Lauren A. Colby
Chapter 07, The Surgeon General's Reports
|© 1996, Lauren A. Colby. Version 2.0||HTML-version by Kees van der Griendt|
At this point, the reader will likely ask, "But what about the Surgeon General's Reports? Don't they prove that smoking causes lung cancer?". Actually, they don't.
It's not easy to get copies of these Reports. When I started my research, I combed the local libraries without success, and called major libraries all over the country. Nobody had any copies. One reason the Reports may be so difficult to obtain is that they contain material which might be embarrassing to the anti-smoking lobby, e.g., the data on pipe and cigar smoking.
Ultimately, I found a small company in Alexandria, VA, which was able to supply copies of the reports from 1964 through 1982, on microfilm. During that time frame, there were a total of 15 Reports, issued sporadically between 1964 and 1982. The largest, most massive Report was issued in 1979, and dealt with programs to "educate" (force) people not to smoke. The last Report that I have was entitled the "Changing Cigarette", and dealt with such things as filters, tar content, etc. The basic "science", purporting to show that smoking causes lung cancer was set forth in the first Report, in 1964, and for that reason I will concentrate here on an analysis of the 1964 Report.
The 1964 Report was issued by a committee of ten "scientists", picked from a list of 150 scientists and physicians, heavily weighted towards government agencies and large organizations active in public relations, with a low representation from the scientific community. Prior to the writing of the Report, numerous experiments had been conducted, attempting to induce lung cancer in laboratory animals by painting their lungs and trachea with cigarette tars, forcing the animals to inhale vast quantities of tobacco smoke, etc. All of these experiments failed, miserably!. Consequently, at page 165 of its Report, the Committee was obliged to concede that "Bronchogenic carcinoma has not been produced by the application of tobacco extracts, smoke, or condensates to the lung or the tracheobronchial tree of experimental animals with the possible exception of dogs".
The phrase "possible exception of dogs" related to a single experiment, of which the Committee wrote that "this work has not yet been confirmed". To this day, it remains unconfirmed and it remains true, to this day, that despite hundreds of experiments 17 . , nobody has been able to induce a single cancer in lab animals by exposing them to ordinary tobacco products or smoke.
Other researchers attempted to induce lung cancer in lab animals by using nasty combinations of industrial strength carcinogens. They used mixtures of ozonized gasoline and mouse-adapted influence viruses; polycyclic aromatic hydrocarbons, directly applied to the lungs of rats; mixtures of benzo(a)pyrene and iron oxide dust; radioactive cerium; and beryllium oxide. Even with these noxious brews, the results were not entirely successful. For one thing, some of the experimenters reported "distant metastases", i.e., tumors occurring in sites far from the lungs (which makes me wonder whether the "treatments" had simply weakened the animals' immune systems to the point at which cancers were springing up spontaneously throughout their bodies). Moreover, not all the animals got sick. For example, two out of ten rhesus monkeys injected with beryllium oxide developed cancers but 8 did not.
The animal experiments having failed, the Committee was left with retrospective studies and prospective studies. Retrospective studies are studies in which cancer patients are interviewed about their smoking habits and compared with another group of controls from the general population, whose smoking habits are likewise identified. In prospective studies, a population is sampled, their smoking habits are ascertained, and they are then followed for a number of years, to determine who develops the disease.
The Committee had a number of retrospective studies available, but wisely decided not to rely much upon them, because of well known problems with such studies. Instead, it chose to rely upon seven prospective studies, as follows:
(1) British doctors, a questionnaire having been sent to all members of the medical profession in the U.K. by Doll and Hill, in 1956.
(2) White American men in 9 states, enrolled by American Cancer Association volunteers, each of whom enlisted 10 white males between 50 and 60 years of age. Hammond and Horn, 1958.
(3) Policy holders of U.S. Government Life Insurance policies. Dorn, 1958.
(4) Men, 35-64 in nine occupations in California which were suspected of having a high occupational risk of lung cancer. Dunn, Linden and Breslow, 1960.
(5) California members of the American Legion and their wives. Dunn, Buell, and Breslow, 1961.
(6) Canadian War Veterans. Best, Josie and Walker, 1961.
(7) American men in ten states, enrolled by volunteers from the American Cancer society, each of whom was asked to enroll about ten families containing at least one person over 45. Hammond, 1963 18 . .
Now, right off the bat, there were several sources of bias immediately apparent in the manner in which the surveys were conducted. It was obvious to everyone, including the participants and their doctors why these studies were being conducted, i.e., to prove that smoking causes lung cancer. Thus, an element of detection bias was introduced. I'll return to that point shortly.
There was also the matter of the selection of the survey participants. Not all the holders of U.S. Government Life Insurance policies participated; not all the British doctors participated, etc. Taking the five studies for which it had data on the non-response rate, the Committee concluded that the average non-response rate was about 32%. Then, at page 116 of its Report, the Committee made the following curious observation. Citing a paper by Berkson 19 , the Committee said, "The death rate in the complete population (3.000) was 42% higher than the respondent death rate. The non-smoker death rate was over 38 times as high among non-respondents as among respondents (60.1221/1.553), whereas among smokers it was only 1.8 times as high. [Berkson's] calculations referred to an early year of the study, in which the differential entry of ill persons among smokers and non-smokers are likely to be most marked. Further, as we interpret his writing, the example was intended as a warning against the type of subtle bias that can arise whenever a study has a high proportion of non respondents, rather than a claim that this numerical estimate of the bias actually applied to these studies".
Thus, the Committee was confronted with what should have been a red flag: a finding that the death rate amongst non responding non-smokers was 38 times as great as the rate amongst responding non-smokers, whereas the death rate among non-responding smokers was only 1.8 times as great as the death rate among corresponding respondents. It is apparent, even to a layman, that such a major discrepancy could greatlyskew the results of the surveys. Yet, the Committee brushed the point aside, saying, in substance, that it didn't think that Berkson meant what he wrote!
There were troublesome discrepancies. The Committee found that the most potent carcinogen present in tobacco smoke is benz (a) pyrene (p. 27). According to the Committee, cigar smoke has 4 times as much benz (a) pyrene as cigarette smoke, and pipe smoke ten times as much as cigarette smoke (p. 58). Yet, the Committee found pipe and cigar smoke to be pretty much innocent of causing lung cancer, and even concluded that pipe smokers live longer than non-smokers (unless they quit - the Committee concluding that those pipe smokers who quit had done so because they were already ill).
Some would argue, of course, that cigar and pipe smokers inhale less than cigarette smokers (although, in my case, I inhale both pipes and cigars). If, however, inhalation is a factor in the development of disease, it should show up in relative inhalation rates for cigarette smokers. A study was, in fact, conducted by Hill and Doll, which sought to classify cigarette smokers as inhaling vs. non-inhaling. At page 188 of the Report, there is a reference to a "negative association" between inhaling and lung cancer, based on the "early" Hill and Dole studies.
In 1959, in fact, R.A. Fischer analyzed some of the Hill and Doll data and concluded that inhalers have a lower rate of lung cancer than non-inhalers 20 . Fischer's findings were incorporated into Table 8 of the 1982Surgeon General's Report, but the Report did not deal with this apparent paradox.
The Committee did, to some extent, recognize the effect of socio-economic status on the various prospective studies which it analyzed. Table 26 at page 109 of the Report showed incidents of morbidity, derived from all seven prospective studies, for 25 different causes of death. In all but two categories (cancer of the rectum and intestines), smokers showed an increased risk of death, as opposed to non-smokers. Indeed, it was claimed that smokers have increased risks of dying from such diverse causes as accidents and suicide, cirrhosis of the liver and bladder cancer, as opposed to non smokers. This troubled Brownlee, because he failed to see the "specificity" of smoking to the disease which the Committee claimed to be "caused" by smoking, i.e., lung cancer. After all, common sense would seem to show no connection between smoking and prostate cancer, or smoking and cirrhosis of the liver. Perhaps, what the studies were really studying was social class. Cigarette smokers tend to come from lower socio-economic strata than cigar or pipe smokers, or non smokers. Perhaps it is socio-economic status that accounted for the paradoxical finding that pipe smokers lived longer than non smokers and that cigar smokers lived the same.
Studies published in recent years (and therefore not available to the 1964 Committee) bear out the relationship between socio-economic status (SES), smoking and morbidity. A 1990 study 21 showed the following relationships between smoking and levels of education:
|Percentage who Smoke (U.S.)|
|Years of Education||Males||Females|
A 1973 Study 22 correlated morbidity with educational levels, as follows:
|Ratio of Observed to Expected Deaths, U.S., ages 21-65|
|Years of Education||Males||Females|