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Comments by Philip l1i L.-)rscti. I•1.D. , FACP. FCCP On EPA IlLaft Docuracnt " EnvironntChta1 Tobacco Smokc: A Guide To Workl,lace Smoking Policies " (Draft DocumCnc datcd Jui'ic 25, 1990) 9 m CS ~

The following comments are limited to those portions of the EPA's draft Guide to Workplace Smoking Policies addressing health effects of ETS. Since it is my understanding that the issues of lung cancer and resoiratory effects in young children are being addressed elsewhere, this paper will not address those two issues. Introduction In the introduction to the Guide, it is stated that "field studies, controlled experiments and mathematical models have shown that environmental tobacco smoke (ETS) is one of the most widespread and harmful (emphasis added) indoor air pollutants and is a major contributor to particulate indoor air pollution." [page 1, first paragraph]. The validity of "most widespread" and "major contributor" is at least arguable. More significantly, the use of "harmful", with the implication of "most harmful" (at least to the scientifically unsophisticated reader to whom this Guide is apparently addressed), inappropriately implies a relationship that remains to be established scientifically and is, thus, potentially misleading. How "harmful" ETS may be, if at all, and its relative potential "harmfulness" compared to other indoor air pollutants remains a matter of considerable legitimate scientific controversy. 2

While there may be "field studies" (presumably referring to epidemiological studies) that have been interpreted by some as suggesting that ETS exposure is associated with adverse health effects, the validity of such interpretations are open to serious question. There are very few "controlled experiments" addressing health effects of ETS, and the validity of the results of these and their interpretation are also a matter of some debate. As for mathematical models, those used by Repace and Lowery, Wells, and others, are dependent upon arguable assumptions of causation. Questions regarding the pre-existing validity of these assumptions notwithstanding, risk assessments that depend upon such assumptions cannot legitimately be used to "prove" the very assumptions upon which they rest. To do so represents an inappropriate and scientifically unacceptable exercise in circular reasoning. The technique of meta-analysis and the validity of its application to the epidemiological studies of spousal smoking by the NRC.and others have been seriously questioned and the interpretation and validity of the results of such analysis are highly controversial. The Guide's characterization of such mathematical manipulations as "mathematical models" showing that ETS is "harmful" implies a degree of scientific credibility and validity (especially to the intended lay, scientifically unsophisticated reader/user of this Guide) that is unjustified and inappropriate. Furthermore, in the absence 3

of comparative data relative to health effects of ETS and other indoor air pollutants, the conclusion that ETS is "one the most ... harmful" is premature, at best, and incorrect, at worst. The introductory statement, especially considering its strategic placement at the beginning of a document directed at unsophisticated non-scientists, therefore suggests an inappropriate bias on the part of the authors of the Guide. This statement also serves to misinform and mislead the unsophisticated reader/user to whom the Guide is directed. The introduction also states that both the 1986 Surgeon General's Report and the 1986 National Research Council (NRC) Report concluded that exposure to ETS "aggravates the conditions of people with heart disease." (page 1, paragraph 5]. Unfortunately, this statement does not accurately represent the conclusions of those reports. With regard to aggravation of heart disease, the 1986 Surgeon General's Report stated: "One study (Aronow, 1978, a, b,) suggested that involuntary smoking aggravates angina pectoris. This study was criticized because the endpoint, angina, was based on subjective evaluation and because factors such as stress were not controlled for. (Coodley, 1978; Robinson, 1978; Waite, 1978; Wakehan, 1978.) More important, the validity of Aronow's work has been questioned (Budiansky, 4

19831." [Page 106]. In the conclusion of the chapter on Health Effects in the Surgeon General's Report. the only statement made that was relevant to heart disease was: "Further studies on the relationship between involuntary smoking and cardiovascular disease are needed in order to determine whether involuntary smoking increases the risk of cardiovascular disease." [pages 107-108]. There were no conclusive statements even implying an opinion that ETS exposure "aggravates the condition of people with heart disease," and, in fact, a careful reading of the Surgeon General's Report would suggest the contrary. Similarly, the 1986 NRC Report, in commenting on the Aronow work, concluded: "The findings of this study, in the absence of a true double-blind approach, require verification by other research workers." [pages 260-261]. The NRC Report concluded that: "Existing studies have not provided evidence of serious harm in people with heart disease. With regard to angina onset, the findings are uncertain and need to be repeated." [page 266]. Further along in the introduction, the Guide states that "there is mounting evidence of heart disease mortality in non- 5

smokers from passive smoking." [page 2, paragraph 3]. Both the 1986 Surgeon General's Report and the 1986 Report of the NRC found the available data inadequate to conclude that ETS exposure was associated with increased mortality from heart disease. The Surgeon General's Report pointed to major problems and deficiencies in the studies reviewed [pages 105- 106] and concluded as noted above. The NRC found the published data to be wanting [pages 262-265] and concluded: "With respect to chronic cardiovascular morbidity and mortality, although biologically plausible, there is no evidence of statistically significant effects due to ETS exposure, apart from the study by Hirayama in Japan." (page 265). With respect to the Hirayama study, the NRC Report noted: "The potential biases inherent in this study (see Chapter 12) limit the weight that can be placed on these results." [page 264]. Since the publication of these two reports, there have been no additional significant data that would justify modifying the conclusions that they reached with respect to cardiovascular disease and ETS. Chapter 1: What is ETS? In the section entitled "Differences between Mainstream and Sidestream Smoke", the Guide indicates that, compared to 6

mainstream smoke, more ETS gets into the lungs. more of it remains there, and what is absorbed remains in the body longer (page 7]. This information is not accurate and its implications are potentially misleading, especially to a lay, scientifically unsophisticated reader. In fact, the available data indicate that differences in the physical properties of mainstream and sidestream smoke result in less retention of sidestream smoke particles (and, therefore, presumably, ETS) in the lungs compared to particles of mainstream smoke [Reasor, M., J Environ Hlth, 1987, 50:20-24]. . In support of the assertion that the chemicals absorbed from ETS remain in the body longer than those absorbed from mainstream smoke in active smokers, the Guide cites a papej: by Wells. While Wells may offer this opinion, he provides no data to support it. The only plausible basis for such a statement is the demonstration that nicotine metabolism is somewhat more rapid in active smokers than in non-smokers, presumably related to enzyme induction. Whether this has any relationship to other substances, including other chemicals and particulates, remains to be determined and is, at best, speculative. 7

Chapter 3: Health Effects of ETS Chapter 3 states that susceptible "sub-populations (those with special sensitivity to ETS) are at greater risk". [page 15, paragraph 1]. This is an assumption that remains to be supported by scientific data. In this regard, it should be noted that the 1986 NRC Report concluded: "Data are not available as to possible adverse cardiovascular effects in susceptible populations, such as infants. elderly, or diseased individuals." (page 11]. Similar conclusions have been reached by others in more recent reviews of the relevant literature (Mahajan, V.K. and Huber, G.L., Seminars in Respiratory Medicine, 1990, 11:87-114]. The Guide further states that "also potentially at risk are people with allergies, other respiratory conditions, heart disease and circulatory disease. All of these conditions may be aggravated by exposure to ETS." (page 16]. As was noted in both the 1986 Surgeon General's Report and the 1986 NRC Report, there were no data then available to support such an assumption. Since the publication of those two reports, there have been no further significant data addressing these issues and no reason to alter the essentially negative conclusions of the Reports. m ~ .~ Also on page 16 of the Guide is the statement that "strong m ~ W 8

irritants in ETS may exacerbate conditions in especially sensitive individuals. These include children and the approximately 10% of the population suffering from asthma, emphysema, bronchitis, and chronic sinusitis." Here again, with the exception of the question of asthma (which is discussed below), there is no body of data supporting such an assumption, as was noted in both the 1986 Surgeon General's Report and the 1986 NRC Report. The absence of such data has also been noted in more recent reviews of the area [Mahajan, and Huber, 1990, cited above; Witorsch, P., in Proc Int'l Symposium at McGill Univ, 1989, p.169-186; Witorsch, R.J., in McGill Symposium, 1989, p.205-226; Wexler, L.M., in McGill Symposium, 1989, p.139-152]. The Guide further states that "ETS may also cause respiratory disease in adults." (page 16]. It refers to several studies that "have reported small declines in lung function in non-smokers exposed to ETS". It neglects to refer, however, to the at least equal number of studies that fail to report such declines, as well as to the fact that neither the 1986 Surgeon General's Report nor the 1986 NRC Report could come to such a conclusion. The Guide also fails to note more recent reviews of the literature in this area, which similarly could find no good evidence to support a causal relationship QD I between ETS exposure and respiratory disease or dysfunction in ~ adults [Witorsch, P, in McGill Symposium, 1989]. GD %I SA 9

On page 17, in commenting on effects in asthmatics, the Guide concludes that "the data are too limited to draw conclusions." While this is a reasonably accurate statement, it is interesting to note that as a matter of fact the data with regard to asthma, although far from conclusive, are arguably less open to challenge than the data relative to other areas where the document nevertheless makes more definitive assertions, such as cardiovascular disease, susceptible individuals, adult respiratory disease, and cancer at sites other than the lung. Relative to cancer at sites other than the lung, while the Guide accurately states that "the data are too limited to be conclusive," (page 18] it then goes on to discuss the reported findings of several studies in this area in some detail, without pointing out the major deficiencies in these studies. The way in which this information is presented can leave the impression, especially to the scientifically unsophisticated reader to whom this document is directed, that these studies may be more valid and significant than is generally held to be the case. (Surgeon General's Report, 1986; NRC Report, 1986; Mahajan and Huber, 1990]. A more appropriately balanced treatment of this area would have ended after the statement that the data are too limited to be conclusive or, alternatively, if it was felt necessary to discuss the results 10