The story I have long believed is that it is nicotine that addicts smokers to tobacco products but that it is the other compounds in tobacco (e.g. tobacco specific nitrosamines) which cause medical problems such as cancer.
Hence one way to encourage people to stop smoking is to provide NRTs (nicotine replacement therapies) such as nicotine patches, gums, nasal sprays or inhalers to deal with the chemical dependence and, by so doing, eliminate the ingestion of other health-damaging compounds from cigarette smoke. The idea is to use NRTs to break the physical dependence of nicotine as the smoker breaks the behavioural cues that trigger smoking.
In fact these sorts of pharmaceutical interventions have been tried often without a great deal of success (Balfour and Fagerstrom). The reasons are various – the NRTs may be inappropriately used, may release nicotine to the brain too slowly or be used by low-intensity smokers who are smoking-dependent but not dependent on nicotine.
There are in fact over 4000 chemicals in cigarette smoke many of which could potentially contribute to dependence on tobacco. The consensus has been that nicotine is the major component of tobacco responsible for addiction.
Commenter ‘dany le roux’ suggested (in remarks on an earlier post) that nicotine may not be the only addicting agent when tobacco is smoked. Nicotine definitely seems to be a major addicting agent through its action on nicotinic acetylcholine receptors and the downstream release of dopamine. However non-nicotinic components of tobacco smoke may also play a role by inhibiting monoamine oxidase (MAO) activity and subsequently altering neurotransmitter levels – this might enhance the addictiveness of nicotine by providing anti-depressant effects.
As I understand it dopamine releases can be stimulated in the brain directly by nicotine or other chemicals may inhibit the action of those chemicals which destroy dopamine. It is conjectured that both processes go on when cigarette smoke is ingested. A simple discussion is here.
A survey of recent research in this area is provided in the survey article by A. Lewis, J.H. Miller & R.A. Lea. Understanding these issues may lead to more effective pharmacotherapies for smoking cessation that utilise these MAO inhibitors. Several MAO inhibitors have already been trialled – these are discussed in the Lewis et al. paper.
The issue of policy importance here is that it may be fallacious to put all weight on NRTs as a cessation therapy. They have not performed that well to date perhaps for the reasons discussed above. It would be interesting to find out whether 'smokeless tobacco' products such as snus outperformed NRTs in delivering MAO inhibitors or if these products are only delivered by smoke.
I’ll keep a watchout on this literature – thanks to dany for the tip on MAOs.