Snus, nicotine and nicotine addiction
The amount of nicotine absorbed by the individual is determined by complex links between several different but interacting factors. Significant product characteristics include nicotine content, pH values, moisture levels, particle size and physical form. The consumer’s behavior also affects how much nicotine is absorbed.
Swedish snus includes finely ground tobacco with a total nicotine content of about 1.5 to 2.5 percent and it has a pH target value of about 8.5. These levels are traditional for Swedish snus and have remained unchanged for years. However, the pH level of the products declines as they age, meaning concurrently with the storage time. The pH level never increases. In Sweden, snus is stored in coolers before it is sold, which means that the pH levels are more stable than, for example, those of American snuff, which is fermented and is not stored in coolers. For reasons related to process engineering, pH levels are also allowed to vary somewhat in the finished product.
Of the total nicotine content in snus, it is the “free” unbound nicotine that is most easily absorbed by the oral mucous membranes. The pH value of the snus indicates the proportion of free nicotine versus bound (protonated) nicotine. The proportion of free nicotine tends to increase as pH rises.
From an addiction perspective, the rate at which nicotine is absorbed is essential. The daily total nicotine absorption among snus users is about the same as it is among smokers, but for smokers, the brain is exposed within seconds to extremely high levels of nicotine for every cigarette smoked. This is linked to the rapid transfer of nicotine from cigarette smoke to the blood, which is pumped almost directly from the lungs to the brain. Among snus users, the nicotine absorption occurs in the oral mucous membranes first. The blood there does not flow directly to the brain; instead, it must first pass through the entire blood circulation system. Accordingly, the nicotine absorption from snus can never be as rapid as it is from smoking. Because snus users and cigarette smokers have about the same total exposure to nicotine, the EU’s assessment of the health impacts of smoke-free products (SCENIHR, 2008) includes a discussion of whether the higher nicotine absorption rate from cigarette smoking could mean that cigarettes are more addictive than smoke-free tobacco products.
For snus, the nicotine absorption process entails that nicotine is extracted from the snus portion and is then absorbed by the blood vessels in the oral mucous membranes. On average, only about 10 to 20 percent of the nicotine content in a snus portion reaches the bloodstream. Absorption studies also show that nicotine absorption varies greatly among individuals. In a study by Lunell and Lunell (2005), blood levels were monitored during a day of controlled usage of snus, and it was observed that the variation in extraction rates among different snus users was 50 to 300 percent greater than the variation from portion to portion in the same snus user. This contributes to the relatively extensive spread in the results for nicotine absorption. The variation in extraction rates in the study can be partially attributable to the individual’s behavior, meaning the intensity with which the portion is manipulated in the mouth can influence the amount of nicotine extracted. Differences in the production and composition of saliva may also have contributed to the variation.
Like smokers, snus users may experience abstinence-related problems, caused mainly by nicotine withdrawal, when they stop using snus. Studies conducted in the US have shown that the symptoms are the same for smokers as for users of smoke-free tobacco products, but that users of smoke-free tobacco products experienced depression less frequently (Hatsukami and Severson, 1999).
In a study by Holm et al. (1992), smokers and snus users were asked to answer questions about their tobacco habits and various measures of subjective nicotine addiction. No differences were revealed between the snus users and the smokers in terms of self-experienced addiction, the need for tobacco and difficulties in cessation of tobacco use. This result was later confirmed in a snus withdrawal study by Gilljam et al. (2003), which showed equivalent results for snus users and smokers.
Many ex-smokers who now use snus feel that it was less difficult to switch from cigarettes to snus than it is to switch from snus to “nothing”. It is likely that such experiences have contributed to the misconception that snus results in a stronger nicotine addiction than smoking does. A more likely explanation is that it is more difficult to stop using nicotine completely than it is to switch between different tobacco products.
Nicotine addiction caused by tobacco are not governed by product characteristics and consumer behavior alone. Hereditary factors may also be highly significant. In a study by True et al. (1997) that included identical and fraternal twins, it was observed that 50 percent of the probability that an individual would begin smoking could be explained in terms of hereditary factors, and that continued smoking was determined by genetic background to an even greater extent (70 percent). Genetic differences in the ability to release dopamine and other signal substances in the brain could be part of the explanation for these results.
To sum up, it is evident that a specific nicotine content in a snus product with a specific proportion of free nicotine (depending on the pH level) does not result in a given nicotine absorption in an individual snus user. Rather, there is extensive individual variation. In a snus user, nicotine absorption can also vary from portion to portion. Other product characteristics and consumer behavior that is partially determined by underlying genetic factors also play a major role.
REFERENCES
Andersson, G., Björnberg, G., and Curvall, M. 1994. Oral mucosal changes and nicotine disposition in users of Swedish smokeless tobacco products: A comparative study. J. Oral Pathol. Med. 23:161-167.
Andersson, G., Axéll, T., and Curvall, M. 1995. Reduction in nicotine intake and oral mucosal changes among users of Swedish oral moist snuff after switching to a low-nicotine product. J. Oral Pathol. Med. 24:244-250.
Gilljam, H., Rankka, M., and Langworth, S. 2003. Smokeless tobacco cessation with NRT: a feasabilty study. Poster at the Fifth European Conference of the Society for Research on Nicotine and Tobacco, Padova, Italy.
Hatsukami, DK., and Severson, HH. 1999. Oral spit tobacco: addiction, prevention and treatment. Nicotine Tob. Res. 1:21-44.
Holm, H., Jarvis, M.J., Russell, M.A.H., and Feyerabend, C. 1992. Nicotine intake and dependence in Swedish snuff takers. Psychopharmacology 108:507-511.
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Lunell, E. and Lunell, M. 2005. Steady-state nicotine plasma levels following use of four different types of Swedish snus compared with 2-mg Nicorette chewing gum: A crossover study. Nic. Tob. Res. 7:397-403.
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SCENIHR Report: Health effects of smokeless tobacco products, 2008
True, WR., Heath, AC., Scherrer, JF., Waterman, B., Goldberg, J., Lin, N., Eisen, SA., Lyons, MJ., and Tsuang, MT. 1997. Addiction 92:1277-1287.
