NOT PEER REVIEWED Perhaps inflaming social confrontation has become so common that people no longer care what they say to each other any longer. Many feel it is all temporary posturing in order to stake out a claim in the impersonal electronic landscape. It is a reflection of unbridled identity rather than thought. In the electronic communications environment, opinionated commentators have started to believe they are speaking truths to the uninitiated. Thus, social change is not difficult; it is just continuing to live out perceptions of self. It takes only being, not commitment, courage or camaraderie.

In contrast, there are those who take hatred personally. Given that the tobacco industry has proven itself untruthful, unethical and criminal, one would hope that some would want to do their personal utmost to rid the earth of the corrupting influence of tobacco and those who represent it. As reflected in the recent financial prognosis by Citigroup (See News Analysis, March 2011), I see it is a social change that even economists don't feel improbable. I urge countering hatred with mindful action. Even now, the cacophony of controversy subsides.

Conflict of Interest:

None declared

NOT PEER REVIEWED This paper, although the authors may well have found evidence in line with their intent, could also open our eyes to another distinct and obvious perspective. One which may well be glossed over, in our determination to find the target perspective many seek. What if a smoke free environment could substantially increase population mortality and morbidity health risks? Is it too late to rethink our position, or to mitigate that risk? The idea is most often met with immediate dismissal. However there is indeed biological plausibility and physical routes by which the argument could be made and made quite convincingly.

The sediment studied in this paper adds significantly to that argument, by the measures of physical evidence which were found, although viral matter or sub micron toxic particulate from ambient air sources was not thoroughly investigated. It is a perspective we have been neglecting by lack of investigation. When people congregate, if one in the room carries a contagious disease and he coughs or sneezes, emitting into the room a virus that would then be inhaled by others within the room, the virus spreads infecting others exponentially. Cigarette smoke acts by its physical properties as a sticky mask that hangs in the air, collecting sub micron particulate and biological toxins. Which even if inhaled could be rendered to the larger extent, ineffective in promoting harms.

Fine particulate cigarette smoke is sticky in nature, in the 2-3 micron range with a capacity to collect large amounts of sub micron particles, with unique velocities and trajectories swirling around within that space. Considering the increased mass by combining the virus or sub micron particulate with tobacco smoke; viral and ultra fine particulate matter in the majority is either excavated from the room by increased ventilation potentials or earned filtering potentials. Within systems which otherwise would have no effect, or even a contributing effect to the toxic particle volumes contained in that space. Traditionally ventilation rates have been increased to limit the tobacco smoke odors and are in turn decreased when it is less pervasive or not noticeable. The viral or sub micron particulate is either evacuated more efficiently in a smoking allowed environment, or is attached firmly to any solid object in the room, as demonstrated by the authors herein. As the study indicates that adhesion will last for months after smoking has ceased which is well beyond the lifespan of the hardiest of viruses.

Thus we see a large degree of mitigation, of both harm and risk. With smoke in the room the chances are much less that someone in that room will become infected by contagions, or poisoned by the most dangerous of non ETS ambient air contaminants, compared to the substantial increased risk without the smoke. The same arguments could be made in relation to any sub micron particulate, with a large array of carcinogens and toxins found in ambient air which have no proper risk assessment to date, which will only increase the potential for adverse effects. The limited evidence of increased risk by Environmental Tobacco Smoke [ETS] is based primarily in "lifetime exposure" estimates. Most within the precautionary principle of assessment, or "worst case", with few of the immediate variety of health risks, demonstrating any substantial or significant numeric effect, which could be remotely comparable to a larger effect by pollen or Diesel exhaust, which are for the most part unavoidable.

According to the American CDC; the common Flu alone kills more than 35,000 annually within the American population, a risk that is immediate and sees its effect within hours or a few days. Can we simply dismiss that immediate risk as implausible? Were the numeric value increased, by what ever means, the mortality impact among the millions at risk would be substantial. The actual population risks understandably carry a potential to provide a much more devastating risk than anything surmised by the most aggressive estimate of mortality and morbidity, which could possibly be caused by tobacco smoke or its sediments.

Unintended consequence is an argument in need of discussion and investigation, evolved by the warning; "be careful what you wish for, because you just might get it".

Conflict of Interest:

None declared

NOT PEER REVIEWED Funding: While this assessment was funded by RJ Reynolds Tobacco Company, it is the product of independent scientific thought, and it expresses solely the opinions of the authors. When data are lacking, models that simulate population health events under different exposure scenarios may serve to inform policy by providing the basis for decision making. In order for models to be used in this manner, their underlying assumptions must be as realistic as possible, and the data used to define the starting point, or "base case", must be accurate. If these criteria are met, then using the model to describe the potential effects of extreme scenarios (i.e., "worst case" and "best case") can provide useful information about the magnitude of effects to be expected for more reasonable scenarios. In a recent publication, Mejia et al. described a model using Monte Carlo simulations, to evaluate the population level health effect that might be expected if smokeless tobacco products were successfully promoted in the US as a safer alternative to cigarettes, resulting in substantial changes in the patterns of use of tobacco products (Mejia, Ling, et al. 2010). The authors concluded that "promoting smokeless tobacco as a safer alternative to cigarettes is unlikely to result in substantial health benefits at a population level". We investigated the methods described by Mejia et al. (2010), and evaluated their conclusion using three approaches: (1) critiquing the assumptions underlying the model and its input data; (2) comparing the published model estimates with estimates developed using the model as described, but with more realistic input data; and (3) using the original input data in a more realistic model, and comparing those results to the published model estimates. We used the results of this investigation to evaluate the utility of their model.

CRITIQUE OF MODEL ASSUMPTIONS AND INPUT DATA

Model transitions:

Mejia et al. (2010) describe their model as beginning with a hypothetical population of non-users of tobacco who are then allowed a very limited number of possible transitions between exposure states. People are allowed to initiate cigarette smoking or smokeless tobacco products, cigarette and smokeless tobacco initiators are allowed to continue use, quit use; switch to the other product, or to become users of both products ("dual users"). Return to cigarette smoking or smokeless product use after cessation, switching from continued cigarette use to a smokeless product or switching from continued smokeless product use to cigarette smoking are not modeled. The model also does not allow non- users of tobacco to initiate cigarette smoking.

Transition probabilities:

A crucial aspect of any model-based evaluation of the effectiveness of a health policy is the model input. Any data selected for the model, and the rationale for their selection, must be clearly documented for the model to be useful in evaluating the potential effectiveness of a proposed policy. In the tobacco harm reduction arena, model results depend heavily on the transition probabilities selected to describe movement between different tobacco exposure states that are expected to result from policy changes. For their base case scenario, Mejia et al. estimated transition probabilities based on multiple populations that differed with respect to age, calendar year and region, even though patterns of tobacco use have been shown to depend strongly on these factors (e.g. (CDC 2007; Gilpin, Pierce, et al. 1992; Nelson, Mowery, et al. 2006; Roth, Roth, et al. 2005; Tomar 2003). The estimated probabilities were applied to the entire hypothetical population, and did not account for age or gender. In addition, some transition probabilities were based on the estimated lifetime prevalence of ever use, others on the prevalence of current use, and yet others on the 2-year incidence of initiation, even though incidence and prevalence are not interchangeable measures or concepts. * The incidence of smokeless product initiation (4%) was based on the arithmetic average of: the prevalence of smokeless product use among adults in 2005 based on the National Survey on Drug Use and Health (3.3%) (NSDUH 2005); the prevalence of smokeless product use among adults (2.3%) based on data from the National Health Interview Survey (NHIS) conducted in 2000 (Nelson et al., 2006); and the prevalence of smokeless product use among 9-12th graders in 2003 (6.7%) based on NHIS data (Nelson et al., 2006). Mejia et al. (2010) averaged these prevalence estimates without taking the differences between the source populations into account.

* To estimate transition probabilities from smokeless tobacco use to other exposure states, Mejia et al. used data from Oregon boys in grades 7 and 9 who were followed for 2 years in the late 1990s. The implicit assumption was that the hypothetical population of smokeless product "initiators" (which in their example was the population of current smokeless product users) was like Oregon 7th and 9th grade boys in terms of their tobacco use patterns.

* The incidence of cigarette smoking initiation was assumed to be equal to the lifetime prevalence of ever smoking among US adults in 2006 (40%). Mejia et al (2010) then divided the group of cigarette "initiators" (i.e., ever smokers in 2006) into categories of continuing smokers, quitters, smokeless product users and dual users based on their motivation to quit smoking in future. The transition probabilities were chosen such that "the end state reflected the current smoking and smokeless use prevalence and quit ratio in the 2006 NHIS survey" (page 298), although the NHIS 2006 survey data were not used by Mejia et al. to provide estimates of smokeless use. The end state distribution of continuing smokers and quitters was approximately even (47% and 53%, respectively) based on the NHIS estimate that 50% of current smokers were able to quit smoking.

Discussion of the motivation to quit smoking in the future (will never quit; is health concerned; is affected by smoke-free regulations; and is price sensitive) comprised a substantial part of the Mejia et al. paper. However, motivation to quit is irrelevant to the stated purpose of the model, which was to estimate the population-level health effect to be expected under different distributions of cigarette smoking and smokeless tobacco use. The proportions of subjects in each motivation category were reportedly based on a study of adult smokers who had smoked for at least 5 years in 1987 (Gilpin, Pierce, et al. 1992). This cross-sectional study used data from the 1987 NHIS and reported the distribution of reported reasons for quitting smoking in the past 5 years among former smokers, and not motivation to quit smoking in the future among current smokers. The Gilpin et al. study did not consider a "smoke-free environment" category, it included a "health concerned and price sensitive" category because of considerable overlap between the two categories among their respondents, and it included several additional categories not considered by Mejia et al. (e.g., "lost interest" and "miscellaneous", among others). The proportion of the population of former smokers reporting reasons for quitting smoking that were not considered by Mejia et al. was almost 50% in the Gilpin et al. (1992) data. Further, according to Gilpin et al., the proportion of subjects that had never tried to quit smoking was 18% among ever smokers and 33% among current smokers, values that are very different from the 10% estimated by Mejia et al. (2010).

* Finally, Mejia et al. calculated the probability of remaining a non -user of tobacco (56%) as the remainder after accounting for the 40% of the population identified as smoking "initiators" and the 4% of the population identified as smokeless tobacco "initiators". The model allowed cigarette "initiators" (i.e., ever smokers) and smokeless product "initiators" (i.e., current users) to transition to other tobacco exposure states, but those initially defined as non-users of tobacco were not allowed to transition into tobacco use.

Tobacco-related health effects:

Mejia et al. created an artificial "tobacco-related health effects" variable to place the different tobacco exposure categories on a continuum of risk, where non-users of tobacco were at zero, former smokers, current smokeless product users and current dual users were log- normally distributed with means of 5, 11 and 90, respectively, and smokers were at 100. References to justify these values were only provided for smokeless product users; even in this case, the value of 11 (standard deviation = 5) was not directly derived from data but was a consensus estimate. Neither duration of use nor cessation was considered in estimating tobacco-related health risk.

Scenarios and results:

Mejia et al. modeled a number of scenarios to represent different levels of adoption of smokeless tobacco products due to varying hypothetical levels of successful smokeless product promotion. The modeled results under each of the scenarios produced wide posterior intervals that overlapped with one another and the base case scenario, indicating that none of the point estimates could be interpreted as demonstrating statistically significant differences in health risk resulting from differences in the exposure distributions. Under the "aggressive smokeless promotion" scenario considered by Mejia et al. to be the most extreme example, the transition probabilities and other assumptions in the model (e.g. that half the smokeless product users came from never tobacco users) were so unrealistic that even though a much lower health risk was assumed for smokeless product users than for cigarette smokers, the model suggested (statistically non-significant) net harm at the population level.

Mejia et al. acknowledged that their transition probabilities were less than ideal, but claimed that better data were unavailable. However, we found several examples that could have been used: Lundqvist et al. reported on patterns of tobacco use in a population of middle-aged Swedes that included initiation, cessation and rates of transition among cigarettes, smokeless tobacco and dual use over a ten year period (Lundqvist, Sandstrom, et al. 2009). Transitions between exposure states among adults in the United States, including cessation of smokeless tobacco and dual use, were provided by Zhu et al. in analyses of the Current Population Survey-Tobacco Use Supplement for 2002 and 2003 (Zhu, Wang, et al. 2009). Smoking initiation rates are available from the National Health Interview Survey (Escobedo and Peddicord 1997). The National Survey on Drug Abuse provides estimates of smoking initiation in the US (Office of Applied Statistics, 1998 and 1999); its successor, the National Survey of Drug Use and Health, provides estimates of cigarette and ST initiation for people aged 12 and older as recently as 2008 (http://oas.samhsa.gov/nsduh/2k8nsduh/2k8Results.pdf); and Davis et al. provided estimates of smoking initiation specifically for youth smokers (Davis et al., 2009). The study of Oregon teenagers that Mejia et al. relied on for smokeless tobacco product transition rates (Severson, Forrester, et al. 2007) also reported the probability of cigarette and smokeless tobacco initiation and the transition probabilities for those who used smokeless products at baseline, but these estimates were not used by Mejia et al.

From these alternative sources, we selected the three papers (Lundqvist et al., 2009; Severson et al., 2007 and Zhu et al., 2009) that provided the most complete sets of initiation, cessation and transition probabilities for comparison with the data used by Mejia et al. (2010). Compared to the probabilities presented by Lundqvist et al. (2009) for Swedish adults and the probabilities observed by Severson et al. (2007) among teenage boys in Oregon, Mejia et al. considerably underestimated the proportion of persons remaining non-tobacco users and greatly overestimated the smoking initiation probability among non-tobacco users. The estimate used by Mejia et al. (2010) was similar to that provided by Escobedo and Peddicord (1997) based on data from the early 1980s, but greater than that provided by Davis et al. (2009) based on students in grades 6-12 who participated in the ALLTURS study between 2000 and 2002. Further, contrary to evidence reported by Zhu et al. and Lundqvist et al. (2009), Mejia et al. (2010) assumed that (i) cessation of use was much lower among smokeless product users than cigarette smokers while initiation of dual use was much higher among smokeless product users; and (ii) switching from one product to the other was much more common among smokeless tobacco users than cigarette smokers.

Model validation:

Mejia et al. did not report any attempt to validate their model, although they did successfully replicate results, using similar model input, produced by another technique (Gartner, Hall, et al. 2007). Some problems underlying the model whose results Mejia et al. chose to replicate have been discussed elsewhere (Sulsky, Bachand et al., 2010)

SENSITIVITY ANALYSIS

Having identified problems with the data selected as model input by Mejia et al., we attempted to assess the model assumptions by using more defensible input and evaluating the difference in results. Although the authors provided the full model input, via a spreadsheet accessible to journal (Tobacco Control) subscribers through its web site, the spreadsheet does not perform any calculations. However, we had already used the WinBUGS computer program to create a simulation model that estimates mortality or morbidity for a hypothetical population of persons who have never used tobacco and who, as they age, may transition into and out of 33 possible tobacco exposure states, including current and former smoking or smokeless product use and recidivism for those who had quit. A brief description of this model is available (Bachand, Curtin, et al. 2010); a full description is currently being prepared for peer review. We were able to use the data documented in the spreadsheet provided by Mejia et al. in a simplified form of our simulation model to replicate their results. We then tested the sensitivity of their model by modifying the input documented by Mejia et al. and using it in the simplified form of our model.

Alternative results:

We simplified our model to restrict it to the transitions described by Mejia et al. (2010). After cigarette smoking initiation, only one change in tobacco exposure was allowed, and only one change was allowed after smokeless product initiation unless the subject switched to cigarettes; in this case, one additional change could be made. For transitions not modeled by Mejia et al., we used transition probabilities of 0. Using the model input specified by Mejia et al. (2010) was difficult to accomplish for several reasons: (i) Mejia et al. did not take age into account, while our model does; (ii) We did not use prevalence as an estimate of incidence in our model. Whenever their transition probabilities were prevalence estimates, we used incidence estimated from the National Household Survey on Drug Abuse (Office of Applied Studies, 1999), instead; and (iii) The proportions used by Mejia et al. to describe the distribution of motivations to quit were not useful for the stated purpose and were not based on reliable information; therefore, we calculated the weighted average of their transition probabilities for each of the four end states: quitting, continuing cigarette use, switching to a smokeless product and dual use. For this example, we used Mejia et al.'s comparison of the "aggressive smokeless promotion" scenario to their base case scenario. To approximate the input used by Mejia et al., we kept the ratios between the transition probabilities the same as the ratios between the "aggressive smokeless promotion scenario" and the transition probabilities in their base case scenario. It is important to keep in mind that their base case scenario assumed that 4% of the population used smokeless products while we assumed no form of tobacco use at baseline, but allowed proportions of the population to initiate cigarette or smokeless tobacco use at user-defined, age-specific rates. In our analysis, follow-up started at age 13, the youngest age at which a non-negligible proportion of tobacco users initiates use, and ended at age 72. The width of each age category was five years. To allow for validation of the model results against current mortality data accounting for adequate disease induction time, we based age category-specific smoking initiation rates on the 1980 National Household Survey on Drug Abuse (Office of Applied Studies, 1999). Age category-specific smoking cessation rates for 1980 were based on data from The California Tobacco Control Program's effect on adult smokers: (1) Smoking cessation (Messer K et al., 2007). More recent data could be used to model prospective future population health effects, if desired. For smoking initiation, we used 11.25%, 10%, 1.25% and 0.25% for age categories 13-17, 18-22, 23-27and 28- 32 years, respectively, and 0 for older age categories. For smoking cessation, we used 2.5% for age 13-17, 4.5 for the next 3 age categories, 5.0 for category 33-37 years, 5.5 for categories 38-42 and 43-47 years, 7.5% for category 48-52 years and 8.5% for the remaining 4 age categories. Mejia et al. used tobacco use patterns reported by 145 7th and 9th grade boys to estimate the transition probabilities for the whole population following the use of a smokeless product. Therefore, we also used the transition probabilities reported for the 7th and 9th grade boys for all ages in our model. Our model uses age-, years of smoking- and years of quitting-specific mortality rates based on the coefficients from a Poisson model estimated using data for men from the Kaiser Permanente Cohort study (Friedman, Tekawa, et al. 1997). The ratio of excess risks for current smokeless tobacco users versus smokers (0.08) was based on a consensus estimate reported by Levy et al. (Levy, Mumford, et al. 2004), and the ratio of excess risks for former smokeless product users versus smokers was set to 0.05. While Mejia et al. combined men and women in their analysis, we restricted our analysis to men because tobacco use patterns vary considerably between genders (see paragraph two of "Limitations", page 303 in Mejia et al. and reference numbers 5, 6, 12, 22, 29, 30, 31, and 36 from Mejia et al.).

Using data that replicated, as closely as possible, the flawed input and transition probabilities used by Mejia et al. to define a "worst-case" scenario of aggressive smokeless tobacco promotion, we, like them, observed statistically non-significant net harm. That is, there were more deaths estimated at the end of follow-up under the test scenario compared to the base-case, but the difference was not statistically significant.

We then made a slight change in the transition probabilities, such that the probabilities for transitions from smokeless tobacco use reported by Severson et al. for 7th and 9th grade boys were applied only to the youngest two age categories (13-<18 and 18-<23 years). For all other age groups, we used the transition probabilities reported by Lundqvist et al. or by Zhu et al. This change resulted in statistically significant net benefit , i.e., there were fewer deaths estimated at the end of follow-up under the test scenario compared to the base-case. Thus, running the model with only slightly more realistic input produced statistically significant estimates that suggested a benefit of aggressive smokeless tobacco promotion, rather than harm, at the population level.

As described above, the model used by Mejia et al. incorporated a very limited number of possible transitions between exposure states. Therefore, we wanted to determine the effect of using the flawed transition probabilities suggested by Mejia et al., but allowing all possible transitions in our model. For transitions not modeled by Mejia et al., we assumed that transition probabilities for "no change in tobacco use" were 95%, while transition probabilities for "changes in tobacco use" were 5%; when more than one type of change was possible, the transition probability of 5% was divided between them. For example, the probability of remaining a cigarette smoker (no change) after several previous changes in tobacco use was set to 95% while the probability of switching back to a smokeless product and the probability of quitting were set to 2.5% each. We repeated the analysis allowing a 25% probability for "change in tobacco use" while the transition probabilities for "no changes" were 75%. Allowing for a small degree (5%) of recidivism and switching from one to the other product after previous changes in tobacco use (while using Mejia et al.'s input, to the extent possible, for transitions considered in their model), we observed a net benefit (i.e., a reduction in mortality) at the population level. The benefit was statistically significant, based on the 95% posterior intervals, even when the transition probabilities for the 7th and 9th grade boys were applied to all ages. Allowing for a greater degree (25%) of recidivism and switching from one to the other product resulted in an even more pronounced, statistically significant, population benefit.

CONCLUSIONS

The model proposed by Mejia et al. model is overly simplistic in its use of only a limited number of exposure states and transitions: 56% of the starting population, identified as non-tobacco users at baseline, are not allowed to become tobacco users; no one who quits tobacco use is allowed to revert to a tobacco use state; the model uses the same initiation, cessation and transition rates for the whole hypothetical population, regardless of age or gender; and, the risk of tobacco related health outcomes "measured" by the health index is assumed to be the same regardless of duration of tobacco use or cessation.

The sources used by Mejia et al. (2010) to define the initial exposure distribution and the transition probabilities are difficult to justify. The authors mixed estimates for adult men and women, drawn from a nationally representative sample of current and former smokers, and for 145 7th and 9th grade boys who attended secondary school in one of a few towns in Oregon. The transition probabilities used by Mejia et al. incorrectly implied that smokeless tobacco users were very unlikely to quit (a beneficial transition) and very likely to switch to smoking or to initiate dual use (harmful transitions) while smokers were very likely to quit or to switch to smokeless tobacco (beneficial transitions) and unlikely to initiate dual use (a harmful transition).

The health index is of questionable validity, and does not seem to be based on empirical data. The data purportedly used to justify the values assigned to the health index comprised a mix of diseases and causes of death, measures of effect (incidence and prevalence), and exposures (product types). Furthermore, the Mejia et al. model assumes that risks associated with each type of tobacco product are the same for all users, i.e., the risk of experiencing a tobacco-related health outcome "measured" by the health index is assumed to be the same for males, females, all ages, and any duration of use or former use of tobacco. The results reported by Mejia et al. did not indicate statistically significant differences between exposure groups, yet the authors interpreted the results as showing no benefit of smokeless tobacco. An objective interpretation of their results is that the model provides no evidence for either benefit or harm to the population associated with increased promotion of smokeless tobacco use.

Due to the significant shortcomings of the methods employed by Mejia et al., their conclusion that "promoting smokeless tobacco as a safer alternative to cigarettes is unlikely to result in substantial health benefits at a population level" does not follow from the results. Small changes to Mejia et al.'s model input or assumptions led to the opposite conclusion. Because of its flaws, the simulation model proposed by Mejia et al. does not provide information that can be used in evaluating or setting tobacco control policy.

BIBLIOGRAPHY

Bachand AM, Curtin G, et al. 2010. Development of a dynamic simulation model to estimate population mortality effects resulting from the availability of smokeless tobacco products. Ann Epidemiol 20: P70. CDC. 2007. Cigarette smoking among adults--United States, 2006. MMWR Morb Mortal Wkly Rep 56: 1157-1161. Escobedo LG, Peddicord JP. 1997. Long-term trends in cigarette smoking among young U.S. adults. Addict Behav 22: 427-430. Friedman G, Tekawa IS, Sadler M, Sidney S. 1997. Smoking and mortality: the Kaiser Permanente experience. In: Shopland DR, Burns DM, Garfinkel L, Samet J, editors. Changes in Cigarette-Related Disease Risks and Their Implication for Prevention and Control. Rockville, MD: US Department of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute.p 477-499. Gartner CE, Hall WD, et al. 2007. Assessment of Swedish snus for tobacco harm reduction: an epidemiological modelling study. Lancet 369: 2010-2014. Gilpin EA, Pierce JP, et al. 1992. Reasons smokers give for stopping smoking: do they relate to sucess in stopping? Tob Control 1: 256-263. Levy DT, Mumford EA, et al. 2004. The relative risks of a low-nitrosamine smokeless tobacco product compared with smoking cigarettes: estimates of a panel of experts. Cancer Epidemiol Biomarkers Prev 13: 2035-2042. Lundqvist G, Sandstrom H, et al. 2009. Patterns of tobacco use: A 10-year follow-up study of smoking and snus habits in a middle-aged Swedish population. Scandinavian Journal of Public Health 37: 161-167. Mejia AB, Ling PM, et al. 2010. Quantifying the effects of promoting smokeless tobacco as a harm reduction strategy in the USA. Tob Control 19: 297-305. Nelson DE, Mowery P, et al. 2006. Trends in smokeless tobacco use among adults and adolescents in the United States 7. Am J Public Health 96: 897-905. Roth HD, Roth AB, et al. 2005. Health risks of smoking compared to Swedish snus 4. Inhal Toxicol 17: 741-748. Severson HH, Forrester KK, et al. 2007. Use of Smokeless Tobacco is a Risk Factor for Cigarette Smoking. Nicotine Tobacco Research 9: 1331-1337. Tomar SL. 2003. Trends and patterns of tobacco use in the United States 1. Am J Med Sci 326: 248-254. Zhu SH, Wang JB, et al. 2009. Quitting Cigarettes Completely or Switching to Smokeless: Do U.S. Data Replicate the Swedish Results? Tobacco Control 18: 82-87.

Conflict of Interest:

Competing interests: The authors are preparing an alternative tobacco harm reduction model. This work was supported by RJ Reynolds Tobacco Company.

We are mildly flattered that Philip Morris found it worthwhile to have Peter Lee criticize our framework [1] for assessing the likely population effects of aggressive promotion of smokeless tobacco as a harm reduction strategy in the USA. Peter Lee is a longtime tobacco industry consultant who has a history spanning decades criticizing important studies demonstrating the harms of tobacco and secondhand smoke [2], including the landmark Hirayama study [3-5] and publishing papers or letters to the editor contesting the health effects of secondhand smoke on cardiovascular disease [6], cancer [7], SIDS [8] and more recently the health effects of smokeless tobacco [9, 10] and menthol [11]. Lee's role in industry efforts to discredit the Hirayama study has been well documented in the literature [12, 13]. As Lee notes, "one would intuitively expect a substantial benefit if increasing snus promotion led to many smokers switching to snus." The whole point of our analysis was to move beyond "intuition" and make predictions based on data in a way that explicitly accounts for the uncertainty in the data on tobacco use behavior and the associated health costs. The fact that the likely health cost ranges overlap is what leads to the conclusion that, accounting for this uncertainty, the market changes likely to accompany aggressive smokeless promotion would not confer population-level health benefits.

Lee, a statistician, simply ignores the uncertainty associated with the estimates that form the core of the model.

He criticizes the fact that we do not account for the temporal dynamics of changes in tobacco use behavior and the associated risks over time. He is correct that our model is a steady-state, not a dynamic, model. We considered a dynamic model, but doing so conflicted with our fundamental goal of basing the results on data rather than the rhetoric and "intuition" that have characterized the harm reduction debate to date. We were unable to find the data necessary to model the dynamics Lee seeks. It is noteworthy that Lee did not provide citations to the data that one could use to develop the model he desires.

Lee found the justification for the health cost we used for snus as 11 to be "unclear." In our paper, we clearly stated that this estimate came from an expert consensus panel estimate of the health effects, reference 9 in our paper [14]. As we noted in our paper, the estimate that this panel produced is probably low because subsequent research has found higher risks for heart disease, that are larger than those considered in this reference, a case that has only grown stronger as evidence has continued to accumulate [15]. If anything, we are almost certainly underestimating these risks.

Lee questions our assumption of a risk of 90 for dual use. He is correct that there is little data available on dual use (a subject worthy of study). The reason we assumed a modest reduction in risk was that there might be less exposure to cigarette smoke, which could lower cancer risk but would have little effect on heart disease risk because of the highly nonlinear relationship between smoking and heart disease risk, with most effect occurring at low levels of smoking.

Lee criticizes us for including what he sees as unacceptably high levels of dual use (i.e., concurrent use of smokeless tobacco and cigarettes) in our scenarios. (It is important to define "dual use" as use of either product on some days rather than both products on all days. This latter definition does not reflect actual dual use, particularly as the snus products are being promoted for use when one cannot "light up", and substantially underestimates dual use.) The base levels of dual use we used in our model are from surveys of actual use patterns in the USA. The fact that we model large increases in dual use reflects the actual marketing of smokeless products by the tobacco companies, who are promoting snus products as cigarette line extensions, packaging them together, and explicitly promoting dual use in their marketing. Dr. Lee could make a real contribution to the debate if he were to present an analysis based on the market targets that his client, in this case Philip Morris, has established for both Marlboro snus and dual use of Marlboro snus and cigarettes together.

Finally, we were surprised that Dr. Lee did not simply put the health costs he asserts are accurate into the model and present the results to demonstrate that his assertions are correct and supported by actual data. (The full model is available on the Tobacco Control website at http://tobaccocontrol.bmj.com/content/19/4/297/suppl/DC1, something we pointed out to him when he contacted us asking for a copy of the model.) The whole object of this enterprise is to move beyond the "intuitive" arguments Lee presents to making decisions based on quantitative estimates of likely population effects: Lee failed to provide credible estimates demonstrating that smokeless promotion would actually be likely to reduce harm on a population level.

Adrienne Mejia

Pamela M. Ling

Stanton Glantz

University of California, San Francisco San Francisco, CA 94143

REFERENCES

1. Mejia AB, Ling PM, Glantz SA. Quantifying the Effects of Promoting Smokeless Tobacco as a Harm Reduction Strategy in the USA. Tob Control. 2010 Aug;19(4):297-305.

2. Lee PN. Many Claims About Passive Smoking Are Inadequately Justified. BMJ. 1997 Feb 1;314(7077):371.

3. Hirayama T. Non-Smoking Wives of Heavy Smokers Have a Higher Risk of Lung Cancer: A Study from Japan. Br Med J (Clin Res Ed). 1981 Jan 17;282(6259):183-5.

4. Lee PN. "Marriage to a Smoker" May Not Be a Valid Marker of Exposure in Studies Relating Environmental Tobacco Smoke to Risk of Lung Cancer in Japanese Non-Smoking Women. Int Arch Occup Environ Health. 1995;67(5):287-94.

5. Ong E, Glantz SA. Hirayama's Work Has Stood the Test of Time. Bull World Health Organ. 2000;78(7):938-9.

6. Lee PN, Forey BA. Environmental Tobacco Smoke Exposure and Risk of Stroke in Nonsmokers: A Review with Meta-Analysis. J Stroke Cerebrovasc Dis. 2006 Sep-Oct;15(5):190-201.

7. Lee PN, Hamling J. Environmental Tobacco Smoke Exposure and Risk of Breast Cancer in Nonsmoking Women: A Review with Meta-Analyses. Inhal Toxicol. 2006 Dec;18(14):1053-70.

8. Lee PN. Passive Tobacco Exposure and Sudden Infant Death Syndrome. Pediatrics. 1993 Sep;92(3):505-6.

9. Lee PN, Hamling J. Systematic Review of the Relation between Smokeless Tobacco and Cancer in Europe and North America. BMC Med. 2009;7:36.

10. Sponsiello-Wang Z, Weitkunat R, Lee PN. Systematic Review of the Relation between Smokeless Tobacco and Cancer of the Pancreas in Europe and North America. BMC Cancer. 2008;8:356.

11. Werley MS, Coggins CR, Lee PN. Possible Effects on Smokers of Cigarette Mentholation: A Review of the Evidence Relating to Key Research Questions. Regul Toxicol Pharmacol. 2007 Mar;47(2):189-203.

12. Hong MK, Bero LA. How the Tobacco Industry Responded to an Influential Study of the Health Effects of Secondhand Smoke. BMJ. 2002 Dec 14;325(7377):1413-6.

13. Yano E. Japanese Spousal Smoking Study Revisited: How a Tobacco Industry Funded Paper Reached Erroneous Conclusions. Tob Control. 2005 Aug;14(4):227-33; discussion 33-5.

14. Levy DT, Mumford EA, Cummings KM, Gilpin EA, Giovino G, Hyland A, et al. The Relative Risks of a Low-Nitrosamine Smokeless Tobacco Product Compared with Smoking Cigarettes: Estimates of a Panel of Experts. Cancer Epidemiol Biomarkers Prev. 2004 Dec;13(12):2035-42.

15. Piano MR, Benowitz NL, Fitzgerald GA, Corbridge S, Heath J, Hahn E, et al. Impact of Smokeless Tobacco Products on Cardiovascular Disease: Implications for Policy, Prevention, and Treatment: A Policy Statement from the American Heart Association. Circulation. 2010 Oct 12;122(15):1520 -44.

Conflict of Interest:

None declared

INTRODUCTION Mejia et al1 argue that a harm reduction strategy based on promoting snus, the form of smokeless tobacco widely used in Sweden, is unlikely to result in any substantial health benefit to the US population. They divide the population into five tobacco groups (never tobacco users, former tobacco users, current cigarette smokers, current snus users, and current dual users), attaching to each group an estimate of the "tobacco-related health effect" (TRHE). By definition, TRHE is 0 in never smokers and 100 in current cigarette smokers, with other smoking groups having intermediate TRHE values, proportional to their relative excess disease risk. Mejia et al consider various scenarios (e.g. "aggressive smokeless promotion") which result in different predicted distributions by tobacco use, and hence different estimates of the overall average TRHE for the whole US population. For the "base case", with tobacco use distributions as they currently are, this is estimated as 24.2, and under the various scenarios considered the estimates lie between 19.2 and 30.5.

Their conclusion that snus promotion probably provides little health benefit seems surprising. Given the strong evidence that health risks from snus are much less than from smoking, one would intuitively expect a substantial benefit if increasing snus promotion led to many smokers switching to snus. It is useful therefore to look at the methodology used and assumptions made.

FAILURE PROPERLY TO ACCOUNT FOR PATTERNS OF TOBACCO USE

There are some deficiencies in the approach. First, there are clealy more than five relevant tobacco groups. Limiting attention to snus use and cigarette smoking, there are nine main groups, representing each combination of never, former and current use of each product. And within some combinations, there are subgroups by sequence of events. Why, for example, should TRHE be assumed similar in former tobacco users regardless of whether snus or cigarettes were previously used, or similar in current snus users who have or have not previously smoked cigarettes? Other deficiencies include failure to consider age, sex, amount used, and other tobacco products such as pipes or cigars. However, these are minor compared to the failure to account for time in its various guises - time since quit, time since switch, and time used snus or cigarettes. It is unsound to assume TRHE is the same for all former users of tobacco regardless of time quit, or the same for current snus users regardless of previous smoking history. Failure to consider time undermines the validity of the TRHE estimates for the different tobacco groups.

ESTIMATES OF TRHE BY SMOKING GROUP Quitters No justification is given for the TRHE estimate of 5 used by Mejia et al. It seems very low. Relative all-cause mortality rates for current, former and never smokers from the well- known CPS-II study2, indicates former smokers have about 40% of the excess all-cause mortality rate of current smokers, not 5%. The appropriate TRHE would be higher still for short- term quitters. Was the value of 5 intended to relate to long-term quitting?

Snus users The justification for the TRHE estimate of 11 is unclear. It is much too low, if applied to recent switchers from cigarettes, particularly following long-term smoking. However, if intended only to quantify effects of snus, it seems too high. Updates of published meta-analyses for snus use for heart disease3 and cancer4 (details available on request) suggest little or no increased risk, with combined relative risk (95% confidence interval) estimates of 1.01 (0.91-1.12) for ischaemic heart disease, 1.05 (0.95-1.15) for stroke, 0.97 (0.68-1.37) for oropharyngeal cancer, 1.10 (0.92-1.33) for oesophageal cancer, 0.98 (0.82-1.17) for stomach cancer, 1.20 (0.66-2.20) for pancreatic cancer, and 0.71 (0.66-1.76) for lung cancer. Given it is implausible that snus use might increase COPD risk, given the lack of confirmed reports of increased risks for other diseases, and given the much stronger relationships seen with smoking, the excess risk from snus use is probably no more than 2% of that from cigarette smoking and not as great as 11%.

Dual use The estimated TRHE of 90 derived from INTERHEART 5 is not relevant to snus, the smokeless tobacco use reported in that study being predominantly in Asian and African countries. Though data are lacking, one might imagine that if lifetime dual users get about half their required nicotine dose from each source, a TRHE of about 50 might be appropriate. Again, however, this would not apply to those changing from long-term smoking to dual use.

HIGH ESTIMATES OF DUAL USE The proportion of dual users predicted in some of the scenarios of up to about 20% seem implausibly high. Recent Swedish surveys (e.g.6,7 give estimates less than 3%. While adolescents in Sweden often try both products, adults usually only use one. Models based on studies in adolescents that do not take this into account may result in misleading predictions of the tobacco use distribution, especially when the data used8 relate to smokeless tobacco use, not snus.

SNUS AND INITIATION OF SMOKING Some Swedish retrospective studies9,10 claim snus users are less likely to initiate smoking than never tobacco users. While these claims are questionable (failing to adjust for time available to initiate), evidence that few Swedish smokers used snus before they started smoking9,10, and that most dual users started on cigarettes, suggest snus can be at most a minor determinant of smoking.

SNUS AND QUITTING SMOKING In theory snus use might discourage rather than encourage quitting. No published study in Sweden suggests discouragement, but many 9,11-15suggest encouragement. Although these studies have some limitations, concern regarding discouragement seems unjustified.

FURTHER THOUGHTS AND A SIMPLER APPROACH The approach of Mejia et al is complex and does not validly allow assessment of the effect on health of the various scenarios considered.

One problem is that promotion of snus cannot affect the risk resulting from past smoking (particularly so for those who quit before the promotion started), so that inclusion of this risk in the overall TRHE estimates obscures estimation of the effects of the various strategies discussed. It would seem better to compare the decline in risk for the given scenario of snus promotion with that in a comparable scenario where those assumed to switch to snus quit instead.

A second problem is that while their approach is complex, it ignores many factors, such as time quit or switched, age, sex, and quantity used. However, attempting to improve the model to account for these would likely be valueless, given the uncertainties involved.

Also Mejia et al do not define what they call a substantial health benefit. The strategy "aggressive promotion with most new users from smokers" reduces the overall TRHE from 24.2 to 19.2, i.e by about 20%. This seems quite substantial, especially so if it is a relatively short- term effect. Would strategies directly encouraging quitting do better?

To my mind, they have obscured a simple situation. Complete switching to snus seems likely to have a health effect virtually equivalent to quitting, with partial switching (dual use) having an intermediate effect. For smokers unwilling or unable to give up their nicotine, switching to snus is clearly a much better health alternative than continuing smoking. Promoting snus may produce some new tobacco users, but these will have little or no excess risk of disease, and be no more likely to take up smoking than are those who have never used tobacco.

(WORD COUNT: 1213)

REFERENCES

1. Mejia AB, Ling PM, Glantz SA. Quantifying the effects of promoting smokeless tobacco as a harm reduction strategy in the USA. Tob Control 2010;19:297-305.

2. US Surgeon General. Reducing the health consequences of smoking. 25 years of progress. A report of the Surgeon General. Rockville, Maryland: US Department of Health and Human Services; Public Health Services; 1989. DHHS Publication No. (CDC) 89-8411. http://www.surgeongeneral.gov/library/reports/index.html

3. Lee PN. Circulatory disease and smokeless tobacco in Western populations: a review of the evidence. Int J Epidemiol 2007;36:789-804.

4. Lee PN, Hamling JS. Systematic review of the relation between smokeless tobacco and cancer in Europe and North America. BMC Med 2009;7:36:

5. Teo KK, Ounpuu S, Hawken S, Pandey MR, Valentin V, Hunt D, et al. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: a case-control study. Lancet 2006;368:647-58.

6. Persson J, Sj?berg I, Johansson S-E. Bruk och missbruk, vanor och ovanor. H?lsorelaterade levnadsvanor 1980-2002 (Health related habits of life 1980-2002). Statistiska centralbyr?n; 2004, (Accessed Oct 2010). (Levnadsf?rh?llanden (Living conditions).) 105. http://www.scb.se/statistik/le/le0101/1980i02/le0101_1980i02_br_le105sa0401.pdf With additional data supplied by E H?gstorp, Statistiska centralbyr?n, 2005.

7. Wadman C. Levnadsvanor - Tobaksvanor. Statens Folkh?lsoinstitut; 2009, (Accessed Oct 2010). http://www.fhi.se/sv/Statistik- uppfoljning/Nationella-folkhalsoenkaten/Levnadsvanor/Tobaksvanor/

8. Severson HH, Forrester KK, Biglan A. Use of smokeless tobacco is a risk factor for cigarette smoking. Nicotine Tob Res 2007;9:1331-7.

9. Furberg H, Bulik CM, Lerman C, Lichtenstein P, Pedersen NL, Sullivan PF. Is Swedish snus associated with smoking initiation or smoking cessation? Tob Control 2005;14:422-4.

10. Ramstr?m LM, Foulds J. Role of snus in initiation and cessation of tobacco smoking in Sweden. Tob Control 2006;15:210-4.

11. Lindstr?m M, Isacsson S-O. Smoking cessation among daily smokers, aged 45-69 years: a longitudinal study in Malm?, Sweden. Addiction 2002;97:205-15.

12. Lundqvist G, Sandstr?m H, ?hman A, Weinehall L. Patterns of tobacco use: a 10-year follow-up study of smoking and snus habits in a middle-aged Swedish population. Scand J Public Health 2009;37:161-7.

13. Rodu B, Stegmayr B, Nasic S, Cole P, Asplund K. Evolving patterns of tobacco use in northern Sweden. J Intern Med 2003;253:660-5.

14. Gilljam H, Galanti MR. Role of snus (oral moist snuff) in smoking cessation and smoking reduction in Sweden. Addiction 2003;98:1183 -9.

15. Ramstr?m L. Is snus a model for harm reduction: the scientific evidence from Sweden. In: The 13th World Conference on Tobacco OR Health: Building capacity for a tobacco-free world, The 13th World Conference on Tobacco OR Health: Building capacity for a tobacco-free world. Washington DC, July 12-15 2006. 2006;

Conflict of Interest:

I am a long-term consultant to the tobacco industry, and this work was supported by Philip Morris

Snus is threatening not only for Sweden also other parts of Europe. We have anecdotal information that UK tourists in Sweden(who are smokers) are trying Snus quite frequently. Therefore, there is a threat of cross-border transmission of Snus addiction. Some of the reports claim that Snus is less injurious to health comparing smoking, but, the evidence shows there is a higher risk for the occurrence of oral cancer (OSCC) and development of Metabolic Syndrome [MS] (MS=Central Obesity, hypertriacylgycerolemia, low HDL cholesterol concentration, elevated BP and fasting glucose concentration). To date, a couple of studies have been published on Quid chewing related metabolic syndrome (1-3). Therefore, we cannot ignore the similar potential consequences of Snus consumption. Again, the claim regarding an antioxidant effect of wet- Snus to prevent cancer is misleading information. Obviously, such information is again misleading for a person who wants to consume Snus, and that needs to be stopped by removing the vested information deliberately quoted by the manufacturers to promote their Snus business in Europe, and probably extending to the other parts of the world. Therefore, any form of the Smokeless Tobacco (SLT) whether it's Indian/Chinese/Taiwanese/Japanese- is a major public health concern today. It needs to be mentioned that in 2010 Japan started marketing a new form of SLT: 'Zerostyle mint' targeting adolescents. And also for the smokers who wants to switch from smoking to 'Zerostyle Mint'- a refillable cartridge (4). It may be incorrect to say that Quid Chewing, Snus consumption or Zerostyle mint will be less injurious than smoking, because it is established that any form of SLT may contribute to the higher risk of oral and oro-pharygeal cancer and Metabolic Syndrome (MS). Therefore, Chewing Quid, Zerostyle Mint or Swedish Snus needs to be properly controlled under the WHO FCTC framework convention (5). We have undertaken an interventional study on Quid/Snus consumption and development of metabolic syndrome especially among the cases suffering from Quid induced oral sub-mucosal fibrosis (OSF)- a cause of high rate of morbidity and mortality in the risk group population. References. 1. Amy Ming-Fang Yen, Yueh-Hsia Chiu et al. A population-based study of the association between betel-quid chewing and the metabolic syndrome in men. Am. J Clin Nutr. 2006; 83:1153-60. 2.Boucher BJ, Mannan N. Metabolic effects of consumption of Areca catechu. Addiction Biol 2002;7: 103-10. 3. Boucher BJ, et al. Betel nut (areca catechu) consumption and induction of glucose intolerance in adults CD 1 mice and in their F1 and F2 offspring. Diabetologica 1994;37: 49-55. 4. JT to Launch New Style of Smokeless Tobacco Product "Zerostyle Mint" http://www.jt.com/investors/media/press_releases/2010/0317_01/index.html 5. WHO Framework Convention on Tobacco Control http://www.who.int/fctc/en/

Link/Contact: Professor Chitta R Choudhury, PhD, MPH, FFDRCS, FRSPH, BDS, DND Lead : OPCL/OSF study team

International Centre for Tropical Oral Health, PHT NHS Dept Max Fac, England & Oral Biology, Genomic Studies, Nitte University, Mangalore, India. President, Institute of Health Promotion & Education (IHPE), UK cr_choudhury@yahoo.co.uk

Conflict of Interest:

None declared

The approach by Ayo-Yusuf and Connolly (2010) to evaluate cancer risks of smokeless tobacco products (STP) addresses issues that could be relevant to modified risk claims for Swedish snus tobacco products. We disagree with the authors' conclusions, and in some cases they simply have the facts wrong. Nonetheless, the issues presented warrant consideration by the tobacco science community, including the FDA Center for Tobacco Products and the newly formed Institute of Medicine committee on modified risk.

The authors' use of the EPA risk assessment process is intriguing. In the hands of someone familiar with the process it may have resulted in a useful contribution to the scientific literature. Unfortunately the authors do not seem to understand the process because they did not follow the well documented EPA guidance.

Recently a National Academy of Sciences committee issued a report examining the EPA risk assessment process (Science and Decisions: Advancing Risk Assessment, 2009). The committee cited the importance of making risk assessments data driven, and when data are unavailable ensuring that default assumptions are accurately characterized. When there is an abundance of information - particularly epidemiological data - the credibility and utility of the risk assessment increases significantly.

There is extensive health-related information available for Swedish snus. That is why an EPA risk assessment approach is worth pursuing. However, the authors did not use all the available data, particularly not the epidemiological documentation. EPA scientists have some flexibility in choosing "critical" studies, but they must justify their decisions, and use "all the relevant and available scientific information." EPA scientists cannot disregard data simply because of personal biases.

Also, instead of comparing life-time use of STP with only 12-weeks medicinal nicotine, the authors should have made a comparison with long- term cigarette smoking. This could then be expanded to comparisons with selected smoke components. It would be enlightening, for example, to determine risk assessment values for the carcinogenic potential of such components as 1, 3-butadiene compared with the authors' claims for tobacco -specific nitrosamines and benzo(a)pyrene.

In summary, we support the application of risk assessment in the regulatory science process. However, if the EPA risk assessment model is used to evaluate potential modified risk tobacco products, it should be done so by scientists experienced in the EPA process who have an understanding and appreciation of the available data.

References: Ayo-Yusuf, O., A., Connolly, G., N. Applying toxicological risk assessment principles to constituents of smokeless tobacco products: implications for product regulation. Tob Control, published online Oct 5, 2010. doi: 10.1136/tc.2010.037135

Science and Decisions: Advancing Risk Assessment. Committee on Improving Risk Analysis Approaches Used by the U.S. EPA. Board on Environmental Studies and Toxicology. Division on Earth and Life Studies. National Research Council of the National Academies. National Academic Press, Washington D.C., 2009.

Conflict of Interest:

Lars E. Rutqvist is employed by Swedish Match AB. Chris Coggins acts in a consulting role to the company.

Smokers will smoke more cigarettes and inhale more deeply should the nicotine content of cigarettes be reduced. It is the burning tobacco which kills - not the nicotine. Each smoker has his own comfortable level of nicotine. Perhaps high nicotine cigarettes are safer?

The speculation that dependence can result from smoking 1 - 2 cigarettes a day is at odds with the more extreme claims by anti tobacco campaigners about passive smoking. Is 5 hours a day in a smoky atmosphere equivalent to 10 cigarettes a year as measured directly by independent scientists or is it several cigarettes a day as is often claimed? If so, why don't non smoking pub-goers become nicotine dependent?

Conflict of Interest:

None declared

It is totally true that tobacco control is funded very little compared to the profits derived by the tobacco companies and the taxes collected by governments. At one point (in the 80s?), WHO had suggested that 1% of the tobacco taxes be allocated to fund tobacco control activities. Then this suggestion "disappeared": I wonder if you know why as it would be a simple request that remains valid.

It is also true that Bloomberg and Gates have provided since 2007 and 2008 a significant amount of money to promote tobacco control worldwide: 500 millions is not small change (325 millions from Bloomberg and 125 millions from Gates). How has this money been used? I don't think I have seen yet a detailed evaluation. Is that normal?

Philippe Boucher Tobacco Control in Africa - The investigative blog http://blogsofbainbridge.typepad.com/africa

PS: I should add that when French people were polled and asked if they were in favor of taking 1% of the tobacco taxers to fund tobacco control activities they were overwhelmingly in favor (including smokers) but that was not the opinion of the Finance Ministry

Conflict of Interest:

None declared

How might those estimates change if we all told smokers the truth?

What if the government changed the warning labels to read "THIS PRODUCT IS NOT A 100% SAFE ALTERNATIVE TO SMOKING"? See what a difference one tiny change can make? This would lead folks to ask, "Well if it's not 100% safe, how much safer is it?"

The way the message is worded now, 85% of the people who read it conclude it means that smokeless tobacco products cause just as much disease and premature deaths as smoking. [1] We know it isn't true. But smokers don't know that.

And then what if the American Cancer Society, American Heart Association, American Lung Association, American Medical Society, and the Centers for Disease Control and Prevention informed smokers that their excess risk of lung disease would be totally eliminated if they switched from smoking to smokeless? What if they provided comparisons between smoking and smokeless of the odds of developing various types cancers, having a heart attack or a stroke?

We know that users of smokeless tobacco products have a lower mortality rate from all these diseases than continuing smokers. [2,3] We know that for most diseases, the Swedish snus user's mortality risks are reduced to the level of those who gave up all use of tobacco. [4] We know all that. But the smokers do not know that.

Most smokers do not read medical journals. They rely on the popular press and information provided by respected organizations that claim to have public health as a mission.

Curiously, most physicians are just as misinformed as their smoking patients. What if the doctors were to learn that their patients could reduce their risk of developing a smoking-related disease by 90 to 99% if they switch completely to a smokeless form of tobacco? Might not more smokers give snus a try if their own doctor told them it was safer than smoking?

What if the FDA required the tobacco companies to develop and conduct advertising campaigns aimed at convincing smokers to switch to smokeless products?

What if we did all these things? What effect would that have on the number of U.S. smokers who switch and consequently on the smoking-related morbidity and mortality rates? Factor in truth-telling and run those Monte Carlo simulations again.

References:

[1] Phillips, C.V. et al. You might as well smoke; the misleading and harmful public message about smokeless tobacco. BMC Public Health 2005, 5:31doi:10.1186/1471-2458-5-31.

[2] Accortt, N.A., et al. Chronic Disease Mortality in a Cohort of Smokeless Tobacco Users. American Journal of Epidemiology 2002; 156:730- 737

[3] Roth, H.D. et al. Health Risks of Smoking Compared to Swedish Snus. Inhalation Toxicology, 17:741-748, 2005.

[4] Gartner C.E, et al., Assessment of Swedish snus for tobacco harm reduction: an epidemiological modeling study. Lancet. 2007 Jun 16;369(9578):2010-4

Conflict of Interest:

None declared

I read with interest your article affirming public support in England for dedicated cigarette price increases and especially highlighting the finding that almost 50% of smokers supported the measure.

As proposed by the authors, the support for the price hike seems likely to be contingent on allocating funds to tobacco control activities (Surveys from United States, Australia, New Zealand and several European and Asian countries show this). Why else would a non- smoker be keen on increasing the price of a product he or she does not even use? Or would anyone who uses a product regularly 'simply' favour increasing its price without a reason (understanding that it would only create a bigger hole in his or her pocket)?

Arguments exist that dedication of tobacco taxes for tobacco control activities not only serves as a means to muster support for increasing taxes, but is also a very effective investment with a high return (1).

Now, understanding a non-smoker's perspective for this support may be easy... Smoking is clearly a public health hazard and any steps to help restrict or reduce the same would be very welcome. But understanding a consumer's support for making his 'favourite' product more expensive is definitely more complex.

Can this support from smokers be taken as an indication of an indirect help-seeking behaviour? (After all, a large majority of smokers who stop smoking do so without any form of assistance (2))

Or is it merely a 'Feel Good' factor which is the undercurrent?

Imagine this: A smoker buys a pack of cigarettes (obviously with the intention to smoke) but says, 'I'm willing to throw in an extra 20p to help control smoking'! Isn't it easier to say that I'll instead smoke one cigarette less (thereby directly protecting myself, my family and the public from this huge health hazard)?

A similar study from China (3), the world's largest producer and consumer of tobacco, which analysed attitudes and behaviour towards tobacco control activities, mirrored the results of this study, revealing good support for increasing tobacco taxation (about 70%); but when the intention to change smoking behaviour was measured independently, the proportion of respondents who intended to change behaviour was only about 25%. Another study from New Zealand (4) however, revealed a significant association between the strength of intention to quit and the support for increasing taxation.

The second issue is that of bias. It has been found that people answering surveys involving moral/ethical dilemmas have a tendency to agree more with answers that are deemed 'morally' correct or in agreement with the view of the majority or in other words, answers which people 'want to hear'.

So, considering the above issues, is this support from smokers genuinely a form of help-seeking behaviour?

The answer to the above question remains intriguing.

Perhaps there should be a proposal to make cigarette packs priced the same, but containing one cigarette less. And the cost of that cigarette 'given up for the good cause' could be used for tobacco control activities. And then a survey could be conducted, examining support for that (indirect) price hike.

References:

1. Thomson G: Dedicated tobacco taxes - Experiences and arguments. Wellington, NZ. Smokefree Coalition, 2007. http://www.sfc.org.nz/pdfs/DedicatedTaxNovember.pdf.

2. Chapman S, MacKenzie R: The Global Research Neglect of Unassisted Smoking Cessation: Causes and Consequences (2010). PLoS Med 7(2): e1000216. doi:10.1371/journal.pmed.1000216.

3. Wilson N, Weerasekera D, Edwards R, Thomson G, Devlin M, Gifford H: Characteristics of smoker support for increasing a dedicated tobacco tax: National survey data from New Zealand. Nicotine & Tobacco Research 2010 12(2):168-173.

4. Yang T, Wu Y, Abdullah A, Dai D, Li F, Wu J, Xiang H: Attitudes and behavioral response toward key tobacco control measures from the FCTC among Chinese urban residents. BMC Public Health 2007, 7:248.

- Dr. Jonas S. Sundarakumar, M.B.,B.S., D.P.M., (MRCPsych)

Conflict of Interest:

None declared

I refer to the recently published paper- 'Scott L Tomar, Hillel R Alpert and Georgery N Connolly. Patterns of dual use of cigarettes and smokeless tobacco among US males: findings from national surveys. Tob Control 2010;19:104-109'.

The rising trend of smokeless tobacco (ST) use, among adolescent and young adults is not only a problem in the USA, it is equally affecting the same age group population in India and SE Asian Countries. In India, this age group (10-24 years old) has 315 million people (30% of total population), since India is home to just over 1.18 billion, the second largest population in the world (1). Although this cohort is healthier, and their literacy rate is higher, unfortunately, this population group is at the highest risk of chewing tobacco related fatal consequences and developing nicotine addiction. Alarmingly, a significant proportion of Indian youths is developing chewing tobacco related oral/dental diseases of high morbidity rate, and of them, oral sub-mucosal fibrosis (OSMF/OSF), a disabling oral health problem, manifested with the burning mouth sensation, restricted mouth opening, dysarthria, dysphagia and sometimes loss of hearing functions, especially in advanced cases. OSF has got high malignant transforming potential (2-10%, thus risking of full blown oral cancer (20~25% of all cancers in India, varies at locations and the regional countries).

It is a serious public health concern in India. Now-days smoking tobacco (Beedi-Indian version of smoking tobacco and conventional cigarette) is gradually being replaced with smokeless tobacco (SL). The product is marketed in various brands of chewing tobacco sachets; among them, Gutkha, Kaini, Paan-parag are common (2). These products are extremely popular, cheaper (compared with cigarettes), commonly available in every corner of the countries, and use is unrestricted in public places, unlike smoking. We studied 9,288 hospital attending cases, measuring their knowledge, attitude and practice (KAP score). The study reveled that a significant proportion of this population is unaware of the ill-effects of chewing tobacco, and a high proportion of the population both chews and smokes tobacco (2). In India SL is classified in five groups (3). Although none of the SL products in India is exactly similar to Swedish wet Snus, or up-coming Japanese ST 'Zerostyle Mint' (4), but Khaini is one which is wet. Khaini is commercially available and could be prepared at home or work-places, just by buying a sachet of tobacco flecks and a mini-tube of calcium hydroxide (slaked lime). This wet variety of SL, ie. Khaini is a very dangerous product. A study revealed that Khaini causes loss of hyterozygocity (LOH) of the chromosomes, and may delete and mutate a number of tumor suppressor genes 'TSGs'(5). ST use is now a global problem, not only confined within the SE Asian population (including SE Asian migrants in USA and Europe), but also in China, Taiwan, Indonesia, Malaysia, Sigapore, Phillipines, and Africa. In my opinion, the FCTC of WHO should come forward with a special focus and strategic plan to prevent and control ST and ST related health problems. A small interest /working group is in progress to study ST related OSF in India and regional countries. The group welcomes any advisory support and participation.

References.

(1). Ministry of Statistics & Programme implementation, East Block 10, R K Puram, New Delhi-110066 http://mospi.nic.in/ (visited 20.05.2010).

(2). Chitta Ranjan Choudhury. Effects of KAP intervention on oral mucosal lesions associated with personal habit(s). In. Publisher Nitte University, India in association with Bournemouth University, UK ; pp.59- 63, 1st ed. February 2010. BDA (British Dental Association) Lib Cat. No. Class No: D 781 CHO http://bdalib.answeb.co.uk/amlibweb/webquery.dll

(3). Chitta Ranjan Choudhury. Classification of marketed quid sachets based on composition In. Handbook of Oral Cancer Screening & Education. Publisher Nitte University, India in association with Bournemouth University , UK ; pp.11,12 & 65-67. 1st ed. February 2010. BDA (British Dental Association) Lib Cat. No. Class No: D 781 CHO http://bdalib.answeb.co.uk/amlibweb/webquery.dll

(4). Japan Tobacco Inc. (JT) (TSE: 2914). JT to Launch New Style of Smokeless Tobacco Product 'Zerostyle Mint'. http://www.jt.com/investors/media/press_releases/2010/0317_01/index.html (Visited 21.05.2010)

(5). Nobuharu Y, Tsukasu K, Akia K, Takahiko S and Chitta Choudhury. Loss of Heteozygosity (LOH) on Chromosomes 2q, 3p and 21q in Indian squamous cell carcinoma. Bull Tokyo Dent Coll (2007) 48 (3): 109-117.

Authors

1. Chitta Ranjan Choudhury*

(Correspondence) Professor & Director, International Centre for Tropical Oral Health Poole Hospital NHS and Bournemouth University, England, UK. And Dept Oral Biology & Genomic Studies, ABSM Dental Sciences, Nitte University, Mangalore, India.

Lead, OSF interventions: a multicentric study initiative.

cr_choudhury@yahoo.co.uk chittarc@bournemouth.ac.uk

2. Dr. Ashoka Dey, Registrar, Paediatrics, King's College Hospital, London.

3. Avidyti C, St Georges Mecical School, University of London.

4. Tadaaki Kirita, Professor & Chairman, Oral & Maxillofacial Surgery, Nara Medical University, Nara, Japan.

Conflict of Interest:

None declared

Dear Daniel

A very interesting paper confirming the exceptional value of NSD to UK society. The obvious conclusion we should draw is that NSD is too valuable to only happen once a year. In Somerset last year we started a Somerset Stop Smoking Day on 1st October, aiming to encourage quit attempts before the onset of winter with the slogan "Don't be left out in the cold this winter", making a play on the smoking ban requirement to smoke outside. I would suggest that a national stop smoking day in the autumn could only be a good thing.

Stewart Brock

Conflict of Interest:

Commissioning stop smoking services

To the editor:

Ms. Keller asks a straightforward question: "Why was [I] so surprised to find very low levels of nicotine in the blood of subjects who had taken 10 puffs from an electronic cigarette?".

The straightforward answer is that I, perhaps naively, was influenced by marketing materials such as this:

http://www.ecigsadvisor.com/ecigs-review.php?keyword=ablw1

This advertisement, seemingly describing all e-cigarettes and still available on-line today, clearly states:

"Get the same amount of nicotine as a regular cigarette"

and

"...around 10 to 15 puffs are equivalent to the same amount of nicotine delivered by a tobacco cigarette."

and

"A cartridge is equivalent to about one pack of cigarettes."

The data I report in the letter in question (Eissenberg, 2010) and those reported in the SRNT poster Ms. Keller describes (Bullen et al., 2009) clearly contradict these advertising claims. In the context of these generic claims, the data regarding the specific products tested were surprising to me. Indeed, readers who examine the Bullen et al (2009) data will likely be struck, as I was, by the consistency in results across laboratories, methods, and devices tested: neither study provides any support for advertising claims such as these.

Interestingly, Ms. Keller is a board member of an organization called the Consumer Advocates for Smoke-free Alternatives Association (CASAA; see http://www.casaa.org/about/board.asp). CASAA's press release of Jan 26, 2010 notes that "CASAA is a non-profit organization that works to ensure the continued availability of products such as electronic cigarettes and to provide smokers and non-smokers alike with truthful information about these and other alternatives." The second of these goals suggests that CASAA welcomes rigorous scientific data that reveal important product characteristics such as nicotine delivery profile. I hope that CASAA is now working to correct misleading marketing materials such as those cited above.

Respectfully submitted,

Dr. Thomas Eissenberg Virginia Commonwealth University

Conflict of Interest:

None declared

Correspondence Earmarking part of cigarette tax revenues for tobacco control programs has public support, but will it lead to more spending for tobacco control? Anthony P. Polednak Connecticut Department of Public Health, Hartford, Connecticut USA (Retired)

Re: Smoker support for increased (if dedicated) tobacco tax by individual deprivation level: national survey data. Wilson et al., Tob Control 2009;18:512.

Public support among smokers for dedicating (earmarking) all of tobacco tax increases to smoking cessation programs and other prevention programs has been shown in New Zealand, but governments should ensure equitable access to high-quality cessation services.1 Surveys in the U.S. have shown public support for earmarking for tobacco control (TC) programs.2 Earmarking could increase total state expenditures for TC,3 which should enhance the decline in tobacco use.4

For U.S. federal fiscal year (FY) 2009,5,6 of all 50 states and the District of Columbia, 12 (i.e., Arizona, California, Colorado, Idaho, Iowa, Louisiana, Michigan, New Jersey, Oklahoma, Oregon, South Dakota, and Utah) earmarked part of their state tobacco tax revenues in FY 2009 for TC (starting in 1989 in California). Remarkably, seven of the 12 states used none (and all used <18%) of their FY 2009 Master Settlement Agreement (MSA) funds for TC (mean 3.9%, median 0.0%). Of the 39 other states, 11 used 0% and seven used >18% of MSA funds for TC (mean 8.1%, median 5.1%). As a proportion of the Centers for Disease Control and Prevention (CDC) target for TC expenditures for each state7 (using a methodology that should be applicable to other countries),3 the average for total TC spending from all sources in FY 2009 for the 12 earmarking states (mean 27.4%, median 25.5%) was similar to that for the 39 others (mean 29.2%, median 21.3%).

Why have the earmarking states not done better in TC spending? With 100% earmarking for TC, a recent taxes increase of only $0.58 in California and $0.31 in Oregon could have resulted in attainment of their CDC targets.3 During the entire 14-year period of 1995-2009, however, the average state cigarette excise tax for all states increased from $0.33 to $1.20.8 Also, only as much as 25% (California) of a state tax increase has ever been used for TC. For the two states reaching 50% of their CDC target, Colorado earmarks 16% of monies from a cigarette tax increase imposed by a constitutional amendment, while South Dakota dedicates $5 million annually from tobacco tax revenues (vs. $11.3 million target).5

Fourteen U.S. states plus the District of Columbia approved legislation in 2009 for increasing cigarette excise taxes, but only New Jersey earmarked for TC.4 Although New Jersey statutes had stipulated $30- 45 million per year in 2002-2005 for ÃÆ’ƒÃ‚¢ÃÆ’‚€ÃÆ’‚Ãâ€Â¦Ãƒ‚“anti- smoking initiatives,ÃÆ’ƒÃ‚¢ÃÆ’‚€ÃÆ’‚ï¿Â½9 actual spending for TC declined to 10.2 million in FY 2009 (or only 9% of the CDC target).5

Recurring state fiscal crises have affected TC spending, including use of MSA funds for TC,10 while prompting tobacco tax increases to help balance budgets. Despite declining use of MSA funds for TC in Colorado, a statewide coalition promoted a successful ballot initiative in 2004 that allocated at least $25 million annually from tobacco tax revenues to TC programs3,11 (reaching $27.5 million in FY 2009 or 51% of the CDC target),5 but a ÃÆ’ƒÃ‚¢ÃÆ’‚€ÃÆ’‚Ãâ€Â¦Ãƒ‚“fiscal crisisÃÆ’ƒÃ‚¢ÃÆ’‚€ÃÆ’‚ï¿Â½ declared for FY 2010 permits use of these funds for any health-related purpose.5 Evidence for health-care costs savings from one comprehensive statewide TC program in the U.S. (and applicable to other countries)12 could be used by coalitions trying to convince governments to earmark substantial proportions of tobacco taxes for TC while not reducing (but increasing) TC expenditures derived from the MSA. State budget deficits and balanced budget requirements would complicate this effort.

A U.S. National Action Plan for Tobacco Cessation called for a $2.00 increase per pack in the federal cigarette tax, with at least 50% earmarked for funding the plan.2 All funds from the federal cigarette excise tax increase of $0.62 per pack in 2009 were earmarked for another health-related priority (health insurance for uninsured children). For the U.S. governmentÃÆ’ƒÃ‚¢ÃÆ’‚€ÃÆ’‚â„¢s ongoing civil- racketeering lawsuit against the tobacco industry, a group of national organizations filed legal briefs in 2005 calling for remedies including funds earmarked for TC programs.13 Funding: None. Conflicts of interest: None declared. Corresponding authorÃÆ’ƒÃ‚¢ÃÆ’‚€ÃÆ’‚â„¢s e-mail: appoled7@yahoo.com.

References

1. Wilson N, Weerasekera D, Edwards R, Blakely T. Smoker support for increased (if dedicated) tobacco tax by individual deprivation level. Tob Control 2009;18:512. 2. Fiore, MC, Croyle, RT, Curry, SJ et al., 2004. Preventing 3 million premature deaths and helping 5 million smokers quit: A national action plan for tobacco control. Am. J. Public Health 94, 205-210. 3. Lum KL, Barnes RL, Glantz SA. Enacting tobacco taxes by direct popular vote in the United States: Lessons from 20 years of experience. Tob Control 2009;18:377-86. 4. Farrelly MC, Pechacek TF, Thomas KY, Nelson D. The impact of tobacco control programs on adult smoking rates. Am J Public Health 2008;98:304- 309. 5. American Lung Association. http://www.lungusa.org. 6. Campaign for Tobacco Free Kids. A decade of broken promises: The 1998 state tobacco settlement ten years later. http://tobaccofreekids.org. 7. Centers for Disease Control and Prevention. Best Practices for Comprehensive Tobacco Control Programs ÃÆ’ƒÃ‚¢ÃÆ’‚€ÃÆ’‚â€ÂÅ“ 2007. Atlanta GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office of Smoking and Health, 2007. 8. Centers for Disease Control and Prevention 2009a Federal and state cigarette excise taxes- United States, 1995-2009. MMWR 58, 524- 527. 9. New Jersey Permanent Statute Database. Statute 26:2H-1858g. Disposition of revenue collected from cigarette tax. http://lis.state.nj.us. 10. Sloan FA, Carlisle ES, Rattliff JR, Trigdon J. Determinants of statesÃÆ’ƒÃ‚¢ÃÆ’‚€ÃÆ’‚â„¢ allocations of the Master Settlement Agreement payments. J Health Polit Policy Law 2005;30:643-86. 11. Nelson DA, Reynolds JH, Luke DA et al. Successfully maintaining program funding during trying times: Lessons from tobacco control programs in five states. J Public Health Management Practice 2007;13:612-20. 12. Lightwood J, Dinno A, Glantz S. Effect of the California tobacco control program on personal health care expenditures. PLoS Med 2008;5:e178. 13. Campaign for Tobacco Free Kids, 2009b. Special reports: Justice department civil lawsuit. Updated 06/01/09. http://www.tobaccofreekids.org/reports/doj.

Conflict of Interest:

None declared

I find it intriguing that the eCigarette samples found no discernible nicotine content. I have personally conducted my own (albeit uncontrolled) blind-study using a lower nicotine brand (12mg) of "e-cigarette Juice" and a higher nicotine content brand (36mg).

The two brands were largely identical in terms of content and taste but the differences in terms of their satisfaction in relieving the stress of not smoking for long periods was noticeable.

Might I suggest that a longer scale study using a variety of differing eCigarettes and brands of eJuice would be fruitful in allaying concerns that the results listed in the study are simply those you would expect to see if the machines in use were faulty or an ultra-low nicotine brand of e-Juice was used.

Conflict of Interest:

None declared

According to the US Centers for Disease Control and Prevention (CDC), smoking is the single most preventable cause of disease, disability, and death in the United States (http://www.cdc.gov/nccdphp/publications/aag/osh.htm). Each year, an estimated 443,000 people die prematurely from smoking or exposure to secondhand smoke, and another 8.6 million have a serious illness caused by smoking. And as aptly demonstrated by Lee et al. in Tobacco Use Among Sexual Minorities in the USA, 1987 to May 2007: A Systematic Review (Tobacco Control 2009:18), certain specific populations continue to be disproportionately affected. The meta-analysis documents statistically a significant higher prevalence of cigarette smoking among sexual minorities than among the general population. Further, within this group, the review also reveals evidence of higher cigarette smoking prevalence among bisexuals, non-college respondents, and black males. Since the existing literature includes minimal information specific to gender minorities, the authors did not, however, assess tobacco use among this particular sub- population and cite this as a limitation. Additionally, little information was found on the use of tobacco products other than cigarettes among sexual minorities.

Sexual and gender minorities (SGMs) include lesbians, gay men, bisexuals, and other persons who do not self-identify as heterosexual; groups defined by sexual behavior, such as men who have sex with men (MSM) and women who have sex with women (WSW); and gender minorities (i.e., persons who do not identify with the gender usually associated with the assigned sex at birth), such as transgender male-to-female or female-to- male. CDC funds efforts by the Lesbian, Gay, Bisexual, and Transgender Tobacco Control Network (http://www.lgbttobacco.org/), a network aimed at raising awareness about the especially high rates of tobacco use among SGMs, and conducts activities to reduce SGM tobacco use prevalence.

As with other historically hard-to-reach populations, SGM research is known to face notable but surmountable methodological challenges. Some national probability surveys, such as the National Survey of Family Growth and parts of the National Health and Nutrition Examination Survey--both conducted by the CDC National Center for Health Statistics--periodically collect data on sexual orientation (i.e., whether respondents self- identify as heterosexual or as straight, homosexual or gay, or lesbian, bisexual, something else, or not sure) but do not ask questions about gender identity. Likewise, some states have sometimes included questions on sexual orientation on their CDC-supported Behavioral Risk Factor Surveillance Survey or Youth Risk Behavior Survey. Survey questions about sexual behaviors such as MSM and WSW are more commonly found, but again, this information is not universally collected. And overall, sexual minority and tobacco use variables are not being consistently defined.

Because of documented higher smoking prevalence among sexual minorities, CDC supports concerted and sustained efforts to enhance the methodological rigor of SGM tobacco-related research. To further document SGM tobacco use disparities, reduce tobacco use initiation, target tobacco cessation efforts, and monitor progress towards reducing tobacco use prevalence, routine collection of both sexual and gender minority demographic data as part of tobacco prevention and control efforts is needed--using consistent and comparable methodologies and definitions. We further agree with the authors that there is a need for additional research to assess reasons for SGM smoking prevalence differences by studying

-Causes of differences in tobacco initiation (e.g., violence, stress, discrimination)

-Tobacco use by sexual identity development

-Tobacco use in SGM social spaces

-Barriers among SGMs to tobacco use cessation (e.g., access to care), and

-The impact of tobacco marketing targeted to SGMs.

Suzanne M. Marks, MPH, MA, Epidemiologist and Chair CDC/ATSDR Sexual and Gender Minorities Work Group

Heather Ryan, MPH Health Scientist CDC Office on Smoking and Health

Bridgette E. Garrett, PhD, MS Senior Health Scientist, Advisor for Health Disparities CDC Office on Smoking and Health

Conflict of Interest:

None declared

In "Tobacco-related disease mortality among men who switched from cigarettes to spit tobacco" Tob Control 2007; 16: 22-28, Henley, et al compared mortality rates for smokers who switched to spit tobacco to the rates for those who quit all forms of tobacco. This is useful information. However, the fact that the number of smokers in the US has remained relatively unchanged for the past 20 years tells us that there are tens of millions of smokers who cannot or will not overcome their dependence on nicotine. Thus, it is vital for tobacco policy makers to establish viable harm-reduction plans. Was there mortality data collected on the group who continued smoking? If so, it would be very useful for the authors to publish a follow-up article that compares the mortality rates for switchers to the rates of those who continued smoking.

In our study in remote Indigenous communities in Arnhem Land we have now interviewed 305 smokers. Of these, 181 had quit intentions and 37 were trying to quit at the time of interview. The effectiveness of more intensive support compared with brief advice has not been evaluated in these populations. However, the need for more intensive support is highlighted in smokers’ own words, for example:

“I’m trying to find a way.” and “I can’t do it on my own.”

In our survey, smokers and non-smokers alike called for more intensive community-based support for smokers to quit, for example:

“… form support groups ….. away from the clinic because they are too busy doing other djama [work].” and “… we need house to house education, every house, clan by clan …”

Our research is trialing interventions that are not limited to quit support. We agree with Thomas and Johnston that population-level interventions have been associated with the steepest declines in smoking prevalence in Australia generally. For Indigenous Australians, especially those living in remote communities, it is not yet known if such smoking reduction initiatives can work. High smoking rates that have not changed in 20 years is evidence that impacts of wider initiatives have not been felt in remote communities.

If we understand him correctly, Ramstrom considered our findings on what has happened in the U.S. too obvious to be interesting. It is obvious because, for over 50 years, Sweden has had a particular smokeless tobacco product, snus, that the US did not have [1]. He apparently considered the history of U.S smokeless tobacco use (which is over 100 years) of no significance and he was confident that the U.S. smokeless tobacco products cannot possibly work to help American smokers quit cigarettes. We did not approach the problem with that perspective. That is why we conducted the study. In our paper, we have considered product difference as part of the explanation in the discussion section [2]. But logic requires us not to attribute the different results between the U.S and Sweden to a single factor when there are so many other contributing factors, including significant cultural differences between the two countries. The way that Ramstrom placed all his confidence in a single factor explanation without making an effort to rule out other strong alternative explanations strikes us as rather unscientific.

Ramstrom also did not like our caution that a significant increase in population smoking cessation may not come from promoting smokeless tobacco in places like the U.S. We believe that the results found in our study justify caution in prediction. The results do not suggest that it will be impossible to increase population smoking cessation rates by promoting smokeless tobacco use. They do suggest that it would require a much more aggressive marketing campaign to get more Americans to use smokeless tobacco than simply getting rid of misinformation about the relative risks of smokeless tobacco and cigarettes. An aggressive promotion of smokeless tobacco products, especially if it comes from both the public health community and the tobacco industry, could change the landscape of tobacco control in a rather unpredictable manner. In many countries nowadays, the tobacco control activities and people’s attitude toward tobacco use are very different from those of Sweden’s in the 1970’s, when snus started to be used by more Swedish men. In fact, we do not even know whether the observed effects of snus on smoking cessation in Sweden were mainly due to the large price differential between cigarettes and snus, which had nothing to with snus being perceived as safer [2]. Again, Ramstrom’s confidence in predicting the future with such limited information seems unfounded.

We welcome Ramstrom’s attempt to present empirical data to compare quitting among current smokers in Sweden and the U.S. It is difficult to find two surveys from two countries that are directly comparable, so some estimation is necessary at this point. However, we have difficulty following his method of analysis because he switched between quit ratio and annual quit rate in his comments. The former is an accumulative rate of former smokers among ever smokers, typically obtained in cross- sectional surveys and not adjusted for population change over time when they are reported from different surveys (for example, if there is a sudden influx of young smokers from year 1 to year 2, the quit ratio of the population can actually go down if analyzed using cross-sectional surveys). The latter is confined to the same cohort of smokers for a particular year, and in our case is followed up longitudinally in 12 months. Ramstrom computed the quit ratio using two cross-sectional surveys and he believed that he has proved the annual quit rates for Swedish men are higher than those of their American counterparts and that this is attributable to the fact that Swedish men used snus. This really doesn’t work. One cannot directly deduce an annual quit rate from the quit ratio in this manner. Since this issue is technically subtle it would be preferable if Ramstrom could present his detailed calculations with a description of the data sets used for calculation as a regular research article. The e-letters format, which does not use a regular peer review process, is not conducive to careful examination of the methodology used. We have tried, but we cannot judge from Ramstrom's comments how he decided that the annual quit rate for the time period considered was higher for Swedish than for U.S male smokers. Our statement that U.S. smokers appear to have higher quit rate is based on the fact that the 6-month abstinence rates are 7.6% and 6.6% for U.S. males and females, respectively, which compared favorably to Rodu et al.’s report of 6.0% and 4.1% for Swedish male and female smokers. These results were reported on page 85 in Zhu et al.’s study [2]. The rates reported in the Rodu et al. study included those who had quit for a long time as well as those who had just quit at the time of the survey [3]. Given that the relapse rate between 6 and 12 months is low, it seems reasonable that the 12-month abstinence rate in the U.S. would not be too much lower than those reported. In any case, we would certainly welcome any empirical analysis that can shed light on this issue. It would be a nice change from continuing this route of debate based on preference of how optimistic or pessimistic one is in predicting the future.

Conflict of Interest: None declared.

Reference:

1. Ramstrom LM. Potential utility of switching to smokeless tobacco. Tob Control eLetter published online June 18, 2009 http://tobaccocontrol.bmj.com/cgi/eletters/18/2/82#2899

2. Zhu S-H, Wang JB, Hartman A, Zhuang Y, Gamst A, Gibson T, et al. Quitting cigarettes completely or switching to smokeless: Do U.S. data replicate the Swedish results? Tob Control. 2009;18:82-87. doi:10.1136/tc.2008.028209 http://tobaccocontrol.bmj.com/cgi/content/full/18/2/82

3. Rodu B, Stegmayr B, Nasic S, et al.. Evolving patterns of tobacco use in northern Sweden. J Intern Med 2003;253:660–665

The study by Zhu et al. "Quitting Cigarettes Completely or Switching to Smokeless Tobacco:Do U.S. Data Replicate the Swedish Results?" has raised a number interesting questions. [1] However, the conclusions of the study need further scrutiny in addition to the previously published comments.

The main conclusion “The Swedish results are not replicated in the U.S.” is certainly true, but not very interesting since it just lays down something very obvious. Sweden’s last 50 years’ development of increasing snus use is built on quite old Swedish traditions and could not possibly have been replicated in a country where Swedish type moist oral smokeless tobacco has not until recently been available altogether and misleading pieces of discouraging information have dominated over evidence-based statements regarding the characteristics of the product.[2]

The statement “Both male and female U.S. smokers appear to have higher quit rates for smoking than have their Swedish counterparts, despite greater use of smokeless tobacco in Sweden.” has very little support in the study, at the same time as there is evidence of the opposite in other scientific sources. The Zhu et al. study reports that 11.6 % of the men who were smoking at baseline declared that they were not smoking at the end of the observation period. But this does not mean that there has been a 11.6 % rate of sustained smoking cessation. It just means that 11.6 % of the initial smokers have started quit attempts that have remained successful up till the end of the observation period. But, it must be assumed that a number of these attempters will relapse, particularly those who started their quit attempt in the later part of the observation period. This assumption is further supported by the observation that a 11.6 % decrease of smoking from 2002 to 2003 appears to deviate from the actual US pattern. The nationwide Behavioural Risk Factor Surveillance Survey, BRFSS, reports a decrease in male prevalence of smoking of just 4.6 % from 2002 to 2003.[3] Further, none of these figures tell us anything about quit rate (ratio between Former Smokers and Ever Smokers). However, from BRFSS data it can also be calculated that in 2003 quit rates in the U.S. population were 0.53 for men and 0.51 for women. Swedish data representing variables defined exactly as these BRFSS data are not available in published sources but present in the more comprehensive database of FSI, The Research Group for Societal and Information Studies. From these data it can be calculated that corresponding Swedish quit rates are 0.63 for men and 0.54 for women. So, Swedish quit rates are markedly higher than those in the U.S. as far as men are concerned and slightly higher for women. Further, the pattern of differences in quit rates between countries and genders is consistent with the corresponding patterns of differences in snus use. A large population study in Sweden has demonstrated that: 1) the gender difference is absent both in the subgroup with snus use and in the subgroup without snus use, and 2) in each gender the quit rates are substantially higher in those with than in those without snus use. [4] These observations, and findings from other Swedish population-based studies, [5, 6, 7] do suggest that the inter-country differences in quit rates may be associated with the use of snus in Sweden. The above statement by Zhu et al. is not consistent with actual evidence.

The statement “Promoting smokeless tobacco for harm reduction in countries with ongoing tobacco control programs may not result in any positive population effect on smoking cessation.” would be true if promotion of smokeless tobacco were seen as a priori unable to achieve actual use of smokeless tobacco for smoking cessation purposes. But, the relevant question is whether or not actual use of smokeless tobacco for smoking cessation purposes can yield a positive population effect on smoking cessation. As pointed out above, Swedish population studies have consistently found a positive association between snus use and increased smoking cessation, particularly in men. These findings are also recognized by various international expert reviews. [8, 9 (p. 109), 10] Similar patterns have been demonstrated in Norwegian population studies. [11,12] A recent US population study suggests that also in the U.S. there are signs that use of smokeless tobacco for smoking cessation purposes are emerging and have higher success rates than those using NRT, just as found in Sweden and Norway. [13] All of these findings come from population-based studies and do then apply to the population level. They also come from countries with ongoing tobacco control programs. These programs do then appear to have taken advantage by being supplemented by the use of smokeless tobacco. Consequently, the above statement by Zhu et al is severely weakened by relevant evidence that is actually available.

After noticing that that the Swedish results have not yet been replicated in the U.S., it is natural to look into a possible future. In that respect Zhu et al. appear to be too pessimistic. Norway has already come quite a bit and, as mentioned above, there are emerging signs of progress in the U.S. as well, and this development may be accelerated if evidence-based public information is strengthened. It should thereby be kept in mind that, according to the Swedish experience, snus can both be an effective temporary aid towards total freedom from nicotine, and, a low -toxicity form for continued nicotine intake for the largely neglected group of smokers who can’t quit using nicotine. Their situation has recently been discussed in a British expert report. [14] For these smokers, quitting nicotine completely is no option. Why not then promote the other option, switching to low-toxicity smokeless tobacco. From health point of view this may be almost as beneficial as quitting completely. [15, 16] This potential utility of switching to smokeless tobacco may eventually, if promoted in a responsible manner, save lives in the U.S. just as in Sweden.

Lars Ramstrom PhD Director Institute for Tobacco Studies Stockholm, Sweden

Email: lars.ramstrom@tobaccostudies.com

Conflict of interest. Owner of shares in Pfizer Inc. Never any funding from tobacco industry sources.

References

1. Zhu S-H et al. Quitting cigarettes completely or switching to smokeless tobacco: Do U.S. data replicate the Swedish results. Tob. Control published online 23 Jan 2009; doi:10.1136/tc.2008.028209.

2. Phillips CV et al. You might as well smoke; the misleading and harmful public message about smokeless tobacco. BMC Public Health. 2005 Apr 5;5:31.

3.National Center for Chronic Disease Prevention and Health Promotion, Behavioral Risk Factor Surveillance System. Prevalence and Trends Data, Nationwide (States and DC) – 2003. (Available at: http://apps.nccd.cdc.gov/brfss/page.asp?cat=&yr=2003&state=UB# accessed June 13, 2009.)

4. Ramström L et al. Role of snus in initiation and cessation of tobacco smoking in Sweden. Tob. Control, 2006 Jun;15(3):210-4.

5. Furberg H et al. Cigarettes and oral snuff use in Sweden: Prevalence and transitions. Addiction 2006:101;1509-1515.

6. Rodu B et al. Evolving patterns of tobacco use in northern Sweden. Journal of Internal Medicine 2003;253:660-665.

7. Furberg H et al. Is Swedish snus associated with smoking initiation or smoking cessation? Tob. Control, 2005 Dec;14(6):422-4.

8. Tobacco Advisory Group of the Royal College of Physicians. Ending tobacco smoking in Britain: Radical strategies for prevention and harm reduction in nicotine addiction. Royal College of Physicians, London, 2008.

9. SCENIHR, Scientific Committee on Emerging and Newly Identified Health Risks. Health Effects of Smokeless Tobacco Products. Brussels: European Commission; 2008. (Available at: http://ec.europa.eu/health/ph_risk/committees/04_scenihr/docs/scenihr_o_013.pdf, accessed June 13, 2009).

10.The European Respiratory Society. Tobacco Smoking: Harm Reduction Strategies - An ERS Research Seminar. Brussels, 2006.

11. Lund K E. The role of snus in the decline of smoking in Norway. Presentation at the 14th World Conference on Tobacco or Health, Mumbai, India, 2009.

12. Scheffels J. Snus as a strategy for smoking cessation. Presentation at the 14th World Conference on Tobacco or Health, Mumbai, India, 2009.

13. Rodu B et al. Switching to smokeless tobacco as a smoking cessation method: evidence from the 2000 National Health Interview Survey. Harm Reduction Journal 2008, 5:18 doi:10.1186/1477-7517-5-18.

14. Tobacco Advisory Group of the Royal College of Physicians. Harm reduction in nicotine addiction: Helping people who can't quit. Royal College of Physicians, London, 2007.

15. Levy DT et al. The relative risks of a low-nitrosamine smokeless tobacco product compared with smoking cigarettes: estimates of a panel of experts. Cancer Epidemiol Biomarkers Prev 2004; 13: 2035-42.

16. Gartner CE et al. Assessment of Swedish snus for tobacco harm reduction: an epidemiological modelling study. Lancet, 2007; 369: 2010- 2014.

We appreciate Dr. Nitzkin’s desire to improve the current FDA bill. Our paper clearly stated that smokers are generally uninformed about the relative risk of various tobacco products and that is an issue that the public health community still must address (1). However, it is important not to equate providing accurate risk information with promoting the use of specific tobacco products. Nitzkin does not seem to make this distinction very clearly (2, 3).

The chief aim of our paper is to provide empirical analysis of available data to increase understanding of what has happened in the U.S. People differ in their predictions of what the overall population effect on smoking cessation will be if smokeless tobacco products are promoted for harm reduction. We believe results reported in Zhu et al. justify the cautionary note in our conclusion (1).

1. Zhu S-H, Wang JB, Hartman A, Zhuang Y, Gamst A, Gibson T, et al. Quitting cigarettes completely or switching to smokeless: Do U.S. data replicate the Swedish results? Tob Control. 2009;18:82-87. doi:10.1136/tc.2008.028209 http://tobaccocontrol.bmj.com/cgi/content/full/18/2/82

2. Nitzkin JL, Rodu B. Promoting snus will save lives in the USA. Tob Control eLetter published online February 6, 2009.

3. Nitzkin JL. Response to Zhu February 24 e-letter. Tob Control, eLetter published online March 24, 2009 http://tobaccocontrol.bmj.com/cgi/eletters/18/2/82#2891

First, an apology is in order for taking so long to respond to the online discussion surrounding the review by Foulds et al. [1] and the opinion piece by Bates et al. [2]. As we had promised in our earlier reply to Foulds et al. (19 December 2003) and have been reminded by Bates, we are belatedly responding to the specific points raised by Foulds et al. in their e-letter dated 5 December 2003:

1. “Misrepresentation of our review.” Our commentary did not misrepresent the conclusions reached by Foulds et al. [1]. We cited their direct quote that snus had “...a direct effect on the changes in male smoking and health” and made the observation that their review added little additional evidence to support that conclusion beyond the spotty evidence cited by Bates et al. (and those two papers had several co-authors in common). Yes, we read their 11 journal pages, 8 figures, 2 table, and 66 references, as well as the 8 journal pages Tobacco Control generously devoted to Bates et al. [2]. No one in the mainstream scientific community questions the underlying premise that exclusive use of snus conveys lower risks for death and disease than does exclusive cigarette smoking. The primary question is whether snus was responsible for the decline in smoking in Sweden and related disease patterns. In support of that hypothesis, Foulds et al. cite sales data from Swedish Match, trend data for tobacco use among men and women age 18–70 years that was unadjusted for age, and cross-sectional data from two northern Swedish counties. That evidence for the role of snus in improving public health does, in fact, provide little additional evidence to what was cited by Bates et al. Foulds et al. make much of the sex differences in use of tobacco products in Sweden to support their hypothesis, yet their reliance on crude (unadjusted) patterns actually masks recent trends in tobacco usage in Sweden and undermines their conclusions. In reality, true age-adjusted smoking initiation rates and cessation rates for males and females in Sweden are essentially equal [3].

2. “Selective reporting of findings”. Foulds et al. acknowledge that they omitted several studies because they were from a part of the country where snus usage was low, claiming that “(b)asing conclusions about snus use in Sweden on a study based exclusively in Malmo is like basing conclusions on smoking and smokeless use in the USA on studies in Utah.” Fair enough, although Foulds et al. had fewer concerns with drawing conclusions about the role of snus in Sweden as a whole based on patterns in northern Sweden.

We stand corrected on our statement that “between 1981 and 2001 daily smoking declined more rapidly for 15-16 year old girls (23% to 16%) than boys (13% to 10%), snus use remained rare among girls, and the sex difference in smoking prevalence decreased.” As the figure presented by Foulds et al. in their electronic letter indicates, the rate of decline in smoking among 15–16-year-olds was about the same for boys and girls. However, that pattern, coupled with a high and increasing level of snus usage among adolescent males in Sweden and very low levels of usage among adolescent girls, provides little support for the conclusion reached by Ramstrom and Foulds [4], two of the authors of the 2003 review paper, that use of snus in Sweden is “associated with a reduced risk of becoming a daily smoker.” If that were truly a causal association, we would expect the initiation rate to be declining more rapidly among boys than among girls due to the much greater growth is snus usage among boys, but it is not. Although there was a 10-fold difference in snus usage between 15–16 year-old boys and girls (20% vs. 2%), smoking initiation exhibited a rather constant and much more modest 3–6 percentage point difference during that time period. Foulds et al. did not respond in their e-letter to broader national trends in Sweden for young males and females that we mentioned in our commentary. We present here more recent data for 16–24-year-olds in Sweden, the age range during which nearly all smoking initiation occurs [3]:

Figure 1. Trends in proportion of persons age 16–24 who used snuff daily or currently smoked (daily or occasionally), by sex. Sweden, 1988–1989 to 2004–2005. Data from Statistics Sweden ULF Surveys.