I first encountered this temporal anomaly after reading an article in the Globe & Mail newspaper, authored by Andre Picard, on December 22, 2003. In that article, Picard stated:
"New research shows, for the first time, just how seriously non-smokers can be affected by secondhand cigarette smoke, even by casual exposure in a public place. The study, published in the medical journal Cancer Epidemiology Biomarkers and Prevention, found that, after only four hours in a casino, non-smokers had dramatically increased levels of carcinogens circulating in their blood. Kristin Anderson, of the University of Minnesota's division of epidemiology, said the levels of two well-known tobacco-based carcinogens , known as NNK and NNAL, rose two to four times on average in non-smokers. She said that until now, a direct link between exposure to smoke and cancer-causing agents had been shown only in a laboratory setting, not in a commercial one."
Globe & Mail story
Reading those words, I had a distinct impression of deja-vu. There was something so familiar about, as if I had read the same words on the same subject sometime in the past. I started searching through my files and - lo & behold - discovered a Las Vegas Review-Journal story about an amazingly similar study to the one referred to in the Globe & Mail article, which appeared on Wednesday, September 10, 1997.
Not only was the subject of the studies referred to in both articles very similar, some specific phrasings in both articles were nearly identical and both articles - published some 6 years apart - contained an identical "first time ever" occurence.
Globe & Mail, 2003 article:
"New research shows, for the first time, just how seriously non-smokers can be affected by secondhand cigarette smoke, even by casual exposure in a public place....Kristin Anderson, of the University of Minnesota's division of epidemiology, said the levels of two well-known tobacco-based carcinogens , known as NNK and NNAL, rose two to four times on average in non-smokers. She said that until now, a direct link between exposure to smoke and cancer-causing agents had been shown only in a laboratory setting, not in a commercial one"
Las Vegas Review-Journal 1997:
"Nonsmokers who work in a smoking environment have shown physical evidence of a cancer-causing substance in their urine, according to a new study released Tuesday. According to the author, the study, presented at the American Chemical Society convention in Las Vegas, marks the first time research has been conducted in the workplace rather than in a laboratory environment"
"The substance, called NNK, was detected in the urine of nine nonsmoking hospital workers caring for patients in a smoking area of a Canadian veterans hospital, said Dr. Stephen Hecht of the University of Minnesota Cancer Center."
"This is the first time that a metabolite of a tobacco-specific lung carcinogen has been found in the urine of nonsmokers exposed to environmental tobacco smoke under field conditions," Hecht said."
Initially, I wondered if reporter Andre Picard - who is openly a partisan advocate for the Health Promotion industry - might have plagarized his story from the Review-Journal story of 1997. However, a little more research revealed the source of Picard's story to be a news item on the University of Minnesota's website:
Inhaling tobacco smoke in public places
wherein the wording is even more identical to the 1997 Review-Journal story:
"A new study by University researchers is the first to measure tobacco-specific carcinogens in nonsmokers exposed to environmental tobacco smoke in a public setting."
"This study by University researchers is the first to measure tobacco-specific carcinogens in nonsmokers exposed to ETS in a public setting"
Apparently, this unique circumstance - "the first time that a metabolite of a tobacco-specific lung carcinogen [specifically, NNK] was found in the urine of nonsmokers exposed to environmental tobacco smoke under field conditions" - occured twice, the first time in 1997 and then again in 2003. Both times, the study in question was conducted and publicized by Dr Hecht and his team at the University of Minnesota. How could this be? Were they trapped in a time-loop, repeating the same discovery over & over?
Obviously not, but they did report and publicize the same discovery multiple times and claimed to be making the discovery "for the first time" in both instances. Why would they do this?
What does "the importance" of Stephen Hecht's research work reveal about "the purpose" of his work -
In 2006, Hecht was awarded the American Association for Cancer Research (AACR)-Cancer Research and Prevention Foundation (CRPF) Award for Excellence in Cancer Prevention Research: Hecht honored
"Dr. Hecht has been the most cited author on tobacco carcinogenesis, and is generally recognized as the world's leader in research on tobacco-specific human carcinogens called nitrosamines, found in cigarette smoke and smokeless tobacco. Other work in his laboratory, showing that exposure to second-hand tobacco smoke resulted in the presence of tobacco-specific carcinogens in nonsmokers has had a profound impact on clean indoor air laws critical for tobacco control.
"Stephen Hecht's ground-breaking and detailed research on tobacco-specific nitrosamines has enhanced our understanding of tobacco carcinogenesis," said Dr. Margaret R. Spitz, chair of the Department of Epidemiology at The University of Texas M. D. Anderson Cancer Center and co-chair of the award selection committee. "His research has provided a strong scientific rationale for public policies on smoking restriction."
In honoring Hecht with this award, the AACR clearly states the importance of his work to be the impact it has had on advancing the Tobacco Control public policy agenda. Hecht himself describes the importance of his work: From basic research to tobacco control
"We have quantified total NNAL in amniotic fluid of mothers who smoke, in the urine of newborns of mothers who smoke, in infants exposed to parental cigarette smoke, in elementary school children, in women living with men who smoke, in hospital workers exposed to patients who smoke, in people who frequented smoking sections of gambling casinos, and in restaurants and bars where smoking was permitted. The results of these studies consistently show uptake of NNK greater than in non-exposed non-smokers, with levels of total NNAL about 1-5% as great as in smokers. These data provide very strong supporting evidence for the epidemiologic studies showing elevated risk of lung cancer in non-smokers exposed to cigarette smoke. These studies also have impact, because they inevitably attract media attention. This work has contributed to the legislative momentum for smoke free restaurants and bars, which, along with taxation and anti-tobacco advertising, is a mainstay of current tobacco control strategies. The regulation of indoor smoking can reduce cues for smoking, reduce the amount smoked, and ultimately can change social norms. In summary, some basic research questions involving nicotine chemistry and mechanisms of carcinogenesis of the tobacco-specific lung carcinogen NNK led to more applied studies which have had an impact on tobacco control."
One rather subtle understatement in Hecht's words above is particularly revealing:
"These studies also have impact, because they inevitably attract media attention".
It is particularly important, both to Hecht and to the entire Tobacco Control industry, that his studies attract media attention, that they are widely publicized as a result, and that fear-mongering assessments of the implications of his work be widely disseminated through the mass media. This is essential, as it generates public sympathy toward the Tobacco Control public policy measures that Hecht's research will serve as a justification for. But, why do Hecht's studies "inevitably attract media attention". Is there something about the ways that Hecht and his team promote their studies that media find seductively appealing? Is there something about "the framing" manipulations that Hecht et al use to describe their studies that grabs media attention?
How about, if they were to describe their study as "groundbreaking", "for the first time", or "the first time 'X' carcinogen was measured in non-smokers in the workplace rather than a laboratory". Would that get the media's attention? And if that worked, in 1997, why not use it again in 2003? That could be a deceptive manipulation, but does that really matter?
What Hecht's work really tells us -
In 1999, Stephen Hecht summarized & reviewed the research on tobacco smoke carcinogens and cancer: Tobacco Smoke Carcinogens and Cancer
The importance of Hect's work, for Tobacco Control and apparently in his own eyes, is that he has developed a plausible biological explanation for how tobacco and tobacco smoke might cause cancer - particularly lung cancer - and demonstrated that his most viable culprit carcinogen, NNK, is absorbed by and can be measured in non-smokers. Widespread dissemination of these finding has resulted in a widespread belief that Hecht's work therefore proves that second-hand smoke causes cancer in non-smokers, and that widespread belief has generated public support for a range of Tobacco Control public policy measures. In this 1999 summary, however, what Hecht tells us does not in fact justify belief that second-hand smoke causes cancer in non-smokers:
"...exposure to environmental tobacco smoke (ETS) is widely accepted as a cause of lung cancer, although the risk is far lower than that of smoking and can be difficult to demonstrate, even in large studies".
Even in the writings of distinguished scientists with great expertise in cancer causes and mechanisms, one can read statements such as: "The carcinogenic mechanisms of tobacco smoking are not well understood".
This review will attempt to provide the generally informed cancer scientist with a distillation of mechanistic information on the subject of tobacco smoke carcinogens and lung cancer and to convince the reader that we know a great deal about the mechanisms by which these carcinogens cause lung cancer. While it is true that we may never be able to map each detail of the complex process by which cigarette smoking causes lung cancer and that there is unlikely to be a single mechanism of tobacco carcinogenesis, there are general principles that have emerged from intensive research in the past four to five decades."
"The tobacco-specific N-nitrosamine NNK is a potent lung carcinogen in rats, mice, and hamsters.
It is the only [nitrosamine] compound that induces lung tumors systemically in all three commonly used rodent models.
Cigarette smoke contains substantial amounts of NNK and the total dose experienced by a smoker in a lifetime of smoking is remarkably close to the lowest total dose shown to induce lung tumors in rats.
The long-term exposure of smokers to the genotoxic intermediates formed from these carcinogens is consistent with our present understanding of cancer induction as a process which requires multiple genetic changes. Thus, it is completely plausible that the continual barrage of DNA damage produced by tobacco smoke carcinogens causes the multiple genetic changes that are associated with lung cancer. While each dose of carcinogen from a cigarette is extremely small, the cumulative damage produced in years of smoking will be substantial".
Note this: "the total dose [of NNK] experienced by a smoker in a lifetime of smoking is remarkably close to the lowest total dose shown to induce lung tumors in rats".
In other words, the smallest dose of NNK that can induce cancer in a rat is equivalent to the total dose of a lifetime of smoking. But Hecht's studies on NNK absorbtion by non-smokers finds that they absorb only 1-3% of the NNK absorbed by the person doing the smoking. That means, a non-smoker would have to suffer 33 - 100 liftimes of second-hand smoke exposure to accumulate the equivalent of the smallest dose that can induce cancer in a rat. If something in tobacco smoke is causing lung cancer in non-smokers, it can't possibly be NNK.
Research scientists should be judged on the basis of their published work and how they represent that work to the public, not on the basis of who provides their funding. If a researcher makes false claims about their work for the sake of attracting media attention - such as claiming to make the same discovery "for the first time" more than once, or allowing their work to be misrepresented as conclusive evidence that something causes cancer in a specific population (when if fact it is merely suggestive of such a relationship) for the purpose of advancing public policy agendas - then it seems fair and appropriate to raise questions about whether or not "the importance" of their work to certain interest groups, or to a sponsor or client, might be influencing the content of that work.