Comments to the CASAC Ozone Review Panel for the 

Reconsideration of the 2008 NAAQS

Robyn Prueitt, PhD 

Prepared on behalf of 

American Petroleum Institute 

1220 L Street NW 

Washington, DC 20005-4070

February 7, 2011
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1 Introduction 

 US EPA is in the process of reaching a final decision on the reconsideration of the 2008 ozone 

NAAQS and seeks to ensure that this decision is based on the most appropriate interpretation of the 

scientific evidence. These comments will focus on issues related to epidemiology studies that examined 

the association between short-term ambient ozone exposure and respiratory effects, particularly in 

asthmatics, and are relevant to charge questions 5 and 6 that US EPA (Wegman, 2011) has provided to 

CASAC to solicit advice on the strengths and limitations of the scientific evidence for the reconsideration 

of the 2008 primary ozone NAAQS. 

Charge question 5: "...how can we appropriately use the results of...epidemiological 

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

susceptible populations?" 

Charge question 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?"

 The epidemiology studies relied on by US EPA as evidence for respiratory effects in the 2008 

rulemaking examined associations between short-term exposure to ambient ozone and (1) lung function 

deficits; (2) asthma symptoms and/or medication use; and (3) respiratory-related emergency department 

(ED) visits and hospital admissions. These studies do not report robust associations, as the US EPA 

(Wegman, 2011) memorandum states, and the many issues inherent to these studies still remain in the 

proposed reconsideration. 

 Most of the epidemiology studies of short-term respiratory effects of ozone were conducted in 

asthmatics, and they do not provide robust evidence that ambient ozone exposures below the current 

standard are associated with adverse effects in this population. Regarding charge question 5, the 

inconsistency of results within and among the studies and their inherent methodological issues preclude 

their use as a reliable basis to inform a judgment on the effects of ozone in asthmatics. Regarding 

question 6, there should be little confidence that any of the associations between short-term ozone 

exposure and respiratory effects are attributable specifically to ozone, regardless of whether they were 

observed in areas with ozone levels near the lower or higher end of the proposed range. The uncertainty 

surrounding the proposed ozone range has not been clearly stated. The majority of positive associations 

were observed in single-pollutant models, and thus cannot be attributed specifically to ozone. Exposure 

measurement error, from the use of central ambient monitors as a surrogate for personal ozone exposure 
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in almost every study, obscures the actual ozone levels at which any individual is exposed to, which can 

bias the results in either direction. 

 Arguments supporting these responses to the charge questions that are specifically related to the 

general methodological limitations of the epidemiology studies and US EPA's inappropriate assessment 

of the findings in documents related to the 2008 rulemaking are described in more detail below. 

2 Methodological limitations 

2.1 Confounding by other pollutants 

Confounding by particulate matter is a major issue in studies of ozone health effects, particularly 

in the summer, when outdoor ozone and PM2.5 concentrations are correlated, so outdoor ozone 

measurements may be a surrogate for personal PM2.5 exposure. Indeed, most studies report stronger 

associations in summer, when ozone levels are higher, and usually null or negative associations in winter. 

Most studies of short-term exposure to ozone and respiratory morbidity evaluated in the 2006 AQCD (US 

EPA, 2006) and 2007 Staff Paper (US EPA, 2007) used single pollutant models, so any reported 

associations cannot be attributed specifically to ozone. For those that used multi-pollutant models, 

associations were not robust and were often confounded by PM or sulfates. 

2.2 Exposure measurement error 

 An assessment of the epidemiology evidence must consider the inadequacy of using ambient 

ozone measurements from central monitors as a surrogate for personal exposure to ambient ozone. Many 

studies have been published that confirm a very weak correlation between ambient and personal ozone 

exposure (Sarnat et al., 2001, 2005, 2006). Reasons for this include: (1) uneven distribution of ozone 

attributable to local sources; (2) monitoring sites may represent a nearby source and not human exposures 

a small distance away; (3) pollution patterns can be affected by terrain features and weather; and (4) daily 

variations in ozone concentrations at a central monitoring site may differ from variations experienced by 

individuals. These factors may bias the results of an epidemiological analysis in either direction. Some 

individuals in the population will have greater exposures than others for any given central-site ambient 

concentration. Brauer et al. (2002) noted that for pollutants with poor personal-ambient correlations, it is 

not possible to accurately assess C-R relationships and thresholds in observational studies, particularly at 
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low levels where the presence of other pollutants will confound the findings for ozone. The possibility 

that exposure measurement error obscures thresholds limits the ability to draw conclusions about effects 

of ozone at low exposure levels. 

 All of the epidemiology studies of respiratory morbidity relied on ambient ozone measurements 

as a surrogate for personal exposure to ambient ozone, which could have biased results in either direction. 

This exposure measurement error has profound implications for assessing both causality and ozone 

concentration-response considerations. 

2.3 Lag times are often not based on biological plausibility 

The extensive human clinical and mechanistic data do not support a long lag between ozone 

exposure and pulmonary function changes; rather, they indicate that the respiratory effects of ozone occur 

soon after exposure; therefore, findings for 0-1 day lags or for cumulative ozone exposure over a few days 

should carry more weight in an assessment of the evidence. In many cases, studies that examined 

multiple lag times reported positive associations only from one or a few biologically implausible lag 

times, but not from plausible lag times. These studies should carry less weight in an assessment. 

2.4 Unreliability of self-reported effects 

Many published studies have documented the general unreliability and inaccuracy of selfreported peak expiratory flow (PEF) measurements, as discussed in detail by ExxonMobil (2007) in 

comments on the 2008 ozone NAAQS review. Some of the key studies from the last review used PEF 

measurements as the outcome, including those by Mortimer et al. (2002), Ross et al. (2002), Neas et al. 

(1999), and Naeher et al. (1999). Because of the unreliability of PEF measurement, studies using this 

method to assess pulmonary function should be given less weight when evaluating the evidence. There 

are also several limitations of symptom reports used in studies of self-reported respiratory symptoms and 

medication use, including recall error, biased reporting, and small sample sizes. 
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3 Assessment of the epidemiology evidence 

3.1 Studies of lung function 

 The 2006 AQCD evaluated acute ozone-related lung function effects in panel studies of 

asthmatics and healthy individuals and stated that these studies provide "clear evidence of causality for 

the association observed between acute ozone exposure and relatively small, but statistically significant 

declines in lung function" (US EPA, 2006). The majority of studies reported no association between 

frequently-studied measures of lung function and short-term ozone exposure, however, even in asthmatic 

children. Studies that did report a positive association generally used only single pollutant models and 

calculated estimates over a broad number of lag and ozone exposure metrics and found mixed results. 

 The Staff Paper states that the most representative data for lung function effects comes from the 

panel study of hikers by Korrick et al. (1998). This study reported small, albeit statistically significant, 

declines in pulmonary function tests (FEV1 and FVC), and noted that hikers with asthma or a history of 

wheeze had four-fold greater responsiveness to ozone than others. There are several concerns that 

weaken the results of this study, however. The authors used five different statistical models to assess the 

relationship between ozone and pulmonary function changes, which increases the possibility of chance 

findings from the issue of multiple comparisons. In addition, the mean FEV1 change attributed to 50 ppb 

ozone in this study is a 2.6% decrement, a very small change that is not considered clinically significant 

by both the ATS (2000) and the ERS (Pellegrino et al., 2005). Using the normal convention of change 

per 10 ppb ozone, this FEV1 change is reduced to 0.5%, which is even further below the accepted criteria 

for clinical significance. When adjustment for PM2.5 and aerosol acidity were included in the models, the 

pulmonary function changes attributed to ozone were not statistically significant. Thus, this study 

provides no evidence for an ozone-specific change in pulmonary function. 

 It is noteworthy that US EPA did not cite the study of lung function in hikers by Girardot et al. 

(2006) as a key study in the Staff Paper, as it has a similar study design to that of Korrick et al. (1998). 

Girardot et al. (2006) reported no statistically significant associations between ozone exposure and 

changes in FEV1 or FVC and, thus, does not confirm the small, statistically significant changes reported 

by Korrick et al. (1998). Consideration of these results provides greater confidence that the small 

changes reported in the study by Korrick et al. (1998) were not likely attributable to ozone. 
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 In studies examining the effects of ozone on PEF measurements, most reported null results, with 

the few positive associations being reported almost exclusively with single pollutant models. The AQCD 

states that results from the study of asthmatic children by Mortimer et al. (2002) provide key evidence for 

a significant relationship between ozone and PEF changes among asthmatics. Mortimer et al. (2002) did 

not present multi-pollutant models for ozone-associated PEF changes, however, so it cannot be 

ascertained whether those changes are attributable to ozone or another pollutant. In addition, the 

reported PEF changes are small and clinically insignificant, as the group changes in PEF are less than 

1%. Furthermore, the authors used multiple lag times with no biologic justification. For a decline of 

≥ 10 % in PEF, null associations with ozone were reported for 1, 2, 3, 5, or 6 day lags, and statistically 

significant associations were reported only for a 4-day lag and the average of 1-5 day lags. Choosing one 

day with a positive association among the various lags examined increases the likelihood of false positive 

effects. 

 The panel studies of ozone exposure and lung function effects do not provide clear evidence of 

causality, as US EPA suggests. Conclusions about these studies should reflect the evidence cited, which 

demonstrates no association with lung function in asthmatics or healthy individuals, in most cases. 

3.2 Studies of respiratory symptoms or asthma medication use 

 In the 2006 AQCD, US EPA reviewed several panel studies of the association between short-term 

ambient ozone exposure and respiratory symptoms or asthma medication use, mostly conducted with 

children. Overall, a number of studies found no association, with those reporting an association often 

using only single pollutant models, reporting very small associations, and having mixed findings across 

respiratory symptom effect measures, ozone exposure metrics, subpopulations, and lag times. US EPA 

cites the studies by Mortimer et al. (2002) and Gent et al. (2003) as key studies providing evidence of 

robust associations between acute ozone exposure and respiratory symptoms in asthmatics. The 

associations reported in this study were not statistically significant in multi-pollutant models, however. 

The study by Gent et al. (2003) relied on subjective reporting of symptoms by mothers, whereas 

associations with more objective symptoms were not generally statistically significant and do not support 

the more subjective respiratory symptom findings. US EPA did not cite the large, multi-city study by 

Schildcrout et al. (2006) that reported no associations between short-term ozone exposure and daily 

asthma symptoms and rescue inhaler use in asthmatic children across the various lag periods examined. 
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 Although the AQCD notes that a number of well-conducted, small studies have not reported 

associations with asthma symptoms, the Staff Paper discounts these studies as having less statistical 

power than the multi-city study by Mortimer et al. (2002) or because they are conducted in areas with 

relatively low ozone levels, and concludes that the panel studies, as a group, indicate a positive 

association with respiratory symptoms. Because of the inconsistent results across studies and the limited 

number of associations that are statistically significant in multi-pollutant models, the evidence does not 

support a positive association between ozone and respiratory symptoms. 

3.3 Studies of respiratory-related ED visits and hospital admissions 

 In the 2006 AQCD, US EPA evaluated a number of studies of respiratory hospital admissions and 

emergency department (ED) visits and concluded that "the overall evidence supports a causal relationship 

between acute ambient ozone exposures and increased respiratory morbidity resulting in increased ED 

visits and [hospital admissions] during the warm season" (US EPA, 2006). Studies cited in the 2006 

AQCD in support of this conclusion often reported very small associations and did not appropriately 

control for confounders and had many other limitations, and in some cases included positive but nonstatistically significant risk coefficients. In the 2006 AQCD, US EPA stated that positive but inconsistent 

associations were observed between ozone and respiratory-related ED visits. The results of studies 

regarding respiratory-related hospital admissions are also generally inconsistent, with many reporting no 

association. Study results were often mixed within and across effect measures, and varied depending 

upon the model parameters selected, including lag time. 

 Regarding respiratory-related ED visits, the AQCD states that of the studies reporting positive 

associations, three key studies reported effects that were robust to adjustment for other pollutants, 

including PM10 (Lin et al., 1999; Peel et al., 2005; Tenias et al., 1998). The AQCD also states that 

several studies reported at least one positive association with ozone, but these associations were 

inconsistent and depended upon the model specifications and analysis approach, the length of the study 

period, or the methods to control confounding by seasonal patterns and co-pollutants. In addition, several 

studies reported null associations, but the AQCD erroneously stated that overall, the studies report 

generally positive associations for asthma-related ED visits in the warm season. 

 Regarding respiratory-related hospital admissions, the AQCD notes some positive associations, 

some inconsistent effects, and some null studies, and concludes that the evidence generally supports 

findings of significant and robust effects. The AQCD also states that co-pollutants do not generally 
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confound the reported associations, particularly in the key, multi-city study conducted in Canada by 

Burnett et al. (1997), which reported statistically significant associations in models including PM10 and 

PM2.5. Not all studies examining effects in multi-pollutant models reported statistically significant 

associations, however, and another key, multi-city study reporting positive associations only used singlepollutant models (Anderson et al., 1997). 

 Overall, studies of short-term exposure to ozone and respiratory-related ED visits and hospital 

admissions provide inconsistent findings that do not support a causal relationship. US EPA should not 

interpret null results from these studies as positive associations. 

4 US EPA's assessment of the evidence 

 As described above, the epidemiological evidence for short-term effects of ozone exposure is 

generally weak and inconsistent. US EPA's assessment of this evidence in the 2006 AQCD and 2007 

Staff Paper is not scientifically appropriate, however, and does not adequately consider the various 

uncertainties associated with epidemiological data of air pollutants. 

 US EPA uses risk estimates that are above null but not statistically significant as evidence for an 

overall positive association. This is inappropriate because only statistically significant results should be 

used as evidence for a positive association. The few positive and statistically significant associations that 

are cited in the AQCD are in many cases from studies that calculated risk estimates across multiple lag 

time and ozone exposure metric combinations. Often, these same studies also reported negative and/or 

null risk estimates, thus providing inconsistent, rather than overall positive, results. US EPA also ignored 

certain negative studies in favor of those with positive results. An example of this can be seen in the 

review of the panel studies. The key studies cited by US EPA (Mortimer et al., 2002; Gent et al., 2003; 

Korrick et al., 1998) reported small respiratory effects but other studies of similar design (Schildcrout et 

al., 2006; Girardot et al., 2006) reporting no association between ozone exposure and respiratory effects 

were not cited as key studies. These latter studies were not included by US EPA in their 2008 review; 

rather, they were cited by the public in their comments on the proposed ozone NAAQS. Thus, it is 

unclear if US EPA considers them as "new" studies or part of the 2008 review. 

 US EPA did not adequately take into account the biological plausibility of lag times for effects on 

pulmonary function, as the long lag periods used in many of these studies are not biologically plausible. 
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Instead of basing the "best" estimates for lag times on biological plausibility, US EPA often emphasizes 

the largest positive association, particularly for the panel studies. 

 US EPA did not appropriately take into consideration the uncertainties associated with flaws in 

the time-series and panel studies, such as their use of ambient ozone measurements as a surrogate of 

personal ozone exposures in spite of the weak correlation between ambient and personal ozone exposures. 

Most studies of short-term exposure to ozone and respiratory morbidity evaluated in the 2006 AQCD 

used single pollutant models. For those that used multi-pollutant models, associations were usually not 

robust and were often confounded by PM or sulfates. Single pollutant estimates were often cited by US 

EPA as support of an association even though it has been demonstrated that co-pollutants can be 

significant confounders of the relationship between ozone and health effects. In addition, many of the 

panel studies, including the study by Mortimer et al. (2002) on which US EPA places high reliance, used 

self-reported peak expiratory flow rate (PEFR) measurements which, as noted above, have been 

demonstrated to be highly unreliable. Because of this unreliability, studies using PEFR data to assess 

pulmonary function should be given less weight when evaluating the evidence. 

 While US EPA has requested that CASAC consider only the data available at the time of the 

2008 ozone NAAQS review, CASAC should at least be aware of the general results of highly relevant 

studies that have been recently published in the peer-reviewed scientific literature. US EPA is aware of 

these studies, as they have been summarized in a rough draft Integrated Science Assessment document for 

the next ozone review (US EPA, 2010). CASAC should recognize that these new studies cast further 

uncertainty on US EPA's conclusion that current levels of ozone cause respiratory morbidity. For 

example, in a study sponsored by the National Institute of Allergy and Infectious Disease (NIAID), the 

National Institute for Environmental Health and Safety (NIEHS), and US EPA, O'Connor et al. (2008) 

reported no consistent associations between ambient ozone exposure and pulmonary function, asthma 

symptoms, or school absences in 861 inner-city children with persistent asthma. In contrast to previous 

studies that relied on PEF measurements, this study assessed pulmonary function using FEV1, a more 

reliable measurement technique. 

 Other studies not included in the last review that evaluated the potential for ambient ozone to 

exacerbate symptoms in asthmatics reported no association between ozone exposure and asthma 

exacerbations. These include a study reporting no association between ozone exposure and asthma 

exacerbation in children and adults in Toronto (Burra et al., 2009), and a study reporting no associations 

between ozone exposure and a wide variety of effect measures, including nighttime symptoms, asthma 
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exacerbations, symptom scores, PEF measurements, and bronchodilator use, a more objective measure of 

effect (Rabinovitch et al., 2004). 

 All three studies not included in the last review that evaluated the potential association between 

ambient ozone and airway inflammation also reported no associations. These include studies in elderly 

individuals (Adamkiewicz et al., 2004), nonsmoking high school athletes evaluated after exercising 

(Ferdinands et al., 2008), and asthmatic children (Liu et al., 2009). 

 Three of the four new studies that evaluated the association between short-term ambient ozone 

exposure and lung function, as measured by changes in FEV1 and FVC, reported no associations. These 

include studies of highly-exposed outdoor groups such as lifeguards (Thaller et al., 2008) and healthy 

hikers, as noted above (Girardot et al., 2006), as well as potentially susceptible subjects with COPD, 

asthma, or ischemic heart disease (Lagorio et al., 2006). Together, many of the studies not included in 

the previous ozone NAAQS review provide significant evidence that current levels of ambient ozone do 

not cause respiratory morbidity. 

5 Conclusions 

 The epidemiological evidence for short-term respiratory effects of ozone in asthmatics and 

healthy individuals is methodologically flawed and was not appropriately assessed by US EPA in the 

most recent review of the ozone NAAQS. Confounding by particulate matter (PM) is a common issue 

among studies of ozone health effects, but the vast majority of studies used only single pollutant models. 

Almost every study also used ambient monitors as surrogates of personal ozone exposures in spite of the 

weak correlation between ambient and personal ozone exposures. Because of these and other limitations 

noted above, two of the charge questions that US EPA (Wegman, 2011) provided to CASAC regarding 

the strengths and limitations of the scientific evidence for ozone-related health effects can be addressed as 

follows: 

5. "...how can we appropriately use the results of...epidemiological studies of 

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

populations?" 

 Most of the epidemiology studies of short-term respiratory effects of ozone were conducted in 

asthmatics, and they do not provide robust evidence that ambient ozone exposures below the current 

standard are associated with adverse effects in this population. The inconsistency of results within and 
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among the studies and their inherent methodological issues preclude their use as a reliable basis to inform 

a judgment on the effects of ozone in asthmatics. 

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?" 

 There should be little confidence that any of the associations between short-term ozone exposure 

and respiratory effects are attributable specifically to ozone, regardless of whether they were observed in 

areas with ozone levels near the lower or higher end of the proposed range. The uncertainty surrounding 

the proposed ozone range has not been clearly stated. The majority of positive associations were 

observed in single-pollutant models, and thus cannot be attributed specifically to ozone. Exposure 

measurement error, from the use of central ambient monitors as a surrogate for personal ozone exposure 

in almost every study, obscures the actual ozone levels at which any individual is exposed to, which can 

bias the results in either direction. Only the controlled ozone exposure studies can address effects that are 

specifically attributable to ozone. These studies indicate transient and minor lung function changes that 

are not likely to be responsible for more serious morbidity effects, such as increases in respiratory-related 

ED visits or hospital admissions, at least not at very low ambient ozone levels. 

 
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