Authors: Richard Kluger
The argument that smoking was not a freely chosen activity because it typically began before the onset of awareness of how brief at best is life’s candle—and was for many devilishly hard to shake thereafter—did not command widespread support. The use of cigarettes, on the contrary, was granted a favored status and exempted from government scrutiny at the opening of the century—a tribute to the power of federal legislators from the leaf-growing states and their allies in the Midwest Farm Belt. Given the congressional seniority system and the long sway of the one-party South, tobacco-state lawmakers only added to their potency during the Democrats’ New Deal era and retained it when the activist era of government waned, thus accustoming the cigarette industry to unique liberty from bureaucratic oversight.
As the 1960s dawned, a young Democratic President faced a crowded social agenda on which a preventive public-health policy against the dangers of cigarettes was among the least pressing items. The product was hugely popular,
consumed by 60 to 70 million Americans—a record number—in 1963. Tobacco was an immensely profitable industry, and several million drew at least part of their livelihood from it. The delights of smoking were hammered into the popular consciousness through advertising that saturated the electronic and print media, and were fiercely defended in the political citadels, which themselves mined billions in excise taxes from the habit that greased the wheels of government. Who, moreover, could get greatly exercised about a product that nobody accused of killing children and rarely struck at people in their prime? A 1962 Gallup survey found that only 38 percent of respondents believed that smoking caused lung cancer. The following year the Food and Drug Administration, empowered by the 1960 Federal Hazardous Substances Labeling Act to determine whether suspect substances—toxic, irritating, corrosive, flammable, strongly sensitizing and pressure-generating—required regulations, ruled that cigarettes were not hazardous in any of those ways.
The American Cancer Society continued to provide the spearhead—somewhat dulled by now and never very pointy—for the antismoking movement at the beginning of the new decade. But in the ’Sixties, the giant agency was at pains to enlist as allies three other prominent private health groups: the American Heart Association, the National Tuberculosis Association, and the American Public Health Association. Together, the four voluntaries addressed a letter on June 1, 1961, to President Kennedy, still reeling from the Bay of Pigs fiasco and struggling to frame a coherent legislative program, to appoint a national commission on smoking, “seeking a solution to this health problem that would interfere least with the freedom of industry or the happiness of individuals” yet address the responsibilities of business, government, and the health community.
The President bucked the letter to Health, Education, and Welfare Secretary Abraham Ribicoff, whom the voluntaries then asked to meet with to explore the subject. When, after four months, no formal reply had been received, the ACS-led coalition flexed its muscles uncharacteristically and threatened to advise the press of the administration’s foot-dragging. The result was a meeting in the first week of 1962 between officials of the four voluntaries and the new top government health officer, Surgeon General Luther L. Terry, a honey-voiced Alabaman who, as a youngster, had picked tobacco. Terry was named after his father’s physician, Luther Leonidas Hill, whose son, Lister, became a U.S. senator chairing the subcommittee in charge of health matters. A beneficiary of Hill’s patronage, Terry was a Public Health Service careerist with a record of competence in hospital administration and some research work in the treatment of hypertension. As Surgeon General, he promised to consider the proposed commission on smoking and health but failed to act with dispatch.
At about that time, Oregon’s junior senator, Democrat Maurine Neuberger, introduced a joint congressional resolution directing the President to name a
group to formulate a comprehensive program to check smoking-caused disease. When Neuberger’s husband, Richard, a liberal idealist, died before completing his first Senate term, she ran for and won his seat. Plucky and principled, she nevertheless proved an ineffectual lawmaker, unwilling to bend to the Senate’s clubby ways. Neuberger won six co-sponsors for her resolution on the smoking problem, but it went nowhere in Congress. Still, hers was a persistent voice, the first in Congress since Representative John Blatnik five years earlier to speak out clearly on the smoking issue. Neuberger’s proposed resolution helped push Surgeon General Terry to suggest to the HEW Secretary in April 1962 a national commission that would make a rigorous assessment of the scientific case against the cigarette. Senator Neuberger, meanwhile, pursued the subject in an adroit letter to the new chairman of the Federal Trade Commission, Paul Randall Dixon, an affable Tennessean, who, like Luther Terry, owed his appointment to the influence of powerful Southern lawmakers. Neuberger urged the FTC not only to rescind what most public-health people now took to have been the commission’s ill-advised ban on any mention of tar and nicotine strengths in cigarette advertising but also to hold as inherently deceptive all such advertising that failed to include a warning on the health hazards of smoking. In mid-May, Neuberger carried her case to Terry, urging the Surgeon General to take a more forceful stand on the smoking peril.
When the President himself was finally asked at his May 23, 1962, press conference about the growing concern over smoking and health and what his administration intended to do to address the issue, Kennedy replied, “That matter is sensitive enough and the stock market is in sufficient difficulty without my giving you an answer which is not based on complete information, which I don’t have.” Confronted with the Cold War, civil rights, Medicare, and other monumental issues, the President was conceding a low rank to the smoking issue but promised to answer the question at his next meeting with the press. Two weeks later, Surgeon General Terry announced that it was indeed “timely to undertake a review of all available data” on the smoking question and that he planned to appoint a committee of experts to advise him on their findings. The cigarette makers, he said, would be allowed to blackball nominees so long as there were substantive grounds for the objection.
Just how weighty the judgment of the Surgeon General’s committee would prove was foreshadowed by the response Senator Neuberger finally received in July to her appeal to FTC chairman Dixon to mandate health warning labels in cigarette advertising. “If the Commission is able to secure competent probative scientific evidence including that furnished by the Public Health Service” of the harmful effects of smoking, Dixon wrote, then an FTC order to include health warnings in cigarette ads would likely “be upheld in appellate courts.” In short, the FTC wanted the official backing of the government’s chief health officer before it would consider such a bold initiative.
II
THE
closest thing to an official endorsement of the medical case against smoking had come earlier that spring from Great Britain. A nine-member panel chosen by the 444-year-old Royal College of Physicians (RCP), an honorary society numbering some 7,000 of the kingdom’s most prominent practitioners, issued a seventy-page report to a nation in which three-quarters of the men and half of the women smoked. Stressing that the high statistical association between smoking and disease had lately been strengthened by compatible if not conclusive laboratory evidence, the RCP said the weight of the findings in some 200 studies was that smoking was a major cause of lung cancer, was causal in bronchitis, and probably contributed to the development of coronary heart disease. And while air pollution intensified the health problems induced by smoking, the toll in disease and death was proportionate to the level of cigarette use, regardless of where an individual lived in the United Kingdom. Among the therapeutic measures proposed were a ban or limits on cigarette advertising, curbs on smoking in public places, and the stamping of tar and nicotine yields on every pack accompanied by the caveat that no brand was necessarily safer than any other.
British cigarette manufacturers were minimally responsive to the doctors’ urgings by agreeing to cease broadcast advertising before 9 p.m. The American industry, through the Tobacco Institute, brushed off the British report, saying it was based on old data. But more objective students of the subject were struck by the implications of two investigations soon reported in the
New England Journal of Medicine
, which dealt a punishing blow to the industry’s defense.
The April 16, 1962, issue of the
NEJM
disclosed results from the thirteen-year-old continuing study established in Framingham, Massachusetts, by the Public Health Service and later expanded to include a cohort from Albany, New York, to monitor the long-term health histories, especially cardiac, of more than 4,000 subjects. The new report focused on the association between smoking and heart disease, long suspected but little documented. Both the total death rate and the fatal toll from coronary heart disease among smokers in the Framingham-Albany cohort were five times higher than the rate among non-smokers. The disparity with regard to heart attack in the forty-to-forty-nine-year-old category was greater still. And the more one smoked, the greater the incidence of disease. The article concluded, however, that the “mechanism” behind these striking figures “is obscure”.
But the numbers, combined with findings in microscopic studies at autopsy by Oscar Auerbach, were enough to prompt his ACS collaborator, epidemiologist
Cuyler Hammond, to tell the annual American Medical Association meeting in July that the lung cancer toll exacted on cigarette smokers might prove “relatively unimportant” compared with the damage to them from other forms of disease, in particular those of the heart. In that month’s
Scientific American
, Hammond wrote a long article in which he hypothesized a systemic, interlocking pathology that frighteningly suggested how the heart and lungs were mutually affected by cigarettes. Smoke irritants thickened the walls of the small blood vessels and pulmonary veins carrying the oxygenated blood from the lungs to the heart, thus making the heart muscle work harder to obtain and distribute the vital oxygen the body needed for survival. The smoke also made thicker and less elastic the linings of the alveoli, the grapelike cluster of tiny air sacs used to feed oxygen to the cardiopulmonary system, greatly reducing their efficiency. Smoke toxins that additionally destroyed the cilia also triggered an apparently compensatory hypersecretion of the mucous cells and glands. This excess discharge often plugged the smaller airways, making it harder to breathe and forming a seedbed for infectious diseases, especially pneumonia. To clear these clogged passages, the sufferer coughed and sneezed, sometimes causing so great an increase in the pressure of the trapped air that the alveolar walls ruptured, further reducing the lungs’ capacity to process oxygen. Since normal lungs house some eight times as many alveoli as they need, a minor loss could be easily compensated for, but in smokers experiencing chronic insults to their tissues, the eventual loss in this vital function was both large and irreparable. When these functional complications were added to the previously known biochemical effects of tobacco smoke—in particular, a loss of 5 to 6 percent in the oxygen capacity of heavy smokers’ hemoglobin because of the high binding with it by carbon monoxide from the burned cigarette, the quickening of the heartbeat during and up to twenty minutes after smoking, and the constricting of the peripheral blood vessels—it was clear why smokers’ chronically overworked hearts often broke down prematurely.
That same month, Hammond co-authored a report in the
New England Journal
, for which Auerbach was the lead investigator, adding clinically explicit evidence of the part smoking played in the development of cancer. Examining the dissected tissue from 1,522 bodies autopsied at twelve hospitals over a seven-year period, Auerbach found obvious changes in the structure and arrangement of the bronchial cells four times as often in male smokers and three times as often in female smokers as in nonsmokers, regardless of their causes of death. Hyperplasia, the abnormal thickening of the airway walls, occurred in 88 percent of the male smokers and 83 percent of the female smokers, compared to 11 percent and 18 percent respectively in nonsmokers. Atypical cells with enlarged and darkened nuclei were found in an overwhelming 97 percent of male smokers and 81 percent of female smokers, compared
to less than 1 percent among nonsmokers of either sex. Cell changes closest in form to frank invasive carcinoma—lesions composed entirely of atypical cells with their cilia absent—were found in lung cancer victims and almost as frequently in the bronchial epithelium of heavy cigarette smokers who died first of other causes. Thus, Auerbach’s use of the term “preinvasive” for such tumors gained credibility.
A still more striking finding, this one unexpected, grew out of a subsidiary study Auerbach had included in his investigation in order to learn what effect, if any, quitting the habit had on the pathogenic condition of smokers. Observing the cell changes in three sets of seventy-two subjects—smokers, ex-smokers (defined as those who had quit five years or longer before their deaths), and never-smokers, with none in any of the groups having died of lung cancer—Auerbach found hyperplasia in 93 percent of the smokers, 57 percent of the ex-smokers, and 12 percent of the nonsmokers. The contrast was still greater with regard to atypical cells: they were present in 93 percent of the smokers, only 6 percent of the quitters, and 1.2 percent of the nonsmokers.
But there was something else. In 43 of the 72 ex-smokers, Auerbach observed a condition present in none of the 144 other subjects, whether smokers or not: lung cells with nuclei that appeared to be shrinking, fading, or just disintegrating. It was not clear whether these had been atypical cells before their hosts had quit smoking, but it was noted that the number of atypical cells in continuing smokers increased until their terminal illness. Thus, Hammond and Auerbach hypothesized that smoke might alter the environment of the bronchial passages in a way that favored the survival and reproduction of cells with atypical nuclei once the mutation process that generated such cell changes had been set in motion. And by extension, they reasoned, an environment in which smoke had ceased its steady assault was unfavorable to sustaining such atypical cells, so quitting caused them to atrophy or disintegrate, thereby reducing the number of cells present that might evolve into invasive cancer. Such a suspected sequence of events would help explain the drop in lung cancer rates in quitters and led Auerbach and Hammond to write: