In the early 1990s, I had been a member of the EPA panel charged with evaluating the evidence for an association of passive smoking with lung cancer. It was clear that the leadership of the committee was intent on declaring that passive smoking caused lung cancer in non-smokers. I was the sole member of the 15-person panel to emphasize the limitations of the published studies—limitations that stemmed from the rudimentary questions used to characterize exposure. Many members of the committee voiced support for my comments, but in the end, the committee endorsed what was clearly a predetermined conclusion that exposure to secondhand smoke caused approximately 3,000 lung cancers per year among never-smokers in the United States.

This is where things stood in the late 1990s, when I was contacted by James Enstrom of UCLA. He asked if I would be interested in collaborating on an analysis of the American Cancer Society’s “Cancer Prevention Study I” to examine the association between passive smoke exposure and mortality. I had been aware of Enstrom’s work since the early 1980s through the medical literature. We were both cancer epidemiologists interested in lung cancer occurring in people who had never smoked, and we had both published numerous studies documenting the health risks associated with smoking as well as diet and other behaviors. In addition, Enstrom had begun his collaboration with the American Cancer Society with Lawrence Garfinkel, the vice president for epidemiology there from the 1960s through the 1980s. Garfinkel was one of the advisors on my (later published) master’s thesis on the topic of lung cancer occurring in never-smokers, which I completed at the Columbia School of Public Health in the early 1980s.

From his work, I had a strong impression that Enstrom was a rigorous and capable scientist, who was asking important questions. Because I had been involved in a large case-control study of cancer, I welcomed the opportunity to work with data from the American Cancer Society’s prospective study, since such studies have certain methodologic advantages. In a case-control study, researchers enroll cases who have been diagnosed with the disease of interest and then compare the exposure of cases to that of controls—people of similar background, who do not have the disease of interest. In a prospective study, on the other hand, researchers enroll a cohort, which is then followed for a number of years. Since information on exposure is obtained prior to the onset of illness, possible bias due to cases reporting their exposure differently from controls is not an issue.

After several years of work, our paper was published by the BMJ on May 17th, 2003, addressing the same question Takeshi Hirayama had posed 22 years earlier in the same journal: whether living with a spouse who smokes increases the mortality risk of a spouse who never smoked. Based on our analysis of the American Cancer Society’s data on over 100,000 California residents, we concluded that non-smokers who lived with a smoker did not have elevated mortality and, therefore, the data did “not support a causal relation between environmental tobacco smoke and tobacco related mortality.”

The publication caused an immediate outpouring of vitriol and indignation, even before it was available online. Some critics targeted us with ad hominem attacks, as we disclosed that we received partial funding from the tobacco industry. Others claimed that there were serious flaws in our study. But few critics actually engaged with the detailed data contained in the paper’s 3,000 words and 10 tables. The focus was overwhelmingly on our conclusion—not on the data we analyzed and the methods we used. Neither of us had never experienced anything like the response to this paper. It appeared that simply raising doubts about passive smoking was beyond the bounds of acceptable inquiry.

The response to the paper was so extreme and so unusual that it merits a fuller account, which I will offer below.

Grab a coffee.