Cigarette smoke contains over 4,000 substances, including at least 50 carcinogens. Levels of tar and nicotine in cigarettes have decreased in the past few decades; however, levels of certain carcinogens have increased. Cigarette smoking is the major cause of chronic bronchitis and emphysema. Approximately one fifth of heart disease-related deaths are attributable to cigarette smoking. Lung cancer caused by smoking is currently the leading cause of cancer deaths in the United States. Smoking also contributes to the development of at least 10 other types of cancer, including cancers of the oral cavity, larynx, esophagus, pancreas, stomach, bladder, and cervix.

Recent literature indicates that certain cultural, genetic, and other factors may provide important information about causes of smoking initiation and progression to nicotine addiction.

Prevalence rates for cigarette smoking also have shown important ethnic and gender differences. For example, smoking initiation is more common among White high school students than among non-White students. This discrepancy is especially pronounced in adolescent females. Over two times as many White females smoke compared to African American females. Ethnic and gender differences in risk factors for initiation may include differential effects of peer and family influence and different perceptions of the negative consequences of smoking. Different cultural expectations from smoking may also contribute to these differences; for example, White female adolescents may be at increased risk due to expectancies that smoking helps control weight and mood.

Researchers have not been able to identify an addictive personality or a group of personality factors that are common to all cigarette smokers. However, certain personality traits are consistently associated with smoking behavior, including higher stress, lower arousal, higher impulsivity and sensation seeking, and neuroticism.

Results from family, adoption, and twin studies indicate that smoking initiation results largely from genetic influences (about 50–60%) and shared environmental influences (about 20%, higher for adolescent onset). Factors contributing to progression to nicotine dependence are primarily genetic (about 70%). Current research on candidate genes for nicotine dependence has focused on genes that may influence the rewarding effects of nicotine, craving for nicotine, and sensitivity to nicotine.

Treatment for nicotine dependence includes self-help, psychological, and pharmacological interventions. Unaided attempts to quit have shown less than a 10% success rate in leading to long-term abstinence. Advice from a physician has been found to lead to cessation rates of up to 10%. Behavioral therapy alone has demonstrated quit rates of 20%. The most promising results have been shown by combined use of medication and behavioral therapy.

Psychological interventions for quitting smoking include psychoeducation (information about smoking and health, quit strategies, and group discussion), behavioral skill training (monitoring situations, practicing cigarette-refusal skills, and relaxation techniques), and cognitive exercises such as reframing thoughts about smoking and smoking situations.

The most common pharmacological treatment used for nicotine addiction is nicotine replacement therapy (NRT). NRT involves administration of nicotine in various forms, including a skin patch, a nasal spray, an oral inhaler, and a chewing gum. These medicinal forms of nicotine prevent symptoms of nicotine withdrawal without inducing the reinforcing effects of smoking. Long-term (6–12 months) abstinence rates for treatment with NRT alone are about 20–25%. Higher abstinence rates may occur when several NRT methods are used together (e.g., patch and gum). Combined with behavioral therapy, long-term abstinence rates may be up to 35–40%.

Another pharmacologic treatment for nicotine dependence is bupropion hydrochloride or Zyban, the first nonnicotine agent approved for cessation of smoking. Cessation rates using bupropion range from 10% to 25%, depending on the dose. The proposed mechanism of bupropion involves reduction of craving and a decrease in the physiological symptoms of nicotine withdrawal.

Finally, researchers are currently examining the possibility of a nicotine vaccine. In animal models, antibodies specific to nicotine have been shown to alter the distribution, and thus the pharmacological effects, of the substance. The proposed vaccine may act by either reducing the uptake of nicotine by the brain or inhibiting the reinforcing effects of nicotine. This vaccine, if effective, is expected to be most beneficial to adolescents who smoke but have not yet become dependent. Other groups that may benefit from such a vaccine are adolescents who have not yet begun smoking, current smokers who are trying to quit smoking, and former smokers interested in avoiding relapse.

Annie R. Peters, Kent E. Hutchison, University of Colorado at Boulder