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I I I I I I I I I I I I U.S. SENATE COMMITTEE ON ENVIRONMENT & PUBLIC WORKS SUBCOMMITTEE ON CLEAN AIR & NUCLEAR REGULATION SENATOR JOSEPH I. LIEBERMAN, CHAIRMAN Hearing to discuss the possible health effects to non-smokers of environmental tobacco smoke Wednesday, May 11, 1994 9:30 a.m. Hart Senate Office Building, Rm. 216 WITNESS LIST Panel I The Honorable Carol M. Browner Administrator U.S. Environmental Protection Agency Washington, D.C. The Honorable M. Joycelyn Elders, M.D. Surgeon General U.S. Public Health Service Washington, D.C. Panel II I I I I I I Dr. Christopher Coggins Principal Research & Development Toxicologist R.J. Reynolds Winston-Salem, North Carolina Dr. Aubrey Taylor Professor and Chairman Department of Physiology University of Southern Alabama School of Medicine (On behalf of the American Lung Association) (Over)

I Panel III Dr. Jane Gravelle Senior Specialist in Economic Policy Congressional Research Service Washington, D.C. (Accompanied by Dr. Dennis Zimmerman Specialist in Public Finance Congressional Research Service) Dr. William Blot National Cancer Institute Consultant, EPA, Science Advisory Board Bethesda, Maryland I I I I I I I I I I I I I I I I

I I I I 63 How about that? SENATOR LIEBERMAN: Thank you, Senator Lautenberg. I actually have more questions but I'm going to submit them to you in writing, and hope that my colleagues will do the same, so we can move on to the third panel. It's been waiting quite a while. , I want to thank you, Dr. Taylor and Dr. Coggins, for being here and for your testimony. I I I I I I I I I I I DR. TAYLOR: Thank you, all, very much. SENATOR LIEBERMAN: Our third panel, Dr. Jane Gravelle, Senior Specialist in Economic Policy, Congressional Research Service, accompanied by Dr. Dennis Zimmerman, who's a Specialist in Public I can. DR. TAYLOR: Thank you all very much. SENATOR FAIRCLOTH: Dr. Taylor? DR. TAYLOR: Yes, sir. SENATOR FAIRCLOTH: I want a yes-or-no answer. DR. TAYLOR: Okay. SENATOR FAIRCLOTH: Is suntanning dangerous to your health? DR. TAYLOR: Suntanning can cause skin cancer. It certainly SENATOR FAIRCLOTH: All right. DR. TAYLOR: But everybody, I think, is quite aware of that. But see, I don't have to go into the sun unless I want to. I have that prerogative. I have the prerogative to also put on some suntan protection agent. But I don't have any prerogative when I go take my grandson -- I tell you what I really [unintelligible]. I have a grandson who has asthma. SENATOR FAIRCLOTH: I'm sorry. DR. TAYLOR: No. Let me -- I want to get this out. I have a grandson who has asthma. And what I did is that I walked -- we go into a restaurant, and if someone's smoking back in the smoking section, which isn't all the restaurant, he will immediately start wheezing. This is my grandson. And I've seen a lot of people wheezing, get sick, but it scares the hell out of me when my grandson gets sick. SENATOR LIEBERMAN: You made your point. Thank you. I

I 64 Finance; and Dr. William Blott of the National Cancer Institute, a consultant to EPA and its Science Advisory Board, from Bethesda, Maryland. Folks, thanks for your patience. Some of you have been referred to earlier on. So we look forward to hearing from you at this point. Dr. Gravelle, you're first. DR. JANE GRAVELLE: Mr. Chairman and members of the committee, my colleague Dennis Zimmerman and I would like to thank you for the invitation to discuss the statistical basis for estimates of the health effects of passive smoking. I would like to begin by noting that we're economists and our area of expertise relates to economic analysis and the associated areas of statistical inference and quantification of effects for purposes of the cost-benefit analysis and related economic_ policies. Our involvement in this issue was the result of a research paper on the proposed cigarette tax. In order to assess economic efficiency issues, it was necessary to examine any costs that smokers might impose on nonsmokers. This led us to a review of the methodology used to assess the scientific evidence on passive smoking. We realize that this passive-smoking issue is a controversial one. Let us begin by emphasizing what we are not saying. We are not saying the Environmental Protection Agency's analysis was done incorrectly or that the studies they analyzed were done incorrectly. We are not reaching conclusions about the biological and medical issues, which are outside our area of expertise. And we do not intend any numbers that we have calculated to represent a risk assessment. Our evaluation of the statistical evidence on passive smoking let to two conclusions. First, the evidence that passive smoking causes disease is far less certain than the effects for active smoking. Second, the health costs of these potential passive- smoking effects, which we translated into a tax per pack, are likely to be small, although there is likely to be some uncertainty attached to these estimates. The reasons for that view our outlined in our written testimony, which we would like to submit for the record. And I would like to highlight the major points made in that testimony. SENATOR LIEBERMAN: Fine. GRAVELLE: Now that I've said all the things we can't do, let me say what we can... SENATOR LIEBERMAN: Go ahead. I I I I I I I I I I I I I I I ~ ~ ~ I

I I I I I I I I I I I I I I I I I 65 GRAVELLE: ...say about it. The evidence of a health effect from passive smoking with no threshold observed for health damage -- excuse me. The evidence of a health effect from active smoking with no threshold observed for health damage is not sufficient to demonstrate a passive-smoking effect, since a threshold effect could occur between the lightest active-smoking level studied and the smaller level of passive- smoking exposure. Since theory is not certain, one approach to studying passive-smoking effects is to examine epidemiological or statistical studies. Given the small risks that are often found for passive smoking, the statistical problems are of greater concern for passive smoking than for active=smoking studies. That is, when the effects are small, it is more likely that some error in design or specification could be responsible for the results. And given this greater uncertainty, consistently of the results with alternative evidence becomes more critical. In the case of lung cancer, most recently summarized by the Environmental Protection Agency, 30 studies which examined the incidence of lung cancer among nonsmoking wives, depending on whether or not their husbands smoked, were combined into an aggregate study. The following are some of the issues discussed in our written statement that might bring some uncertainty to bear no these statistical studies. Let me say these tend to extend to things other than lung cancer: children's respiratory diseases, heart disease, and other diseases that have been studied. First, some method of aggregating these studies is necessary, but there are certain subjective aspects to performing such a combined analysis. Second, some uncertainty attaches to the estimates in most of the individual studies due to the need to rely on interview data to measure exposure. Third, there is a possibility that results reflect the effects of active smoking due to possible misclassification of former or current smokers as never-smokers. Fourth, the failure to account for other lifestyle factors that might be correlated with marriage to a smoker and that might be independently associated with lung cancer, leading to possible spurious correlation exists. And five, two large new studies which were not included in the EPA study do not seem to us to add certainty to the statistical I

I 66 evidence. Indeed, the results of the largest study finds no overall risk from passive smoking. Now, a possible alternative approach to examining the passive- smoking effects would be an extrapolation for the levels of active smoking, and it is discussed because it provides an alternative measure that might or might not corroborate the direct statistical evidence. The average exposure to passive smoking, as indicated in the EPA study based on cotinine (?) in the urine, is about one-half of one percent, or the equivalent of one-tenth of a cigarette per day. A linear extrapolation produces an estimate of 600 never-smoker deaths, compared to the 2000 never-smoker deaths estimated by the EPA based on statistical studies. * A non-linear extrapolation yields virtually no deaths. These differences are even more pronounced -- these discrepancies between the two approaches are even more pronounced for heart disease, where a linear extrapolation yields about a thousand deaths and the statistical studies show in excess of 30,000 deaths. These results I'll leave to you to judge what you think about these, but we see them as subject to question, since the statistical estimates for passive-smoking heart disease represent 26 percent of active-smoking attributable deaths, despite the much lower level of physical exposure. It's also much, much larger than the lung-cancer, estimated lung-cancer deaths. And the EPA rejected this extrapolation approach for several reasons, and I can elaborate on these later if you'd like, although they did review the literature -- and there's a literature using this linear extrapolation method -- and they actually used the approach themselves with passive smoking, extrapolating from female never-smoker deaths that could be estimated directly from their statistical risk ratios to workplace and other exposures. And I'd like to close by adding that -- I'd like to remind you of the fact that both of these methodologies, direct statistical evidence and physical extrapolation, have inherent problems, but currently they're the only recourse we have in providing you with information on the issues before you. We'd be happy to elaborate further on any of these issues. Thank you. SENATOR LIEBERMAN: Thank you, Dr. Gravelle. Thanks for your testimony and indicating the context in which you entered this discussion. I I I I I I I I I I I I I I I I

I I I I I I I I I I I I I I I I I 67 Dr. Blott, welcome. We look forward to your testimony now. DR. WILLIAM BLOTT: Thank you. Good morning, Senator Lieberman and members of the subcommittee. My name is William Blott. I am Chief of the Biostatistics Branch at the National Cancer Institute. I've been on the staff of NCI for about 20 years conducting epidemiologic research on the environmental and host determinants of cancer. Many of these research studies have evaluated the role of tobacco in cancer risk. I'm pleased and honored to be here today to discuss the conclusions of the EPA Science Advisory Board in its review of the EPA draft report on the health effects of passive smoking. In 1990 I was asked to serve as one of about nine consultants to a standing Science Advisory Board at EPA and was requested to address several issues in the draft report on passive smoking. Perhaps the most important issue was whether the evidence was sufficient to conclude that environmental tobacco smoke -- and occasionally I might refer to that as ETS -- is causally related to lung cancer. The Science Advisory Board met in December of 1990 and again in the summer of 1992 to discuss the EPA report and to review testimony on the health effects of ETS exposure. I helped the board prepare its recommendations, which were delivered to the EPA in the fall of 1992; and then the EPA, in January of 1993, released its final report. The Science Advisory Board unanimously concluded, based on the review of the totality of evidence available, that the EPA was justified in categorizing environmental tobacco smoke as a Class A carcinogen. That is, as a substance which can cause cancer in people. The board also concurred with the EPA's assessment that the severity of asthma and the risk of other respiratory diseases in children could be increased form exposure to environmental tobacco smoke. But I will restrict my remarks to its association with cancer. Over 30 epidemiologic studies conducted in the United States and abroad have evaluated risk of lung cancer among nonsmokers exposed to environmental tobacco smoke, primarily by studying lung cancer among nonsmoking women married to smokers. Not all of the studies have reported an excess risk linked to environmental tobacco smoke but the great majority have. This consistency of findings across studies throughout the world establishes that exposure to environmental tobacco smoke is indeed associated with a small but a measurable increase in lung cancer. I

I 68 Several additional features of the data led the Science Advisory Board, myself included, to conclude that the relationship was likely to be causal. That is, that it was the environmental tobacco smoke that was responsible for the increase in lung cancer among passive smokers. First, virtually all of the studies that examined dose- response trends found rising risk of lung cancer with increasing level of exposure to environmental tobacco smoke. The more the spouse smoked, the greater the risk to the nonsmoking partner. This is what would be expected if, in fact, environmental tobacco smoke were a carcinogen. Second, there was no compelling evidence that the association was simply due to bias or to confounding by other risk factors for lung cancer. Although only a few studies adjusted for dietary or other risk factors, those that did tended to show little change in the magnitude of the association between environmental tobacco smoke and lung cancer. Third, increased risks of lung cancer were actually observed at exposure levels found in typical environmental settings. Thus the risk assessment that was performed by EPA did not have to rely on extrapolations from high-dose settings, as is sometimes done when relevant low-dose data are not available. And finally, there is a biological plausibility of the association. We know that cigarette smoking is the dominant cause of lung cancer in this country, and in fact in most others, with upwards of a 20-fold excesses in risk in heavy smokers. Nonsmokers exposed to environmental tobacco smoke inhale many of the same substances that smokers do, although in smaller amounts. Components of tobacco smoke have been detected in the blood and in the urine of nonsmokers, With some of the carcinogenic compounds in tobacco bound to the hemoglobin of passive smokers. Thus there is no doubt that tobacco components are absorbed and metabolized by ETS-exposed nonsmokers. There are differences in the chemical compositions, quantitative differences in the chemical compositions of environmental tobacco smoke and inhaled cigarette smoke, but there are a great man qualitative similarities. It is therefore biologically plausible that this lower level of exposure to tobacco from environmental tobacco smoke results in an increase in lung cancer risk. There is uncertainty as to extent of the increased risk and the exact numbers of cancers among Americans that might result from passive smoking. Such imprecision is a common trait in epidemiologic studies and reflects variations in sample sizes and other characteristics of the available data. Thus the estimate that 3000 lung-cancer deaths per year are due.to environmental I I I I I I I I I I I I I I I k`Ca ~ ~tt I

I I I I I I I I I I I I I I I I I I 69 tobacco smoke exposure is reasonable but it is an approximate figure. The Science Advisory Board recommended that such uncertainty be recognized, but this did not alter our scientif ic judgment that prolonged exposure to environmental tobacco smoke can increase the risk of lung cancer. This was the fundamental conclusion that was drawn by EPA and also by reviews of the National Academy of Sciences and the Surgeon General, and one with which the Science Advisory Board and myself fully concurred. Thank you for this opportunity to come before you. I'll be happy to answer any questions. SENATOR LIEBERMAN: Thank you, Dr. Blott. Let me ask you a question that I'm going to submit in writing to Dr. Coggins, who was on the last panel, because I thought that -- I want you to respond, if you would, to what I thought was at the center of his critique of the EPA study and some of the other evidence, some of the other allegations about the effect of secondhand smoke on people. And that was this whole question of volume, or as he -- dose. DR. BLOTT: Dose. SENATOR LIEBERMAN: In other words, yes, perhaps the chemical components of the smoke that people inhale when they smoke and the chemical components of secondhand smoke are similar, but the dose is so different that it stretches the imagination to think that secondhand smoke could actually be such a determinant of cancer. He testi -- Dr. Coggins indicated in his testimony that the maximum amount of secondhand smoke to which a nonsmoker is exposed is equivalent to approximately one to four or one to five, I think he said, cigarettes per year. And he described -- he said that was such a trivial dose that it is, quote, scientif ically implausible that they can result in meaningful toxicological activity. And I'd say again, playing the -- not playing the role, but as a layman, the thought of one to four cigarettes a year doesn't sound like it could cause all the illness and disease and death that we've heard testified to. So, I know that -- I gather, from having gotten into -- that's the top of the iceberg. That's what we see. Underneath is all this complicated statistical inquiry and methodology. And I gather that some of this may have to do with the physical extrapolation method that Dr. Coggins used. But I wanted to ask you if you would respond to those allegations, because I think they go to the heart of what's at issue here. I

I 70 DR. BLOTT: Well, I think this one to -- the equivalent of one to four cigarettes per years is definitely a minority view. It's the first time I've heard this today. And I think the evidence that's available suggests that the amount of exposure to environmental tobacco -- from environmental tobacco smoke in a nonsmoker... SENATOR FAIRCLOTH: Would you come a little closer to the microphone? DR. BLOTT: That the actual levels experienced by nonsmokers are much greater than that. A comment that was made by Dr. Gravelle was if you lboked at cotinine levels, which cotinine is a metabolite of nicotine, in nonsmokers who are exposed to environmental tobacco smoke, compared to smokers, the ratio might be in the order of somewhere between one to a hundred or one to two hundred. That is, these nonsmokers have a much lower amount of cotinine in their body. But if you figure an average cigarette smoker smokes a pack a day of cigarettes pez year -- a pack of cigarettes per day and there are 365 days per year, you multiply 20 times 365 and you take one percent of that, it's going to be a number much greater than the one to four. The problem in the extrapolations from biomarkers, as they're called, is that there are so many different compounds in cigarette smoke. There may be 4000 different compounds. There are 40 or so carcinogens. And it depends -- the answer you get as to the relative exposure for a smoker, compared to a nonsmoker, exposed to environmental tobacco smoke depends upon which of these biomarkers you choose. If you choose the extreme that Dr. Coggins mentioned, you'll get this bay (?), which I think is not reasonable. You take a cotinine level... SENATOR LIEBERMAN: What's the extreme? DR. BLOTT: Well, that you get the equivalent of one to four cigarettes per year. SENATOR LIEBERMAN! Yeah. Are you familiar with the method used by Dr. Coggins? DR. BLOTT: In general. SENATOR LIEBERMAN: Yeah. DR. BLOTT: The extrapolation method. I I I I I I I I I I I I I I I I I I