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Bast RC Jr, Kufe DW, Pollock RE, et al., editors. Holland-Frei Cancer Medicine. 5th edition. Hamilton (ON): BC Decker; 2000.

Cover of Holland-Frei Cancer Medicine

Holland-Frei Cancer Medicine. 5th edition.

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Chapter 25Prevention of Tobacco-Related Cancers

, MD, , PhD, , PhD, and , PhD.

In the United States, approximately 46.3 million people smoke, and nearly 400,000 people die prematurely each year from tobacco-related diseases. This includes 151,000 deaths from cancer, 179,800 from cardiovascular diseases, and 84,500 deaths from respiratory diseases. Cigarette smoking remains the greatest cause of preventable mortality in the United States.1

Americans have dramatically altered their smoking behavior since the first Surgeon General’s report on tobacco was released in 1964. At that time, approximately 40% of the U.S. population smoked; in 1987, it was 29%. The smoking rate is higher among African Americans (34%) than among whites (29%). Smoking is inversely related to level of education; 36% of those without a high school diploma, 33% with a high school diploma, 26% with some college, and 16% of college graduates smoke.1 There also is a similar pattern of higher smoking rates among blue-collar and service workers compared with whitecollar workers. Tobacco use is influenced heavily by the tobacco industry’s $2-billion annual advertising and marketing campaigns. Women, minorities, blue-collar workers, adolescents, and even children are bombarded by clever and often insidious marketing and advertising gimmicks.

Richard Peto2 estimates that worldwide, 3 million deaths were attributed to smoking in 1995, and that by 2025, there will be approximately 10 million such deaths, 7 million of which will occur in the developing world. For instance, more than 70% of men aged 25 and older in the People’s Republic of China smoke cigarettes. At current smoking rates, there will eventually be approximately 2 million deaths per year directly related to smoking. Worldwide cigarette smoking is the largest single cause of premature death.

This chapter reviews the pathogenesis and epidemiology of smoking-related cancer. It also discusses addiction, prevention, and cessation of tobacco use.

Physiochemical Composition of Tobacco Smoke

In 1992, the U.S. Environmental Protection Agency classified environmental tobacco smoke as one of the most dangerous cancer-causing agents in humans, a group A carcinogen. Tobacco smoke consists of more than 4,000 chemical compounds and approximately 60 known carcinogens. Half of these compounds occur naturally in the green tobacco leaf while the remainder are generated when the tobacco is burned. The complex mixture of chemicals in tobacco smoke includes carbon monoxide, hydrogen cyanide, benzene, formaldehyde, N-nitrosamines, nicotine, phenol, polycyclic aromatic hydrocarbons (PAHs) and tobacco-specific nitrosamines (TSNAs). It should be noted that only the particulate phase, approximately 5% of the cigarette’s total output, is visible.

For risk assessment, tobacco smoke has been classified as either mainstream smoke or sidestream smoke. Mainstream smoke is that which is inhaled through the column of the cigarette and filter tip. In contrast, sidestream smoke is emitted from a burning cigarette between puffs and inhaled by nonsmokers. Although the chemical compositions of mainstream and sidestream smoke are similar, the concentration of many constituents is higher in sidestream smoke. The primary source of environmental tobacco smoke is sidestream smoke.

Nicotine, the second most abundant constituent of tobacco smoke, is responsible for the addictive properties of tobacco and represents a major source of TSNAs.3 It is present in both mainstream and sidestream smoke and is rapidly absorbed in the alveoli of the lungs. Nicotine is concentrated in the pulmonary veins as a bolus and circulated throughout the body. Subsequent activation of cholinergic receptors in the brain and modulation of hormones such as epinephrine and cortisol4 is believed to lead to nicotine dependence. Recent studies from Spitz and colleagues5 have suggested that polymorphisms in the D2 dopamine receptor gene may contribute to nicotine dependence.

Carcinogenic and Genotoxic Effects of Tobacco Constituents

Both tobacco smoke and smokeless tobacco contain compounds that can initiate tumors, promote the development of previously initiated tumors, or act as cocarcinogens. Tumor initiation has been associated with the neutral subfractions rich in PAHs, while promotion has been associated with the weakly acidic subfractions.3 Cancer types appear to be compound specific. For example, an association between TSNA exposure and cancers of the lung, larynx, esophagus, and pancreas has been suggested. In contrast, exposure to 4-aminobiphenyl and certain arylamines has been linked to bladder cancer.6 The involvement of benzene (from tobacco smoke) in smoking-induced leukemia has been implicated.7

Efforts to study the carcinogenic effects of cigarette smoke in animal models have been met with limited success. Classic tobacco carcinogenesis studies have been performed by painting cigarette smoke condensate (CSC) onto the skin of rodents. Although CSC itself failed to cause tumors under these conditions, CSC significantly increased the incidence of skin tumors in animals previously exposed to β-irradiation.8 One explanation for this exclusive tumor-promoting activity of CSC is that rodent skin is unable metabolically to activate the tumor initiators (PAHs) present in tobacco smoke. In contrast, exposure of xenotransplanted human bronchial epithelial cells to CSC in vivo has produced invasive neoplasms.9

Subsequent use of animal inhalation models to evaluate the carcinogenic effects of tobacco smoke has been compromised by the inability of most animals to inhale as deeply as humans. In these studies, animals are placed in chambers and exposed to alternating short periods of tobacco smoke and dilute air, followed by air alone. An excess incidence of respiratory tumors has been observed in smoke-exposed mice, rats, dogs, and hamsters (the latter develop laryngeal tumors only) as compared to unexposed controls. The overall incidence has been low, and tumors have been predominantly adenomas and alveologenic adenocarcinomas.3

Of all of the compounds in tobacco smoke, the potent carcinogenicity of PAHs (i.e., benzo(a)pyrene) and TSNAs, specifically 4-(methylnitrosamino)-l-(3-pyridyl)-l-butanone (NNK), has been most extensively documented. Polyaromatic hydrocarbons and NNK induce pulmonary tumors in rodents at doses similar to those experienced during a lifetime of smoking.10 Metabolic activation of PAHs and NNK leads to the irreversible binding of these carcinogens to DNA or the formation of bulky DNA adducts. While chemical carcinogens prefer to bind to guanine, the specific position within this base is dependent upon the chemical properties of the carcinogen. Aromatic amines such as 4-amino-biphenyl prefer to bind to the C8 position, while PAHs such as benzo(a)pyrene bind preferentially to the N2 position of DNA. When left unrepaired, these adducts can induce gene mutations, converting cells to a preneoplastic phenotype. The resulting G-to-T (B(a)P and NNK) and G-to-A (NNK) transversions have been detected in lung tumors from smokers.11 Activation of oncogenes and tumor suppressor genes by these adducts has been suggested. PAHs such as benzo(a)pyrene induce G-to-T transversions in the 12th codon of the ras proto-oncogene.12 Administration of NNK to hamsters leads to mutational activation of Ki-ras in resulting lung tumors.13 A direct correlation has been established between mutations in the tumor suppressor gene p53 and extent of tobacco smoke exposure.14

DNA adducts from tobacco exposure are present in many tissues from smokers, including lung, bronchus, larynx, kidney, bladder, esophagus, liver, aorta, and placenta.15 Adduct levels correlate with the amount smoked and the duration of exposure,16 and they decrease in a time-dependent manner following smoking cessation. The rate at which adducts are removed from DNA is dictated by the activity of DNA repair enzymes. Deficiencies in the repair enzyme O6-alkyl-DNA-alkyltransferase have been observed in fibroblasts from lung cancer patients.17 The potential use of DNA adduct levels as biomarkers of cancer risk remains to be determined.

Genetic Variation in Cancer Susceptibility

Detoxication enzymes play a pivotal role in protecting individuals from environmental carcinogens, including the PAHs found in tobacco smoke. These enzymes have been categorized into two groups based on their functional properties. Phase I enzymes, including the cytochrome P450s, metabolically activate xenobiotics as well as endogenous substances (i.e., fatty acids, steroid hormones) to highly reactive electrophiles (i.e., epoxides and reactive oxygen species). Phase II enzymes inhibit the activity of these oxidative intermediates both by competing with the phase I carcinogen-activating enzymes and catalyzing the conversion of reactive electrophiles to inactive, water-soluble conjugates. It is the cellular balance between phase I and phase II enzymes that profoundly influences one’s risk of developing chemically induced cancer.

Several enzyme systems involved in the metabolism and detoxication of xenobiotics exhibit genetic polymorphisms that have been associated with differential susceptibility for cancer. Epidemiologic and clinical data continue to suggest that polymorphisms in select phase I and II detoxication enzymes may serve as biomarkers of increased risk for smoking-related cancers.

Phase I Enzymes


Cytochrome P450 2D6 (CYP2D6) is responsible for converting the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone to highly reactive metabolites.18 Debrisoquine, an antihypertensive agent, is metabolized solely by CYP2D6 and serves as a phenotypic marker of enzyme activity. Numerous polymorphisms in this gene have been identified and correlated with variability in the extent of drug metabolism. This has led to the classification of individuals as either recessive poor metabolizers (approximately 9%) or homozygous/heterozygous dominant extensive metabolizers.19 Initial studies demonstrated that individuals who exhibited the extensive metabolizer phenotype (as determined by the ratio of unchanged debrisoquine to 4-hydroxydebrisoquine in the urine) had an increased risk of lung cancer as compared to poor metabolizers.20,21 In contrast, several additional phenotypic analyses have failed to confirm the contribution of this polymorphism to lung cancer susceptibility.22–24 Although the mutation responsible for variable drug metabolism has been identified,25 results from DNA-based assays remain equivocal.26

An association between the extensive metabolizer phenotype and increased risk for bladder and cervical cancer has been suggested.27–29 Stratification of drug-metabolizing activity by stage of bladder cancer revealed a stronger association with the more aggressive stage III disease.27 In addition, high debrisoquine recovery ratios were found to correlate with bladder tumor recurrence.28 Female smokers who were extensive metabolizers were at increased risk of developing cervical intraepithelial neoplasia.29 In contrast to bladder cancer, progression of cervical intraepithelial neoplasia to squamous cell carcinoma occurs less frequently in extensive metabolizers.29


Cytochrome P450 1A1 (CYP1A1) is an inducible microsomal enzyme that oxygenates carcinogenic PAHs such as benzo(a)pyrene to facilitate their ultimate detoxication and excretion.30 CYP1A1 is expressed in normal and malignant lung tissue from smokers, while low expression is detected in nonsmokers.31 Nicotine has been identified recently as a potent and rapid inducer of pulmonary CYP1A1, suggesting its ability to accelerate the metabolism of carcinogens in cigarette smoke.32 High inducibility of the gene product, aryl hydrocarbon hydroxylase, in select individuals has been attributed to polymorphisms in the CYP1A1 gene33 and correlated with high DNA adduct levels.34 Several studies have demonstrated that a point mutation in exon 7 of CYP1A1 (NcoI polymorphism) occurs more frequently in lung cancer patients than in noncancer controls.35,36 The documented increased risk for lung cancer among female smokers has been attributed in part to gender-based differences in CYP1A1. The frequency of the CYP1A1 (NcoI) polymorphism was significantly greater among female lung cancer patients than among controls.37 Findings from an independent study indicate that CYP1A1 expression is significantly elevated within the lungs of female smokers as compared to males.34

Initial studies in Japanese patients with an enzyme’s restriction fragment length polymorphism(RFLP), an MspI RFLP in the 3', noncoding region of CYP1A1, reported a relative risk of 3.21 for squamous cell lung cancers.38 Additional investigations in similar Japanese populations have confirmed the association of the MspI polymorphism with increased lung cancer risk.33 Studies to examine this polymorphism in Caucasian lung cancer patients have produced negative results.39–42 Recent evaluation of smoking data from the Nurse’s Health Study suggested that females with the MspI polymorphism who start smoking before age 18 may be at increased risk for breast cancer.43

A polymorphism in CYP1A1 that is unique to African Americans has been described.44 Data from Taioli and colleagues45 indicate that individuals with the variant allele are at increased risk for adenocarcinoma of the lung (OR 2.6, 95% CI, 1.1–6.3). A strong interaction with smoking was also apparent. In contrast, no association was observed between this polymorphism and lung cancer risk in a larger African American population when individuals were stratified for other risk factors, including occupational exposure and micronutrient intake.46


Cytochrome P450 2E1 (CYP2E1) catalyzes the oxidation and DNA adduct formation of benzene, nitrosamines, and other carcinogens.47 A polymorphism in the CYP2E1 gene has been associated with lung cancer in Japanese populations.48 A cigarette dose-dependent effect was noted in one of these studies.48 This association has not been replicated in Caucasians. However, the CYP2E1 polymorphism, when combined with polymorphisms in either the CYP2D6 or GSTM1 gene, has been strongly associated with lung cancer risk, producing odds ratios of 14.0 and 6.0, respectively.49

Phase II Enzymes


Although N-acetyl transferase is classified as a phase II enzyme, its ability to both inactivate and activate arylamines has been suggested.50 Corresponding acetylation rates (slow versus rapid) are controlled by a single gene. Slow acetylation is an autosomal recessive trait that occurs in approximately 50 to 60% of Western populations, compared with 10% among Asians. Slow acetylators are less efficient in detoxifying arylamines, which are potent bladder carcinogens.51 The prevalence of bladder cancer among male smokers in the United States has been attributed to the carcinogenic arylamines in tobacco smoke.52 Slow acetylators possess higher levels of tobacco-related arylamine hemoglobin adducts than rapid acetylators, and adduct levels increase with the number of cigarettes smoked per day.53 Data from several studies provide further support for these observations and suggest that slow acetylators are at increased risk for bladder cancer.54,55 In contrast, most phenotypic and genotypic analyses of lung cancer patients have failed to reveal an association between acetylator status and cancer risk.56,57 Drozdz et al.58 found that a significant proportion of patients with cancer of the larynx (84%) possessed the slow acetylator phenotype as compared to 60% of controls. An association between risk for postmenopausal breast cancer and the slow acetylator genotype has been established with respect to smoking dose.59


The glutathione S-transferases (GSTs) are a family of enzymes that catalyze the conjugation of PAHs and other toxic intermediates with glutathione. The resulting conjugate is more water soluble and more readily excreted from the body. The gene encoding the M1 isozyme is absent in approximately 50% of the general population.60 This polymorphic expression, when combined with the ability of M1 to inactivate highly reactive epoxides such as the benzo(a)pyrene-4,5-oxide,61 has prompted a detailed investigation of the role of the null genotype in determining personal susceptibility to a variety of cancers. Several studies have suggested an association between the GSTM1-null genotype and increased risk for various smoking-related cancers. A recent meta-analysis of the relationship between GSTM1 status and lung cancer risk in 12 case-control studies classified the GSTM1-null genotype as a moderate risk factor for all histologic subtypes of lung cancer (OR = 1.4).62 The unavailability of standardized data on smoking history prohibited the analysis of this variable. Several independent investigations have demonstrated that patients with both the mutant CYP1A1 and GSTM1-null genotypes are at a significantly increased risk of developing lung cancer.33,63 Individuals with the combined genotype metabolically activate carcinogens at a fast rate but are less efficient in providing cellular protection from the resulting reactive intermediates.

Strategies for Cessation

Upwards of 46% of adult smokers make at least one “quit” attempt annually, yet fewer than 14% are able to remain abstinent for 30 days.64 Hence, identifying effective treatments to help boost short- and long-term cessation rates has become increasingly important. The past decade has witnessed a burgeoning of research aimed at achieving this goal65–68 by exploring the therapeutic elements predictive of abstinence (e.g., motivation to quit, pros and cons for quitting, social support, problem-solving skills, tailored treatments) and by evaluating the effectiveness of behavioral and pharmacologic treatments.

A thorough review of smoking cessation interventions was recently conducted by the Agency for Health Care Policy and Research (AHCPR).67,68 With regard to behavioral cessation treatments, this review concluded that while self-help treatments do not produce notably high cessation rates, individual or group cessation interventions and physician-based treatments that provide support and encouragement, education, and problem-solving skills training can produce substantial smoking abstinence rates. Also, since there is a dose-response relationship between the intensity and duration of behavioral smoking cessation interventions and their effectiveness,69 more intense behavioral interventions (i.e., more sessions and therapeutic modalities) are considered to be more effective in producing long-term smoking abstinence. Moreover, the most effective behavioral interventions are those which are tailored to characteristics of the population, such as individuals’ readiness to change, their unique health risks, or their specific ethnic/cultural barriers.67

The AHCPR guidelines also reviewed the efficacy of pharmacologic therapies,67 including nicotine replacement therapies (NRTs; i.e., nicotine patch, gum, nasal spray, inhaler), while other literature reviews have assessed the benefits of bupropion (Zyban), an antidepressant that operates as a dopamine reuptake inhibitor.66 Currently, accumulated data indicate that the spectrum of available NRTs and non-nicotine treatments (e.g., Zyban) significantly enhance behavioral smoking cessation treatments,65 supporting their use in a comprehensive smoking cessation treatment.

Therefore, current state-of-the-science treatment guidelines indicate that all smokers should be offered a combination of behavioral therapy (i.e., social support, education, and skills training) and adjunctive pharmacologic treatment.68,70 The effects of behavioral and pharmacologic treatments are independent and additive, with the combination of the two modalities yielding the highest cessation rates.68 Although the additive effects of tailored behavioral approaches and pharmacologic treatments have yet to be fully explored, current research suggests that such an approach would be uniquely effective at promoting smoking abstinence. Next, we review the current literature concerning a variety of behavioral and pharmacologic interventions for smoking cessation.

Self-Help Methods

The majority (80–90%) of smokers interested in quitting or of those who have successfully quit report using a self-help method,71 including “cold-turkey” or self-help manuals (e.g., Clear Horizons).72 The popularity of self-help manuals is due to their low cost, easy access, and absence of the barriers that accompany assisted forms of smoking cessation treatments (e.g., lack of insurance reimbursement), rather than to their greater efficacy.66 On the one hand, a meta-analysis of self-help cessation studies concluded that self-help manuals result in a 20% abstinence rate at 1 year post treatment.73 On the other hand, the AHCPR review of this literature reported that self-help materials were no more effective at producing smoking abstinence than no intervention, since they resulted in a cessation rate of about 9% versus the 8% rate produced by no intervention.67,68

The effectiveness of self-help guides can be increased by tailoring manuals to the individual’s stage of change or to specific barriers to cessation. Prochaska et al.74 compared the effects of standard self-help manuals to those individualized to the person’s stage of change on long-term smoking abstinence. Whereas 9% of smokers who received standard manuals remained abstinent at an 18-month follow-up, close to 20% of smokers who received tailored manuals remained abstinent. Likewise, the inclusion of telephone counseling with self-help manuals has been shown to boost cessation rates. Curry et al.75 found that smokers who received telephone counseling in addition to self-help manuals reported significantly higher abstinence rates than smokers who received self-help manuals only. Similarly, Orleans, Schoenbach, et al.76 reported that self-help manuals plus telephone counseling outperformed self-quitting materials alone, with 18% of smokers receiving telephone counseling reporting 7-day point prevalence abstinence versus 11% of smokers receiving self-help manuals alone. Finally, two studies have demonstrated the benefits of including computer-generated, tailored-feedback messages with a self-help manual. Prochaska et al.74 found that computer reports (i.e., based on stage-appropriate processes of change) in addition to a self-help guide more than doubled point prevalence abstinence rates when compared to a generic self-help manual by itself (25% versus 10%). Strikingly, the computer-enhanced condition almost tripled the maintenance rates of a standard self-help guide at an 18-month follow-up (14% versus 4%). More recently, Velicer et al.77 compared a stage-matched computer intervention that provided tailored written cessation instructions (i.e., the expert system) to a stage-matched self-help manual alone. Among smokers who received a stage-matched manual, 7-day point prevalent abstinence at an 18-month follow-up was 15.5%, with 6.4% remaining abstinent for at least 6 months. In contrast, among smokers in the expert system condition, 7-day point prevalent abstinence at 18-months was 21.3%, with 9.3% remaining abstinent for at least 6 months.

Formal Smoking Cessation Clinics

In general, these programs offer tailored help in the form of social support, education, and problem-solving/skills training.68 The social support component involves the provision of encouragement to quit (e.g., setting a quit date), the development of the smoker’s sense of self-efficacy to quit, the expression of concern about the individual’s desire to quit, and provision of the opportunity for the smoker to discuss cessation worries and concerns (e.g., weight gain, irritability) as well as cessation achievements (e.g., quitting for 24 hours). Education involves the provision of information about the harmful effects of continued smoking, what to expect from withdrawal, and various methods available to assist with smoking cessation. Finally, training in coping skills consists of relapse prevention through identifying and avoiding high-risk situations (e.g., being with smokers, and at bars and parties), teaching smokers how to employ specific coping strategies (e.g., distraction), encouraging rewards for abstinence, assisting smokers with managing the adverse emotional effects of quitting with stress reduction techniques, and arming smokers with strategies to stave off potential negative outcomes from smoking (e.g., monitoring diet to avoid weight gain).

Overall, a review of close to 40 studies by the AHCPR concluded that assisted smoking cessation programs that offer these three therapeutic elements are generally effective at producing long-term smoking abstinence. Averaging across studies, compared to a no-contact control group, individual and group counseling resulted in cessation rates of 15.1% and 15.3%, respectively.68 These rates are significantly better than the 9.3% rate of those assessed with self-help interventions. Also, a dose-response effect exists such that quit rates are positively correlated with the intensity and duration of the given intervention.67 Whereas minimal contact interventions (i.e., < 3 minutes per contact) resulted in an estimated cessation rate of 10.7%, the rate for interventions that lasted for more than 10 minutes per contact yielded a cessation rate of 18.7%. Likewise, interventions that lasted 2 to 4 weeks yielded a cessation rate of 15.6% whereas treatments lasting more than 8 weeks produced a cessation rate of 23.8%.

Scheduled smoking, a behavioral technique that has recently been incorporated into assisted smoking cessation treatments, may further boost the cessation rates of formal assisted programs. This technique allows smokers to gradually reduce their dependence on tobacco by having them smoke on a predetermined schedule in which the interval between cigarettes is progressively lengthened. The assumption is that individuals can wean themselves of the physiologic dependence by reducing tobacco intake. In addition, since smoking is scheduled, it takes place without the environmental cues to smoke (e.g., after dinner), thereby removing contingency reinforcements associated with smoking. Cinciripini et al.78 found that, when paired with stress management, coping skills training, and relapse prevention, 44% of smokers who quit according to scheduled smoking remained abstinent at 1 year, compared to 18% who quit using a nonscheduled gradual reduction method and 22% who received only the cognitive-behavioral cessation program. This result suggests the need to further examine the benefits of scheduled smoking technique within formal behavioral smoking cessation programs.

Physician-Based Interventions

Since approximately 70% of all smokers visit their primary care physician at least once each year, it has been increasingly recognized that physician-based smoking cessation messages represent a viable approach to boosting abstinence rates.79 In fact, several professional and government agencies have been outspoken in an attempt to convince physicians to play a larger role in the implementation of smoking cessation interventions.67

A sizable literature illustrates the effectiveness of physician-based smoking cessation treatments even when such interventions are extremely brief. A study by Morgan et al.80 compared a group of primary care practices that received a brief training program based on the AHCPR guidelines (i.e., ask, advise, assess, assist, and arrange) to a matched comparison group that later received the intervention. Six-month follow-up data showed that 15.4% of patients who received the physician-based intervention reported 7-day abstinence in comparison with 8.3% of control patients. More recently, Leischow et al.81 compared the abstinence rates associated with the nicotine patch to those produced when brief physician smoking cessation advice was added. While abstinence rates for the NRT condition reached 9% at a 1-year follow-up, the rates for NRT plus physician advice reached 12.5%. Likewise, Secker-Walker et al.82 compared abstinence rates for pregnant women who received a physician-based smoking cessation intervention to women who received a self-help manual at the first prenatal visit. At 1 year post partum, 18% of women provided with the physician-based intervention were abstinent, compared to 11% of women provided with a self-help manual. In addition, while 40% of women in the physician-based smoking cessation intervention reduced their smoking consumption by at least 50%, only 25% of women in the self-help condition reported such a reduction.

Unfortunately, physician-based interventions are not common. Recently, Goldstein et al.83 questioned over 3,000 smokers who had seen primary care physicians in the preceding 12 months. The findings showed that 51% of smokers were talked to about their smoking, 45.5% were advised to quit, 14.9% were offered assistance, 3% were provided with a follow-up appointment to track smoking cessation, and 8.5% were provided with an NRT or a non-nicotine pharmacologic medication. Likewise, a larger study evaluated trends in the treatment of smokers by U.S. ambulatory care physicians.84 The proportion of visits in which a patient’s smoking status was identified dropped from 67% in 1994 to 61% in 1995. Of the 17,632 physician visits by smokers, 3,302 (or 22%) provided smokers with smoking cessation counseling, and NRT was provided to 161 patients (or 1%). In order to facilitate the assessment of smoking status and the provision of cessation material and referrals by physicians, the AHCPR recommends that (1) health-care delivery practices must change so that smoking cessation interventions are institutionalized; (2) clinicians and their patients must be reimbursed by insurers for counseling and pharmacotherapy; (3) the content of interventions must be tailored to the patient’s readiness to quit; and (4) the standards of health care must include an obligation to provide timely and effective smoking cessation assessments and interventions.

Pharmacologic Interventions

There has been extensive research in the area of pharmacologic smoking cessation treatments over the past decade. Currently, a broad range of NRTs (e.g., nicotine gum) and non-nicotine pharmacotherapies (i.e., Zyban) are available. The AHCPR recommends that all smokers be offered some form of NRT unless there is a clear medical contraindication.67 Although NRTs are effective at reducing smoking, they are recommended in conjunction with behavioral therapies.65 More recently, in light of strong evidence that depression plays a significant role in determining smoking cessation rates,85 the Food and Drug Administration (FDA) approved buproprion (i.e., Zyban), a dopamine reuptake inhibitor, for use in smoking cessation. Although the efficacy of Zyban has not been extensively examined, recent studies suggest that it represents a promising new treatment for nicotine addiction that should be incorporated into behavioral smoking cessation treatments.65

Nicotine Gum

One of the most used and well-researched NRTs is nicotine gum (e.g., Nicorette). The AHCPR, after reviewing three meta-analytic studies concerning the efficacy of nicotine gum, concluded that (1) nicotine gum improves cessation rates by 40 to 60% at a 1-year follow-up, compared with control interventions; (2) abstinence rates are highest when the gum is paired with a behavioral therapy (e.g., skills training), compared to the gum only; and (3) there is a dose-response effect for heavy smokers, with the 4-mg dose being more effective than the 2-mg dose.68 However, the efficacy of nicotine gum decreases over time and is largely dependent on the contribution of adjuvant behavioral therapies.65 Indeed, the efficacy of this NRT has been shown to be related to the intensity (i.e., duration) of accompanying behavioral therapy.67 Moreover, the gum’s efficacy is limited by low compliance due to such factors as inconvenience, side effects (e.g., burning, nausea), and bad taste. Consequently, although nicotine gum has been shown to be an effective NRT (versus placebo or a no-gum control), it should be viewed as only one dimension of a comprehensive cessation program.

Transdermal Nicotine Patch

“The patch” (i.e., Nicotrol and Nicoderm) is also a popular and well-researched NRT. Compared to the gum, the patch is associated with fewer compliance problems, produces fewer side effects, and requires less clinician involvement for patient training. Hence, this NRT is considered preferable to nicotine gum.69 Further, meta-analytic studies show that the patch can double cessation rates when compared with placebo and can significantly increase cessation rates when added to a behavior therapy.67 For instance, 2-month abstinence rates among smokers provided with the patch was 36% compared to 20% among smokers given a placebo.86 Further, Cinciripini et al.87 examined the effects of behavior therapy alone to behavior therapy plus the patch on 1-year cessation rates. In the behavior therapy condition, 22% of participants were abstinent at 1 year, compared to 38% of those who received the patch in addition to behavior therapy. Moreover, Fiore et al.88 showed that 19.5% of smokers given the patch and low-intensity behavior therapy remained abstinent at 6 months, compared to 26.5% of smokers given a high-intensity behavior therapy along with the patch. Finally, in recent studies that examined the combined effects of nicotine gum and the patch, data revealed that despite immediate benefits of combining these NRTs, the advantage disappeared at 1-year follow-ups, indicating this approach to have an inconsequential effect on long-term smoking rates.89,90

Nicotine Nasal Spray

Nicotrol NS—a nicotine nasal spray—is one of the most recent NRTs available to help smokers remain abstinent. The spray is thought to be effective since it closely mimics the delivery process of smoking and has a faster nicotine uptake rate compared with other NRTs.65 To date, little systematic research on the spray has been conducted, and the spray can produce adverse side effects (e.g., nasal irritation). In a placebo-controlled study, analyses at a 3-month follow-up showed that 10% of smokers given a placebo spray were abstinent, compared to 24% of smokers given the spray.91 However, the difference in abstinence rates was not significant at 6- and 12-month follow-ups. Further, in a randomized double-blind study,92 there was no difference in abstinence rates at 1 week following study initiation between the nicotine nasal spray and a placebo nasal spray. Likewise, a study with smokers who had relapsed after using other NRTs indicated that the nasal spray was ineffective at producing significant abstinence rates.93 Based on these data, no unequivocal conclusions can be formulated concerning the effectiveness of the nasal spray for producing smoking abstinence, though additional research to examine the immediate and long-term impacts of the nicotine nasal spray on abstinence rates is warranted.70

Nicotine Vapor Inhaler

Like the nicotine nasal spray, the inhaler is a newly developed NRT that may be more effective than the patch or the gum since it was devised to meet the psychological as well as the physiologic needs of those addicted to cigarette smoking.94 Unfortunately, since the inhaler has been only recently developed and marketed, it has not been adequately researched. One study, however, did indicate that the inhaler may be effective in producing short-term gains in smoking abstinence. Schneider et al.91 randomly assigned smokers to either an active (i.e., inhaler) or placebo condition and tracked abstinence rates for 12 months. At 3 months, significant differences in abstinence rates were noted, with 24% of smokers using the inhaler reporting abstinence versus 10% of placebo smokers. Although individuals in the inhaler condition had higher abstinence rates at 6 months (17% versus 9%) and at 12 months (13% versus 8%), these differences were not statistically significant. Despite these initial encouraging results, additional systematic research concerning the efficacy of the inhaler is needed before more conclusive recommendations can be offered.

Non-nicotine Medications (Zyban)

Several lines of research suggest an association between a greater likelihood of being a smoker and having more difficulty with quitting on the one hand and a history of (or current) depressive symptoms on the other.85 These findings have sparked interest in, and the recent development of, non-nicotine pharmacotherapies for use in smoking abstinence (e.g., the antidepressant bupropion, sold under the brand name Zyban). Unpublished marketing data from Glaxo Wellcome, the manufacturer of Zyban, indicate that Zyban can improve cessation rates over a placebo, when paired with behavioral therapies.65 One independent double-blind placebo-controlled study with a 1-year follow-up randomly assigned 615 smokers to receive placebo or sustained-release bupropion at a dose of 100, 150, or 300 mg/day for 7 weeks.95 Participants in all conditions also received physician advice to quit, self-help guides, encouragement to set a quit date, and follow-up cessation messages throughout the study. The findings showed that each of the Zyban dosages outperformed the placebo up to 3 months (24.2%, 26.1%, and 29.5%, respectively, versus 14.4%). At the 6-month and 12-month assessments, only the 150 mg/day and the 300 mg/day dosages outperformed the placebo (27.5% and 26.9% versus 15.7%, and 22.9% and 23.1% versus 12.4%, respectively). In addition, Jorenby et al.96 randomly assigned 244 smokers to receive a placebo, the patch alone, bupropion alone, or both bupropion and the patch and followed the sample for 12 months. Abstinence rates at 12 months were 15.6%, 16.4%, 30.3%, and 35.5%, respectively. These findings indicated that treatment with bupropion either alone or in combination with the patch produced abstinence rates that were significantly greater than those produced by either the nicotine patch or placebo. Although the combination treatment produced the highest abstinence rate (35.5%), it was not significantly different from bupropion alone (30.3%). Overall, these data indicate that Zyban represents a promising new pharmacologic smoking cessation aid.

Tailoring Smoking Cessation Interventions for Special Populations

Certain segments of the population exhibit disproportionately higher rates of smoking,97 report lower rates of success with cessation,98 and are uniquely susceptible to certain adverse smoking-related health consequences.67 Further, there is substantial variability in the degree to which an individual is prepared or “ready” to quit—a motivational variable that affects sustained smoking cessation.99 Finally, population-specific barriers to quitting and motives for smoking must be considered when targeting interventions to subgroups of smokers most in need of cessation aids.67 Few controlled, randomized studies, however, have evaluated the comparative impact on cessation rates of tailored versus generic cessation interventions.67 Nevertheless, several studies have shown that cessation treatments that (1) are tailored to the individual’s readiness to change,99 educating individuals about their distinctive vulnerability to tobacco-related health problems;100 (2) are designed to consider culturally-relevant barriers or motivators to quitting101 or age-relevant barriers and motivators to quitting;102 or (3) are targeted towards inpatient medical populations103 can significantly enhance intention and self-efficacy to quit and boost abstinence rates. The following sections summarize the literature concerning the effects of tailored interventions to stage of change and for minority smokers, women, adolescents, older smokers, and cancer patients.

Stage of Change

Much of the development and implementation of behavioral smoking cessation interventions has been guided by the transtheoretical model (TTM).104 The TTM uses a five-stage classification scheme to categorize individual “readiness to change,” with lower stages (e.g., precontemplation) reflecting current use and low intention to quit and higher stages (e.g., action, maintenance) representing smoking cessation and the intention to stay abstinent. In addition to staging individual motivation to quit, the TTM provides a conceptual framework for understanding the key psychosocial variables (i.e., processes of change) related to movement through the stages towards abstinence. These include cognitive processes (i.e., consciousness raising, weighing of the pros and cons, self-efficacy), social factors (i.e., social support), and behavioral and problem-solving strategies (i.e., removing reminders of smoking). These variables have been linked to progression towards smoking abstinence,105 converging with the AHCPR outline of the key therapeutic elements of effective behavioral cessation interventions.

Stage-matched interventions recognize that different processes of change promote cessation more effectively with individuals at different stages. For instance, while behavioral processes such as counter-conditioning (i.e., choosing healthy behaviors instead of smoking) may prove beneficial for those in later stages, such processes can reduce the likelihood of cessation among individuals in earlier stages. For individuals in the stage of precontemplation, enhancing their awareness of the detrimental effects of continued smoking has been shown to be more effective at progressing them to the stage of contemplation. Overall, little data are available to fully evaluate the relative benefits of stage-of-change-tailored interventions and generic treatments. Nevertheless, one study did indicate that such an individualized intervention can effectively help individuals progress through the TTM stages and promote higher rates of cessation. This large controlled intervention study compared a generic self-help manual to three different stage-matched conditions.74 Each of the stage-matched interventions outperformed the generic condition at an 18-month follow-up assessment. Analyses of point prevalence abstinence rates indicated that about 17% of smokers in the tailored self-help manual condition were abstinent, compared to approximately 10% in the standard self-help manual condition. Stage-matched interventions which target TTM processes (e.g., pros and cons, self-efficacy, avoiding tempting situations) appear to effectively help individuals progress through the TTM stages, in turn producing a significant increase in successful quitting, compared to non-stage-matched interventions. This approach also provides a way to effectively intervene with entire populations, not just motivated quitters. Nevertheless, additional research is needed to replicate these findings and to extend them to more diverse populations.

Minority Smokers

Certain ethnic groups exhibit disproportionately higher rates of smoking and suffer higher tobacco-related morbidity and mortality (e.g., lung cancer), compared with the majority population.64 Although smoking prevalence has begun to decline in the United States among whites, this decrease has been much more gradual among minorities.64 While 24% of American adults are current smokers, 36% of American Indians, 26% of African Americans, 18% of Hispanic Americans, and 51% of Laotian and 42% of Vietnamese Americans are current smokers.64 Further, rates of smoking among African Americans with low socio-economic status and certain Hispanic groups (e.g., Cuban Americans) are as high as 40-50%.64 The United States Department of Health and Human Services report106 indicated that certain minority groups are at greater risk for certain tobacco-related health consequences (e.g., lung and cervical cancer). Moreover, ethnic minorities, particularly African Americans, exhibit low quit rates and are less knowledgeable about the adverse health consequences of smoking.107 The tendency to smoke brands higher in nicotine, poor access to health services, high rates of life stress, and exposure to tobacco advertising, more common among minority groups, hinders smoking cessation efforts as well. Hence, there is a critical need for cessation programs tailored to be more pertinent, unique, and available to these groups, and which address the specific factors that contribute to smoking among minorities.64

Smoking cessation materials and programs tailored to the cultural and linguistic characteristics of several ethnic groups have been developed.106 Few such programs, however, have been systematically compared to generic approaches. One study developed and evaluated an intervention for African American smokers, randomizing 1,422 smokers to either a generic self-help manual or to a cessation guide tailored to the unique smoking patterns and quitting needs and barriers of this under-served population.101 At 6-months following the intervention, smokers in the tailored condition reported significantly more quit attempts and greater use of pre-quitting strategies (i.e., setting a quit date, reducing the numbers of cigarettes smoked per day, and switching to cigarettes with lower nicotine). Although there was no difference in 1-week abstinence rates, quit rates at the 12-month follow-up were significantly higher among smokers in the tailored intervention, compared with quit rates for smokers in the generic condition (25% vs. 15.4%).

Hispanic smokers have also been targeted by smoking cessation initiatives with tailored programs including: a self-help manual addressing the specific attitudes, beliefs, and values of Hispanic smokers, emphasis on using the family as a source of support for cessation, a Spanish electronic media campaign, community outreach services, quit-smoking raffles, and culturally-tailored cessation counseling. An evaluation of this program showed that exposure to the intervention correlated with fewer cigarettes smoked per day, more quitting attempts, and greater knowledge concerning sources of quitting materials.108 However, cessation rates were unaffected, and no comparison condition was studied. A more recent study suggests that this program’s effectiveness can be improved by including mood management information. Munoz et al.109 compared the effectiveness of the self-help guide to the self-help guide plus a mood management audiotape intervention. While only 11% of smokers provided with the cessation guide reported abstinence at a 3-month follow-up, 23% of smokers provided with the guide and mood management instructions were abstinent.

Finally, the paucity of studies with high-risk Asian American and Native American smokers is discouraging. A recent study did target a smoking cessation campaign towards Vietnamese American men.110 The treatment included Vietnamese-language antitobacco billboards, television ads, and self-help manuals and kits, a continuing medical education course on smoking cessation counseling methods for Vietnamese physicians and antitobacco ordinances. The risk of becoming a smoker was significantly lower, and the probability of quitting smoking significantly higher, among members of the intervention community compared with rates observed in a no-contact control community. Likewise, a recent study used a physician-based intervention to promote cessation among Native American smokers.111 Smokers were assigned to receive either brief physician advice to quit and cessation materials (e.g., self-help and NRT instruction) or standard medical care. Although intervention smokers reported higher self-reported abstinence rates (7.1% versus 4.9%), a greater number of quit attempts and a higher intention to quit, urinary cotinine-validated abstinent status was equal across the groups (6.7% and 6.8%, respectively). Further evaluations of smoking cessation interventions that include counseling and pharmacologic cessation aids is needed for ethnic groups. Counseling should address the unique barriers to quitting common across ethnic groups, namely, lack of knowledge concerning the harmful effects of tobacco, lack of information about how to quit, a tendency to attribute the etiology of cancer to non-tobacco-related causes, social norms that facilitate smoking, lack of social support, high stress and competing life priorities, lack of financial resources, and the use of smoking as a coping strategy.98

Women Smokers

The decline in smoking evident over the past several decades has been much slower among women.112 At the same time, the rates of lung cancer among women have been steadily increasing, with women smokers 1.5 times more likely to develop lung cancer than men.113 Lung cancer is now the leading cause of cancer deaths among women, killing about 68,000 women each year.114 Female smokers have the added risk of the health consequences of smoking during pregnancy, such as an increased risk for low infant birth weight, spontaneous abortion, stillbirth, and maternal complications such as placenta previa and abruptio placentae.115 Although smoking among pregnant women has dropped in recent years, the rate among pregnant women 15 to 19 years of age has increased between 1990 and 1996.116 In light of these data, cessation programs targeted towards women smokers, especially those who are pregnant, is a priority highlighted in the AHCPR report.

Increasing women’s awareness of the adverse health effects of smoking can boost cessation rates.100 For instance, the strongest motivator to quit among women smokers undergoing Pap smear tests was the awareness that smoking might cause cervical cancer.117 Motivation to quit can also be influenced by having the support of others who want the smoker to quit. A recent intervention study assessed the efficacy of a multi-component cessation program that emphasized support and encouragement to quit.118 The data showed that while 14.5% of the 516 female smokers provided with the cessation program were abstinent several months following the intervention, only 7.7% of control subjects had quit. Lastly, since concern about weight gain can diminish the effectiveness of cessation programs for women, adding weight management components to cessation programs could boost abstinence rates. A recent study demonstrated that 10% of women randomly assigned to receive behavioral cessation counseling (e.g., education) were abstinent at the end of treatment, compared to 19.4% of women provided with exercise instruction in addition to the behavioral counseling.119 Follow-up at 3 and 6 months also showed higher abstinence rates among the group with exercise plus counseling cessation condition (16.4% and 11.9%), compared to women receiving only cessation counseling (8.2% and 5.4%).

With regard to predictors of smoking among samples of pregnant smokers, awareness about the harmful effects of continued smoking and partner support for quitting have also been identified as key predictors of abstinence.120 Further, several meta-analytic studies have shown that randomized controlled studies of smoking cessation interventions for pregnant smokers effectively reduce smoking rates.121 Even minimal-contact interventions—especially when they are tailored—can significantly reduce smoking behavior.122 For instance, a study of 393 pregnant smokers examined the effectiveness of formal physician cessation advice combined with individual smoking cessation counseling with that of a self-help manual.82 A higher quit rate among the women who received the physician advice (18%) compared to the self-help manual (11%) was noted; moreover, a greater proportion of women in the physician advice condition reported a 50% or more reduction in their cigarette consumption by the second prenatal visit, compared to women in the self-help group. In a similar study, Secker-Walker et al.123 compared prenatal cessation advice, a tip sheet, and a cessation video (that modeled how to deal with bad feelings and urges to relapse and how to elicit social support) to cessation advice and a tip sheet. While 19% of the women in the videotape condition were abstinent at the end of their pregnancy, 0% of the women in the comparison group had quit.

Although the use of NRTs may improve cessation rates, their use among pregnant smokers remains controversial. Nicotine given to female rats during gestation can produce loss of tolerance to neonatal hypoxia, thereby causing sudden infant death syndrome.124 The potential harmful effects of NRTs for pregnant women may be outweighed by the range of health benefits to be accrued from smoking cessation among women, especially pregnant smokers. However, given the unknown potential for nicotine-caused changes in fetal brain structure and brain function, caution still is indicated. To date, treatments that include physician advice, boosting the women’s awareness of the harmful effects of smoking, and instruction in coping strategies and methods for eliciting support have proven successful. Adding weight management components to cessation programs may further improve quit rates.


Dr. David Kessler, the former head of the U.S. Food and Drug Administration (FDA), characterized tobacco addiction as a “pediatric disease” and has stated that “adolescents are the gateway through which tobacco addiction enters the population.”125 Indeed, upwards of 90% of adult smokers begin tobacco use before age 18, and four out of five persons use tobacco before they reach adulthood.125 More alarming are data indicating that the overall prevalence of cigarette use among adolescents increased from 27.5% in 1991 to 36.4% in 1997.126 With nearly 3,000 young people beginning to smoke each day, an estimated 6.1 million adolescents are current smokers.127 Of additional concern among male adolescents is the 6 to 8% prevalence rate of smokeless tobacco use.128,129

Most tobacco control studies with adolescents have examined strategies to prevent adolescent smoking, rather than focusing on cessation.130 The few cessation programs for adolescents that have been examined have mostly been school-based programs, which provide adolescents with information about the adverse health impact of smoking and teach adolescents skills to combat the pressure of peers and the media. Descriptive evaluations of these programs suggest that smoking rates decline; however, comparison groups are rarely included.127 A more innovative study examined the efficacy of a cessation clinic which used the expert system to provide computerized cessation messages tailored to the individual’s stage of change.131 High 6-month cessation rates (20%) among adolescents randomly selected for the intervention were reported. The paucity of research in this area indicates a substantial need for additional evaluations of tobacco cessation interventions for adolescents.127 Such interventions hold promise for reducing smoking rates since they can capitalize on the high level of interest in cessation reported by adolescents.132 Since cognitive (e.g., quitting self-efficacy, perceived benefits of quitting), emotional (e.g., low levels of depression), and social (e.g., number of friends who smoke) factors have been identified as predictors of successful cessation among adolescents,133–135 these processes should be the targeted by adolescent tobacco cessation programs.

Similarly, few systematic evaluations of smokeless tobacco cessation programs have been conducted.127 Moreover, although the intervention studies that have been conducted have generally yielded successful results, the data are limited by small sample size and lack of comparison groups.136 One study evaluated the efficacy of a smokeless-tobacco cessation self-help manual for high school seniors, which urged social contracting and peer education and provided relapse prevention advice.137 The results showed that 26% of participants completely quit and that 42% of participants made at least one quit attempt. Moreover, studies of the use of dental visits as an opportunity to provide smokeless tobacco cessation messages have provided encouraging results (see Smokeless Tobacco, below). In the context of smokeless-tobacco use, cigarette smoking and participation in sports are strong predictors of continued use, as well as psychosocial factors such as use and approval by peers and self-described risk-taking personality.129,138 Cognizance of these predictors should guide the implementation and evaluation of smokeless-tobacco interventions for adolescents.

A recent Blueprint for Action for youth and young adult tobacco cessation provides a framework to guide research in this area.139 Consistent with this report is the need for the study of interventions that use brief, physician-based cessation messages that emphasize the economic, health, and physical-appearance benefits of cessation. Further, these interventions should be tailored to address the specific barriers to smoking cessation among adolescents (e.g., peer pressure) that affect regulation. Lastly, although NRTs are not specifically approved for use with adolescents, including NRTs with behavioral therapies may enhance cessation rates, although their effectiveness in this population remains largely unexplored.

Older Smokers

Upwards of 13% of individuals over the age of 50 smoke,140 and the rate of decline in smoking has been much slower among older adults compared to younger adults.141 With much of the focus today on smoking prevention in youths, older smokers are at risk for being ignored by tobacco control researchers and health professionals, despite being uniquely vulnerable to several adverse health consequences such as cardiovascular disease and, among men, erectile dysfunction.142 Since older smokers started smoking at a time when smoking was marketed as safe, fashionable, and glamorous, they are less convinced of the adverse effects of smoking on health, report lower perceptions of risk from their smoking, and are more likely to believe that smoking has not negatively affected their health.143

Studies have shown that cessation among longtime smokers can still reduce the risks for cardiovascular disease and cancer among older individuals.144 Although few well-controlled intervention studies have targeted this population, some evidence suggests that physician-based interventions can effectively promote cessation. One randomized study compared standard medical care to a brief physician-based cessation intervention that included physician advice to quit and counseling.80 At a 6-month follow-up, 15.4% of intervention participants had quit smoking, compared with 8.2% of control participants. Other research has utilized the Clear Horizons self-help guide, a manual specially designed to educate older smokers about the benefits of quitting, to help these individuals overcome the barriers unique to them, and to provide them with detailed quitting advice and support. One study compared this manual to a generic self-help guide and to a condition of receiving Clear Horizons and two cessation support calls.102 The findings indicated a cessation advantage for smokers randomized to the tailored guide plus the phone calls, compared with the other two conditions. Future research is needed to systematically assess the added benefits of NRT as an adjunctive cessation tool to these behavioral treatment modalities for older smokers.

Cancer Patients

Most cancer patients continue to smoke after their diagnosis.145 This is of particular concern since smoking cessation among cancer patients can significantly improve survival, reduce the likelihood of disease recurrence and the development of a second primary tumor, diminish treatment-related complications, and reduce the risk of noncancer smoking-related diseases, such as heart disease.66 In light of such data, AHCPR guidelines encourage the implementation of hospital-based smoking cessation interventions. These interventions may be particularly effective since hospital visits represent a “window of opportunity” when the smoker is particularly aware of their susceptibility to the adverse consequences of smoking and is uniquely motivated to participate in cessation treatments.146

Unfortunately, few data are available concerning predictors of smoking abstinence among patients, making it difficult to tailor interventions for this population.103,147 The few available studies have focused mainly on medical (e.g., extent of disease), demographic (e.g., age), and smoking (e.g., extent of addiction) variables,145 without assessing the role of key psychosocial variables. Moreover, despite the fact that physician-based interventions have been shown to be effective in producing high cessation rates, only two controlled studies have been conducted in the cancer context. Gritz et al.148 randomized patients with head and neck cancer to either usual care (that included physician advice to quit) or a smoking cessation intervention that included a written date-to-quit contract, tailored self-help booklets, and booster advice to remain abstinent. Although the results showed high quit rates among both conditions (usual care, 77%; intervention, 64%), there was no distinct advantage to the intervention. A second study randomized cancer patients to either a brief smoking cessation intervention (e.g., discussion of the physiologic and psychological benefits of cessation, the importance of setting a date to quit, and techniques to manage withdrawal symptoms) or a usual-care condition.149 Despite a small sample, 21% of intervention patients were abstinent at a 6-month follow-up, compared with 14% in the control group. In light of the well-documented benefits associated with smoking cessation for cancer patients, coupled with high patient motivation to quit, cessation programs with this population is an important direction for researchers to pursue.

Smokeless Tobacco

The use of smokeless tobacco among men, especially athletes and those in the military, is a serious public health concern. Since 1970, smokeless tobacco has changed from a product used by older men to one for which younger men make up most of the market. In 1970, the prevalence of smokeless tobacco use was 12.7% among males over the age of 65 and 2.2% among college-age males.128 By 1991, use among young males had more than tripled to 8.4% while rates among older males decreased to 5.6%.128 Currently, upwards of 8.8% of young males use smokeless tobacco127 while approximately 7 to 9.3% of military personnel150 and almost 50% of college athletes are self-classified users of smokeless tobacco.151

Smokeless tobacco contains known cancer-causing agents, such as nitrosamines and polycyclic aromatic hydrocarbons, as well as 30 metals and a radioactive element, polonium-210. The most recurrent health problem of the use of smokeless tobacco is leukoplakia, a precancerous oral lesion of the soft tissue. One study found that 79% of 245 smokeless tobacco users undergoing dental procedures had observable leukoplakia, 85% of which cases were in the most advanced stage.152 Three to six percent of leukoplakia lesions appear to have the potential to convert to oral squamous cell carcinomas, with a 5-year survival rate of 54%.151 Also, use of smokeless tobacco increases risk for cancers of the mouth, esophagus, pharynx, larynx, stomach, and pancreas.153 Important, early-stage leukoplakia can dissolve upon cessation of smokeless tobacco.154

Although smokeless tobacco is addictive,127 70% of current users report an interest in quitting, and 33% of users indicate that they have made at least one serious attempt to quit.64 The dental visit has been viewed as an optimal time to introduce smokeless tobacco cessation messages,155 since more than one-half of the population routinely visit a dentist and since the early adverse consequences of smokeless tobacco use can be easily detected during an oral examination.156 Although few systematic studies have evaluated the effectiveness of dentists to promote smokeless tobacco cessation, one study suggests that such interventions can reduce the prevalence of smokeless tobacco use. Stevens et al.152 randomized 518 male users of smokeless tobacco either to (a) an intervention that included an oral examination to assess for leukoplakia, cessation advice, information about the link between lesions and use of smokeless tobacco, a short video that described the health consequences of smokeless tobacco use and attempted to reduce defensiveness about quitting, attempts to get the patient to set a date to quit, the provision of a self-help manual, information about a 24-hour hotline for advice, oral substitutes (e.g., gum, nontobacco chew), and a tip sheet with specific strategies for quitting; or to (b) usual care. Additionally, intervention patients received follow-up phone calls to reinforce cessation messages and to support quitting attempts. Whereas 32.2% of intervention patients were abstinent (based on biochemical validation of saliva) at a 3-month follow-up, 21.3% of control patients had ceased use of smokeless tobacco. The 12-month follow-up data also showed that a significantly larger proportion of intervention subjects had stopped using smokeless tobacco, compared to the control subjects (33.5% versus 24.5%).

Another study targeted a cessation intervention towards college athletes.157 Three hundred sixty college athletes who reported using smokeless tobacco were randomized to either a minimal-contact control group or an intervention condition. The intervention group received an oral examination, counseling to help the individual avoid cravings and triggers for use, and follow-up telephone calls to encourage quitting. At a 3-month follow-up, 24% of the intervention participants were abstinent, compared to 16% in the control group. A 1-year follow-up showed that 35% of intervention participants were abstinent, compared to 16% in the control group.158 Finally, only one study has compared the cessation benefits of behavioral and pharmacologic treatments for smokeless tobacco use. Hatsukami et al.159 randomized 234 smokeless tobacco users to (1) behavioral treatment plus 2 mg of nicotine gum, (2) behavioral treatment plus placebo gum, (3) minimal contact plus 2 mg nicotine gum, or (4) minimal contact plus placebo gum. Behavioral treatment involved learning self-control behaviors (e.g., self-monitoring events associated with use), use of coping strategies to manage the cues associated with use (e.g., relaxation, alternative behaviors, avoidance of tempting situations), and learning to reward abstinence. At a 6-month follow-up, the abstinence rate for those given behavior therapy and nicotine gum was 47.3%, compared to 28% for those given behavior therapy plus placebo gum, 19.6% in the condition of minimal contact plus nicotine gum, and 31.5% in the condition of minimal contact plus placebo gum. Although comparisons at a 1-year follow-up were not significant, the abstinence rate (34.5%) for those given behavioral therapy plus nicotine gum was greater than for all of the other three groups. Since the abstinence rate for the condition of minimal contact plus nicotine gum was lower than the rate for the condition of minimal contact plus placebo gum, NRTs may not be an effective cessation approach for users of smokeless tobacco. The authors suggest that either the 2-mg dosage was not sufficient to promote cessation, or the similarities between the gum and smokeless tobacco in terms of absorption may “prime” lapses and relapses, as has been seen in the context of other drugs of abuse. Additional research is needed to replicate these data and to assess the use of other NRTs. Specific research is also needed to identify the predictors of sustained smokeless tobacco cessation.

Tobacco Addiction

That nicotine is highly addictive is unequivocal.160 Virtually all smokers exhibit the classic diagnostic symptoms indicative of drug addiction as outlined by the Diagnostic and Statistical Manual of Mental Disorders,161 including dependence, tolerance, and withdrawal syndromes.162 Nevertheless, while many individuals who experiment with tobacco products become addicted, many others can either become occasional users or decide to refrain from use entirely.163 Since only one-third to one-half of those who experiment with tobacco become habitual smokers,164 researchers suggest that genetic factors account for some of the variability in the risk of becoming addicted to tobacco.165

Recently, a meta-analysis of five twin studies showed a heritability factor (i.e., the degree to which a behavior can be attributed to genetic factors) of 60% for the risk of becoming a regular smoker.166 One genetic theory of tobacco addiction centers around biologic differences in dopaminergic regulation.167 The re-inforcing and motivating properties of nicotine addiction have been directly linked to nicotine’s stimulation of dopamine release in the nucleus accumbens.168 In particular, nicotine stimulates dopamine release and inhibits uptake, in turn providing the physiologic “euphoria” that accompanies tobacco use.169 These data have sparked recent investigations into the role of genetic variation in the dopaminergic regulatory system as a determinant of the propensity to become an habitual smoker. The assumption underlying these studies is that individuals with genetic polymorphisms which cause a “shortage” of dopamine are more likely to become smokers in order to facilitate the release and circulation of dopamine than individuals with genetic polymorphisms that increase circulating dopamine.

Two studies in this area examined genetic variations in the dopamine receptor (DRD2) and dopamine transporter (SLC6A3) genes—alterations that determine concentrations of synaptic dopamine. In the first study, Lerman et al.170 compared 289 smokers to 233 nonsmokers with regard to genetic variations in DRD2 and SLC6A3 genes. It was hypothesized that DRD2-A2 and SLC6A3-9 genetic variants (which allow for greater concentrations of synaptic dopamine and functioning receptors, respectively) would be more prevalent among nonsmokers than among smokers. The data showed that smokers were significantly less likely to have SLC6A3-9 genotypes (46.7%) than were nonsmokers (55.8%). However, there was not a significant difference between smokers and nonsmokers with regard to the prevalence of DRD2-A2 variants (39.1% versus 41.7%). Additional analyses indicated that smokers with the SLC6A3-9 variant reported a significantly longer average duration of abstinence, compared with smokers without this variant (472 versus 230 days), when controlling for age, race, education, and use of psychotropic medications. The second study also examined the link between SLC6A3-9 and DRD2-A2 genotypes and the likelihood of being a smoker.171 Although the analyses showed no association between smoking initiation and SLC6A3-9 genotype, there was a nonrandom relationship between smoking cessation and SLC6A3-9 genotype. Specifically, while 42% of current smokers exhibited this genotype, 52% of former smokers were found to have the SLC6A3-9 genotype. Those with the SLC6A3-9 genotype were about 1.5 times more likely to have quit smoking than those without the variant. As in the Lerman et al.170 study, no effect for DRDR-A2 genotype was detected.

While these studies are important pioneering efforts toward explaining genetic contributions to tobacco addiction, they represent only the initial steps towards understanding the complex and multi-determined causes of tobacco addiction. Although the findings from these studies suggest that addiction to smoking is influenced by the individual’s constitutional ability to regulate dopamine, the dopaminergic system is likely to be one of a number of determinants, genetic and environmental, of smoking behavior. First, the effect size of these genetic variants is small (i.e., about 2%).170 Further, over one-half of smokers studied to date exhibited the genetic polymorphism associated with lower risk of smoking. Nonetheless, these data have important implications for the treatment of tobacco addiction, especially in light of the wider availability of Zyban, which inhibits the reuptake of synaptic dopamine.

Prevention of Tobacco Use

Tobacco use is the single leading preventable cause of death in the United States.126 Tobacco-related deaths outnumber those caused by AIDS, car accidents, alcohol, homicides, illegal drugs, suicides, and fires, combined.172 Yet, nearly 50 million American adults and children continue to smoke.173 Fortunately, the past decade has been one in which data concerning predictors of tobacco use initiation and approaches to tobacco use prevention have been accumulating.

Factors that influence the onset of smoking are complex and numerous, and a better understanding of these factors is needed to reduce the rate of smoking.130 Some predictors are predetermined, such as age, socioeconomic status, and family background.174 Younger individuals with less fortunate socioeconomic backgrounds and from single-parent homes are at higher risk of initiating smoking and experimenting with cigarettes and smokeless tobacco.175 On the other hand, adolescents who have friends and parents who smoke are significantly more likely to initiate smoking themselves.176,177 Moreover, several psychological factors, including higher rates of depression and sociability, have been linked with a higher probability that an adolescent will start smoking.178 Lastly, the impact of the tobacco industry’s targeting of adolescents with aggressive advertising, marketing, promotional campaigns, and sponsorships on youth smoking initiation rates should not be overlooked.179 One study reported that 88% of seventh graders reported exposure to cigarette advertising, including billboards and magazines, and at events.180 One-quarter of these adolescents reported owning tobacco industry promotional items, and owning such paraphernalia was associated with a 2.2 times greater likelihood of being a smoker. Moreover, a strong correlation between smoking rates among adolescents and sales promotion expenditures by tobacco companies has been documented.181

Prevention initiatives have had two thrusts: (1) school-based programs, and (2) community-wide approaches. School-based programs encourage students who have yet to experiment with tobacco to abstain from use through (1) enforcement of antitobacco policies (e.g., prohibitions against tobacco use and tobacco advertising on campus); (2) education about the adverse health and social consequences of tobacco use (e.g., cancer risk, exacerbation of asthma, stained teeth and foul-smelling breath and clothing, and ostracism by nonsmoking peers); (3) education regarding the reasons that adolescents smoke (e.g., peer acceptance, stress management) and about alternative methods for attaining such goals; (4) education concerning the social influences on smoking, such as media, adults, and peers, and strategies for resisting such influences (e.g., refusal skills, assertiveness); (5) the use of teachers and peer leaders as health counselors; and (6) support for students who abstain from smoking as well as for those students who have quit.A meta-analysis of school-based prevention studies showed that programs involving peer and social elements can reduce adolescent smoking rates by as much as 30%.182 A large Norwegian study showed that when students were provided with an intensive school-based prevention program involving classroom education and parental partnerships, smoking increased by 1.9% after 2 years, compared with an 8.3% increase among students randomized to a control group.183 Likewise, in a Finnish study, schools were randomly chosen to receive a prevention program focusing on teaching students to resist social pressures to smoke.184 The results showed a 22% reduction in lifetime cigarette consumption among intervention participants at a 15-year follow-up, compared with controls. A randomized study conducted in the United States reported significantly lower 24-hour, 7-day, and 30-day abstinence rates among students receiving a prevention program that provided education about the harmful effects of smoking and taught skills to resist social pressures to smoke, compared with students who received only education.185

Community-wide smoking prevention programs involve approaches that include counteradvertising (e.g., antismoking billboard ads) and antitobacco policies (i.e., restricting access, raising taxes, instituting bans).173 Evaluations of the benefits of counteradvertising media campaigns suggest that this approach can effectively reduce smoking initiation rates.186 One study showed that cigarette consumption in California diminished by 12% following the California media antismoking campaign.187 An assessment of the effectiveness of antismoking advertising messages for youths and adults showed that “highly effective” messages concerned industry manipulation (e.g., the tobacco companies have deceived you in order to increase their profits) and the effects of secondhand smoke. “Non-effective” messages for youth were those that focused on restricting youth access to tobacco products, the long-term adverse health consequences of smoking, or romantic rejection, while “non-effective” messages for adults concerned short-term adverse health effects (e.g., yellow teeth) or romantic rejection.186

The past several years have witnessed a burgeoning of antitobacco legislation. Initiatives to restrict access to tobacco among children and adolescents were strengthened in 1997 with the creation of a new federal law prohibiting the sale of tobacco products to individuals younger than age 18 and requiring all retailers to check the identification of anyone appearing to be under the age of 26.188 Prior to this federal law, over two-thirds of minors were able to purchase tobacco products illegally.189 Three studies have shown that the sale of tobacco products to minors was significantly reduced in communities that instituted strict tobacco sales restrictions to minors, compared to communities which did not enforce such legislation.190–192 Further, one randomized study demonstrated that an intervention designed to strengthen community restrictions on the sale of tobacco products to minors (e.g., by mobilizing citizens to monitor retailer compliance) resulted in a significant decrease in the prevalence of smoking among adolescents under age 18.193

Other antitobacco legislation involves boosting tobacco taxes. Studies from Canada provide convincing data that taxes can influence the prevalence of tobacco use. The cost of tobacco products has been directly linked to the probability of becoming a smoker,194 with one study showing that the rates of tobacco use were higher, and the rates of quitting lower, in provinces where taxes were reduced, compared to provinces where taxes remained unchanged.195 In the United States, tobacco taxes have also led to a significant decrease in the prevalence of tobacco use.196 The tobacco tax in California led to a 17% drop in smoking rates, the tobacco tax in Massachusetts diminished tobacco sales by 18%,173,189 and an 11.3% decrease in cigarette consumption in Oregon was detected after Oregon instituted its cigarette excise tax.197

Finally, the prevalence of work-site, hospital, and restaurant and bar smoking bans in the United States have increased over the past decade. Evaluations of the effects of work-site198 and hospital199 smoking bans indicate that cigarette consumption is significantly reduced by such policies, with the rate of secondhand smoke exposure completely eliminated. Although studies have yet to evaluate the impact on cessation rates of restaurant and bar smoking bans, such policies undoubtedly eliminate exposure to secondhand smoke for many Americans. Despite the vigorous protestations from the tobacco and restaurant and bar industries that such policies would adversely impact revenues, studies have shown that smoking bans in California, New York City, and Vermont have actually increased, rather than decreased, tourism and restaurant revenues.200,201


Over the past decade, the growing national commitment to reducing the prevalence of tobacco use has resulted in a substantial growth in the scientific literature and availability of clinical interventions concerning the promotion of smoking cessation and prevention. Never before has there been a more hospitable climate for conducting empirical research into the determinants and treatment of tobacco addiction and for the implementation of cessation and prevention programs. Today, the commitment to support tobacco control research and initiatives from federal and state government agencies and from private granting institutes has never been stronger. Support for researchers as well as community-wide prevention and cessation initiatives has been greatly strengthened by the results of litigation between the states and the tobacco companies. The 1998 settlement with the tobacco industry (1) prohibits the targeting of youths with advertising, marketing, and promotions (e.g., banning cartoons, and restricting corporate sponsorship at sporting events); (2) provides $25 million annually for 10 years to support the study of programs designed to reduce the use of tobacco products by adolescents and $1.45 billion to establish a national, sustained advertising and education program to counter youth tobacco use and to educate all consumers about the harmful effects of tobacco use; (3) requires a commitment from the tobacco industry to reduce youth access to tobacco products (e.g., establish principles to reduce youth access and designate employees responsible for tracking corporate achievements in this area); (4) prohibits the suppression or misrepresentation of any research concerning the harmful or addictive nature of tobacco products, and (5) restricts lobbying by tobacco companies.202

Despite many advances in treating tobacco addiction and preventing initiation of tobacco use, the rate of decline in smoking among adults has slowed, and the prevalence of tobacco use has actually increased among certain subgroups, namely, adolescents and Native Americans. More research and wider availability of cessation and prevention initiatives are necessary if there is any hope of eradicating tobacco use among all Americans. Specifically, the psychosocial and sociodemographic determinants of smoking initiation must be systematically identified. Further, additional research concerning genetic and gene-environment interaction determinants of tobacco addiction is essential. Finally, since current data indicate that optimal cessation programs can produce modest 20 to 40% cessation rates at best, a greater emphasis on evaluating more comprehensive, multi-component cessation interventions could greatly improve upon current efficacy.

Achieving greater tobacco abstinence rates may only be realized with a nationwide comprehensive approach to tobacco cessation and prevention. This approach should involve the widespread availability of tailored (e.g., to stage of change, or to ethnic-based unique barriers), formal- and minimal-contact (e.g., physician-based), behavioral and pharmacologic cessation programs; the implementation of school-based and work-site health promotion and prevention programs; and the upholding of federally mandated legislation that reduces access to tobacco products and institutes disincentives for initiation of tobacco use. One important step would be a broader commitment among physicians to evaluating and managing patients in their practice who smoke. This commitment could be guided by the step-by-step approach depicted in Table 25.1and Figure 25.1. These guidelines are consistent with AHCPR recommendations and are based on the accumulated data concerning the treatment of nicotine addiction. The landscape for implementing a more comprehensive national smoking cessation and prevention initiative as described above has never been as fertile, given that the antismoking movement has been buttressed by the tobacco settlement. The eventual realization of this broad approach should facilitate lower rates of tobacco initiation and sustained use, thereby reducing the human costs of addiction to tobacco products.

Table 25.1. A Physician’s Guide to the Evaluation and Management of Smokers.

Table 25.1

A Physician’s Guide to the Evaluation and Management of Smokers.

Figure 25.1. Guideline for physician minimal-contact treatment using the stepped-care model (see Table 25.

Figure 25.1

Guideline for physician minimal-contact treatment using the stepped-care model (see Table 25.1). Based on AHCPR report in Fiore et al.


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Bookshelf ID: NBK20866


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