State of the Art Smoking and Smoking Cessation 1 •2

EDWIN B. FISHER, JR., DEBRA HAIRE-JOSHU, GLEN D. MORGAN, HEATHER REHBERG, and KATHRYN ROST Contents Introduction Multiple Determinants of Smoking Stages of the Smoking Career Nicotine Addiction Conditioning of Smoking Cigarette Marketing The Social Differentiation of Smoking Multiple Determinants and the Persistence of the Smoking Career Influences on Smoking Cessation Personality Variables Peer, Family Factors, and Social Support among Adults Health Effects of Smoking Weight and Smoking Contemplation of Quitting, Quitting, and Relapse Smoking Cessation Interventions Temptation Management Cue Extinction Aversive Techniques Contingency Management "Self-Help" Results of Stimulus Control, Contingency Management, and Social Support Programs Pharmacologic Interventions Interventions for Maintenance and Relapse Social Support Worksite Programs Implications for Health Professionals Clinical Interventions for Smoking Cessation Pulmonary Disease and Smoking Cessation Smoking and Cardiovascular Disease Smoking and Diabetes Comparative Study of Smoking Cessation across Types of Disease Introduction

The average25-yr-old, pack-a-day smoker will die six to eight years younger than his nonsmoking peer (1). Smoking kills more people each year through cardiovascular disease than it does through cancer. Chronic obstructive lung disease might well be renamed "chronic smoking disease" because estimates attribute as many as 85010 of cases to smoking (2). Fortunately, however, smoking is declining. In 1965, 52% of the adult male and 702

34% of the adult female population in this country smoked. The 1989 Surgeon General's Report (3) estimated those figures to have declined to 29.5 and 23.8%, respectively. Considering the billions spent on marketing cigarettes and the addictive nature of cigarette smoking, the reduction in the prevalence of smoking must be viewed as a major triumph for public health and medicine. As Dr. C. Everett Koop noted in his preface to the 1989 report, "This achievement has few parallels in the history of public health. It was accomplished despite the addictive nature of tobacco and powerful economic forces promoting its use" (3). Most smokers eventuallydo quit smoking. Although individual interventions may have modest, short-term impacts, ranging from five to 40% abstinence, one survey indicated that 55% of adults who had ever been regular smokers had quit, for an average of 7.4 yr and without regard to whether they had been heavy or light smokers (4). National figures also suggest high rates of quitting. The 1989 Surgeon General's Report estimated that 50% of all adults who had ever smoked regularly had quit. The goal of this report is to acquaint readers with the "state-of-the-art" in smoking cessation research. Before doing this, it is necessary to reviewthe stateof-the-art of research into the nature of smoking. This section of the report will emphasize the multiplicity of determinants, from biochemical aspects of addiction to financial determinants of cigarette marketing, as they influence the "career" of the smoker. Research into general strategies and procedures for smoking cessation will then precede review of smoking cessation activities in clinical settings. Finally, the report will emphasize interventions with patients with chronic lung disease and patients with other chronic diseases, especially heart disease and diabetes. In addition to focusing on research most pertinent

to the activities of readers of the REVIEW, this section will emphasize commonalities across smoking interventions for chronic disease as well as ways in which characteristics of specific diseases influence the impact of smoking cessation programs. Multiple Determinants of Smoking

Awareness of the many determinants of smoking has increased substantially since smoking became a health concern. At the level of basic physiologic processes, we now have a sharper understanding of the role of nicotine addiction. At the other end of the spectrum of causes, we can also articulate the influence of the impact of cigarette profits on advertising budgets. Guiding the development of our understanding of smoking, considerable evolution has taken place in models of causal inference in psychology and behavioral science. With perspectives ranging from behaviorism to general systems theory to hermeneutics, there has been increased understanding of how multiple causes, none of them necessaryor sufficient, may interact to bring about complex behavior patterns such as smoking. Within such models, concerns for the key or underlying or sufficient cause are put aside in favor of identifying and understanding the relationships among contributing causes. In line with this, current explanations assume that smoking

(Received for publication April 23, 1990) 1 From the Center for Health Behavior Research, Washington University, St. Louis, Missouri; the Wyoming ValleyFamily Practice Residency Program, Kingston, Pennsylvania; the Research Division, Department of Psychiatry and Behavioral Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas. 2 Correspondence and requests for reprints should be addressed to Edwin B. Fisher, Jr., Washington University, Center for Health Behavior Research, 33 South Euclid, St. Louis, MO 63108.

AM REV RESPIR DIS 1990; 142:702-720

703

STATE OF THE ART: SMOKING AND SMOKING CESSATION

is determined by multiple causes, no one sufficient, no one necessary. In addition to being determined by a wide range of influences, smoking is a set of behaviors that evolve over time. To emphasize this idea, smoking has even been described as a "career" (5). Borrowed from the sociology of the use of other addictive drugs (6, 7), "career" includes periods of initiation of use, development of an ongoing habit, habitual use, and often, several phases leading to cessation (8). The concept of career helps clarify that smoking is not just a simple process that may be turned on and off with ease. Rather, it is a complex, evolving process, the stages of which may be differentially influenced by the many factors that determine smoking. As it has a natural history, the career resembles the course of a disease; however, course is often viewedas the expression of factors intrinsic to the disease. In contrast, it is the interplay of intrinsic and social or environmental factors that direct the natural history of a career. How society reacts to the career influences the nature of that career. The career entails intrinsic factors, such as core skills or habits, as well as social reactions to those intrinsic factors and the interaction of these intrinsic and social factors (6, 7). In fact, the natural history of a career is only "natural" in the sense that the social factors that influence it (e.g., rights, privileges, responsibilities, professional standards, prejudices, myths, laws, sanctions, etc.) are viewed themselves as natural or as obeying natural laws of social influence (9). A school system's restrictions on smoking; parental actions to punish or model or encourage it; advertisements' presentations of smokers as daring, sophisticated, successful, or attractive; workplace smoking policies; insurance regulations and other social and governmental responses to smoking will interact with its intrinsic characteristics to determine smokers' experience of their habit and to direct their smoking careers. Amid the multiple determinants of a smoking career is the interplay of psychologic and biologic forces. Their relative importance has been a recurrent issue in biology, medicine, psychology, and social science. In smoking research, this has centered on the roles of nicotine and addiction. The 1988 Surgeon General's Report (10) focused on nicotine. It presented numerous findings indicating that nicotine, conditioning, and social determinants interact in the determination of smoking. Indeed, the biologic potency

of nicotine may make the habits that comprise smoking patterns stronger and more resistant to change. At the same time, the plenitude of daily circumstances, activities, and emotions conditioned to smoking tie this addiction to so many circumstances of daily life as to contribute to it being an unusually difficult addiction to break. This interplay between habit and physiology, between psyche and soma is mirrored in research on smoking cessation in which nicotine replacement may enhance the impact of psychologic interventions while psychologic support and attention to habit change enhance the impact of nicotine replacement (11-13).

Stages of the Smoking Career A variety of stages may be identified in the smoking career: initial use, experimentation, and transition to habitual use refer to the development of smoking (14). Precontemplation and contemplation of quitting, action, maintenance, and relapse refer to cessation (8). At different stages, different influences and different actions are prominent. For instance, the smoker in precontemplation is not responsive to directive encouragement to quit or advice on how to do so. The person in the action stage, on the other hand, is receptive to cessation advice and is focused on ways of breaking smoking habits. In the use of any stage or developmental theory, there exists the risk of overly concrete interpretation. The stages are not explanations but descriptions of smokers' and quitters' behavior. The several stages of the career of a smoker themselves develop and wax and wane over time; their order is not rigid. For instance, some may proceed from the stage of transition to habitual use to the stage of action and, then, maintenance without ever going through the phases of habitual use, precontemplation, or contemplation. Of course stages can be repeated, as with relapse and action. Indeed, the average successful quitter reports several and often many failed attempts before achieving maintained abstinence (5).

Nicotine Addiction As in the 1964Surgeon General's Report, smoking was formerly viewed as an "habituation" rather than an "addiction." This distinction rested largely on the presence or absence of chronic intoxication, whether desire is overpowering and compulsive, presence of physical dependence,

and whether detrimental effects are to society or primarily to the individual. The following paragraphs review revisions of these criteria since the time of the first Surgeon General's Report and evidence that smoking meets these as well as current criteria for addiction. The criterion of chronic intoxication has been replaced by a criterion that an addictive drug have psychologic effects, a criterion met by nicotine. Rapid absorption of nicotine into the bloodstream and consequent delivery to the central nervous system is a common feature of all popular forms of tobacco use. Recent evidence indicates nicotine is absorbed in the brain, which contains receptors specific to nicotine (15-17). Within the brain, nicotine has euphoric effects and perhaps sedative or other anxiolytic effects of neurohormonal processes (18). It is also capable of reinforcing behavior, even among animals or human subjects blind to whether they were receiving saline placebo or nicotine (10). That such psychoactive effects are observed across human and even animal subjects argues against nicotine addiction resting in some peculiar personality characteristic - the basis for nicotine addiction is nicotine. The criterion of compulsive use in addiction is contradicted by more recent evidence, such as reviewed in the 1988 Surgeon General's Report (10). In fact, studies indicate substantial rates of cessation of addictive drug habits, even spontaneously, such as by heroin-addicted Vietnam veterans upon their return to the United States (10, 19). In contrast, smoking may be maintained against substantial awareness of its harm, as by pregnant women or chronic lung disease patients. Many persist even after heart attacks attributable to smoking (20, 21). Physical dependence is still a criterion for addiction, but the various psychologic and physical withdrawal symptoms following smoking cessation appear to meet it (10). The crucial role of nicotine is clear from the reduction of these symptoms by the delivery of nicotine through buccal absorption from nicotine polacrilex (22). The substance of the last of the old criteria of addiction, detrimental effects on society, is determined as much by laws and customs that pertain to a drug's use as by its direct psychologic and biologic effects. Even if the criterion of detrimental effects on society is retained, the toll of death, disability, and lost productivity and income attributable to cigarettes must meet this criterion. Also indicative of addiction is that the

704

FISHER, HAIRE-JOSHU, MORGAN, REHBERG, AND ROST

rate of smoking is driven by nicotine. Smokers smoke more after deprivation (23) and less after nicotine "preloading," even if through administration other than by cigarettes (24-26). Moreover, the dose of nicotine governs tobacco taking or smoking, apparently within a range of blood levels from those characterizing deprivation to those characterizing satiation. This control of smoking by nicotine ingestion defies the myth that cigarette smoking is a casual habit, governed only by the desire or whim of the smoker. As with other addictive drugs, prolonged ingestion of nicotine leads to tolerance, a tendency to consume increasing amounts of a drug, presumably to achieve a desired euphoric or other effect. The 1988 Surgeon General's Report concluded "... cigarette and other forms of tobacco are addicting. An extensive body of research has shown that nicotine is the drug in tobacco that causes addiction. Moreover, the processes that determine tobacco addiction are similar to those that determine addiction to drugs such as heroin and cocaine" (10). The finding that smoking is an addiction prompted popular criticism of placing cigarette smoking in the same category as addiction to alcohol, heroin, cocaine, or other drugs. It is important to note that the 1988 Surgeon General's Report's criteria of addiction do not include social deviance, psychopathology, personal deterioration, and the like, characteristics that many associate with addiction to illegal drugs. Thus, the finding that smoking is an addiction does not imply that smokers take on such characteristics. The career concept highlights the roles of extrinsic as well as intrinsic determinants of the career of drug taking, clarifying that social deviance, personal deterioration, and the like are as much the products of social reactions to drug use rather than of drug use per se. They are products of external or social influences on the career rather than of intrinsic characteristics of addiction or smoking.

Conditioning of Smoking An interesting exception to the reduction of withdrawal symptoms by nicotine is its modest effect on desire to smoke. Subjects giving up cigarettes for 3-day periods received varying doses of nicotine or placebo. Nicotine reduced several withdrawal symptoms, supporting the viewof smoking as a specific addiction to nicotine. Relative to placebo, however, nicotine did not achieve statistically signifi-

cant reductions of subjects' reported desire to smoke (22). Desire to smoke was apparently more dependent on cues and circumstances associated with previous smoking than it did on blood nicotine levels. Thus, circumstances associated with smoking may become cues for desires for cigarettes following abstinence, even with nicotine substitution. Indeed, Henningfield and Nemeth-Coslett (22) identify as a "misconception" of drug dependence the idea that "the drug is the only relevant factor driving the behavior and the only relevant factor in treatment. Use of all dependence-producing drugs occurs in the context of a variety of environmental stimuli ... the desire to use the drug ... may be elicited by environmental stimuli relatively independent of physiologic state or need...." Conditioning of nicotine to cues associated with its delivery has been demonstrated in place conditioning studies (27) and conditioned taste aversion (28). Gritz (29) found reductions of smoking with elimination of cues associated with it, such as ambient smoke and the sight of the cigarette. Katz and Goldberg (30) found environmental stimuli trigger smoking after previous association with smoking. The range of possible conditioning effects surrounding nicotine addiction is great. First, of course, the effects of nicotine may reinforce those behaviors that lead to them. Second, the circumstances in which smoking occurs may become discriminative stimuli for smoking, signaling the likelihood of reinforcement of smoking. Third, the circumstances surrounding smoking may also become conditioned to nicotine so that they evoke conditioned responses that resemble the organismic response to nicotine itself. The complexity of these conditioning effects is increased by the fact that smoking is a sequence of behaviors. Thus, behaviors in the middle of the smoking chain may (1) elicit conditioned responsesresembling the pharmacologic effects of nicotine, which may (2) reinforce previous behaviors that had led to them, (3) be reinforced themselves by the conditioned responses they elicit, (4) serve as discriminative stimuli for subsequent links, signaling the likelihood of their reinforcement by nicotine. As an example, reaching for a cigarette may be elicited by noticing the cigarette pack on the table. Reaching for the cigarette may then, itself, elicit conditioned responses that resemble the effects of nicotine. These may reinforce having reached for

the cigarette and having noticed thecigarette pack. Reaching for the cigarette and the conditioned responses that it elicits may both serve as cues for subsequently lighting and inhaling the cigarette, Thus, a chain of behaviors is linked by the basic psychologic processesof conditioning, reinforcement, and stimulus control (31). Withdrawal symptoms may be conditioned to the circumstances in which smoking has occurred (32, 33). This sets the stage for withdrawal being psychologically prolonged. Stimuli associated with prior drug taking elicit withdrawal symptoms and cravings even after the organismhas returned to physiologic homeostasis after cessation of drug ingestion. With smoking, greater withdrawal symptoms have been noted when cessation occurs in natural rather than artificial environments, presumably because those natural environments contain numerous cues associated with prior smoking (34). Further complication of the conditioning of smoking arises from the varied effects of nicotine (35). As nicotine may reduce arousal, reduce anxiety, or function as a stimulant, arousal, anxiety, or lethargy may come to serve as a discriminative stimulus for smoking and a conditionedstimulus for withdrawal symptoms or cravings after cessation. The effect of such association would be for such moods to elicit urges to smoke (36), an effect mirrored in reports of antecedents of relapse (37, 38). Additionally, the circumstances that give rise to such emotions or moods, e.g., time of day, work demands, family conflict, or loneliness may come to signal the occasion for smoking or elicit conditioned withdrawal symptoms. Finally, moods or arousal states, which merely resemble those that have been associated with smoking, may come by stimulus generalization to signal occasions to smoke. If the effects of smoking improve those moods or states, the individual will have extended his or her smoking repertoire. The biologic potency and speed of action of nicotine also contribute to the strength of conditioning that surrounds smoking. Research in classical conditioning has established that stronger unconditioned stimuli, as measured by intensity, amount, etc., lead to more rapid conditioning, stronger conditioned responses, and greater resistance to extinction (39). Consequently, the many and easily discriminated effects of nicotine (10)would be expected to lead to the powerful conditioning of cues that accompany them.

STATE OF THE ART: SMOKING AND SMOKING CESSATION

This should be especiallytrue after a period of deprivation. For instance, the cues surrounding the first cigarette in the morning should be especially strongly conditioned to smoking because the nicotine-unconditioned stimulus, which they accompany, will be especially strong after overnight deprivation. In addition to the strength of nicotine as an unconditioned stimulus, its delivery to the central nervous system is rapid, approximately 7 s from inhalation (35). This should support stronger classic conditioning of cues that accompany smoking. Brief intervals between such cues and the unconditioned stimuli and responses to which they are conditioned enhance that conditioning. Rapidity of delivery should also make nicotine an effective reinforcer of behaviors that lead to inhalation because delay may reduce the effects of reinforcers, especially in the early phases of learning (39). In contrast, most disincentives for smoking are subtle, insidious, or much delayed, reducing their ability to discourage it. A subtle but important distinction is whether resumption of smoking is reinforced by reduction of withdrawal symptoms or by the positive consequences of nicotine ingestion. Niaura and colleagues (40) reviewed the evidence on this issue and concluded that the positive consequences of nicotine drive relapse, often cued by stimuli associated with smoking and these consequences. Thus, the exsmoker is prone to relapse not in order to reduce withdrawal symptoms but because of the likelihood of reinforcement by nicotine. This analysis does not mean that negative affect cannot be a cue for smoking. Mild depression, for instance, may cue smoking and reinforcement by nicotine's euphoriant effects. The reinforcer, though, is not the reduction of a withdrawal symptom but the euphoriant effects of nicotine that may have been cued and enhanced by the prior low mood. This analysis suggests treatments should not focus on supposed withdrawal symptoms but should minimize cues associated with smoking and should teach alternative skills for dealing with affects that have come to trigger it. As can be seen, the many waysin which smoking is conditioned to circumstances around it explain "... the thorough interweaving of the smoking habit in the fabric of daily life" (35). The sheer repetition of smoking also strengthens such interweaving. It is estimated that the average, pack-a-day smoker of 20 yr has inhaled cigarettes over one million times

(41),each inhalation providing opportunity for conditioned smoking to many settings or situations of daily life. The million conditioning trials link the many actions of a smoking career. As the person recently retired from a job or business career may "not know what to do with myself," so the quitter may feel overwhelmed by the ubiquity of cues and cravings, complaining that smoking is almost constantly "on my mind."

705

The linkage of smoking to the women's movement is apparent. Among white adolescent females surveyed in Louisiana in 1981,31% named Virginia Slims" as their preferred brand. Paradoxically, this brand is still less popular within this group than the macho brand Marlboro'" (46). In addition to smoking prevalence and brand choice, other features have been related to group differences. Black smokers report fewer cigarettes per day than white smokers but choose brands with Cigarette Marketing higher tar/nicotine yields (47). Heavy Cigarettes are the most heavily market- smoking is apparently rare among Hised consumer product in our nation. panics (48, 49). Observed group differences may be (Marketing includes advertising as well as other promotions such as distributions misleading if they cause us to conclude of samples, point-of-sale displays, or dis- wrongly that intrinsic characteristics of tribution of product-related goods such those groups are responsible for high or as cigarette lighters, 'l-shirts, etc.) In 1986, low prevalences. For instance, there is no $2.38 billion was spent marketing ciga- evidence that central characteristics of rettes in the United States (42). Adjust- black culture are responsible for higher ing for inflation, Davis (43) estimated a prevalences than those observed among threefold increase from 1974to 1984, or, white groups. Indeed, observed differin terms of 1974dollars, an increase from ences by race and sex are attributable to 1 to 3.3¢ per pack sold. This amount of effects of income and education (3, 50). money on marketing may discourage me- Income and education effects are, themdia coverageof cigarette-related risks and selves, quite substantial. For instance, disease (44). The average citizen may con- results of the 1985 National Health Include that cigarettes are "not really all terview Survey indicated a 35.4% prevathat bad" because the government "surely lence among adults with less than a high wouldn't allow" their vigorous promo- school education, over twice the 16.50/0 prevalence among those with postgraduate tion (43). The direct effects of tobacco market- training. Among unemployed men, the ing are hard to characterize. That recruit- prevalence is 44.3% (to). Within the miliment of new or reenlistment of former tary, smoking is more prevalent among smokers is among them is suggested by enlisted ranks than officers. Pack-years the extent of the marketing effort and (packs per day multiplied by years smokthe apparent need to replace smokers ing) range from 1.6to 10.5 for pay grades who quit - 500/0 of all adults who have among enlisted ranks and from 0.9 to 3.6 ever smoked (3) - or die. In contrast, the for pay grades among officers (51). (The tobacco industry maintains that adver- increase in pack-years with increasing pay tising is directed to brand preference grade among both enlisted and officer among current smokers, not to recruiting ranks reflects the association of the packnew smokers; however, only to% of years measure with age and seniority.) smokers switch brands each year (43). Even among health professionals, soThis seems a modest impact for the most cioeconomic status appears related to extensive marketing effort in our culture. smoking. Physicians smoke less than registered nurses who, in turn, smoke less The Social Differentiation than licensed practical nurses (52). of Smoking Beyond the general associations of Marketing and advertising of cigarettes smoking with education and income, sevare highly segmented according to race, eral specific characteristics of its distriethnicity, and gender (43). This segmen- bution suggest it is especially common tation is reflected in numerous brand among those not doing well in our culpreferences. Three menthol brands have ture. Divorced or separated men had the an aggregate share of 60% of the ciga- highest prevalence of smoking, 48.2%, rette market of the black population (45). of the 38 subgroups defined by gender Even greater market shares may result in and economic, educational, vocational, some groups. For instance, among black or marital status in the 1988 Surgeon adolescent males and females surveyed General's Report (to). Given the prevain Louisiana in 1981,56 and 77% report- lence among divorced men, it is interested Salem" as their preferred brand (46). ing to note that divorce and separation

706

among men have also been linked to suicide and alcoholism (53). Among a sample of psychiatric outpatients, 52010 reported smoking. Prevalence varied with diagnosis, e.g., 88% with schizophrenia, 49% with major depression (54). Among male frequenters of a churchsponsored soup kitchen in Charleston, South Carolina, 76% reported smoking cigarettes (55). Whereas smoking may be more common among those not doing well, smoking cessation seemsmore common among those who are succeeding and who have greater personal and socioeconomic resources. Prospective studies indicate that among a wide sample of health maintenance organization (HMO) subscribers, for example, those who quit were likely to have been those with fewer health problems (56). That is, smoking cessation may be part of a pattern including other individual efforts to enhance health. Congruent with the likelihood of cessation being associated with fewer health problems, those with other personal advantages are also more likely to quit. Prospectivestudiesindicatethat education level, income, and skills in self-management or personal coping are significantly related to success in self-initiated efforts to quit (57, 58). Racial prejudice, low income, less education, poverty, adolescent problem behavior, lack of optimistic plans for the future, identity as working class, breakdown of affectional bonds, psychopathology - these correlates of smoking suggest a role in response to psychosocial adversity. The effects of stress on initiation of smoking, on smoking rate, and on relapse after smoking cessation as well as the stress-reducing effects of nicotine, all reviewed in the 1988 report (10), support such an analysis. Indeed, the pharmacologic characteristics of nicotine and the delivery characteristics of inhaled tobacco smoke make the cigarette wellsuited as a drug for mitigating stress and other psychologic reactions to adversity in our culture.

Multiple Determinants and the Persistence of the Smoking Career As an example of the interdependencies among wide-ranging determinants of the smoking career, consider the response of a recent quitter coming across a cigarette advertisement in a magazine. To the extent the quitter is part of the "market segment" targeted by the advertisement, he or she may find within the ad a number of symbols closely associated with his or

FISHER, HAIRE.JOSHU, MORGAN, REHBERG, AND ROST

her own recent smoking habits. Previous conditioning of these symbols causes them to elicit some of the individual's responses to cigarettes,experienced as urges to smoke. The symbols and the conditioned responses to them may serve as strong cues for smoking. The conditioned responses to the advertisement are enhanced by the strength of nicotine as an unconditioned stimulus. Further smoking behaviors that are cued by the advertisement and by responses conditioned to it may be reinforced by nicotine. Of course, the placement of such advertisements, billboards, point-of-sale marketing displays, free samples, and other instances of cigarette marketing at numerous points in the daily life of the quitter is supported by the great profits associated with the sale of cigarettes. Thus, cigarette profits make worthwhile the placement of advertisements and other marketing efforts throughout the daily circumstances of the quitter's life. These advertisements and promotions trigger numerous biologic and psychologic responses to make it hard to stay off cigarettes. The smoking career is maintained by forces ranging from physiology to corporate profits. Influences on Smoking Cessation

Considering the easy availability of cigarettes, the enormous resources devoted to marketing them, the ease with which they are consumed in almost every setting of daily life, and their strongly addictive properties, it is no wonder that over a quarter of the adult population smokes. Considering all of these forces, however, it is remarkable that a campaign of public information and related community efforts to encourage nonsmoking has been able to reduce the prevalence of smoking as much as weobserve. Though far underestimating the uniquely enormous dimensions of the risk of smoking, the public has come to understand that smoking is risky. Although the physiologicallyaddictive nature of smoking makes it resistant to social and educational influence, smoking has become undesirable, even by most smokers, 95% of whom report wishing to quit. Since the 1964 Surgeon General's Report, the national campaign to reduce smoking has had substantial impacts on smoking in this country. These impacts are especially impressive when compared to levels of smoking projected from trends apparent before 1964and the first Surgeon General's Report, levels that might have been reached were it not for the national cam-

paign against smoking. Warner (59) estimated that because of the campaign, 35 million Americans were nonsmokers in 1985 who otherwise would have been smokers. Projected to the year 2000, the campaign will have postponed over 2 million deaths. On balance, then, the observed reduction in the prevalence of smoking from 1964 to 1989, from approximately 42 to 27% of the adult population, constitutes a unique achievement in public health efforts to encourage mass behavior change as well as a remarkable testimony to the ability of Homo sapiens to pursue its own betterment.

Personality Variables Over the years, research has linked smoking to rebelliousness, impulsiveness, and identity assertion in adolescence and adulthood (3). Psychology, however, no longer sees such variables as the explanation for or sufficient cause of change; rather, it sees them as mediators of other determinants of change. For instance, negative-affect smoking has been found to predict relapse at an extended followup of a smoking cessation program (60). This does not mean that the absence of negative affect causes long-term abstinence. Rather, low levels of negativeaffect smoking may aid cessation efforts, whereas high levels may undermine efforts or magnify the effects of other barriers to abstinence. Nevertheless, some with high negative-affect smoking succeed in spite of it and some with low levels fail, for reasons unrelated to this variable. In addition to viewingpersonality variables as mediators of change, psychology also views them as the results of programs to promote change. For instance, self-efficacy or confidence in one's own ability to cope with situations likely to trigger relapse has been found predictive of abstinence (61). Other research has found some cessation programs more effective than others in promoting selfattribution of cessation, conceptually similar to self-efficacy (62, 63). These studies have also found self-attribution related, in turn, to abstinence. That is, interventions lead to heightened selfattribution of change, which predicts greater outcomes. From a deterministic or positivistic perspective,self-attribution is not an independent cause of cessation but a marker of impacts of interventions (62, 64). The difference has clinical import. The causes of smoking cessation are not inferred motives and personality characteristics but treatments, education-

STATE

OF THE ART: SMOKING AND SMOKING CESSATION

al campaigns, interpersonal persuasion, and the like. It is these causes that cessation campaigns need to address. As noted above, prevalence of smoking is heightened among those in poor personal, social, and economic circumstances, including psychiatric outpatients. Recent evidence indicates the possibility of specific links between smoking and psychologic problems in addition to the more general linkage of smoking and distress. Glassman and colleagues (65) reported greater than expected lifetime prevalence of depression in smokers and that depression tended to predict failure at cessation attempts. While further studies are needed to confirm this result, Hughes (66) suggests that quitters with a history of depression may require nicotine to prevent depressive episodes. Another possibility is that smokers may develop depression as a component of the tobacco withdrawal symptom (67).

Peer, Family Factors, and Social Support among Adults Family and peer smoking habits are related to the uptake of smoking among adolescents, but they are also related to smoking and resistance to cessationamong adults. Supporting the importance of friends' smoking across the life-span, its impact was not significantly influenced by subject age (68). Those who fail to quit or relapse are more likely to be married to a smoking spouse and/or to report high prevalence of smoking among their friends (69-71). Quitters who work with nonsmokers are more likely to be successful in maintaining their abstinence than are quitters who work with smokers (72). Several studies of smoking cessation clinics have found abstinence related to participants' ratings of support from spouses, living partners, other family members, or friends (73-76). Others' own smoking habits as opposed to their support for smoking cessation may have different impacts. Mermelstein and coworkers (75) found social support related to 3 months of abstinence, but smoking habits of those in participants' social networks related to 12months of abstinence. Health Effects of Smoking Eighty-seven percent of current smokers now understand that smoking is harmful to their health (77). One might wonder, then, why so many persist in smoking, even granted its addictive properties. After all, the 25-yr-old, pack-a-day smok-

er who doesn't quit will die, on average, 6 to 8 yr earlier than someone who has never smoked (1). Smoking accounts for about 400,000 deaths, or one of every six or seven deaths, each year in this country (3). These are outstanding impacts on death for one behavior pattern. They dwarf the effects of other risks. One explanation for the persistence of smoking even with widespread awareness of its riskiness is, of course, its addictive properties. Another is widespread failure to appreciate just how dangerous smoking is (78). In fact, smokers' knowledge of their risks is less than one might conclude from the fact that 87070 acknowledge it as harmful. In contrast to the 87070 of smokers, 97 and 98% of former smokers and nonsmokers, respectively, acknowledge it as harmful. More striking, only 75% of smokers in the same surveyindicated agreement with the proposition that smoking is "one of the causes of lung cancer." In contrast, 94% of nonsmokers and 90% offormer smokers indicated agreement. In a similar pattern, 75% of smokers agreed that smoking is a cause of emphysema, in comparison to 91 and 90% of former smokers and nonsmokers, respectively (77). Furthermore, surveys indicate general insensitivity to the unique levelof risk associated with smoking. That the public does not adequately appreciate the risky nature of smoking was clarified in a Harris survey in 1985. Health professionals rated not smoking as the first priority among things Americans can do to protect their health. The public rated not smoking as tenth, behind such worthy but, for most Americans, less critical habits as consuming adequate vitamins and minerals and drinking water of acceptable quality. Economic factors in public knowledge. Why have many smokers not gotten the message? One answer is that they have not been given it. Warner (44) has documented persistent efforts of tobacco companies and their representatives to suppress media coverage of the uniquely risky nature of smoking. Their ability to do this is enhanced by being part of conglomerates with substantial advertising budgets for nontobacco products. The possibility of loss of advertising revenues from these nontobacco products, as well as from cigarettes, is an effective threat to print and electronic media (44). It is also a threat to others in the communication business. In the spring of 1988, one tobacco conglomerate canceled nontobacco product accounts with an advertising agency that had prepared adver-

707

tisements for an airline's nonsmoking policy. Why would a highly diversified conglomerate manipulate its nontobacco marketing and economic power to advance the interests of its cigarette division? The answer may be in the great profitability of cigarettes in comparison to other product lines. Based on profit and sales data from one conglomerate in 1981, the profit per dollar gross sales of cigarettes was four times that of nontobacco products such as alcoholic beverages and food (41). Indeed, the 1988bid to "take private" the R.J. Reynolds Company was reported to rest on a plan to sell off nontobacco brands, such as Nabisco, to pay the debts of acquisition. This would have left the bidders with full, private ownership of a tobacco company, reversing a 25-yr trend toward diversification of such holdings apparently instigated by the 1964 Surgeon General's Report. The profits of cigarettes are great and motivate substantial contortions in corporate policy and action. That information regarding its health effects might discourage smoking has not always been clearly recognized. Popular views of health education have held that information about health risks or "scare tactics" are ineffective in promoting change. Such views encouraged many smoking cessation programs to focus on how to quit rather than why. However, the level of information versus the level of arousal may mediate the effectiveness of information about smoking risks. Calmpresentation of risk information may increase decisions to quit. Scare tactics, on the other hand, may raise arousal to the point that the individual is simply motivated to reduce that arousal, even at the cost of ignoring the information provided (79). The effects of information may also be mediated by the stage in the smoking career. The contemplator of quitting may take in and benefit from information resisted by the precontemplator (8). The person maintaining abstinence may consolidate change through risk information that confirms its value (80). Again, it is important to recognize that the several stages of a smoking career differ in their responses to external influences, such as information about health risks.

Weight and Smoking On average,smokers weigh less than nonsmokers (81, 82). Paradoxically, however, initiation and continuance of smoking may cause harmful patterns of weight

708

distribution despite lower overall weight (83). Appetite and hunger (84) as well as increased preference for sugar (85) are common withdrawal symptoms. The fear of weight gain after cessation may be particularly a problem for women who report using cigarettes as a method of appetite and weight control (86). Evidence indicates nicotine's utility in maintaining lower body weight is especially important to women (87). Hall and colleagues (88) studied nutritional patterns and body weight before and after quitting. Initial impacts of quitting included increased total calorie intake, sucrose intake, and fat intake. No changes were noted for protein or nonsugar carbohydrates. Increased caloric intake predicted later weight gain. Rodin (82) found increased proportion of calories from sugar related to postcessation weight gain. Among subjects abstinent through the 6-month follow-up, Hall and associates (88) found caloric intake had returned to baseline for women and had fallen below baseline for men. Nevertheless, both groups showed net weight gains at the 6-month follow-up, 8.71bs (105010 baseline body weight) for men and 10.34 lbs (108010 baselinebody weight)for women. Thus, weight gain after cessation appears to be a complex result of changes in total intake, changes in specific food intake, and changes in nutrient metabolism or fat storage (89-91). Several studies have reported nicotine replacement via nicotine polacrilex suppresses weight gain after cessation (84, 92). Gross and colleagues (93) randomized quitters to active nicotine polacrilex or placebo conditions and objectively measured abstinence and weight gain. After 10 wk, those receiving nicotine polacrilex gained 3.8 lbs, whereas those receiving placebo gained 7.8 lbs. Results indicated a dose-response relation between polacrilex use and suppression of weight gain as well as lessened increases of hunger and eating among those receiving nicotine polacrilex. Unfortunately, the 23-wk follow-up found weight gains of 6.8 and 8.7 lbs among subjects still abstinent who had received nicotine polacrilex and placebo. The difference was not significant, leading the investigators to conclude "that nicotine replacement delayed but did not prevent typical postcessation weight gain, an outcome that is consistent with the physiological effects of nicotine on dietary intake, physical activity, and resting or basal metabolic rate" (93).

FISHER, HAIRE-JOSHU, MORGAN, REHBERG, AND ROST

Contemplation of Quitting, Quitting, and Relapse Just as with smoking in general, smoking cessation needs to be viewed as a career taking place amid multiple internal and external influences, ranging from physiology to economics and politics. As noted earlier, there appear to be five stages of cessation: precontemplation, contemplation, action, maintenance, and relapse (8). These five stages may recur in the smoker's career because repeated relapses and efforts to quit are common, many successful quitters reporting several prior attempts and relapses. Thus, the career of cessation may develop over a number of years. As with other career paths, the influences that have the greatest impacts on quitting vary from stage to stage. At the precontemplation stage, matter-offact information is most likely to be effective, whereas exhortations or extensive advice on quitting may only provoke resistance to change. At the contemplation stage, further information about reasons to quit encourages movement toward a commitment. At the action stage, concrete information about tactics in quitting and direct assistance are most helpful (8). There are many reasons whypeople fail to cease smoking or relapse after an attempt to quit on their own or in a clinic. A popular explanation is lack of motivation. This is only an apparent explanation. It renames the problem as "low motivation" but leaves unexplained the reason "motivation" may be low. A more robust explanation of failure is needed. Among possible explanations of relapse are stress, interpersonal conflict, and dysphoria (37, 94) as well as failure to use skills for coping with stress and gaps in social support for nonsmoking. Relapse crises are often precipitated by stress and negative affect. Bliss and coworkers (95) found 56010 of relapsers attributed their first slip to negative affect, and O'Connell and Martin (96) found a comparable figure of 600;0. Subjects surveyed by Marlatt and Gordon (94) and Lichtenstein and associates (97) attributed about 80010 of smoking relapse to interpersonal conflict. In a prospective study of quitters, Ashenberg and colleagues (98) found level of stress to predict subsequent relapses. Life stress coupled with a firmly established pattern of using cigarettes to alleviate anxiety or other negative affect (60) may increase relapses.

The evidence that stress often precedes relapses might lead us to assume that relapserslack skills for coping with stress, but relapsers in one study did not differ from smokers in their stress coping skills (98). Relapsers reported failing to use the skills they did have in the specific situations in which they relapsed. Shiffman (37) found that subjects using strategies for coping with temptations, almost regardless of the strategies chosen, were less likely to relapse than subjects who did not use any strategies. Additionally, it appears that the number of strategies used predicts maintenance (95). Thus, stress as well as failure to use available skills to cope with it and with other sources of temptation appear to be important antecedents of relapses. An interesting finding links the importance of using coping strategies and the likelihood of relapses in the presence of other smokers previously observed (96). Quitters reported less use of coping strategies in the presence of smokers. When the significant effects of coping on relapse were accounted for, the effect of smokers' presence was no longer significant (95). Thus, others' smoking may trigger relapse by discouraging coping with temptation. Marlatt and Gordon (94, 99) present a model that has been very popular in understanding relapse. In addition to being under stress, the quitter may also receivesocial prompts, encouragement, or direct facilitation by peers to resume smoking. After a slip, Marlatt suggests that an "abstinence violation effect" may compound the problem. This may occur in the followingsequence: (1) negativeaffect leads to lowered self-confidence, which in turn leads to a smoking slip; (2) the slip, one or two cigarettes, leads to a further reduction in self-confidence; (3) further lowered self-confidence leads to the conclusion that the case is "hopeless," and abandonment of the quit attempt. Critical to the abstinence violation effect is weighing too heavilythe implications of a single slip, justifying the conclusion that one's case is hopeless. Different influences have been found effective in triggering or preventing relapse at different periods of quitting, maintenance, and relapse. High levelsof daily hassles (100) were predictive of relapse shortly after cessation (98). In the first months after quitting, interpersonal emotional support (73-76) predicted abstinence. Long-term abstinence of a year or more has been tied to the number of

STATE OF THE ART: SMOKING AND SMOKING CESSATION

smoking friends and relatives(69, 70, 75). (Note especially the parallel between consolidation of long-term abstinence and consolidation of smoking in adolescence. Just as the initiate who goes on to a career of drug use will tend to have friends who are also users, so the long-term abstainer is more likely to have friends who are also nonusers.) Failure to maintain long-term abstinence has also been associated with pretreatment measures of "negative-affect smoking" (60). Smoking Cessation Interventions

As the career of smoking cessation includes a number of phases with different influences varying in their importance from stage to stage, so the range of influences marshaled to discourage smoking is great. Nonsmoking efforts now range from the living room to the legislature and many public areas. Health education efforts include home videotapes, TV broadcasts of cessation courses designed to trigger viewers' efforts, cessation manuals that target specificgroups, such as pregnant women, and a range of settings for nonsmoking efforts that include the worksite, the community, the classroom, and the family. Worksites, hospitals, and schools have implemented smoke-free policies. Legislation has been introduced that would restrict marketing of smoking or alter the tax incentives for advertising of cigarettes. Mirroring this breadth, cessation programs themselves have grown to address nicotine addiction, stress management, selfcontrol, fantasy and personal meaning, means to recruit support from friends and relatives, and means of resisting peer pressure to begin or resume smoking. The following sections review a variety of specific tactics that are often included in comprehensive, group smoking cessation courses. These include temptation management, cue extinction, aversive techniques, and contingency management. For some tactics, such as the aversive technique of rapid smoking, there exist data validating its specific impact for smoking cessation. For others, little data support specific contributions to smoking cessation. Nevertheless, they are routinely included in programs because of their general utility in the behavior therapy literature (e.g., contingency management) or because they are part of a standard package that is widely used and of which the aggregate impacts appear appreciable (e.g.,temptation management).

Temptation Management Popular in weight loss (101) as well as in smoking cessation and other behavior change programs, temptation management entails avoiding or minimizing exposure to temptations, preventing consumption, or manipulating incentives so that temptations remain less powerful than desired behavior. The first step in temptation management is often monitoring of the time, place, and reason for each cigarette. The next step is to limit exposure to these. For example, if coffee is a cue, the quitter may drink tea in its place during the initial period of abstinence. Avoiding the coffee break, perhaps by going for a walk, may be another strategy. Incentives may be manipulated by tactics such as alerting all coworkers to a cessation effort so that fear of embarrassment may pose a counterforce to temptation. What is critical to temptation management is anticipating and acting in advance of the temptation; trying simply to avoid a present and salient temptation is unlikely to be successful (102). Cue Extinction Unless the smoker is to make many radical changes in lifestyle, he or she must eventually face those situations in which temptation is strong. According to basic processes of classic conditioning (39), extinction of a conditioned response requires exposure to the conditioned stimulus without the unconditional stimulus. For instance, extinguishing urges conditioned to coffee requires exposure to coffee without a cigarette. "Cue extinction" may be implemented before actual cessation to diminish the impact of powerful cues before having to abstain from smoking altogether. Seven to ten days before giving up cigarettes altogether, smokers select several cues, such as coffee, that they feel will be most difficult for them to endure without a cigarette. Until they quit, they continue smoking at their normal rate, but do not smoke in the presence of the selected cues. A guideline for this is to wait at least 10 minutes until after the cue has passed before lighting a cigarette. Observations in our own programs indicate reduced "pull" of these cues after cessation (5, 103). Aversive Techniques Several smoking cessation research programs (104) included rapid smoking as a tactic designed to condition the stimuli of the cigarette and the act of smoking to an aversive response. Participants in

709

rapid smoking smoke a series of cigarettes (frequenty three) in rapid succession, inhale frequently (i,e., every 6 s), and hold the smoke in their mouth for some time. By the end of this procedure, most participants feel dizzy and/or nauseated. This is repeated several times per session and/or for several sessions around the time of quitting. The purpose of such a technique is to have the smoker come to associate the thought/sight/ smell of a cigarette with the feelings of nausea. Subsequent thoughts or cues of cigarettes should elicit unpleasant images rather than favorable ones. Early results of rapid smoking wereimpressive (104). Replication, however, was not always easy (105, 106), and concerns over safety and smoker acceptance have led to little use as a core method for community smoking cessation clinics. Nevertheless, milder variants of rapid smoking, such as normal-paced aversivesmoking or smoke holding, are commonly included in treatment packages (11, 106). It appears that concerns for the safety of rapid smoking are overstated and that it may be especially effective for patients with disease in whom cessation is an immediate priority. One study found a 2-yr continuous abstinence in 50070 of cardiopulmonary patients receivingrapid smoking as opposed to zero percent among control subjects. Regarding safety, there was no evidence of myocardial ischemia or significant cardiac arrhythmia attributable to rapid smoking as opposed to either normal smoking or abstinence for 12 h (107). Use of electric shock as an aversive stimulus has received little support as a smoking cessation tool (108) and is now rarely employed.

Contingency Management Contingency management has been used in outpatient (109, 110) and worksite settings (111,112). The quitter arranges that some reward or punishment be contingent upon critical behavior during a specified period, for instance, smoking no cigarettes between the fourth and seventh days after cessation. This may be established informally or by written contract, shared perhaps with friends and family or with a professional. Generally, private contracts are less effective "than those known to at least one other person. Contracts will generally be more effective if they reward desirable behavior rather than punish undesirable behavior. Contracts should not be based on longterm outcomes; rather, they should spell

FISHER, HAIRE.JOSHU, MORGAN, REHBERG, AND ROST

710

out a frequent, clear, and contingent reward. The reward doesn't have to be large but it should be frequent.

"Self-Help" An often quoted statistic is that 95070 of all smokers quit on their own. This is an undocumented figure, first used in a government pamphlet in 1977 (113) and since then quoted frequently. Self-help is actually a misnomer - no one quits in a void. Behavior results from the interaction between the person and the environment. Those who are viewed as having quit through self-help will often have been encouraged by a variety of sources such as individual counseling from a physician or a TV show on quitting. Self-help may be a damaging myth because it may cause people to focus too much on supposed personal sources of change, such as determination and insight. They may wait for some imagined insight that they expect to make quitting automatic. Instead, they need to instigate changes in their routines or obtain help from friends or professionals in order to quit. The importance of actively changing routines or otherwise coping with temptations to smoke was clarified in a recent study of individuals quitting independently of any organized program. The strongest predictor of outcome (abstinence at the end of one month) was the number of coping mechanisms employed by the smoker. Although the specific type of mechanism (e.g., engaging in some distracting activity rather than smoking, chewing gum, telling oneself how hazardous smoking is) was unrelated to outcome, the number of different strategies used by individuals was significantly associated with outcome. Of 96 who reported using no coping mechanism, only one remained abstinent (95). The myth of self-help may also lead to ascriptions of failure to presumed immutable forces such as a supposed "lack of willpower." Especially after relapses, the self-control rhetoric may be damaging. The attribution of failure to "lack of willpower" often goes hand-in-hand with the assumption that willpower is something "you either have or you don't." Putting the two together, a single cigarette may become evidence for lack of a necessary condition for success that cannot be acquired. Such an analysis of relapse is unlikely to prompt renewed efforts to quit. Results of Stimulus Control, Contingency Management, and Social Support Programs At Washington University, St. Louis,

Missouri, we developed a 15-sessionprogram that included such techniques as target-date quitting (in which participants select their own quit date) (114), cue extinction, and self-management of cues and incentives. The program also included covert sensitization (115) in which subjects practiced imagining aversiveconsequences of smoking (coughing, choking, nausea) in order to establish the use of such images as a self-control tactic to counter urges (116). The program included no aversive smoking procedures. At the 6-month follow-up, participants' reports of abstinence, no cigarettes during the previous 7 days, were validated by analyses of salivary thiocyanate. By this criterion, 33% of participants were abstinent (103). This study demonstrated that a comprehensive behavioral and educational program could obtain validated, appreciable abstinence rates among heavy smokers (minima: 20 cigarettes per day for at least 5 yr; means: 32 cigarettes per day for 22 yr). Others have also reported successful programs using such multicomponent behavioral and health education, groupbased interventions (117). One of the most successful programs (106) achieved current abstinence with 45% of smokers at the 12-month follow-up. These programs also included aversive smoking procedures. The smoking intervention of the Multiple Risk Factor Intervention Trial (MRFIT) program, described in detail below, was in most respects a multicomponent, behavioral group program without aversive procedures. By the end of the four-year program, 40% of initial smokers were no longer smoking. Integrating state-of-the-art procedures such as described above, the Freedom from Smoking® program of the American Lung Association (ALA) was developed in the late 1970s through a joint committee of the American Thoracic Society (ATS) and ALA staff and volunteers. The program includes both a sevensession, outpatient group clinic as well as a self-help alternative consisting of two self-help manuals. The Freedom from Smoking group clinic has been evaluated by ALA from 1982through 1985.Across 135 offerings of the clinic for which data were available, the percent of individuals reporting no smoking at the end of the clinic ranged from 47 to 55% with an average of 51%. The prevalence of reported nonsmoking during the month preceding the 12-month follow-up ranged from 25 to 32% with an average of29% (118). Most local Lung Associations, or other agencies such as the American Cancer Soci-

ety or American Heart Association, include professionals eager to work with physicians in identifying sources of referrals to these or similar smoking cessation programs. The self-help version of ALA's Freedom from Smoking includes a cessation manual, "Freedom from Smoking in 'Iwenty Days," which offers participants the choice of reducing their smoking gradually or quitting cold turkey. In addition to the cessation manual, there is a maintenance manual, "A Lifetime of Freedom from Smoking." This includes material for coping with tension, social cues for cigarettes, weight gain, and other obstacles that arise during maintenance. Distributed by mail, the combination of the two manuals attained an 18% prevalence of reported nonsmoking for the month preceding the 12month follow-up, assessed by telephone interview (119). What was most interesting about the follow-updata for the ALA self-helpprogram was that the quit rate was 12% at the 1and 3 month follow-up. It then rose to 15% at six months, 19010 at nine months, and 18% at 12 months. The manuals appeared to have continued to recruit smokers to cessation during the course of the follow-up. In contrast, most cessation clinics reported in the literature are followed by a continuing diminution in the prevalence of nonsmoking at greater durations of follow-up. There may be two reasons that the self-help manuals instigated a reversal of this pattern. One is the natural history of individuals' attempts at quitting on their own. It may be the nature of self-help for people to try it, go back to it, try again, and gradually reach their goal. In contrast, smokers joining a highly structured comprehensive cessation clinic may perceive themselves as having failed if they do not quit according to the schedule of the program. Following the inferences of the abstinence violation effect, such participants may even feel that there is no point in trying again, having failed with what they view as a state-of-the-art program. A second reason for the continued increase in the prevalence rate of nonsmokers using the ALA manuals may be that they are very attractive and well produced. High production values may be important in encouraging the smoker or would-be quitter to keep the materials for subsequent use (as opposed to discarding them). Recently, the ALA has developed another "self-help" manual, Freedom from Smoking for You and Your Family", This manual reflects emphasis on easier readability and a clearer

STATE OF THE ART: SMOKING AND SMOKING CESSATION

presentation of material, and includes instruction on adjunctive use of nicotine polacrilex (120).

Pharmacologic Interventions Pharmacologic treatment of tobacco dependence has received renewed attention in the last decade. This has been prompted by increased recognition of the role of nicotine and its psychoactive properies. Three approaches have received significant attention: nicotine antagonists (blockade therapy), symptomatic treatment of smoking withdrawal, and nicotine replacement. Among nicotine antagonists, mecamylamine hydrochloride, an antihypertensive, acts both centrally and peripherally. Data from animal studies and preliminary clinical trials support further empiric investigation of its use for smoking (121). Although not a nicotine antagonist, clonidine is also an antihypertensive that reduces symptoms of opiate and alcohol withdrawal (122). Several studies have noted the significant effect of clonidine on withdrawal symptoms during brief periods (1 to 3 days) of smoking cessation (123, 124). A double-blind, randomized trial compared clonidine and placebo. All participants received individual counseling based on ALA materials. In the group receiving clonidine, 52070 of heavy smokers (mean = 31.2cigarettes/day) achieved continuous abstinence at the end of a 4-wk treatment, as opposed to 21% of those receiving placebo (65). The advantage of clonidine was interestingly limited to female participants. Six months after treatment, 27% of those who received clonidine reported nonsmoking in comparison to 5% of those receiving placebo; however, a randomized trial in a primary care setting found no advantage of clonidine over placebo (125). When combined with minimal contact instead of with individual counseling, clonidine showed a nonsignificant trend to exceed the effects of placebo (126). Of pharmacologic approaches to smoking, nicotine replacement therapies have shown the most promise. At present, nicotine polacrilex is the only nicotine substitute product that has Food and Drug Administration (FDA) approval. A number of studies have compared the combination of behavioral counseling and nicotine polacrilex with counseling plus placebo gum or counseling alone (84, 127). Approximately half of these studies have shown significantly higher abstinence rates for active gum at the 6- or 12-month follow-up. The inconsistency in findings may be due, in part,

to varying patient characteristics, subject selection, and intensity of treatment. Three recent randomized, double-blind, placebo-controlled studies illustrate this diversity. A study that randomized 70 family physician practices to three treatment conditions investigated the effect of training physicians in brief smoking intervention skills in combination with nicotine polacrilex administration. Polacrilex plus physician training was superior to polacrilex alone or usual care conditions at the 3-month follow-up (p < 0.05), yet fell short of statistical significance at the 1-yrfollow-up (p < 0.07) (128). Rather atypical recruitment criteria were used in this study. Subjects were eligible for entry if they smoked one or more cigarettes per day and did not have to commit to attempt to stop smoking. Nicotine polacrilex showed no advantage over placebo when combined with a brief physician and nurse intervention (129). This study is noteworthy in that patients were selected according to their desire to quit (as indicated by willingness to set a quit date within a 2-wk period), physicians were carefully trained and monitored, and criteria for outcome were rigorous (1yr continuous abstinence). In a third study, the effectiveness of 2 and 4 mg nicotine polacrilex was evaluated in combination with six sessionsof group counseling. Highly dependent smokers were randomized to 2 or 4 mg nicotine polacrilex; others were randomized to 2 mg nicotine gum or placebo gum. All comparisons at the 1- and 2-yr followups were significant with the exception of the 2-mg nicotine gum versus the placebo at one year. Interestingly, this study diverged from others in that its counseling component was not specifically behavioral. The "important elements" were described as "nonspecific support and encouragement and an atmosphere of acceptance" (130). Many of the interventions utilizing nicotine polacrilex have been in concert with behavioral counseling protocols that may be more extensive than those likely to be replicated in physicians' offices. Importantly, nicotine replacement seems ineffective if administered outside of a more comprehensive treatment or counseling intervention. For instance, when simply prescribed in a dispensary setting without counseling for proper use and other cessation efforts, it failed to exceed the effects of placebo (13). In another study, nicotine substitution did no better than placebo when participants were told that the placebo contained nicotine (131). Thus, the 1988 Surgeon General's Report devoted to nicotine addiction con-

711

eluded, "Nicotine polacrilex gum has been shown in controlled trials to relieve withdrawal symptoms. In addition, some (but not all) studies haveshown that nicotine gum, as an adjacent to behavioral interventions, increases smoking abstinence rates" (10). As desirable as it may be to combine pharmacologic interventions with appreciable behavioral counseling, minimal contact protocols are more attractive to many smokers and likelyto be more feasible for practitioners. Some research has addressed this. In combination with nicotine polacrilex, eight self-administered relapse prevention modules, mailed weekly,'achieved 7-day sustained abstinence rates 1.5times greater than placebo (132). This study employed an unusual inclusion criterion: subjects were required to have quit smoking for 48 hours before entry into the program. This abstinence requirement was established because the study's focus was on maintaining abstinence and to exclude quitters who were likely to fail early. Forty-nine percent of those scheduled for a postquit visit did, in fact, relapse within 48 h. Though this requirement significantly limits comparison to other studies, it is striking in its suggestion of alternative strategies for patient selection. To summarize research on nicotine replacement, positive outcomes appear more consistently when nicotine polacrilex is utilized with counseling or psychologic programs to encourage and provide structure for cessation. Nevertheless, several investigators have questioned the utility of nicotine polacrilex in general medical practice (127, 129). In primary care settings, the best results generallyappear more often with more intense treatment efforts (130) and when a patient selection procedure is utilized (132). The development of a transdermal nicotine patch presents a new possibility for nicotine replacement after smoking cessation. This approach provides continuous nicotine delivery that is less reliant than nicotine gum on patient adherence. An initial study demonstrated 3-month abstinence rates of 36% for the nicotine group versus 23% for the placebo group (133). Severalgroups have published detailed protocols for administration of nicotine gum (134-136).

Interventions for Maintenance and Relapse Perhaps the greatest trend in smoking programs in the recent past has been their attentiveness to relapse prevention. Many different types of programs or self-help techniques can be effective in aiding peo-

712

pie in quitting for 24 h to several days. It is not uncommon for quit rates at the end of a 1-to 2-month program to exceed 50070; however,when subjects are assessed 6 to 12months later, cessation rates have generally fallen back to around 30%. Thus, research explores a wide variety of techniques to prevent relapse. Social support interventions, skills training, aversion techniques, or simply extending the schedule of meetings have all been tried but often with disappointing results (137). As noted earlier, one of the best predictors of maintained abstinence is self-efficacy (61).The chief determinants of selfefficacy are not mere verbal reassurances but pertinent experiences and opportunities to learn and practice skills (138, 139). Similarly, attributing quitting to personal characteristics (such as a personal decision to quit or one's own skill) as opposed to external characteristics has been a predictor of long-term abstinence (62, 63). Thus, counseling should emphasize an individual's skills, strengths, and decision to quit. Attempts to teach skills for coping with relapse temptations have been successful in several studies (117). In one, quitters identified explicit tactics for coping with situations most likely to tempt them. They then rehearsed these tactics in four weekly, 2-h group meetings. This treatment led to a I-yr continuous abstinence of 41.3%, significantly greater than that of control subjects (140). Thus, encouraging use of skills for coping with relapse temptations may enhance maintenance. As noted in the discussions of relapse and of self-help above, the choice of particular coping skills is not critical to successful resistance.Their use as opposed to their neglectis what predicts maintenance. Rather than teaching new coping skills, interventions may best emphasize practice and use of skills already available.

Social Support As early as 1971, research indicated the importance of peer smoking in adult smoking and its cessation (69, 70). These factors, however, did not receive the attention they long enjoyed in discussions of smoking among adolescents, probably reflecting popular notions that adolescents are especially influenced by their peers but that adults are more autonomous. While peer influences on adults were relatively ignored, the popularity of self-control procedures and rhetoric (64) was manifested in smoking cessation programs of the 1970s, which stressed the individual's control over smoking by manipulating its triggers or antecedents.

FISHER, HAIRE..JOSHU, MORGAN, REHBERG, AND ROST

However, research directed at such pro- been promising. For instance, the Johncedures failed to yield appreciable im- son and Johnson Live for Life program provements in program impacts (141). included a comprehensive, group smokThis led to a search for important vari- ing cessation clinic. At the 2-yr followables that had been ignored. The 1980 up, 22.6% of those smoking at baseline and 1982Surgeon General's Reports (142, reported no longer smoking. In worksites 143)each identified social support as pos- receiving only screening, this figure was sibly important in mediating cessation 17.4%. The difference was more proamong adults. A number of papers have nounced among smokers at high risk for continued to explore its effects (73-76, cardiovascular disease, 32 versus 12.9% 111). In their efforts to quit, women may (148). Klesgesand Cigrang (149) reviewed benefit from interpersonal support more worksite smoking cessation research and than do men (29, 144). Social influence found multicomponent behavioral promay also be negative. Quitters' reports grams at the worksite to yield reports of of smokers offering cigarettes or smok- no smoking among 33070 of participants ing in front of them predicted subsequent at their conclusion and 20% at followrelapse (76). up. That these abstinence levels are someAs recently reviewed by Lichtenstein what lower than those reported in group and colleagues (145), social support programs offered in the community may measures have been repeatedly correlat- reflect that as many as 70% of smokers ed with abstinence, but social support in- entering worksite programs would not terventions have not been found to im- have sought out similar programs in their prove markedly on other procedures. For communities (150). instance, an emphasis on group cohesion The biggest problems associated with to enhance social support led to initial worksite intervention are the low numbut not long-term advantages over a con- bers of smoking employees who choose trol group receiving standard interven- to join the programs and then a fairly tion (146). high attrition rate after joining (149, 151). The failure of attempts to manipulate This has prompted research into factors group cohesion or partner support to that differentiate joiners from nonjoinlead to long-term improvements in treat- ers as well as studies of incentives for ment outcome (147) may be understood joining, such as competitions among through considering the nature of peer companies or work groups (152, 153). factors that do correlate with long-term Community organization approaches abstinence. As noted above, the smoking seek to involve target audiences in planprevalence in the social network has reli- ning and implementing their own proably been associated with nonsmoking or grams in order to increase social support long-term abstinence (69-71). Indeed, re- for desired changes among their memcent research indicates that numbers of bers (154). Application to worksite smokfriends and family members who smoke ing cessation has led to programs in may be a better predictor of long-term which steering committees of employees abstinence (e.g., 12 months) than short- and managers guide a broad-based proterm (e.g., 3 months) (75). It may be more gram to promote cessation. Professioneffectiveto interveneto manipulate norms als consult to these committees and train and standards of networ ks than to teach selected coworkers to run smoking cessasupportive strategies to a few significant tion clinics. Such a program, Employer others. Assisted Smoking Elimination (EASE), was developed with support from the Worksite Programs ALA of Eastern Missouri. In this proThat social support and changed norms gram, broad promotion and peer support and standards may need to be sustained in appeared more important than a proorder to promote continued nonsmoking gram's formal cessation clinic. Across has encouraged programs at the worksite. four worksites completing long-term Smokers spend large portions of their follow-up in EASE, 9.5 to 25% of those time at work. Coworkers may be impor- who didn't join the formal clinic reported tant sources of social support. Managers current nonsmoking at follow-up rangmay be cooperative with cessation pro- ing from 12 to 24 months after program grams in order to reduce health costs and initiation. Overall prevalence of reportto provide workers a benefit. Worksite ed nonsmoking among all baseline smokprograms havebeen encouraged by regula- ers ranged from 16 to 24% (150, 155). tions restricting smoking in public buildImplications for Health ings and by many privatecompanies workProfessionals ing toward a smoke-free environment. Outcomes of worksite programs have Smoking is a chronic behavior that ex-

STATE OF THE ART: SMOKING AND SMOKING CESSATION

tends over time, influenced by biologic, psychologic, social, economic, and political forces in a career of several stages. Part of the career is quitting itself, developing and continuing through different stages, including failed attempts. Because of these characteristics of the smoking career, health professionals may take diverseroles ranging from discouraging the adolescent who is contemplating to initiate smoking to provoking the interest of the adult precontemplator, to reassuring the relapser, to continuing to support and encourage the long-term quitter. The dimensions of smoking and quitting are broader than anyone profession or provider can encompass. Conventional clinical activities such as a brief explanation of risks and encouragement of corrective action, prescription of nicotine polacrilex, and follow-up to encourage success may be adequate for many smokers. For others, referral to self-help or group cessation programs may be worthwhile. Within this range of conventional clinical activities, from explanation to referral, the health professional can have a very constructive impact. Given the vast array of smoking cessation influences outside health care settings and their potential interactions with clinicians' advice, counseling, or referral, the professional may be best viewed not primarily as the direct provider of a wide range of smoking cessation services but as a powerful catalyst of the patient's progression through the career of quitting. Clinical Interventions for Smoking Cessation

Counseling by health professionals has contributed to a substantial proportion of the 90% of quitters who claim to have quit outside formal group treatment programs (143). Based on data from the 1983 Health Interview Survey, Ockene (157) reported that physicians contact at least 700/0 of all smokers each year, including a majority of smokers who consider themselves to be in "excellent" health. A review of 12 studies (157) of American physicians published since 1983 concludes that, on average, less than twothirds of providers report advising all their patients to stop smoking. Ockene concluded that "only a very small percentage of physicians actually go beyond providing advice to stop smoking," utilizing written materials and referrals that assist smokers interested in quitting (157). Thrning to patients' reports, one study found that two-thirds of primary care patients who smoked cigarettes reported

ever having been advised to quit (78). Citing an earlier report (158), Ockene (157) suggested that this figure represented an increase over responses a decade ago when only 20% of smokers reported they had ever been advised to quit. Studies have found that the presence of a smoking-related illness, a longer duration of cigarette smoking, a greater number of prior quit attempts, and a higher number of cigarettes smoked predict whether a smoker reports having been advised to quit (45, 78). That less than two-thirds of physicians and other providers report advising all smoking patients to quit and that only about two-thirds of patients report receiving such advice indicates a need for greater instigation of professionals in this area. Accentuating the importance of this, the potential of physicians to contact large numbers of smokers makes even a modest impact of their efforts of substantial public health significance. Initially encouraging this perspective was work by Russell and coworkers (159) with general practitioners in England. Twoto three minutes of professional advice to quit along with a brief cessation pamphlet and the physician's stated plan to follow up on patients resulted in cessation rates of approximately 5% (159). Although seemingly a modest effect, Russell and coworkers noted that the adoption of such a simple intervention by primary care providers would have much greater effects than a great many smoking cessation group clinics. In a randomized, controlled study that included biochemical validation of smoking status, Li and colleagues (160) demonstrated the incremental impact of 3 to 5 min of counseling by a physician over a simple warning about smoking. Advice to quit and structured counseling (setting a target quit date, discussing coping strategies) achieved current abstinence at the ll-month follow-up among 8.4% of workers exposed to asbestos compared with 3.6% in a minimal warning group. More recent studies have continued to support the utility of advice and cessation counseling for smoking patients. Kottke and colleagues (161) reported a metanalysis of 39 smoking cessation intervention studies conducted in medical settings to determine which attributes of clinical interventions were most strongly associated with successful quitting. As predictors of program success, metanalysis included a number of variables, including treatment modalities (counseling, nicotine polacrilex, or written materials), face-to-face counseling, repetition and duration of

713

intervention sessons, and whether counseling was provided by physicians, nonphysicians, or both. Six months after intervention, the average difference in cessation rates between experimental and control groups was 8.4% with the largest reported difference being 37% (162). Among treatment modalities, face-toface counseling or advice had the best results, followed by nicotine polacrilex, written materials, and miscellaneous other interventions; however, multiple regression analyses showed that the number of such treatment modalities was more predictive of success than was the presence or absence of anyone. Similarly, more frequent contacts over a longer period of time and incorporating both physician and non-physician contact were predictive of success at the 6- and 12month follow-ups. The failure to identify any single key ingredient but, instead, to find the range and repetition of advice predictive of success has substantial implications for practice. As the investigators concluded, "Success was not associated with novel or unusual interventions. It was the product of personalized smoking cessation advice and assistance, repeated in different forms by several sources over the longest feasible period" (161). Supporting the importance of individualized interventions repeated over time are two of the most successful interventions that have been reported in clinical settings, the Whitehall Civil Servants Study and the MRFIT study. The Whitehall Civil Servants Study (163) used a randomized controlled design to investigate 1,445 smokers among a larger group of employees, all at high risk for cardiopulmonary disease. After comprehensive cardiopulmonary assessment, physicians (1) provided individualized feedback regarding test results and family history, (2) informed smokers of evidence that, for them, smoking represented more than the average risk to future health, and (3) advised them to quit. During three subsequent 15-min counseling sessions, the physicians provided advice on steps to stop smoking, brief manuals, and encouragement. Reporting abstinence from all smoking at the 3-yr follow-up were 23% of those receiving the intervention versus 10% in usual care. These rates need to be interpreted conservatively because they werebased on self-reports in a clinical setting with a high implicit demand on patients to report positive change. Even assuming a rate of false reports of 20 to 30%, however, they are still striking. The MRFIT included extensive screening and individualized counseling regard-

FISHER, HAIRE.JOSHU, MORGAN, REHBERG, AND ROST

714

ing risk profiles, regular follow-up, repeat treatment, a treatment package including a full range of stimulus control and contingency management techniques, involvement of spouses, buddy systems, and other social support procedures, all continued over a 4-yr period. Forty-four percent of all 4,103 smoking men in the MRFIT had stopped by the end of the initial, 4-month intensive cessation program. Of these,929or 23% remained nonsmokers throughout the 4-yr follow-up period. Continued treatment and followup helped still more to quit. The nonsmoking prevalence at the 4-yr followup was 40070 (164, 165). Several large-scale studies are currently developing and testing programs to help physicians incorporate smoking cessation interventions into their routine practice. The results of two of these studies published to date suggest that such training programs can indeed increasethe frequency of physician counseling about cessation and the frequency of patients' quit attempts. Unfortunately, the programs do not appear to result in a significantly higher rate of verified cessation at the I-yr follow-up (166,167). Kottke and colleagues (167) explained these problematic findings by noting that even trained physicians in the context of an intensive month-long campaign discuss quitting with only half of their smoking patients. Furthermore, the impact of their advice on quit attempts is minor in comparison with the number of spontaneous quit attempts smokers make. Because of the frequency of spontaneous quit attempts, Kottke and colleagues suggested physicians can have a greater impact by working to prevent relapse than by providing more advice to quit. To help prevent relapse, the investigators suggested helping to identify family and friends who are willing to provide emotional support during a quit attempt. Because both of the trials published to date were designed to increase the frequency with which physicians counseled smokers to quit in the context of a shortterm campaign, less is known about how to sustain high rates of physician intervention over time. Earlier studies (168) showed that the frequency of physician counseling deteriorated markedly in the nine months after training, with some physicians concentrating primarily on the heavy smokers. These investigators demonstrated that monthly monitoring and the provision of feedback when performance declined was necessary to maintain a high rate 0 f physician intervention. Others have demonstrated that patient

chart stickers and the provision of free nicotine polacrilex increase the time physicians and dentists spend counseling their patients about smoking (169). Patient health characteristics have alse been investigated as predictors of successful cessation. Studies that have followed samples at risk or patients with disease have tended to show the presence, symptoms, or severity of smoking-related disease to increase rates of cessation (78, 170). Longitudinal population-based studies, on the other hand, indicated greater rates of cessation among those with fewerhealth problems or complaints at initial assessment (56, 171). Thus, information about risks or the occurrence of disease may be the occasion that provokes cessation in many smokers. Yet, smoking cessation may be associated with having fewer health problems when evaluated on a population basis.

Pulmonary Disease and Smoking Cessation Eighty-five percent of chronic obstructive lung disease can be attributed to cigarette smoking, far outweighing other etiologic factors (2). Smoking cessation often reverses changes seen in small airway function and slows the rate of decline in lung function in those individuals with significantly reduced expiratory airflow (52). In nonpatient samples, former smokers achieve similar lung function as never smokers after smoke-free intervals of 7 yr or more (172). Smoking cessation is clearly critical for the patient with respiratory disease. Both retrospective and prospective studies have investigated cessation among patients that have been either identified as high risk for or have been diagnosed with pulmonary disease. Conclusions from these studies, however, are limited by the heterogeneity of interventions, outcome measures, and subject selection. Because some studies group together patients with pulmonary disease, cardiac disease, or the combination, inferences specific to pulmonary patients and smoking cessation are difficult. Tworetrospective, cross-sectional studies assessing smoking status at admission to treatment centers found more than 65070 of the patients indicating they were former smokers (173, 174). Pederson and associates (175) evaluated retrospectively the impact of brief smoking cessation counseling upon the patient panel of a single pulmonary physician. Six months to 7 yr after advice to give up smoking and information regarding techniques weredelivered, 27% of 117 patients reported continuous abstinence for

6 months or longer. All three of these studies relied on patient reports of smoking status, included no control group, and in the latter, may have reflected the enthusiasm or diligence of the single physician whose patients were studied. There have been relatively few experimental intervention trials with pulmonary patients that employ randomization, control groups, and biochemical validation of outcome.The study by Roseand Hamilton (163) of high-risk patients, reviewed in the previous section, met these criteria with the exception of verification of smoking status. One year after receiving a noncontrolled clinic intervention, 50070 of pulmonary and/or cardiac patients who had smoked at baseline reported current abstinence (176). Three randomized, controlled intervention studies of cardiopulmonary patients have reported biochemically verified follow-up abstinence rates. In a study comparing health motivation treatment with normal-paced aversive smoking, group differences failed to achieve significance (177). However, Hall and colleagues (107) found 50070 continuous abstinence at the 2-yr follow-up of rapid smoking, compared to zero percent for a wait list control. No subject developed untoward consequences from rapid smoking as shown by extensive cardiac testing and monitoring. These results prompted the investigators to conclude rapid smoking is safe and efficacious for patients with mild to moderate cardiopulmonary disease. A study comparing the addition of behavioral skills to nicotine gum in a VApopulation found no differences between groups but an overall abstinence rate of 46070 at the 3-month follow-up (178). Although relatively little research has targeted smoking cessation among pulmonary patients, a current major investigation should help redress this imbalance. The Lung Health Study is a national clinical trial investigating the impact of smoking cessation and bronchodilator therapy in patients at high risk for chronic lung disease. Approximately 6,000 smokers with early airway obstruction have been randomized to control or treatment groups and are to be followed 5 yr. This study will evaluate treatment effects in terms of smoking cessation, compliance with bronchodilator regimens, and lung function. The Lung Health Study is the first prevention trial for lung disease as well as the largest clinical trial of nicotine polacrilex. Pulmonary patients' efforts and success at cessation have been associated with demographics, social influences, and pa-

STATE OF THE ART: SMOKING AND SMOKING CESSATION

tient perceptions or beliefs. Consistent with other research regarding the relationship between demographic factors and smoking cessation, older patients (179) and men (178, 180) are more likely to become ex-smokers. The psychosocial assets or adaptive behaviors of pulmonary patients were significantly related to smoking cessation before hospitalization (181) and with permanent cessation (182). In a prospective study of 308 newly diagnosed respiratory patients who were given advice to cease smoking by a pulmonary physician, a logistic regression model correctly classified smoking status 92070 of the time (183). Variables predicting follow-upsmoking status wereincreasing age, desire to quit, the patient's prediction of his or her own likelihood of quitting, being married, and higher socioeconomic status. A subsequent study cross-validated this model on a newgroup of patients with prediction accuracy of 89.6% (184). In a follow-up of the original cohort of patients 4 to 7 yr after advice to quit, the original model was less useful for predicting success (67% classification accuracy) than was a model that also incorporated self-reported 6-month abstinence rates and "reasons for smoking other than addiction" (185). Although social, demographic, and psychologic factors have predicted cessation, it is surprising that disease characteristics have not been strongly related to cessation among pulmonary patients. Several studies have found little impact from subjective or objective evidence of early respiratory disease. Asbestosexposed smokers with abnormal pulmonary function tests were no more likely to quit than were those with normal pulmonary function tests (160). Worse than not inducing cessation, the presence of chronic respiratory symptoms appeared inversely related to cessation among 467 coal miners who smoked. Those who initially reported symptoms of smokingrelated illness were more likely to remain smokers at a 5-yr follow-up than were those who initially denied respiratory symptoms (186). Subjects in both studies were men. Other research with both pulmonary and cardiovascular patients indicates women are more likely than men to be ex-smokers, given the presence of disease (78).

Smoking and Cardiovascular Disease Smoking cessation reduces the risk of myocardial infarction to that of nonsmokers quite rapidly, perhaps as quickly as 3 to 5 months after cessation (187). Reviewingstudies of smokers who devel-

op cardiovascular disease, Rigotti and Tesar (188) found one-quarter to one-half of survivors of myocardial infarctions abstinent from smoking at extended followups. They identified as contributing to cessation the presence and severity of disease as wellas symptoms related to smoking. Three to five years after myocardial infarctions, 51% of survivors who had smoked at the time of their infarct reported currently not smoking (189). The impact of heart disease on cessation is also demonstrated by a study by Ockene and coworkers (190) in which 27% of subjects hospitalized with an initial coronary event were ex-smokers, whereas 44% of those hospitalized for their second or subsequent event were ex-smokers; the difference of 17% is presumably attributable to cessation after the initial event. That myocardial infarction may motivate cessation was also demonstrated by a study of intensive advice to quit while the patient was still in the early phase of recovery. Of those receiving intensive advice,63% reported nonsmoking 3 yr later in comparision to 27.5% receiving conventional information (170). The severity of myocardial infarction is related to long-term abstinence. Many of those who suffer less severe infarcts return to smoking relatively quickly after the acute stage of their illness (189), in many cases resuming before hospital discharge (20).

Smoking and Diabetes Diabetes mellitus results in accelerated macrovascular and microvascular atherosclerotic disease, doubling the risk for stroke, myocardial infarction, and peripheral vascular disease. In the presence of smoking, this risk increases from fourto elevenfold (191). Looking at some of the specific interactions between smoking and other risks, diabetes has been found to increase the risk of hyperlipidemia (192) and double the risk of hypertension (193). In turn, the combination of these two risk factors with smoking increases the risk for death from coronary disease elevenfold (194). Cigarette smoking contributes to the presence of arterial vasoconstriction, increasing the risk of peripheral vascular disease in diabetes. In one study, diabetic patients with gangrene were smokers in nearly all cases and, when compared to nonsmokers, had peripheral vascular disease rates of 33 versus 16% (195). Diabetic persons who stopped smoking for at least 2 yr had a 30070 lower prevalence of lower extremity arterial disease than did those who continued to smoke.

715

As noted in the previous sections, relatively little work has been done to characterize smoking patterns in chronic disease populations. This is true also with diabetes. Jones and Hedley (196) conducted a detailed assessment of the smoking habits of 1,930diabetes clinic attendees in Great Britain. Overall, the prevalence of smoking in diabetics was not different from that of a 1982 survey of the general population; however, the prevalence of smoking in the diabetic population older than 50 yr of age was found to be significantly less for both men (p < 0.001) and women (p < 0.001) with fewer diabetic men older than 60 yr of age having ever smoked. Although interventions may have played some part, the investigators concluded that the multiplicative effects of smoking and diabetes had produced a high mortality rate in diabetic smokers. A recent report (197) reviewed the smoking status of 703 Type I and II diabetic patients who received regular treatment for diabetes through a university clinical research center over a 5-yr period. Subjects ranged in age from 17 to 82 yr (mean = 42 yr). Although not a representative sample, it is striking that 34.8% of patients (245 of 703) had reported they currently smoked. Of the subset of patients admitted from January 1988 to March 1989, 39% (66 of 168) reported smoking. Since 1983, there was less than a 1% annual cessation rate with only 13 patients having reported cessation. This compares to a 3 to 5% annual rate in the general population as reported in an earlier section of this report. Smokers were more likely than nonsmokers to be diagnosed with some form of diabetic complication (62 versus 54%) with a trend for smokers to exhibit higher rates of neuropathy (61 versus 42%). As smoking may be viewed as a career, so may diabetes. Family and personal characteristics (198), in combination with external factors such as health insurance regulations and worksite characteristics (199),may interact with the disease to determine the career of diabetes for an individual. Fear of complications, complex regimens for metabolic control, adjustment to limitations on activities, and foregoing preferred foods all make diabetes an especially difficult disease to which to adjust. There is little research that directly addresses smoking among those with diabetes; however, what we know about smoking and what we know about diabetes suggest problems unique to the combination of the two such as: (1) exacerbation of general underesti-

716

Other research indicates poorer results among patients with disease. For instance, the rates of cessation among pulmonary patients havebeen disappointing. In one study, 16% of patients with chronic lung disease versus 45 % of healthy subjects were currently abstinent 22 months after receiving a treatment combining group counseling and nicotine gum (210). Similarly, a multicomponent treatment of a group composed primarily of patients with chronic lung disease achieved 202-204); abstinence for 1 wk before assessment (5) smoking ameliorating stress as- among only 17070 of participants (177). sociated with poor metabolic control or Although there is little cessation research with efforts to maintain good metabolic with diabetic smokers, the prevalence control and high levels of family stress among diabetic adults appears to be at or diminished social support, which may least equal to that of the general adult be exacerbated in diabetes (98, 205-208); population, indicating little encourage(6) the use of smoking to enhance task ment of cessation by the presence of diaperformance frequently required to man- betes or its routine care. age a complex diabetic regimen of mediTaking just these three groups - chronic lung disease, cardiovascular disease, and cation, diet, and activity (60, 204). These and other issues pertinent to smok- diabetes - it appears that cessation is ening, smoking cessation, and diabetes are couraged by cardiovascular disease but reviewed in a recent special series of re- not by the others. This may be related printed articles and commentaries in Di- to the consequences of cessation that patients with these diseases may expect. As abetes Spectrum (1990). Given the high rates of smoking we these consequences of smoking may vary have found among diabetic adults and according to coexisting disease, so the inthe obvious deleterious effects of smok- centives for quitting may vary. It may be ing and diabetes, it is striking that almost explicable, then, that different rates of no research has been published on smok- cessation occur among varying diagnosing cessation in this group. In one study, tic groups. Cooperstock and Thom (180) 60 diabetic smokers were randomly as- categorized patients with chronic diseases signed to routine advice stressing general and a history of smoking into broad smoking hazards or intensive advice with groups based on their diagnosis. Paralinformation on smoking and diabetic lel to the trends noted here, those with complications. Only one patient in the respiratory or musculoskeletal disorders group receivingintensive advice and none were less likely to have stopped smoking in the group receiving routine advice quit than those with circulatory disorders. smoking. Somewhat extremely, perhaps, People with circulatory disorders were the investigators concluded "convention- more likely than others to mention that al antismoking strategies are completely cessation followed a frightening episode, ineffective in persuading diabetic patients usually a heart attack, that may partialto stop smoking" (209). ly account for the greater proportion of quitters. Comparative Study of Smoking The incentive for cessation associated Cessation across TYpes of Disease with a particular disease may entail sevAs reviewed earlier, disease related to eral dimensions. Patients' motivation to smoking may facilitate cessation. The quit smoking may be affected by appraisal greatest abstinence rates seem to be of personal exposure to elements that inamong patients with cardiovascular dis- teract with smoking risk (e.g., coal dust, ease. As noted earlier, for instance, sev- asbestos), abnormal tests, early respiraeral studies have reported greater rates tory symptoms, or the disease diagnosis. of cessation among cardiovascular pa- Supporting this analysis, Pederson and tients, including postmyocardial infarc- coworkers (211) found such appraisals tion patients, than among general clinic and other elements of the health beliefs or nonclinical samples (78, 190). Others model (212) of value in understanding have reported abstinence rates of about pulmonary patients' smoking cessation 50070 for postmyocardial infarction pa- after physician advice. Those patients tients (188, 189), well above cessation who believed their diagnosis, thought rates generally reported in the literature. they were susceptible, considered the dismation of risks of smoking (200) prompted by attention to risks of diabetes; (2) distraction from smoking cessation by professionals' attention to metabolic control; (3) fear of weight gain (81, 82, 84, 87, 91, 201), which may be exacerbated by concern for weight control in diabetes management; (4) utility of nicotine's mood elevating effects in reducing depressed moods commonly found in diabetes (54, 65,

FISHER, HAIRE.JOSHU, MORGAN, REHBERG, AND ROST

ease serious, and thought quitting would help prognosis were more likely to be abstinent from smoking 6 months after physician counseling. This pattern of results appears parallel to that noted above for cardiovascular patients with more serious disease to be more likely to quit smoking (20, 189). Variations in risks of smoking and payoffs for cessation may make sense of the variations in cessation rates among patients with cardiovascular disease as opposed to lung disease and diabetes. The prospects of full recovery from myocardial infarction, for instance, may be advanced substantially by smoking cessation and other lifestyle changes. In contrast, the impacts of cessation for the patient with chronic lung disease are likely to be on course and symptoms, not mortality. Those with diabetes are often told they will"die of diabetes." The smokers among them may see little risk from lung cancer or other smoking-related diseases and, so, see little point in smoking cessation. As the early sections of this review stressed the multidimensionality of smoking, so even cessation interventions for those with chronic disease have effects that vary according to a number of individual and disease characteristics. Although results of smoking cessation interventions in chronic disease are cause for only cautious optimism, a number of characteristics of current care for pulmonary and cardiovascular disease and diabetes should promote effective smoking cessation counseling. First, current care entails extensive patient education and counseling regarding such diverseregimen components as nutrition, complicated medication adjustment, exercise, and stress and emotional issues. Smoking histories and counseling could easily be incorporated into such topics. Care for chronic disease is often provided by a team of professionals accustomed to differing role responsibilities that ensure implementation of both medical and educational or counseling services. Professionals in chronic care understand that medication prescription does not obviate behavioral adherence to regimens and patient responsibility for daily management. This should facilitate their use of nicotine replacement or other medical approaches to cessation without them mistakenly thinking that these approaches eliminate the need for patients' efforts in cessation. Professionals in chronic care are also familiar with referring to other services so should have little difficulty identifying and using referral resources for

STATE OF THE ART: SMOKING AND SMOKING CESSATION

smoking cessation. Finally, it should be an advantage that chronic care is coordinated over time because consistent followup and contact have been shown to encourage smoking cessation (161, 213). Thus, the setting of chronic disease care should be hospitable to developing and evaluating improved methods of smoking cessation. References 1. u.s. Department of Health, Education, and Welfare. Smoking and health: a report of the Surgeon General. Rockville, MD: U.S. Department of Health, Education, and Welfare,1979.DHEW Publication No. (PHS)79-50066. 2. Holland WW. Chronic obstructive lung disease prevention. Br J Dis Chest 1988; 82:32-44. 3. U.S. Department of Health and Human Services. Reducing the health consequences of smoking: 25 years of progress. A report of the Surgeon General. Rockville,MD: U.S.Department of Health and Human Services, Office on Smoking and Health, 1989. DHHS Publication No. (CDC)89-8411. 4. Schacter S. Recidivism and self-cure of smoking and obesity. Am Psychol 1982; 37:436-44. 5. Fisher EB Jr, Bishop DB, Goldmuntz J, Jacobs A. Implications for the practicing physician of the psychosocial dimensions of smoking. Chest 1988; 93(2):69S-78S. 6. Becker HS. Outsiders: studies in the sociology of deviance. New York: The Free Press, 1963. 7. Goffman E. Asylums. Garden City,NY:Doubleday, 1961. 8. Prochaska JO, DiClemente CC. Stages and processes of self-change of smoking: toward an integrative model of change. J Consult Clin Psychol 1983; 51:390-5. 9. Krasner L, Ullmann LP. Behavior influence and personality: the social matrix of human action. New York: Holt, Rinehart and Winston, 1973. 10. U.S. Department of Health and Human Services. The health consequences of smoking: nicotine addiction. A report of the Surgeon General. Rockville,MD: U.S. Department of Health and Human Services,Office on Smoking and Health, 1988. DHHS Publication No. (PHS)88-8406. 11. Hall SM, Tunstall C, Rugg D, Jones RT, Benowitz N. Nicotine gum and behavioral treatment in smoking cessation. J Consult Clin Psychol 1985; 53:256-8. 12. Killen JD, Maccoby N, Taylor CB. Nicotine gum and self-regulation training in smoking relapse prevention. Behav Ther 1984; 15:234-48. 13. SchneiderNG, JarvikME, ForsytheAB, Read LL, Elliott ML, Schweiger A. Nicotine gum in smoking cessation: a placebo-controlled, doubleblind trial. Addict Behav 1983; 8:256-61. 14. Biglan A, Lichtenstein E. A behavior-analytic approach to smoking acquisition: some recent findings. J Appl Social Psychol 1984; 14:207-23. 14a. U.S. Public Health Service. Smoking and health. Report of Advisory Committee to the Surgeon General of the Public Health Service.Washington, DC: U.S. Government Printing Office, 1964. Publication No. (PHS)1I03. 15. Schmiterlow CG, Hansson G, Andersson L, Appelgren E, Hoffman Pc. Distribution of nicotine in the central nervous system. Ann NY Acad Sci 1967; 142:2-14. 16. London ED, Waller SB, Wamsley JK. Autographic localization of 3H nicotine binding sites in rat brains. Neurosci Lett 1985; 53:179-84. 17. London ED, Connolly RJ, Szikszay M, Wams-

ley JK. Distribution of cerebral metabolic effects of nicotine in the rat. Eur J Pharmacol 1985; 110: 391-2. 18. Pomerleau OF, Pomerleau CS. Neuroregulators and the reinforcement of smoking: towards a biobehavioral explanation. Neurosci Biobehav Rev 1984; 8:503-13. 19. Robins LN, Helzer JE, Davis DH. Narcotic use in southeast Asia and afterward. Arch General Psychiatry 1975; 2:955-61. 20. Baile WF Jr, Bigelow GE, Gottlieb SH, Stitzer ML, Sacktor JD. Rapid resumption of cigarette smoking following myocardial infarction: inverse relation to MI severity. Addict Behav 1982; 7:373-80. 21. Burling TA, Singleton EG, BigelowGE. Smoking following myocardial infarction: a critical reviewof the literature. Health Psychol1984; 3:83-96. 22. Henningfield JE, Nemeth-Coslett R. Nicotine dependence - interface between tobacco and tobacco-related disease. Chest 1988;93:37S-55S, 385-95. 23. Henningfield JE, Griffiths RR. A preparation for the experimental analysis of human cigarette smoking behavior. Behav Res Meth Instrum 1979; 11:538-44. 24. Herman CPo External and internal cues as determinants of the smoking behavior of light and heavy smokers. J Pers Soc Psychol1974; 30:664-72. 25. Gritz ER. Smoking behavior and tobacco abuse. In: Mello NK, ed. Advances in substances abuse: behavioral and biological research. Greenwich, CT: JAI Press, 1980; 91-158. 26. Sachs DPL. Pharmacologic, neuroendocrine, and biobehavioral basis for tobacco dependence. In: Simmons DH, ed. Current pulmonology. Chicago: Year Book Medical Publishers, Inc., 1987; 371-405. 27. Fudala PJ, Teoh KW, Iwamoto ET. Pharmacologic characterization of nicotine-induced conditioned place preference. Pharmacol Biochem Behav 1985; 22:237-41. 28. Etskorn F. Sucrose aversions in mice as a result of injected nicotine or passive tobacco smoke inhalation. Bull Psychonomic Soc 1980; 15:54-6. 29. Gritz ER. Patterns of puffing in cigarette smokers. In: Krasnigor NA, ed. Self-administration of abused substances: methods for study. Washington, DC: U.S. Government Printing Office, 1978; 221-35. National Institute on Drug Abuse Research Monograph No. 20. 30. Katz JL, Goldberg SR. Second-order schedules of drug injection: implications for understanding reinforcing effects of abused drugs. In: Mello NK, ed. Advances in substance abuse. Vol.3. Greenwich, CT: JAI Press Inc., 1987. 31. Skinner BF. Science and human behavior. New York: MacMillan, 1953. 32. Wikler A. Requirements for extinction of relapse-facilitating variables and for rehabilitation in a narcotic-antagonist program. Adv Biochem Psychopharmacol 1973; 8:399-414. 33. Wikler A, Pescor FT. Classical conditioning of a morphine abstinence phenomenon, reinforcement of opioid-drinking behavior and "relapse" in morphine-addicted rats. Psychopharmacology (Berlin) 1967; 10:255-84. 34. Hatsukami DK, Hughes JR, Pickens RW. Blood nicotine, smoke exposure and tobacco withdrawal symptoms. Addict Behav 1985; 10:413-7. 35. Pomerleau OF, Pomerleau CS. A biobehavioral view of substance abuse and addiction. J Drug Issues 1987; 17:111-31. 36. Leventhal H, Cleary PD. The smoking problem: a review of the research and theory in behavioral risk modification. Psychol Bull 1980; 88:370-405. 37. Shiffman S. Relapse following smoking ces-

717 sation: a situational analysis. J Consult Clin Psychol 1982; 50:71-86. 38. Shiffman S. A cluster-analytic classification of smoking relapse episodes. Addict Behav 1986; 11:295-307. 39. Rachlin H. Introduction to modern behaviorism. 2nd ed. San Francisco: W.H. Freeman, 1976. 40. Niaura RS, Rohsenow DJ, Binkoff JA, Monti PM, Pedraza M, Abrams DB. Relevance of cue reactivity to understanding alcohol and smoking relapse. J Abnorm Psychol 1988; 97:133-52. 41. Fisher EB Jr, Rost K. Smoking cessation: a practical guide for the physician. Clin Chest Med 1986; 7:551-65. 42. FederalTrade Commission. Report to Congress pursuant to the Federal Cigarette Labeling and AdvertisingAct, 1986.Federal Trade Commission, May 1988. 43. Davis RM. Current trends in cigarette advertising and marketing. N Engl J Med 1987; 316: 725-32. 44. Warner KE. Cigarette advertising and media coverage of smoking and health. N Engl J Med 1985; 312:384-8. 45. Cummings KM, Giovino G, Mendicino AJ. Cigarette advertising and racial differences in cigarette brand preferences. Public Health Rep 1987; 102:698-701. 46. Hunter SM, Croft 18, Burke GL, Parker FC, Webber LS, Berenson GS. Longitudinal patterns of cigarette smoking and smokeless tobacco use in youth: the Bogalusa heart study. Am J Public Health 1986; 76:193-5. 47. Orleans CT, Schoenbach VJ, Salmon MA, et al. A survey of smoking and quitting patterns among black Americans. Am J Public Health 1989; 79:176-81. 48. Samet JM, Schrag SD, Howard CA, Key CR, Pathak DR. Respiratory disease in a New Mexico population sample of Hispanic and non-Hispanic whites. Am Rev Respir Dis 1982; 125:152-7. 49. Stern MP, Haskell WL, Wood PDS, Osann KE, King AB, Farquhar JW. Affluence and cardiovascular risk factors in Mexican-Americans and other whites in three northern California communities. J Chronic Dis 1975; 28:623-36. 50. NovotnyTE, Warner KE, Kendrick JS, Remington PL. Smoking by blacks and whites: socioeconomic and demographic differences. Am J Public Health 1988; 78:1187-9. 51. Bray RM, Guess LL, Marsden ME, Herbold JR. Prevalence, trends, and correlates of alcohol use, nonmedical drug use, and tobacco use among U.S. military personnel. Milit Med 1989; 154:1-11. 52. U.S. Department of Health and Human Services. The health consequences of smoking: chronic obstructive lung disease. A report of the Surgeon General. Rockville,MD: U.S. Department of Health and Human Services, Office on Smoking and Health, 1984. DHHS Publication No. (PHS) 84-50205. 53. Kaplan HI, Sadock BJ, eds. Comprehensive textbook of psychiatry. 4th ed. Baltimore: Williams & Wilkins, 1985. 54. Hughes JR, Hatsukami DK, Mitchell JE, Dahlgren LA. Prevalence of smoking among psychiatric outpatients. Am J Psychiatry 1986; 143: 993-7. 55. McDade EA, Keil JE. Characterization of a soup kitchen population. Proceedings of the American Heart Association Conference on Epidemiology, Sante Fe, New Mexico, March 1988. 56. Friedman GD, Siegelaub AB, Dales LG, Seltzer CC. Characteristics predictive of coronary heart disease in ex-smokers before they stopped smoking: comparison with persistent smokers and non-

718

smokers. J Chronic Dis 1979; 32:175-90. 57. Blair A, Blair SN, Howe HG, et al. Physical, psychological and sociodemographic differences among smokers, ex-smokers, and nonsmokers in a working population. Prev Med 1980; 9:747-59. 58. Perri MG, Richards CS, Schultheiss KR. Behavioral self-control and smoking reduction: a study of self-initiated attempts to reduce smoking. Behav Ther 1977; 8:360-5. 59. Warner KE. Effects of the antismoking campaign: an update. Am J Public Health 1989; 79:144-51. 60. Pomerleau 0, Adkins D. Pertschuk M. Predictors of outcome and recidivism in smoking cessation treatment. Addict Behav 1978; 3:65-70. 61. Condiotte MM, Lichtenstein E. Self-efficacy and re!apse in smoking cessation programs. J Consult Clin Psychol 1981; 49:648-58. 62. Fisher EB Jr, Levenkron JC, Lowe MR, Loro AD Jr, Green L. Self-initiated self-control in risk reduction. In: Stuart R, ed. Adherence, generalization, and maintenance in behavioral medicine. New York: Brunner/Mazel, 1982. 63. Harackiewicz JM, Sansone C, Blair LW, Epstein JA, Manderlink G. Attributional processes in behavior change and maintenance: smoking cessation and continued abstinence. J Consult Clin Psychol 1987; 55:372-8. 64. Fisher EB Jr. A skeptical perspective: the importance of behavior and environment. In: Holroyd KA, Creer TL, eds, Self-management of chronic disease: recent developments in health psychology and behavioral medicine. New York: Academic Press, 1986; 541-65. 65. Glassman AH, Stetner F, Walsh T, etal. Heavy smokers, smoking cessation, and clonidine: results of a double-blind, randomized trial. J Am Med Assoc 1988; 259:2863-6. 66. Hughes JR. Clonidine, depression, and smoking cessation. JAm Med Assoc 1988; 259:2901-3. 67. Flanagan J, Maany I. Smoking and depression. Am J Psychiatry 1982; 139:541. 68. Gottlieb NH, Baker JA. The relative influence of health beliefs, parental and peer behaviors and exercise program participation on smoking, alcohol use and physical activity. Soc Sci Med 1986; 22:915-27. 69. Eisinger RA. Psychosocial predictors of smoking recidivism. J Health Soc Behav 1971;12:355-62. 70. Graham S, Gibson RW.Cessation of patterned behavior: withdrawal from smoking. Soc Sci Med 1971; 5:319-37. 71. West OW, Graham S, Swanson M, Wilkinson G. Five year follow-up of a smoking withdrawal clinic population. Am J Public Health 1977; 67:536-44. 72. Bishop DB, Cook TLW, Fisher EB Jr, Ashenberg Z, Cappello M. Grass-roots steering committees in worksite smoking cessation. Proceedings of the Society of Behavioral Medicine, New Orleans, Louisiana, March 1985. 73. Coppotelli HC, Orleans CT. Partner support and other determinants of smoking cessation maintenance among women. J Consult Clin Psychol 1985; 53:455-60. 74. Mermelstein R, Lichtenstein E, Mclntyre K. Partner support and relapse in smoking-cessation programs. J Consult Clin Psychol 1983; 51:465-6. 75. Mermelstein R, Cohen S, Lichtenstein E, Baer JS, Kamarck T. Social support and smoking cessation and maintenance. J Consult Clin Psychol1986; 54:447-53. 76. Morgan GO, Ashenberg ZS, Fisher EB Jr. Abstinence from smoking and the social environment. J Consult Clin Psychol 1988; 97:238-45. 77. American Lung Association. Survey of attitudes toward smoking. Princeton, NJ: Gallup Organization, July 1987.

FISHER, HAIRE-JOSHU, MORGAN, REHBERG, AND ROST

78. Ockene JK, Hosmer DW, Williams JW, Goldberg RJ, Ockene IS, Raia TJ. Factors related to patient smoking status. Am J Public Health 1987; 77:356-7. 79. Janis IL, Mann L. Decision making: a psychological analysis of conflict, choice, and commitment. New York: Free Press, 1977. 80. Best JA. Tailoring smoking withdrawal procedures to personality and motivational differences. J Consult Clin Psychol 1975; 43:1-8. 81. Hall SM, Ginsberg D, Joans RT.Smoking cessation and weight gain. J Consult Clin Psychol1986; 54:342-6. 82. Rodin J. Weight change following smoking cessation: the role of food intake and exercise. Addict Behav 1987; 12:303-17. 83. Shimokata H, Muller DC, Andres R. Studies in the distribution of body fat. J Am Med Assoc 1989; 261:1I69-73. 84. Fagerstrom KO. Efficacy of nicotine chewing gum: a review. Prog Clin Bioi Res 1988;261:109-28. 85. Grunberg NE, Bowen OJ, Maycock VA, Nespor SM. The importance of sweet taste and caloric content in the effects of nicotine on specific food consumption. Psychopharmacology 1985; 87: 198-203. 86. Sorenson G, Pechacek TF. Attitudes toward smoking cessation among men and women. J Behav Med 1987; 10:129-37. 87. Abrams DB, Monti PM, Pinto RP, Elder JP, Brown RA, Jacobus SI. Psychosocial stress and coping in smokers who relapse or quit. Health Psychol 1987; 6:289-303. 88. Hall SM, McGee R, Tunstall JD, Benowitz N. Changes in food intake and activity after quitting smoking. J Consult Clin Psychol 1989; 57:81-6. 89. Carney RM, Goldberg AP. Weight gain after cessation of cigarette smoking: a possible role for adipose-tissue lipoprotein lipase. N Engl J Med 1984; 310:614-6. 90. Comstock GU, Stone RW. Changes in body weight and subcutaneous fatness related to smoking habits. Arch Environ Health 1972; 24:271-6. 91. Wack J, Rodin J. Smoking and its effect on body weight and the systems of caloric regulation. Am J Clin Nutr 1982; 35:366-80. 92. Emont SL, Cummings KM. Weight gain following smoking cessation: a possible role for nicotine replacement in weight management. Addict Behav 1987; 12:151-5. 93. Gross J, Stitzer ML, Maldonado J. Nicotine replacement: effects on postcessation weight gain. J Consult Clin Psychol 1989; 57:87-92. 94. Marlatt GA, Gordon JR. Determinants of relapse: implications for the maintenance of behavior change. In: Davidson PO, Davidson SM, eds. Behavioral medicine: changing health lifestyles. New York: Brunner/Mazel, 1980; 410-52. 95. Bliss RE, Garvey AG, Heinold JW, Hitchcock JL. The influence of situation and coping on relapse crisis outcomes after smoking cessation. J Consult Clin Psychol 1989; 57:443-9. 96. O'Connell KA, Martin EJ. Highly tempting situations associated with abstinence, temporary lapse, and relapse among participants in smoking cessation programs. J Consult Clin Psychol 1987; 55:367-71. 97. Lichtenstein E, Antonuccio DO, Rainwater G. Unkicking the habit: the resumption of cigarette smoking. Proceedings of the Western Psychological Association, Seattle, Washington, April 1977. 98. Ashenberg ZS, Morgan GD, Fisher EB Jr. Psychological stress and smoking recidivism. Paper presented at Society of Behavioral Medicine, Philadelphia, Pennsylvania, May 1984. 99. Marlatt GA, Gordon JR, eds. Relapse prevention: maintenance strategies in the treatment ofaddictive behaviors. New York: Guilford Press, 1985.

100. Kanner AD, Coyne JC, Schaefer C, Lazarus RS. Comparison of two modes of stress measurement: daily hassles and uplifts versus major life events. J Behav Med 1981; 4:1-39. 101. McReynolds WT, Green L, Fisher EB Jr. Selfcontrol as choice management with reference to the behavioral treatment of obesity. Health Psychol 1983; 2:261-76. 102. Rachlin H, Green L. Commitment, choice and self-control. J Exp Anal Behav 1972; 17:15-22. 103. Lowe MR, Green L, Kurtz S, Ashenberg Z, Fisher EB Jr. Alternatives to rapid smoking: selfinitiated, cue extinction, and covert sensitization procedures in smoking cessation. J Behav Med 1980; 3:357-72. 104. Lichtenstein E, Harris DE, Birchler GR, Wahl JM, Schmahl DP. Comparison of rapid smoking, warm, smoky air and attention placebo in the modification of smoking behavior. J Consult Clin Psychol 1973; 40:92-8. 105. Danaher BG. Research on rapid smoking: interim summary and recommendations. Addict Behav 1977; 2:151-66. 106. Lando HA. Successful treatment of smokers with a broad-spectrum behavioral approach. J Consult Clin Psychol 1977; 45:361-6. 107. Hall R, Sachs D, Hall S, Benowitz N. 1\voyear efficacy and safety of rapid smoking therapy in patients with cardiac and pulmonary disease. J Consult Clin Psychol 1984; 52:574-81. 108. Russell MAH, Armstrong E, Patel UA. Temporal contiguity in electric aversion therapy for cigarette smoking. Behav Res Ther 1976; 14:103-23. 109. Paxton R. The effects of a deposit contract as a component in a behavioral programme for stopping smoking. Behav Res Ther 1980; 18:45-50. 1I0. Winett R. Parameters of deposit contracts in the modification of smoking. Psychological Record 1973; 23:49-60. Ill. Fisher EB Jr, Lowe MR, Levenkron JC, Newman A. Reinforcement and structural support of maintained risk reduction. In: Stuart R, ed, Adherence, generalization, and maintenance in behavioral medicine. New York:Brunner/Maze!, 1982; 145-68. 112. Rosen GM, Lichtenstein E. An employee incentive program to reduce cigarette smoking. J Consult Clin Psychol 1977; 45:957. 113. U.S. Department of Health, Education, and Welfare. The smoking digest: progress report on a nation kicking the habit. Bethesda, MD: National Cancer Institute, National Institutes of Health, 1977 (reprinted 1979). NIH Publication No. 79-1549. 114. Flaxman J. Quitting smoking now or later: gradual, abrupt, immediate and delayed quitting. Behav Ther 1978; 9:260-70. 115. Cautela JR. Behavior therapy and self control: techniques and implications. In: Franks C, ed. Behavior therapy: appraisal and status. New York: McGraw-Hill 1969; 323-40. 116. Bandura A. Principles of behavior modification. New York: Holt, Rinehart and Winston, 1969. 1I7. Hall SM, Rugg D, Tunstall C, Jones RT. Preventing relapse to cigarette smoking by behavioral skill training. J. Consult Clin Psychol1984; 52:372-82. 118. American Lung Association. Update Vol. X, December 11, 1987; 6-7. 119. Davis AL, Faust R, Ordentlich M. Self-help smoking cessation and maintenance programs: a comparative study with 12-month follow-up by the American Lung Association. Am J Public Health 1984; 74:1212-7. 120. Strecher VJ, Rimer BK, Monaco KD. Development of a new self-help guide - Freedom from Smoking'" for you and your family. Health Educ Q 1989; 16:101-12.

STATE OF THE ART: SMOKING AND SMOKING CESSATION

121. Jarvik M, Henningfield JE. Pharmacological treatment of tobacco dependence. Pharmacol Biochem Behav 1988; 30:279-94. 122. Sees K, Clark HW. Use of clonidine in nicotine withdrawal. J Psychoactive Drugs 1988; 20: 263-8. 123. Ornish S, Zisook S, McAdams L. Effects of transdermal clonidine treatment on withdrawal symptoms associated with smoking cessation. Arch Intern Med 1988; 148:2027-31. 124. Glassman A, Jackson W, Walsh BT, Roose S. Cigarettecraving,smoking withdrawal,and cJonidine. Science 1984; 226:864-6. 125. Franks P, Harp J, Bell B. Randomized, controlled trial of clonidine for smoking cessation in a primary care setting. J Am Med Assoc 1989; 262:3011-3. 126. Davison R, Kaplan K, Fintel D, Parker M, Anderson L, Haring O. The effect of clonidine on the cessation of cigarette smoking. Clin Pharmacol Ther 1988; 44:265-7. 127. Lam W, Sacks H, Sze P, Chalmers T. Metaanalysis of randomised controlled trials of nicotine chewing-gum. Lancet 1987; 2:27-9. 128. Wilson DM, Taylor DW, Gilbert JR, et al. A randomized trial of a family physician intervention for smoking cessation. JAm Med Assoc 1988; 260:1570-4. 129. Hughes J, Gust S, Keenan R, Fenwick J, Healey M. Nicotine versus placebo gum in general medicalpractice.JAm MedAssoc 1989; 261:1300-5. 130. Tonnesen P, Fryd V, Hansen M et at. Effect of nicotine chewinggum in combination with group counseling on the cessation of smoking. N Engl J Med 1988; 318:15-8. 131. Gottlieb AM, Killen JD, Marlatt GA, Taylor CB. Psychological and pharmacological influences in cigarette smoking withdrawal: effects of nicotine gum and expectancy on smoking withdrawal symptoms and relapse.J Consult Clin Psychol1987; 4:606-8. 132. Fortmann S, Killen J, Teich M, Newman B. Minimal contact treatment for smoking cessation. J Am Med Assoc 1988; 260:1575-9. 133. Abelin T, Muller P, Buehler A, Vesanene K, Imhof PRo Controlled trial of transdermal nicotine patch in tobacco withdrawal. Lancet 1989; 1:7-10. 134. Fisher EB Jr, Rost K, Gaponoff-Berson BG, Nett LM. Smoking. In: Cherniack RM, ed. Current therapy of respiratory disease- 3. Toronto: B.C. Decker, 1989; 311-9. 135. Nett LM, Dingus SM. Smoking cessation techniques. In: Kacmarek R, Stoller JK, eds. Current respiratory care. Toronto: B.C. Decker, 1988; 107-16. 136. Sachs DPL. Nicotine polacrilex: practical use requirements. In: Simmons DH, ed. Current pulmonology. Chicago: Year Book Medical Publishers Inc., 1989; 141-57. 137. Glasgow RE, Lichtenstein E. Long-term effectsof behavioral smoking cessation interventions. Behavior Therapy 1987; 18:297-324. 138. Bandura A. Self-efficacy: toward a unifying theory of behavioral change. Psychol Rev 1977; 84:191-215. 139. Bandura A. Self-efficacy mechanism in human agency. Am Psychol 1982; 37:122-47. 140. Stevens VJ, Hollis JE Preventing smoking relapse,using an individually tailored skills-training technique. J Consult Clin Psychol1989; 57:420-4. 141. Lichtenstein E. The smoking problem: a behavioral perspective. J Consult Clin Psychol1982; 50:804-19. 142. U.S.Department of Health and Human Services.The health consquences of smoking for women. A report of the SurgeonGeneral. Rockville, MD: U.S. Department of Health and Human Services,

Office on Smoking and Health, 1980. 143. U.S.Department of Health and Human Services. The health consequences of smoking: cancer. A report of the Surgeon General. Rockville, MD: U.S. Department of Health and Human Services, 1982. DHHS Publication No. (PHS) 8250179. 144. Fisher EB Jr, Bishop DB. Sex roles, social support, and smoking cessation. Paper presented at Society of Behavioral Medicine, San Francisco, California, March 1986. 145.Lichtenstein E, Glasgow RE, Abrams DB. Social support in smoking cessation: in search of effective interventions. Behavior Therapy 1986; 17:607-19. 146. Etringer BD, Gregory VR, Lando HA. Influence of group cohesion on the behavioral treatment of smoking. J Consult Clin Psychol 1984; 52:1080-6. 147. McIntyre-KingsolverK, Lichtenstein E, Mermelstein RJ. Spouse training in a multicomponent smoking-cessation program. Behavior Therapy 1986; 17:67-74. 148. Shipley RH, Orleans CT, Wilbur CS, Piserchia PV, McFadden DW. Effect of the Johnson & Johnson Live for Life program on employee smoking. Prev Med 1988; 17:25-34. 149. Klesges RC, Cigrang JA. Worksite smoking cessation programs: clinical and methodological issues. In: Hersen M, Eisler RM, Miller PM, eds. Progress in behavior modification. Newbury Park, CA: Sage Publications, 1988; 36-61. 150. Fisher EB Jr, Bishop DB, Mayer J, Brown T, White-Cook T. The physician's contribution to smoking cessation in the workplace. Chest 1988; 93(2):56S-65S. 151. KlesgesRC, Brown K, Pascale RW,Murphey M, WilliamsE, Cigrang JA. Factors associated with participation, attrition, and outcome in a smoking cessation program at the workplace.Health Psychol 1988; 7:575-89. 152. Cummings KM, Hellmann R, Emont SL. Correlates of participation in a worksite stopsmoking contest. J Behav Med 1988; 11:267-77. 153. GlasgowRE, Klesges RC, Klesges LM, Somes GR. Variables associated with participation and outcome in a worksite smoking control program. J Consult Clin Psychol 1988; 56:617-20. 154. Minkler M. Improving health through community organization. In: Glantz K, LewisF, Rimer B, eds. Health behavior and health education: theory, research, and practice. San Francisco: JosseyBass, 1990; 257-87. 155. Fisher EB Jr, Bishop DB, Levitt-Gilmour T, Newman E, Lankester L, Tormey B. Impacts on smoking prevalence of organizational and social support in worksite smoking cessation. Paper presented at Society of Behavioral Medicine, Boston, Massachusetts, April 1988. 157. Ockene JK. Physician-deliveredinterventions for smoking cessation: strategies for increasing effectiveness. Prev Med 1987; 16:723-37. 158. Stewart AL, Brook RH, Kane RL. Smoking conceptualization and measurement of health habits for adults in the health insurance study. Vol. 1. Santa Monica, CA: Rand, 1979. 159. Russell MAH, Wilson C, Taylor G, Baker G. Effects of general practitioners' advice against smoking. Br Med J 1979; 28:231-5. 160. Li VC, Kim YJ, Ewart CK, et al. Effects of physician counseling on the smoking behavior of asbestos-exposed workers. Prev Med 1984; 13: 462-76. 161. Kottke TE, Battista RN, DeFrieseGH, Brekke ML. Attributes of successful smoking cessation interventions in medical practice: a meta-analysis of 39 controlled trials. JAMA 1988; 259:2883-9. 162. Glasgow RE, Schafer L, O'Neill HK. Self-

719

help books and amount of therapist contact in smoking cessation programs. J Consult Clin Psychol 1981; 49:659-67. 163. Rose G, Hamilton PJS. A randomized controlled trial of the effect on middle-aged men of advice to stop smoking. J Epidemiol Community Health 1978; 32:275-81. 164. Hughes GH, Hymowitz N, Ockene JK, Simon N, Vogt TM. The multiple risk factor intervention trial (MRFIT). Prev Med 1981; 10:476-500. 165. Ockene JK, Hymowitz N, Sexton M, Broste SK. Comparison of patterns of smoking behavior change among smokers in the multiple risk factor intervention trial (MRFIT). Prev Med 1982; 11: 621-38. 166. Cummings SR, Hansen B, Richard RJ, Stein MJ, Coates TJ. Internists and nicotine gum. JAMA 1988; 260:1565-9. 167. Kottke TE, Brekke ML, Solberg LI, Hughes JR. A randomized trial to increase smoking intervention by physicians: doctors helping smokers, round 1. JAMA 1989; 261:2101-6. 168. Ewart CK, Li VC, Coates TJ. Increasing physicians' anti-smoking influence by applying an inexpensive feedback technique. J Med Educ 1983; 58:468-73. 169. Cohen SJ, Stookey GK, Katz BP, Drook CA, Smith DM. Encouraging primary care physicians to help smokers quit: a randomized controlled trial. Ann Intern Med 1989; 110:648-52. 170. Burt A, Thornley P, Illingworth D, White P, ShawTRD, Turner R. Stopping smoking after myocardial infarction. Lancet 1974; 1:304-6. 171. Seidell JC, Bakx KC, Deurenberg P, Burema J, Hautvast JGAJ, Huygen FJA. The relation between overweight and subjective health according to age, social class, slimming behavior and smoking habits in Dutch adults. Am J Public Health 1986; 76:1410-5. 172. Tashkin DP, Clark VA, Coulson AH, et al. The UCLA population studies of chronic obstructive respiratory disease. Am Rev Respir Dis 1984; 130:707-15. 173. Daughton DM, Fix AJ, Kass I, Patil KD. Smoking cessation among patients with chronic obstructive pulmonary disease (COPD). Addict Behav 1980; 5:125-8. 174. Dudley DL, Aickin M, Martin CV.Cigarette smoking in a chest clinic population - psychophysiologic variables. J Psychosorn Res 1977; 21: 367-75. 175. Pederson LL, Williams 11, Lefcoe NM. Smoking cessation among pulmonary patients as related to type of respiratory disease and demographic variables. Can J Public Health 1980; 71:191-4. 176. Sirota AD, Curran JP, Habif V.Smoking cessation in the chronically ill medical patient. J Clin Psychol 1985; 41:575-9. 177. Hall SM, Bachman J, Henderson JD, Barsdoe R, Jones RT. Smoking cessation in patients with cardiopulmonary disease: an initial study. Addict Behav 1983; 8:33-42. 178. Carmody T, Loew D, Hall R, Breckenridge J, Hall S. Nicotine polacrilex: clinic-based strategies with chronically ill smokers. J Psychoactive Drugs 1988; 20:269-74. 179. Pederson LL. Compliance with physicianadviceto quit smoking: a reviewof the literature. Prev Med 1982; 11:71-84. 180. Cooperstock R, Thom B. Health, smoking and doctors' advice.J R Coli Gen Practitioners 1982; 32:174-8. 181. Daughton DN, Fix AJ, Cass I, Patil KD. Smoking cessation among patients with chronic obstructive pulmonary disease (COPD). Addict Behav 1980; 5:125-8. 182. Dudley DL, Aickin M, Martin CJ. Cigarette

720 smoking in a chest clinic population - psychophysiologic variables. J Psychosom Res 1977; 21: 367-75. 183. Pederson LL, Baskerville JC, Wanklin JM. Multivariant statistical models for predicting change in smoking behavior following physician advice to quit smoking. Prev Med 1982; 11:536-49. 184. Pederson LL, Baskerville JC. Multivariant prediction of smoking cessation following physician advice to quit smoking: a validation study. Prev Med 1983; 12:430-6. 185. Pederson LL, Wanklin JM, Lefcoe NM. Selfreported long-term smoking cessation in patients with respiratory disease: prediction of success and perception of health effects. Int J Epidemiol1988; 17:804-9. 186. Ames RG, Hall DS. Smoking cessation among coal miners as predicted by baseline respiratory function and symptoms: a five year perspective study. Prev Med 1985; 14:181-6. 187. Rosenberg L, Kaufman DW, Helmrich MS, Shapiro MB. The risk of myocardial infarction after quitting smoking in men under 55 years of age. N Engl J Med 1985; 313:1511-4. 188. Rigotti NA, Tesar GE. Smoking cessation in the prevention of cardiovascular disease. Cardiol Clin 1985; 3:245-57. 189. Havik OE, Maeland JG. Changes in smoking behavior after a myocardial infarction. Health Psychol 1988; 7:403-20. 190. Ockene JK, Hosmer D, Rippe J, et al. Factors affecting cigarette smoking status in patients with ischemic heart disease. J Chronic Dis 1985; 38:985-94. 191. Rytter L, Troelsen S, Beck-Nielsen H. Prevalence and mortality of acute myocardial infarction in patients with diabetes. Diabetes Care 1985; 8: 230-4. 192. Gordon T, Castelli WP, Hjortland MC. High density lipoprotein as a protective factor against

FISHER, HAIRE.JOSHU, MORGAN, REHBERG, AND ROST

coronary heart disease: the Framingham study. Am J Med 1977; 62:707-14. 193. Christlieb AR. Diabetes and hypertensive vascular disease. Am J Cardiol 1973; 32:592-606. 194. Kannell WB, Schatzkin A. Factor analysis. Prog Cardiovasc Dis 1984; 26:309-32. 195. Lithner F. Is tobacco of importance for the development and progression of diabetic vascular complications? Acta Med Scand [Suppl] 1983; 687:33-6. 196. Jones RB, Hedley AJ. Prevalence of smoking on a diabetic population: the need for action. Diabetic Med 1987; 4:233-6. 197. Haire-Joshu D, Fisher EB Jr. The prevalence and clinical impact of smoking in diabetic subjects. Presented at Society for Behavioral Medicine, Chicago, Illinois, April 1990. 198. Fisher EB Jr, Delamater AM, Bertelson AD, Kirkley BG. Psychological factors in diabetes and its treatment. J Consult Clin Psychol 1982; 50: 993-1003. 199. Heins J, Arfken D, Padgett D, Nord W. Management of diabetes mellitus (DM) at work. Presented at American Diabetes Association, Atlanta, Georgia, June 1990. 200. Dolicek TA, Schoenberger JA, Oman JK, Kremer BK, Sunseri AJ, Alberti JM. Cardiovascular risk factor knowledge and belief in prevention among adults in Chicago. Am J Prev Med 1986; 2:262-7. 201. Hall SM, McGee R, Thnstall C, Duffy J, Benowitz N. Changes in food intake and activity after quitting smoking. J Consult Clin Psychol1989; 57:81-6. 202. Lustrnan PJ, Griffith LS, Clouse RE. Depression in diabetes. Diabetes Care 1988; 11:605-11. 203. Popkin MK, Callies AL, Lentz RD, Colon EA, Sutherland DE. Prevalence of major depression, simple phobia, and other psychiatric disorders in patients with longstanding type I diabetes

mellitus. Arch Gen Psychiatry 1988; 45:64-70-. 204. Henningfield JE. Pharmacologic basis and treatment of cigarette smoking. J Clin Psychol 1984; 5:24-34. 205. Stabler B, Surwit RS, Lane JD, Morris MA, Litton J, Feinglos MN. Type A behavior pattern and blood glucose control in diabetic children. Psychosom Med 1987; 49:313-7. 206. Glasgow RE, Toobert DJ. Social environment and regimen adherence among type II diabetic patients. Diabetes Care 1988; 11:377-86. 207. Hansen CL, Henngeler S, Burghen GA. Model of associations between psychosocial variables and health outcome measures of adolescents in IDDM. Diabetes Care 1987; 10:752-8. 208. McCaul KD, Glasgow RF, Schaefer DC. Diabetes regimen behaviors: predicting adherence. Med Care 1987; 25:868-81. 209. Ardron M, MacFarlane lA, Robinson C, Van Heyningen C, Calverley PMA. Anti-smoking advice for young diabetic smokers: is it a waste of breath? Diabetic Med 1988; 5:667-70. 210. Tennesen P, Fryd V, Hansen M, et al. Tho and four milligramnicotine chewinggum and group counseling in smoking cessation: an open randomized controlled trial with a 22-month followup. Addict Behav 1988; 13:17-27. 211. Pederson LL, Wanklin JM, Baskerville JC. The role of health beliefs in compliance with physician advice to quit smoking. Soc Sci Med 1984; 19:573-80. 212. Becker MH. The health belief model in personal health behavior. Health Educ Monogr 1974; 214:409-19. 213. Thompson RS, Michnick ME, Friedlander L, Gilson B, Grothaus Le, Stover B. Effectiveness of smoking cessation interventions integrated into primary care practice. Med Care 1988; 26:62-76.

Smoking and smoking cessation.

State of the Art Smoking and Smoking Cessation 1 •2 EDWIN B. FISHER, JR., DEBRA HAIRE-JOSHU, GLEN D. MORGAN, HEATHER REHBERG, and KATHRYN ROST Conten...
3MB Sizes 0 Downloads 0 Views