for many debilitating or fatal diseases. Smoking tobacco, using snuff, and ingesting
other smokeless tobacco have become pervasive around the world.
The primary active ingredient in tobacco is nicotine, which has stimulant properties
that appear to increase SNS arousal and alertness and to reduce appetite.
Once tobacco use is established as a habit, it is highly resistant to change.
Among tobacco users, the relief from withdrawal, appetite suppression,
arousal, and sensation of well being associated with tobacco make it a very desirable
behavior (Kassel 1997, Parrott et al 1996).
Smoking and other forms of tobacco use are major contributors to heart disease,
hypertension, stroke, cancer, and several serious diseases of the lungs
and airways. These effects are generated by a combination of constituents and
smoke associated with smoking tobacco as well as by tobacco itself. Tobacco
use also affects endocrine and immune system activity (e.g. Canals et al 1997,
Mol et al 1993). Direct effects of tobacco use underlie its broad negative impact
on health (e.g. Lykkesfeldt et al 1997). Passive exposure to tobacco
smoke is also a problem, and research suggests that it has many effects consistent
with exposure to nicotine (Hausberg et al 1997).
Because of the difficulty in getting people to stop using tobacco once they
have started, considerable attention has been paid to prevention, particularly
with children and adolescents (e.g. Chassin et al 1997). Risk factors for smoking
vary by culture, but in the United States, adolescent cigarette smoking has
been associated with perceived availability of cigarettes, cost, social models,
social pressures, and mental health (Robinson et al 1997, Milberger et al 1997,
Wang & Chou 1996, Unger et al 1997). The combination of social pressures
and immediate reinforcers may induce people to try smoking when they do not
intend to smoke (Engels et al 1997). Prevention efforts are most effective when
continued for long periods (Eckhardt et al 1997), but a recent meta-analysis
suggests that the average effect of social programs is small (Rooney & Murray
1996). Stress is one cause of tobacco use. Smoking and tobacco use appear to
reduce stress or ameliorate its aversive effects (e.g. Viinamaki et al 1997, Todd
et al 1996, Naquin&Gilbert 1996, Ogden&Mitandabari 1997). Smoking also
alters acute stress responses. Smokers exhibit greater increases in peripheral
resistence than nonsmokers during challenge (Girdler et al 1997). The synergistic
effects of stress and smoking may heighten the negative effects of smoking
and increase the incidence of tobacco-related illnesses (Maser 1997).
Stress increases the amount and frequency of tobacco use (e.g. Steptoe et al
1996, Acierno et al 1996, Beckham et al 1996).
Stress also appears to be a major cause of relapse after cessation and often
leads to resumption of smoking (Shiffman et al 1996, Matheny&Weatherman
1998). Newer approaches to cessation and relapse prevention hold some promise
for success, appropriate motivation, and pharmacological adjuncts, while
addressing individual level of addiction and recognition of barriers and supports
(Lichtenstein & Glasgow 1997). Consideration of openness to change
may also increase the efficacy of interventions by matching people to all ap-propriate intervention and fashioning changes in pre-contemplation behavior
(e.g. Parrott et al 1996).
