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Snuff – how dangerous is it? The controversy continues

2001; Wiley; Volume: 250; Issue: 6 Linguagem: Inglês

10.1046/j.1365-2796.2001.00918.x

1365-2796

Kjell Asplund,

Cardiovascular Effects of Exercise

Whereas cigarette smoking is pandemic, the use of snuff and other forms of smokeless tobacco can best be described as endemic. It is largely restricted to certain geographical areas such as North America [1], the Scandinavian countries [2, 3], India, Bangladesh and Southeast Asia [4, 5] and parts of Africa [6, 7]. In the United States, moist snuff is the only tobacco product with increasing sales during the last decade [8–10]. Snuff is often used in certain subsets of a population, such as athletes [11, 12], male adolescents and young adults [3, 10, 13], and people in professions where smoking is not allowed (firemen!) [14]. Acting on a WHO recommendation to prevent snuff dipping in countries where oral tobacco use is not yet established, the European Union has prohibited the sales of snuff in its members states, Sweden exempted. There have been three main arguments for banning snuff: (i) it is hazardous, (ii) it may introduce young people to smoking and (iii) it is yet another dubious product from the cynical tobacco industry. The discussion and research on potential health hazards of smokeless tobacco have focused on the risks for cardiovascular disease, cancer and addiction. The cardiovascular chapter of the story started with a 12-year follow-up study of a very large cohort of Swedish construction workers that were investigated in 1971–1974. Those who used snuff at baseline had a 40% higher risk of cardiovascular death compared with nontobacco users [15]. Obviously, this finding was in agreement with what was previously known about cardiovascular hazards conferred by tobacco smoking. In more recent studies, however, it has been very difficult to confirm that snuff use accelerates the atherothrombotic process or involves increased risk for cardiovascular disease. In this issue of Journal of Internal Medicine, Wallenfeldt and her collaborators present data indicating that snuff dippers do not have more carotid or femoral atherosclerosis by ultrasound than men that have never used tobacco [16]. This finding concurs with previous observations that firemen who regularly use snuff, in contrast to their smoking colleagues, do not have more carotid intima thickening than nontobacco users do [14]. Other intermediary variables that are abnormal in smokers but not in snuff users include plasma levels of antioxidant vitamins [17], fibrinogen [18] and fibrinolytic variables [18]. Wallenfeldt et al. now add normal plasma levels of C-reactive protein in snuff dippers (as opposed to smokers) to this list [16]. In exploring the risk for hard end-points, two large case–control studies in Sweden have failed to show an excess risk of myocardial infarction in male snuff users compared with men who never used tobacco [19, 20]. There are many possible explanations for the discrepancy between the results of the first cohort study on construction workers by Bolinder et al. [15] and the ensuing studies. The cohort study was based on causes of death recorded by official vital statistics. Nicotine has immediate effects on the heart rate [21] and there is a possibility that snuff is arythmogenic, hence enhancing the risk of sudden death. Later studies have not had the statistical power to detect a small increase in the risk for cardiovascular death. Also, there has been a change in snuff use amongst Swedish men during the last decades, the high-prevalence groups gradually shifting from elderly low-educated men [22] to young and middle-aged men with a high level of education [20]. In the construction worker study, smokers had higher body mass index and higher resting blood pressure levels than nontobacco users [15]. Elevated resting blood pressure in snuff dippers has not been possible to confirm in studies performed during the 1990s, including a population-based study of middle-aged people in Sweden [18], a study on Swedish male students [23], an investigation amongst snuff-dipping baseball players in the United States [11] and now the Wallenfeldt study [16]. A third possible explanation for the apparent discrepancies between the results of the construction worker study and the more recent studies is that the composition of moist snuff has changed over the years. The content of tobacco-specific nitrosamines was reduced by half in Swedish snuff from 1983 to 1992 [24], and this could perhaps be associated with reduced health hazards from the use of snuff. To summarize the research on smokeless tobacco and cardiovascular disease, there is now evidence that snuff (i) does not adversely influence known mediators of atherosclerosis the way smoking does, (ii) has little, if any, effect as promoter of atherosclerosis, (iii) does not increase the risk of myocardial infarction, but (iv) the question whether or not snuff is arythmogenic and thus enhances the risk of sudden death is not yet settled. Much of the discussion on possible health hazards of smokeless tobacco has focused on cancer. Tobacco-specific nitrosamines can be absorbed from snuff to a considerable extent [25], and snuff dippers have as high levels of haemoglobin and DNA adducts of tobacco-specific nitrosamines as cigarette smokers have [26]. In a Swedish study conducted during the 1930s, it was described that the great majority (70%) of patients with cancer in the anterior part of the mouth used smokeless tobacco [27]. When a consensus panel under the auspices of the US National Institutes of Health reviewed the available evidence in a report published in 1988, smokeless tobacco was pointed out as a culprit in the causation of oral cancer [28]. In analogy with cigarette smoking, smokeless tobacco has been implicated as a possible causative factor in other upper gastrointestinal and urological cancers. All snuff packages sold in Sweden have been carrying the label 'Snuff causes cancer'. Several studies published in recent years have, however, failed to confirm the suspicion that snuff marketed in Western countries causes cancer [15, 29–32]. The cancer forms in focus are, however, not very common, and the studies do not have the statistical power to exclude a very modest excess risk. More recently, the interest in snuff as a pathogenetic factor has turned to diabetes. Long-term use of nicotine gum has been associated with insulin resistance and hyperinsulinemia in a dose-dependent manner [33]. In agreement with such metabolic disturbances, Wallenfeldt et al. now report that plasma levels of triglycerides are elevated in snuff users [16]. In a recent cohort study published in the Journal, the risk of developing type 2 diabetes (but not glucose intolerance) was increased in snuff dippers compared with nontobacco users [34]. Contrary to these observations, no increased prevalence of hyperinsulinemia was found in a population-based sample of snuff dippers [18], and mean blood glucose and plasma insulin levels were not elevated amongst snuff dippers participating in the Wallenfeldt study [16]. The finding of an excess risk of diabetes in snuff dippers need to be confirmed (or refuted) in larger studies. The most obvious medical effect of snuff dipping is that of addiction. Nicotine peaks in the circulation reach very high levels in snuff dippers [35], and snuff seems to be at least as addictive as cigarette smoking. The success rate amongst people who try to quit using snuff is no better than that amongst cigarette smokers [36]. Intervention programmes to help people quit using smokeless tobacco have been used with reasonable success when compared with the effects of antismoking interventions [37–39]. The marked difference in risk for myocardial infarction and cancer between cigarette smoking and snuff dipping provides important information in how the effects of smoking are mediated. It is unlikely that differences in nicotine content and absorption account for the differences [35]. It therefore appears that nicotine is not an important contributor to myocardial infarction (and not to atherothrombotic mechanisms in general) and malignancy. It is more likely that moieties specific to tobacco smoke mediate the excess risk. Many of the components of tobacco smoke are produced when tobacco is heated and burned. The process of smoking itself contributes to endogenous nitrosation [21] and some tobacco components are better absorbed through airways than through the buccal mucosa. Amongst the about 2500 chemical substances identified in tobacco smoke, tobacco-specific nitrosamines and polycyclic aromatic hydrocarbons are some of the candidates as aetiological agents for cardiovascular disease [24, 40, 41]. A specific compound, 1,3-butadiene, that accelerates atherosclerotic plaque has been identified in environmental tobacco smoke [42]. In addition, carbon monoxide has been implicated in the pathogenesis of smoking-related cardiovascular disease [43], although the clinical and experimental evidence to support this hypothesis is not very robust. The composition of smokeless tobacco varies greatly around the world. It may be chewed or snuffed. Various substances are added (such as 'natrone powder' in the Sudanese variant toombak), and some of the additives may contain exceedingly high concentrations of tobacco-specific nitrosamines [25]. In the United States, snuff production involves a fermentation process, whereas Swedish snuff is nowadays prepared by a heating process without traditional smoke-drying, yielding a semisterile product with a lower content of polycyclic aromatic hydrocarbons than previously [24]. It must be noted, however, that even within a country, there are wide variations in the content of nicotine and carcinogenic tobacco-specific nitrosamines between different brands of moist snuff [40, 44]. In young people, snuff and other forms of smokeless tobacco may be a gateway to smoking. A cohort study of US Air Force recruits showed that the risk to start cigarette smoking amongst smokeless tobacco users was twice that of nontobacco users [45]. Switching from smokeless tobacco to smoking is common also in US college students [46]. In Finland, a substantial proportion of young snuff users turned to cigarette smoking when sales of snuff were banned in 1995 [47]. Switching in the other direction, from cigarettes to snuff, is also common. The great majority of middle-aged snuff users in Sweden are ex-smokers [19]. In people who still smoke, concomitant snuff use may help to reduce cigarette consumption to about half [20]. In northern Sweden with a tradition of widespread snuff use, the prevalence of cigarette smoking is amongst the lowest in the world (and lower than in the south of the country with less use of snuff) [48]. It is evident that the use of snuff involves much lower risks of cardiovascular disease and cancer than cigarette smoking does. Proponents of snuff have applied the concept of harm reduction [49]: can snuff be tried in inveterate smokers who failed to quit using nicotine patches (or similar)? Some have made the analogy with the well-known interaction between radon and smoking as a cause of lung cancer. Eliminating all exposure to radon in buildings is very costly and hardly feasible. A much more pragmatic way of reducing harm is to eliminate smoking. Only one intervention study has been reported so far. In an open, uncontrolled, small study, a quarter of heavy smokers that were recommended to use snuff instead of cigarettes were smokefree at 1 year. Nearly all quitters had previously tried nicotine patches or gums, and all of them still used snuff at the 1-year follow-up [50]. Clearly, if this disputatious strategy is to be tried further, high-quality, controlled intervention studies are needed. We are confronted with extremely difficult questions: Are there circumstances that could justify doctors to recommend the use of smokeless tobacco? What about the smoking patient who asks if he/she should try snuff dipping instead? And even more challenging: in pragmatic public health work, is snuff friend or foe? People involved in the fight against tobacco intuitively refute the idea of treating cigarette smoking with smokeless tobacco as being 'flawed' [51]. The antisnuff position is sometimes worded even more dramatically: 'To promote smokeless tobacco in place of cigarette smoking would be like encouraging sniffing cocaine as a safer alternative to mainlining heroin' [52]. So, the concept of harm reduction by use of snuff is complicated and controversial. Faced with antismoking campaigns and restrictions on sales of cigarettes, it is tempting for the tobacco industry to turn to less deleterious alternatives, i.e. various forms of smokeless tobacco. In the United States, the Smokeless Tobacco Council contributes considerably to the total lobbying by the tobacco industry [53]. The increased sales of smokeless tobacco in countries like the United States and Sweden during recent years are, at least partly, the result of a determined effort by the industry to promote consumption. The manufacturers of moist snuff, the dominating ones being US Tobacco and Swedish Match, are creating a market amongst young boys and girls [54]. Obviously, from a medical point of view, the only reasonable norm is nonuse of tobacco. The goal should be a tobacco-free society. On the route towards this goal, we face enemies that are more perilous than others. My personal opinion is that we should not squander our forces. We should concentrate them on the fight against cigarettes – they are the overwhelming threat to people's health, snuff being only a mini-monster in comparison.