Snus, nicotine and nicotine addiction

Snus and other smokefree tobacco products contain nicotine, which can lead to addiction through its effect on the neurotransmitters in the brain’s reward system. Some important considerations in this context are how much of the nicotine in the portion pouch that is absorbed into the bloodstream and how quickly it reaches the brain. Genetic factors have also been shown to be extremely important in the development of nicotine addiction.

A person’s absorption of nicotine is the result of a complex interaction between several different factors. Product characteristics such as nicotine content, pH value, moisture content and particle size and physical shape are important. The consumer’s behavior also affects how much nicotine is absorbed.

Swedish snus is finely ground. It has a total nicotine content of about 1.5–2.5%, and a standard pH of about 8.5. These levels are traditional for Swedish snus, and have remained unchanged over the years. But the pH value of the products declines as they age, in other words with time spent in storage. The pH never rises. In Sweden snus is kept refrigerated before it is sold, which does more to stabilize the pH value than is the case with American snus, which is fermented and not refrigerated. The pH is also allowed to vary somewhat in the finished product for process engineering reasons.

Out of the total nicotine content of snus, “free” unbound nicotine is most easily absorbed via the buccal mucosa. 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 the pH rises.

The speed of absorption of nicotine is extremely important from an addiction standpoint. The daily total nicotine absorption among users of snus is roughly the same as for smokers, but smokers’ brains are exposed to extremely high nicotine levels within seconds with each cigarette. This is due to the rapid transfer of the nicotine in the cigarette smoke to the blood, which is pumped directly from the lungs to the brain. Users of snus absorb nicotine in the buccal mucosa. The blood does not go directly to the brain — it must first pass through the entire circulatory system. Therefore nicotine can never be absorbed as rapidly from snus as from smoking. Since users of snus and cigarettes exhibit roughly the same total nicotine exposure, an EU report on the health effects of smokefree products (SCENIHR, 2008) discusses whether the more rapid absorption seen with smoking could mean that cigarettes are more addictive than smokefree tobacco products.

Nicotine absorption from snus involves the extraction of nicotine from the portion pouch, followed by the absorption of the extracted nicotine into the blood vessels in the buccal mucosa. On average only 10-20% of the nicotine in the portion pouch reaches the blood vessels. Absorption studies also demonstrate that nicotine absorption varies widely between individuals. In Lunell and Lunell’s study (2005), where blood levels were monitored during a day of controlled snus usage, it was observed that the variation in the degree of extraction between different users of snus was 50-300% greater than the variation from portion to portion for the same user of snus. This contributes to the relatively large distribution in the results for nicotine absorption. The variation in the degree of extraction in this study can be partially explained by the fact that individuals can affect how much nicotine is extracted through their behavior, in other words how energetically they “work” the portion in their mouths. Differences in saliva production and composition may also have played a role.

Users of snus can experience difficulty with abstinence as smokers do when they stop using their respective product, which is primarily caused by nicotine addiction. Studies performed in the US have demonstrated that the symptoms are the same for smokers and users of smokefree tobacco products, with the exception that users of smokefree products experience depression less frequently (Hatsukami and Severson, 1999).

In a study by Holm et al. (1992), smokers and users of snus were asked to answer questions about their tobacco habits and various measurements of subjective nicotine addiction. There was no difference between users of snus and smokers concerning self-perceived addiction, the need for tobacco or difficulties in stopping its use. These results were later confirmed in a study of snus withdrawal by Gilliam et al. (2003), with equivalent results for users of snus and smokers.

Many former smokers perceive the experience of moving from cigarettes to snus as less difficult than moving from snus to “nothing.” Experiences like these have probably contributed to the misconception that snus produces a stronger nicotine addiction than smoking. The more likely explanation is that it is more difficult to stop using nicotine entirely then to switch between different tobacco products.

Nicotine addiction caused by tobacco is not determined by product characteristics and consumer behavior alone. Genetic factors are also extremely important. In a study by True et al. (1997), the subjects were identical and fraternal twins. It was observed that the probability that a person would start smoking was 50% attributable to genetic inheritance, and that continuing to smoke was determined by the inherited background to an even greater extent (70%). These results may be partially explained by genetic differences in the ability to release dopamine and other neurotransmitters in the brain.

In summary, a given nicotine content in a snus product with a given share of free nicotine (depending on the pH value) does not imply a given amount of nicotine absorption by an individual user of snus. This varies widely between individuals. It can also vary from portion to portion for an individual user of snus. Other product characteristics and individual consumption behaviors, partly determined by underlying genetic factors, also play a large 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.
Lund, KE. 2008. Presentation at the 51st Conference of the International Council on Alcohol and Addictions.
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.
Ramström, L.M. and Foulds, J.  2006.  Role of snus in initiation and cessation of tobacco smoking in Sweden.  Tobacco Control 15:210-214.
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