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Calculating the comparative mortality risk from smokeless tobacco versus smoking Carl V Phillips, Dunsi Rabiu, Brad Rodu University of Alberta School of Public Health Alberta Smokeless Tobacco Education and Research Group (ASTER) University of Louisville Background and Motivation Smoking is bad for your health. We assume we do not have to expand on that. The use of smokeless tobacco (ST), which includes moist snuff (“dip”), chewing tobacco, and various new sachet and lozenge-type products, is much less risky than smoking, and provides a dose of nicotine similar to that from smoking. For simplicity, the present analysis is restricted to men, who are more likely to consider using ST, though there is not believed to be any substantial sex difference in the comparative risk. All calculations are for the 35+ year-old population, divided into age categories 35-44, 45-64, 65+. This follows the methods used in the US government reports. There is overwhelming epidemiologic evidence to support the claim that the risk of life-threatening disease from ST use is much lower than that from smoking. Sources of Inputs Estimated mortality from smoking was taken directly from the CDC/SG reports. This observation has led some public health advocates, ourselves included, to suggest that smokeless tobacco might be a promising substitute for smoking and that this “harm reduction” strategy could benefit the large number of smokers who are never going to quit nicotine entirely. Baseline mortality, by disease, was calculated by subtracting smoking attributable mortality from total mortality. Such substitution has worked very well in Sweden, where a large portion of male smokers switched to ST, resulting in the lowest smoking rate for any comparable population. New smokeless tobacco products are easy to use; in particular, they do not require spitting. This makes the harm reduction option socially feasible. Unfortunately, for reasons that are not entirely obvious, a large, well-financed cadre of anti-tobacco abolitionists opposed the harm reduction strategy. Sometimes their arguments imply that the total risk reduction would be too modest to be sufficient. How much would substitution of smokeless tobacco for cigarettes change health risks? The U.S. Center for Disease Control and Prevention (CDC) attributes the deaths of more than 400,000 Americans a year to smoking and reports 46 million people smoke in the U.S. Health Canada reports 6 million smokers and attributes 45,000 annual deaths. How many deaths would there be if all those people used smokeless tobacco instead? Some tobacco abolitionists would like people to believe that there is no health difference, regardless of the actual epidemiologic evidence. People who attend to the actual science come to rather different conclusions about the approximate fraction of the risk from smoking resulting from smokeless tobacco use: Royal College of Physicians (UK): between 0.1% and 10% Levy et al. (2004), based on a survey of selected researchers close to the issue: average for the group: about 10% Rodu, calculated based on early risk estimates: 2% Phillips, based on rough calculation: 1% These estimates show broad agreement that risk from ST is very small compared to that from smoking (the Levy average is pulled up by inclusion of some people who apparently fall into the “regardless of evidence” category). However, the estimates are based on some combination of guesses, unpublished back-of-the-envelope estimates, or (in the case of Rodu) an early estimate based on then-current wisdom that can now be updated. Because knowing the comparative risk is important in making public health policy, and because existing estimates are not terribly robust, we set out to develop a more robust and transparent estimate. Methods Our calculation, with the exception of the relative risk (RR) estimates for ST use, is based on the reports and data used by the recognized authorities on smoking in the United States. Diseases and Mortality Estimates for disease specific mortality and smoking-attributable mortality are from the CDC, as reported in the 2004 US Surgeon General’s (SG) report on smoking. These appear in Table 1. For purposes of our calculation, we divided these into oral and pharyngeal cancers, esophageal cancer, pancreatic cancer, other cancers, cardiovascular diseases, and other lung diseases. We chose to ignore neonatal effects, fires, and secondhand smoke. Those who believe there is substantial mortality from secondhand smoke should adjust the comparative risk from ST downward accordingly. The division into disease categories was based on the fact that oral cancer is most widely believed to be a risk from ST use. There have been some recent claims about pancreatic cancer, and esophageal cancer seems to be next most common. Cardiovascular diseases are included as a possible risk from ST and combined because there is not sufficient epidemiology to justify separating them. Other lung diseases are included only in the deaths from smoking. Baseline mortality was divided among the age ranges using age-specific rates from SEER (Surveillance Epidemiology and End Results) database. Portion of the population who were current and former smokers is reported in the SG report. For former smokers, we divided the population based on number of years since quitting (Table 2) based on data from NHIS (National Health Interview Survey). (continued) The spreadsheet used to carry out these calculations is available for customization during the poster session. Anyone who prefers a different scenario or assumption can enter their preferred numbers. The spreadsheet will be published with our results, ensuring that they are transparent and maximally flexible. Pancreatic Cancer Esoph. Cancer All other Cancers CVD Total mortality risk compared to smoking Scenario Description Oral Cancer 1 No extra risk 1 1 1 1 1 0.0% 2 Current cancer rhetoric 1.5 1.5 1 1 1 0.6% 3 Old cancer rhetoric 4 1 1 1 1 0.4% 4 All-cancers risk 1.5 1.5 1.1 1.1 1 0.7% 5 CVD risk 1 1 1 1 1.1 1.9% 6 Combined 1.5 1.5 1.1 1.1 1.1 2.5% 7 Pessimistic but plausible case 1.2 1.2 1.1 1.05 1.05 1.2% 8 Unrealistic case 1.8 1.8 1.2 1.2 1.2 5.0% Estimated risks from ST are described below Our estimates are based on plausible results from our extensive comprehensive reviews of the literature (detailed elsewhere). There are no definitive estimates for the mortality risk from ST. Indeed, contrary to popular misconceptions, ST use has not been convincingly linked to any mortality endpoint, including oral cancer. Of course, the nature of epidemiologic analysis is that it is impossible to distinguish between a sufficiently small risk and zero risk. However, it is possible to rule out strong associations (using the same logic as ruling out the null – a fact that many health researchers seem woefully unaware of). A few outlier studies have found strong associations, but modern high-quality studies of ST and oral cancer have shown the association to be null or close to it. An RR 1.1 or 1.2 for this rare cancer is compatible with the data, but an RR as high as 1.5 seems implausible. (For comparison, the RR from smoking is about 10.) . Two recent studies claim to shown an association with pancreatic cancer, though as we have pointed out elsewhere, both of these studies are suspect. Those studies showed RRs above the null but below 2 (which is the usual estimate for smoking). For other cancers, the literature does not even suggest an association. For cardiovascular disease, most studies have show null associations, but two or three studies (notably one large study that is analyzed in Phillips’s other poster in this session) have shown some positive association. The highest plausible RR estimate based on the evidence appears to be in the range of 1.1 (compared to about 2 from smoking). Calculation For each baseline mortality (by disease and age category), we calculated the portion of baseline mortality attributable to current and former smokers. Using the estimated relative risks from ST use (scenarios described below), we calculated mortality above baseline that would occur if all current smokers used ST instead. We calculated the effect of former use as follows: For former smokers, we assume they would be former ST users in the hypothetical world where smokers use ST instead. We assume those who had quit within 4 years has the same additional cancer risk as current users; those who quit 15 years earlier had no additional risk (and so are not included in the calculation); and those in between had half the risk of current users. For cardiovascular disease risk, we estimated no increase risk for former users (the usually posited biological mechanism for any such risk is short-term acute blood pressure effects of nicotine). We summed the resulting estimated increased mortality and divided it into the extra risk from smoking, getting a comparative risk (which applies to an individual or a population) Scenario 1 is obviously trivial, but it is worth including as a reminder that there is no clear evidence of an elevated risk, and so the other scenarios are based on speculative risks. Scenario 2 reflect one thread of current anti-smokeless-tobacco rhetoric, that seems to emphasize the two cancers, without claiming any specific relative risks (the relative risks reflect the highest remotely plausible value). Scenario 3 reflects an older, more naïve popular claim about oral cancer risk (based on one outlier study). Scenario 4 adds a small risk for other cancers to Scenario 2, though there is not really evidence that supports that claim. The key lesson from these three scenarios is that any plausible level of cancer risk (and even somewhat implausible levels) does not produce total risk as large as 1% that from smoking. The rhetorical emphasis on cancer risk from ST, particularly when used as an argument against tobacco harm reduction, is misguided. Scenario 5 shows the effect of a speculative level of cardiovascular disease risk. As anyone familiar with mortality statistics for North American nonsmokers could predict, a bit of CVD risk overwhelms plausible levels of cancer risk increase in nonsmokers. Scenario 6 combines Scenarios 4 and 5. Scenario 7 is intended to approximate the worst plausible case that is consistent with the epidemiologic literature. We consider both of these scenarios to be pessimistic. Scenario 8 increases the risks beyond any supported estimates for relative risk. This are presented not because we believe the inputs are plausible, but to show that even extreme estimates produce results no higher than about 5% from that from smoking. Conclusions Any estimate of comparative risk is going to be as uncertain as the input parameters, but the variety of scenarios we present should make clear the plausible range of estimates. It is not absolutely necessary to carry out this calculation to be able make the argument that the comparative risk favors a harm reduction strategy, since the rough, it adds robustness to the argument. Table 1: Annual smoking-attributed and other-cause mortality, US males, age 35+ Disease Total Deaths Smoking Attributable Not Smoking Attributable Oral and pharynx cancer 5200 3900 1300 Esophageal cancer 8600 6300 2300 Pancreatic cancer 13400 3100 10300 Other cancers 120000 92600 27400 Cardiovascular disease 424000 87600 336400 92000 53700 38300 663200 247200 416000 Other respiratory diseases Total Population Our estimates are based on statistics for the U.S. population. Because population size divides out in our calculation (which comes out in a per-person basis), the result will extrapolate to similar populations. Results Table 2: Smoking status, U.S. males, age 35+ (percent of population) Age Current Smoker Quit within 4 years Quit 5-14 years before 35-44 27.60% 10.2% 10.0% 45-64 27.60% 4.4% 8.0% 65+ 10.50% 5.0% 8.7% Our scenarios show that estimates in the range of 1% or 2%, and possibly less, are most consistent with the epidemiologic evidence. Perhaps most important, our calculation shows that comparative risk estimates as high as 5%, let alone 10% or more, cannot be justified based on the evidence. This has not been so clearly demonstrated before. We will make our calculation tool available so that others who disagree with inputs can redo the calculations. With that available, anyone claiming that the risks from ST are a substantial fraction of those from smoking will be obliged to show their version of the inputs and calculations (which can then be shown to be patently implausible). While anti-harm-reduction advocates have proven that they do not necessarily let little matters like overwhelming evidence interfere with their efforts, this calculation will make their errors more apparent to those who are interested in improving the public health. For further reading www.TobaccoHarmReduction.org ASTER (Phillips et al.) www.SmokersOnly.org (Rodu)