February 7, 2011 

Testimony to the EPA Clean Air Science Advisory Committee (CASAC) Ozone Review 

Panel for the Reconsideration of the National Ambient Air Quality Standard 

February 18, 2011 

Bruce Copley, Ph.D. 

ExxonMobil Biomedical Sciences, Inc. 

My name is Bruce Copley. I am an epidemiologist with ExxonMobil Biomedical Sciences, Inc. I 

would like to thank EPA and CASAC for the opportunity to address the Committee today. My 

remarks focus on whether or not there is adequate scientific support for the theory that current 

levels of ambient ozone cause acute cardiovascular mortality and morbidity. Based on data from 

the 2008 review, EPA concluded that the data support this causality conclusion. The most 

current studies on the health effects of ozone--excluded from recent deliberations on the ozone 

NAAQS discussion--clearly do not support this causality conclusion. I will summarize the 

findings from these studies and also address why EPA’s acute mortality risk estimates are not 

accurate and, thus, do not justify lowering the current ozone standard. 

First, new scientific evidence clearly demonstrates that in contrast to EPA’s conclusion, the 

ozone acute mortality association is significantly confounded by exposure to other 

pollutants. 

I note that this new scientific evidence is especially critical to answering EPA charge question 

number 6, which asks "to what extent the effects observed in epidemiology studies should be 

attributed specifically to ozone alone?". In a Health Effects Institute (HEI) sponsored study, 

Katsouanni et al. (2009) reported that when PM10 was included in a two-pollutant models, the 

"all-cause mortality" for ozone in the U.S., using data from the National Morbidity, Mortality 

and Air Pollution Study (NMMAPS), was reduced by 68-88% depending on the age group 

considered. Also, the cardiovascular mortality attributed to ozone was reduced by 155% (Table 

24). 

Similarly, using data from NMMAPS, Smith and Switzer (2009) reported a 22-33% reduction in 

the ozone mortality coefficient when PM10 was included in a two-pollutant model. This study 

also indicated regional heterogeneity of effect that suggests that a derived single national risk 
February 7, 2011 

estimate is unreliable for standard-setting. Franklin and Schwartz (2008) reported that including 

sulfate PM in a two-pollutant model decreased the ozone mortality by 33% and that the ozone 

association was not statistically significant. 

Second, a large body of new scientific information clearly suggests that, in contrast to 

EPA’s conclusion, current levels of ozone do not cause cardiovascular morbidity. 

This new scientific evidence is highly relevant to answering EPA charge question 9. 

Question 9 asks CASAC to provide their perspective on the occurrence and public health 

importance of various ozone induced health effects, including cardiovascular morbidity and 

mortality at alternate ozone standards. Numerous new epidemiology studies report no 

association between current ambient ozone levels in the U.S. and cardiovascular hospital 

admissions. These studies include those focusing on cardiovascular morbidity alone (such as 

those reported by Szyskowicz (2008), Symons et al. (2006), Villeneuve et al. (2006), Wellenius 

et al. (2005), Tolbert et al. (2007), Zanobetti and Schwartz (2006), and Katsuyanni et al. (2009)), 

as well as those focusing on combined cardiovascular and respiratory causes (Tolbert et al 2007, 

Zanobetti and Schwartz, 2006). 

As noted by the HEI Review Committee in their commentary on the findings from the study by 

Katsouyanni, this marked lack of an association for cardiovascular morbidity provides little 

coherence for the ozone-cardiovascular mortality association. The Katsouyanni study also 

demonstrated that the risk estimates used for standard-setting are particularly sensitive to the 

specification of statistical models. 

In both the Risk and Exposure Assessment (REA) and the Regulatory Impact Assessment (RIA) 

prepared by EPA for the ozone NAAQS reconsideration, EPA adopted the theory that the ozonemortality association was causal and also estimated the risks of ozone exposure and the benefits 

of reducing this pollutant, based on single-pollutant model results. The new scientific data cast 

doubt on these assumptions and approaches. In order to facilitate the most scientifically sound 

decision on the ozone NAAQS, a thorough assessment of all relevant scientific data, including 

new scientific information, is required. Again, we would like to thank EPA and CASAC for the 

opportunity to provide these comments. 
February 7, 2011 

References

 

Franklin M. and Schwartz J. (2008). The impact of secondary particles on the association 

between ambient ozone and mortality. Environmental Health Perspectives. 166(4): 453-458. 

Katsouyanni et al. (2009). Air Pollution and Health: a European and North American Approach 

(APHENA). HEI Report 142. 

Smith et al. (2009). Reassessing the relationship between ozone and short-term mortality in U.S. 

urban communities. Inhalation Toxicology 29:37-61. 

Symons et al. (2006). A case-crossover study of fine particulate matter air pollution and onset of 

congestive heart failure symptom exacerbation leading to hospitalization. Am J Epi 164:421-

433. 

Szyskowiz et al. (2008). Ambient air pollution and daily emergency department visits for 

ischemic stroke in Edmonton, Canada. Int. J. Occup Med Environ. Health 21:295-300. 

Tolbert et al. (2007). Multipollutant modeling issues in a study of ambient air quality and 

emergency department visits in Atlanta. J. Expo. Sci. Env. Epid. 17 Supple 2: S29-35 

Villeneouve et al. (2006). Associations between outdoor air pollution and emergency 

department visits for stroke in Edmonton, Canada. Eur. J. Epid 21:689-700 

Wellenius (2006). Effects of ambient ozone on functional status in patients with chronic 

congestive heart failure. A repeated-measures study. Environ Health: 6-26. 

Zanobettei and Schwatz (2006). Air pollution and emergency admissions in Boston, MA. J. 

Epid. Comm. Health 60:890-895.