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SMOKING AND HEALTH ISSUES AUGUST 21, 1989 CONFIDENTIAL ATTORNE¥-CLIENTMEMORANDUM CONTAINING OPINION AND IMPRESSIONS OF RETAINED COUNSEL

TABLF. OF CONTENTS INTRODUCTION ......................... 1 THE SCIENTIFIC DEBATE ON SMOKING AND HEALTH ......... 5 SMOKING AND' ADDICTION ..................... 60 THE NONSMOKER: ENVIRONMENTAL TOBACCO SMOKE .......... 76 PRIOR TOBACCO INDUSTRY POSITIONS ON SMOKING ANDHEALTH 9¸0 CONFIDENTIAL 10125996 - i -

INTRODUCTION The controversy over the claimed health effects of smoking is as old as the practice of smoking itself. There is no publ~ic health topic that has received as intense and prolonged scrutiny by the Congress, various federal agencies, the medical profession, and the press as has the issue of smoking and health. Smokers and non-smokers alike have been inundated with information about the health risks associated with smoking. The Surgeon General's Office, for example, in addition to releasing its well-known annual report dealing with health issues associated with. tobacco use, has for the last several years been pursuing a highly publicized campaign directed toward school-age children to achieve a "smoke free society" by the year 2000. Every pack of cigarettes sold in this country for the last 23. years has borne a Congressionally-mandated warning label. For the last 17 years, this same warning has appeared on all cigarette advertising. Yet the scientific evidence that smoking cigarettes (and other forms of tobacco use)~ causes cancer, heart disease, and other chronic illnesses is not so one-sided as is often claimed. Reputable independent scientists over the years have questioned the validity of the various charges made against smoking. Brown & Williamson. and the other major cigarette manufacturers have consistently maintained, with. considerable support, that it has CONF ]DENT IAL

not been proven that smoking causes any chronic disease. The industry's position is often misunderstood to be that smoking has been proved not to cause any disease. This is not the industry's position. The ~ndustry believes that the question, is still unanswered. This is not to say that Congress has acted inappropriately in continuing its scrutiny of the "public health" aspects o~ smoking. The "standard of proof" in a public health sense is quite different -- and rightly so-- than that required by science, or that mandated in. a courtroom. Particularly where the question is whether the public has sufficient information about a particular product, the government may decide to act before the scientific "case" regarding the product is complete. Many products carry with them claimed health risks-- butter, eggs, red meat, and milk are familiar examples. Many other products carry known health risks -- automobiles, knives, and whiskey are again familiar examples. The public awareness as to the claimed risks of these products is much less than that with regard to cigarettes. Moreover, with the possible exception, of alcohol, no product other than cigarettes has been subj~ected to as vehement and concerted an effort to restrict or deny its availability to the adult consuming public. Thus, the use of ~ONF |'DENT |AL - 2 -

cigarettes in light of this awareness (and in the face of this effort) is uniquely a ma£ter of personal and informed choice. Brown & Williamson and other cigarette manufacturers market their product for adults precisely because the question of whether to smoke is one based on an informed personal choice. The industry recognizes that the consumer has a great deal of negative information through which he or she must sort in making the decision to smoke. Because this topic has been so thoroughly and publicly canvassed,. Brown & Williamson does not agree with those opponents of smoking who wish to place greater restrictions on the availability of cigarettes -- those who wish to make the adult consumer's choice for the consumer, in the mistaken belief that only the choice not to smoke can be "right" for any individual, no matter how well informed he or she may be. The road down which some anti-smoking advocates wish to take American society is dangerous. Once the government begins to ban "life-style choices," it is impossible to predict where it will end. Who will draw the line dividing those products and activities that are "healthful," and thus "permissible," from those that are claimed to be "unhealthful," and thus "forbidden?'" More fundamentally, what will happen to the quality of life for members of such a society, under the heavy hand of such extraordinarily intrusive government action? CONFIDENT IAL

The following material outlines some potential topics for discussion should Brown & Williamson. determine to pursue a program of legislative contacts. This program would be designed to. provide governmental decision-makers with an understandingand appreciation. of Brown & Wi~liamson's position on smoking and health. At the same time, Brown & Williamson would acknowledge its understanding of positions Congress has taken. CONF ];DENT IAL - 4 -

THE SCIENTIFIC DEBATE ON SMOKING AND HEALTH CONFIDENTIAL - 5 -

Although it is assumed by many people, and often asserted by anti-smoking advocates, that the scientific community has long: been unanimous in concluding that smoking "causes" various diseases, the fact is that respected scientists have stated that the question of whether cigarette smoking causes disease remains unanswered. The passage of time has not diminished the flaws in the case for causation; many of the reasons for skepticism that were cited by scientists in. the 1950s and 1960s are sti~l valid concerns in the 1980s. At the same time, Brown. & Williamson and the other companies in the industry have behaved responsibly in funding substantial research efforts by independent scientists into the wide-ranging issues of "smoking and: health." Those efforts -- as described below -- have not always resulted in findings favorable to the industry. Much of that research -- favorable and unfavorable -- has nonetheless been published. CONFIDENT IAI. - 6 -

THE NATURE OF THE SCIENTIFIC EVIDENCE ON SMOKING AND HEALTH. A. Lunq Cancer i. Epidemioloqical Data The most important scientific part of the industry's critics' case is the various epidemiological studies associating cigarette smoking with certain chronic diseases.1 A number independent scientists, however, have expressed concern about the interpretation of such epidemiological data. These scientists have been unimpressed by the numbers of such studies,, because of concern about the underlying validity of the evidence. For example, in the early ~980s, Dr. Laurence Kupper, in criticizing many of these studies said: i. These studies have two primary methods of approach: retrospective and prospective. A retrospective study selects a group of lung cancer patients, then tries to backtrack in time to determine smoking histories. A prospective study identifies a specific group, determines their smoking habits, and then observes the disease patterns that develop. Both types of studies then arrange the raw data into various categories, and run statistical tests to determine if one group (smokers) differs from another (nonsmokers) with respect to a particular disease. These studies have generally shown that smokers are more likely to get lung cancer than non- smokers. Approximately 90% of lung cancer cases are smokers; less than 5% of smokers, however, get lung: cancer. CONF ],DEN] ],AL - 7 -

The main. prospective (i,.e., follow-up) studies concerning smoking and its relationship to mortality and morbidity from certain diseases (as discussed in the latest Surgeon. Genera~ reports) d~o not address the issue of causality. The claim that the conclusions reached are 'impressively uniform and consistent' does not mean that a causal relationship has been established, but only that approximately the same observed associations keep appearing. I_~n fact, the biases inherent in these studies preclude the riqht to claim that causality has been demonstrated. Actually, one could arque that the same associations keep appearinq because the same biases are present in each study. The fact that so: many studies have produced a positive association between smoking and lung cancer has led many people to make the false conclusion that 'quantity means quality.' The truth of the matter is that repeatability (!i.e., the ability to produce the same estimated association) does not imply accuracy (i.e., the ability to produce a valid estimate of the true association). In this regard, one study free from all bias and producing a valid measure of the true smoking-lung cancer association is worth more than a thousand biased studies, all of which provide the same distorted estimate of the true association.. (I) And, a recent editorial in the International Journal of Epidemioloqy suggested the following: CONFIDENT ]AL We trust that the global differences in cancer incidence will finally be explained by the interplay between the environment and our genes. Thereby, it is certain that molecular biologists will have to face the challenge to help explain these variations in. incidence. A question remains whether cancer epidemiology, and maybe epidemiology in general, will have to fall to the same leve~ of academic disrepute as miasma - 8 -

theory, to facilitate this scientific process of integration . The way out for epidem~ology would be to explicitly recogn,ize the challenge, anddirect research to programmes that focus specifically on the envi, ronment- gene interaction. (2') Specific criticisms of using epidemiological studies to "prove" causation, include the following points: First, epidemiological studies can show a statistical association between factors, but they cannot demonstrate a causal relationship. Even the 196.4 Surgeon General's Report conceded this: "Statistical methods cannot establish proof of a causal relationship in an association." (p. 20) This is self-evident because "cancer is a biologic, not a statistical problem." (3) Second, in epidemiological studies smokers, ex-smokers and nonsmokers are not randomly assigned to their study groups. Instead, they make their own decisions about smokingi,~ and they, therefore, constitute "self-selected" samples. Such self-selection Can introduce considerable bias into an ep~demiological study. Third, many of the large-scale prospective studies examining the relationship between smoking and disease do not adequately account for the potential effects of other factors that can affect the results. These factors include general l~ifestyle, CONFIDENT IAL -- 9 --

alcohol consumption, occupational and envi.ronmental exposures,2 genetics,~ aging and the immune processes. As one statistician has commented: In general it is ironic that while studies of environmental or occupational health effects are constrained to take population smoking habits into account, studies on smoking effects seldom bother to search for a report on occupational exposures. (4) Fourth, if smoking causes lung cancer, it would be reasonable to expect more of the disease in countries where more cigarettes are smoked per capita. That does not always happen. For example, Austria, Belgium, and Finland report higher lung cancer rates but considerably lower per capita tobacco consumption than the United States, Canada, and Australia. (5) Fifth, if cigarette smoking does cause cancer, then the earlier a person starts to smoke and the more he smokes, the sooner he would be expected to get lung cancer. Yet nonsmokers and smokers (whether they smoke a lot or a little) all appear to develop the disease at approximately the same age. (14) According to one expert: "that both the age of starting to smoke, and the rate of smoking, should have no appreciable influence on the average age Indeed, some environmental exposures that now may be considered significant -- such as radon gas in the home -- were not recognized as potentially hazardous at the time the studies were conducted. CONFIDENT IAL

of onset of lung cancer greatly taxes, if it does not destroy, any causal hypothesis." (6) Similarly, one major study indicated that inhalers had a lower lung cancer rate than non-inhalers. Sixth, the same type of epidemiological information used: to suggest that lung cancer has increased in. smokers, suggests that it may also have increased in nonsmokers. In an April 1979 report on this phenomenon, a scientist who believes that smoking causes lung cancer nonetheless conceded that factors besides cigarette smoking must have had a "significant effect" on the mortality rate of lung cancer. (7) Seventh, if cigarettes do cause lung cancer, one might reasonably expect that heavy smoking would lead invariably to the disease. Yet, the studies relied upon by the industry"s critics show that less than 5% of all smokers ever develop lung cancer. From the first to the most recent hearings .regarding smoking and health, Congress has heard scientists and physicians express their skepticism about the relationship between smoking and lung cancer. In 1957, Dr. Joseph Berkson, of the Mayo: Clinic, testified that "there is serious doubt as to the scientific validity" of the conclusion that smoking causes lung cancer. (8) In 1964, Dr. Thomas Burford, Chief of Thoracic and Cardiovascular Surgery at Barnes Hospital in St. Louis, Missouri, said "carefu~l CONF]DENTIAL - ii --

study of the literature will reveal that many thoughtful studies by competent people concur in the opinion that the. cause of lung cancer, or of cancer in any organ, is unknown. Without needlessly belaboring the issue, it is obvious that there is a large volume of good scientific evidence which tends to refute the premise that cigarette smoking is causally related to cancer of the lung." (9) Almost 20 years later, in 1983~ Dr. Walter Booker said "Despite what those in the legislative arena might believe, the cause or causes of cancer of the lung (and other organs) remain unknown. Both smokers and nonsmokers contract cancer and other diseases often associated with cigarette smoking, and we still don't know why." (110)3 The opinion of these scientists that smoking has not been proven to cause lung cancer rests not only on certain of the generic criticisms of the epidemiological "case" described above, but also on factors specific to that particular disease. For example, ostensibly parallel increases in the 20th century between the consumption of cigarettes and the incidence of lung cancer have been cited as one piece of evidence that smoking causes lung cancer. Yet, both pathologists and thoracic surgeons have repeatedly Indeed, the fundamental biological mechanisms of cancer are still largely a mystery. As an a.rticle ~n the Journal of the National Cancer Institute recently acknowledged: "Although a large number of factors have been associated with the development of malignant neoplasms in humans, the mechanisms are still largely unknown." (Ii) CONF )DENT IAL

testified before Congress that the data on lung cancer trends over time are not dispositive because dramatic improvements in physicians' ability to diagnose lung cancer caused more lung cancer to be reported in official health statistics. As Dr. Rosenblatt said in 1965, "statistics showing a tremendous increase in lung cancer during the past 30 years are misleading. The increase is only apparent and is [in part] the result of greater skill in the detection of the disease." (12) Similarly, changes in the International Classification of Diseases in the mid-20th century have inappropriately combined data for cancers that originated in the lung with cancers that spread to the lung from another part of the body. Since majlor internal cancers frequently spread to the lung, these secondary lung cancers have been included in the statistics on. smoking and lung cancer. This combination of primary and secondary lung cancers in some statistics has made it impossible accurately to establish a statistical relationship between primary lung cancer and any agent, including cigarette smoking. In sum., the use of epidemiological data to indict smoking as a "cause" of disease has many flaws, and neither the industry nor independent scientists have acted irresponsibly in noting those problems in the public debate over smoking and health. CONF ]DENT |AL

o Animal Studies Those claiming that cigarette smoking causes lung cancer also rely upon the experiments by Ernst Wynder and other scientists who. claim to have produced skin cancers by painting the skin of certain animals (usually mice)with tobacco '"tar." For several reasons, such skin-painting: studies are not directly applicable to the human smoking experience. First, the mice used in many of the experiments have been specially bred to be extremely sensitive to any possible carcinogenic activity. They therefore may react positively to many substances which are not carcinogenic in humans. Further, in the 1950s, Dr. Jonathan Hartwell of the National Cancer Institute compiled a list of animal carcinogen studies which included such common items as fructose (fruit sugar), glucose (processed sugar), and even lactic acid (made naturally by the human, body). He found that 481 of the 2,.108 common chemical compounds tested (23%) were "carcinogens'" in such. animal studies. But, neither Dr. Hartwell nor any other responsible scientist ever concluded that these many "animal carcinogens" were therefore human carcinogens. Second, the substance that is applied to the backs of mice in such. skin-painting experiments -- condensate created by solidifying tobacco smoke and m~xing it with a chemical solvent -- CONF ]DENT

is not the same substance as the fresh whole smoke a smoker inhales. It is for this reason that Brown & Williamson and the other tobacco companies sponsored animal studies by independent scientists which more closely resemble the human smoking condition- - i.e., experiments in which the animals inhale fresh, whole smoke. Despite numerous animal experiments involving many different species, reproducible human-type lung cancers have never been found in the lungs of animals as the result of inhaling fresh whole tobacco smoke. Third, the organ involved -- mouse skin -- is obviously quite different from a human lung. For example, animal skin lacks the intricate clearance mechanisms of the lungs, such as the mucus blanket which coats the lining of the major airways of the lung. Even the summary report of a study sponsored by the United States government utilizing skin painting techniques conceded that there is an "uncertain relationship between tumors resulting from mouse skin painted with condensate and human lung cancer." (13)i Once again, all scientists recognize the importance of inhalation studies which could tend to support, or as has been the case, cast doubt on the skin-painting results. Finally, the doses applied~ in, mouse skin painting are massively greater than the amounts of particulate matter which a smoker would encounter in a normal smoking situati~on. Such. CONF ]DENT [AL - 15-

experiments involve applying '"the wrong material, in the wrong form,~ in the wrong concentration, to the wrong tissue of the wrong animal." (14) As Dr. Greene. stated at the 1957 hearings, "the [skin-painting] experiments demonstrated that tobacco tar extracted by a special technique induces cancer in the skin of CAF mice, and! nothing more. This point is of little significance to workers in the fiel, d who have found that under certain conditions a multiplicity of substances in everyday use will induce cancer in m~ce of highly susceptible strains." For these reasons, the industry has properly insisted that animal inhalation experiments are more relevant to the question of whether cigarette smoking causes human lung cancer. Over the years, many researchers -- both supported by industry grants and completely independent of any industry connection -- have conducted such experiments where test animals have been forced to take in. large doses of whole smoke. One study recently concluded by Microbiological Associates (with funding from the Council for Tobacco Research) involved thousands of animals, in a lifetime experiment. These studies have not found any significant pathological changes, and none have found credible evidence of cancer CONF ] DEI~T, IAL -- 16 --

production.4 As Arthur Furst, the Director Emeritus of the University of San Francisco's Institute of Chemical Biology, said "For many years, I tried to induce lung cancer in animals with cigarette smoke, with no success, despite the most sophisticated smoking machines available. Not only were my colleagues and I unsuccessful, but every other investigator who. attempted to induce lung: cancer in animals by inhalation of fresh smoke also fail, ed." Thus, he said: "I have concluded that no reliable, reproducible animal studies have shown that the inhalation of cigarette smoke causes lung cancer." In sum, the totality of the evidence fails to establish that smoking is a cause of lung cancer. B. Cardiovascular Disease Independent scientists have similarly expressed skepticism about the alleged causal link between smoking and heart o One of the most thoroughly discussed animal studies was the beagle dog inhalation study conducted by Dr. Auerbach. Dr. Auerbach claimed to find changes which he labeled as cancerous, but his study was severely criticized. Dr. Victor Buhler stated in 1982: "That experiment suffered from. severe design defects, and the photomicrographs published with the article would not permit most pathologists to reach the conclusions stated by the authors." Significantly, Dr. Auerbach and others were unable toreplicate his results in later studies. CONFIDENT I~AL -- 17 --

disease. They have noted the inconsistent statistical correlations between smoking and heart disease in various populations; the strong: genetic influence in heart disease; and the failure of the critics of smoking to establish a mechanism to explain how tobacco smoke might cause heart disease. In 1964, Dr. Henry Russek testified before Congress that "statistical findings linking the tobacco habit to coronary disease afford no proof of a causal relationship.;" and that his research had shown that emotional stress was far more significant than cigarette smoking! in the development of heart attacks. (15) In 1982, Dr. Carl Seltzer, a Fellow of the American Heart Association's Council on Epidemiology, similarly said that the statement "'cigarette smoking is a major cause of heart disease,', is not scientifically valid." (16) Anti-smoking advocates blame nicotine for the development of heart disease. Yet no mechanism by which nicotine, or any other agent, is involved in heart disease has been demonstrated. Serious questions about what role, if any, nicotine plays have been raised as a result of autopsy findings of fatty deposits and other changes in the arteries of individuals who either have not smoked or could have smoked only briefly, such as infants, children, and young men killed in battle. (17) Even the 1983 U.S. Surgeon General's Report, which focused on cardiovascular disease, concedes that "the evid~ence for and against a primary role for nicotine in the development or acceleration of atherosclerosi, s is not conclusive." CONF [DENT [~AL

(18) That opinion was shared by Dr. H. Schievelbein, a German researcher who conducted research o:n the relationship between nicotine and the clogging of arteries. After reviewing the literature, he and his co-author concluded that "there is n_~o established evidence which supports the hypothesis that nicotine has any influence on the development" of those changes. [emphasis added] (19) The role of nicotine in the development of heart disease posited by anti-smoking advocates is further undermined by two epidemiological studies. In. 1983, a study that dealt with myocardial infarction (heart attack) reported finding -- contrary to what the authors expected -- that the nicotine and carbon monoxide levels of the cigarettes smoked by the study's subj~ects were not related to the risk of heart attack. (20) The second study, chaired by Dr. N. Wald, a well-known British scientist opposed to cigarette smoking,: examined the serum. (blood) levels of cotinine, a nicotine metabolite, in male nonsmokers and smokers of cigarettes only, cigars only, and pipes only. The study determined that the mean cotinine level for pipe smokers was significantly higher than the levels for cigarette and cigar smokers. Since studies of pipe smokers generally have not reported an increased risk of coronary heart disease, the researchers concluded that "niicotine is unlikely to be the major CONFIDENT I,AL

cause of the excess coronary heart disease mortality in cigarette smokers." (21) After re-evaluating their methodology in response to anti-smoking criticism of their study, the researchers agai, n concluded, "we can be reasonably confident that exposure to high systemic concentrations of nicotine is not a cause of the disease." Although the researchers argued that their data "cannot completely exonerate" nicotine, they added that the data do "substantially reduce the weight of evidence suggesting that nicotine is a cause of coronary heart disease." (22) Animal studies which purport to establish a causal role for nicotine in heart disease have been soundly criticized for their unrealistic and excessive test conditions. An American researcher who conducted animal studies on this subject has noted: "There have been some studies that have exhibited minor or questionable changes with the use of 6:00 or more cigarettes a day in man. This is such a large number that I think man would find it difficult to find the time to smoke them." (23) Tn contrast, animal studies using realistic doses of nicotine have "failed to initiate, exacerbate, or otherwise influence" the process leading to the clogging of arteries in test animals. (24) In one such study, which was funde~ by the United States government, mal!e beagle dogs fed a special diet to induce this process were exposed for two years to cilgarette Smoke containing low. or high levels of COMF |DENT |AL - 20-

nicotine and, in some cases, enriched with CO. According: to the final report of the research laboratory which conducted the study, "the results of this study lent no support to the suggestion that cigarette smoking increases the rate of development" of this process. (25) The foregoing authorities demonstrate the validity of one researcher"s summary: "While many studies have been done in this field, none [sic] have established nicotine as contributing to the causation, aggravation or precipitation of any cardiovascular disease." [emphasis added] (26) C. Chron,ic Obstructive Lunq Di, sease ~Emphysema) The failure of experiments to produce emphysema in animals that have inhaled cigarette smoke casts serious doubt on the statistical associations beween Chronic Obstructive Lung Disease (COLD) and smoking, in various epidemiological studies. At the 1982 House hearings, Dr. Domingo Aviado described his efforts over many years to induce emphysema in laboratory animals exposed to cigarette smoke. None of the experiments produced emphysema in the animals. Dr. Aviado therefore questioned "the logic of finding cigarette smoke the major cause of pulmonary emphysema when primary air pollutants [such. as sulfer oxides] have been shown to cause CONF ]DENT,|kL - 21 -

pulmonary emphysema in experimental animals, and. with the same models, cigarette smoking has not." (2:7) The 1984 Surqeon General's Report focused on COLD.~ According to the Report, mortality ratios of heavy smokers to nonsmokers are as high as 30 in published studies, and 80-90% of deaths from these, diseases are attributable to smoking. The Report concluded, however, that only 10-15% of smokers woul~d develop '"moderate or severe airflow obstruction." The Report al.so conceded: that "an animal model for the development of emphysema using the inhalation of cigarette smoke alone has not been convincingly demonstrated." As with lung cancer and heart disease, COLD appears to be "multifactorial." The literature has identified possible genetic factors associated with COLD,. familial and socio-economic factors, occupational and environmental exposures, poor nutrition, and~ infection. (28) II. RISK FACTORS: THE ISSUE AND ANALYSIS The anti-smoking forces, including the Surgeon General, claim that tobacco kills 350,000 to 400,000 persons per year. The claim is now so commonplace that most of the people repeating it CONF |DENT:IAL - 22 -

have no idea where it came from or what it really means. In, fact, the number and the computation, upon which it is based are subject to serious scientific challenge. The various calculations of numbers of disease cases or deaths have nothing to do with laboratory research or the biological mechanisms underlying the disease processes. These numbers are based solely on statistical associations obtained from epidemiological studies. Consequently, when a number of excess deaths is calculated, for example, deaths from lung cancer attributed to smoking, this number tells nothing about whether an individual smoker"s lung cancer "~is due" to smoking or some other factor, nor does it even tell which smokers in a group of lung cancer patients "developed" their disease because of smoking. Underlying the calculation of excess deaths due to. smoking is the scientifically unjustified interpretation of the reported statistical association between smoking and disease as a causal relationship. A comment in a recently published book titled~ Statistical Methods In Cancer Research provides a cautionary note in regard to the interpretation of excess deaths and attributable risks: CONF;]DENT|AL Unfortunately, the only way to be absolutely certain that a causal relationship exists is to intervene actively inthe system, by removing the disputed factor. In the absence of such - 23 -

evidence, a more cautious interpretation of the attributable risk measures would be terms of the proportion of risk explained by the given factor, where "explain' is used in the limited sense of statistical association. (29) In the context of smoking, this observation is pertinent because the claimed causal relationships between cigarette smoking and certain diseases, as discussed above, have not been scientifically established. The calculations of excess deaths due to smoking hawe been. subject to criticism over the years throughout the world. The Report of the Advisory Committee to the Surqeon General on Smokinq and Health (the Terry Report) published in 1964 did not provide a calculation of a number of excess deaths causally related to smoking in the population because, as the Report noted,, it "cannot be accurately estimated." (p. 31) In fact, the Committee, in preparing the report,~ considered the possibility of performing such calculations but, according to a doctor who attended their deliberations, decided not to because "it involves making so many assumptions that the Committee felt it should not attempt this, that it might be as misleading as it was informing." (30) Subsequent Reports have, however, made these calculations. In 1969, a distingu.ished physician testifying before a U.S. congressional committee said "the widely publicized accusa- CONF ],DENT ]~AL - 24 -

tions of hundreds of thousands of deaths caused by cigarettes, and of shortening life expectancy a specific number of minutes per cigarette smoked, are fanciful extrapolations and not factual data." (31) In 1986, a critical essay published in The Journal of Medical Sciences addressed the claim by the Health Education Council and the British Medical Association that 77,774 deaths in England and Wales were caused annually by smoking. These were 77,774 deaths from heart disease, lung cancer, emphysema and bronchitis among men and women. After a careful scientific analysis of the assumptions underlining the calculation, the researcher concluded: his essay by noting that "the notorious 77,774 deaths per year have to be consigned to the realm of fantasy " (32) In 1988, a New Zealand statistician published in the New~ Zealand Medical Journal criticism of the use of the attributable risk calculations in regard to that country. He described the estimates of death per year due to smoking as of "spurious accuracy" because they are based on disease rates subject to error and the assumption that statistical association is equivalent to causation. (33) An examination of the epidemio~ogical concepts used in the excess deaths cal, culation will highlight the uncertainties CONF ]~DENT ]:AL

mentioned above. The attributable risk percentage for smoking is. calculated by using two numbers -- the smokers' "relative risk" for a disease and the percentage of smokers in the population:. Both of these components contribute to the uncertainty in the attributable risk percentage. "Relative risk" is a statistical term. It represents the ratio of the number of deaths in a given population exposed to a substance over the number of deaths in a population that has not been exposed to the substance. For example, assume that the death rate for lung cancer among asbestos workers is 60 per i00,000; assume also that the lung cancer death rate for non-asbestos workers is I0 per i00,000. The "mortality ratio" is 6:1. Therefore, the "relative risk" for lung cancer among asbestos workers is 6. The 1989 U.S. Surqeon General's Report indicates that the nonsmoker death rate for lung cancer per i00,000 for males is 13.6 and for females is 11.4. These figures are divided into the smoker death rates for lung cancer per i00,000 to give relative risk for males of 11.94 and for females of 4.69. Relative risks are obtained from. epidemiological studies based on information regarding smokers'~ death rates and nonsmokers' death rates.5 Consequently, a~l the biases and variations in. those The epidemiologica~ studies relied upon most heavily in the 1989 Report are the American Cancer Society's CPS-I (1959-1965) and CPS-II (1982-~986) studies. CONF IDENT IAL - 26 -

calculations are transferred to the attributabl~e ri, sk calculation. In particular, if the population in an epidemiological study is not representative of the general population, the relative risks obtained from the non-representative group can be challenged when used to calculate attributable r~sk in general. Moreover,. the measurement of the prevalence of smoking in the population is frequently difficult to estimate accurately. A 1987 statistical methods text noted: "It is difficult to obtain estimates of attributable risk. Even cohorts such as the British doctors or US veterans d~ffer sufficiently from the general population., in terms of economic level for example, to. make extrapolation in terms of attributable risk hazardous." (34) The attributable deaths figure -- 390,000 in 1985 according to the 1989 Report -- is derived by projecting the expected non-smoker death rates for various chronic diseases onto the 1985 population,, subtracting the "expected" number of deaths from the actual deaths caused by those diseases, and attributing the difference to smoking. The breakdown o.f extra deaths in the 1989 ~eport is as follows: COM F i DENT~! AL - 27 -

Cancer Cardiovascular Disease COLD Other (e.q., residential fires)! 136,100 142,500 571,000 531,000 388,600 This technique has a number of inherent flaws. First, it assumes that causation, is fully established for lung cancer, a variety of other cancers, and heart disease; second, it also assumes that the ACS samples are not only representative of the entire United States population, but can be projected forward; and third, it assumes that smoking is the sole and only cause of "extra" smoker deaths -- an obvious fallacy which renders the 390,000 number virtually meaningless. The 1989 Report listed and discussed various "uncertainties" in its attributable risk calculations. The list includes the following points: "errors of classification of exposure levels (e.g., amount smoked, length of time quit),. representativeness of populations studied, failure to take into account confounding variables (e.g., occupational exposures), potential errors in estimating current or past cigarette use or non-use, and errors in classification of causes of death." (135). CONF I:DENT |AL

These sources of uncertainty, however, did not prevent the well- publicized claims of 390,000 excess deaths. One disquieting problem with the attributable risk calcu- lation for smoking arises when another attributable risk calculation is made for the same group for another exposure (e.g., occupational, diet). The two attributable, risk percentages can add up to over i00 percent, causing severe interpretational problems. For example, a report that in a group 60 percent of the deaths are due to smoking: and 70 percent of the same deaths are due to an occupational exposure presents problems. This occurs because an attributable risk percentage for smoking does not and cannot take into account any suspect other than smoking for the disease in question. An. epidemiologist pointed this out in discussing attributable risk as a fraction instead of a percent: "For any given individual, however, this estimate is fraught with difficulties. For one, the attributable fraction can have no unique value; when there is overlap and interaction with other factors, the estimate can always be eroded." (36) When the attributable risk formula was examined from a statistical perspective in view of its possible adoption by the U.S. Congress as a method of compensation in radiation and cancer cases, a statistician concluded that " . it is inappropriate CONF ),DEMT IAL - 29 -

either as a statistical measure of probability of causation or as a guide to share in causation." (37) No one denies that cancer and, most particularly, heart disease are multi-factorial diseases. Nor can anyone deny that smokers, as a class, are more exposed to many of these "other factors" than are non-smokers. These factors are "lifestyl:e," the same k~nds of choices or personality characteristics or environmental influences that may lead people to smoke. In 1988, the Public Health Service ("PHS"')I issued a report seeking an answer to the question "whether smokers have other unhealthy habits that may . . increase their probability of succumbing to serious illness, disability and even death.." The report concluded that "smoking is related to other unhealthy behaviors." Included in the survey were hours of s~eep (31% of heavy smokers got less than six hours, compared to 21% of never smokers); breakfast habits (48% of heavy smokers never eat breakfast, compared to 18% of never smokers); exercise (65% of heavy smokers were "sedentary," compared to 55% of never smokers); and alcohol consumption (22.5% of heavy smokers averaged two drinks a day, compared to 3.5% of nonsmokers). The big surprise was over- eating, where it was expected that smoking would have a uniformly favorable effect. In fact, ~t turned out that male heavy smokers snack more and are not significantly di~fferent in weight. CONF, IDENTIAL

The PHS results are more notable for their source than for their substance. Had the PHS surveyed the existing literature, it would have found evidence for smoker exposure to a wide variety of "other" risks: socio-economic factors (blue collar, education, income); geographical factors (urban versus rural); environmental factors (water and air pollution); alcohol; coffee; dietary habits (Vitamin A); drug use; lack of exercise; Type-A personality (aggressive or ambitious); stressed personality (idepressed or anxious); situational stress (unemployment and divorce); lack of preventive health care,, suicide, accidents, violence and overall risk-taking. The gross error in the attributable risk studies is that they are "univariate." They take into account only one health behavior, whereas there are many associated with smoking that might influence mortality. One way to demonstrate this error is to take another health behavior, apply a univariate analysis, and see where it leads. For instance, a recent preliminary report from the University of Minnesota finds that heavy coffee drinkers have a relative risk for lung cancer of about 7 to 1 (compared to 10 to 1 for smokers). If it is assumed that the only important variable is coffee and that a substantial portion of heavy coffee drinkers are smokers,~ a calculation can be made that re-attributes a very large portion of lung cancer deaths from smoking to coffee. The CONFIDENT IAL - 31 -

same sort of calculation could be done with. respect to exercise or stress or Type-A behavior or any of the other factors mentioned above -- if the data were available. Of course, the result of each of the univariate analyses would be wrong. Each would fail to take into account the "confounding" effects of all the others. A "multivariate" approach is more appropriate. In fact, many epidemiological studies include a lot of the relevant behavioral data. Nonetheless, the Surgeon General and others have chosen to focus only on smoking. In the Cipo~lone pretrial discovery, the defendants obtained (for the first time): the underlying American Cancer Society data (ACS Million Persons Study) relied upon in the 1989 Surgeon General's Report and many. other "excess death" calculations. Statistician Irwin Miller put the data (for women and lung cancer) into a computer and did a "multivariate" analysis -- ~.e., the computer juggled all the health-related behaviors simultaneously to see which ones were related to lung cancer. Dr. Miller'.s conclusion was that a great portion of Hhe apparent relationship between smoking and. lung cancer disappeared when other factors were taken, into account. He is doubtful, given the in.terdependence of all the health behaviors and the absence of full data, that any clear multi-variate conclusion can be drawn. CONF:IDENT |AL

III. THE INDUSTRY RESPONSE Notwithstanding the indictment by its critics, Brown & Williamson and the tobacco industry responded in an appropriate fashion to health issues raised about smoking by funding numerous independent research efforts. These efforts have involved hundreds of outside institutions and thousands of independent scientists who have added markedly to science's understanding of a number of diseases and any possible link between them and smoking. Council for Tobacco Research In 1954, the chief officers of nine tobacco products manufacturing companies in the United States, and five organizations of growers of leaf tobacco and operators of tobacco warehouses formed the Tobacco. Industry Research Committee (TIRC). The purpose of the TIRC was to investigate the connection between tobacco use and human health. Although the name, TIRC, was changed in. 1964 to the Council for Tobacco. Research (CTR), the organization continues to pursue the goals that were established by its founders in 1954. Seeking to promote objective, independent research on smoking and health, the TIRC formed a group of independent scientists called the Scientific Advisory Board (SAB):. This group CONF ]DENT:]AL

is composed o.f highly-regarded scientists who come fromwell-known universities, laboratories, and medical centers throughout the country. The SAB decides what research will be funded. CTR has been fortunate in that it has been guided by independent scientists of the highest reputation. The current members of the SAB are: Richard J. Bing, M.D., Professor of Medicine,. University of Southern California School of Medicine; Roswell K. Boutwell, Ph.D., Professor of Oncology, University of Wisconsin; Drummond H. Bowden, M.D., Professor and Head of Pathology, University of Manitoba; Michael J. Brennan, M.D., President and Medical Director, Michigan Cancer Foundation; Joseph D. Feldman, M.D., Editor, Journal of Immunoloqy; Jeffrey R. ~dle, Ph.D., Professor of Pharmacogenetics, University of Newcastle upon. Tyne; Leon O. Jacobson, M.D., Professor of the Department of Medicine, University of Chicago; Manfred L. Karnovsky,: Ph.D., Professor of Biological Chemistry, Harvard Medical School; Alfred G. Knudson, Jr., M.D.,. Ph.D., Fox Chase Cancer Center, Institute for Cancer Research; Henry T. Lynch, M.D., Professor and Chairman, Department of Preventive Medicine and Public Health, President,: Hereditary Cancer Institute, Creighton University Schoo~ of Medicine; G. Barry Pierce, M.D., American Cancer Society Centennial Research Professor, University of Colorado Health Sciences Center; Gordon H. Sato, Ph.D., Director,. W. Alton Jones Cell Science Center; Sheldon C. Sommers, M.D., C~inical Professor of Pathology, Columbla CONF I DENT | AL - 34 -

University; Peter K. Vogt, Ph.D., Chairman, Department Microbiology, University of Southern California School of Medicine. When an application reaches CTR, the scientific staff assigns a subcommittee of the SAB to each application. At the SAB meeting, each application is discussed. A member of the subcommittee assigned to the application is asked to present a critique of the proposal. Other critiques are read and a general discussion is held regarding the application. A vote is then taken as to whether to. approve the application. If the application is approved, each SAB member rates the application, as to. its relevance to smoking and health.. The Scientific Director must fol~low the advice of the SAB, giving preference to. those applications given high ratings. The administrative work of CTR is carried out by a permanent scientific and administrative staff located in New York City. CTR has always had distinguished researchers who have served as its Scientific Director. The first was Dr. Clarence Cook Little, a prominent researcher in the field of genetics. Others who have served in this role are Dr. William U. Gardner, a former Professor of Anatomy at Yale University School of Medicine, and Dr. Sheldon C. Sommers, a former Professor of Pathology at Columbia University College of Physicians andSurgeons. The present Scientific Director is James F. Glenn,~ M.D., former Dean of the Mount Sinai School~ of CONFIDENTIAL "~ - 35 -

Medicine. The Scientific Director of CTR is responsible for administering funds for medical and laboratory research. The funds are appropriated by CTR only upon the recommendation~ of the SAB. The Industry Technical Committee (ITC), composed of the research directors of the member companies, acts as an advisory panel for the Scientific Director and the SAB. They provide technical information from industry sources about cigarettes and tobacco. A representative of the ITC may attend SAB meetings, but has no vote on, research grants. The overall administration of CTR has been the responsibility of the Board of Directors, whose members are designated executives of the companies that belong to CTR. The Board of Directors is responsible for administrative decisions such as determining the budget, voting on the bylaws and selecting office space. The directors, however, have no control over the research decisions of the SAB. CTR does not operate its own research facility. Rather,~ research support has been achieved primarily through a program, of grants-in-aid, supplemented by contracts with institutions and laboratories. As of the end of 1988, grants and contracts have been approved totalling more than $136,.000,000. Grants have been awarded to 1,053 independent scientists in some 30Omedical schools, CONF ]DENT - 36 -

hospitals and research institutions. Much of this research was jointly funded by non-tobacco interests such as the U.S. Public Health Service, the National Institutes of Health, and the National Cancer Institute. CTR grantees have made significant contributions to scientific research. They have presented their findings at scientific and medical society meetings too numerous to list. They are free to publish any of these research results as long as the research meets the criteria of peer reviewed journals. In fact, CTR grantees have published over 3000 papers and articles, some of which have been cited by critics of the industry such as the Surgeon General. Since the beginning, CTR has supported research that would identify and define factors that may be involved in the causation of certain chronic diseases associated with cigarette smoking. Approved research has covered a wide range of human diseases, including many types of cancer, respiratory and cardiovascular diseases. CTR also approved investigation into other medical,~ chemical, biochemical and pharmacological areas. In addition, CTR has sponsored the study and development of basic laboratory and research, techniques and has underwritten reviews of research literature in specific areas. CONF:IDENT,%AL - 37 -

Research funded by CTR has added much to the present knowledge about cigarette smoking and health. For example, the research has: (i) tested the hypothesis that cigarette smoke acts as a direct contact carcinogen; (2) identified smoke components that may affect cilia; (3) investigated whether smoking or nicotine causes cardiovascular disease; (4) attempted to produce pulmonary squamous cell carcinoma in animal inhalation studies.6 These studies and other published research demonstrate CTR'~s commitment to examining the relationship between cigarette smoking and disease causation. ~Dstitutional Research Brown & Williamson has demonstrated its interest in smoking and health issues by supporting research efforts at prestigious institutions with nonrestrictive funding. Most notably, three separate multi-million dollar projects have been sponsored at three universities: Harvard University, the University of California at Los Angeles, and Washington University. 6o Microbiological Associates, for example, conducted a CTR-funded nine-year study, costing some $12 million dollars, in which over i0,000 mice inhaled the smoke of approximately 800,000 cigarettes. Inhalation of the smoke did not produce any squamous cell lung cancers. Furthermore, mice in which, cancers were chemically induced! did not get significantly increased lung cancers when later exposed to long-term cigarette smoke inhalation. Experiments were performed using high tar/low nicotine cigarettes and high tar/high nicotine cigarettes. CONF |D£1~T - 38 -

A unique and important aspect of this industry grant research is the flexibility in the utilization of the funds. This flexibility has made it possible to provide funding for the initiation of research programs which are then supported by grants from the National Institutes of Health and other agencies as well as providing certain items of core equipment that are shared by the investigators. Harvard In September 1972, Harvard Medical School was awarded a broad-based institutiona~ grant by Brown & Williamson and other tobacco companies to launch a five-year investigation into pulmonary and cardiovascular diseases. In 1977, the grant was renewed for an additional three-year period. The project was under the direction of Dr. Gary Huber, Assistant Professor of Medicine and Director of the Respiratory Diseases Clinic at Boston City Hospital's Channing Laboratory. At the time the project was launched, Dr. Huber was already directing a well-established research program for the study of host defenses in the lung. With the aid of the grant~ Dr. Huber was able to expand his program to include studies on the relationship between tobacco smoke and health, on differences in, host CONF ]DENT IAL - 39 -

susceptibility to disease,, and the effect of other environmental influences, such as air pollutants, on the lung. Dr. Huber's research proj, ect was designed to contain four phases. First, he intended to redirect his existing program. toward the study of possible biological effects of cigarette smoke on the lung with the, objective of determining what role,~ if any, cigarette smoking might play in. the development of pu,lmonary disease. Second, he sought to expand existingi resources to incl~ude more comprehensive studies in the areas of biochemistry, pathology and epidemiology. Third, Dr. Huber p~anned to develop resources for the study of potential relationships between cigarette smoke and lung cancer. Fourth, he intended to study possible relationships between cigarette smoke and cardiovascular diseases. During the eight-year period in which the industry sponsored the project, Dr. Huber and his co-workers published approximately 90 articles on their work. The Harvard grant also made it possible for Dr. Huber and his group to obtain government funding for other smoking-relating projects. With funds received! from the Nationa~ Cancer Institute and the National Institutes of Health, he was able to develop a method of monitoring respiration and smoke inhalation patterns of human smokers. CONF %IDENT IAL -- 40 --

Unfortunately, Dr. Huber was unable to complete the project because of difficulties with the animal inhalation facility used by his group. In 1977, the animal facility was closed on the advice of Harvard veterinarians. A large number of the animals had developed infections. Although Dr. Huber spent many months attempting to find other facilities and the sponsoring companies were making plans for long-term support, a practical solution could not be found. Consequently, Dr. Huber finished pending research.,. and the program was terminated in June 1980.. UCLA The commitment of the cigarette companies to broad-based research is also demonstrated by their support of a biomedical research project from 1974 to 1982 at the UCLA School of Medicine. The UCLA project, under the direction of Dr. Martin J. Cline, Chief of the School of Medicine's Division of Medical Ontology and Hematology, facilitated the expansion of the Division and supplemental ongoing research in three major areas, including the investigation of a possible relationship between tobacco usage and disease, particularly lung cancer, as well as exploration of methods for early cancer detection and therapeutic techniques involving immunotherapy and chemotherapy. -41 -

The project researchers determined that the ability to define alveolar macrophage function could aid in, the analysis of environmental factors and diseases that might influence macrophage function. They could not identify any significant abnormalities or adverse effects of smoking on the performance of human alveolar macrophages. The UCLA researchers collaborated with others in an. attempt to determine whether activation of cancer genes is important in: causation of tumors. Preliminary data suggested that these genes may be important in the initiation and maintenance of certain tumors. The UCLA project also provided, new information in the treatment of refractory malignant disease. The researchers in the project were among the first to develop the concept of freezing bone marrow for long-term storage in patients with malignant disease. As this brief summary suggests, physicians and scientists involved in the UCLA project were able to address fundamental problems of human health and disease. Their efforts have resulted in, the publication of numerous articles in scientific and medi, cal journals, in which the support of the participating tobacco companies was acknowledged. CONFIDENT IAL

Washinqton University The third of the broad-based institutional grants was awarded in March 1971, to Washington University in St. Louis for a basic research program on the immunological properties of cancer. The project is still being funded today by three tobacco companies. Initially, the project was conducted under the direction of Dr. Lauren Ackerman, an international authority on cancer, and Dr. Paul E. Lacy, head of the University's Department of Pathology and one of the world's leading experts on cell structure. The initial purpose of the program was to find and analyze "foreign" substances or antigens within the cancer cell and to utilize those antigens for the early detection, treatment and possible prevention of cancer. This focus eventually led to immunology studies, on the role of antibodies in the growth and development of neoplastic cells; the cellular events involved in antibody production; the morphologic and biochemical structure of the cell membrane; the effect of viruses on the genetic information in the cell; and the effect of physical and chemical carcinogenic agents on the genetic information in cells. CONF ]DENT ]AL - 43 -

The research findings from this program, reported in more than 300 publications, have made significant contributions to ongoing work aimed at understanding the basic cause,, development and treatment of cancer and other diseases. The understanding of the immune system made possible by this research is relevant not only to cancer, but it can also be expected to provide insight into diseases such as lung emphysema, rheumatoid arthritis, lupus and diabetes. C. AMA-ERF The America Medical Association Education and Research Foundation Project for Research on Tobacco and Health (AMA-ERF) was funded by six clgarette manufacturers from 1964 through 1972,. with contributions totaling over $15 million. All administrative, scientific and policy decisions, screening of grant applications, and distribution of funds were the responsibility of the AMA-ERF Board of Directors and the scientific advisory committee appointed by the board. Other than funding, the project was entirely independent of the tobacco industry. In 1963, the AMA House of Delegates adopted a recommendation from, its Board of Trustees that the AMA-ERF undertake a comprehensive research program on tobacco and health. The AMA- ERF was an existing organization within the AMA, primarily CONF; ! DE NTI] AL 4!4 -

responsible for supporting medical education and scientific and medical research. fostering An AMA announcement indicated that the project would be financed by a contribution from the AMA and solicited contributions. Only unrestricted contributions would be accepted. The tobacco industry wrote the AMA early in 1964, offering to contribute $10 million to the project over a five-year period. The industry was responding to the Surgeon General's suggestion that more research was needed. The contributions were made with the understanding the money would be used only for research on smoking and health. The AMA-ERF Board of Directors appointed a committee of distinguished scientists, the Committee for Research on Tobacco and Health (CRTH), to develop guidelines on research policies and procedures, to identify significant areas of research, and to screen applications for research grants. Three of the original five members .of the CRTH had also served on the Surgeon General's Advisory Committee that produced the 1964 Report to the Surgeon General. Grantees were required to publish their findings in the medical or scientific journal of their choice so that the information would become public through the scientific medila. Grantees were also expected to participate in workshops convened COMF tDENT:]AL - 45 -

by the AMA-ERF committee in 19661, 1970 and 1972 for the purposes of presenting oral reports on their research projects, stimulating an exchange of ideas, and delineating new areas for investigation. In 1968, during the AMA's Annual Meeting in San Francisco, a presentation was made by some of the grantees to report on their progress. At that time, the AMA-ERF committee indicated that more research was still needed to clarify many of the issues surrounding tobacco and health, including statement become controversial interpreted as casting doubt questions of causation. This because at the time it was on the Surgeon General's 1964 conclusions. The AMA-ERF committee then. clarified its position in. a statement pubiished in JAMA two months after the annual meeting, affirming that research completed under this project in no way challenged the .conclusions of the 1964 Surgeon General's Report. In August 1971, seven years after the project had begun, the tobacco companies and AMA began to consider phasing out the project. By July 1972, they had agreed to conclude the project by making no more new grants. The grants then in existence were allowed to wind down over the next several years. The findings of the AMA-ERF project were well publicized both in the medical, and scientific literature and in a final summary report by the AMA-ERF committee, produced in 19:78 under the title Tobacco and Health,. The information in the final summary was not new, since the research COMF ]DENT IAL - 46 -

results had been published by the grantees in scientific journals over the previous 14 years. According to the summary, the foundation had sponsored 219 separate research projects that resulted in 795 publications and reports. Copies of the report were provided free of charge to institutional members of the Medical Library Association. The AMA also sent copies to those who wrote to request one. During the life of the AMA-ERF project, anti-smoking critics became more vocal. The project did not escape these criticisms, especially those attacking the AMA for associating itself with the tobacco industry. The project was concluded in large measure because of the AMA's embarrassment over these attacks. In sum,, the AMA-ERF project represents a substantial effort on the part of the tobacco industry to sponsor broad-based research on smoking and health. Tobacco Workina Group The Tobacco Working Group (TWG) was formed in 1968, to. provide support to the National Cancer Institute's Less Hazardous Cigarette (LHC) research program. The goal of the LHC research program initially was, as its name suggests, to identify means of developing a "less hazardous cigarette;''~ the goal of the TWG was CONFIDENT IAL - 47 -

to develop a research program to identify how this product could be achieved. Thus, the TWG's purpose was to. provide scientific and technical assistance in designingand developing the experiments that were being conducted under the LHC program, at the National Cancer Institute. The LHC program itself was federally funded and inspired. It lasted approximately Ii years and spent over $32 million dollars on research, on both a grant and a contract basis. The open and cooperative attitude of the tobacco industry in investigating smoking and health issues is illustrated by the participation of company scientists in the TWG and the sharing o£ tobacco industry technical expertise and research results. Company scientists provided technical advice, reviewed research proposals, and conducted seminars on topics such as smoke chemistry and techniques of cigarette manufacturing. This expertise was not generally available outside the tobacco industry and was, of course, of particular relevance to the work of the TWG. The companies also shared technology with the TWG. For example, A.D. Little's improved smoking machine, developed as a part of its work for Liggett, was utilized in TWG animal inhalation. experiments. Moreover, various companies encouraged tobacco industry suppliers to share new product ideas with the TWG, i.e., various new cigarette papers, processes for producing reconstituted~ tobacco sheets, technology concerning expanded tobacco, etc. The CONF [DENT - 48 -

suppliers were, of course, dependent upon the tobacco industry for the potential use of their respective new products. They would not have shared these concepts for "safer cigarettes" with the TWG if the cigarette companies had discouraged them. The work of the TWG began by forming numerous subgroups to address a number of complex scientific questions central to smoking and health research: (~) the parameters of ci~garette manufacturing that influenced smoke constituents; (2) a review of available bioassay systems; (3) a review of epidemiology; (4.) smoking machine technology; and (5) the proper method for generating tars and fresh cigarette smoke for experiments. Then, TWG designed a series of experiments funded by the National Cancer Institute and conducted under the auspices of the LHC research program to identify cigarette characteristics that could be incorporated into a "less hazardous cigarettes" Eventually, over 150 cigarette variables were tested. The bulk of the work actually performed focused on investigating the biological activity of cigarettes with the goal of producing oigarettes with lowered biological activity. Lowered biological activity was sought by changing cigarette manufacturing parameters to modify smoke composition, by use of tobacco substitutes, varying paper porosity, varying tobacco processing methods, and varying methods in cutting tobacco. The result was n__Qo significant scientific "breakthroughs" toward the development of a "less hazardous cigarette." CONF IDEN%|AL

Following the 1976 elections, the National Cancer Institute's new leadership determined they should not be funding what they considered "product development research" for the tobacco industry in view of the government's position that smoking should be discouraged. The TWG was formally disbanded in August 1977. TWG members consulted as individuals on LHC research projects until the research program ended in 1979. TWG issued four topical~ reports, a fifth report summarizing the skin-painting research, and separate annual reports, but never issued a final summary report of all activity. The results of the TWG-LHC experiments pointed out that regardless of how cigarette design characteristics were modified, the changes in the tumorigenicity of the smoke condensate would be marginal, at best. CO#F ]DENT [AL

END NOTES (i) I_~d. at 656. (2) Vandenbroucke, J., "Is 'The Causes Of Cancer' A Miasma Theory For The End O:f The Twentieth Century?" 17(4) International Journal of Epidemioloqy 708, 709 (11988). (3) (4) Berkson, J., "Smoking & Lung: Cancer: Some Observations on Two Recent Reports," Journal of the American Statistical Association 53(281):28-38132], March 1958. Sterling, Cigarette Smoking and Disease, 1976 Hearings before Senate Subcommittee on Health, p. 456. (5) Lee, P. (ed.), "Tobacco Consumption in Various Countries," Tobacco Research Council, Research Paper, No. 6 (4th ed.; Edinburgh: T. and A. Constable, Ltd., 1975). "'76.' Cancer Facts and Figures, American Cancer Society," (New York: The American Cancer Society, 1976). (6) Buhler, V., Statement, U.S. Congress, House, Committee on Interstate and Foreign Commerce, Ciqarette Label:inq and AdvertisinqD-1969, Hearing, 91st Cong., 1st Sess., April 15-30, CON£IDENT IAL

and May I, 1969 (Washington: 1969), pp. 769-774. Government Printing Office, Burch, P., "Smoking and Cancer," Lancet I- 1316, June 9, 1973. (17) Burch, "Smoking and Cancer." (8) (9) False and Misleading Advertising, Hearing Before House Committee on Government Operations, 75; Cigarette Labeling and Advertising, Hearings Before House Committee on Interstate and Foreign Commerce, 201-02. Enstrom, J., Ph.D., "Rising Lung Cancer Mortality Among Non- Smokers," Journal of the National Cancer Institute 62:4 [755] (April, 1979). (i0) Smoking: Prevention Health and Education Act, Hearings Before Senate Committee on. Labor and Human Resources, 287. (ii) JNCI, June, 1988. (12) Cigarette Labeling and Advertising Hearings Before Committee on Interstate and Foreign Commerce, 248-49. House CONF ]DENT IAL - 52 -

(13) Hockett, R., "Where Do We Go from Here in Tobacco and Health Research?," Presentation before the Burley and Dark Leaf Tobacco Export Association, Lexington, Kentucky, October 2, 1967. (14) Furst 1983 Senate, pp. 465, 467. (15) NCI Report No.. 5,. "Toward Less Hazardous Cigarettes,'" p. 2 (Sept. 1980). (16) Seltzer, 1982 House Appendix, p. 757 (emphasis added). (17) Benditt, E., "The Origin of Atherosclerosis," Sci Amer 236(2): 74-85, February, 1977. Blumenthal, S., et al., "Risk Factors for Coronary Artery Disease in Children of Affected Families," Pediatr 87(6, Pt. 2): 1187-1192, 1975. Newman, W., et al., "Relation of Serum Lipoprotein Levels and Systolic Blood Pressure to Early Atherosclerosis: The Bogalusa Heart Study," N Enql J Med 314(3): 138-144, 1986. CONF ]DENT IAL - 53 -

Rifkind, B., and C. Lenfant,. "Cholesterol Lowering and the Reduction of Coronary Heart Disease Risk," JAMA 256(20): 2872-2:873, 1986. Strong, J., "Coronary Atherosclerosis in Soldiers: A Clue to the Natural H~story of Atherosclerosis in the Young," JAMA~ 256(20): 2863-2866, 1986.. Enos, W., et al.~ "Coronary Disease Among United States Soldiers Killed in Korea: Preliminary Report," JAMA 152(12): 1090-1093, 1953. Enos, W., "Pathogenesis of Coronary Disease in American Soldiers Killed in Korea," JAMA 158(11): 912-914., 1955. Enos, W., et al.~ "Pathology of Coronary Arteriosclerosis,." Amer J Cardiol 9(3.): 343-354, 1962. McNamara, J., et al., "Corona~9 Artery Disease in Combat Casu- alties in Vietnam," JAMA 216(7): 1185-1187, 1971. (18) U.S. Public Health Service, Office on Smoking and Health, The Health Consequences of Smokinq: Cardiovascular Disease. A Report of the Surgeon General: 1983, Department of Health and CONFIDENT I:AL - 54 -

Human Services, Washington, DHHS Publication No. 50204, 1983, p. 50. (PHS) 84,- (19). Schievelbein, H. and G. Heinemann, "Nicotine and Athero- sclerosis," Atherosclerosis VI: Proceedinqs of the Sixth International Symposium, ed. F. Schettler, et al. (Berlin: Springer-Verlag, 1983), pp. 899-902. (20) Kaufman, D., et al., "Nicotine and Carbon Monoxide Content o~ Cigarette Smoke and the Risk of Myocardial Infarction in Young Men," N Enql J Med 308(8): 409-413, 1983. (21) Wald, N., et al., "Serum Cotinine Levels in Pipe Smokers: Evidence Against Nicotine as Cause of Coronary Heart Disease," Lancet II(8250): 775-777, 1981. (22) Wald, N., et al., "Urinary Nicotine Concentrations in Cigarette and Pipe Smokers," Thorax 39(5): 365-368, 1984.. (23): Fisher, E., Statement, United States House of Representatives Committee on Energy and Commerce, Subcommittee on Health and the Environment, Smokinq Prevention Education. Act, Hearings, 98th Congress, First Session, March 9 and 17, 1983 (Washington: Government Printing Office, 1983), pp. 4.06-423. CONF |'DENT

(24) I_~d. (25) Hazleton Laboratories America, Inc., "Final Report -- Inhalation Bioassay of Ciqarette Smoke in Doqs: Effects of Nicotine and Carbon Monoxide on Atheroqenesis," Project No. 976-904, Contract No. ECI-SHP-75-112, Submitted to the National Cancer Institute, Division of Cancer Cause and Prevention, Smoking and Health Program, Washington, D.C., June i0, ~981. (26) Hockett, Statement, 1976. (27) 1982 House Appendix, p. 540. (28) Burrows, B., et al., "The Relationship of Childhood Respiratory Illness to Adult Obstructive Airway Disease," Am Rev Resp Dis 115: 751-60, 1977. Fletcher, C., et al.,~ The Natural History of Chronic ~ronchitis and EmDhvsema, Oxford Univ Press, Oxford, 1976, 272 pp. Lebowitz, M.D., "The Relationship of Soci.o-Environmental Factors to the Prevalence of Obstructive Lung Diseases and Other Chronic Conditi.ons," J Chron Dis 30: 599-611, 1977. CONF]DENTI]AL

Moser, K.M., Bordow, R.A., "Chronic Obstructive Pulmonary Disease: Definition, Epidemiology, and Pathology," in Manual of Clinical Problems in Pulmonary Medicine, Bordow, R.A., e__t al. (eds.), Little, Brown and Company, Boston, 1980. Openbrier, D.R., et al.~ "Nutritional Status and Lung Function in Patients with Emphysema and Chronic Bronchitis," Chest 83: 17-22, 1983. Quanjer, Ph.H., et al., "Maximal Expiratory Flow-Volume Curves in a Follow-Up Study," Scan J Resp Dis 57: 309-310, 1976. Salvaggio, J.E., "Overview of Occupational Immunologic Lung Disease," J Allerqy Clin Immunol 70: 5-10, 1982. Tager, I., et al., "Studies of the Familiar Aggregation of Chronic Bronchitis and Obstructive Airways Disease," Int J Epidemiol 7: 55-62, 1978. Tisi, G.M., Pulmonary Physioloqy in Clinical Medicine, Second Edition, Williams & Wilkins, Baltimore/London, 1983. U.S. Public Health Service, Smokinq and Health: Report of the Advisory Commilttee to the Surqeon General of the Public Health Service, DHEW, Pub. No. Ii03,: 1964. CONF [iDENT |AL - 57 -

U.S. Public Health Service, Smokinq and Health: A Report of the Surqeon General, DHEW, Pub. No. (PHS)79-50066, 1979. U.S. Public ~ealth Service, The Health Consequences of Smoking, Cardiovascular Disease: A Report of the Surqeon General, 1983, DHHS,. Pub. No. DHH(PHS) 84-50204'. U.S. Public Health Service, Advance, Report of Final Mortality Statistics, 1980, Monthly Vital Statistics Report, National Center for Health Statistics, Vol. 32, No. 4 (Sup.), Aug. ii, 1983. (29) I N!. Breslow & N. Day, Statistical Methods in Cancer Research, 78 (IARC 1980). (30) Hundley, J., M.D., Assistant U.S. Surgeon General, U.S.P.H.S. news conf. i/ii/~4. (31) Cigarette Labeling and Advertising Hearings Before House Committee on Interstate and Foreign Commerce (1969), 1256. (32) Burch, P., M.D., "Can Epidemiology Become A Rigorous Science?" Journal o~ Medical Sciences 14, 956-951 [!960] (1986). CON F I DENT

(33!) Mullins, P., Ph.d.~ "The Cost of Cigarette Smoking," Zealand Medical Journal 27 July 1988, 491. New (34) II N. Breslow & N. Day, Statistical Methods in Cancer Research 21 (IARC 1987). (35.) "Reducing the Health Consequences of Smoking: Progress," 122-161 (Surgeon General 1989). 25 Years of (36)i Susser, M., "Rules of Inference in Epidemiology," Regulatory Toxicology & Pharmacology, 6:1:16-128 [119] (June 1986). (37)! Cox, L., "Statistical Issues in the Estimation of Assigned Shares for Carcinogenesis Liability," Risk Analysis,~ 7"1, 71-80 [72] (April 1987). CONFIDENTIAL -- 59 --

SMOKING AND ADDICTION CONFIiDENT]AL - 60 -

Tobacco smoking is an activity that has been engaged in by people from a variety of cultures for hundreds of years. It is a behavior involving innumerable individual choices, which, are reflected in each person."s decision of whether, when, where and in what manner he or she will smoke. As with many other aspects of personal lifestyle, smoking appeals to some, but is displeasing to others; some seem to enjoy smoking only during certain periods of their lives, and eventually decide tot and do, quit. Among those who dec~de to. smoke, the activity takes a variety of forms and patterns. Some smokers only smoke at certain times, or in association with specific activities, e.q., only in the evenings, following meals, or during an intellectual activity like reading. Given such idiosyncratic patterns, it is not surprising that behavioral scientists have had great difficulty in explaining individual motivations for smoking. Nevertheless, some researchers with apparent biase~ against smoking seem to pay little attention to the complexities of smoking behavior. Instead, they focus on a single ingredient in tobacco smoke, namely nicotine, and say that it is the reason why people smoke. They observe that some persons smoke frequently and seem to value the opportunity to smoke and infer that smokers are "dependent on" c~garettes. Some anti-smokers go so far as to call smoking a "drug addiction..'" This claim is clearly CONF !DENT |AL - 61 -

inappropriate, but one that often gets media attention when made by the Surgeon General and others. Just what is meant by the claim that cigarette smoking is an "addiction?" A meaningful response to this question must deal with the term "addiction" as more than merely a term of convenience used to describe any frequently occurring behavior. One must put aside, for example, statements by exercise enthusiasts that they are "addicted" to running, or announcements of parents that their children are addicted to television. Consider also that there are books that describe a "love" addiction.. Former Surgeon General Koop also contributed to the debasement of the term when he said in 1982 that video games are ":addicting.'" (I) It is obvious that the word addiction is on the verge of losing its scientific meaning. Some, in fact, would argue that the battle has already been lost. Dr. David M. Warburton, of Reading University, England, commented in. 1985 on the disturbingly broad usage the term "addiction" has received: Thus we can see that addiction in ordinary usage can refer to work and business, sport and revels, melancholy and study, Sack and vice, prayers and virginity. Certainly, it is a very broad concept which has been applied to CONF ]DENT XAL - 62 -

a wide variety of behavioral phenomena. (P. 285) (2) Rampant misuse aside, what is meant by the term"addict" in a technical sense? Generally, there is a consensus that an addict is a person whose repeated drug use is primarily motivated: by avoidance or reduction of adverse physical (physiological) symptoms. In other words, people are, said to be "physically dependent" on the drug,, because if they do not receive their "fix," their bodies will go through an agonizing "withdrawal." Their behavior is further characterized by ever greater leve~s of drug intake, as they try to: gain the intoxicating "high" which is so important in. the addict's life. Yet~ this. is more and more difficult to do because the addict has developed a "tolerance" to the drug. Addiction thus leads to the pitiful situation of having a compelling physical need for a drug, which provides little pleasure beyond meeting this need. From a practica! point of view, the addict, when on the drug, becomes intoxicated and is often unable to function normally. There is intellectual and social impairment. His "need''~ for the drug! overrides everything else. not. Does the cigarette smoker fit this picture? Of course CONFIDENTIAl. - 63 -

Even researchers who are vehemently opposed to smoking recognize that the scientific evidence for addiction -- for physical dependence -- to smoking is highly equivocal. But this has not stopped many of these same researchers from. advocating an "addiction" label for smoking. Unfortunately, as a result it seems that the scientific evidence becomes scientists, along with everyone else, surrounding the term "addiction." camouflaged and these add to the confusion Some examples of this confusion are instructive. In 1983, Dr. William Pollin, former Director of the National Institute on Drug Abuse (NIDA):, testified before Congress that tobacco smoking was "addictive." Yet, almost in the same breath, he also stated: [e]vidence is not yet conclusive as to whether or not there is physiologic dependence or what type of withdrawal syndrome is associated with cigarette smoking. (Pp. 99-100) (3) Similarly, much publicity surrounded release of a Public Health Service Pamphlet purporting to explain, "Why People Smoke Cigarettes." (4) The pamphlet describes cigarette smoking as "addictive." Dr. Jack Henningfield of the NIDA, commenting on the pamphlet,~ is quoted as claiming that "we had filled in all the gaps in the research" (p. 36) on the issue of addiction in smoking:. (5) Yet, Henningfield had, only 2 years before, expressed in CONF | DEN1 IAL - 64 -

writing that whether physiological diependence is an important factor in smoking was only "suspected." (P. 212) (6) The real issue is camouflaged by such blatant statements that cigarette smoking is an "addiction." Even advocates of th~s position concede that scientific demonstration of the necessary element of addiction -- physical dependence -- is "not yet conclusive" or is only "suspected." How do advocates of the smoking addiction hypothesis explain the inconsistency of their positions? They have changed the "name of the game." They now say that physical dependence is not a prerequisite for addiction. They emphasize instead some sort of nebulous, psychological analogue to addiction -- namely, "dependence." "Dependence" is an inexact term. It must not be confused with "physical dependence," which specifies the precise and objective characteristics of withdrawal and tolerance. The term "dependence" often seems to be applied merely when some repetitive behavior is observed which seems to have some importance to a person, as reflected by indications that the behavior is difficult to forego. It is a subjective label often referring to vague, psychological characteristics. CONF[DENTIAL - 65 -

An eloquent statement of the near scientific meaninglessness of the term "dependence" comes from the British scientist,. Dr. David Warburton, of Reading University: We all are 'dependent' for our ordinary happiness, gratification, emotional well-being and general quality of life on a whole range of people and objects. We are in this sense clearly dependent on things like our family and friends, our job,~ our motor car, our favorite armchair and the television set. (Pp. 287- 2s8) (7) The vagueness and broadness of the general notion of "dependence" can be avoided by focusing on "physical dependence" as a critical feature of "addiction." When a person is "physically dependent" on a drug, then abstinence from the drug leads to a consistent set of physical disturbances, which together constitute a uniform withdrawal syndrome. As noted above, no such physical syndrome has been. established: for smoking. Any symptoms experienced by one who stops smoking are the same as or similar to those experienced by someone giving up a habit or by someone dieting. It is probably more difficult for the dieter to give up certain foods because he or she needs food to survive. In the absence of solid evidence for withdrawal, an attempt is sometimes made to keep the physical dependence concept of addiction alive by claiming '"tolerance" to smoking. "Tolerance" means that an increasing amount of a substance is needed to achi~eve the same "high~" or effect on a person. CONFIDENTIAL - 66 -

Tolerance claims concerning smoking tend to be highly anecdotal. For example, it is often pointed out that novice smokers take a period of time before becoming accustomed to the habit, and it is ~mplied that this is related to nicotine. However, this is an obvious misuse of the concept of tolerance. All habits need a formative period to become established. The concept of "tolerance" clearly is inapplicable when considering the typical pattern of smoking, which tends to remain at a fairly constant level throughout the smoker's life. In addition, there is a category of smokers who smoke only a few cigarettes a day or only in social situations. Given the lack of credible evidence for physical dependence in smoking, it is not surprising that those who advocate the "addiction" hypothesis rely on indirect arguments. For example, some have maintained that most smokers would like to quit smoking. The relevance of this point is questionable for at least two. reasons. First, even if one accepted that a large percentage of cigarette smokers say they want to quit, that indicates nothing about their motivations for continuing. Second, there is evidence that reports of smokers' desires to quit smoking are highly unreliable. Even Lynn T. Kozlowski, a scientist well-known for his anti-tobacco views, commented on this, noting that "answers to questions on 'wanting to stop' and 'trying to stop' have regu.larly been. used uncritically. " (P. 699) He "encouraged caution CON F I!DENT IAl - 67 --

in what is made of what smokers say about their wish to give up smoking and their attempts to do so," (p. 699). and advised that "[b]oth what smokers say about their smoking and: what researchers make of these statements should be read skeptically." (Pp. 699- 70.0.) (8) The objective observer should have this sort of skepticism in evaluating such indirect arguments. Some imply that quitting smoking is a herculean task, at which only a few succeed. This forms the basis for the c~aim that the "drug" nicotine has overcome a person's ability to choose whether or not to smoke. But this is an incredible position. In fact, as noted by the U. S. Surgeon General,~ over 41 million people in this country have chosen to quit smoking, and have done so. (9) The effort involved in quitting smoking is often highly exaggerated. This is .recognized by even many of the more well- known opponents of smoking. For example, consider the following: GONF IDENT IAL It may also be that, for the general public, the stories circulating about the agony of abstinence serve as a self fulfilling prophesy: smokers expect it to be painful and therefore it is. Many give up their attempts to break the habit at the first sign of discomfort,~ anticipating greater pain., which, in reality is not forthcoming. (P. 34.7). (i0) [I]t is quite apparent that most smokers can stop wi.thout formal help. (P. 16)i (ii) I deplore those who characterize quitting smoking as a tortured, almost impossible - 68 -

process.. For many people, it is easy; for most it is somewhere between, easy and difficult; and only for a minority is it really difficult. (P. 25) (12) Much has been made of the alleged high relapse rates among quitters. However, studies of such rates have been almost exclusively based on therapeutic samples -- that is, people who have had difficulty in. quitting smoking. Those people able to quit on their own rarely come to the attention of researchers. However, when dealing with nontherapeutic samples, a different picture emerges. In the words of one researcher,~ a conclusion to the effect that cigarette smoking is highly intractable "is a conclusion based largely on the results of numerous studies of single therapeutic interventions with populations of self-selected subjects who had actively sought help." (P. 436) (113) Dr. Pollin is one of those who states that smokers lose their ability to choose whether or not to smoke. However, even his own comments argue otherwise. For example, he points out that the smoking quit rates for physicians and other health care professionals are far greater than among other segments of the population. If loss of personal control to a pharmacological master explains cigarette smoking, then one would expect uniform quit rates among: all segments of the population. CON F ~iDENT ! AL

A similar argument could be made in regard to the social class gradient for cigarette quitting rates. This was noted in a 1978 New Scientist article, as a challenge to the view that people smoke for pharmacological reasons: One of the strongest challenges to the theory of 'physiological' cigarette dependence is the simple observation that those who are most likely to. stop smoking are determined far more by social class than by individual psychology or physiology. (P. 148) (14) Clearly, the social and cultural factors impinging on individuals have major impacts on their choices of whether to continue or to quit cigarette smoking. Thus, there are serious unanswered questions and inconsistencies in the smoking addiction hypothesis. Despite these problems, former Surgeon General Koop released a new report on "Nicotine Addiction" on May 16, 1988. (15) Dr. Koop took a categorical position regarding cigarettes and addiction. He stated: This Report shows conclusively that cigarettes and other forms of tobacco are addicting the same sense as are drugs such as heroin, and cocaine. (p. vi). This "conclusion" was biased by a number of factors, including: use of the vague term "dependence" which blurs the distinctions from actual "addiction'"; selective application of CONE !DENT IAL - 70 -

data to support his preconceived opinions; and restricting the review to pharmacological literature which ignores the complex psychological aspects of smoking. Because of these and other types of bias, the position of the Surgeon General's Report has been criticized in the press and by several respected scientists before a Congressional subcommittee in July, 1988. What has occurred in recent years is an increasingly vociferous attack on smoking, and an attempt to label it an addiction. Lacking scientific demonstration of physical dependence, these attacks have taken on a distinct emotional and political tone. Consider, for example, the comments of Dr. Morris A. Lipton, one of several scientists who performed a review for the U. S. National Institute on Drug Abuse of the evidence for "cigarette addiction." He gave the following reason for NIDA's choice of "addiction" as applicable to cigarette smoking: It was selected because it's sort of a dirty word. ~P. 5B) (23) Obviously, this implies that the label of "addiction" is applied to smoking for social and political reasons, with little regard for its scientific meaning. CONF]DEN;]AL - "71 -

Cigarette smoking is more accurately classified as a "habit." As when giving up any habit, a smoker needs the desire and the motivation to quit. There is nothing in cigarettes which interferes with a smoker's ability to decide to quit and to carry out that decision. COI,/F | DENT ! AL - 72 -

END NOTES ( 1)~ Mattiace, P., "Surgeon General Says Video Games May Harm Children," The Associated Press, November 9, 1982, A.M. cycle. (2) Warburton, D.M., "Addiction, Dependence and Habitual Substance Use,." Bulletin of The British Psycholoqical Society 38: 285- 288,~ 1985. (3) Pollin, W., Statement for the Record, Smoking Prevention Health and Education Act of 1983, Hearings before the Committee on Labor and Human. Resources, United States Senate, May 5 and 12, 1983, pp. 98-103. (14,) U. S. Department of Health and Human Services, "Why People Smoke Cigarettes," U,. S. Government Printing Office, 1983. (5) Anonymous, "At Last, The Government Calls Smoking an (6) Addiction," Medical World News 24(6),, March 28, 1983, pp. 36- 3¸7 . Henningfield, J. E., Griffiths, R. R. and Jasinski, '"Human Dependence on Tobacco and Opioids: Common Factors, '"In: Behavioral Pharmacoloqy of Human Druq Dependence, T. CONF I!DENT

Thompson and C. H. Johanson (eds.), NIDA Research Monograph 37, July, 1981, pp. 210-234. (7) Warburton, D. M., "Addiction, Dependence and Habitual Substance Use," Bulletin of The British Ps¥choloqical Society 38: 285- 288, 1985. (8): Kozlowski, L. T., Herman, C. P. and Frecker, R. C., "What Researchers Make of What Cigarette Smokers Say: Filtering Smokers' Hot Air," The Lancet, March 29, 1980, pp. 699-700. (9) U. S. Department of Health and Human Services (1988), The Health Consequences of Smoking: Nicotine Addiction, A Report of the Surgeon General, Publication No. DHHS (CDC) 88-8406. U. S. Government Printing Office, Washington, D.C.: (i0) Pertschuk, M. J., Pomerleau, O. F., Adkins,. D. and Hirsh, C., "Smoking Cessation: The Psychological Costs," Addictive Behaviors 4(4): 345-348, 1979. (ii) Jaffe, J. H. and Kanzler, M., "Smoking As An Addictive Disorder," In: Ciqarette Smokinq as a Dependence Process, N. A. Krasnegor (ed.), NIDA Research Monograph 23,~ January, 1979, pp. 4-213. CONF[DENTIAL - 74 -

(12) Horn, D., "Psychological Analysis of Establishment and Maintenance of the Smoking Habit," In: Ciqarette Smokinq as a Dependence Process, N. A. Krasnegor (ed.), NIDA Research Monograph 23, January, 1979, pp. 24-29. (13) Schachter, S., "Recidivism and Self-Cure of Smoking and Obesity," American Psychologist 37(4): 436-4.44., 1982. (14)i Anonymous, "Addiction or No?" New Scientist, April 20, 1978, pp. 148-149. (15)! U. S. Department of Health and Human Services (1988), The Health Consequences of Smoking: Nicotine Addiction, A Report of the Surgeon General, Publication No. DMHS (CDC). 88-8406. U. S. Government Printing Office, Washing, D. C. (16) Christensen, R., "Cigarettes Addictive, Panel Says," The News and Observer, Raleigh, N.C., Wednesday, September 3, 1980, pp.. 1 and 5B. CONF[DENT]AL - 75 -

OCR for 2023235876 does not yet exist

Environmental tobacco smoke (ETS), a~so sometimes referred to as "passive (or involuntary)! smoking", is a shorthand reference to the presence of diluted side-stream smoke (smoke from the burning end of the cigarette) and exhaled mainstream smoke in the ambient air, and, more particularly, to the public controversy over the effect such smoke has, if any, on non-smokers who are exposed to. it. Industry critics contend that exposure to ETS both causes disease in non-smokers and exacerbates existing health conditions for individuals who suffer from heart and lung disease. A great deal of public attention has recently been focused on efforts to curb smoking in the workplace, in restaurants and other public accommodations, and in airplanes and other forms of public transportation. There. also has been a good deal of press attention given to the claim that parents harm their children by smoking at home. The question of whether ETS exposure is a health risk for non-smokers is rarely discussed or decided on the basis of the scientific evidence; rather politics, speculation, and emotion-laden arguments have replaced open scientific discussion of ETS' alleged health effects. In a number of instances, investigators have simply assumed that ETS is. a health risk and have gone on to attempt to estimate the magnitude of the assumed risk. Such. reports claim that hundreds or even thousands of non- smokers die of diseases due to ETS. However, these investigators COXF |,DENT |AL

fail to acknowledge the serious methodological problems underlying: their estimates. At several recent meetings, experts on ETS have reported the lack of valid scientific data to support such health claims and the difficulty of interpreting the available scientific data on the subject. For example, the summary of a report on an international workshop held at the University of Geneva in March 1983, contains the statement, "an overall evaluation based upon available scientific data,~ leads to the conclusionthat an increased lung cancer risk for non-smokers from ETS exposure has not been established." (I) Likewise, the organizer of an international symposium on the medical perspectives of ETS, organized and sponsored by United States and European private and governmental bodies, and held in, Vienna, Austria,~ in 1984 notes: Summarizing all of the results presented here, I come to the con,clusion that up to now there is no scientific evidence of a causal relationship between passive smoking and lung cancer. In my opinion, all the epidemiological studies carried out so far lack the appropriate methods to determine the extent of exposure to passive smoking. So, I do not think any epidemiological investigationwi~l be performed convincingly in the future until the problem of determining the extent of exposure to passive smoking has been solved satisfactorily. (12). CONFIDENTIAl.

A 1983 U.S. Government sponsored review of research on possible respiratory effects of exposure to ETS concluded: A review of the data from the studies which have been carried out or are in progress which address the effect of passive smoking on the respiratory system suggests that the effect varies from negligible to quite small. From this review, it was not possible to determine whether there is a specific group which is at increased risk or what the mechanisms of the effect (if any) may be. (3) In 1986, the Surgeon General published a report on ETS which concluded that ETS is harmful to non-smokers. It specifically reported that ETS exposure causes lung cancer. Close examination of this report, however, shows that the conclusion is based on. studies which even the report acknowledges to have serious methodological flaws. The report also acknowledges the need for more accurate data on exposure than simply using a spouse's smoking: habits. On the question of the possible effects of ETS exposure on the adult respiratory function, the report concedes: CONFIDENTIAL The physiologic and clinical significance of the smal~ changes in pulmonary function found in some studies of adults remains to be determined. The sma~l magnitude of effect implies that a previously healthy individual would not develop chronic lung disease solely on the basis of involuntary tobacco smoke exposure in adult life.

With regard to ETS and acute respiratory illness, the report notes "there are no studies of acute respiratory illness experienced in adults exposed to environmental cigarette smoke." The report also acknowledges the lack of data to support claims that exposure to ETS can induce asthmatic attacks in sensitive individuals. It notes th, at studies to date used artificial test settings, unrealistically high levels of smoke, and inadequate control of psychological facts. The report concludes that exposure to ETS has not been shown to contribute to cardiovascular disease or to be hazardous to patients with pre-existing heart disease: 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. The studies cited by industry critics as evidence of health claims from ETS exposure contain serious methodological inadequacies. Questions have arisen because in no epidemiological study to date has the alleged r~sk to non-smokers been assessed by actual measurements of ETS in the home, in the workplace or in public. Other problems arise because of the failure to account and control for the many factors associated with the diseases in CONFIDENT ]AL - 80-

question. Such factors commonly overlooked include diet, lifestyle, heredity, and the wide variety of chemical, physical, and biological contaminants common to the modern indoor and outdoor environment. Failure to account and control for these factors makes interpretation of study results questionable. British researchers,, for example, examined epidemiological studies on ETS and lung cancer for possible bias and errors which could explain the reported increased risk among non-smoking women married: to smokers. They concluded: In summary, when a spouse's smoking status is used to estimate a non-smoker's ETS exposure,, 'a considerable amount of misclassification' may resu~It. Since selection bias and confounding must also. be considered, extreme caution is required in interpretation of these studies. This is especially so when [the] literature as a whole contains several studies reporting no significant association between ETS exposure and lung cancer, as well as various inconsistencies, both among and within studies. (4) In a paper presented to the U.S. Air Pollution Control Association meeting in 1986, an American researcher examined the epidemiological data on ETS and lung cancer and concluded: The epidemiological data concerning any cause and effect relationship between ETS and lung cancer is, at best, equivocal. The most persistent weakness is the absence of adequate exposure information. This precludes the CONFIDENT |AL - 81 -

evaluation of dose response relationships-- a critical element of the test for causality. Moreover, the problems of sampling bias and misclassification complicate interpretation of studies done to date. (5) Critics argue that asthmatics and individuals with pre- existing heart and lung diseases are particularly vulnerable to various environmental influences, including ETS. Reviews on the health effects of environmental tobacco smoke exposure, however, report that the data are limited and conflicting on this subject. The Surgeon General's 1984 report on chronic obstructive lung disease contains a chapter on ETS which concludes, among other points,, that "the limited existing data yield conflicting results concerning the relationship between passive smoke exposure and pulmonary function changes in patients with asthma." The report further explained: There are very limited data on the effects of passive smoke exposure in patients with pre- existing pulmonary disease, and the available data are conflicting. Clinical studies have suggested a relationship, between respiratory symptoms in asthmatics and exposure to parental cigarette smoke, but methodologic problems complicate the interpretation of the limited available data. CONFIDENTIAL - 82 -

The 1986 Surgeon General's Report on ETS similarly acknowledges conflicting data on ETS exposure in children and adults with asthma. On children it states: Epidemiologic studies of children have shown no consistent relationship between the report of a doctor's diagnosis of asthma and exposure to involuntary smoking. Although one study showed an association . . ., others have not. On the question of whether ETS exposure affects adults with asthma, the report reviewed three studies on the subject and acknowledged conflicting results and methodological problems. It states: Acute exposure in a chamber may not adequately represent exposure in the general environment.. Biases in observation and [in the] . selection of subjects and the subject's own expectations may account for the widely divergent results. Studies of large numbers of individualswith measurement of the relevant physiologic and exposure parameters will be necessary to adequately address the effects of environmental tobacco smoke exposure on asthmatics. The plausibility of the claim that ETS exacerbates symptoms in those with existing cardiovascular disease rests on the observations that ETS contains carbon monoxide and nicotine. Actual measurements, however, suggest that carbon monoxide and nicotine in the ambient air do not substantially increase lewels of these substances in the blood of non-smokers. (6) CONFIDENT I!AL - 83 -

The evidence linking parental smoking and children's health problems is contradictory and weak. There is no agreement that the reported associations are in fact due to parental smoking and not to a variety of so-called confounding factors such as socio- economic status, and the use of gas cookers and heaters. Surveys and studies on this subject have produced conflicting results. (7) Some studies report that children whose parents smoke have more respiratory symptoms and illnesses than those whose parents are non-smokers. Others report no such effects. Although some individuals are annoyed by the sight and smell of tobacco smoke and a few even report experiencing irritation, the existence of human allergens in tobacco smoke has not been established. (8) In many cases, the sensitive individual may be responding to high room temperatures, lack of ventilation, or even to the mere sight of tobacco smoke. A review of the scientific literature on. the subject indicates that it must be questioned what people really mean when they say they are "~allergic" to tobacco smoke. They may simply not like the sight and smell of tobacco smoke and interpret this to mean that they are '"allergic'" to tobacco smoke. Tobacco smoke is only one of many possible contributors to indoor air quality. Other suspected factors affecting indoor CONF [:DENT IAL

air quality include allergens such as dust mites and spores from fungi, and chemicals such as formaldehyde, ozone, and nitrogen dioxide. (9). To ban one suspected constituent because it is visible and commonplace is unjustifiable. Reaction to tobacco smoke may merely indicate a more general ventilation problem. The alleged health hazards of ETS exposure in the workplace have also received considerable attention in the media. There is very little data on ETS exposures at the workplace; nonetheless, some reports strongly recommend workplace smoking restrictions. These recommendations are often implicitly based on the desire to force smokers to reduce their smoking, rather than on any sound scientific data. Scientists who have studied the air quality in office buildings have concluded that tobacco smoke does not play a major role in the quality of indoor air. (i0) It has been reported that neither pollution levels nor complaints about "stale" air are higher in buildings where smoking is permitted than in buildings where it is prohibited. (II) Although smoking restrictions that apply to offices and public places are being considered, none to date is based on actual air quality studies. When actual measurements in real life situations are made, the results suggest that ETS is not a significant factor of indoor air quality, and that smoking regulations are unnecessary to assure adequate indoor CONF ]DEN~'IAL - 85 -

air quality. (12) Current studies suggest that inadequate ventilation is the most important factor determining indoor air quality. (13)! Since the data on ETS are inconclusive, public smoking laws constitute unnecessary government intervention in matters of individual behavior. To the extent that scientific debate on ETS is suppressed and data misused,~ the public may accept coercive or punitive laws it would not otherwise accept. There is a need for a balanced discussion on, ETS. Some of the press coverage given to ETS issues tends to highlight the most alarming or sensational claims, often without regard to the critical limitations of the methodologies and data used in the studies. Brown & Williamson appreciates the desire of some members of the non-smoking public for "separation" from smokers. The easiest and best response to this desire is polite courtesy on the part of smoker and non-smoker alike. CONFIIOENIIAL

(1) Rylander, R. et al. (Ed.), ETS--Environmental Tobacco Smoke, Report from a Workshop on Effects and Exposure Levels, March 15-17, 198.3,. University of Geneva,. Switzerland, published in European Journal of Respiratory Diseases (1984) Supplementum No. 133, Vol. 65, page 144.. (2) Lehnert, G., Chairman, "Round-Table Discussion," Preventive Medicine (November 1984) 13:6, p. 746. (3) U.S. Department of Health and Human Services, Report of Work Shop on Respiratory Effects of Involuntary Smoke Exposure: Epidemiologic Studies, May 1-3, 1983, Public Health Service, National Institute of Health (December 1983). (4,), Lee, P.N. et al., "Relationship of Passive Smoking to Risk of Lung Cancer and Other Smoking Associated Disease," British Journal of Cancer (1986) 54.:167. (5) Balter, N.J. et al., "Causal Relationship Between Environmental Tobacco Smoke and Lung Cancer in Non-Smokers: A Critical Review of the Literature," paper presented at the 79th Annual Meeting of the U.S. Air Pollution Control Association, Minneapolis, Minnesota, June 22-27, 1986, p. 13. CONFIDENTIAL -- 87 --

(6) Schievelbein, H. & Richter, F., "The Influence of Passive Smoking on the Cardiovascular System," Preventive Medicine (November 1984) 13:626. (7) U.S. Surgeon General, The Health Consequences of Smok~ng-- Chronic Obstructive Lung Disease (1984), pp. 387-389, 392, 401; U.S. Department of Health and Human services,. Report of Workshop on Respiratory Effects of Involuntary Smoke Exposure: Epidemiologic Studies,. May 1-3, 1983, Public Health Service, National Institute of Health (December 1983) p. 3; U.S. National Research Council, Environmental Tobacco. Smoke-- Measuring Exposures and Assessing Health Effects, prepared by the NRC Committee on Passive Smokin,g, Board on Environmenta~ Studies and Toxicology (1986), National Academy Press, Washington, D.C. (8)i Lehrner, S., et al., "Tobacco Smoke Sensitivity: A Result Allergy?" Ann. Allerqy 56:1-10, 1986. (9) Anderson, I. & Korsgaard, J. "Asthma in the Indoor Environment--Assessment of the Health Implications of High Indoor Air Humidity," pp. 79-86; Berglund,~ B., et al. (Eds.).,~ Proceedings of the Third Internationa~ Conference on Indoor Air Quality and Climate, held in Stockholm, Sweden, August 20-24, 1984. CONF | DENT - 88 -

(i0) Sterling, T.D. et al., "Environmental Tobacco Smoke and ~ndoor Air Quality in Modern Office Work Environments~" Journal of Occupational Medicine (January 1987), 29:5.7. (ii) "Statement of Gray Robertson,~ President, ACVA Atlantic, Inc.," (December I0, 1987), Statement Accompanying Tobacco Institute press release. (12)i Sterling, T.D. et al., ,,Environmental Tobacco Smoke and Indoor Air Quality in Modern Office Work Environments," Journal of Occupational Medicine (J~anuary 1987),. 29:61. (13) ~d. CONF ]DENT |AL

PRIOR TOBACCO INDUSTRY POSITIONS ON SMOKING AND HEALTH CONFIDENTIAL - 90 -

This section reviews the positions taken by the tobacco industry on smoking and health issues, both in testimony before Congress and in publications and programs of The Tobacco Institute. Not surprisingly, the positions of the industry have changed to some extent over the years as the scientific studies and debate on smoking and health have evolved.. This paper merely outlines these positions and notes some of the specific statements that may be challenged by industry critics. In general, the industry has taken a consistent position that proof is lacking of adverse health effects from smoking, passive smoking, or any of the constituents found in tobacco smoke. Industry research expenditures have generally been characterized: as substantial, more generous than those of other private groups, and having no restrictions. In addition, the industry has denied any addictive qualities of smoking. Finally, advertising of cigarettes has been stated to be merely related to brand preferences, and to have no effect on recruiting youth, or non-smokers, to smoke. I. WHETHER SMOKING CAUSES DISEASE The industry has consistently taken the position, that it is an "open question" whether there is a causal link between smoking and various diseases, and that further research is necessary.. This position has been maintained throughout the various CONF ]DENT ]AL - 91 -

congressional hearings and industry publications. Industry members have admitted that statistical associations exist between smoking: and certain diseases, but they have emphasized that such a statistical relation does not establish causation. Industry spokespeople have consistently denied that there is sufficient proof of a causal link between smoking and lung cancer; cardiovascular disease (including stroke and high blood pressure); chronic obstructive lung diseases (including emphysema and bronchitis)i; cancers of the pancreas, larynx, esophagus, bladder, and urinary tract; oral and pharyngeal cancer; ulcers (including peptic ulcers); and overall mortality rates. The industry has similarly criticized the claim that there are 400,000~ excess deaths per year due to smoking, characterizing this claim as "sheer speculation." (i) There have been similar statements on the effect of smoking on women, especially during pregnancy. The industry has acknowledged that "smoking mothers, on the average, have slightly lighter weight babies." (2) But the industry has denied that there is proof of a causal link to the following conditions which have been statistically linked to tobacco use: increased perinatal mortality, abortion, stillbirth, birth defects, early menopause, decreased child development, and disease in those using oral contraceptives. CONFIDENTIAL -- 92 --

The industry has likewise stated that there is no scientific evidence linking passive smoking to any disease. Statements on passive smoking tend to be stronger than those regarding primary smoking. (3) The questioning of adverse health effects includes questioning any effect on children of smoking parents. (4) There are also, however, some industry statements which may raise questions as to adverse health effects, including the following: (i) Dr. Little, testifying for the Tobacco Industry Research Committee ("~TIRC") at 1957 congressional hearings, stated that any chronic irritation '"is a bad risk in any form of cancer" and that "inhalation of smoke" is an irritant. Dr. Little also referred during his testimony to an. article in which he said "it would seem unwise to fill the lungs repeatedly with the suspension of fine particles of tobacco products of which smoke consists." (2) Industry statements have acknowledged that smoking has a role "in depressing ciliary mobility" but have denied that this has any proven relation to the development of lung cancer. (5) (3.) Joseph Cullman., speaking as Chairman of the Executive Committee of TI at 1969 congressional hearings (April/May hearings),. CONF|~DENT ~AL - 93 -

stated that "Caution: Introduction of polluted air into lungs, including cigarette smoke, is injurious to health" was "a fair statement,~" but then also said "I don't think people really know" if smoking is injurious. (4) Dr. Robert Hockett, in October 5, 1978 testimony, stated that it is a "plausible possibility" that smoking has "an effect on small airways," that smoking causes "a certain amount of irritation," that for a small group of persons who "for genetic reasonsare highly susceptible to chronic pulmonarydisease" smoking can be "a grave danger" and that smoking reduces muscle and tissue production in youth. (5) In May 1983 congressional testimony Dr. Sheldon Sommers stated that those with preexisting emphysema should not smoke and that for them. smoking "is going to cause difficulty." In addition, the industry has stated that "[.y]oung people should not smoke." (6)i In October 5, 1978 congressional testimony, Dr. Robert Hockett similarly stated that nicotine '"and perhaps other ingredients in smoke reduced somewhat the efficiency of the production of muscle and other body tissues" in youth, such. that smoking could cause harm absent adjustments to diet. CONFIDENTI,AL

There has also been some conflict as to whether smoking can cause an allergic reaction.. Thus, Science and Smoke (1978), quotes testimony that "it has not been clearly established that allergens for man are present in tobacco smoke." A TI newsletter, however, merely states that "True tobacco allergy is rare." (7)i A CTR report, introduced in the 1965 congressional hearings (April/May hearings), notes research that "certain tobacco effects • may be due to specific allergic susceptibility of particular individuals," and an exhibit to testimony fn 1972 by Horace Kornegay states that "there may be people who have an unusual hypersensitivity to tobacco smoke.''~ As noted above, the industry has acknowledged that there is a statistical link between smoking and various diseases, even if statistics do not prove causation. In some ~nstances, however, even the statistica~ link of smoking to disease has been d~sputed. For example in The Ciqarette Controversy: Why More Research is Needed 9 (Feb. 1984), statistical links to "perinatal problems, including low birth weight, fetal growth retardation, perinata~ mortality and congenital abnormality" are questioned in light of recent studies. (8) Some industry statements also argue that if a causal relation of cigarettes to disease were ever established, the industry would take action to modify its product: "If one or more CONF IDENTI,A1 - 95 -

of these compounds, as found in smoke, can be proved harmful, modern technology certainly would be applied in efforts to modify the product accordingly." (19) As Dr. Little stated at the 1957 congressional hearings, "I don't think there is one of them [li.e., tobacco executives] that is stupid enough to want to bluff for a minute" regarding any adverse health effects. In responding to these criticisms, the industry has noted that there are a variety of other factors which may be causal agents for the diseases that have been statistically linked to smoking. Most emphasis has been placed on the role of heredity and personality, as well as the role of viruses and of environmental pollution. One often-cited position is that it is not smoking that causes disease~ but rather the underlying personality of those who are most likely to smoke. (I0) Finally, the industry sometimes noted the potential benefits of smoking, particularly in the area of stress reduction. One publication in particular, The Smokinq Controversy: A Perspective (Dec. 1978), argues for the beneficial effects of smoking, including the risk that some persons m~ght be subject to "critical levels of hypertension" if they could not smoke. Dr. Robert ~ockett, in October 5, 1978 congressional testimony, similarly notes benefits from smoking in the areas of relieving anxiety and tension, aidi~ng in. digestion, and reducing the number CONF ]DE~T ]AI.

of cases of Parkinson's disease and ulcers. The testimony of Dr. Sheldon Sommers on March 12, 1982 notes beneficial effects of smoking for those with "severe psychic or psychologic problems." II. INDUSTRY RESEARCH EFFORTS The industry's descriptions of its research efforts usually consist of statements regarding the amount of money spent on research (either during the prior year or since the establishment of CTR) and the names of recipients of grant money. Industry spokespersons also consistently stress that the grantees have complete freedom, in their research and in the decision whether to publish the results. The research funding is usually described as "no-strings-attached," with "complete freedom and autonomy'" g~ven to the researchers. The nature of the research is also usually described only in general terms. Some publications have described tobacco industry research as directed at "smoking and health," and congressional testimony has used similar phrases, such as "the relationship between tobacco use and health." Among the stronger statements is one (repeated on several occasions by Dr. Sheldon Sommers) that from 1970 to 1982 $14 million was spent on "whether cigarette smoking causes lung cancer in animals," and the results "proved negative." Dr. Sommers also stated in March 1983 testimony CONF ~,DEII T ~AL

that two-thirds of CTR's research grants were spent on cancer research. In 1972 testimony, Dr. Sommers, speaking as Chairman of the Scientific Advisory Board of CTR, noted that grants are awarded based on, "competitive scientific merit and relevance of the proposals received to smoking and health problems." Nevertheless, Dr. Little, in 1957 congressional testimony, stated that grant money is given out in a "very, very broad" range of ideas "not confined to the effects of tobacco or any tobacco product." Dr. Robert Hockett of CTR stated in 1969 testimony (April/May hearings) that CTR is "concentrating study on the diseases that have been reported to be associated statistically with tobacco use." Industry statements have also criticized research by private organizations active in anti-smoking work, such as the American Cancer Society. One paper characterizes the research of these organizations by saying that "there is good reason to suspect waste and misdirection." (ii) The usual citations are more mild, however, and merely note that the tobacco industry has spent more on smoking and health research than any of the other organizations interested in these issues, such as the American Cancer Society. II~. INGREDIENTS/CONSTITUENTS OF SMOKE The industry has stated that no constituent of tobacco. smoke has been shown to be a cause of cancer in humans as found in CONFIDENTIAL - 98 -

smoke. The statements have encompassed the following substances: "tar," nicotine, carbon monoxide, benzpyrene, nitrosamines and nitrogen oxides, hydrogen cyanide, and beta naphthylamine. The industry has repeatedly emphasized the need for "whole smoke" research. The precise formulation of this position varies. Most often, the industry has made the general statement that the concentrations of these substances in smoke are so minute as to be inconsequential, and that only sophisticated research tools can detect some of these constituents. (12) At other times, the focus in on the absence of any smoke inhalation, studies finding adverse health effects., or the absence of studies on primates. For nicotine there have been further statements that not only is nicotine not harmful, but also that it may have beneficial effects,, including that it "stimulates the learning process." Nicotine's effect is often paralleled to that of '"mild exercise." (13) Statements regarding "tar" focus on arguments that "tar''' is not actually an ingredient in smoke, and that analysis of it is not an accurate method of research. Similarly, there is repeated criticism of skin-painting of "tar" as a method of research, since such studies "involve the wrong material [that is, the condensate instead of whole smoke], in the wrong dose, and ~n the wrong form, applied to the wrong tissue of the wrong animal!." (~4) CONF | DENT - 99 -

By contrast, Dr. Little, at the 1957 congressional hearings, admitted benzpyrene is carcinogenic, although only "[i]f you get enough of it at the right place." In addition, there is at least one reference in congressional testimony to the presence of insecticides and pesticides on cigarettes. Joseph. Cullman, speaking at 1969 congressional hearings (April/May hearings), stated that it was unclear "what if anything of these insecticides or pesticides get through to the products." Statements regarding the ingredients used in, the manufacture of cigarettes, as opposed to the natural constituents of tobacco smoke, are more rare. Beyond broad references to supplying information to the government, specific ingredients are not mentioned, and their health effects are not discussed. Instead:,~ there are broad statements that no causal link between disease and any cigarette ingredient has been proven. The distinction between ingredients and constituents is often blurred in these statements. (15) IV. ADDICTION/WHY PEOPLE SMOKE There are very few industry statements on the issue of addiction. To the extent such statements exist, they deny any addictive effect. (16) CONFIDENT ]AL - I0'0 -

More often there are statements regarding why people smoke, and in particular why young people begin to smoke. In this regard, the industry position has been that young people begin to smoke primarily because of peer pressure, and other social influences, and not as a result of advertising. (17) The industry explicitly states that it is not aiming its products at youth, and that smoking is an "adult practice." ADVERTISING AND PROMOTIONAL ACTIVITY Industry statements in this area focus on the argument that the claimed harmful effects from smoking have been. w~dely stated and are known to more than 90% of the population. (18) Conversely, Mr. Cullman has stated that reductions in advertising do not decrease consumption of cigarettes. (19) Finally, the industry position has been that smoking is an adult habit, and that advertisements should not be and are not directed toward young people. CONF ]'DENT ]AL

END NOTES (i) See, e.g., The Cigarette: Controversy, Eight Questions and Answers 26. (2) The Cigarette Controversy 8 (1974.). (3) See, e.g., Testimony of Horace Kornegay 633 (1972) (c~a~m "seems extremely far-fetched"). (4) Cf. Women and Smoking 7 ("Is it true that smoking mothers can harm their children by smoking around them? Studies in this area report conflicting results.'"). (5) See, e.g., Testimony of Dr. Robert Hockett 810 March/April hearings). ( 1965- (6) Fact or Fancy? 51. (7) Smokinu and: the Public 5. (8) See also Testimony of Dr. Sheldon Sommers 1080 (19,69 -- April/May hearings) ("evidence both favoring and opposing'" statistical links). CONF I'DENT IAL - 102 -

(9) The Ciqarette Consumer Controversy 13 (Jan. 1981). See also Testimony of Bowman Gray 160 (1964) (if harmful effects were found "We get awfully fast to work to see what we can do about it"); Testimony of George Allen 943 (1965 -- March/April hearings) ("If there is something in tobacco that is causally related to cancer or any other disease, the tobacco industry wants to find out what it is"). (i0) See, e.q., Fact of Fancy? 29 ("It may be the smoke__r rather than the smokinq that should be investigated"). (ii) The, Smokinq Controversy: A Perspective 19 (Dec. 1978). (12)i Cf. Testimony of Dr. Robert Hockett 105 (1972) (cigarette smoke is "about 2 or 3 percent carbon monoxide by volume"). (13)i See, e.q., Testimony of Dr. Robert Hockett i~12 April/May hearings) ("effects similar to those exercise on the work of the heart"). (1969 -- of light (14)i Testimony of Dr. Robert Hockett 102 (1971). (15)i See, e.q., Testimony of Bowman Gray 251 (1965 -- March/April hearings) (i"have not been. able to establish that any particul~ar CONF IDENT ]AL - 103 -

ingredient or compound in cigarette smoke is the cause illness. ") (16) See, e.q., Testimony of Edward Horrigan 390 (1982 -- March 5, ii, and 12 hearings) ("absolutely no proof that cigarettes are addictive"); Testimony of Dr. Robert Hockett 22 (1978 -- October 5 and 61 hearings)("there is an adjustment" to smoking over time and issue of dependence is "a very tough question").. (17) See, e.q., Testimon~ of Horace Kornegay 190 (1978 -- February hearing) ("I do not believe . . that cigarette advertising induces young people to smoke"); On Tobacco: 21 Questions and Answers 7 ("complex physiological, cultural and socioeconomic factors"). (18) See, e.~., Testimony of William Kloepfer 674 (1969-- April/May hearings) ("Never has any product been so extensively publicized with an increasing crescendo of inflammatory insistence that its use is hazardous"). (19) See, e.q., Testimony of Joseph Cullman 114 (1969 -- July hearings) ("[t]here isn't any evidence around the world that reduction in advertising or discontinuance of advertising will materially affect cigarette consumption,). CON F |:DENT I AI,. - 104 -

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