 (Dec. 13, 1996). 152 61 Fed. Reg. at 65,740. 
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uncertainties in models to estimate economic values associated with attainment of alternative 

standards.”153 

 Discussing the quantitative analyses carried out at that time, the proposal indicated that 

“the Administrator acknowledges the significant uncertainties in these analyses and recognizes 

that these benefits should be regarded as rough approximations.”154 Because of the lack of new 

data or substantive improvements in the risk assessment, these same issues remain today, 

contributing a similar degree of uncertainty, as was the case in the prior review. 

 The 1996 CASAC Panel did not reach consensus on key issues regarding protection of 

vegetation. Of the four Panel members with expertise in ozone vegetation effects, two indicated 

that the open-top chamber experiments produced results that overestimated the effects of ozone 

on plant yield; the other two did not agree with there being a positive bias.155 With regard to the 

seasonal cumulative metric under consideration at that time, SUM06, two of the experts thought 

the cumulative form was appropriate but they disagreed as to the appropriate level. The other 

two experts were uncomfortable with a SUM06 form because they felt it lacked a biological 

basis.156

 The main reasons given for the lack of agreement were lack of sufficient rural ozone data 

and the lack of relevant plant exposure studies. The Panel concluded that “[f]ive years 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, to avoid the shortcomings of the 

open-top chamber experiments, then 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 at the most 

reasonable cost.”157 

 Ten years have now elapsed, and the same concentration-response functions from the 

open-top chamber studies of the 1980s are still the only viable data to use to estimate crop loss 

and the called-for increase in rural ozone monitoring has not taken place. The 1996 CASAC 

Panel agreed that the estimates of crop loss at that time were highly uncertain.158 

 Although the current CASAC panel recommends a stringent cumulative secondary 

standard, there is little in the new data that reduces the uncertainty recognized in 1996. In fact, 

the current CASAC panel’s recommendations for the appropriate range of the standard come 

from a 1997 workshop on secondary ozone standards.159 If the workshop recommendations are 

to be used for standard setting, then the studies underlying their basis, as well as the method for 

reaching the recommended values, should be stated in more detail than in the cited workshop 

 

153 61 Fed. Reg. at 65,740. 154 61 Fed. Reg. at 65,743. 155 G. Wolff, CASAC Letter, EPA-SAB-CASAC-LTR-96-006, Apr. 4, 1996 at 2 (“1996 CASAC Letter”). 156 1996 CASAC Letter at 3-4. 157 CASAC Letter 96-006, Apr. 4, 1996, at 5. 158 1996 CASAC Letter at 3. 159 See W. Heck and E. Cowling, The need for a long-term cumulative secondary ozone standard – an ecological 

perspective, Environmental Manager, pp. 23-33, January 1997. 
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summary. The basis for establishing a standard should be transparent and reproducible. One of 

the current CASAC Panel points out that the state of the science regarding vegetation effects has 

not changed very much since the last review and, in a minority view, indicates that the case has 

not been made for a biological basis for either the SUM06 or W126 metric.160 

2. There are problems, flaws and concerns with the SP analysis and 

vegetation risk assessment that preclude the establishment of a 

separate secondary standard to protect vegetation. 

a. Extremes of background ozone concentrations were not 

considered. 

 The same analyses, arguments, and data that apply to consideration of background for the 

primary standard also apply to the secondary standard. As discussed above, 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 Multi-Scale Air Quality (CMAQ) modeling 

system , which EPA evaluated when developing an “as-is” W126 exposure surface performed 

extremely poorly in predicting the observed 2001 SUM06 and W126 in the west. When the 

model was used to predict the SUM06 values at 300 western locations, it had over 300 percent 

normalized mean error and almost a 300 percent normalized mean bias. This means that the 

sources and processes that contribute to substantial levels of both SUM06 and W126 in rural and 

remote areas in the Western U.S. are not well-captured in state-of-the-art chemical transport 

models. Since CMAQ was developed to focus on the impact of U.S. man-made pollution 

sources, the poor prediction performance suggests other sources and processes are responsible 

for a substantial portion of the elevated SUM06 and W126 levels observed in rural and remote 

western areas. 

b. The pattern of current W126 levels suggests contributions from 

both man-made emissions and uncontrollable background. 

 The map of “as-is” W126 levels included as Figure 7-6 at 7-28 of the SP shows W126 

levels exceeding 7 ppm-hr throughout many areas of the country. Although some areas of 

elevated W126 occur in and downwind of major man-made source areas, other elevated W126 

areas occur in less populous areas including: Utah, New Mexico, Wyoming, Kansas and 

Oklahoma, states where population and density of man-made emissions are only a small fraction 

of that in the Eastern U.S. 

 The overall pattern of W126 suggests both a contribution from U.S. man-made emissions 

and a background component that could involve biogenic emissions, agricultural emissions, 

long-range transport from non-U.S. sources and a stratospheric component. In particular, W126 

levels greater 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. These 

 

160 2007 CASAC Letter at C-17- C-18. 
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levels could be explained in part by NOx emissions from soils due to microbial processes. 

Jaegle, et al.161, using satellite observations of NO2 columns, found that soil NOx emissions were 

twice as high as assumed in the GEOS-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. 

c. EPA and CASAC relied on an inadequate model in recommending 

secondary standards that fall within the range of uncontrollable 

background. 

 EPA and CASAC assume, incorrectly, based on the Fiore et al. 2003 global modeling 

analysis, that SUM06 or W126 is not confounded by background ozone. However, substantial 

levels of both SUM06 and W126 in rural and remote areas are not obviously related to known 

man-made source areas, and are likely due to such factors as soil NOx emissions. As noted 

above, both models and observations must be used when determining the extent of 

uncontrollable ozone. Otherwise, a secondary ozone standard may be implemented that is 

unattainable in reality. 

 In Figure 3, longer-term W126 data are plotted for a series of sites across the Western 

U.S. from the California/Oregon border across Idaho, Wyoming and into South Dakota. All of 

these sites are substantially removed from major emission sources and have W126 values 

generally in the range of 0 to 20. Note also that there are wide variations from year-to-year. 

There are several important implications from this data. 

i. Even sites removed from obvious source areas have a substantial number of hours 

annually at or above 0.06 ppm, often on the order of 100 to 200 hours per year. 

Importantly, all these sites have 8-hour design values of 0.06 or greater. 

ii. The W126 metric varies substantially from year-to-year even in rural and remote 

areas lacking any obvious influence from anthropogenic sources. In addition, in 

2001, the year used by EPA to model “as-is” W126, it appears to be an anomaly 

compared to all the other years. Thus, the ranges recommended for a W126 

standard are even more stringent and more likely confounded by background than 

apparent at first glance. With such large variations, if a W126 or other cumulative 

standard is set using only one year’s data, areas could bounce in and out of 

attainment, causing havoc with implementation planning efforts. Even three years 

of data does not appear to provide a stable statistic for implementation planning. 

 

161 L. Jaegle, et al. (2005) at 130, 407-423. 
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0

2

4

6

8

10

12

14

16

Calendar Year

Butte, ID

Campbell, WY

Custer, SD

Jackson, OR

Jackson, SD

Minnehaha, SD

Pennington, SD

Siskiyou, CA

Teton, WY

W126 Trends by Rural County

Air Improvement Resource, Inc.

Figure 3 

d. There is no new data on vegetation effects suitable for establishing 

secondary standards. 

 The vegetation risk assessment utilizes the crop yield loss and seedling growth data used 

in the previous review. Due to the lack of new data, the vegetation risk assessment does not 

materially reduce the major uncertainties that were acknowledged in the 1996/1997 review. 

e. The choice of an appropriate ozone metric to protect vegetation is 

difficult. 

 Although cumulative ozone metrics offer advantages over the form of the primary 

standard to protect vegetation, the limitations and simplifications involved with cumulative 

ozone metrics are still of concern. For example, the simplifying assumptions that plant exposure 

to ozone equals plant response, and that there is a uniform threshold or response function for 

plant injury are both known to be incorrect. In spite of these issues, EPA staff and CASAC 

recommend a seasonal cumulative secondary ozone standard. Although more biologically-based 

flux-based models offer promise, there are insufficient data to apply them at present. The 

decision to ask for comments on establishing a suite of secondary standards is an implicit 

acknowledgement of the problems with a national seasonal cumulative standard. However, there 

is insufficient data to establish a suite of standards that would vary with vegetation type and/or 

location and it is not clear how such a suite of standards could be implemented under the current 

CAA. 
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f. The European experience with cumulative standards has been 

disappointing. 

While both EPA staff and CASAC recommend a cumulative ozone metric, the European 

experience with cumulative ozone metrics has been disappointing. In a series of recent papers,1

European researchers have acknowledged that the AOT402

 critical level adopted in Europe has 

proven to be unrealistic and unattainable and have called for revisions to the approach. In 

addition, it has been reported that visible symptoms at 83 sites in five countries had no relation to 

the cumulative exposure metric and that crown defoliation of beech was only related to ozone 

exposure at very high exposure levels, seven times the European critical level for forests. 

In fact, in the European approach, the cumulative seasonal metric was chosen as a first 

step that evaluated the potential risk to vegetation, while recognizing that it does not take into 

account environmental factors that modify ozone uptake, plant defense mechanisms, or 

differences in ozone tolerance between species. The Europeans are now working on their second 

level approach which will be flux-based. 

g. The analysis used to discriminate between cumulative standards 

and the current 8-hour standard is flawed. 

 A major consideration in the choice of a seasonal standard was the assessment of the 

extent to which an 8-hour standard would provide protection for vegetation. The assessment 

involved a comparison of the “as-is” W126 exposure (Figure 7-6 of the SP) with the W126 

exposure rolling back 8-hour ozone concentrations to meet the current standard (Figure 7-7 at 7-

30 of the SP). This comparison is misleading, because the rollback approach assumes that there 

will be no reduction in ozone at sites that currently attain the 8-hour standard. In reality, there 

are many national and regional emission reduction programs that will reduce man-made ozone 

throughout the country, and measures adopted through the SIP process that will also reduce 

ozone in current attainment as well as nonattainment areas. 

 The Agency is fully aware that the rollback approach underestimates the benefits of 

attaining the alternative standards. The RIA used the monitor rollback approach for some of its 

calculations, and the Agency acknowledges that the approach understates the benefits that would 

occur due to implementation of actual controls because controls implemented to reduce ozone 

concentrations at the highest monitor will result in reductions in ozone at attaining monitors and 

other nonattaining monitors.3 If the rollback approach understates the benefits of alternative 

standards it also overstates the risk remaining after just meeting the standard. 

 

1

 See M. Ferretti, F. Bussotti, V. Calatayud, M. Schaub, N. Krauchi, B. Petriccione, G. Sanchez-Pena, M. Sanz and 

E. Ulrich, Ozone and forests in South-West Europe – What have we learned? Environmental Pollution, 145, 652-655 

(2007), that summarizes the findings from monitoring of forest conditions and ozone at 83 sites in France, Italy, 

Luxembourg, Spain and Switzerland over the years 2000-2002. 

2

 The AOT40 metric is the seasonal accumulated dose of the hourly concentrations above a threshold of 0.040 ppm. 

3

 RIA at 6-99, 8-15 
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 The form of the current 8-hour standard, while not designed to protect vegetation, does 

focus control on the precursors of man-made ozone and consequently will reduce the overall 

level of man-made ozone throughout the country. EPA’s analysis to date does not evaluate the 

impact of the nation’s ozone control program on W126 in a scientifically sound manner. Before 

a decision regarding the protectiveness of an 8-hour standard is made, a realistic evaluation of 

the ozone reductions throughout the country must be made using state-of-the-art photochemical 

models. The draft RIA did not include such an analysis. 

 In addition, the EPA analysis has focused on determining if the proposed seasonal air 

quality targets could be exceeded in areas where the 8-hour standard is met. Starting with the 

basics, however, an analysis of the exposure-response data to determine if effects are observed 

for exposures which do not exceed the 8-hour standard has not been presented. The ecological 

effects data are provided generally as seasonal means or cumulative (SUM06, W126) values, 

which may include multiple exceedances of the 8-hour standard. This is particularly true for the 

crop studies that form the basis of the EPA and CASAC recommendations, which have multiple 

hourly peaks > 0.10 ppm. 

h. The estimates of crop loss are substantially lower than those of the 

previous review. 

 The SP acknowledges that the estimates of crop loss for the species evaluated are 

substantially lower than in the previous review. As a result, the economic benefits associated 

with attaining various alternative standards have been substantially lowered from previous ozone 

yield loss studies.4

 It is now widely accepted that ozone concentrations at the “standard 

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. 

i. Studies of foliar injury do not support a cumulative metric. 

 The map of locations where foliar injury was present and absent in 2001 (Figure 7-19 at 

7-62 of the SP) shows a patchwork of responses that, in many cases, are not obviously correlated 

to major areas of man-made precursor emission. Although foliar injury is observed in areas that 

meet the current 8-hour standard, there are also high and low SUM06 areas that experience foliar 

injury and areas that do not. Similarly, the European experience indicates that there was little or 

no relation between a cumulative metric, AOT40, and foliar injury at 83 sites in five countries. 

 At a site in the Northeast Corridor of the U.S. where ozone levels are elevated, Davis and 

Orendovici5 report that there was no readily apparent relationship between SUM06 ozone levels 

and incidence of ozone stipple. SUM06, by itself, was not a reliable predictor of ozone foliar 

injury, but when included with N100 (the number of hours of 0.100 ppm or higher) and drought 

stress, a cumulative ozone metric such as W126 did have substantial predictive power. 

 

4

 SP at 7-52. 

5

 D. Davis and T. Orendovici, Incidence of ozone symptoms on vegetation within a National Wildlife Refuge in New 

Jersey, Environmental Pollution, 143, 555-564, 2006. 
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Although the SP mentions the possible use of N100 along with a cumulative ozone metric, it 

took no position on the question. Clearly, this is an important issue that should be evaluated 

fully by EPA. 

j. CASAC made its recommendations based on the draft SP that 

contained errors overstating the magnitude of vegetation effects. 

There were major errors in the translation of the results of the vegetation risk assessment 

in the Second Draft SP, overstating the magnitude of crop loss from ozone. For example, the 

table summarizing the results of the crop loss risk assessment in the appendices to the second 

draft SP (Table 7E-4) reported the maximum yield loss for various crops (8 crops and 7 fruits 

and vegetables) but labeled the numbers as the median yield loss. This grossly overstated both 

the yield loss from current ozone levels, as well as the yield gain from attaining any of the 

alternative secondary standards under consideration. While this was corrected in the final SP, 

CASAC made its recommendations concerning the secondary standard based on the draft text 

that contained numerous errors overstating the magnitude of vegetation effects. Moreover, the 

SP still only discusses the maximum yield loss figures. The actual distribution of yield loss/gain 

can only be found in Section 5.4.1 and Appendix G of the TSD,6

 which indicates that the mean 

and median yield gains from attaining any of the alternatives under consideration are quite small 

– the order of 1 percent or less for even the most stringent standards. For example, the mean 

yield gain for cotton (compared to the 2001 “as-is” baseline) from attaining a 13 ppm-hr W126 

standard is 0.19 percent and the mean yield gain for soybeans from attaining a 13 ppm-hr W126 

standard is 0.14 percent. In contrast, the second draft SP had indicated that there would be the 

orders of a 7 % mean yield gain for cotton and 2.5 % for soybeans. 

k. The recommended range for a cumulative standard needs to be 

adjusted upward. 

The CASAC suggestions for the range of a SUM06 or W126 standard come from a 

consensus-building workshop held in 1997. The EPA staff’s recommended range also 

considered the results of the 1997 Review and risk assessment. Since neither of these sources 

considered the difference between the ozone monitored in the network and the ozone exposure at 

plant height, these ranges should be re-evaluated accordingly. 

 If ozone monitoring is continued under the current guidelines, the ranges for a seasonal 

secondary standard would have to be adjusted upward. Based on the reduction in ozone 

exposure at plant height of a factor of 2 compared to that at measurement height, the range 

should be increased by roughly a factor of 2. Neither CASAC nor EPA took this into account in 

making their recommendations concerning the level of the secondary standard. 

 

6

 J. Lehrer, M. Bacou, B. Blankespoor, D. McCubbin, J. Sacks, C. Taylor and D. Weinstein, Technical Report on 

Ozone Exposure, Risk, and Impact Assessment for Vegetation, EPA 452/R-07-002, Jan. 2007, Appendix G. 
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l. The tools needed to implement a seasonal ozone standard are not 

in place. 

 The placement of current ozone monitors is not appropriate for evaluating vegetation 

exposure in terms of either spatial coverage or monitor height. Therefore, a new monitoring 

network must be designed and implemented before designations of attainment or nonattainment 

occur. Based on work-to-date, a model suitable for developing control strategies for a 

cumulative seasonal standard, particularly in the Western U.S., is not available. In addition, 

major improvements would be needed in grided emission inventories throughout the U.S. 

particularly for agricultural emissions. Therefore, the tools needed to implement a seasonal 

ozone standard are not in place. 

 When the timeframe required implementing a new monitoring network, to collect data for 

several years, and to develop and approve an implementation plan is considered, the next ozone 

review will have been completed before implementation plans will be in place. Ozone reviews 

are required every five years and EPA recently changed the review process dramatically to meet 

the statutory requirement. As an example of the timeframe needed to implement a standard 

when a new monitoring network is required, the PM2.5 standards were set in 1997 and the SIPs 

are due to EPA in 2007. 

 All this assumes that tools are available when needed, sources responsible for the 

nonattainment can be identified, and the standard is attainable in the sense that reduction or 

elimination of the identified sources is at least theoretically possible. To the extent that any of 

these steps are not possible, the setting of a seasonal secondary standard will not be fruitful and 

will not aid materially in the protection of vegetation. 

 
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III. Comments on EPA’s Regulatory Impact Analysis for the Agency’s Proposal to 

Revise the National Ambient Air Quality Standards for Ozone. 

The Regulatory Impact Analysis (RIA) EPA issued on August 2, 2007 estimates potential 

incremental benefits and costs of reaching a standard in the year 2020 in the range EPA proposed 

(0.070 to 0.075 ppm, and at two other levels on which the Agency is taking comment (0.065 and 

0.079 ppm). 

The RIA concludes that the annual net benefits for implementation of the proposed 

standards (i.e., 0.070 to 0.075 ppm) in 2020 range between -$20 billion and +$23 billion. 

Because of the high degree of uncertainty in these calculations, EPA cannot estimate whether 

costs will outweigh benefits, or vice versa.

168 An analysis of the RIA suggests that many of the 

potential benefits may not be realized while the estimated cost is likely to be significantly greater 

than the estimates suggest. The RIA shows that attainment of any alternative ozone standard is 

going to require massive new control programs that will affect most parts of the country and 

many sectors of life. After the application of every known control measure, substantial areas of 

the country still fail to attain the current standard. 

 

A. EPA’s Alleged Benefits From Lowering the Ozone NAAQS Are Not Likely to 

Occur. 

Most of the benefits estimated in the RIA are due to the avoidance of premature 

mortality. For the upper-end estimate of the benefits, EPA assumes that premature mortality is 

linked causally to both ozone and PM2.5. The Alliance takes issue with both of these causal 

assumptions. For the lower-end estimate, EPA assumes premature mortality is only linked to 

PM2.5 and not to ozone. Because emissions of NOx will need to be reduced to meet any of the 

proposed alternative ozone standards, ambient concentrations of fine particulate nitrate, a 

component of PM2.5, will also be reduced. In fact, estimated benefits from reduced PM2.5

pollution make up between 13 and 99 percent of the estimated benefits of meeting the alternative 

standards. 

Since only observational studies are used in the RIA, judgments are necessary in 

selecting the health endpoints and concentration-response functions to include from a wide range 

of available associations in the literature. As indicated above, there are major issues of model 

selection and potential biases involved in interpreting the air pollution epidemiologic literature. 

The current practice of using central station monitoring data, central station weather data, and 

available health statistics yields many weak positive associations for various pollutants in timeseries analyses. However, the full range of associations in the literature is very wide, with both 

positive and negative associations, and it is known that the methodology is subject to problems 

of measurement error and exposure misclassification, as well as severe collinearity between 

weather and pollution variables. When the uncertainty due to model selection issues is added 

and the potential biases are considered, the interpretation of a subset of positive findings as 

 

168 RIA at 8-10. 
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causal becomes problematic. Therefore, the use of epidemiological studies for health effect 

benefit estimation is highly uncertain. 

 The most important uncertainty relates to the assumption of causality. The second most 

important uncertainty is due to the assumption of no threshold for most of the evaluated 

endpoints. The SP indicates that the bulk of estimated premature mortality accrue at 24-hour 

concentrations below 0.04 ppm which is close to the background assumed in the previous 

review. The CD and SP acknowledge that only a few ozone studies have examined the shape of 

the concentration-response function. The Special Panel of the Health Effects Institute Review 

Committee recently raised several cautions in interpreting epidemiological concentrationresponse results. They point out169 that measurement error could obscure any threshold that 

might exist and note that city-specific concentration-response curves (for particulate matter, in 

this instance) exhibited a variety of shapes. They also caution that the standard approach of 

minimizing the Akaike Information Criterion may not be appropriate for choosing between 

models. The HEI Panel finally cautions that lack of evidence against a linear model should not 

be confused with evidence in favor of it. CASAC has raised similar concerns regarding the 

inability of time-series studies to identify the presence or absence of thresholds. The use of a 

linear ozone effect model as the default should not be accepted until it is demonstrated with 

controlled studies that low doses within the range of background are capable of eliciting 

significant biological effects. 

There are specific concerns with each of the health endpoints included in the RIA, as 

discussed in detail in the following sections. 

1. EPA’s estimates of acute mortality rely on weak epidemiology 

evidence and incorrectly assume causality. 

The RIA acknowledges considerable uncertainty in the ozone/mortality relationship 

including the possibility that the ozone/mortality association may not be causal. However, the 

RIA inappropriately goes on to include estimates of health benefits that presume acute mortality 

from exposure to ozone. These estimates are based on the Bell et al. 2004 NMMAPS analysis, 

and the three meta-analyses sponsored by EPA in 2005. Since the proposed rule acknowledges 

that the three meta-analyses are subject to publication bias, those results should not be included 

in the final RIA. 

There are several reasons why even the NMMAPS results are not consistent with a causal 

relationship and should not be used as the basis of a health benefits analysis. The RIA notes 

CASAC’s concern that time-series analysis is a blunt tool that implicates all pollutants and it 

notes EPA’s request that the National Academy of Sciences (NAS) evaluate the evidence. 

 

 

169 See Commentary by Health Review Committee in M. Daniels, F. Dominici, S. Zeger and J. Samet, National 

Morbidity, Mortality, and Air Pollution Study, Part III: Concentration-Response Curves and Thresholds for the 20 

Largest U.S. Cities, Health Effects Institute Research Report Number 94, Part III, May 2004. 
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The CD and SP acknowledge that there is a lack of consistent effect on respiratory 

mortality. Although this is blamed on a lack of statistical power, CASAC questions this 

interpretation.170 In addition, the Anderson et al. 2004 study reported no association of 

respiratory mortality with ozone in a meta-analysis of European studies. There were no 

statistically significant associations of ozone with respiratory mortality in the 12 studies 

evaluated. The overall risk was 1.000 per 10 #g/m3 increase in ozone. While there was a weak 

signal of an association of ozone with cardiovascular mortality, the finding of a cardiovascular 

but not respiratory mortality signal from ozone in single-pollutant models is hard to explain as a 

causal relation. It is not coherent with the staff conclusion that the ozone signal in hospital 

admissions is with respiratory not cardiovascular admissions. In the Anderson study, the 

combined association of ozone with respiratory hospital admissions was not statistically 

significant for the five cities available for analysis. 

Anderson discusses the issue of publication bias acknowledging that it is a common and 

possibly universal problem in our research culture. Furthermore, they note that there are 

particular reasons why it might occur in time-series studies. These include the large number of 

associations evaluated and the possibility for a selection bias involving the results included in a 

paper. They also mention a lag selection bias that can be overcome with multi-city studies such 

as NMMAPS. They further point out that publication bias can result in false conclusions being 

drawn in the hazard identification stage of a risk assessment and result in an inflation of the 

magnitude of the health impacts. They also recognize that the methods of detecting publication 

bias are not without problems. 

In an earlier meta-analysis, Levy et al. 2001 describe their result as providing weak 

epidemiologic support for ozone mortality and as potentially biased because it excludes studies 

that found ozone to be insignificant. After listing a number of such studies and noting that nearly 

all the studies found ozone not to be a predictor of mortality including all studies in warmer 

climates, Levy et al. concludes this information must “...give one pause in using our pooled 

estimate as a representative measure of ozone mortality risks.” Levy et al. also discuss the 

difficulties of separating temperature or weather and ozone effects, cautioning that “possible 

confounding by weather leaves lingering doubt about whether the ozone findings are causal, an 

issue that would be difficult to resolve epidemiologically.” 

Although the RIA relies on the Bayesian adjusted summer ozone/mortality associations 

from the Bell et al. 2004 NMMAPS analysis, the individual-city data shown in Figure 7-17 of 

the CD demonstrate a much wider range of associations. Such a wide range with many negative 

associations and few statistically significant positive associations is not consistent with a causal 

ozone effect on mortality. There is another NMMAPS analysis that also raises important 

concerns. The NMMAPS re-analysis171 reported a small positive combined association for 

ozone with mortality in the summer, but a small negative combined association in the winter at 

lag 0. The lag 0 results were stronger than the lag 1 and lag 2 results. However, an association 

 

170 October 2006 CASAC Letter at 10. 171 F. Dominici, A. McDermott, M. Daniels, S. Zeger and J. Samet, Revised analyses of the National Morbidity, 

Mortality, and Air Pollution Study: Mortality among residents of 90 cities, J. Toxicology and Environmental Health, 

Part A, 68, 1071-1092 (2005). 
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of ozone at lag 0 may be problematic since the ozone peaks in the afternoon and mortality is 

distributed throughout the day, so that a lag 0 association potentially runs afoul of the 

temporality requirement that the cause precede the effect. 

 

The wide range of individual city results in NMMAPS, the overall negative winter 

association demonstrated in NMMAPS, and the lack of a significant summer combined 

association for the 90 largest U.S. cities in the NMMAPS multi-pollutant models all erode the 

RIA case for causality. The only reported NMMAPS ozone results in multi-pollutant models 

were for the summer. In each case, when other pollutants were included, the ozone association 

was reduced and became non-significant. If the ozone associations are not robust to inclusion of 

other pollutants in the summer when there was a combined small positive association in single 

pollutant models, it is very unlikely that they could be causal. 

2. The RIA incorrectly bases benefit estimates from reduced hospital 

admissions for respiratory disease on selective studies. 

 The RIA inappropriately uses selected positive associations of ozone with respiratory 

hospital admissions from the literature. As discussed in the comments above concerning this 

endpoint, there is less consistency in the hospital admissions and emergency department 

ozone/association data than EPA acknowledges. As shown in the NMMAPS mortality analyses, 

the range of individual city results in multi-city analyses with a consistent methodology is very 

large (with both positive and negative associations) and not biologically plausible. The wide 

range of positive and negative associations in Ito 2003 also indicates that assuming that selected 

individual city positive associations are real health effects overstates the situation. The timeseries studies in the literature can be used to implicate many different air pollutants as potentially 

causing respiratory hospital admissions and emergency department visits, but as Anderson et al.

1998 point out there is lack of consistency in the pollutant responsible or the specific respiratory 

endpoint affected. 

 

This conclusion is consistent with the emerging realization in the scientific community 

that there is increasing evidence for caution in interpreting weak air pollution associations. In 

order to fully consider the range of ozone/hospital admissions associations in the literature, the 

presence of negative studies and studies with negative associations must be acknowledged and 

the lower limit of estimated zero should be zero. In fact, the RIA acknowledges that the 

confidence limits for the pooled estimate for asthma-related emergency room visits includes 

negative values, so the lower limit for this endpoint is indeed zero.172 

 

172 RIA at 6-16. 
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3. The data on school absences are weaker than noted in the proposed 

rule and are not reliable for purposes of estimating benefits. 

The RIA uses associations between school absences and ozone from Chen et al. 2000 and 

Gilliland et al. 2001. However, both the SP and CD indicate that further replication is needed 

before firm conclusions can be drawn regarding the presence of ozone effects on school 

absences. The Gilliland et al. study of school absences reported a large effect but there is a 

question of residual seasonal confounding in the study. Furthermore, Gilliland et al. report a 

substantially larger effect in low ozone communities versus the effect in high ozone 

communities, a highly counterintuitive result that necessitates additional explanation. Potential 

confounding by bioaerosols was not evaluated in the study. Thus, it would be particularly 

important to replicate the study in another cohort and over all seasons. 

The many issues with model selection that have arisen in recent years raise additional 

concerns that the result may not be robust. Specifically, the final CD discusses three analyses of 

the school absence data from the Southern California Children’s Health Study (Gilliland et al.

2001, Berhane and Thomas 2002, and Rondeau et al. 2005) that used different statistical 

approaches and assumptions and came to very different conclusions concerning the presence and 

magnitude of an ozone effect using the same data set. This is an indication that the choice of the 

statistical approach used to analyze the data can change the findings dramatically. Overall, the 

evidence for school absence associations with ozone is weaker than noted in the proposed rule. 

The large reported ozone effect on respiratory absences in Southern California is 

disproportional to the lack of substantial effects on respiratory symptoms seen in school children 

residing in the Basin. There are several studies of respiratory symptoms in California that failed 

to detect symptomatic effects. These include Delfino et al. 1996, Delfino et al. 1997b, Linn et 

al. 1996 and Ostro et al. 2001. There is a particularly important study of asthmatic, wheezy and 

healthy children in Southern California that is not considered by EPA. The HEI study by Avol 

et al.173 evaluated potential acute respiratory effects of ambient ozone in the spring and summer. 

About 200, 10- to 12-year old children from Lancaster, San Dimas, Upland, Mira Loma, 

Riverside and Lake Arrowhead were studied in the spring and late summer of 1994 with 

monitored hourly ozone levels exceeding the federal 1-hour standard in each season, and with 

peak hourly levels up to 0.20 ppm in the summer period. 

Furthermore, there was no consistent or clear role of ozone in producing changes in 

reported symptoms or medication use. There was also no discernible pattern of diurnal lung 

function changes by season, ozone level, or health group. The authors note that failure to detect 

clear evidence of acute pulmonary effects in the three groups may be due to insufficient 

elevation of ozone levels during the study, although ozone concentrations exceeded 0.08 ppm 

during the study. The authors note that children in their study on average did not spend a 

comparable amount of time outdoors or exercising at high levels to the time used in the chamber 

studies. 

 

173 E. Avol, W. Navidi, E. Rappaport and J. Peters, Acute effects of ambient ozone on asthmatics, wheezy, and 

healthy children, Health Effects Institute Report Number 82, 1998. 
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Finally, the lack of a substantial respiratory symptom signal in several California studies 

is inconsistent with the large effect on school absences reported by Gilliland et al. This 

difference needs to be acknowledged and discussed in the RIA. 

 

4. EPA should include a lower bound of zero for the benefits of minor 

restricted activity days. 

The RIA uses an association of 2-week average ozone with minor restricted activity days 

from Ostro and Rothschild 1989 for this endpoint. The authors note that the association with 

ozone was highly variable but statistically significant. They also note that there was no 

association with respiratory-related restricted activity days (RRADs). Minor Restricted Activity 

Days (MRADs) are days when people reduce their activity but do not miss work or school. 

Levy et al. 2001 point out some statistical issues with the study. Levy et al. raise 

concerns that the study may not properly measure an independent ozone effect. Levy et al. note 

that of the six years in the study, 1976-1981, the regression coefficient was significantly negative 

in 1977 and 1981. Although the combined result was significantly positive, Levy et al. caution 

that the magnitude of the ozone impact on MRAD should be considered somewhat uncertain 

given that “only one older study with statistical issues is available.” 

Since ozone was not significantly associated for any year with RRAD, it is difficult to 

discern what the actual health effect on a MRAD might be and how it could be caused by ozone. 

Given these issues and the presence of negative as well as positive study results in different 

years, the lower bound estimate should be zero. 

 

5. Given questions of PM speciation and other uncertainties, the lower 

bound of the ancillary PM2.5 benefits should also be zero. 

The RIA acknowledges that ancillary benefits from reduced PM2.5 pollution make up 

between 13 and 99 percent of the estimated benefits of meeting the alternative standards. (RIA at 

8-10) Because emissions of NOx will need to be reduced to meet any of the proposed alternative 

ozone standards, ambient concentrations of fine particulate nitrate, a component of PM2.5, will 

also be reduced. Since the baseline for the RIA assumes sufficient controls to attain the new 

PM2.5 standards, there are several reasons why reduced nitrate concentrations, especially at 

concentrations below the new PM standards, would not be expected to impact mortality. 

" The toxicology of nitrate and other PM components indicates that nitrate is among the least 

toxic PM components. PM air pollution is a mixture of many different kinds of particles 
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that vary by three orders of magnitude in toxicity per unit mass (AICGH, 2006)174 and 

nitrate is among the least toxic of these components. (Schlesinger and Cassee, 2003).175 

" Nitrate exposures of the frail population are substantially below that measured in ambient 

air. Ammonium nitrate is known to decompose to gaseous nitric acid and ammonia as it 

penetrates indoors where people spend 90 percent of their time with the nitric acid formed 

being lost on surfaces.176 Numerous studies report substantially reduced nitrate 

concentrations indoors compared to ambient concentrations with lower indoor/outdoor (I/O) 

ratios for nitrate than for other ambient PM components such as sulfate. 

" Spatial and temporal distribution of nitrate is opposite to the acute health effects signal from 

PM. Ambient nitrate is highest in winter and higher in the west than in the east. A seasonal 

NMMAPS analysis is available (Peng et al. 2005)177 with updated mortality data from 

1987-2000 in 100 cities. Summer was the only season for which the combined effect of 

PM10 was statistically significant. An analysis by geographic regions showed a strong 

seasonal pattern in the northeast with a peak in the summer. The authors note several 

possible explanations. One obvious hypothesis is that the most toxic particles have a 

spring/summer maximum and are more prevalent in the northeast. The acute PM health 

effects signal from this large multi-city study is not consistent with nitrate-caused mortality. 

" The spatial distribution of nitrate is also not consistent with causation of cardiovascular 

hospital admissions based on the results of the Dominici et al. (2006)178 study of PM2.5

hospital admissions associations for 204 U.S. urban counties. Dominici et al. report a clear 

difference in the combined associations between the eastern and western regions of the 

country. The combined hospital admissions association is positive for cardiovascular 

outcomes in the east but negative in the west except for heart failure, which is positive in 

both areas. However, there is an ample literature of small positive associations of hospital 

admissions in single pollutant models with a wide range of air pollutants, particularly for 

heart failure, for which the most consistent associations are reported.179 The Dominici et al.

results are not consistent with an effect of either generic PM2.5 or nitrate on cardiovascular 

hospital admissions and, indeed, the authors point out the need to shift the focus of research 

 

174 American Conference of Governmental Industrial Hygienists, 2006 Threshold Limit Values and Biological 

Exposure Indices, Cincinnati, Ohio. 

175 R. Schlesinger and F. Cassee, Atmospheric secondary inorganic aerosols: The toxicological perspective as a 

basis for health effects risk assessment, Inhalation Toxicology, 15, 197-235 (2003). 176 M. Lunden, T. Thatcher, D. Littlejohn, M. Fischer, T. Kirchstetter, N. Brown, S. Hering and M. Stolzenburg, 

Building a Predictive Model of Indoor Concentrations of Outdoor PM2.5 in Homes, Report under U.S. Dept. of 

Energy Contract No. DE-AC03-76SF00098, prepared by Lawrence Berkeley National Laboratory and Aerosol 

Dynamics Inc., Berkeley, CA, September 2001. 

177 R. Peng, F. Dominici, R. Pastor-Barriuso, S. Zeger and J. Samet, Seasonal analyses of air pollution and 

mortality in 100 U.S. Cities, Am. J. Epidemiol, 161, 585-594 (2005). 178 Dominici F., Peng, R., Bell M., Pham.L., McDermott, A., Zeger, S. and Samet, J., Particles, Air Pollution and 

Hospital Admissions for Cardiovascular and Respiratory Diseases, J. American Medical Association, 2006, 295, 

1127-1134. 

179 See M. Goldberg, et al., Env. Res., 91, 8-20 (2003) which reports similar small associations with congestive 

heart failure for every pollutant included in the analysis. 
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to identifying those characteristics of particles that determine their toxicity. The authors 

also note that their combined result is several-fold lower than other hospital admission 

associations they cite from the literature, suggesting publication bias in that literature. 

The implications of these two large multi-city studies are that the PM2.5 associations in the 

RIA inflate the magnitude of potential benefits from control of generic PM2.5 and that the 

associations should not be applied to estimate the benefits of nitrate reductions. 

 

" Regional differences in the chronic mortality signal are inconsistent with nitrate causing 

chronic mortality. There is a major difference in the chronic PM2.5 mortality signal between 

the east and west in the data the RIA relies on that is inconsistent with nitrate-causing 

chronic mortality. The RIA relies on the Pope et al. 2002 update of the Pope et al. 1995 

American Cancer Society Study (ACS) to estimate the ancillary nitrate benefits. However, 

the lack of a PM2.5 association with mortality in western cities in the ACS cohort was noted 

by EPA (Grant 2001)180 in a presentation to the CASAC PM Panel. Staff indicated an 

excess risk from 10 #g/m3 PM2.5 of +29 percent in the industrial midwest, +25 percent in the 

southeast, +14 percent in the northeast, and –9 percent in the west (west is a combination of 

cities in the northwest, southwest, upper midwest, and Southern California NMMAPS 

geographic regions). The different regional signals and other findings from the HEI reanalysis181 of the chronic PM health studies all raise questions concerning the interpretation 

of the chronic PM2.5 associations as a universally applicable chronic PM health effect. For 

the RIA, the lack of a chronic mortality signal in the west, where nitrate is a major 

component of ambient PM, is not consistent with the assumption that nitrate causes chronic 

mortality. 

" The expert solicitation that the Agency uses in a sensitivity analysis never addressed the 

experts’ views on causality of ammonium nitrate or other specific PM components. 

Therefore, the sensitivity analysis regarding causality is incomplete, as it applies to ancillary 

nitrate reduction impacts. 

" As noted above, all the estimated ancillary PM2.5 benefits from more stringent ozone 

standards accrue from PM2.5 concentrations below the new PM2.5 NAAQS that the 

Administrator decided was protective of public health with an adequate margin of safety. 

For all these reasons, the lower bound of ancillary PM2.5 benefits due to NOx reductions 

should be zero. 

 

180 Grant, L.; EPA Staff Presentation to CASAC, July 23, 2001; Key Revisions and Scientific Issues for Second 

External Review Draft of Air Quality Criteria for Particulate Matter, Slide 46. 181 For example, the Krewski et al. 2001 re-analysis showed that the increased risk was cardiovascular not 

respiratory, that one gaseous pollutant, SO2, had a strong association with mortality, that when SO2 was included in 

the model the PM all-cause mortality association was materially reduced and became non-significant, and that the 

increased mortality was experienced in the portion of the cohort that had a high school education or less. 
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B. Even Though the Benefits Are Uncertain, the Costs of Meeting a More 

Stringent Ozone Standard Will Occur and the EPA Analysis Likely 

Underestimates Those Costs. 

In order to conduct the RIA, EPA used a photochemical grid model to model two 

different scenarios and then used selected grid modeling results to extrapolate and estimate the 

number of additional tons of precursor control that would be needed for attainment of the 

alternatives under consideration. 

1. The RIA shows many existing nonattainment areas will not attain the 

current standard with all known control technologies, even when 

applied to regions outside the nonattainment area. 

The first modeling scenario, designated as the 2020 Baseline includes all national 

emission control programs that are on the books or being proposed and many additional local 

and regional NOx and VOC control programs that are thought necessary to bring most of the U.S. 

in attainment with the existing 8-hour ozone NAAQS of 0.08 ppm. The RIA reports (Figure 3.4 

of the RIA) that ten counties would not attain the current standard by 2020 with all these known 

or available controls. The remaining nonattainment areas include counties in the Houston 

metropolitan area, the Lake Michigan area, the Northeast Corridor, and the South Coast and San 

Joaquin Valley areas of California. Although only ten counties would actually experience ozone 

levels above the current standard in 2020 in this simulation, the areas affected by such 

nonattainment are much larger. For the baseline, the geographic areas where additional known 

controls were applied are extensive, including much of the midwest and the Northeast Corridor 

and all of Texas and California. This baseline analysis also shows that the application of all 

known controls would result in 82 counties that exceed 0.075 ppm standard, which is the highend of the range in the proposed rule. 

The second model simulation added a hypothetical national control strategy for attaining 

a 0.070 ppm standard by 2020 to the controls in the baseline case. Although described as 

applying all known or demonstrated controls, this emission scenario is a mix of adding known 

controls in additional geographic areas, adding controls assuming that current technologies can 

be applied to smaller and smaller sources of the same type, and adding hypothetical controls that 

are extensions of existing technology that EPA assumes will be available and effective in the 

needed time-frame. After applying the hypothetical “known” controls over most of the Eastern 

U.S. and throughout five additional western states -- Nevada, Utah, Colorado, Arizona and New 

Mexico -- the simulation was only able to show partial attainment of the 0.070 ppm goal. In fact, 

after these hypothetical controls were added to the baseline, nine counties still exceeded the 

current standard, 50 exceeded 0.075 ppm and 126 exceeded the 0.070 ppm goal as shown in 

Figure 3.13 of the RIA. No estimates for the number of counties exceeding the 0.060 ppm 

alternative recommended by many environmental activists were reported. 

To summarize, the RIA acknowledges that known and reasonably anticipated controls 

would likely be insufficient to bring many areas into attainment with either the current or 
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alternative standards.182 In other words, the Agency does not know how the current standard 

can be attained throughout the country. 

2. The RIA relies on unknown control technology to demonstrate 

attainment. 

Since the measures in the hypothetical national control strategy were not sufficient to 

bring much of the country into compliance with the alternative standards, a third emissions 

scenario for 2020 was developed using unknown technology to further reduce NOx emissions so 

that all places (except two areas in California) would be in compliance with the alternative 

standards by 2020. This exercise involved developing estimates of the emissions needed to 

provide full attainment but it did not involve testing in the grid model whether those emission 

reductions would, in fact, provide full attainment. 

The emission reductions in this scenario were estimated from grid modeling runs of the 

impact of NOx reductions. A single national estimate of the reduction in NOx and VOC in terms 

of parts per billion ozone reduced per kiloton of precursor reductions was used together with the 

extent of remaining nonattainment to estimate that several million additional tons of NOx 

reductions would provide for attainment of the more stringent alternatives under consideration in 

the RIA. The cost of full attainment was then estimated based on historical experience with NOx 

controls in terms of dollars per ton of NOx removed. Even though EPA does not know how these 

reductions will be achieved, the costs are estimated by extrapolating the cost from known 

technologies. 

3. The RIA correctly characterizes this extrapolation of costs from 

known to unknown technologies as a highly speculative exercise. 

Actual costs are likely to be significantly higher. 

The RIA characterizes the extrapolation of costs from known to unknown technologies as 

a highly speculative exercise, 183 and describes the resulting estimates as providing guidance on 

the general magnitude of costs and benefits not precise predictions. As standards across multiple 

pollutants with overlapping precursors are tightened, states and affected industries will move 

further down the list of cost-effective known and available controls, until uncontrollable 

background and anthropogenic emissions are reached. The nation has had a major national effort 

to develop and apply controls to reduce ozone and particulate matter emissions for over 40 years. 

Although much progress has been made, achieving even the current ozone standard throughout 

the country will require either the invention and application of substantial additional technology 

or curtailment of economic activity. Thus, the current standard is a very stringent standard. 

The estimated costs in the RIA, as large as they are, may significantly underestimate the 

true costs of the alternative standards. As the RIA notes, the estimated emission reductions are 

based on generalized precursor ozone relationships while the actual relationships are highly 

 

182 RIA at 8-11. 183 RIA at 8-11. 
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variable across the country.184 The full attainment emission reductions were restricted to NOx 

controls, but the remaining ozone problems tend to occur in areas with the greatest population 

and emissions density (modified by the extent to which the area’s meteorology is conducive to 

ozone formation). These areas are the large metropolitan areas where portions of the domain are 

VOC-limited and NOx reductions can both increase and decrease ozone formation.185 Thus, full 

attainment in these areas may be more difficult than EPA has assumed in the RIA. The 

generalized precursor relationships were derived from 36 km grid modeling runs which tend to 

exaggerate the benefits of NOx control and mask the benefits of VOC control. 

All the remaining major nonattainment areas have sophisticated ongoing grid modeling 

efforts supported in many cases with extensive field studies. Some of these areas were not able 

to develop and submit attainment demonstrations for the current standard by the June 2007 

deadline due to modeling issues and the lack of known controls. Others did develop attainment 

demonstrations that depended on the black box for as yet unidentified controls. The RIA 

acknowledges that in urban areas with a high population density, ozone is often VOC-limited 

(RIA at 2-1) and that in these areas NOx reductions can increase ozone. The RIA also notes that 

between the NOx-limited and VOC-limited extremes there is a transitional region where ozone is 

relatively insensitive to changes in NOx and VOC. To the extent that the mix of national and 

local controls results in areas being in the transitional region, where ozone formation tends to 

maximized, it may take massive reductions in one precursor or the other to come into attainment. 

Given the large biogenic emissions of both VOC and NOx that need to be included in the 

modeling, such massive reductions may not be feasible or achievable in some locations. In the 

final RIA EPA needs to test its full attainment strategies in a nested grid model to insure that 

attainment of the ozone standard is feasible. 

In conclusion, the RIA notes that tightening the ozone standard will incur significant but 

uncertain costs.186 The RIA concludes that the hypothetical national strategy to attempt to attain 

the 0.07 ppm alternative would cost $3.9 billion per year and that the estimated reductions for 

full attainment of the 0.07 ppm alternative would cost $13 to $26 billion per year. (For the 

0.065 ppm standard the estimated national cost, excluding full attainment in California, is $17 to 

$46 billion per year. No estimate for the 0.060 ppm standard was made. While, as documented 

above, the benefits of an 0.07 ppm standard (or any of the alternatives) depend on highly 

questionable assumptions concerning causality, it is, without question, demonstrably clear that 

achieving such a standard will require massive additional emission reductions costing the order 

of several tens of billions of dollars per year on top of the already massive national costs of 

attaining the current standard. The RIA acknowledges that the direct benefits from ozone 

reduction itself are $190 million per year for the 0.07 ppm alternative if it is assumed that ozone 

does not cause premature mortality.187 Since the morbidity effects of ozone in the RIA are 

 

184 RIA,, at 8-16. 185 See J. Heuss, D. Kahlbaum and G. Wolff, Weekday/Weekend Ozone Differences: What Can We Learn from 

Them? J. Air & Waste Management Association, 53, 772-778 (2003); G. Yarwood, K. Bonyoung, T. Stoeckneius, 

and J. Heiken, Modeling Weekend and Weekday Ozone in Southeast Michigan, ENVIRON International 

Corporation Draft Final Report prepared for National Renewable Energy Laboratory, Golden, CO, July 30, 2007. 

186 RIA at 8-16. 187 RIA at 6-2. 
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highly exaggerated as demonstrated above, all the alternative standards below the current 

standard are expected to be highly cost-ineffective.