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Environmental Tobacco Smoke Overview Many people have recently come to believe that environmental tobacco smoke (ETS) is a cause of disease. It is the considered opinion of British- American Tobacco that this belief is not supported by the science. The vast majority of epidemiological studies on ETS do not repor~ overall statistically significant increases in risk. Therefore, in our view, not only has it not been proven that ETS causes disease, but ETS has not even been established to be a risk factor for diseases such as lung cancer and heart disease. Nevertheless, some now argue for increased restrictions on where people can smoke in order to protect non-smokers from exposure to ETS. This is particularly so in countries where smoking has become less socially acceptable. It is our view that the debate has become more political than scientific. British-American Tobacco accepts that some non-smokers find ETS annoying, and, because of this, supports the sensible accommodation of the interests of smokers and non-smokers alike. British-Ame6can Tobacco rejects the notion that smoking bans are needed to protect th~.health of.n_on- smokers. In our view, the science, when reviewed in a.~'_air.__and com_p|~te~= .'~' manner, does not prove that exposure to ETS causes disease in non- smokers; indeed, the science does not even establish a pattern of consistent statistical associations between ETS and the development of disease in adult nonsmokers. This view is shared by many scientists. What Is Environmental Tobacco Smoke? When someone lights up a cigarette in a room, smoke is released into the air from the burning end of the cigarette and by the smoker when exhaling. The smoke quickly mixes with the air and hence is highly diluted. AQ12885

Indoor air contains a huge number of substances at low levels, whether or not ETS is present. These substances originate from outdoor sources (dust, pollen, bacteria, traces of vehicle emissions and other pollution, etc.) and from indoor sources (cooking, heating, and other activities). Tests indicate that the actual types of substances found in indoor air are very similar with or without the presence of ETS.1 .There a~e some basic differences between mainstream smoke and ETS with respect to their physical and chemical properties. 2 Hence, exposure to the air in a room where someone is smoking is different from smoking itself, and the term "passive smoking" is therefore misleading. Measuring ETS Scientists have tried to measure the ETS exposure of a typical non-smoker. These experiments have been difficult for three reasons. First, there is actually very little smoke in the air. To collect enough to measure exposure can typically take several hours or longer. Most of the substances that have been measured in mainstream smoke are present at too low a level~o measure in ETS.. Second, there is very little known to be in ETS that is not already present in indoor air. Thus, when a measurement is token, it is often uncertain how much of a particular substance is actually derived from ETS. Third, ETS is a mixture of substances that constantly change in their relative concentrations as dissipation, dilution, ageing and removal occur. Therefore, a marker substance for ETS, such as airborne nicotine, cannot be related directly to total ETS exposure,~: ~ ;,~,~ ~ ~ ~ ~ ~. Despite these problems, scientists have devised methods to estimate typical ETS exposures. Overall, this research suggests that exposures are low. Recent studieK undertaken by Oak Ridge National Laboratories in the US and Coming Hazelton Laboratories in the UK confirm the view that exposure to ETS is extremely low.3 For example, the Hazelton study reported that, on average, non-smokers are exposed to a yearly exposure that is less than the amount delivered to a smoker ~om just five cigarettes (given a typical UK cigarette delivery of 12 mg tar, 1 mg nicQtine). AQ12885 O0 0 0 I~O

ETS and Disease Over the past 15 years or so, scientists in many different parts of the world have tried to answer the question of whether a non-smoker's exposure to ETS can cause disease. Lung cancer The majority of the research addressing the question of whether exposure to ETS causes lung cancer has been epidemiological - that is, statistical studies that have cdmpared the incidence of lung cancer in non-smokers exposed in some way to ETS with that in non-smokers not exposed. There is no scientific way to measure lifetime exposure accurately, so the. statistical studies rely on asking their subjects to remember when they might ~- have been around smokers through questions such as "Did your spouse smoke?" or "Did your colleagues smoke at work?" Inevitably, these methods are subject to a great deal of error. Most of the studies have looked at women who say they never smoked. These studies typically compare women married to a smoker with women married to a non-smoker. Over ,tO such statistical studies were published between 1980 and 1995. The overwhelming majority of these studies have not reported an overall statistically significant increase in lung cancer risk in the women married to smokers. That is, ETS exposure was not found to be a risk factor. A small minority of these studies have reported that ETS is a risk factor for lung cancer, but in these studies the reported relative risk was so small as to be in the range that, by generally accepted epidemiological standards, would be considered inconclusive. Some of the ETS and lung cancer studies also asked the non-smoking women whether they were exposed to ETS at work. Around 15 such studies have been published. A11 but one reported that there was no overall statistically significant increase in lung cancer for those non-smoking women exposed to ETS at work. In other words, ETS exposure at work was not a risk factor for lung cancer. In the one study that did report an overall statistically significant increase, the relative risk was 1.39. Recently the US National Cancer Institute said "[In epidemiological research] relative risks AQ12885

of less than two are considered small and usually difficult to interpret. Such increases may be due to chance, statistical bias, or the effect of confounding factors that are sometimes not evident.''4 Some of the studies have also looked at exposure in social settings and during childhood. Again the overwhelming majority do not report an overall statistically significant increase in risk for lung cancer. Whilst scientists continue to research whether ETS causes lung cancer, our view is that the relevant science today does not demonstrate that ETS exposure is a risk factor for lung cancer, let alone a cause. Childhood Disorders Statistical studies have also been used to try to determine whether exposure to ETS causes disease in children. Typically, such studies compare children from households where one or both parents smoke with children from households where neither parent smokes. The studies have looked at a variety of diseases, from minor respiratory ailments (coughs and wheezes) to asthma and sudden infant death syndrome ("cot death"). A number of the studies have reported an increased incidence of temporary respiratory symptoms and infections (such as coughing, wheezing, colds and bronchitis) among the pre-school age children of smoking parents compared with the pre-school age children of non-smoking parents. The increase in these symptoms and infections is not usually observed in studies that have looked at slightly older, school-age, children whose parents smoke. In the case of pre-school age children, it is uncertain whether these symptoms and infections are caused by ETS or by potential confounding factors i.e. other risk factors for disease that differ between smoking and nonsmoking households. These factors include diet, housing conditions and the availability and quality ofpre-natal care.5 The studies comparing the incidence of asthma in children" in households where one or both parents smoke with children in households where neither parent smokes generally fail to find ETS to be a risk factor for the AQ12885

development of asthma. Some studies do report that asthmatic children with parents that smoke have a higher incidence of symptoms of exacerbation. Again it is not certain whether this is because the parents smoke or because of other factors that differ in smoking households compared to nonsmoking households. Other studies have reported that smoking in the home is associated with sudden infant death syndrome (cot death). Those reporting that sudden infant death syndrome may occur more frequently in families where there is a smoker have been unable to establish ETS as the cause. No one fully understands the reasons behind sudden infant death syndrome. ~~: In our view, looking at all the relevant science, it has not been proven that exposure to ETS is a cause of disease in children. Adult respiratory disease Research has also looked at whether exposure to ETS might cause respiratory disease in non-smoking adults. There has been both statistical and clinical research on this issue. The statistical studies overall do not support the claim that ETS exposure is a risk factor for respiratory disease in non-smokers. The clinical research has focused on assessing the reaction of particularly sensitive individuals to high concentrations of ETS in chambers. Researchers have experienced difficulties in prompting a measurable response even from avowed "smoke-sensitive" asthmatics in these chambers. In our view, considering all the relevant science, it has not been proven that ETS exposure causes adult respiratory disease; nor has it been established to be a risk factor(REF Witorsch). Heart disease There has been much less research on the question of whether ETS exposure might cause heart disease. Most of that research h.as again been epidemiologieal. The most substantial data on this issue comes from three US databases - two from the American Cancer Society's Cancer Prevention Study Database (called CPSI and CPSII) and the US National Mortality AQ12885 0 0 0

Followback Survey. These studies, which together are ten times larger than all other pertinent studies combined, report no association between ETS exposure and heart disease (REF). In our view, considering the entirety of the relevant data, it has not been proven that ETS is a risk factor for heart disease, let alone a cause. Science or.Politics ? Despite the lack of convincing scientific data, several government bodies in the US, UK and Australia have reviewed the science and concluded that ETS is a cause of lung cancer and other diseases. Perhaps the most cited review is that of the US Environmental Protection. Agency (EPA), which issued its report in 1993. The EPA reached the~ conclusion that ETS was a cause of lung cancer in adult non-smokers and respiratory health problems in children. The process by which the EPA reached its conclusions has been questioned for many reasons. For example, an EPA staff member was reported to have said that "to fashion an indictment of lETS], "the ~gency had engaged in "fancy statistical footwork."6 Part of this was apparently to alter the significance level generally accepted by the scientific community from 95% to 90% in evaluating the studies. In essence, this doubles the likelihood that a study's findings are due to mere chance. The EPA's report has been widely criticised for its poor science. For example, an analysis sponsored by the US Department of Energy was critical of the report. The debate about poor science led the US Congress to ask its indet~ndent research arm, the Congressional Research Service (CRS), to look at the EPA report. Following its evaluation, the CRS was highly critical of the EPA's report. Indeed, in testimony given before the US Senate in 1994, Dr. Jane Gravelle of the CRS concluded that "Based on that evidence, as indicated in this testimony, our evaluation was that the statistical evidence does not appear to support a conclusion that there are substantial health effects of passive smoking." 10 Also, the EPA failed to consider two pertinent US studies before it released its final ETS report. One of these had received funding from the US National Cancer Institute AQ12885

and was the largest study of its kind published up to that time. This study reported no overall statistically increased risk of lung cancer from spousal smoking. Had the data from the NCI study been included in the EPA report, it is unlikely that the Agency would have been able to claim any overall statistically significant increased risk. Even ignoring these important studies, the EPA was still only able to calculate a weak relative risk for combined US studies of 1.19 (a relative risk of 1.0 means no increase in risk). Such weak relative risks are difficult to interpret. As a high ranking official of the US Food and Drug Administration once observed: "My basic rule is if the relative risk isn't at least three or four, forget it."8 At the release of an earlier draft of the risk assessment, the chairman of the EPA's science advisory board, Dr Morton Lippmann, speaking about the purported risk of ETS and lung cancer, told journalists that "the possibility of cancer from (ETS) is a small added risk, probably much less than you took to get here through Washington traffic."9 Nevertheless, the EPA's conclusion has been the driving force behind smoking bans in the US. The Science and Environmental Policy Project (SEPP), a Washington, DC- based think-tank, in a January 1996 press release included the EPA's conclusions on ETS as one of the "top five environmental policy 'myths' of 1995."11 The SEPP said that the EPA's position on ETS "represents environmental policies initiated or continued last year despite an absence of sound scientific data..." These criticisms of the EPA's conclusions on ETS are in accord with our view that the debate over whether ETS is a cause of disease has be~me political rather than scientific. Conclusion British-American Tobacco is of the view that it has not been proven that exposure to ETS is a cause of disease; nor has exposure, to ETS been established to be a risk factor for diseases such as lung cancer and heart disease. This view is shared by many scientists. AQ12885 ~0 0 0 ~0

British-American Tobacco supports the sensible accommodation of smokers and non-smokers alike. In view of the science, we do not believe that government regulations are needed to protect the health of non-smokers. In our view, common sense and courtesy can go a long way toward resolving problems some non-smokers may have with ETS. Smokers should make considerate decisions about when to refrain from smoking in the presence of those who find it annoying, or who may consider themselves to be particularly .sensitive. December9,1996December96 AQI2885 0 0 ~0

References Proctor, C, Warren, N D, Bevan, M J, "Measurement of Environmental Tobacco Smoke in an Air Conditioned Office Building," Present and Future of Indoor Air Quality, eds C Bieva et al (Amsterdam: Excerpta Medica, 1989): 167-172 (1989); Bayer, C, Black, M, "Thermal Desorption/Gas Chromatographic/Mass Spectrometric Analyses of Volatil~ Organic Compounds in the Offices of Smokers and Nonsmokers," Biomed Environ Mass Spect 14(8): 363-367 (1987). Guerin, Met al, The Chemistry of Environmental Tobacco Smoke: Composition and Measurement, Arm Arbor, M I, Lewis Publisher, at p. $0 (1992). Jenkins, R Aet al, "Determination of Personal Exposure of Non- Smokers to Environmental Tobacco Smoke in the United States," Lung Cancer 14(I, Suppl): S195-$213 0Vlareh 1996); Phillips, K et al, "Assessment of Personal Exposure to Environmental Tobacco Smoke in British Nonsmokers," Environmental International 20(6): 693-712 (1994). 4. Fumento, M, "Dirty Water," Reason 28(1): 52 (May 1996). Hood, R, Wu, J M, Witorsch, R, Witorsch, P, "Environmental Tobacco Smoke Exposure and Respiratory Health in Children: An Updated Critical Review and Analysis of the Epidemiologieal Literature," Indoor Environ 1:19-35 (1992); Witorseh, P, Witorseh, K, "Analysis of Potential Confounding Variables in Epidemiological Studies Of Parental/Household Smoking And Respiratory Health in Preschool Children,~ Indoor Environ 2(2): 71-91 (TVlareh 1993); Ecobichon, D J, Wu, J M, Environmental Tobacco Smoke, Lexington, M A, Lexington Books at 236 (1990). 6. Stone, R, "Bad News on Second-Hand Smoke," Science 257:607 (July 1992). AQ12885

10. Taubes, G, "Epidemiology Faces Its Limit," Science 269: 164-169, at 168 (July 14, 1995). Bocchino, F, "EPA Using 'Political Math' to Subtract from Tobacco," Tobacco International 14-16, at 14 (February 1, 1993). Gravelle, J, Zimmerman, D, "Statement Before Subcommittee on Clean Air and Nuclear Regulation, Committee on Environmental and Public Works,' United States Senate on Environmental Tobacco Smoke," Congressional Research Service, at CRS-16 (May 11, 1994). Press Release of The Science & Environmental Policy Project "TOP FIVE ENVIRONMENTAL POLICY 'MYTHS' OF 1995 TO BE RELEASED BY SCIENCE AND ENVIRONMENTAL POLICY PROJECT: List Challenges Costly Policies Not Supported By Sound~ Scientific Data," .~anuary 10, 1996 AQ12885 10