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DRAFT ONLY THE EPA AND THE SCIENCE OF ENVIRONMENTAL TOBACCO SMOKE by Dr. S. Fred Singer S Professor of Environmental Sciences (on leave) University of Virginia and Senior Fellow Alexis de Tocqueville Institution and Mr. Kent Jeffreys Adjunct Scholar Alexis de Tocqueville Institution

About this study... "The EPA and the Science of Environmental Tobacco Smoke" is the first in a series of evaluations of the science that forms the basis of the Federal government's environmental regulatory decisions. Given the growing costs of compliance for environmental regulation on individuals, businesses, and state and local governments, it is extremely important that the public be made aware of the precise degree of potential health and ecological risks based on sound scientific principles. This in turn would result in more rational -- and perhaps less costly -- environmental regulation. The final report entitled "Science and Environmentalism" -- scheduled to be completed in mid-June -- will evaluate the science behind several of the most current environmental questions. The goal of the report is to provide policy-makers, the media and the general public with information that will help improve and rationalize environmental policy decisions. The Center on Regulation aind profit, non-partisan Alexis de Toquevill on the costs and benefits of regulation. omic.Growth, a research project of the non- tution, was established to conduct research Conda, executive director of the Alexis Ze 4969. Address: 2000 15th Street North, S: 5 ----------------------------------------------------------------- rther information, contact Cesar V. viilie Institution: Phone No: (703) 351- gton, Va. 22201 Note: Nothing written here should be construed as necessarily reflecting the views of the Alexis de Tocqueville Institution or its co-chairmen and directors, or as an attempt to aid or hinder legislation before Congress.

DRAFT ONLY The EPA and the Science of Environmental Tobacco Smoke f Introduction Il- The downward trend of cigarette F- ~ /F `E:_. ..1 g in~America has been going on for many years. Whereas almost half of all adults: on~ ed~. now fewer than three out of ten American adults smoke, and thrs rate~~(~,tinuig to decline. This everY ~'~ ~ downward trend is the result of a combination of•,factorsz greater knowledge of the health risks associated with smoking, increased federal' and state taxes, and a general reduction of tolerance for smoking on the part of nonsmokers, among other things. Ironically, as smoking has declined, the federal government has increased its campaign against smoking. Undoubtedly, many view this effort as beneficial to society. However, it now appears that the federal government has gone beyond its traditional anti-smoking efforts, consisting mainly of education and health warnings, and is now moving toward a (de facto) ban on smoking. The vehicle by which this ban may take effect is an Environmental Protection Agency (EPA) study which allegedly found harmful effects on non-smokers from environmental tobacco smoke, ETS, which is also called "second-hand smoke" and "passive smoking." If this were the case, it would be difficult to stop the government from banning smoking in the name of protecting innocent non-smokers. Unfortunately, in its zeal to abolish smoking, science has been sacrificed. The EPA's finding that second-hand smoke is harmful to human health is based on a lower threshold of risk assessment than what the agency normally uses for other substances. In short, the EPA study relied on methodologies different from those which have been historically used in such analyses. Scientific standards were seriously violated in order to produce a report to justify a political agenda, namely to ban smoking. Before the government takes action to ban some substance on the basis of its 1 W. Kip Viscusi, Smoking: Making The R_isky Decision, (New York: Oxford University Press, 1992), p.1. 1

danger to health, it is extremely important that we know the precise degree of danger based on generally accepted scientific principles. If science is debased in an effort to "do good," society ultimately may be left worse off. There are two reasons for this. First, if we debase the scientific method in pursuit of a political agenda, we are opening a Pandora's Box. Second, the number of dangers everyone encounters in everyday life are so numerous that if we do not carefully delineate the government's role in regulating , such dangers there is essentially no lim.iYto,how much government can ultimately control ` ~ . our lives. '' The health risk from smokii'tg.is explores the EPA's analysis of ETS or\seco and highly variable mixture of substances whA foaus of this paper. Instead, this paper dsmoke. By any name, it is a complex se~.through the air. And ETS has elicited a complex and highly variable political reaction:" . The Environmental Protection Agency h;is,compiled several studies and reports which examine various aspects of the ETS issue. Two in particular are considered at length in this paper; one examined the respiratory health effects of ETSZ and the other examined the economic consequences of a proposed restriction on smoking.3 In brief, EPA makes certain assumptions about ETS which are then used to buttress EPA's scientific and economic conclusions. Moreover, the science as presented is insufficient and the economic claims are similarly unsupportable. They will be dealt with in turn. First, we will examine EPA's use of the scientific research surrounding ETS. EPA and the Science of ETS There are certain things about smoking which sound science can demonstrate. 2 U.S. EPA, Office of Health and Environmental Assessment, Office of Research and Development "Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders" Washington, D.C., December 1992. Hereinafter cited as "U.S. EPA, Report." g U.S. EPA, Indoor Air Division 6607J, Office of Radiation and Indoor Air, "The Costs and Benefits of Smoking Restrictions: An Assessment of the Smoke-Free Environment Act of 1993 (H.R. 3434), Washington, D.C., April 1994. Hereinafter cited as "U.S. EPA, Costs and Benefits." 2

For example, active smoking may be detrimental to the health of millions of smokers. Nevertheless, EPA has no official role when it comes to regulating smoking. Yet, EPA lately has taken the leading role in publicizing the potential health risks from smoking. According to EPA Administrator Carol M. Browner, "Although EPA has no regulatory authority over tobacco products, it does have a responsibility to inform the public about dangers it finds in the environment.i4 In particular, EPA has gone far beyond its authority in making ETS an "environmental" issue within its regulatory jurisdiction. In the process, it has engaged in both scientific overreach and regulatory overreach. Admittedly, trying to prove that second-hand smoke carries a measurable risk of lung cancer and determining preciselywvhaIth`af~risk is are difficult tasks. It is accepted that smoking is linked to several forms o46r,'particularly of the lungs, and also to ~±iig, or ETS, should be based upon heart disease. Similar conclusions about pasl' i o c evidence. To that en A has undertaken a review of the equally strong scient'f'i , ,,~F ~ scientific literature to determine the effects of ETS on the lungs of nonsmokers. The .. ;~ EPA's major finding was that "ETS is a human lungcarcinogen, responsible for approximately 3000 lung cancer deaths,annually in U.S. nonsmokers."S The question addressed by this section is whether or not that statement is justified. Crossing the Threshold It is well-established that "the dose makes the poison." That is, almost any chemical substance will harm a person's health if administered in sufficiently large quantities. Even substances which are necessary for life itself become deadly at high doses. Unfortunately, the EPA ignores this fact in most of its risk assessments by applying a "linear no-threshold" theory of environmental harm. In essence, the linear no-threshold theory holds that high-dose effects can be extrapolated back to a zero dose 4 Carol M. Browner, Letter to the Editor, Washington Post (May 6, 1994). 5 U.S. EPA, Report, at page 1-1. 3

without searching for a threshold below which no health effect will be elicited.6 In other words, if it were found that exposure to a given level of some chemical substance caused one death per 100,000 population, then half the exposure would therefore cause one death per 200,000 population, one fourth the exposure would cause one death per 400,000 population, etc. This flawed assumption underpins almost all of the EPA's work on environmental exposures, from the Superfund program to radon in homes to, I especially, ETS. f The EPA claims to disceriiian "~p arent non-threshold nature of the dose- i response relationship observed betwee e smokung and lung cancer."' Even if this were true for active smoking (and, as i(uestt~^s that. statement is, it is beyond the scope of this paper), it is not automatically valid fo reje,at the possibility of a threshold effect for ETS. For environmental tobacco smokkiAot just a lower dose of the substances inhaled by a smoker; important, if poorly researched, chemical changes occur as tobacco smoke is diluted and cooled in the open air. Researchers recognize three principal types of tobacco smoke. "Mainstream smoke" is produced when the smoker draws air through a cigarette, thereby "fanning" the temperature as high as 900 degrees centigrade. Most of the compounds in smoke change as they cool and as they react with the smoker's mouth, throat and lungs. "Exhaled smoke" is not the same as the smoke that was inhaled. "Sidestream smoke" is that which is produced by the smoldering cigarette between puffs. Because the temperature is significantly lower (perhaps 500 to 600 degrees centigrade), different chemical compounds (or different amounts) are produced. Together, mainstream smoke, exhaled smoke and sidestream smoke produce environmental tobacco smoke, 6 See, for example, Elizabeth M. Whelan, Toxic Terror: The Truth Behind the Cancer Scares, Prometheus Books, Buffalo, NY, 1993. 7 U.S. EPA, Report, at page 5-1. 4

with sidestream smoke accounting for 85 to 90 percent.8 The EPA notes that some potentially carcinogenic compounds are present at much higher levels in sidestream smoke than in mainstream smoke. This is a function of the respective temperatures at which various compounds form. Regardless of the composition of sidestream smoke when it is produced, it rapidly undergoes changes, both chemical and in terms of concentration per liter of air. EPA's report recites several distinctions between ET:: and mainstream, or even sidestream smoke. The most important distinction arises from the significant dilution of the ETS. In addition, the composition and concentration of ETS~,is cihpendent on the number of smokers, their smoking styles, and the number of cigarS^s smbked in a given period of time. According to the EPA, for active MMAY "A clear dose-response relationship exists between lung cancer and amount of •.exp without any evidence of a threshold level.i9 Of course, a strong dose-response r"elatio~p does not rule out the existence of some minimum dose below which there will bp zero:;response. Yet the EPA almost never looks for a threshold for any potentially harmful substance. In fact, it is essentially an unofficial EPA policy to deny that thresholds exist for any potentially hazardous substance. As examples, consider EPA's stance on dioxins, radon gas, or pesticide residues in the food supply.10 What is more, the fact that tens of millions of smokers survive their habit without developing lung cancer seems to suggest that a threshold exists for each individual, regardless of EPA's assumptions concerning aggregate data. Thus, the statement that no evidence for a threshold exists could easily confuse members of the public. 8 Gary L. Huber, Robert E. Brockie, and Vijay K. Mahajan, "Smoke and Mirrors: The EPA's Flawed Study of Environmental Tobacco Smoke and Lung Cancer" Regulation (No. 3, 1993), p. 46. 9 U.S. EPA, Report, at page 4-1. 10 See, for example, Michael Gough, "Reevaluating the Risks From Dioxin," Journal of Regulation and Social Costs, January, 1991, pages 5-23; Bruce N. Ames and Lois S. Gold, "Chemical Carcinogenesis: Too Many Rodent Carcinogens," Proc_eedings of the National Academy of Sci,ence, 87: 7772-76, 1990. 5

As mentioned earlier, essentially every substance to which humans are exposed is potentially harmful. Many ordinary substances -- common table salt, for instance -- are fatal if ingested in sufficiently large amounts. In addition, hundreds of foods in the human diet contain enormous quantities of "natural carcinogens.n11 Because the human species has evolved the ability to self-repair the damage caused by these naturally occurring substances, we are also able to repair the similar damage caused by small amounts of other carcinogens, including the ones found in ETS. In the face of this assertion by EPA that no safe threshold exists for active smoking, it becomes important to examine• how closely EPA links ETS with mainstream smoke. The EPA's Guidelines fo -:Carcin eit,Risk Assessment (U.S. EPA, 1986) sets out "three criteria that must be met bc~fo _pausal• association can be inferred between exposure and cancer in humans: ~-~ 1. There is no identified bias that could.expktim the'association. 2. The possibility of confounding has been considered and ruled out as explaining the association. " 3. The association is unlikely toq be due to chance."12 Under these criteria, one could conclude that mainstream smoke (MS) easily qualifies as a lung carcinogen. However, the EPA asserts that because sidestream smoke is chemically similar to MS and because sidestream smoke is the major constituent of ETS, then by inference ETS is also a Group A carcinogen under the EPA test. However, EPA is well aware that ETS is not identical to mainstream smoke, either qualitatively (chemical makeup) or quantitatively (dose). Nevertheless, EPA seems to adopt the old cliche': "Close enough for government work." It should be borne in mind that even if ETS is legitimately considered a "known human carcinogen," that does not prove that, at actual environmental exposures, it can or does cause lung cancer. In fact, most U.S. studies conducted on ETS and lung cancer .11 Lois S. Gold, et al., "Rodent Carcinogens: Setting Priorities," 258 Science 261, October 9, 1992. 12 U.S. EPA, Report, at page 4-28. 6

have found no statistically significant indications of carcinogenicity. Many observers have questioned whether EPA's conclusions are justified." If this were limited to the question of an internal EPA categorization, it would not be excessively controversial. However, much more is riding on this classification than mere bookkeeping entries. Declaring ETS to be a Group A carcinogen has set in motion a chain of policy events which must ultimately result in widespread federal bans on smoking. To quote the EPA's expressed reasoning in full: "The conclusive evidence of the dose-related lung carcinogenicity of MS [mainstream smoke] in active smokers, coupled with information on the chemical similarities of MS and ETS and evidence of ETS uptake in nonsmokers, is sufficient by itself to establish ETS as a known human lung carcinogen, or "Group system: ~14 A" carcinogen under U.S. EPA's car~ci~,tig.~m classification . , . Similarly simplistic reasoning has` allow e EPA to publicly fret over almost every suggested cancer risk, from electroniagne 'ation to artificial sweeteners.75 tf~a~, Despite the EPA's conclusion that ETS is a~K4&A carcinogen, it is at the very least arguable that ETS would flunk each separate,stepMo6f the t~'iree-prong test. And it is ~. the EPA's effort to cross the final hurdle that has proZiuced~the harshest criticism. When its review discovered that existing U.S. studies of lung cancer and ETS did not support its position, the EPA arbitrarily reduced the traditional standard of proof, or "confidence interval." Only by this manipulation could the EPA claim that its analysis was statistically significant. Why is the concept -of statistical significance so important to epidemiological studies? As valuable as these studies can be, there are well-recognized limitations. For instance, no matter how well designed, epidemiological studies can only show 13 See, for example, Michael Fumento, "Is EPA Blowing Its Own Smoke?" Investor's Business Daily, January 28, 1993, page A- 1. 14 U.S. EPA, Report, at page 1-2, 1-3. 15 For a general discussion, see Michael Fumento, Science Under Siege, (William Morrow and Company, Inc., New York: 1993) 7

correlation, not causation. Only after many studies have found strong correlations covering large populations (as is the case with active smoking and lung cancer) are researchers on firmer ground in asserting direct causation. (Yet even then they may not know the precise mechanism.) Most individual studies, which are expensive and time- consuming, involve only a small number of individuals (or sample size). This reduces the confidence that researchers place in how well the sample population reflects the ,characteristics of the general population. Epidemiologic studies can test the specific hypothesis, for example, whether ETS is a risk factor for lung cancer. While even well designed studies cannot prove beyond any doubt that a particular substance is the cause of cancer, they can indicate that a particular substance is a potential risk facaor. In this case, the EPA assumed -- before it even began its investigation -- that,ETS~is a risk factor for lung cancer; the very question supposedly being asked. However; fhe ffthat most studies of ETS and lung cancer do ~+/ S ti not support this assumption is not entirely ~or~d bMPA. Why else did the EPA adopt unique- manipulations of the data which"4p#Vo l~c e~arly designed to cover up this embarrassing fact? Furthermore, the EPA does not utilize the.:appr6priate "two-tailed" analysis of whether ETS causes lung cancer. In a two-tailed test, a specific assumption is made, for example, that ET S has an effect on human health. (The two "tails" refer to the fact that the hypothesized effect may be harmful or beneficial: the evidence may point in either direction.) In addition, if ETS were found to have no measurable effect either way, that would be called the "null hypothesis." In its examination of ETS, however, the EPA utilizes a"one-tailed" test. That is, the EPA makes the assumption that ETS cannot stimulate the human immune response and thereby produce lower rates of lung cancer than would exist in the absence of exposure. However, several American studies examined by the EPA leave open this very point. Indeed, of the 30 studies considered for inclusion in the EPA report, "six found a statistically significant (but small) effect, 24 found no statistically significant effect, and 8