February 7, 2011

Testimony to the EPA Clean Air Science Ad visory Committee ( CASAC) Ozone Review Panel for the Reconsideration of the Na tional Ambient Air Quality Standard February 18, 2011

Bruce Copley, Ph.D. ExxonMobil Biomedical Sciences, Inc.

My name is Bruce Copley. I am an epidemiologi st with ExxonMobil Biomed ical Sciences, Inc. I would like to thank EPA and CASAC for the oppor tunity to address th e 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 cardiovascula r mortality and morbidity. Based on data from the 2008 review, EPA concluded that the data support this cau sality conclusion. The most
current studies on the health eff ects of ozone--excluded from rece nt deliberations on the ozone NAAQS discussion--clearly do no t support this causal ity conclusion. I will summarize the findings from these studies and also address w hy EPA’s acute mortality risk estimates are not accurate and, thus, do not justify lo wering the current ozone standard.

First, new scientific evidence clearly demonstrat es that in contrast to EPA’s conclusion, the ozone acute mortality association is sign ificantly confounded by exposure to other pollutants. I note that this new scientific evidence is espe cially critical to answ ering 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 PM 10 was included in a two-pollutant models, the "all-cause mortality" for ozone in the U.S., us ing data from the National Morbidity, Mortality and Air Pollution Study (NMMAPS), was reduc ed by 68-88% depending on the age group considered. Also, the cardiovasc ular 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 PM 10 was included in a two-pollutant model. This study also indicated regional heterogeneity of effect that suggests that a derived single national riskFebruary 7, 2011

estimate is unreliable for standard-setting. Frankl in 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 statis tically significant.

Second, a large body of new scientific inform ation clearly suggests th at, in contrast to EPA’s conclusion, current levels of ozon e do not cause cardiovascular morbidity. This new scientific evidence is highly rele vant to answering EPA charge question 9. Question 9 asks CASAC to provide their pers pective on the occurren ce and public health importance of various ozone induced health e ffects, including cardiovascular morbidity and mortality at alternate ozone standards. Numerous new ep idemiology studies report no
association between current ambient ozone leve ls in the U.S. and cardiovascular hospital
admissions. These studies include those focusi ng 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 co mbined cardiovascular and respir atory causes (Tolbert et al 2007, Zanobetti and Schwartz, 2006).

As noted by the HEI Review Co mmittee in their commentary on the findings from the study by Katsouyanni, this marked lack of an associati on for cardiovascular morbidity provides little
coherence for the ozone-cardiovascular mort ality 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 reconsider ation, EPA adopted the theory that the ozonemortality association was causal and also estimate d the risks of ozone ex posure and the benefits of reducing this pollutant, based on single-pollutant model results. The new scientific data cast doubt on these assumptions and appro aches. In order to f acilitate the most sc ientifically sound decision on the ozone NAAQS, a t horough assessment of all relevant scientific da ta, 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 im pact 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 Hea lth: a European and North American Approach (APHENA). HEI Report 142.
Smith et al. (2009). Reassessing the relationship be tween ozone and short-term mortality in U.S. urban communities. Inhalation Toxicology 29:37-61.
Symons et al. (2006). A case-cro ssover study of fine particulate matter air pollution and onset of congestive heart failure symptom exacer bation leading to hospitalization. Am J Epi 164:421- 433.
Szyskowiz et al. (2008). Ambient air polluti on 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 i ssues in a study of am bient air quality and emergency department visits in Atlanta. J. Expo. Sci. Env. Epid . 17 Supple 2: S29-35
Villeneouve et al. (2006). Associations be tween outdoor air pollution and emergency department visits for stroke in Edmonton, Canada. Eur. J. Epid 21:689-700
Wellenius (2006). Effects of am bient 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.