Authors: Richard Kluger
As the cigarette yields were dropping—without explanation—and claims of the implied miraculous powers of the filters—without proof—were escalating, the chairman of the FTC struck a statesmanlike pose and pressured the industry into adopting what he hoped would be an advertising policy in the public interest. It would shortly prove to be just the opposite.
Earl W. Kintner, a twelve-year FTC veteran and its general counsel before assuming the chairmanship, exultantly reported in February of 1960 that the tobacco companies had voluntarily agreed to “a drastic change in the tone of cigarette advertising.” Henceforth, there were to be “no more tar and nicotine claims,” which were being “eliminated simultaneously and on an industrywide basis, because the individual claims were confusing to the public and possibly misleading in view of the absence of a satisfactory uniform testing method and proof of advantage to the smoker.” Where the 1955 FTC cigarette ad guide had ruled out unsubstantiated health claims (which nonetheless continued to be implied by allowable descriptions of filter styles and yield data attributed to reputable sources), the 1960 agreement ended all mention of the smoke yields since their health effects could not be proven. “In my view,” said the FTC head, patting himself on the back, “this is a landmark example of industry-government cooperation in solving a pressing problem.”
Like most forms of censorship, the FTC edict succeeded mainly in promoting ignorance—in this case, on the part of consumers—and retrogression—on the manufacturers’ part. Having somewhat modified their product in order to appear to have reduced its health hazards (that they nevertheless continued to deny existed), the companies now saw no value in continuing the trend. If they could not even imply a reduction in the perils of smoking, under the new FTC rules, further slashes in tar and nicotine strength offered them no possibility of
competitive advantage and might even, if they weakened their brands too much, destroy the addictive power of cigarettes that sustained their economic existence. Soon the yields leveled off or, in some cases, began creeping upward again.
III
HAVING
reduced their intake marginally in the preceding two years, smokers in 1955 resumed their indulgence in cigarettes, as if reassured by the arrival of many new filter brands designed—or so they chose, and were led, to suppose—to diminish whatever health hazard their habit fed. One prominent poll reported that nearly two-thirds of all adult men smoked cigarettes, one-third of all adult women, and half of all eighteen-year-olds. The health “scare” seemed to have eased. Cigarettes were barely linked to the No. 1 killer, heart disease—“the available evidence is not sufficient” to make the connection, said the American Heart Association’s scientific committee, except in the case of those already afflicted with a cardiac condition, and if there was a causal connection, “it is only one of many factors.”
While more convincing evidence had been developed regarding the likelihood that regular use of cigarettes was a major contributor to lung cancer, the February 1955 issue of
Consumer Reports
contended that the case “is still inconclusive.” By the end of 1960, when the death toll from lung cancer surpassed 35,000 a year, or twice the 1950 figure, a different verdict was reaching consensual proportions. The change, based on the extension of the earlier findings from surveys on death rates and laboratory experiments on mice, was due mainly to the work of pathologists and other investigators engaged in microscopic studies of human and animal tissue chronically exposed to tobacco smoke.
If epidemiologists, who had conducted most of the smoking studies in the early ’Fifties, were widely viewed in the medical profession as practitioners of “soft” science, pathologists enjoyed an exalted standing among their peers. Their interpretation after microscopic study of diseased tissue, usually undertaken just before surgery or immediately after death, represented science’s last word on the ravages of nature and how well doctors had coped with them. Pathologists knew better than anyone else the mistakes in diagnosis and treatment common to the healing arts. One such practitioner, in his fiftieth year when he started examining the smoking question, was Dr. Oscar Auerbach, by then a paunchy little pipe smoker admired within his field for a compulsively neticulous work ethic. Where others examined three or four “sections” of tissue before rendering judgment on the precise nature of the suspected disease, Auerbach might examine a dozen or two dozen slides. Well liked and unassuming
(for a pathologist, it was generally added), he was an exuberant and bouncy man who seemed to run rather than walk when outside his laboratory, as if to compensate for the largely sedentary nature of his work, which left him hunched for endless hours over a microscope. He wore thick glasses to correct severe myopia, which, while not affecting the accuracy of his microscopic vision, made him an uneasy motorist who, for his own safety and everyone else’s, commuted to work during off hours. Drawn to pathology while in Vienna for part of his student training because “it seemed to give you all the answers to so many diseases,” Auerbach specialized in lung disease early in his career and so had naturally grown familiar with cancer as it replaced tuberculosis as the prime bronchial menace.
Stationed at the Veterans Administration hospital in East Orange, New Jersey, Auerbach had a thought following one of his regular Tuesday morning clinical conferences in 1953. Part of the session had been devoted to a lung cancer victim whose tissue samples clearly illustrated the progressive stages of the disease. Why not undertake a study at autopsy of the lung cells of smokers who had succumbed to the same disease to see if a comparable progression could be tracked? The implications of such a finding might be profound.
The normal trachea, or windpipe, is divided into two main tubes, or bronchi, which en route to the lungs subdivide into ever smaller air tubes called bronchioles, ending in tiny air sacs, or alveoli, numbering perhaps 400,000 and surrounded by blood vessels with semi-permeable walls through which the vital life function of exchanging inhaled oxygen for exhaled carbon dioxide waste from the bloodstream is conducted. The interior surface of this intricate bronchial system, from the nostrils to the tiniest airways, is lined with a layer of sticky mucus, excreted by deep-lying glands and goblet-shaped cells along the surface to protect the breathing system from infection. The inner lining (or epithelial) cells are topped with a whiplike fringe of hairy filaments called cilia that beat back and forth rhythmically, propelling the carpet of mucus upward and outward in a protective mechanism that traps up to 99 percent of the irritants and toxic substances invading the body; scavenger cells called macrophages generally catch and consume unwelcome invaders not mired in the mucus. Any intrusive force, such as inhaled smoke, that might disrupt this chief line of the body’s defenses against disease was of keen interest to pathologists like Oscar Auerbach.
His lung tissue study, begun with a small grant from the Pfizer pharmaceutical company, would eventually involve four primary researchers who over an eight-year span microscopically examined more than 100,000 samples from some 1,500 cadavers, whatever their cause of death. To assure objectivity, the specimens were examined in a “blind” test, whereby each individual slide was identified only by a serial number so the investigators would have no prior knowledge of the subject’s cause of death. The sole condition in selecting the
subjects was that a reliable history of each one’s smoking habits be made available.
When his initial funding ran out and was not renewed, Auerbach took his project to the American Cancer Society, where chief epidemiologist Cuyler Hammond saw at once how such a careful pathological study might be an ideal complement to the biostatistics emerging from the ACS field survey of nearly 200,000 subjects. If the population study confirmed a close relationship between smoking and health, a microscopic examination at the cellular level might add the vital dimension of explaining how the disease process unfolded. Hammond got Auerbach ACS funding and the added expert counsel of Columbia’s famed pathologist Arthur Purdy Stout, who reviewed Auerbach’s slides and readings. By 1956, the first preliminary findings were reported.
Auerbach and his colleagues found three kinds of cell changes affecting the bronchi of smokers that rarely, if ever, showed up in nonsmokers’ lungs—and the more heavily the subjects had smoked, regardless of their ultimate cause of death, the more frequent and prominent the cell changes. First, some 95 percent of smokers had undergone hyperplasia of the epithelial cells lining their bronchi—an excessive growth
(i.e.
, anything more than two layers) in reaction to chronic irritation of the walls lining the airway and thus thickening them and narrowing the passage. In a number of cases, this had advanced to metaplasia, the abnormal proliferation of cells of altered shape and arrangement, which in turn, if unchecked, sometimes became tumorous lesions that drained nutrients from normal cells and formed what Auerbach and other pathologists called “carcinoma in situ,” meaning cancerous growths that had not yet broken through the underlying tissue of the membrane floor and started traveling to other body sites. Auerbach thus felt justified in terming such lesions “preinvasive,” by way of suggesting that if the subjects lived long enough, the chronic irritants inducing the disease process
(i.e.
, smoking) would cause the fatal spread.
A second phenomenon Auerbach observed in the cells of smokers was the destruction, shrinkage, or paralysis of the cilia during and after hyperplasia. The immobilized mucous lining, its flow arrested by the dysfunction of the cilia, allowed irritants from tobacco smoke, infectious bacteria, and other disease-bearers to accumulate and become ever more deeply embedded to do their mischief against the lungs’ now overmatched other defense mechanisms. Third, Auerbach found atypical cells in disproportionate numbers in the smokers’ lung tissue. The cell nucleus, visible under a microscope in normal cases as a little dark dot that served as the cellular brain directing the chemical processes in the cytoplasm, the surrounding fluid, began to enlarge and grow very dark in smokers’ cells because, as further studies would disclose, they were accumulating abnormal quantities of DNA and RNA, the critical gene materials affecting cell division and mutation. Belief grew that the carcinogens
in smoke constantly assaulting the epithelial cells eventually succeeded in penetrating the nucleus and altering or damaging the genetic material and thus promoted the disease process. The loss of cilia and presence of atypical cells were not found at all in the lungs of Auerbach’s nonsmoking subjects, whereas all lesions found in the heavy smokers’ lungs showed the atypia. In the latter, 11.4 percent of the subjects had all three kinds of changes, and in 14.3 percent of the lung cancer victims,
all
the epithelial cells were atypical. Such numbers were consistent with the emerging epidemiological studies that would show about one in ten heavy smokers contracting lung cancer.
Of further corroborative, or at least highly suggestive, value was the location of the tumorous lesions Auerbach found. As was the case in laboratory experiments using Y-shaped glass tubing to collect smoke condensate, the heaviest collection of which occurred at the joint where the tube bifurcated, so the branching points where the human airways are widest and the surface exposure is greatest proved the prime gathering site for the suspiciously precancerous changes in smokers’ cell samples. Still more persuasive as Auerbach’s studies lengthened was the finding that these cell changes in smokers’ lungs declined markedly after they quit the habit, and the longer they had stayed off it, the fewer cell changes were observed, suggesting that the disease process could be arrested and reversed.
Auerbach’s key investigation was substantiated by smaller contemporaneous studies by others working independently of him, especially on how cigarette smoke interfered with the critical function of the cilia. Anderson C. Hilding, a Minneapolis ear, nose, and throat specialist, used cows’ lungs to show how smoke inhibited ciliary action and that tars and other substances tended to accumulate on the lungs’ surface in places where the cilia had been destroyed and the clearance mechanism thus impaired. Paul Kotin and Hans Falk, working at the University of Southern California, used rabbits and rats to confirm that tobacco smoke curtailed ciliary activity and increased mucus secretion. And at the Arthur D. Little labs in Cambridge, in studies with rabbits paid for by Liggett & Myers, Charles Kensler, Sam Battista, and their coworkers found that the cilia were destroyed or stunted not only by tar solids but also by such toxic compounds in the gas phase of tobacco smoke as ammonia, hydrogen cyanide, formaldehyde, and acrolein. The net effect of these studies was to demonstrate that when one of the body’s chief defense mechanisms was deactivated by smoke, foreign materials of whatever origin—auto exhaust fumes, industrial dust, air pollutants, tobacco smoke carcinogens, or any other airborne pathogenic irritants—readily collected and remained in contact with the bronchial lining for far longer periods in smokers than in nonsmokers. This process greatly enhanced the likelihood that smokers would suffer more diseases, regardless of the specific agent or the precise and not yet understood nature of the mutation process at the cellular level.
In short, smoking was a major promoter of health damage, and probably in a wide variety of forms. This likelihood was underscored, though the investigators did not say it in so many words, by the husband-and-wife team of Cecile and Rudolf Leuchtenberger, pathologists at Western Reserve in Cleveland, working with a grant from the tobacco industry’s own research committee (TIRC) and using mice exposed to tobacco smoke. Their findings included cell changes in lung tissue markedly similar to those Auerbach was finding in human tissue of smokers at autopsy; no such signs were observed in the Leuchtenbergers’ unexposed control animals. However—and to their tobacco industry sponsors it was the saving feature of their investigation—in none of the 600 mice exposed over a two-year study did they uncover any case of invasive carcinoma, thereby casting doubt upon Auerbach’s contention that “carcinoma in situ,” the sizable tumors found in smokers’ lungs, was necessarily “preinvasive” and that such lesions were necessarily a stage in an unstoppable death march. Others argued, with Auerbach, that the only reason the Leuchtenbergers’ mice and other animals comparably exposed did not suffer from invasive cancers was that they died from related or other elements in the smoke before the ineluctably malignant process could play itself out.