Authors: Richard Kluger
If the statistical association between smoking and damaged health was
found to be overwhelming, the SGAC’s next key challenge was to define the criteria for determining whether the undeniable association was causal in nature. What they were after was a set of standards comparable to the postulates set out by Robert Koch, the famed nineteenth-century German bacteriologist, in determining the causative agent in such contagious diseases as typhus, tuberculosis, anthrax, and Asiatic cholera in a period when such single-cause diseases exacted a ravaging toll on humanity. But in the case of chronic, multicausal killers like cancer and heart disease, formulating the criteria to determine the most prominent contributory agents was a far more complex challenge.
To help Leonard Schuman, the SGAC’s epidemiologist, frame the case for causality by testing the statistical association as rigorously as possible, Hamill spirited him and Cochran away for a few days of concentrated brainstorming in the tonic atmosphere of Saratoga Springs in mid-June of 1963. The three were joined by two of the nation’s most respected epidemiologists, the University of Pennsylvania’s Johannes Ipson and the dean of the University of California’s School of Public Health, Reul A. Stallones. After much shooting of pool and talking shop, the little group had its final dinner together, wreathed in smoke from all their cigarettes, and at the end it was Stallones, a witty companion and incisive thinker, who pulled it all together. The question before them had been what criteria had to be met before medical science could conclude that the statistical case against smoking as the prime cause of lung cancer had been proven. “This is what I think we’ve been talking about,” Stallones said and, taking an empty pack of Luckies from his pocket and tearing it apart, scrawled on the inside surface of the wrapper: “The consistency of the statistical association, the strength of the association, specificity of the association, and the coherence of the association.”
The consistency of the association was beyond dispute, Berkson’s mad-dog objections aside. Despite the differences in the sizes of the sampled cohorts, their whereabouts, their social customs and economic status, and the purity or impurity of the air they breathed, the findings were uncannily similar. And the strength of the association was no mere 20 or 30 percent higher for smokers than nonsmokers but on the order of fifty to sixty times higher than that, and even more for the heaviest smokers—a magnitude made all the more persuasive by the dose-response data
(i.e.
, the more one smoked, the greater the chance of contracting lung cancer). The specificity of the association, meaning the precision with which one element in an associated pair (smoking and lung cancer) can be depended upon to predict the occurrence of the other, was of particular concern because lung cancer
did
occur, in twelve to fifteen cases out of one hundred, in nonsmokers while it did
not
strike the majority of smokers—or, to put it another way, it had not struck them at the time of their deaths
from some other cause. But since the risk ratio was more than ten times higher in smokers, to attribute lung cancer to another causative factor would have required its presence in a comparably high ratio (and its absence in nonsmokers); no such factors were ever demonstrated by the defenders of tobacco. The specificity argument was also enhanced when the dose-response factor was more closely examined: it was not only how much one smoked that raised one’s lung cancer risk but how early one began to smoke and how long one kept at it.
Finally, as to the coherence of the association, the committee members had to be satisfied that the statistical case was of a piece with the known facts in the natural history and biology of the diseases as well as environmental and social considerations. For Leonard Schuman, the coherence criterion required determining, for example, upon finding that blue-collar workers suffered more from lung cancer than other groups, whether they in fact smoked more heavily as well. They did. Similarly, if women got the disease a good deal less than men, did they in fact smoke fewer cigarettes a day than men, inhale less, leave longer butts, and as a group begin the habit in earnest several decades later in the century than men had? They did. And if Britons got more lung cancer than Americans but smoked fewer cigarettes per day, did they smoke them further down the butt, where the toxic materials collected in intensified strength, possibly because each fag they drew on was far more heavily taxed than the American cigarette? They did. It was all of a piece.
In the wake of such a searching analysis, as detailed in the SGAC report, to dismiss the case against smoking as “merely statistical” was a preposterous denial of reason itself. The numbers, hard logic, and human experience behind them fused to build a conclusive case.
IX
THE
Surgeon General’s panel had only one lingering concern about the population studies indicting smoking as the most prominent cause of lung cancer. Cuyler Hammond’s results in his big American Cancer Society study seemed almost too perfect. And Hammond himself did not help much by evidencing what the SGAC panel and its staff felt to be a rigid personality and a highly controlling attitude toward sharing the backup materials for his announced results. “He spoke as if he were God, without any doubts about the accuracy of his studies,” Peter Hamill recounted. “And he spoke as he wrote, as if life were predigested and predetermined.”
Pathologist Emmanuel Farber, while enthralled with the stringent analysis by his committee colleague William Cochran of Hammond’s numbers and
those in the other studies, nevertheless wanted to see the supporting clinical evidence for himself. That insistence drew him, Cochran, and Hamill to the East Orange, New Jersey, laboratory of Oscar Auerbach for two days of inspecting the slides that the VA pathologist had painstakingly assembled over seven years and that showed severe changes in the lung cells of smokers. The hovering Auerbach, his mass of work under intense scrutiny now, struck the visitors as inarticulate, obsessive, and opinionated, though hardly close-minded, as Hammond was thought to be. But after two days, the second one beginning at 4:30 a.m and ending at 10 p.m., Farber concluded that his fellow pathologist was honest, dedicated, and very careful in his microscopic tissue examination. The inference to be drawn from Auerbach’s massive studies disclosing the grim cellular metamorphosis in smokers was unmistakable. Comparable cell changes found in experimental animals dosed with smoke were enough to compensate, most SGAC members felt, for the failure to produce frank, metastasized tumors in the animals, which frequently died first from other toxins in the smoke. The case against smoking as the chief perpetrator of lung cancer was closed, and two of Auerbach’s microphotos were borrowed for inclusion in the committee’s report, along with extensive citation of his findings.
Whatever uneasiness may have remained over the almost too precise symmetry of Hammond’s earlier study was routed in the late fall of 1963 as the SGAC knuckled down to committing its judgment to writing. After thirty-four months, Hammond’s second massive population study under the ACS banner—this one involving 1,078,894 men and women, with a 99 percent follow-up rate—had progressed sufficiently to allow the preliminary results to be rushed to the Surgeon General’s committee. Beyond its unprecedented size, what distinguished this project, known as Cancer Prevention Study No. 1 (CPS-I) to epidemiologists, was the way in which Hammond had designed it to counter the criticism of Berkson and others that the first ACS population study was based only on the factors of smoking, age, and residence. This time, using a computer, Hammond matched some 37,000 pairs of subjects, each composed of a smoker and a nonsmoker of a comparable age and otherwise identical or very similar with regard to two dozen possibly confounding factors, including height, weight, race, national origin, marital status, drinking, sleeping, dietary and exercise habits, longevity of parents and grandparents, and occurrence of cancer in other family members.
In Hammond’s paired subsampling, 1,385 of the smokers had died after nearly three years of follow-up, compared with only 662 of the nonsmokers. And in every category examined, whether the subjects had been tall or short, white or black, married or single, those who smoked a pack of cigarettes a day or more died of lung cancer at an appreciably higher rate. The overall risk for
the disease among Hammond’s huge sample was nearly eleven times higher than that for nonsmokers, or almost exactly the median figure that Cochran had calculated in his cumulative computations for the seven prior prospective studies.
This last-minute infusion of clinching data only added to the advisory committee’s unanimous finding on lung cancer. From the first, their hope had been to issue a single consensual document, and that sentiment had grown over the course of their deliberations even as certain irreconcilable differences among them surfaced. All of them conceded that a minority report would emasculate the whole effort. “It was a matter of credibility,” recalled Leonard Schuman, who did more of the writing than any other committeeman. “We didn’t want to be second-guessed, and a minority report would have invited that, with people saying, ‘See, even they had their doubts and misgivings.’”
As a result, the SGAC’s 387-page report had to omit certain judgments that a majority but not all of its members would have endorsed. Every nuanced word was reviewed scrupulously, assuring the most cautious possible language consistent with the evidence. Thus, the panel’s single most indicting judgment read: “Cigarette smoking is causally related to lung cancer in men; the magnitude of the effect of cigarette smoking far outweighs all other factors. The data for women, though less extensive, point in the same direction.” With regard to the cardiovascular peril posed by tobacco, the committee would go no further than to state: “Although the causative role of cigarette smoking in deaths from coronary disease is not proven, the Committee considers it more prudent from the public health viewpoint to assume that the established association has causative meaning than to suspend judgment until no uncertainty remains.” Indeed, such an assumption was the central thrust of the entire document, which was and could be no more than an interim judgment, not a conclusive statement about a subject in which science was constantly generating new evidence. Science, as embodied by the Surgeon General’s learned committee, was saying to the smoking public, “Better safe than sorry.”
For all its collegiality, the SGAC had to settle two substantive clashes within its ranks as the writing proceeded. One involved a disagreement between its two youngest members, LeMaistre and Farber. The former, in charge of drafting the chapter on the effects of smoking on chronic obstructive lung diseases, was satisfied that cigarette smoking was the most important cause of bronchitis, triggering both the inflammation of the bronchial walls that reduced air flow and the hypersecretion of mucus that caused chronic smoker’s cough. But the case against emphysema was a tougher call, even though some 80 to 85 percent of the cases occurred in smokers. Farber thought the evidence was sufficiently clear-cut to call the connection causal, and his concern was intensified by the belief that emphysema was “a far worse sort of disease than lung
cancer.” The latter struck down its victims generally within a few years of their turning symptomatic, but with emphysema “you choke to death for twenty years.”
Little mystery remained about the dysfunctional nature of emphysema, the term applied to the destruction or loss of elasticity of the walls of the alveoli, the tiny air sacs at the end of the bronchioles where the body exchanges carbon dioxide, its chief gaseous waste matter, for life-fueling oxygen. The irreparable damage was rarely discovered until some 60 percent or more of the alveoli were gone, producing chronic shortage of breath and the eventual choking sensation. But just how tobacco smoke broke down the alveoli could only be theorized at the time. One theory held that some toxic substance in smoke turned the macrophages, scavenger lung cells that normally thrived on foreign matter not trapped in the mucus and expelled from the body by the beat of the cilia, into cannibals that devoured the alveolar walls. A second theory posited a smoking-induced imbalance of enzymes in the bronchial cavity which destroyed the elastic nature of the alveolar walls, causing them to rupture when the air pressure got too high. “My opinion was clear,” LeMaistre recounted, “but the corroborative evidence—the proof—was simply not there yet. … We had to put credibility first, not our personal beliefs.” Thus was the reach of the SGAC report shortened in order, as LeMaistre later put it, “to meet the body of evidence then available—it had to conform to what we felt we could justify.” Accordingly, and despite Farber’s fury that LeMaistre was being overly cautious, the consensual language read, “A relationship exists between cigarette smoking and emphysema but it has not been established that the relationship is causal.” A mellower Farber would concede nearly three decades later that LeMaistre had probably been right.
A more serious clash developed after committee members read Walter Burdette’s draft of chapter 9, which dealt with cancer and would make up one-third of the final version of the report. Burdette, the nonsmoking surgeon from tobacco-hating Utah, angered his heavy-smoking colleague, Leonard Schuman, by larding the key chapter with material on the genetics of cancer, inferentially lending substance to the constitutional theory of lung disease favored by the tobacco industry and its apologists while shortchanging the hard epidemiological, chemical, biological, and clinical evidence. If the victims of cancer—bronchial along with other kinds—were foreordained from birth, then environmental and behavioral factors like cigarette smoking were beside the point. To the outraged Schuman, who stopped smoking soon after the SGAC report was issued, this was close to quackery. He told the top staff people and the Surgeon General’s office that he would part company with the committee if the punch was to be pulled so blatantly. Burdette, at first supercilious in his response to the criticism, was diplomatically massaged by the staff until he conceded that perhaps he had not taken into account the full range of evidence.
Schuman was invited to redraft the chapter; his version, as fine-tuned by others on the panel and editors from the Public Health Service staff, became the centerpiece of the report.