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Commentary

Harm reduction: lessons learned from tobacco control

Journal of Psychopharmacology 20(3) (2006) 329–330

By Marcus R. Munafò Department of Experimental Psychology, University of Bristol, Bristol, UK.

The proposal that morbidity, mortality and social costs, associated with alcohol use may be reduced by developing alternatives to alcohol (either as lower-strength versions of existing alcoholic drinks, or by developing pharmacological alternatives to alcohol) is a rational argument applied to an irrational (i.e. addictive) behaviour. The history of harm reduction efforts in the field of tobacco control suggest that likely benefits will be attenuated by the ultimate desirability of correlates of the harm-inducing properties of a substance, such as the psychoactive effects of the substance. How do harm reduction efforts fare when exposed to the harsh realities of the world, and what can be learned from the experiences of the tobacco control community in the implementation of harm reduction strategies?

The delivery device of the cigarette is a large part of the reason behind the addictive potential of smoking, delivering a bolus of nicotine to the brain in approximately 10–15 seconds (Shiffman et al., 2005). This generates marked arterial spikes of nicotine concentration following a puff, which typically occur in the context of a range of multi-modal cues (e.g. tastes, smells, locations, etc.) that themselves acquire incentive salience as a result (Berridge and Robinson, 1998). The best illustration of the results of this process is the relative lack of efficacy of nicotine replacement therapy for smoking cessation, where the odds ratio for active nicotine replacement therapy versus placebo is approximately 2.0 (Stead and Lancaster, 2005), against a backdrop of a base rate for cessation of less than 5% (Stead and Lancaster, 2005). Given the disparity between the delivery of nicotine via cigarette and via nicotine replacement therapy (which offers slow delivery of a relatively low dose), it is little wonder that nicotine replacement therapy is so ineffective – to paraphrase the cigarette advert: ‘It isn’t a Marlboro’.

The powerful control of nicotine over behaviour is illustrated in the most common harm reduction strategies spontaneously employed by cigarette smokers: switching from high tar to low tar cigarettes, or reducing the number of cigarettes smoked. These strategies do not substantially reduce tar exposure (Jarvis et al., 2001; Hecht et al., 2005;), since the tar and nicotine content of manufactured cigarettes is derived from ‘machine-smoked’ readings, and these machines ‘smoke’ cigarettes in a standard way which bears little or no resemblance to how people smoke cigarettes. When a smoker moves from a high tar to a low tar cigarette brand, or cuts down on the number of cigarettes smoked per day, it is possible (often unconsciously) to modify subsequent smoking behaviour to titrate the amount of nicotine (and therefore tar) extracted from each cigarette to suit the smoker’s needs (Hammond et al., 2005). This can be done by taking more puffs, inhaling more deeply, closing the filter vents on the cigarette with one’s fingers, and so on. The greatest irony is that commercially available de-nicotinized cigarettes are potentially the most harmful, as smokers will inhale extremely deeply in a futile effort to extract nicotine (Dunsby and Bero, 2004).

This serves to illustrate the powerful influence, at least in dependent individuals, of the need to maintain circulating levels of the drug, and the extent to which behaviours can be modified, both consciously and unconsciously, to achieve this. Therefore, offering lower strength drugs, for example, may simply lead to an increase in the volumes consumed. While pharmacological alternatives which offer comparable psychoactive effects might be attractive, it is likely that the development of these remains some distance in the future. There is also a question regarding whether marketing a substance as ‘healthier’ (which would almost certainly be done by the manufacturers) may have harmful consequences itself: it should be remembered that filtered and low tar cigarettes were both marketed as ‘healthier’ options (Warner, 2005), as low nitrosamine cigarettes are today.

There is encouraging evidence that harm reduction strategies, such as the promotion of low nitrosamine smokeless tobacco products, may be effective (Levy et al., 2004; Levy et al., 2005), although their implementation remains controversial. Nevertheless, the single most effective means of tobacco control, to date, has been the reduction in availability achieved through taxation and other control measures (Wilson and Thomson, 2005). While this may disproportionately target those for whom health disparities are greatest (Wilson and Thomson, 2005), it is nevertheless the case that increased taxation on tobacco products is associated with reductions in smoking prevalence. Recent exercises in the banning of smoking in public places appear also to be reducing the prevalence of smoking (Frieden et al., 2005) by restricting availability. This is in marked contrast to the recent relaxation of alcohol licensing laws in the United Kingdom. It is likely, therefore, that efforts to reduce the harmful consequences of alcohol will require strong political will.

References


Corresponding author: M. R. Munafò, Department of Experimental Psychology, University of Bristol, 8 Woodland Road, Bristol, BS8 1TN, UK.
Email: marcus.munafo{at}bristol.ac.uk


© 2006 British Association for Psychopharmacology
ISSN 0269-8811
SAGE Publications Ltd, London, Thousand Oaks, CA and New Delhi
10.1177/0269881106063046