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I August 11, 1994 TESTIMONY IN RESPONSE TO OSHA'S IDENTIFICATION OF CARDIOVASCULAR DISEASE AS A HAZARD RESULTING FROM EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE IN THE WORKPLACE Presented by Helen Betty Hubert, M.P.H., Ph.D, My name is Helen Betty Hubert and I am here to present testimony in response to OSHA's contention that workplace exposure to environmental tobacco smoke causes cardiovascular disease in nonsmoking workers. I obtained my Ph.D. in Chronic Disease Epidemiology from Yale University and am currently a senior research scientist at Stanford University in the Department of Health Research and Policy. Prior to joining the staff at Stanford, I served for 4 years as the Director of Research at General Health Underwriting, Inc. in Washington, DC and for 6 years as a Research Epidemiologist at the National Heart, Lung, and Blood Institute of the National Institutes of Health in Bethesda, Maryland. Through these positions, I have gained extensive experience in the design, conduct, and analysis of human health data from large-scale epidemiologic studies and have published numerous articles evaluating cardiovascular disease in these populations. I am currently a member of the American Public Health Association, the Arthritis Health Professionals Association, the American College of Epidemiology, the American Heart Association Fellow Council on Epidemiology, and the Society for Epidemiologic Research and I serve as a peer reviewer for the American Journal of Epidemiology, American Journal of Public Health, the Joarnal of the American Medical Association, Chest, and Archives of Internal Medicine. Based on my experience, I was invited by the Washington Technical Information Group Inc. to review OSHA's statements regarding exposure to environmental tobacco smoke and cardiovascular disease. The following represents my views regarding OSHA's identification of cardiovascular disease as a hazard resulting from workplace exposure to environmental tobacco smoke. I I

I In its recently proposed regulation governing indoor air quality, OSHA identified cardiovascular disease as a major, quantifiable risk_to health in nonsmoking individuals exposed to environmental tobacco smoke in the workplace (59 FR 15968, April 5, 1994). The agency claims that these exposures are capable of inducing changes in cardiovascular parameters in humans and animals and that they are associated with measurable acute and chronic effects on the heart. Consequently, OSHA proposes in this rule to eliminate environmental tobacco smoke from indoor work environments. Based on the premise that environmental tobacco smoke is a cause of cardiovascular disease, the agency then presents precise estimates of the number of heart disease deaths that it claims will be prevented in the United States as a result of this action. I believe, however, that close review of the agency's discussion and of the studies in the rulemaking record reveal that neither the epidemiological evidence nor the experimental toxicology data that OSHA relies upon as justification provide sufficient support for the agency's position. It appears that the agency did not apply a rigorous scientific approach to its analysis of the relevant epidemiological evidence. Furthermore, the experimental animal data and studies - cited in the rulemaking record do not support the agency's conclusions. This testimony addresses the empirical basis of OSHA's conclusions. With regard to epidemiological evidence, it appears from the discussion that OSHA did not apply a rigorous scientific approach to its analysis of the relevant research. The agency failed to conduct a critical review or to evaluate the quality of the epidemiologic data it used to justify its claim that environmental tobacco smoke is statistically associated with heart disease. The agency's discussion of these data in its proposed rulemaking is inadequate, inconsistent, and incomplete and thus not grounded in sound scientific methods. This makes it impossible to either ascertain OSHA's reasoning for the allegation that environmental tobacco smoke is associated with an increased heart disease risk, or to assess the validity of the cited studies from the intbrmation'the agency provides. 2

I I I ~ I I t In addition, OSHA fails to acknowledge relevant factual evidence such as data on workplace exposures. These data do not indicate the existence of a statistically significant association between workplace exposures and risk of heart disease. Instead, OSHA assumes without convincing proof that spousal exposure data are directly applicable to work environments. Spousal data on exposure to envirottmentel tobacco smoke are neither relevant, reliable, nor sufficient to conclude that workplace exposure is associated with a statistically significant increase in the risk of heart disease to the exclusion of alternative hypotheses or explanations. For example, there is published data to suggest that exposure at home may be greater with respect to concentration, frequency, duration, and intake rate than in workplace settings (Guerin et al. 1992, Clayton et al. 1993, OSHA 4-129; Holcom et al. 1993; Siegel 1993; Gephart et al. 1994). In addition, confounding variables may vary in significance between home environment and workplace (Aviado 1993), and it is difficult to extrapolate from general population studies or studies of selected subgroups to working populations since employed populations are healthier on average than comparable nonworking populations (Last 1988). OSHA relies primarily upon the results of five studies (that are based on only four datasets) to derive its conclusions that exposure to environmental tobacco smoke is linked to cardiovascular disease. These are Hirayama (1984); Helsing et al (1988), He (1989); Sandler (1989), who evaluated the same data as Helsing; and Dobson et al. (1991). All five studies report low relative risks (1.5 to 2.5), fail to account for the possible effects of bias or confounding factors, and exhibit other flaws that limit their validity. Hirayarna (1984) and He et al. (1989), for example, are very difficult to assess due to the authors' lack of rigor in reporting their methods and the inherent biases that complicate the interpretation of results from case-control studies. Helsing et al. (1988) failed to fiilly ascertain, and thus may have underestimated, mortality of the study sample which, in addition, did not adequately reflect the overall population of the United States. Furthermore, the Helsing et al. (1988) study, which OSHA uses to estimate the risk of heart disease that provides the impetus for this proposed rulemaking, reported relative risks of mortality 3

I I due to arteriosclerotic heart disease in both men and women of less than 1.5. According to widely accepted standards of epidemiologic investigation, relative risks this low indicate an extremely weak association that may be the result of bias or confounding (Wynder 1990). In fact, Helsing et al. (1988) failed to adjust their analyses for significant heart disease risk factors (including blood pressure, setum cholesterol, glucose intolerance, or obesity) or for other potential residual confounders (including diet and physical exercise). This is a significant flaw, especially because of the low relative risks. Most importantly, Helsing et al. (1988) use data that are now 20 to 30 years old. Major lifestyle changes have occurred in the last 30 years, including major changes in smoking patterns and exposure to environmental tobacco smoke in the workplace. Thus, the data that are used by OSHA to estimate the risk for heart disease in the workplace are likely to be outdated. Reliable evidence of a statistical association, at the exclusion of alternative hypotheses, is only one criterion that OSHA must meet to demonstrate a causal relationship between environmental tobacco smoke and cardiovascular disease. According to standard principles of epidemiological research, other criteria include: (1) an association that is dose dependent where higher doses are consistently associated with higher incidence of disease; (2) consistency of associated risks across comparable studies; (3) specificity of the association in that the exposure is associated with the outcome after controlling for other confounding risk factors for disease; and (4) that the exposure precedes the onset of disease by a reasonable time period. In aggregate, the epidemiological evidence OSHA presents to support its claim that environmental tobacco smoke in the workplace is causally linked to cardiovascular disease fails to meet these criteria. OSHA also provides experimental data from studies in humans and animals, but these data fail as well to provide adequate support for the agenc}'s position. A review of the animat and human experimental studies in the tulemaking record reveals only weak evidence that environmental tobacco smoke can cause cardiovascular disease in animals, or affect the biochemical and physiological processes that may be involved in the formation of blood clots and atherosclerotic I

, I I I 1 plaques in humans or animals. Nor do the studies establish credible mechanisms by which environmental tobacco smoke might act. In general, these data are inadequate because they come from studies in which the effects of active smoking or exposure to mainstream smoke (which is a component of, but not identical to, environmental tobacco smoke) were evaluated, because the effects of environmental tobacco smoke were evaluated in smokers rather than nonsmokers, or because the studies contained serious methodological flaws that compromised their interpretation Furthermore, some reported effects were of such a small magnitude that their biological significance is doubtful. OSHA also makes several claims for which they provide no supporting data (such as the ability of environmental tobacco smoke to stimulate smooth cell proliferation or change blood lipids) and even cites reports with results that do not support its conclusions [such as the use of Dobson et al. (1991) to show increased fibrinogen levels in nonsmokers exposed to environmental tobacco smoke, when in fact no such conclusion may be drawn from the data presented]. Finally, the agency fails to address studies that show results that contradict its position (e.g, NCI 198 1, Coggins et al. 1993). In conclusion, I believe that OSHA fails to provide sufficient, relevant, factual evidence to prove that long-term exposure to environmental tobacco smoke in the workplace presents a significant risk of heart disease for nonsmoking workers. This failure raises serious concerns about the validity of the agency's risk assessment and subsequently of its estimates of coronary heart disease deaths that allegedly will be prevented by this rule.

REFERENCES I Aviado, D.M. 1993. Complex mixtures of tobacco smoke and the occupational environment. In Clayton G.D. and Clayton FE. (eds.). Patty's Industrial Hv¢iene and Toxicology. Fourth Edition. New York: John Wiley and Sons, Inc. Pp. 107-148. Clayton, C.A., Perritt, R.L., PelPu.rari, E.D., Thomas, K.W., Whitmore, R.W., Wallace, L.A., Ozkaynak, H., and Spengler, J.D. 1993. Particle total exposure assessment methodology (PTEAM) study: Distributions of aerosol and elemental concentrations in personal, indoor, and outdoor air samples in a Southern California community. J. Expo. Anal. Environ. Epidemiol. 3:227-249. Coggins, C.R.E., Ayres, P.H., Mosberg, A.T., Sagarez, J.W., and Hayes, A.W. 1993. Subchronic inhalation study in rats using aged and diluted sidestream smoke from a reference cigarette. Inhalation Toxicol. 5:77-96. (OSHA 4-60) Dobson, A.J., Alexander, H.M., Heller, R.F., and Lloyd, D.M. 1991. Passive smoking and the risk of heart attack or coronary death. Med. J. Aust. 154:793-797. (OSHA 4-85) Federal Register. Apti15, 1994. Volume 59. Pp. 15968-16039. (Not Enclosed) Gephart, L.A., Tell, J.G., and Triemer, L.R. 1994. Exposure factors manual. J. Soil Contam: 3:47-117. Guerin, M.R., Jenkins, R.A., and Tomkins, B.A. 1992. The Chemistry ofEnvironmental Tobacco Smoke: Composition and Measurement. Boca Raton: Lewis Publishers. (OSHA 4-129) He, Y., Li, L.X., Fong, C.C., Li, L.S., Chang, X.L., and Qua, Q.L. 1989. Passive smoking in females and coronary heart disease. Chin. Prev. Med. 23:19-22. (OSHA 4-138) Helsing, K.J., Sandler, D.P., Comstock, G.W., and Chee, E. 1988. Heart disease mortality in nonsmokers living with smokers. Am. J. Epidemiol. 127:915-922. (OSHA 4-139) Hirayarna, T. 1984. Cancer mortality in nonsmoking women with smoking husbands based on a large-scale cohort study in Japan. Prev. Med. 13:680-690. (OSHA 8-143) Holcomb, L.C. 1993. Indoor air quality and environmental tobacco smoke: Concentration and exposure. Environ. Int. 19•.9-40. Last, J.M. 1988. A Dictionarv of Epidemioloav. Second Edition. New York: Oxford University Press. 6

National Cancer Institute. 1981. Final Report 3nhalation bioassavQf, ciaarette smoke in dQgL Effects of Nicotine and Carbon Monoxide on Atherpgenesis. Hazleton Laboratories America Inc a I 1 I I Sandier, D.P., Comstock, G.W., Helsing, K.J., and Shore, D.L. 1989, Deaths from all-causes in non-smokers who lived with smokers. Am. J. Public Health 79:163-167. (OSHA 4-277) Siegel, M. 1993. Involuntary smoking in the restaurant workplace. A review of employee exposure and health effects. JAMA 270:490-494. Wynder, E.L. 1990. Epidemiological issues in weak associations. Int. J. Epidemiol. 19:S5-S7. ~ 7 ~ GO ~. 0 co w