Smokeless Tobacco Is For Smokers Only
Tobacco initiation by young people should be stopped in its tracks, but the relative safety of smokeless isn’t a children’s issue. The 8 million Americans who will die from smoking-related illness in the next 20 years are not children today; they are adults, 35 years and older. Preventing youth access to tobacco is vitally important, but that effort should never be used as a smokescreen to condemn smoking parents and grandparents to premature death.
Smokeless Tobacco Use is Not a Gateway to Smoking Among Teenagers
1. Evidence from Sweden Against a Gateway
In Sweden, a country with a very high prevalence of ST use (in the form of moist snuff called snus), there is no evidence that ST is a gateway to smoking, especially among youth. A 2003 policy statement published in Tobacco Control, coauthored by Clive Bates, former director of Action on Smoking and Health (U.K.) and five other eminent tobacco research and policy experts, dismissed the notion that ST use led to smoking in Sweden: “To the extent there is a ‘gateway’ it appears not to lead to smoking, but away from it and is an important reason why Sweden has the lowest rates of tobacco related disease in Europe” (1). Foulds et al. reached a similar conclusion: “This review suggests…that in Sweden snus has served as a pathway from smoking, rather than a gateway to smoking among Swedish men” (2).
A 2005 study by Rodu et al. examined tobacco use among 15- to 16-year old schoolchildren in Sweden over a 15-year period, from 1989 to 2003 (3). The investigators found that the prevalence of regular snus use among Swedish boys increased from about 10% to 13% from 1989 to 2003, but the prevalence of regular smoking was very low and declined, from about 10% to under 4%. The prevalence of smoking among girls was about double that of boys over the entire period (snus use among girls was very low). The authors concluded that snus use did not appear to be a gateway to smoking among Swedish boys but instead was associated with low smoking prevalence.
Other recent studies based in Sweden have come to similar conclusions. In 2005 Furberg et al. investigated whether snus use was associated with smoking initiation or smoking cessation using data from the population-based Swedish Twin Registry. They concluded that snus use was “inversely associated with initiation.” (4)
In 2006 Ramström and Foulds examined data on tobacco use from a national Swedish survey. They found that “Use of snus in Sweden is associated with a reduced risk of becoming a daily smoker…” (5) In 2008, the European Commission’s Scientific Committee on Emerging and Newly Identified Health Risks concluded that “The Swedish data…do not support the hypothesis that…snus is a gateway to future smoking.” (6)
2. Evidence from the U.S. Against a Gateway
Opponents of tobacco harm reduction in the U.S. believe that it will lead to increased teenage ST use, which will function as a “gateway” to smoking (7). It has been observed that teenagers who use ST are more likely than non-users to subsequently smoke (8,9,10,11,12). But a close examination of the evidence suggests only that ST use is one of several behaviors associated with smoking, not that it leads to smoking.
In the U.S., concomitant use of cigarettes is common among ST users (13). However, investigators have not found credible evidence that ST use is a gateway to smoking among American youth. In 2003 Kozlowski et al. analyzed data from the 1987 NHIS survey and concluded that there was little evidence that ST use was a gateway to smoking, because the majority of ST users had never smoked or had smoked cigarettes prior to using ST (14).
The belief that ST is a gateway to smoking is based mainly on two longitudinal studies comparing subsequent smoking among adolescent ST users and non-users (12,15). The first study, which used the 1989 Teenage Attitudes and Practices Survey (TAPS) and its 1993 follow-up, found that young males who used ST were significantly more likely to have become smokers at follow-up than non-users of tobacco (OR = 3.5, CI = 1.8 – 6.5) (12). However, a subsequent analysis revealed that the earlier study did not take into account well-known psychosocial predictors of smoking initiation that were in the TAPS, including experimenting with smoking, below average school performance, household member smoking, depressive symptoms, fighting and motorcycle riding (16). Inclusion of these variables into a multivariate model reduced the odds ratio of smoking among regular ST users to 1.7, which was not statistically significant. The investigators concluded that the earlier “analysis should not be used as reliable evidence that smokeless tobacco may be a starter product for cigarettes.”
The second study found that 7th and 9th grade students who had used ST (in the past 30 days) were more likely than nonusers to be smoking two years later (OR = 2.6, 95% CI = 1.5 – 4.5), after controlling for smoking by family and friends, low grades, alcohol use and deviant behavior (15). However, Timberlake et al. (17) have observed that regression analysis may not adequately control for imbalances in covariate distributions between ST users and nonusers. They analyzed data from the National Longitudinal Study of Adolescent Health after propensity score matching and found that adolescent ST use was not associated with an increased risk of smoking in later adolescence or young adulthood (17).
In 2005 O’Connor et al. examined data from the 2000 National Household Survey on Drug Abuse to determine if ST use caused smoking. They described the impact of ST use on subsequent cigarette smoking initiation as “minimal at best,” and they concluded that the association of ST use and smoking seen in other reports “is likely a manifestation of dual experimentation rather than a causal relationship.” (18)
In 2010 Rodu and Cole examined the gateway issue with data from the National Survey on Drug Use and Health (NSDUH) during years 2003, 2005 and 2007 (19). The NSDUH asks survey participants at what age they used cigarettes or smokeless for the first time. Using this information, Rodu and Cole classified participants as cigarette initiators (meaning they smoked before they used smokeless), ST initiators, or both. They determined the prevalence of current smoking among these groups using established criteria. The analyses were restricted to white men age 18+ years, who are most likely to have used ST. In addition, they looked at white boys aged 16-17 years, since the gateway claim often focuses on teenagers.
Rodu and Cole showed that the prevalence of current smoking among white men who were cigarette initiators was 35% (19). In comparison, the prevalence of smoking among ST initiators was only 28%, a significantly lower statistic (prevalence ratio, PR = 0.80, CI = 0.77 – 0.84). If the gateway effect was real, smokeless initiators would have had smoking rates similar to – or higher than – cigarette initiators.
The results for boys were even more impressive. Current smoking among cigarette initiators was 43%, but only 18% of ST initiators smoked (PR = 0.43, CI = 0.36 – 0.52). This means that boys who had started with ST were less than half as likely to be smoking at the time of the survey.
Claims of a gateway effect persist, even with lack of credible evidence, prompting O’Connor et al. to note in 2005, “Continued evasion of the [harm reduction] issue based on claims that ST can cause smoking seems, to us, to be an unethical violation of the human right to honest, health-relevant information”. (18)
Dual Use of Cigarettes and Smokeless Tobacco
Dual use is the object of persistent complaints by opponents of THR. For example, in 2002 Henningfield et al. described theoretical adverse consequences of dual use (20). Despite their concerns, they acknowledged that “There are virtually no data that currently exist on the safety of such use or the degree to which such use will foster the perpetuation of smoking or contribute to reduced overall smoking…The issue warrants further study.”
In 2010 that study was completed by Frost-Pineda et al, who reviewed 17 published research studies that had data on the health risks from dual use versus those from smoking (21). Frost-Pineda and colleagues conclude that “…there are not any unique health risks associated with dual use of ST products and cigarettes, which are not anticipated or observed from cigarette smoking alone.” The authors further commented that “some data indicate that the risks of dual use are lower than those of exclusive smoking.”
Frost-Pineda et al. also reviewed longitudinal studies in the U.S. and Sweden to determine if dual users had a different trajectory of tobacco use and cessation than that of exclusive smokers. A 2002 study by Wetter et al. found that 11% of dual users were tobacco-abstinent after 4 years of follow-up, compared with 16% of exclusive smokers (22). However, 80% of exclusive smokers were still smoking at the 4-year follow-up, while only 27% of dual users were smoking; 44% were still dual users and 17% were exclusive smokeless users.
Very similar results have been reported in longitudinal studies of dual users in Sweden. For example, Rodu et al. reported the follow-up tobacco status of men in northern Sweden who were either cigarette smokers or dual users when they enrolled in a population-based epidemiological study (23). Among exclusive smokers followed for 5 years, 69% were still smoking, 4% were dual users, 7% used ST, and 19% were tobacco free; the respective percentages among dual users were 6%, 52%, 24%, and 18% (24). Among smokers followed for 9 years, 51% were still smoking, 10% were dual users, 16% used ST, and 45% were tobacco free; the respective percentages among dual users were 4%, 44%, 41% and 11%. Among smokers followed for 13 years, 46% were still smoking, 7% were dual users, 12% used ST, and 36% were tobacco free; the respective percentages among dual users were 9%, 22%, 60%, and 9%.
Frost et al. concluded that, although dual users are less likely than exclusive smokers to be completely tobacco abstinent at follow-up, they are much less likely to be smoking.
References
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2. Foulds J, Ramström L, Burke M, Fagerström K. Effect of smokeless tobacco (snus) on smoking and public health in Sweden. Tobacco Control 12: 349-359, 2003.
3. Rodu B, Nasic S, Cole P. Tobacco use among Swedish schoolchildren. Tobacco Control 14: 405-408, 2005.
4. Furberg H, Bulik CM, Lerman C, Lichtenstein P, Pedersen NL, Sullivan PF. Is Swedish snus associated with smoking initiation or smoking cessation? Tobacco Control 14: 422-424, 2005.
5. Ramström L, Foulds J. Role of snus in initiation and cessation of tobacco smoking in Sweden. Tobacco Control 15: 210-214, 2006.
6. Scientific Committee on Emerging and Newly Identified Health Risks (SCENIHR). Health Effects of Smokeless Tobacco Products. Health & Consumer Protection, Directorate-General, European Commission, 6 February 2008. Available here
7. Tomar SL, Fox BJ, Severson HH. Is smokeless tobacco use an appropriate public health strategy for reducing societal harm from cigarette smoking? International Journal of Environmental Research and Public Health 6: 10-24, 2009.
8. Ary DV, Lichtenstein E, Severson HH. Smokeless tobacco use among male adolescents: patterns, correlates predictors and the use of other drugs. Preventive Medicine 16: 385-401, 1987.
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13. Wetter DW, McClure JB, de Moor C, Cofta-Gunn L, Cummings S, Cinciripini PM, Gritz ER. Concomitant use of cigarettes and smokeless tobacco: prevalence, correlates, and predictors of tobacco cessation. Preventive Medicine 34: 638-648, 2002.
14. Kozlowski LT, O’Connor, Edwards BQ, Flaherty BP. Most smokeless tobacco use is not a causal gateway to cigarettes: using order of product use to evaluate causation in a national U.S. sample. Addiction 98: 1077-1085, 2003.
15. Severson, H.H., Forrester, K.K., & Biglan, A. Use of smokeless tobacco is a risk factor for cigarette smoking. Nicotine & Tobacco Research 9: 1331-1337, 2007.
16. O’Connor RJ, Flaherty BP, Edwards BQ, Kozlowski LT. Regular smokeless tobacco use is not a reliable predictor of smoking onset when psychosocial predictors are included in the model. Nicotine & Tobacco Research 5: 535-543, 2003.
17. Timberlake, D.S., Huh, J., & Lakon, C.M. Use of propensity score matching in evaluating smokeless tobacco as a gateway to smoking. Nicotine & Tobacco Research 11: 455-462, 2009.
18. O’Connor RJ, Kozlowski LT, Flaherty BP, Edwards BQ. Most smokeless tobacco use does not cause cigarette smoking: results from the 2000 National Household Survey on Drug Abuse. Addictive Behaviors 30: 325-336, 2005.
19. Rodu B, Cole P. Evidence against a gateway from smokeless tobacco use to smoking. Nicotine & Tobacco Research 12: 530-534, 2010.
20. Henningfield JE, Rose CA, Giovino GA. Brave new world of tobacco disease prevention: promoting dual tobacco-product use? American Journal of Preventive Medicine 23: 226-228, 2002.
21. Frost-Pineda K, Appleton S, Fisher M, Fox K, Gaworski CL. Does dual use jeopardize the potential role of smokeless tobacco in harm reduction? Nicotine & Tobacco Research 12: 1055-1067, 2010.
22. Wetter DW, McClure JB, de Moor C, Cofta-Gunn L, Cummings S, Cinciripini PM, Gritz ER. Concomitant use of cigarettes and smokeless tobacco: prevalence, correlates, and predictors of tobacco cessation. Preventive Medicine 34: 638-648, 2002.
23. Rodu, B., Stegmayr, B., Nasic, S., Cole, P., & Asplund, K. Evolving patterns of tobacco use in northern Sweden. Journal of Internal Medicine 253: 660–665, 2003.
24. Rodu B. Dual use (letter). Nicotin &Tobacco Research, 2011. doi: 10.1093/ntr/ntq23
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