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Comments on: ENVIROi J1vtENTAL TOBACCO SMOKE: A GUIDE TO WORKPLACE SMOKING POLICIES [Draft] EPA 400/6-90/004 Response Addressing: Chapter 1: What Is ETS? Section: Toxins and Irritants Topic: Carbon Monoxide (CO) Chapter 3: Health Effects of ETS Section: People With Heart Disease Section: Heart Disease Section: Respiratory Disease Prepared by: Arnold T. Mosberg, Ph.D. Master R&D Toxicologist Manager. Animal Biology R.J. Reynolds Tobacco Company October 1990

SUMMARY: The statements in the EPA public review Draft document, "Environmental Tobacco Smoke: A Guide to Workplace Smoking Policies,"concerning alleged toxicity and irritancy of CO and alleged health effects of ETS are irrelevant and alarmist. The minute concentrations of CO measured in ETS fall below all regulatory standards and produce no significant effect on aerobic capacity or cardiovascular function. The unsubstantiated insinuation that ETS is somehow associated with "heart disease," or exacerbates its effects, is at best hypothetical. Studies presented as evidence for positive correlation between ETS and respiratory disease in adults and children are inconsistent and structurally weak. Data concerning children are totally irrelevant for workplace environments. COMMENTARY: Commentary is presented in four parts: (1) Toxins and Irritants - Carbon Monoxide; (2) Health Effects of ETS; (3) Respiratory Disease in Adults; and (4) Respiratory Disease in Children. 1. Toxins and Irritants » Carbon Monoxide Summarv: In contrast to the statements in the EPA document "Environmental Tobacco Smoke: A Guide to Workplace Smoking Policies," the combined evidence that CO concentrations in office buildings do not exceed 9 ppm and that COHb concentrations associated with exposure to as much as 9 ppm CO do not induce any alterations in cardiovascular function, even in cardiovascularly compromised segments of the population, suggests that inclusion of ETS CO as a meaningful toxicant or irritant in the EPA document

is misleading in the context of the EPA discussion. Commentary: The Guide notes "carbon monoxide is a gas that interferes with the ability of the blood to carry oxygen" [The Guide, p. 9] and that ETS adds "to the body burden of carbon monoxide from other environmental sources" [The Guide, p. 9]. The EPA implies that ETS significantly contributes to indoor air carbon monoxide ("CO"), concentrations and results in nonsmokers being deprived of normally available oxygen. This is not an accurate representation of the quantitative impact of ETS CO concentrations on the environment nor is it correct to assume that biological effects associated with exposure to high concentrations of CO are likely to occur at concentrations found in ETS. The highest CO concentration in office buildings reported by Carson and Erickson, 1988, was 8.7 ppm without correction for ambient CO concentrations from outside sources. Even so, all concentrations measured were below EPA's own established standard of 9 ppm [EPA-Air Quality Criterion for CO] and well below the OSHA TLV of 35 ppm for an 8-hour work period [Fed. Reg., January 19, 1989]. In addition, 13 of 23 offices evaluated by Carson and Erikson, 1988, in which smoking took place were below the outdoor concentrations of CO. These data show that CO concentrations in office buildings do not increase significantly as a result of ETS. Thus, the contrnbution of ETS to ambient CO concentrations in the workplace must be considered insignificant. Horvath and Bedi, 1988, exposed nonsmoking men to 0 or 9 ppm CO for 8 hours at both sea level and at a simulated 2134 meters. They measured each individual's ability to perform a maximal aerobic capacity test. Results indicated that COHb 2

concentrations associated with exposure to as much as 9 ppm CO do not induce alterations in cardiovascular functions. Sheps et al., 1987, examined 30 patients with ischemic heart disease and found no significant effects of COHb levels of 3.8% on either resting or exercise hemodynamics. The time to onset of angina, the duration of angina, and electrocardiophysiologic parameters were not altered by this concentration of COHb. This COHb concentration is five times those measured in the Horvath study in which individuals were exposed continuously for 8 hours to CO concentrations greater than those measured by Carson and Erikson, 1988, for office buildings. In their review of CO and the production or aggravation of cardiovascular disease processes, Weir and Fabiano, 1982, indicated that the available studies suggest that concern is largely unwarranted. They found no convincing evidence that chronic CO exposure increases the risk of clinically significant atherosclerotic disease. They also concluded that low to moderate CO exposure does not adversely affect cardiac rhythm in man. In addition, cardiovascular studies that support the national ambient air-quality standards for CO have been investigated by a committee formed by the EPA which concluded that the Agency should not rely on the results. The combined evidence that CO concentrations in office buildings do not exceed 9 ppm, and that COHb concentrations associated with exposure to 9 ppm or more do not induce any alterations in cardiovascular function, even in compromised segments of the population, suggests that the inclusion of ETS CO as a toodcant or irritant in the EPA 3

document is misleading in the context of an ETS discussion. 2. Health Effects of ETS - Heart Disease Summarv: The paucity of meaningful data on the alleged relationship between ETS exposure and heart disease and the failure of EPA, by its own admission, to conduct a complete analysis of the few available data on this relationship necessitate deletion of this section from the EPA document "Environmental Tobacco Smoke: A Guide to the Workplace Smoking Policies." Commentary: The EPA document includes two references to heart disease in Chapter 3; these are heart disease and people with heart disease. In the heading associated with "people with heart disease," [The Guide, p. 17) the EPA suggests that exposure to CO from ETS results in alterations of cardiovascular dynamics in individuals already compromised with coronary vascular disease. The discussion above describes both the extremely minimal exposure to CO that individuals are likely to encounter from ETS and the lack of the effects on both compromised and healthy individuals of concentrations in excess of those found in ETS. Again, the EPA uses the excuse that it has not conducted a complete analysis of the information. In the case of heart disease [The Guide, p. 18], the EPA refers to epidemiologic studies in which the relationship between heart disease and ETS exposure was examined. The EPA itself concludes that these data are insufficient to conclude that ETS 4

causes heart disease. The EPA indicates that it has not conducted a full review of the literature, yet it suggests that an association may exist. This is simply an inadequate reason for the EPA to include the topic of heart disease in the chapter of health effects of ETS. The National Research Council (NRC, 1986) reviewed the studies of Garland, Gillis, Hirayama and Svendsen which are referenced by the EPA. At that time, the NRC concluded that, overall, these studies showed (a) no statistically significant effects of ETS exposure on the heart rate or blood pressure of resting healthy men, women, and school age children, (b) no difference in the cardiovascular changes observed in exercising men and women exposed to ETS and to non-ETS conditions, and (c) despite the plausibility of cardiovascular morbidity and mortality, no statistically significant effects of ETS except for those reported in the Hirayama study of a Japanese population. The Hirayama study has been criticized by many reviewers because of many methodological problems, including the misclassification of smokers and nonsmokers, misclassification of dose response, ignoring workplace exposure, omission of control for indoor air pollution such as cooking with kerosene stoves, and utilization of a non- representative sample of the Japanese population. The inclusion of the heading "heart disease" in a document which, at first review, masquerades as a scientific compilation of accepted fact is misleading and puts undue and unfair emphasis on the completely unproven hypothesis that ETS exposure and the development of heart disease are related. The uncertainty of the current knowledge of the relationship between ETS and the development of heart disease should be presented in the EPA's Policy Guide. 5

3. Respiratory Disease in Adults Summarv: Because the eleven studies in which the relationship between ETS and pulmonary function in adults was examined employed questionable data collection techniques and gave discordant results, it is not possible for the EPA to conclude that any significant relation exists in adults between ETS and pulmonary function. This section in the EPA document "Environmental Tobacco Smoking: A Guide to Workplace Smoking Policies" requires drastic revision. Since the relationship between exposure to ETS and respiratory diseases/symptoms in children is not pertinent to a discussion of workplace concentrations and exposure to ETS, this section should be deleted from the EPA document "Environmental Tobacco Smoke: A Guide to Workplace Smoking Policies." Commentan+: Eleven studies reviewed the relationship between ETS exposure and pulmonary function in adults (Schilling et al., 1977; White and Froeb, 1980; Comstock et al. 1981; Kauffmann et al. 1983; Salem et al., 1984; Lebowitz, 1984; Brunekreef et al., 1985; Hosein and Corey, 1986; Svendsen et a1.,1987; Kauffmann et al., 1989; Hole et al., 1989). Of these numbers, four found differences in one or more parameters of respiratory function associated with ETS exposure, seven did not. In those in which a reduction in one parameter of pulmonary function was reported, the degree of reduction was small (3-15%) and must be considered to be of questionable clinical signif cance (Bates, 1989; Miller,1986). In addition, the majority of these studies employed questionnaires and household or spousal smoking as an index of ETS exposure, both of which predispose to the misclassification of 6

smoking status and exposure estimate. Eight studies evaluated the relationship of ETS exposure and respiratory symptoms and/or disease as endpoints (Schilling et al., 1977; Simecek, 1980; Comstock et al., 1981; Lebowitz, 1984; Gillis et a~., 1984; Kalandidi et al., 1987; Kauffmann et al., 1989; Hole et al., 1989). The findings were equally divided, with four studies reporting positive relationships and four without such relationships. These studies were too variable in their fmdings to support a unified interpretation regarding ETS and respiratory disease in adults. Acute exposure in normal individuals generally fails to demonstrate adverse effects of short term ETS exposure on pulmonary function (Pimm et al., 1978; Shephard et al., 1979a). Similar studies in asthmatics have yielded inconsistent results (Shephard, 1977; Dahms et al., 1981; Knight and Breslin, 1985; Wiedemann et al., 1986; Stankus et al., 1988). Based upon available literature on the subject of respiratory disease and ETS exposure, conclusions regarding potential relationships between ETS exposure and respiratory disease are not possible. In addition, the minimal magnitude of the measurable responses found to be statistically significant suggests that the results are of no clinical significance. 4. Respiratorv Disease in Children Summary: Studies presented as evidence for positive correlation between ET'3 and respiratory disease in children are inaccurate and totally irrelevant. 7

Commentary: Several points must be considered in interpreting the findings regarding the association between parental smoking and increased incidence of respiratory symptoms and diseases in children. Witorsch, 1989, reviews the studies and makes several important observations. He identifies a number of factors that could account for the findings in this area, including socioeconomic status of the participants. Further, the studies relied upon questionnaires which are considered inaccurate. The mechanisms of action for the observed changes are unexplained and the variability of the observations increases with increasing age of the children studied. Finally, data regarding children are not significant to a discussion of workplace concentrations of ETS. 8

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