Thursday, October 29, 2009

Observations on a New Tobacco Harm Reduction Commentary

In August I discussed a comprehensive meta-analysis of smokeless tobacco use and cancer, which was published by Peter Lee and Jan Hamling in the prestigious journal BMC Medicine. Recently that journal published a commentary by David Timberlake and Jason Zell, professors at the University of California at Irvine. The article, available here, will be widely read and will likely promote lots of debate, so I will make some critical comments.

Timberlake and Zell attribute the origin of the “controversy” over the use of smokeless tobacco as a “potential substitute for cigarettes” to the “steep decline” in smoking among Swedish men “over the past two decades.” They conclude that “it is premature to state that the increased use of ‘snus’ is causally associated with tobacco substitution and the decline in morbidity.” Unfortunately, Timberlake and Zell have repeated a common misunderstanding of the Swedish data.

Most commentators describe the “Swedish experience” as a recent phenomenon. This is incorrect. Philip Cole and I published a study earlier this year in the Scandinavian Journal of Public Health and discussed in this blog, which examined lung cancer rates among men and women in all European Union countries for the past 50 years. We concluded “that snus use is inversely correlated with cigarette consumption among men in Sweden, resulting in the lowest [lung cancer mortality rates] in Europe for most of the past 50 years.” Thus, Timberlake and Zell are mistaken that it is “premature to state that increased use of ‘snus’ is causally associated with tobacco substitution and the decline in morbidity.” In fact, nothing else adequately explains the profound and sustained differences between very low lung cancer mortality in Swedish men compared with other EU countries over the past half-century.

Timberlake and Zell correctly observe that clinical trials are starting to address the efficacy of tobacco harm reduction. They describe a Danish quit-smoking trial that used smokeless tobacco as successful at 7 weeks and unsuccessful at 6 months, but they could have explained that the investigators urged subjects to be tobacco-free at 3 months. It is perfectly clear that smokeless tobacco will not be any better for smoking cessation than pharmaceutical nicotine (that is, terrible) IF the ultimate objective is complete nicotine and tobacco abstinence. This objective is the Achilles heel of the conventional quit-smoking mindset, and it is entirely unnecessary. The appropriate objective is for smokers to lead longer and healthier lives, and this can be accomplished by not forcing smokers to abstain completely from nicotine and tobacco.

Timberlake and Zell repeat anti-tobacco extremists’ claims that “[c]arcinogens in smokeless tobacco include high levels of nitrosamines, polycyclic aromatic hydrocarbons and other agents,” and they cite a monograph from the zealous International Agency for Research on Cancer. These contaminants are present in smokeless tobacco, but in miniscule concentrations that aren’t relevant to human health.

Trace levels of contaminants are in virtually every product that humans consume. For example, in 2000 Bruce Ames, a well known expert in carcinogenesis (cancer causation), published an article noting that roasted coffee contains thousands of chemical agents. At that time about 30 of them had been tested as carcinogens, and 21 were positive. Thus, even though coffee contains cancer-causing chemicals, there is no epidemiologic evidence that coffee is a significant risk factor for any cancer in humans who consume it. Similarly, although smokeless tobacco contains trace levels of carcinogens, the cancer risks among smokeless users are so low that they are barely measurable with modern epidemiologic methods.

Timerlake and Zell represent that Lee and Hamling observed “excess risk” for oropharyngeal cancer among smokeless tobacco users, but this is perplexing. As I noted in August, Lee and Hamling found no risk related to smokeless tobacco after adjustment for smoking and alcohol, two risk factors acknowledged by Timberlake and Zell.

In some sections Timberlake and Zell get on the anti-industry train, which may be attractive to anti-tobacco extremists but may not be entirely accurate. For example, they suggest that Philip Morris had a crystal ball as early as 1984 regarding the benefits of smokeless tobacco. This is just short of nonsense, because until 2005, none of the major cigarette manufacturers had ANY stake in smokeless tobacco. Prior to that, cigarette and smokeless manufacturers were absolute competitors, representing a lost opportunity for tobacco control advocates who failed to focus on the most harmful products (cigarettes and other combustible tobacco products).

Timberlake and Zell also appear to agree with the anti-industry complaint that it is “more interested in the dual use of tobacco products, rather than tobacco substitution.” It is true that some ads promote smokeless use during “times when you can’t smoke.” But the industry has been forced into a marketing corner so tight that it doesn’t have any other choice. With the idiotic warning present on smokeless products since 1986 (This product is not a safe alternative to cigarettes), a marketing campaign focusing on substitution would be a ticket to self-destruction. It is depressing to think that FDA regulation is likely to make a science-based switch-to-smokeless pitch even less likely.

I have been critical, but there is much to recommend Timberlake and Zell’s commentary. For the most part, they provide a balanced discussion of key issues, which is absent in many other published articles. With respect to the Lee-Hamling study, they correctly conclude that “the overwhelmingly null (i.e., zero) associations with cancer in this high quality analysis are provocative, if not compelling.” Regarding the gateway issue (the idea that smokeless tobacco use leads to smoking, especially among children), their interpretation is on target: “even if a gateway effect to smoking exists, which is doubtful, only a minority of smokeless-tobacco users would be affected.” They address the role of human papillomaviruses, another commonly forgotten risk factor in oral and pharynx cancer. Finally, they recognize that FDA regulation “may not be the sole determinant of harm reduction’s fate in the USA,” and they “anticipate that much of the debate will shift from the discussion of epidemiologic data to the discussion of the marketing, health communication and economics of smokeless tobacco.” When that happens, it will be long overdue.

No comments: