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I I I I I I I I I I I I I I I CxS-1 i studies, nonsmoking wives of men who smoke have 30 percent more lung cancer than nonsmoking wives of men who do not smoke. This risk is, in turn, only a tiny fraction of the risk from active smoking (probably around 3 percent)7. The risk in the United States epi studies was slightly lower, only about 20 percent. Based on the epi studies' 20 percent risk factors for the U.S., the EPA estimated 3000 lung cancer deaths from passive smoking, 2000 for those who are never-smokers and 1000 for former smokers.8 Extrapolation based on physieal evidence yields smaller effects. According to data in the EPA report, measures of cotinine in the urine indicate that, overall, passive smokers have about 1/2 of one percent of the level of active smokers. Or, to put it another way, given that the average smoker smokes about 20 cigarettes a day, the passive smoking effect is equivalent to smoking a tenth of a cigarette a day. In comparing the physical exposure extrapolation approach to the epi estimates, it is simpler to compare the effects on never-smokers. Since the number of current and former smokers are the same as the number of never-smokers, the estimated premature deaths annually from passive smoking for never-smokers would be about 600 using a linear 7 The risk of lung cancer in smokers and ex-smokers depends on intensity, duration, and, in the case of ex- smokers, time elapsed since quitting. Passive smoking would involve three percent of the risk of active smoking if there is a ten fold active-smoking risk (i.e. smokers have an additional estimated risk of lung cancer that is ten times the disease rate of nonsmokers) which is typical of current estimates of the risk for women as reported in the 1989 Surgeon General's Report, Reducing the Health Consequences of Smoking. U.S. Department of Health and Human Services, DDHS Publication No. (CDC) 89-8411). In generating the estimates of deaths from passive smoking, the EPA actually used the additional risk (of wives married to smokers as compared to wives married to nonsmokers) in the U.S. passive smoking studies, which was about 20 percent. If studies from all countries are considered, the estimated risk from these studies was 30 percent. 8 Actually, the only number that was directly estimated from the epi study was the calculation of slightly under 500 deaths due to increased risks for women married to nonsmokers. This number was, in fact, extrapolated backward using a linear physical exposure method to calculate an additional 1000 deaths from other sources of environmental exposure (e.g. workplace, social), for a total of 1500 female never-smoker deaths. A further extrapolation yielded 500 additional deaths for male never-smokers, and another 1000 for both male and female former smokers. Lung cancer deaths attributable to passive-smoking are two to three percent as large as the estimated 113,000 lung cancer deaths attributed to active-smoking. For data on widely accepted estimated active smoking deaths, see C. S tephen Redhead, Mortality and Economic Costs Attributable to Smoking and Alcohol Abuse, Congressional Research Service Report 93-SPR, April 20, 1993.

I CRS-12 extrapolation.s This number is considerably less than the EPA's estimate of 2000 never smoker deaths.10 There are potential problems with the physical exposure measure as well as with the epi approach. The physical extrapolation method used above assumes a linear relationship between the incidence of a disease and exposure. Based on evidence from the pattern for active smoking, however, a linear method may not be correct. There is some evidence that disease rises with square of the exposure or' even with higher powers in the case of lung cancer.ll If the disease were to rise with the square of exposure, then the estimate based on cotinine levels would be only 3 people rather than 600 people. Thus, in this case-the epi studies suggest 2000 deaths of never smokers and the physical exposure measure suggests 3 deaths and the contrast between the two approaches is even greater. It is also possible that cotinine is not the best measure of exposure; as discussed in the EPA study some exposure measures show larger and some show smaller effects. It is worth noting that the EPA chose the epidemiological studies as a basis of their approach, but they nevertheless relied on the cotinine measures for several aspects of their estimates (such as extrapolating from the effects on spouses of smokers to the population in general). HEART DISEASE AND OTSER CANCER Many of the statistical concerns raised above with regard to lung cancer are relevant to respiratory effects in children and heart disease in adults. Indeed, the conclusions by these 9 To extrapolate, multiply the ratio of cotinine (.005) by the ratio of never-smokers to ever smokers, and by the 113,000 deaths attributable to active smoking. to There is also a section in the EPA study that discusses extrapolations based on the physical exposure to passive smoking; these estimates also tend to.be smaller - in some cases, much smaller-than the epidemiological estimates. 11 Surgeon General's Report, p. 44. I I I I I I I I I I I I I I I I . I I

t I I I I I I I I I I I I I I I CRS-13 Government agencies about passive smoking and lung cancer are generally not extended to heart disease or other health effects in adults. The presence of other factors that may be related to these illnesses that are not controlled for are particularly important in the case of heart disease, general respiratory illness, and cancers in other parts of the body, where the link between active smoking and the disease is not as strong as in the case of lung cancer. In addition, the differences between deaths estimated from epi studies and from physical exposure extrapolations are much more pronounced in the case of heart disease estimates. Recall that the EPA estimate of lung cancer deaths from passive smoking was 3000. There has also been widespread reference to an estimate of 50,000 deaths attributable to passive smoking. The 50,000 estimate has been circulated by non-governm€:.t organizations, and was mentioned in testimony by the American Medical Association which stated that passive smoking "may kill as many as 53,000" Americans annually.12 This statement in turn appears to be ultimately traceable to an article by Wells published in 1988 in Environment International.ig This article used existing epidemiological studies to estimate these deaths which included, under one set of calculations, 3,700 lung cancer deaths, 12,300 deaths from other cancers, and 37,400 deaths from heart disease. (Wells actually reported estimates ranging from 38,000 to 53,000, with a preferred estimate of 46,000).14 12 Statement of the American Medical Association, Health and the Environment Subcommittee, House Committee on Energy and Commerce, Re Adverse Health Effects of Exposure to Environmental Tobacco Smoke, July 21, 1993. 13 A. Judson Wells, An Estimate of Adult Mortality in the United States from Passive Smoking. Environment International. Vol. 14, No. 3, 1988, 249-265. 14 Each issue of Environment International contains an editorial; the one in the issue containing the Wells article was directed at that article. The editorial indicated that the study received mixed reviews from referees (two recommended publication after revision and the third recommended against publication on the grounds that it was too speculative); the editors chose to publish the paper. In the following three years there were a series of critiques and rejoinders related to this paper. Letters from Alan W. Katzenstein, Peter M. Lee, and Larry Holcolm criticizing the Wells results; a clarifying letter from Takeshi Hirayama, a rebuttal to Katzenstein and Lee from James L. Repace and Alfred H. Lowrey, and a response from Wells were published in 1990 (Vol. 16, no. 2, pp. 175-193). In 1991, a letter from Stanton A. Glantz criticizing Lee was published along with Lee's reply (Vol. 17, no. 1, pp. 89-91). Later in 1991, a response of Lee to the 19901etters of Repace and Lowrey, and Wells, a letter from Muin J. Khoury clarifying a point raised in Lee's letter, a joint letter from Glantz and Lee clarifying an issue raised earlier in the I

I CRS-14 While the estimates from at least some of the epidemiology studies of lung cancer are significantly larger than the estimates based on physical exposure, these results are not magnitudes apart. The same cannot be said, however, for the Wells estimates of deaths from heart disease. Using the same type of linear physical exposure extrapolation as in the previous section would result in 700 deaths from coronary disease for never smokers, and perhaps another 350 for former smokers, with a total of about 1000. The comparable portion of the Wells' 53,000 estimate from the epid'emiological studies, even for several years ago, is 37,000, a number that is enormously larger. This large estimate occurs because the epidemiological studies; on the whole, show a very high risk estimate for passive smoking relative to active smoking for heart disease as compared to lung cancer. For example, Wells indicates a 30 percent additional risk for heart disease for males and a 20 percent rise for females resulting from exposure to passive smoke, as compared to a 70 percent risk for smokers. The passive-smoking deaths associated with these relative risks are immense compared to both the physical exposure extrapolation estimates for heart disease and to either method for lung cancer. Note that although the risk ratios are not that different from lung cancer, the absolute risk estimates are much larger. The risk of lung cancer for nonsmokers is very low, and any percentage of a small number is still a small number. The estimated risk for heart disease is much larger initially, and therefore any significant percentage change in the risk is larger. Put another way, even the epidemiological studies of lung cancer produced passive-smoking deaths of less than 3 percent of active-smoking deaths, while the heart disease studies produced estimates that were 26 percent of estimated active-smoking deaths. t~> ~-.~ -4~- . . rn r,~ year, and a response from Repace and Lowrey, and Wells to Lee's letter were pubIished'(VoL 17, no. 4, 379-387). m In 1992 (Vol. 18, No. 3, pp. 315-317, 321-325) another letter from Lee and response from Wells was published. '~ [!! ~ ~ I I I I I I I I I I I I I I 1 , I

I I I I I I I I I I I I I CRS-15 The biological plausibility of passive smoking effects on cardiovascular diseases has been the subject of some discussion.ib A likely explanation of these apparent large risks from passive smoking found in epidemiological studies for heart disease is, however, the absence of control for other factors." There are many important causes of heart disease (e.g. diet, lack of exercise, lack of preventive health care) that may be engaged in by smokers. There is much evidence that smokers tend to be less concerned about health risks in general. In general, studies do not, and perhaps cannot, eontrol for many of these factors. If smokers' wives share in these behaviors, the relationships found in the epidemiological studies are spurious. The Wells estimate of passive-smoking deaths from cancers other than lung cancer is even larger relative to a,~tive-smoking deaths than is the case of heart disease-about 50 percent. Again, these cancers are influenced by many other factors, and the same general criticisms can be made about these epidemiological estimates as in the case of heart'disease. In sum, this analysis s.uggests that the Wells estimates are so high relative to measures of physical exposure that they seem implausible. It also suggests that the absence of controls or the inability to control for other factors may be a. major problem in relying on epidemiological estimates of the health effects of passive smoking. To restate this criticism, if wives or children of smokers share in poor health habits or other factors that could contribute to illness, statistical associations found between disease and passive smoking could be incidental or misleading. 1s The argument has been made for a relationship in which passive smoking can have large effects relative to active smoking in some laboratory settings, which is largely attributed to increased sensitivity of some nonsmokers. See Stanton Glantz and William Parmley, Passive Smoking and Heart. Disease, in Circulation, vol. 53, no. 1, January 1991, pp. 1-12. 16 This position is taken by Gary L. Hubert, Robert E. Brockie, and V~ay K Mahajan in a paper written for the layman: Passive Smoking and Your Heart, Consumers Research, vol. 75., April 1992, pp. 13-19, 32. These authors consider the results in the Wells study and the similar heart diseases study by Steenland (1992) biologically implausible, and also note that six of the nine epidemiological studies show relative risks for passive smokers that are in excess of risks estimated' for active smokers and that most have very few controls for the other factors that might affect heart disease.

CRS-16 CONCLUSION - Our assessment of the existing evidence on passive smoking was made as a basis for drawing conclusions about the efficiency justifications for an increase in the cigarette tax. 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. This finding flows from an analysis of the statistical methodology employed in assessing such health effects andi purports to no technical research or conclusion on the physiology of disease-causing agents. I I I I I I I I I I I I I I I I