Ashes to Ashes (113 page)

The RJR counterpunch began to land in the spring of 1984, when the first ad appeared under the headline “Can we have an open debate about smoking?” Horrigan’s idea of openness was to insist that a “causal relationship” between smoking and disease had not yet been proven. The follow-up ads were a bit more inspired, the most effective one featuring side-by-side messages from prototypical smokers to nonsmokers (“We’re on the spot. Smoking is something we consider to be a very personal choice, yet it’s become a very public issue. We’re confused. … We’re not criminals … ”) and vice versa (“We feel a little powerless. Because you can invade our privacy without even trying. Often without noticing. And sometimes when we speak up and let you know how we feel, you react as if we were the bad guys … ”). The spread said in small italics that it was “brought to you in the interest of common courtesy.”

This raised-fist campaign crossed the line between advocacy and deception, however, with an ad headlined “Of Cigarettes and Science,” which dwelled on the MRFIT study, just as the Tobacco Institute pamphlet had the year before. The Reynolds text said, “After 10 years, there was no statistically significant difference between the two groups in the number of heart disease deaths”—allowing readers to infer in the overall context of the ad that it was referring to the effect on smokers and quitters, not merely on the regular and special treatment groups. As the FTC asserted, when it finally got around to issuing a complaint against RJR for the misleading ad two years later, the company had conspicuously failed to disclose that “men in the study who had quit smoking had a significantly lower rate of coronary heart disease than men who continued to smoke.”

Philip Morris, meanwhile, was pioneering with’a less cerebral form of brainwashing, this one involving subliminal advertising. For a reported payment
of $42,000 the company bought twenty-two exposures of the Marlboro logo in the 1980 movie
Superman II
, aimed largely at the youth market. While neither the extraterrestrial man of steel nor his mild-mannered, earthbound alter ego, Clark Kent, was seen to light up, his girlfriend, Lois Lane, a reporter and role model for teenage girls, had a Marlboro pack on her desk and was shown puffing merrily away. At one point in the film, a character was tossed into a van with a large Marlboro sign on its side, and in the climactic scene the superhero battled numerous foes amid a maze of Marlboro billboards until he zoomed off in triumph, leaving in his wake a solitary taxi with a Marlboro sign on top. So effective was this technique deemed that the company next teamed up with Liggett, its partner in world rights to Lark cigarettes, to buy multiple plugs for that brand in the James Bond thriller
License to Kill
at a cost of $350,000. The method was used in other films by other manufacturers, attracted in part by the added exposure of the brand names on millions of home screens when the movies were shown on television—yet another circumvention of the federal ban on broadcast advertising of cigarettes. The practice continued for several years, until congressional investigators began making unfriendly noises about it, largely because the plugola game was employed in films for which a sizable part of the intended viewership was eighteen and under—a market the tobacco manufacturers swore they were not interested in soliciting.

Even as Philip Morris lobbyists were fighting to remove any reference to tobacco dependency from the rotating warning labels in the federal cigarette legislation being considered in 1983 and 1984, company researchers were coming up with interesting findings on that subject. Starting in the late ’Seventies, its scientists had begun intensified studies of the pharmacological properties of nicotine, looking for an artificial substitute without its negative effects like elevated heartbeat. Among their suspicions was that a second substance in tobacco smoke—acetaldehyde—was as addictive as nicotine, and the two together might be a more powerful addicting agent than either separately; further, that a synthetic compound known as 2-prime methylnicotine caused animals to behave as if they were undergoing a nicotine high without experiencing rapid heartbeat. An important corroborative study was also proving fruitful. Associate senior scientist Victor J. DeNoble, a psychologist who had joined Philip Morris in 1980 and was put in charge of the nicotine explorations, worked with rats that self-administered the substance by depressing a lever for small, rapid doses equivalent to that in a human cigarette puff. The animals became increasingly fond of the nicotine and learned how, when the task of obtaining it was made harder, to depress the lever six or seven times to obtain their momentary fix and to ignore another lever that yielded only a placebo. DeNoble’s rats conditioned themselves to absorb nearly a hundred nicotine jolts in a twenty-four-hour period. He wrote up his findings in a paper
entitled “Nicotine as a Positive Reinforcer in Rats,” of scientific interest because so vivid a demonstration of self-administered addictive behavior from nicotine had not been achieved before with rodents.

Shortly after DeNoble sent off his paper to the scientific journal
Psychopharmacology
in May of 1983, a Little Ferry, New Jersey, woman named Rose Cipollone, dying from lung cancer, filed a product liability suit against three cigarette makers, Philip Morris among them, accusing them of failing to warn her properly of the addictive nature of smoking and its potential lethal effects. DeNoble was summoned to New York to brief top Philip Morris executives on his laboratory’s findings. The highly suggestive conduct of his nicotine-dosed animals worried the Philip Morris brass. One of their rank, according to DeNoble, asked him rhetorically, “Why should I risk a billion-dollar [business] on rats pushing a lever to get nicotine?” On August 30, 1983, DeNoble wrote the editor of
Psychopharmacology
to advise that “due to factors beyond my control I must withdraw our manuscript … .” Publication was suppressed because, accordingly to an account by DeNoble ten years later, his lab was “generating information that the company did not want generated inside the company [and] it was information that would not be favorable to the company in litigation.” Consideration was given to moving DeNoble’s staff and facilities to Switzerland, where the work could have been done at arm’s length from the company, with the scientists funded as independent contractors. Instead, on April 5, 1984, just a few weeks before Mrs. Cipollone’s lawyers filed a massive request for company research documents, DeNoble was told to close down his laboratory, to kill the animals, to suspend all further investigation of possibly less toxic or harmful alternatives to nicotine, never to try to publish or discuss his work on addicting rats, and to find work elsewhere. DeNoble tested the company’s resolve in the matter by submitting his paper, slightly revised, once more the following year to
Psychopharmacology
and was promptly threatened with a court injunction.

About the same time that DeNoble’s work was running its course, Philip Morris scientists were undertaking another project that might have proved similarly vexing to the public, had it not been similarly shielded from its view. The effort, aimed at developing a fire-retardant cigarette, was called Project Hamlet (as in “To burn or not to burn … ”) and was carried out as Congress was expressing concern over the more than 1,000 deaths, many more injuries, and hundreds of millions in property damage traceable each year to some 40,000 cigarette-ignited fires. Public-health officials spearheaded by Andrew McGuire of the trauma center at San Francisco General Hospital had argued that cigarettes could be made far less incendiary if the tobacco was cut finer and packed tighter, the paper was less porous, and additives to quicken the burn rate were dropped. By 1987, the R&D team at Philip Morris had developed a less flammable version of Marlboro, found by a panel of seventy-seven consumers to be
as acceptable in taste as the regular brand. Yet the company did not share details of this development with a special federal commission convened to study the problem, but instead joined with other industry officials in insisting before the inquiry board that the experimental fire-retardant cigarettes their companies had explored were too hard to draw on or had an unsatisfactory taste, making them commercially unviable.

Perhaps the most egregious example of the tobacco industry’s reprehensible tactics in this period was a study undertaken by the Council for Tobacco Research (CTR)—in itself a rare initiative—and presented to the public as something very different from what it actually was: a hugely expensive investigation, flawed in design and mangled in execution, which might have seriously embarrassed the industry if it had been allowed to be completed.

Published by CTR itself in a handsome blue cloth binding in November of 1984, the 187-page study entitled
Chronic Exposure of Mice to Cigarette Smoke
was described in a press release carried in the February 1985 issue of the Tobacco Institute’s house organ, the
Tobacco Observer
, and by the wire services as a nine-year investigation undertaken by Microbiological Associates of Bethesda, Maryland, under contract to the industry’s research council at a cost of $12 million. In the course of the study, 10,000 mice and the smoke from 800,000 cigarettes were used by researchers who performed a reported 11,000 daily manipulations of the test animals, dosing and later autopsying them, studying their tissue under the microscope, and evaluating the data—in short, the last word in completeness and thoroughness, or so it was implied—as part of what CTR’s scientific director, Sheldon Sommers, called in the foreword “a determined effort to develop a suitable animal model” for inhalation tests to learn if tobacco smoke caused cancer. The key finding, Sommers wrote, was that the vast experiment “did not produce any squamous cell lung cancer, a type often reported to be associated with smoking in humans.” The only hint that the smoke might not have been exactly therapeutic was the disclosure that “[t]he incidence of alveolar adenocarcinoma was not different between smoke-exposed and sham-tested [put in the same stock-like holders, though not exposed to the smoke], but appeared sooner in the former.” Even this vaguely cautionary information seemed to be outweighed by the further news that some type of cancer occurred in 27 percent of the smoke-exposed mice but in 29 percent of the sham-tested animals. The overall message, though not explicitly stated, apparently was that the smoke exposure had not harmed the test animals. The 1984 CTR annual report called special attention to the study, as it had done to no other before. Upon careful review, however, the investigation appears to have been based on inadequate science and presented to the public in a misleading and confusing way that was close to fraudulent.

To start with, there was no indication that the findings had ever been peer-reviewed
by outsiders; the report was published by the CTR itself. The same industry that had howled fourteen years earlier when Oscar Auerbach’s study on smoking beagles was made public before it appeared in a scholarly journal was now bringing forth as legitimate science its own self-certified work. Then there was the matter of Sommers’s introductory claim that the study was a “determined effort” to find a suitable animal model for such inhalation studies when (a) no other species but mice was used and (b) it had been well known among experimental biologists for more than twenty-five years that small animals were notoriously poor subjects for such studies because most of them inhaled shallowly when administered smoke and allowed so little of it to reach their lungs that cancers were most unlikely to develop there. Investigators like the Leuchtenbergers and Homburger, on the other hand, had found laryngeal cancers in smoke-dosed hamsters, yet the CTR study neither used hamsters nor examined the larynx tissue in their subject mice. More to the point, mice were known to react badly to being immobilized for inhalation tests and, if dosed too strongly, were prone to die of asphyxiation from the carbon monoxide in the smoke or go into convulsions due to nicotine poisoning. In the case of the Microbiological Associates study contracted for by CTR, researchers apparently failed to conduct dose-response tests to set a tolerable level of smoke, and as a result, by the thirty-second week of the scheduled two-year investigation, 52 percent of the smoke-exposed mice and 19 percent of the sham-tested ones had died from what the report termed “exposure-related problems”—either systemic stress and agitated head movement or “improper air-smoke flow leading to suffocation.” So severe was the agitation problem that some of the animals had to be “rested” from the test to allow their wounds to heal, yet when the research laboratory developed padded holders to reduce the mice’s self-inflicted abrasions, the CTR disallowed their use. This huge premature death toll meant that many fewer smoke-exposed animals were left in the study, greatly skewing the outcome since the subject animals most likely to develop cancers did not live long enough for the pathology to take hold.

Even so, some 77 percent of the smoke-exposed mice developed pulmonary lesions, compared with less than half that percentage among the unexposed animals, and such cellular alterations, as Auerbach and others had posited in work with both dogs and human tissue, might well have turned into malignancies if the mice had lived long enough. Furthermore, despite the impression given by the CTR that all the test animals had been autopsied, fewer than half the smoke-exposed animals were, compared with 82 percent of the unexposed subjects—and none of the smoke-exposed animals that had died prematurely were autopsied, so the investigators could not tell how many of them might have had presymptomatic cancers or precancerous lesions. The first half of the investigation, moreover, was halted after fifteen months, nine short of its planned duration, on orders from CTR’s overseers and without explanation to
the commercial laboratory conducting the project. The high premature death toll was the likely reason; for the second part of the study, the smoke dosage was cut to one-fifth of what had been administered during the first stage—in order, probably, to spare many more of the subject mice, but probably too low an amount to induce cancer.