Tobacco Documents Online

Women and Lung Cancer A comparison of international lung cancer patterns raises serious questions about the claim that the larger number of women smoking today accounts for their rising lung cancer rates. Such a comparison indicates,that lung cancer patterns in women are different in various countries and are dissimilar from male patterns. Even when allowance is made for the later popularity of smoking among women, there is no consistent trend of increasing mortality rates. Some scientists have questioned whether the recent increase in lung cancer mortality is more artificial than real. These queries have been made because physicians appear to be ordering more diagnostic tests for women they know to be smokers. Therefore, it may be possible that more lung cancer among women is being diagnosed because more reliance is being placed on diagnostic techniques not available in the past. In addition, a role for occupational and/or other environmental exposures has been suggested by research con- ducted in heavily industrialized counties. Cancer in the Work Place The almost exclusive focus on individual smoking habits in the study of disease may have delayed needed research into possible occupational and environmental causes. tV Cn 0 ~ ~ ~ w N N 7

The announcement last September by HEW Secretary Califano that at least 20 percent of all cancers may be occupa- tionally related brought angry denials from anti-smoking researchers and organizations whose own estimates differed significantly from the new estimate. The authors of the report referred to by the Secretary actually estimated that between 21 and 38 percent of all cancers were occupationally related. They attributed a sizable proportion of all occupational cancers to asbestos exposure and noted that "perhaps the most important lesson to be learned from the asbestos story is that a major health disaster can develop while its early manifesta- tions are lost by being attributed to other factors." Lung Cancer The failure to consider critically 1) important diag.nostic advances, 2) cha_nges in the r_eQorted frequencies of lunK cancer cell types and 3) trends in cigarette consumption and lunJg cancer mortality data raises serious questions about any conclusions regardinR smoking. What some have called the "epidemic" in lung cancer mortality in this century has been linked by some to the increased popularity of smoking. However, it has been specu- lated that this reported increase may in fact have been created largely by improvements in diagnostic techniques -- in other words, more lung cancer cases have been reported because 8

physicians were better equipped to find them. Even if at least a portion of the "epidemic" is real, trends in lung cancer death rates can not be satisfactorily explained by cigarette consumption patterns. A British researcher has reported a similar phenom- enon in the United Kingdom that he contends is more consistent with the constitutional hypothesis than the smoking-causation theory. An apparent change in the reported frequencies of lung cancer cell types was observed in 1977. A researcher noted a shift in the histologic types of lung cancer found at a major cancer center -- from epidermoid, or squamous-cell, which has been more strongly associated with cigarette smoking, to adenocarcinoma, which is only weakly associated. Up to this point, at least, adenocarcinoma has been the predominant hist'ologic type of lung cancer reported in women and in non- smokers. Because of this reported increase in the lung cancer cell type not generally associated with cigarette smoking, serious doubt is cast on the role of smoking in the development of this disease. Other Cancers The establishment of an Y relationship between smok- ing ng and cancers of the larynx, esophagus and bladder must involve considerable guesswork, because of the vastly different incidence patterns and trends of these diseases and multiQle susQected causes.

Incongruities in the trends of incidence rates for "other cancers," such as cancers of the oral cavity, bladder, esophagus, larynx and pancreas, are almost impossible to reconcile with the cigarette smoking causal hypothesis. These trends, as described last year, include such anomalies as incidence rates that rise, fall or remain stable depending on disease, sex and race. Moreover, new evidence indicates that a number of these cancers may be associated with alcohol consumption and that the association of alcohol with cigarette smoking may not only confound the relationships but may hide other correla- tions. In addition, recent work has implicated occupational exposures and nutritional factors in the etiologies of some of these cancers. Cardiovascular Disease tv ~ 0 ~ A fair appraisal of the evidence, examined in its -~P , entiretY, indicates that the risk of coronary heart disease is strongly associated with genetic CO Cn and lifestyle factors. In 1977, the director of the governmental agency responsible for cardiovascular research told a Congressional committee that "we still don't know the etiology of arterio- sclerosis and hypertension" and that his researchers are still testing the "hypothesis...that lowering cholesterol and cessation of smoking will delay or prevent the onset of 10

heart disease" (emphasis added). Meanwhile, statisticians were finding that death rates for heart disease continued the decline that began in the late 1960s -- in all age groups, in both sexes and in both whites and nonwhites. There was new evidence in 1976, 1977 and 1978 that lifestyles, personality patterns and hormonal imbalances are implicated in coronary disease. An important development in cardiovascular research, was reported in 1977, by a group of researchers who reported that they were unable to duplicate their previous findings, which they said had suggested a causal role of carbon monoxide (CO) in the development of cardiovascular disease. In a presentation describing their findings, they said "no direct toxic effect of CO" could be demonstrated. Chronic Obstructive Pulmonary Disease The uncertainties and unknowns in the medical under- standing of COPD permit no firm conclusions about smoking . Chronic bronchitis and emphysema are highly complex and poorly understood diseases. Despite serious gaps in the medical knowledge in this area, claims abound that these diseases are caused by smoking. The validity of such claims is challenged by a recent National Heart, Lung and Blood Insti- tute statement that "the exact etiology of emphysema and other chronic lung diseases is unknown..." 11

Public Smoking This could have been the shortest chapter in this collection, considering the first item to be presented below. But it won't be, because the myths which have grown up around the whole subject of public smoking (sometimes called "passive smoking") must be discussed. Despite those myths, the recent testimony of the man who has directed the government's smoking and health research program for more than 10 years may well summarize the situation. Dr. Gio B. Gori of the National Cancer Institute was asked by a Congressional committee last October, "Is Other people's smoke has never been shown to cause disease in nonsmokers. there evidence to suggest that there may be an increase in risk of heart and lung disease to a nonsmoker by being in the presence of smokers?" Replied Gori: Well, this is a difficult question to answer, Mr. Chairman, because the answer that I have to give as a scientist may not please always the anti-smoking forces. But the fact remains that we really do not have conclusive scientific evidence about the adverse health effects of passive smoking on the bystander [and] in the usual conditions under which smoking is practiced, the evidence does not indicate that the casual bystander is seriously harmed by smoking (1). 134,

Very recent research -- two papers published in the second half of 1978 -- confirms this appraisal. In one, which appeared in the American Medical Association's Archives of Environmental Health, a Canadian team found that physiological responses to smoke exposure in normal adults could be described only as "minimal" and said "arguments concerning effects rest on symptomatology" -- in other words, on how the subjects said they felt, a highly unreliable standard (2). In the second, Danish and British scientists wrote in International Archives of Occupational and Environmental Health that they found "transitory discomfort" but that con- stituents of neither the gas phase nor the particulate phase of ambient cigarette smoke have "a lasting adverse health effect in otherwise healthy individuals" (3). Like the Canadians, the researchers said their test situations were realistic and typical of rooms in which smokers gather. Carcinogenic effects have not been demonstrated in humans. Nor do any studies to date establish that breathing others' tobacco smoke either causes lung disease or worsens the status of patients with existing disease (4). And it has not been established that atmospheric tobacco smoke has a causal role in coronary heart disease in nonsmokers (5). What evi- dence there is that ambient cigarette smoke may affect CHD sufferers has been called deficient (see below). 14

Nitrosamines A recent technique of some researchers has been to measure levels of specific cigarette smoke components in various public places and then announce that the non- smokers, by merely being present, would inhale of so many cigarettes in so many hours. the equivalent One such experiment in New York was described in 1977 at a joint conference of the American Chemical Society and the Chemical Institute of Canada (6). One of the researchers told how they had isolated tiny amounts of nitrosamines in cigarette smoke from laboratory smoking machines. Then they designed an apparatus to measure the compounds also in the smoke produced between the machine's puffs (the sidesteam smoke, in effect). Next they fitted the apparatus, consisting of two glass jars full of "trapping solution", some tubing and a battery-operated vacuum pump, into an attache case. And they headed, attache case in hand, first for a smoky New York commuter train bar car and then for a small metropolitan bar "frequented primarily by cigarette-smoking clientele." The amounts of nitrosamines they trapped in their glass bottles, they told their fellow chemists, indicated that customers in the bar could have inhaled in an hour the

same amount of nitrosamines as a smoker of nine to 16 nonfilter cigarettes. The researchers then discussed the "shortcomings" of their experiment. First of all, they were dealing with "volatiles" which change swiftly in the atmosphere (if not in a glass bottle with "trapping" solution). Then there were the two assumptions on which their estimates were based: one, that the mode of inhalation in breathing and smoking are comparable and, two, that "man's smoking conditions are synonymous with those of the test machine." Then they admitted that neither assumption was true. And they have yet to publish their results in a scientific journal. The measurement of nitrosamines in tobacco smoke has been controversial. Even the 1971 HEW report to Congress commented that nitrosamines reportedly found in smoke may be "artifacts dependent on the method of smoke collection" (7). A University of California chemist has estimated that at the trace amounts nitrosamines were reported in side- stream smoke, smoking as many as 100 cigarettes in a small room would produce only 3 nanograms (3 one-billionths of a gram) of the compound per liter of air (8). He said that at this concentration a carcinogenic effect could not be demon- PO strated in animals. Cn O ~ A 41 W ~ 1.~' Q

Carbon Monoxide Th ere was considerable furor last July at the publi- cation of an experiment by an avowedly anti-cigarette resear- cher in California -- coincidentally just before that state voted on a proposed statewide restrictive public smoking measure. Dr. Wilbert S. Aronow wrote that remaining two hours at a time in smoke-laden rooms adversely affected 10 patients with angina pectoris (9). The research has been roundly criticized since then for faulty study design as well as unsupported conclusions based on self-described symptoms of severely ill patients who had no doubt been advised, as are most angina sufferers, to avoid stressful situations (5, 10-16). Calling the study "flawed," a Los Angeles chest specialist wrote in The Los Angeles Times: Both investigators and subjects were aware of their exposure to the smoke and, obviously, that such exposure might be harmful. Moreover, the major measurement of the study -- the occurrence of chest pain -- was subjective. In other words, the test subjects' reports of chest pains while exercising could well have been influenced by their belief that they had been harmed by exposure to cigarette smoke. Considering this, as well as the curiously low variation in the subjects' carboxyhemoglobin levels [with and without exposure], I find the study questionable and sorely in need of confirmation (17). N Cn 0 ~ -p ~ W ~ ~ ~ 17