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(p. 272) Tobacco Use and Nicotine Dependence 

(p. 272) Tobacco Use and Nicotine Dependence
(p. 272) Tobacco Use and Nicotine Dependence

Anne E. Smith

and Suchitra Krishnan-Sarin

Page of

date: 25 May 2018

Betty is a 21-year-old Caucasian woman who began smoking at age 13. In adolescence she lived with her mother (a smoker) and younger brother (also a smoker) and had intermittent contact with her biological father (a nonsmoker). She initially smoked only at parties with friends but soon progressed to regular daily smoking. All of her friends smoked cigarettes. In high school, this meant smoking a cigarette at the bus stop, sneaking a cigarette in the school bathroom or behind the athletic building during the school day, and then smoking 4–8 cigarettes after school. Although Betty had been athletic and interested in team sports in elementary and middle school, she found it more and more difficult to keep up in high school and quit all sports at the beginning of her sophomore year. She reports a mild depression during that year which resolved itself without treatment, but she describes herself as generally ‘‘moody.’’ Since graduating and moving into her own apartment, she has smoked nearly a pack a day. Betty has frequently tried to quit out of concern for her health and the expense, but she has never been successful at establishing abstinence for longer than 24 hours. She has never sought help with quitting from a doctor or other health care provider. During previous attempts to quit she felt overwhelmed by cravings to smoke, feelings of restlessness and irritability, and a diminished ability to manage her daily life. She believes that smoking cigarettes helps her calm down when stressed and helps to manage her appetite and keep her on her diet. She worries that if she quits smoking she will gain at least 15 pounds and will be unable to cope with the withdrawal symptoms, particularly the restlessness and irritability. She also admits that she is reluctant to quit because she enjoys smoking— particularly when drinking alcohol—and that many in her social circle smoke and she would feel not only tempted to smoke when they light up but also excluded and isolated from the group. She is presently motivated to quit smoking because of a new relationship with a man who does not smoke and has encouraged her to quit.

Tobacco use is one of the most serious health-related behaviors of North American young adults. Cigarette smoking is the leading preventable cause of death in the United States, accounting for approximately 1 of every 5 deaths (438,000 people) each year and estimated to be responsible for $167 billion in annual health-related economic losses in the United States (CDC, 2002a, 2004, 2005a). Tobacco use is most prevalent in young adulthood with 24.4% of 18–24 year olds reporting current cigarette use (CDC, 2006a), and despite declines in use over recent decades, data suggest that the rate of decline has slowed and positive perception of smoking is increasing once again among young people (Johnston et al., 2007).

Common features of young adult nicotine dependence are illustrated in this case study. In many ways, nicotine dependence and tobacco use follow a developmental progression from initiation in young adolescence that is strongly driven by friends’ use, reduced or infrequent involvement in activities, and the presence of mood symptoms. Once established, tobacco use typically continues despite efforts to quit that are (p. 273) frequently motivated by health concerns and financial expense. Furthermore, tobacco use is often described as a response to stress or negative affect and for weight management. Finally, any withdrawal symptoms are anticipated to be experienced as fairly distressing and intolerable, and a cycle of dosing withdrawal symptoms with nicotine/tobacco use quickly develops.

A complex interaction of biological, behavioral, social, and psychological factors influences initiation and maintenance of tobacco use in the development of nicotine dependence. Influences on the progression and continuation of smoking include not only the aversive and rewarding influences of nicotine but also individual, social, and cultural factors such as heritability, expectancies, peer groups, and economics. This chapter discusses the epidemiology of tobacco use and dependence, briefly describes the neurobiology of nicotine dependence, identifies related issues that are particularly salient to adolescent development and the transition to adulthood, and reviews emerging evidence regarding the interaction between gene and environmental factors in the establishment of tobacco dependence. It concludes with a discussion about behavioral and pharmacological interventions and treatment guidelines.


Recently young adulthood has been recognized as a critical period for tobacco use initiation (Wechsler et al., 1998). For example, 25% of 12th grade ‘‘never-smokers’’ initiated smoking in the year following graduation, and 39% of 12th graders increased their cigarette use in that year (Tercyak, Rodriguez, & Audrain-McGovern, 2007). Similarly, 20% of smokers tried their first cigarette after the age of 18 (Hammond, 2005). As a result, although each day an estimated 4,000 young people between the ages of 12 and 17 years initiate cigarette smoking in the United States, and an estimated 1,140 young people become daily cigarette smokers (CDC, 2006b), a considerable number of smokers initiate the behavior in young adulthood. In fact, current smoking is most prevalent among young adults than any other population subgroup, with 26%–39% reporting current tobacco use (Lawrence et al., 2007; SAMHSA, 2006). Furthermore, although cigarettes account for most reported tobacco use in young adults, the use of cigars and smokeless tobacco is also fairly common, with 8%–17% of young adults reporting either current cigar use or use of other tobacco products (Rigotti et al., 2000; SAMHSA, 2006). Rates of cigarette use differ considerably by gender, race, education, and socioeconomic status. For example, cigarette smoking is more common among men (23.9%) than women (18.1%) (CDC, 2006a), and the use of cigars and other tobacco products is significantly more common among young men than young women, with nearly 16% of young men reporting current cigar use and nearly 9% reporting current use of other products, compared with 4% and 0.4% of young women, respectively (Rigotti et al., 2000). In addition, while some reports suggest that smoking rates are highest among American Indians/Alaska Natives (33%) and whites (31%) than other racial/ethnic groups (Lawrence et al., 2007), others have found smoking prevalence estimates as high as 60% among inner-city African American young adults (Stillman et al., 2007). Less education and concurrent enrollment in school are also related to smoking prevalence among U. S. young adults. Those not enrolled in college or without a college degree have been found to be more than twice as likely to report current and daily smoking (Lawrence et al., 2007). One report found that 48% of young adults with a high school degree or less reported current smoking (Solberg et al., 2007). Data suggest that a higher educational level may increase the likelihood of a quit attempt (Green et al., 2007). However, the number of quit attempts in the past year, level of interest in quitting, and relapse rates have also been found to be similar across education level (Solberg et al., 2007). Finally, blue collar workers, the unemployed, and those reporting an annual household income of less than US$20,000 are more likely to report current, daily, and heavy smoking (Lawrence et al., 2007).

Initial tobacco use is thought to be greatly directed by social and psychological forces, but these influences are quickly reinforced by the development of nicotine dependence, which is strongly driven by the neurobiological effects of nicotine.

(p. 274) Nicotine Dependence

The essential characteristics of nicotine dependence include the emergence of withdrawal symptoms in response to abstinence and unsuccessful attempts to reduce use or quit tobacco use. In order to meet clinical diagnosis of nicotine dependence, a tobacco user must exhibit any three (or more) of the primary symptoms at the same time during a 12-month period. In addition to the primary characteristics described, other criteria include tolerance to the aversive effects of nicotine (i.e., nausea and lightheaded-ness), limiting social or occupational activities because smoking is not permitted in those settings, continued use despite significant health concerns, and greater use than intended. Withdrawal symptoms can occur within 4 to 6 hours following last nicotine use (CDC, 1988). These symptoms, including depressed mood, insomnia, irritability, anxiety, difficulty concentrating, restlessness, and increased appetite and cravings for tobacco/nicotine, can be almost immediately alleviated by tobacco use.

Neurobiology of Nicotine Dependence

Cigarette smoking—the most common form of tobacco use—quickly distributes nicotine to the brain and levels of nicotine peak within 10 seconds of inhalation (Benowitz, 1996). The effects of nicotine are thought to be mediated by the dopamine-containing neurons in the ventral teg-mental area (VTA) that project to the nucleus accumbens and prefrontal cortex and form part of the brain’s ‘‘reward’’ pathway (Laviolette & van der Kooy, 2003). This circuitry is implicated in the rewarding motivational effects of multiple addictive drugs, including cocaine (Phillips et al., 2003), alcohol (Diana et al., 2003), opiates (Nader & van der Kooy, 1997), and nicotine (Pontieri, Tanda, Orzi, & Di Chiara, 1996). Nicotinic acetylcholine (nACh) receptors located throughout the CNS stimulate neurotransmitter release (directly and indirectly) and the resultant increase in dopamine is thought to at least partially underlie the pleasure associated with smoking. Interestingly, the nature of these nACh receptors inherently contributes to a pattern of continued use. Repeated and chronic administration of nicotine—for example, smoking over the course of the day—leads to desensitization and inactivation of nACh receptors (Pidoplichko, DeBiasis, Williams, & Dani, 1997), reducing the neurochemical reward of a cigarette. However, with abstinence—for example, overnight—the receptors may resensi-tize and once again be responsive to nicotine (George & O’Malley, 2004), resulting in frequent positive neurochemical reinforcement of nicotine use (Benowitz, 1996).

Recent data suggest that continued use of nicotine may be a result of the multifaceted influence of nicotine on the dopamine system. For example, dopamine release may not only produce pleasurable effects but also have a role in mediating the aversive effects of nicotine (Laviolette & van der Kooy, 2003). Additionally, the increase in dopamine response to nicotine appears to generalize to behaviors and contexts associated with tobacco use: over time, associated smoking behaviors are sufficient to stimulate dopamine release and act as reinforcement of the behavior even in the absence of nicotine (Balfour, 2004). In addition, repeated exposure to nicotine may result in an increase in functional nicotinic receptors in the brain and a heightened sensitivity of the dopamine response to nicotine (Gentry & Lukas, 2002). Preclinical evidence suggests that even limited exposure to nicotine is sufficient to induce lasting changes in the reward system (Mansvelder & McGehee, 2002), and nicotine may have differential effects in adolescent and adult brains. For example, the rewarding and reinforcing effects of nicotine appear to be enhanced (Belluzzi et al., 2004; Vastola, Douglas, Varlinskaya, & Spear, 2002) and the aversive effects possibly minimized (O’Dell et al., 2006; Shram, Funk, Li, & Le, 2006) in adolescent versus adult rodents. This difference may explain the reporting of symptoms of nicotine dependence in even occasional adolescent smokers (DiFranza et al., 2000).

Once thought to require some period of regular and considerable smoking, emerging precli-nical and clinical evidence suggests that symptoms of nicotine dependence, such as withdrawal and tolerance, can be established following relatively minimal administration of nicotine. For example, two-thirds of occasional (p. 275) adolescent smokers report at least one symptom of nicotine dependence (DiFranza et al., 2000) and nearly half of all daily young adult smokers are nicotine dependent (Breslau, Kilbey, & Andreski, 1994). In addition, considerable neu-rodevelopment occurs during adolescence and young adulthood (Giedd, 2004; Sowell, Thompson, Tessner, & Toga, 2001; Spear, 2000) that may create a particularly accommodating environment for the establishment of a lasting neurological impact of nicotine. For example, reduced prefrontal attentional network activity has been observed in young adult smokers compared with nonsmokers (Musso et al., 2007).

Differences in rewarding properties and withdrawal from nicotine may cause an increased vulnerability to nicotine addiction in adolescent and young adult animals and possibly in the adolescent human. Although the specifics of these neurobiological processes remain to be fully revealed, environmental influences almost certainly interact with biological vulnerabilities to result in smoking behavior in adolescence and adulthood. The following sections of the chapter discuss the influences of peers, mood, expectancies, and genetics on smoking initiation, maintenance, and cessation.

Peers and Tobacco Use

More than two decades of research have established that peer influence is a significant predictor of adolescent and young adult smoking initiation, progression, and maintenance/relapse (Conrad, Flay, & Hill, 1992; Flay, Hu, & Richardson, 1998; Leventhal & Cleary, 1980; McAlister, Krosnick, & Milburn, 1984; Sussman et al., 1998; Tyas & Pederson, 1998). Initiation of smoking generally takes place in a social context, and more than half of teens report that they smoked their first cigarette because they accepted an offer from a peer (Presti, Ary & Lichtenstein, 1992). In young adulthood, the number of high school and college friends who smoke increases the likelihood of smoking (Ridner, 2005). Recently, social smoking, that is, smoking primarily when with others or equally when alone and with others, has been found to describe the smoking behavior of more than 50% of current college student smokers (Moran, Wechsler, & Rigotti, 2004). This type of smoking behavior is associated with less use, less dependence, less intention to quit, and fewer recent attempts to quit (Moran, Wechsler, & Rigotti, 2004).

Mood and Tobacco Use

The links between mood states and smoking have been well documented. For example, in general, smokers retrospectively attribute smoking to negative affective states (Piper et al., 2004), smokers report greater overall negative affect than nonsmokers (Hall et al., 1998), and both increases in, and relative intensity of, negative affect have been identified as specific antecedents to lapse to smoking (Shiffman, 2005). In addition, negative affect has been consistently associated with relapse to smoking during a cessation attempt (e.g., Piasecki, 2006). Perhaps most clinically relevant is the fact that smokers themselves believe that their smoking ameliorates negative affect and increases positive affect (Shadel & Mermelstein, 1993). However, attempts to identify affective cues as immediate antecedents for smoking behaviors in naturalistic settings have been somewhat equivocal. There is some evidence that smoking behavior is preceded by an increased urge to smoke, feeling happy, feeling stressed, and a decrease in hunger (Shapiro, Jamner, Davydov, & James, 2002). In the presence of other smoking cues, both positive and negative affect imagery scripts can produce equivalent reports of urges to smoke (Maude-Griffin & Tiffany, 1996). In contrast, other studies have found no associations between either negative or positive affect and smoking (Shiffman et al., 2002; Shiffman, Paty, Gwaltney, & Dang, 2004).

Much of the research on affect in connection with smoking urges and behaviors has reasonably focused on negative affect, given the negative affective characteristics of withdrawal (such as dysphoria, anxiety, irritability, and restlessness). There is considerable evidence that negative affective states contribute to the smoking behaviors of adults (see Piasecki, 2006, for brief review). However, aspects of the relationship between positive affective states and smoking behaviors may be more relevant to young adult smokers. Although positive affect is less (p. 276) frequently associated with relapse than negative affect (Baer & Lichtenstein, 1988; Shiffman, 1986), when positive affect is predictive of relapse it is generally accompanied by other smoking-related cues (for example, the presence of other smokers smoking). In fact, this appears to be a key distinction between the influences of positive and negative affect on smoking urges: that negative affect alone produces strong urges to smoke, while positive affect appears to require additional cueing in the form of other smoking stimuli (Maude-Griffin & Tiffany, 1996). Evidence of the potentially high salience of positive affect in smoking is found in research on college age smokers. For example, heavier smokers report smoking more in response to feeling low-energy positive affect (i.e., calm, peaceful, content, or relaxed), compared to lighter smoking peers. Interestingly, the lighter smokers smoked a greater proportion of cigarettes in the presence of high-energy positive affect (i.e., happy, upbeat, cheerful, or energetic) compared to heavier smokers, and they were also significantly more likely to be influenced to smoke by having contact with another person smoking (Krukowski, Solomon, & Naud, 2005).

A primary motivation for tobacco use may be smokers’ perceptions of the coping functions provided by tobacco for affect regulation—for example, to increase concentration, counter boredom, enhance positive mood, and reducing distress in anxiety-arousing conditions (Wills & Cleary, 1996). One study found that 40% of adolescent smokers reported that their primary reason for smoking was to manage negative affect (Stevens, Colwell, Smith, Robinson, & McMillan, 2005). Similarly, the majority of smoking girls in one survey reported initiating and maintaining their smoking in response to stress, and they indicated in qualitative interviews that they perceived smoking as helpful in coping with distress at home, with friends, and at school (Nichter, Nichter, Vuckovic, Quintero, & Ritenbaugh, 1997). Among adult populations, there is evidence that expectations of this coping function of tobacco use moderates the relationship of stress to smoking urges and behaviors (Shadel & Mermelstein, 1993) and that smoking helps to modulate negative affect states within ‘‘real-life’’ settings (Jamner, Shapiro, & Jarvik, 1999).

Genetic Influences

Tobacco smoking is a highly heritable behavior—with genetic factors accounting for up to 53% of variability in smoking and up to 67% in variability of nicotine dependence (Sullivan & Kendler, 1998). Indeed, researchers have recently identified particular chromosomes as strongly associated with nicotine dependence (Li et al., 2008). In fact, particular aspects of nicotine dependence appear more highly heritable: tolerance, withdrawal, difficulty quitting, time to first cigarette in the morning, and number of cigarettes smoked per day (Lessov et al., 2004). However, investigations into the specific genes mediating cigarette smoking are complicated by a number of different definitions of the nicotine dependence phenotype (see review by Ho and Tyndale, 2007). Investigations into the specific genes that might explain the heritability of tobacco smoking have focused on genes which influence the reward pathway. Generally, it is thought that specific genetic polymorphisms may contribute to a dopamine deficit, thereby increasing the neurochemical reward of tobacco and other substances of abuse. Indeed, smokers have been found to be more likely to have a particular polymorphism of a dopamine receptor gene (DRD2), which as been associated with lower density of dopamine receptors in the brain (Noble et al., 1994). As a result, these smokers may be more vulnerable to the rewarding aspects of nicotine, thereby increasing their likelihood for repeated use. Another genetic influence on tobacco use and dependence is related to the relative speed of metabolizing nicotine (Malaiyandi, Sellers, & Tyndale, 2005). Individuals with polymorphisms in the genes responsible for encoding the metabolic enzymes (e.g., CYP2A6) tend to smoke fewer cigarettes and are less likely to be current smokers. This may be because slower metabolism of nicotine results in longer impact of the more aversive aspects of nicotine (nausea, etc). It may also be a function of smoking greater amounts in response to faster metabolizing (Audrain-McGovern (p. 277) et al., 2007). Adolescents without such genetic variation (i.e., those who metabolize nicotine more rapidly) have been found to progress to nicotine dependence more quickly than those with the variation (Audrain-McGovern et al., 2007). Additional underlying genetic predispositions or vulnerabilities may also increase risk for nicotine dependence, such as those which are associated with psychiatric or substance abuse comorbidities.

Psychiatric Comorbidity and Tobacco Use

Tobacco use is associated with a range of psychiatric diagnoses in both adults and adolescents; most commonly with depression, schizophrenia, attention-deficit hyperactivity disorder, and substance use disorders. Athough prevalence of tobacco smoking in the general population is approximately 21%, much higher rates have been observed among those with psychiatric disorders (41%) or substance abuse (67%) (Lasser et al., 2000). It is estimated that 70% of adolescent daily smokers have a comorbid psychiatric disorder (Kandel, Johnson, & Bird, 1997), and adults with mental illness consume approximately 44.3% of the cigarettes smoked in the United States (Upadhyaya, Deas, Brady, & Kruesi, 2002). Most common theoretical explanations for the strong links between psychiatric disorders and cigarette use suggest the possibility that there are shared underlying predispositions which may be genetic or environmental and influence neuro-biological pathways in the brain. Relatedly, it is proposed that individuals with serious mental illness, such as schizophrenia, may be ‘‘self-medicating’’ and using nicotine to modulate symptoms related to their illness (again by influencing neurobiological pathways). In any case, these populations not only have higher prevalence of cigarette use but also have substantially greater difficulty quitting, with lifetime quit rates of less than half that in the general population (Lasser et al., 2000).


There is extensive evidence illustrating positive associations between depressive symptoms and diagnoses with tobacco use and nicotine dependence. Adolescents with depressive disorders are more likely to initiate experimental smoking, transition to regular use (Patton et al., 1998), and be nicotine dependent (Breslau, Felm, & Peterson, 1993) than their nondepressed counterparts. The presence of an affective disorder can increase the likelihood of nicotine dependence by 10-fold in adolescents (Dierker, Avenevoli, Merikangas, Flaherty, & Stolar, 2001). In adults, diagnoses of depression and the presence of depressive symptoms are associated with greater likelihood of use (Anda et al., 1990), more severe withdrawal symptoms (Breslau, Kilbey, & Andreski, 1992), and more difficulty with cessation (Glassman et al., 1988; Glassman et al., 1990; Glassman et al., 1993; Niaura et al., 2001). Rates of smoking among population-based samples reporting clinically significant depressive symptoms range from 40% to 60% (Anda et al., 1990). A population-based twin study of female twins suggests that the comorbidity between depression and smoking may be, in great part, due to familial factors that underlie both disorders (Kendler et al., 1999).


Cigarette smoking is highly prevalent among patients with schizophrenia—with as many as 70% to 80% of diagnosed individuals concurrently using tobacco (Degenhardt & Hall, 2001). There is evidence to suggest that nicotine improves particular deficits associated with schizophrenia, including improving attention and working memory. Nicotine and smoking also appear to remediate certain psychophysiological deficits which appear to be mediated by neuro-transmission through nicotinic receptors that may function differently in schizophrenics and their first-degree relatives (Adler, Hoffer, Wiser, & Freedman,1993; Freedman et al., 1997; Leonard et al., 2002; Olincy, Ross, Young, Roath, & Freedman, 1998). In addition, nicotine may interact with the antipsychotic medications frequently prescribed to patients with schizophrenia. For example, certain aspects of motor impairment induced by neuroleptic medication may be ameliorated while other aspects are worsened—possibly by influencing dopamine systems implicated in these gross and fine motor impairments (Decina et al., 1990; Yassa, Lal, Korpassy, & Ally, 1987). Such findings would suggest that individuals with schizophrenia may be particularly prone to reinforcing effects (p. 278) of nicotine, by experiencing improved cognitive and motor processes, beyond the rewarding effects experienced by individuals without schizophrenia.

Attention-Deficit Hyperactivity Disorder

The links between tobacco use and attention-deficit hyperactivity disorder (ADHD) are somewhat equivocal. For example, a higher prevalence of smoking among adolescents and adults diagnosed with ADHD has been reported (Chilcoat & Breslau, 1999; Pomerleau, Downey, Stelson, & Pomerlau, 1995). However, other studies have found no increased risk for smoking related to ADHD (Dierker et al., 2001). Smokers with ADHD have been observed to have more ADHD symptoms than their nonsmoking ADHD peers (Pomerleau et al., 1995). It has been proposed that smokers with ADHD may be using nicotine as a way to improve attention by increasing the release of dopamine (Dani & Harris, 2005). This self-medicating hypothesis is supported by findings that the nicotine trans-dermal patch improved performance on cognitive reaction tasks in adult smokers and nonsmokers with ADHD (Conners et al., 1996; Levin et al., 1996)

Alcohol and Substance Abuse

There is significant comorbidity between tobacco use and the use of alcohol and other drugs. In young adult college students, 98% of smokers drink alcohol and up to 59% of drinkers smoke tobacco (Weitzman & Chen, 2005), and the risk for co-occurrence of use is highest among those students with the highest alcohol consumption, alcohol problems, and symptoms of alcohol abuse. Some reports have observed that more than 80% of alcohol-dependent patients are also cigarette smokers (Burling & Ziff, 1988; diFranza & Guerrera, 1990; Miller & Gold, 1998; Patten, Martin, & Owen,1996). Cigarette smoking is consistently positively, and in a bidirectional nature, associated with alcohol use. For example, smokers are more likely to drink alcohol than nonsmokers, and drinkers are more likely to smoke than nondrinkers. Data also indicate a dose-dependent relationship, with greater use of one substance related to greater use of the other (Zacny, 1990). As adolescents enter young adulthood and reach the legal age to use such substances as tobacco and alcohol, these risks are exacerbated. For example, 22% of college students report starting to engage in heavy drinking during their first semesters in college (Wechsler, Davenport, Dowdall, Moeykens, & Castillo, 1994), which increases their risk for smoking and the development of nicotine dependence.

The comorbidity of alcohol and tobacco use in young adulthood may have its roots in adolescence, as teens’ vulnerability to risk for other substance use appears exacerbated by even minimal use of tobacco. For example, adolescent smokers are more likely to be heavier drinkers and have four times the risk of a comorbid alcohol use disorder than never-smokers; in fact, even those teens who experiment with cigarettes are two times more likely to have an alcohol use disorder than never-smokers (Grucza & Beirut, 2006). Interestingly, twin studies have implicated shared genetic factors as responsible for comorbid nicotine and alcohol dependence (True & Xian, 1999), suggesting an underlying biological vulnerability to dependence on both substances. Indeed, dopamine neurotransmission, particularly in the nucleus accumbens of the mesocorticolimbic system, is central to mechanisms regulating CNS effects of both nicotine and alcohol. Emerging evidence suggests both that the effects of alcohol may be regulated by the same nicotinic receptors which mediate nicotine’s effect on the brain and that alcohol influences nAChR activation (Kalman, Marissette, & George, 2005).

In addition to alcohol use, evidence indicates that cigarette smoking is strongly associated with the use of other substances. Smokers are twice as likely to have ever used drugs compared with nonsmokers (Farrell & Marshall, 2006). In adults, these relationships vary as a function of nicotine dependence, with dependent smokers being at much greater risk for alcohol dependence, cocaine dependence, and cannabis dependence compared with nonsmokers and nondependent smokers. For example, nicotine-dependent (p. 279) smokers were found to have 11 times the risk for cocaine dependence compared with nonsmokers, but non-nicotine-dependent smokers had only 6.5 times the risk compared with nonsmokers (Breslau, 1995).

Prevention, Cessation, and Treatment

Due to the recognition that young adulthood is a period of continued risk of initiation and generally high rates of tobacco use, many college campuses have developed focused campus-wide prevention programs to support their students. These programs typically include combinations of campus policies (such as smoke-free buildings and residences), educational programming, and cessation support. Prevention-focused education programs have been linked to lower smoking rates (Borders, Xu, Bacchi, Cohen, & SoRelle-Miner, 2005), and the establishment of such campus policies as smoke-free residences has been shown to effectively prevent the initiation of tobacco use among young adults who are not already regular smokers (Wechsler, Lee, & Rigotti, 2001). However, there remains a dearth of research on the effectiveness of prevention programs targeted toward young adult smokers. The majority of research has focused on interventions for cessation of use.

Tobacco use is highly resistant to cessation: although 70% of adult smokers report a desire to quit and 42.5% have attempted to quit in the past year (CDC, 2005a), success rates in cessation are generally low, ranging from 5% without intervention to 30% with combined psychological and pharmacological treatment.

Although the overall benefits may be greater for people who stop at earlier ages, cessation is beneficial at all ages (CDC, 1990, 2001). The effects of cessation are nearly immediately beneficial with positive health impacts occurring within hours of the most recent cigarette. Smoking cessation lowers the risk for coronary heart disease, stroke, peripheral vascular disease, and lung and other types of cancer (CDC, 1990). The risk for developing cancer declines with the number of years of smoking cessation and coronary heart disease risk is considerably reduced within 2 years of quitting (CDC, 1990, 2001). Women who stop smoking before or during pregnancy reduce their risk for adverse reproductive outcomes such as infertility or having a low-birth-weight baby (CDC, 2001). However, most smokers find it highly difficult to quit, particularly because of the experience of withdrawal and cravings. In fact, the scientific consensus identifies nicotine as a powerful drug of addiction, comparable to heroin, cocaine, and alcohol (Henningfield, Miyasato, & Jasinski, 1985; Stolerman & Jarvis, 1995). It is an addiction that can require multiple repeated efforts to quit and can require a variety of interventions, including behavioral and pharmacological treatments.

Stages of Change

There is great interest among current smokers to quit smoking. Among current U. S. adult smokers, 70% report that they want to quit completely (CDC, 2006a). In 2005, an estimated 19.2 million (42.5%) adult smokers had stopped smoking for at least 1 day during the preceding 12 months because they were trying to quit (CDC, 2006a).

The extent of a smoker’s motivation to make a quit attempt has been frequently assessed and described by the Stages of Change (SOC) model (Prochaska & DiClemente, 1983). The SOC model includes five progressive stages of motivation and movement toward abstinence, including precontemplation, contemplation, preparation, action, and maintenance. Precon-templation refers to a stage in which the individual has no intention or consideration regarding abstinence in the coming 6 months. Contemplation involves an intention and plan to quit in the future (i.e., in the next 2 to 6 months). Preparation includes having made recent efforts to quit and an ongoing motivation to attain abstinence in the near future (i.e., within the next 30 days). The action and maintenance stages describe individuals who have just recently attained abstinence and maintained abstinence for at least 6 months, respectively.

There is evidence that both adult (Segan et al., 2004) and adolescent smokers (Dino et al., 2004) in the preparation stage, at the initiation of a cessation intervention, are more likely to attain abstinence than those in the contemplation stages. As a result of the potential links between stage of change and cessation success, research has begun to focus on how interventions may be tailored to identify and address the issues and (p. 280) challenges relevant to an individual’s specific stage. Indeed, such tailoring has had some success in increasing abstinence rates (e.g., Dijkstra et al., 2006). However, other research has concluded that there is little evidence that the model provides predictive power for future tobacco use or cessation (Carlson, et al., 2003). Critics of the model have argued that the stage model may minimize concepts highly relevant to addiction—such as neurological and behavioral rewards and the unpredictability of human decision making and motivation (West, 2005). Despite these critiques, the model continues to be used and promoted in the tobacco cessation field.

Certain environmental factors related to smoking that may characterize the developmental period of young adulthood, such as marrying a nonsmoker and a smoke-free workplace, have been found to increase the likelihood of long-term cessation (Macy et al., 2007). In addition, young adults appear to be sensitive to the financial cost of cigarettes. Increased smoking initiation has been observed following price reductions (Zhang, Cohen, Ferrence, & Rehm, 2006), and tobacco taxation has indicated that increased prices result in an increase in quitting (Taurus, 2004).


Interestingly, attempts to quit can be fairly easily encouraged by brief interventions by practitioners and even minimal intervention can increase abstinence rates significantly (Fiore et al., 2000). For example, spending 3 minutes discussing smoking cessation with a practitioner can increase abstinence rates from 11% to 14.4%. A patient who spends up to 90 minutes (not necessarily at the same visit) discussing cessation with their practitioner is three times more likely to succeed in their effort to quit. Furthermore, although 90% of smokers who successfully quit do so without professional help, evidence suggests that consultation with a health care provider can nearly double the likelihood of success. Unfortunately, young adults are less likely to receive advice to quit from a health care provider than other smokers and are less likely to use pharmacotherapy (Curry, Sporer, Pugach, Campbell, & Emery, 2007). In fact, 73% of young adults who attempted to quit in the past year did not receive any assistance in their effort (Solberg et al., 2007).

Despite the apparent need for effective smoking cessation services for young adult populations and the existence of treatments specifically designed for college and university students, treatment is not frequently offered or available. In one study of college students, 77% of smokers reported that a medical professional had asked about their tobacco use, but only 56% had been advised to quit (Koontz et al., 2004). Even fewer received advice about how to quit (22%) or how to set a quit date (5%), and very few were offered follow-up care (4%). On an institutional level, although most health directors perceive smoking cessation as important, over half of surveyed sites did not offer cessation services of any kind and those who did offer some type of intervention simultaneously believed that these programs were only minimally effective (Friedman, Smith, Zhang, Perry, & Colwell, 2004). College students themselves express interest in quitting, with an average report of three attempts to quit smoking and generally moderate to high interest in intention to quit (Black, Loftus, Chatterjee, Tiffany, & Babrow, 1993). One study of factors that would entice students to participate in a smoking cessation program found that accessibility, affordability, convenience, flexibility, social support, and behavioral prompts/cues are important factors to consider (Black et al., 1993). Another found that young adults believed that programs should focus on the addictive nature of nicotine and the benefits of using nicotine replacement therapy (Staten & Ridner, 2007). However, evidence-based treatments, such as pharmacotherapy and/or behavioral counseling, are underused by the young adult population compared with the general population (Curry et al., 2007). One important barrier to treatment may be the perspective that smoking cessation messages portrayed in the media are directed at adults and/or teens, and college students or young adults may not identify with these messages (Staten & Ridner, 2007).

(p. 281) Innovative approaches to behavior change in young adults are in development. For example, Web-based smoking cessation programs (e.g., Escoffery, McCormick, & Bateman, 2004) and quit-to-win programs may be cost-effective and high-impact interventions that can easily target young adult populations. Other programs that incorporate individual counseling, computer-based assessments, individualized feedback, and physiological measurements (such as lung functioning) are showing promise as attractive interventions to young adults (Prokhorov et al., 2007). In addition to individual or group counseling that can be offered on campus, college and university settings have unique opportunities to establish institutional interventions that could influence smoking behaviors. A review of interventions targeted specifically toward college students found that interventions such as campus smoking restrictions, smoke-free policies, anti-tobacco messages, and cigarette pricing can reduce tobacco use (Murphy-Hoefer et al., 2005).

Behavioral Therapy

Behavioral therapies have been shown to be effective in reducing tobacco use and assisting in quit attempts, with reported success rates ranging from 7% to 20% (Lerman, Patterson, & Berrettini, 2005). These interventions have been found to be influential at increasing abstinence rates whether provided in individual or group format. Effective in both individual and group formats (Carlson, Taenzer, Koopmans, & Bultz, 2000), three primary aspects of behavioral therapy have been found to be effective in increasing abstinence rates: the provision of practical/problem-solving skills, the support provided by the practitioner during the counseling, and the assistance the smoker receives in gaining social support for a quit attempt (Fiore et al., 2000). Typically offered in addition to a pharmacological intervention, such as nicotine replacement or medication, behavioral counseling can significantly improve on the effectiveness of the pharmacological treatment (e.g., Alterman, Gariti, & Mulvaney, 2001). However, efficacy is greatly influenced by time spent in counseling, with greater length of sessions, greater number of sessions, or longer contact time resulting in higher efficacy (Niaura & Abrams, 2002).

Motivational Interviewing

Motivational interviewing is another counseling intervention that has shown to be successful in increasing abstinence rates (Butler et al., 1999; Soria, Legido, Escolano, Yeste, & Montoya, 2006). Typically administered in a brief format, the counseling emphasizes the provision of personalized feedback regarding various aspects of the individual’s smoking profile (Mallin, 2002). Topics of discussion may include level and symptoms of nicotine dependence, the individual’s perception of smoking norms, the relative influence of the individual’s social network, the financial cost of smoking, and the impact of smoking on appearance or attractiveness to others. In addition, it might include feedback regarding lung functioning, any pulmonary symptoms, and carbon monoxide concentrations. Finally, the session focuses on how motivated the individual is to change his or her smoking behavior, addresses potential barriers to that change, and, if appropriate, assists in planning a quit attempt. However, despite success with additional risk populations, such as patients diagnosed with diabetes (Persson & Hjalmarson, 2006) or comorbid drug abuse (Richter, McCool, Catley, Hall, & Ahluwalia, 2005), other studies have found motivational interviewing not to be effective with high-risk smokers, such as those living in poverty (Okuyemi et al., 2007), pregnant women (Stotts, DeLaune, Schmitz, & Grabowski, 2004; Tappin et al., 2005), and those diagnosed with cancer (Wakefield, Olver, Whitford, & Rosenfeld, 2004). Further work to determine the efficacy of motivational interviewing on tobacco cessation is necessary (Niarua & Abrams, 2002).

Motivational Incentives

Motivational incentives, also termed contingency management (CM), involve the use of immediate, tangible, and salient rewards in (p. 282) response to proven abstinence from a target drug. For example, a smoker must provide a practitioner with evidence of abstinence, such as a negative level on a breath carbon monoxide assessment or a salivary cotinine measure, in order to receive a reward. Rewards may be cash payments or vouchers to be exchanged for particular goods. These procedures have been effective in increasing abstinence rates in tobacco cessation programs for adults (Stitzer, Rand, Bigelow, & Mead, 1986) and more recently in adolescents (Krishnan-Sarin et al., 2006). Although found to be less effective in reducing tobacco use than in reducing use of other substances (Prendergast, Podus, Finney, Greenwell, & Roll, 2006), this type of motivational incentive intervention may effectively supplement other treatment programs (such as cognitive-behavioral therapies, nicotine replacement interventions, or nonnicotine medications).

Quit and Win

Smoking cessation contests, in which large numbers of participants make simultaneous quit attempts during a specific time period and successful abstainers are eligible to receive prizes, have been shown to be successful in motivating quit attempts among young adult smokers. Quit and Win programs were developed in the early 1980s by the Minnesota Heart Health program and have since been implemented around the world. This type of contest may be particularly useful with young adult smokers, as research indicates that the contest tends to appeal most to younger smokers (Cummings et al., 1990; Hawk et al., 2006) and is most successful with lighter smokers (Hanewinkel, Wiborg, Isensee, Nebot, & Vartiainen, 2006). A report of use of the contest method with young adult smokers (mean age = 21 years) found an intention-to-treat success rate of almost 15% of contestants reporting abstinence at a 4-month follow-up and 7% at 12 months (Hanewinkel, Wiborg, Isensee, Nebot, & Vartiainen, 2006). Another contest held on college campuses, found that 30% of participants were abstinent at the end of 7 weeks and 12% were abstinent at a 6-month follow-up (Rooney et al., 2005). These rates compare favorably with reported typical self-initiated annual quit rates of 2%–4% (Zhu, Sun, Billings, Choi, & Malarcher, 1999).

Nicotine Replacement

Nicotine replacement therapies (NRTs) involve the administration of nicotine in order to attenuate the development of withdrawal symptoms. Considered to be ‘‘first-line’’ pharma-cotherapy treatments, these interventions are packaged in the form of gums, lozenges, trans-dermal patches, inhalers, and nasal sprays and typically provide 30%–50% of the amount of nicotine provided by cigarettes. Nicotine replacement therapies are similar in efficacy to each other regardless of the method of delivery and are 1.5 to 4 times more likely than placebo treatment to result in a successful quit attempt (Fiore et al., 2000). In addition, these interventions may be combined in the event that a patient is unable to quit using a single type—for example, combining the nicotine patch (which can provide a more constant administration of nicotine) with either the nicotine gum or nicotine nasal spray when particular urges arise. Data suggest that the combining of treatment modalities can significantly increase the efficacy of treatment (Bohadana, Nilsson, Rasmussen, & Martinet, 2000).

Nonnicotine Medications

Recently nonnicotine medications such as Bupropion SR (Zyban) and Varenicline Tartrate (Chantix) have been approved for use in the treatment of nicotine dependence. Sustained-release bupropion is a prescription medication considered a first-line treatment to assist in cessation. First approved by the FDA in 1997 for the treatment of nicotine addiction, it is thought to block the reuptake of dopamine and norepinephrine and impact nicotinic receptors. This medication appears to reduce smoking by minimizing cravings and urges to smoke and can be supplemented safely by NRT. Compared with placebo, bupropion can double the odds of successfully quitting (Fiore et al., 2000). However, side effects of the medication include dry mouth, difficulty sleeping, headache, dizziness, and skin rash and the use of the medication is (p. 283) contraindicated for smokers with seizure conditions or eating disorders. Varenicline (Chantix) is a partial agonist of the nicotine acetylcholine receptors and was approved by the FDA in 2006. This medication acts to diminish the emergence of withdrawal symptoms and reduces the reinforcing properties of nicotine. Common side effects of varenicline are nausea, changes in dreaming, and vomiting, and it should not be used by smokers with kidney problems. Varenicline is nearly four times as effective as a placebo in determining abstinence and almost twice as effective as bupropion (Gonzales et al., 2006). Forty-four percent of patients who were administered varenicline were able to attain and maintain abstinence continuously for 4 weeks compared with only 17% of those on placebo and 29% of those administered bupropion. In addition, long-term follow-up rates are increased by varenicline (Jorenby et al., 2006), and maintenance treatment with varenicline (i.e., prolonged medication administration) can significantly reduce the likelihood of relapse (Tonstad et al., 2006).

Special Treatment Considerations

The high comorbidity of nicotine dependence and tobacco use with other psychiatric disorders requires consideration when evaluating treatment options. Typically, combined treatments that are effective at addressing both disorders are most effective. For example, intervention programs for smoking cessation (such as the use of NRTs or other medications) that included a cognitive behavioral adjunct to specifically address depression symptoms resulted in higher success rates for smokers with a lifetime history of major depression (Brown et al., 2001; Hall, Munoz, & Reus, 1994). Medications that may address both a primary psychiatric or substance abuse disorder and nicotine dependence include atypical antipsychotics for schizophrenia, antidepressants for depressive disorders, and naltrexone for alcoholism (Hall et al., 1998; Kalman et al., 2005).

As described, the prevalence of nicotine dependence among alcohol or other substance abusers is extremely high. Smoking cessation is frequently not a focus of clinical interventions for this population and at times is discouraged based on beliefs that smoking cessation may undermine attempts to quit the drug of abuse (Sussman, 2002). Smoking cessation has in fact been found to be associated with greater likelihood of abstinence from other drug use following drug treatment (Lemon, Friedman, & Stein, 2003). Similarly, continued smoking can even adversely impact treatment for marijuana dependence (Sullivan & Covey, 2002). There is evidence to suggest that timing of the cessation efforts may be important to consider: smokers who quit alcohol prior to quitting cigarettes had similar success at quitting tobacco as those who quit concurrently, but alcohol outcomes were better in those who quit cigarettes after some established period of sobriety (Joseph, Willenbring, Nugent, & Nelson, 2004). Young adults who are engaged in treatment to address alcohol or substance dependence should be assessed for tobacco use and strongly encouraged to quit—the prevalence of smoking-related morbidity makes it likely that individuals are more likely to die of smoking-related disease rather than directly from alcohol-related medical disorder or abuse of another substance (Hurt et al., 1996; Hurt & Patten, 2003).

Finally, accumulating evidence suggests that pharmacogenetics could be used to predict response to nicotine replacement and nonnico-tinic therapies for smoking cessation (see Berritini & Lerman, 2005, for a review). Further advances in this exciting field may help advance therapeutic outcomes for smoking cessation for young adult smokers.


Young adulthood is a critical period for the initiation and establishment of tobacco use. Although great gains have been made toward greater appreciation of the needs of this population, better understanding of the potential impact of public policy to reduce initiation and increase cessation, and improved pharmacological and behavioral treatments, there remains an ongoing need for quality research on prevention and intervention for tobacco use in young adults. Indeed, future research will likely prove to be transdisciplinary and incorporate neurobiological, behavioral, psychosocial, and social aspects in the development of effective interventions. (p. 284)


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