8.28Tobacco SmokingMARTIN J. JARVIS

University College London Medical School, UK

and

GAY SUTHERLAND

Institute of Psychiatry, London, UK

8.28.1 INTRODUCTION 646

8.28.2 PATTERNS OF SMOKING PREVALENCE WORLDWIDE 646

8.28.3 SMOKING AS A CAUSE OF DEATH 646

8.28.3.1 Diseases Caused by Smoking 6478.28.3.2 Smoking in Pregnancy 6488.28.3.3 Health Effects of Passive Smoking 6488.28.3.4 The Health Benefits of Smoking Cessation 649

8.28.4 CIGARETTE SMOKING AND NICOTINE DEPENDENCE 650

8.28.5 THE SMOKING CAREER: PATTERNS OF UPTAKE, MAINTENANCE,AND CESSATION OF SMOKING 651

8.28.5.1 Recruitment of Young People to Cigarette Smoking 6518.28.5.2 Adult Smoking: Disadvantage and Dependence 6528.28.5.3 Factors Associated with Smoking Cessation 6528.28.5.4 Rates of Spontaneous Cessation in Smokers 654

8.28.6 PSYCHOLOGICAL SYMPTOMS 654

8.28.7 ASSESSMENT 656

8.28.7.1 Assessing Motivation and Intention to Quit 6578.28.7.2 Assessing Nicotine Dependence 6588.28.7.3 Questionnaire Measures of Dependence 6588.28.7.4 Biochemical Measures of Dependence 660

8.28.8 TREATMENT APPROACHES 661

8.28.8.1 Behavioral and Public Health Approaches 6618.28.8.2 Pharmacological Approaches to Smoking Cessation 663

8.28.8.2.1 Nicotine replacement therapy 6638.28.8.2.2 Non-nicotine pharmacotherapy 666

8.28.9 APPROACHES TO REDUCE SMOKING-RELATED DISABILITY 667

8.28.10 PROSPECTS FOR THE FUTURE 668

8.28.11 REFERENCES 668

645

Copyright © 1998 Elsevier Science Ltd. All rights reserved.

8.28.1 INTRODUCTION

Tobacco smoking presents numerous para-doxes. Despite being possibly the most pre-valent, and certainly the most lethal, form ofdrug dependence in the world, for yearscigarette smoking was regarded as no morethan a social habit and there was little awarenessof its psychoactive component, nicotine. Nico-tine is in many ways an invisible drug, whichlacks obvious effects on users' cognitive per-formance, mood, or social functioning. Yet it isnow regarded by many as the purest pharma-cological dependence, the very paradigm ofdrug addiction. Nicotine is a stimulant drugwhich users say calms them down and sedates.Smoking is often viewed as a form of self-medication to cope with stress, but there is littleevidence that nicotine possesses any anxiolyticor anti-depressant properties. Despite nicotine'slack of euphoriant or other obvious moodaltering effects, smoking is remarkably recalci-trant to change. Most smokers want to give upsmoking, and make numerous attempts to doso. But even those with severe smoking-relateddisease often fail to quit, and even in developedcountries with a strong antismoking ethos,fewer than half of all those who have eversmoked regularly succeed in stopping before theage of 65. It is this feature above all which hasmade smoking a focus of interest for psychol-ogists. It has long been an area of active researchinto methods of achieving behavior change, aswell as for understanding the complex interplaybetween pharmacological, psychological, andsocial determinants of behavior. After yearswhen progress was very limited, there haverecently been genuine advances in developingeffective, and cost-effective, treatment methodsfor smoking cessation. But failure to succeed inquit attempts, or relapse following initialsuccess, are still the norm, and young peoplecontinue to be recruited to smoking in largenumbers. The smoking problem shows no signof going away.

8.28.2 PATTERNS OF SMOKINGPREVALENCE WORLDWIDE

While tobacco use has a long history, withforms such as pipe and cigar smoking, chewingtobacco, and nasal snuff predominating inearlier periods, the manufactured cigarette,and with it the epidemic of smoking worldwide,is essentially a phenomenon of the twentiethcentury. Annual per capita consumption ofcigarettes in adults in developed countries rosesteadily from 600 in 1920 to a peak of over 3000in the mid-1970s, since when there has been amodest decline of some 16% (Collishaw &

Lopez, 1996). In developing countries, on theother hand, cigarette consumption increasedsharply in the 1970s and 1980s, so that the gap inper capita cigarette consumption betweendeveloped and developing countries is narrow-ing. On current trends, per adult consumption indeveloping countries will exceed that of devel-oped countries shortly after the turn of thecentury.Table 1 shows WHO estimates of smoking

prevalence inmen andwomen in various regionsin the world in the early 1990s, and also trends inper capita consumption since the late 1970s.Among men, worldwide prevalence, at 47%,approaches one-half of all adults, with particu-larly high levels being seen in China and in theformer socialist countries of Eastern Europe.Globally, women's smoking is at much lowerlevels than that of men (12%), with relativelyhigh prevalence being seen in developed coun-tries and low rates in Africa, India, China, andother parts of Asia where cultural traditions stillfrown on female smoking. In terms of the totalworldmarket, the decline since 1970 of 1.5%perannum in per capita consumption in theAmerican region and of 0.6% in WesternEuropean countries has been more than offsetby rapid growth in China (4.8%per annum) andother less developed countries, with the resultthat overall the size of the market continues toincrease.

8.28.3 SMOKING AS A CAUSE OF DEATH

Because the magnitude of the risk to healthrises with increased duration of the habit,increases in deaths from smoking show a timelag of about 30±40 years from the onset ofregular smoking. As a result, differing patternsof smoking related deaths are currently seen inmen and women. In the UK, although malesmoking declined from the 1960s onward,smoking deaths have only recently begun todecline; while in women death rates are rapidlyincreasing and will continue to do so for someyears, despite prevalence peaking in the early1970s (Peto et al., 1996).Table 2 gives estimates of the total number of

deaths caused by smoking in developed coun-tries since 1955. In 1955, smoking was respon-sible for about 500 000 deaths per year, mostlyamong men. Since that time smoking-attribut-able deaths have risen dramatically and by 1995almost 2 million people (1.5 million men and500 000 women) in developed countries weredying each year from tobacco. The rate ofincrease is now slowing somewhat among men,but continues to increase rapidly in women. Inthemid 1990s about 25%of all male deaths, and

Tobacco Smoking646

9% of female deaths, in developed countrieswere due to smoking. The proportion of deathsin middle age (35±69) caused by smoking isconsiderably higher, at 36% in men and 13% inwomen. Estimates of smoking related deaths inthe developing world are more uncertain, but itis already clear that the increases in smokingprevalence that have occurred in the developingworld since the 1970s will lead inexorably tomassive increases in deaths. The current world-wide annual figure for deaths caused bysmoking of 3 million (made up of 2 million indeveloped and 1 million in developing coun-tries) is estimated to increase to 10 million peryear by about 2020 or 2030. The great bulk ofthese deaths will be in the developing world(Peto, Lopez, Boreham, Thun, & Heath, 1994).

8.28.3.1 Diseases Caused by Smoking

The link of smokingwith lung cancer was firstreported in prewar Germany (Smith, Strobele,& Egger, 1994), but this work was largelyforgotten, and the findings of Doll and Hill(1950) and Wynder and Graham (1950) stimu-lated the setting up of a number of epidemio-logical studies which established thefoundations of our understanding of smokingas a cause of disease. Based on the 20 yearfollow-up of the British doctors cohort, it was

concluded that a young man who persists insmoking will run a 1 in 4 chance of being killedprematurely by tobacco (Royal College ofPhysicians, 1971). More recent studies, includ-ing the 40 year follow-up of the British doctors(Doll, Peto, Wheatley, Gray, & Sutherland,1994) and the second large study of theAmerican Cancer Society (CPS II) (Thun,Day-Lally, Calle, Flanders, & Heath, 1995)have extended this understanding and forced are-evaluation of the extent of the risk. It is nowapparent that persistent smokers run a 1 in 2risk of being killed by cigarettes, losing onaverage eight years of life.Table 3 summarizes data from the American

Cancer Society study of over 1 million men andwomen aged 35 and over, giving mortality incigarette smokers and life-long nonsmokers forthe main fatal smoking-related diseases. Therelative risk and absolute excess risk is given foreach disease, together with the attributableproportionÐthe proportion of all deaths foreach specified disease that is due to smoking.Smoking is recognized to cause 80% or more ofall lung cancers with a relative risk in men of 22andwomenof 12. In addition it is responsible formost cancers of the upper respiratory tract (lip,tongue, mouth, pharynx, and larynx) and for asmaller fraction of cancers of the bladder,pancreas, esophagus, and kidney. Among bothmen and women, smoking-attributable deaths

Table 1 Daily smoking prevalence in men and women aged 15 and over, selected world regions, early 1990s:WHO estimates.

Men(%)

Women(%)

Annual % change 1970±1972to 1990±1992 per capitacigarette consumption

WHO regionsAfrican region 29 4 1.2American region 35 22 71.5Eastern Mediterranean region 35 4 1.4European region 46 26 0.0Southeast Asia region 44 4 1.8Western Pacific region 60 8 3.0

More developed countries 42 24 70.5Established market economies 37 23 70.6Formerly socialist economies of Europe 60 28 0.6

Less developed countries 48 7 2.5China (1984) 61 7 4.8India (1980s) 40 3 1.5Other Asia and islands 54 7 2.1Middle Eastern crescent 41 8 1.2Sub-Saharan Africa 25 3 1.0Latin America and the Caribbean 40 21 70.4

World 47 12 0.8

Source: Collishaw and Lopez (1996).

Smoking as a Cause of Death 647

from cardiovascular disease (ischemic heartdisease, aortic aneurysm,andstroke)outnumberthose from all other causes, including lungcancer. Over 70% of chronic obstructive lungdisease is attributable to smoking, with a relativerisk inbothmaleandfemale smokersofabout10.Findings from the 40 year follow-up of the

British doctors' study are in general very similar,but additionally indicate a causal effect ofsmoking on stomach cancer and leukemia.Associations between smoking and cirrhosis ofthe liver, suicide, poisoning, and cancer of theliver have been regarded as being due toconfounding (Doll et al., 1994). Similarly, thereis uncertainty whether the association of smok-ing with cervical cancer is causal or attributableto confounding (Phillips & Smith, 1994).As well as being the single largest cause of

preventable premature death, cigarette smokingis a cause of a number of disabling but generallynonfatal conditions (Wald & Hackshaw, 1996).These include peripheral vascular disease,cataracts, Crohn's disease, gastric and duodenalulcers, hip fracture in the elderly, and period-ontitis, the major cause of teeth loss in adults.

8.28.3.2 Smoking in Pregnancy

Smoking is an important hazard in preg-nancy, leading to an increased risk of sponta-neous abortion and doubling the risk of ectopicpregnancy (Poswillo &Alberman, 1992). Babiesof smoking mothers weigh on average 150±250grams less at birth than babies of nonsmokingmothers. This association has been shown to becausal, since randomized trials of smokingcessation in pregnancy have shown that birthweight can be increased (Sexton &Habel, 1984).Smoking by mothers has consistently beenfound to be associated with sudden infant deathsyndrome, although it is uncertain whether pre-

natal exposure, or passive exposure to mother'sand father's smoking postnatally, is moreimportant (Blair et al., 1996; Haglund &Cnattingius, 1990; Klonoff-Cohen et al., 1995).

8.28.3.3 Health Effects of Passive Smoking

The adverse effects of cigarette smoking onhealth are not limited to active smoking. Sincethe early 1980s there has been an explosion ofresearch into the effects on nonsmokers ofbreathing in other people's smoke, and thiswork has had a decisive impact on the debateabout the social acceptability of smoking.Studies of the uptake of smoke constituentsby nonsmokers have shown dose±responserelationships with the extent of exposure topassive smoking (Jarvis, 1989). Cotinine con-centrations in exposed individuals have beenfound to average about 0.7±1.0% of those inheavy smokers (Jarvis, Tunstall-Pedoe, Feyer-abend, Vesey, & Saloojee, 1984; Jarvis et al.,1985). A number of reports by independentscientists have reviewed the evidence linkingpassive smoking with lung cancer in nonsmok-ing spouses exposed to their partners' smoke.All have concluded that passive smoking causeslung cancer in otherwise healthy nonsmokers,with an estimated number of deaths each year of3000 in the USA (US Environmental ProtectionAgency [USEPA], 1992) and about 300 in theUK (Froggatt, 1988). TheUSEPA has classifiedenvironmental tobacco smoke as a knownhuman carcinogen. The association of heartdisease with passive smoking is of similarmagnitude to that observed for lung cancer,with exposed spouses having about a 30%increase in risk. On a causal interpretation ofthis association, passive smoking may kill farmore people through heart disease than throughlung cancerÐup to 60 000 deaths each year in

Table 2 Estimated deaths caused by smoking in developed countries, 1950±2000.

Men Women

Mid-decade year

No. ofdeaths per

year% of alldeaths

% ofdeaths age35±69

No. ofdeaths per

year% of alldeaths

% of deathsage 35±69

1955 447 000 10 20 26 000 51 21965 793 000 17 28 70 000 2 41975 1 119 000 21 31 165 000 3 71985 1 369 000 24 35 317 000 6 111995 1 442 000 25 36 476 000 9 13

Total all deaths caused bysmoking 1950±2000

52 million 20 30 10.5 million 4 7

Source: Peto et al. (1994).

Tobacco Smoking648

the USA (Wells, 1994; Steenland, 1992). How-ever, because of the difficulty in makingappropriate allowance for confounders suchas diet, uncertainty remains about how much ofthe observed association is truly causal.Although the debate about the effects of

passive smoking has largely centered on lungcancer in adults, the main public health burdenis borne by children with smoking parents.Numerous studies have shown that babies fromsmoking households are at increased risk foradmission to hospital with bronchitis andpneumonia (USEPA, 1992). In later childhoodthere is strong evidence of impairments in lungfunction (Strachan, Jarvis, & Feyerabend, 1990;Cook et al., 1993) and of increased risk ofmiddle ear effusion when parents smoke(Strachan, Jarvis, & Feyerabend, 1989).

8.28.3.4 The Health Benefits of SmokingCessation

Stopping smoking benefits health at any age,the more so the younger the smoker stops (USDepartment of Health and Human Services,1989). In the British doctors' study, those whogave up by their mid-30s had a life expectancy

indistinguishable from never smokers, and eventhose who gave up in their late 60s livedsignificantly longer than continuing smokers(Doll et al., 1994). Benefits have been observedfor a variety of conditions. The Lung HealthStudy, a randomized trial of smoking cessationin people at increased risk of chronic respiratorydisease, showed that on stopping smoking therate of loss of ventilatory capacity reverts fromthe accelerated rate characteristic of smokers tothe slower age-related decline of nonsmokers(Anthonisen et al., 1994; Jarvis, 1995). Withlung cancer a somewhat different picture is seen.The extra risk incurred from a smoking career ofa given duration is never lost, but remains at thelevel determined by the duration of smoking atthe time of quitting (Halpern, Gillespie, &Warner, 1993). Since that risk would haveescalated exponentially with continued smok-ing, a marked reduction in risk is observed bycomparison with persisting smoking. For heartdisease the risk in ex-smokers declines towardthat of never-smokers, although there is someuncertainty as to how rapidly the excess risk islost, whether rapidly (Dobson, Alexander,Heller, & Lloyd, 1991; Rosenberg, Kaufman,Helmrish, & Shapiro, 1985) or over many years(Cook, Shaper, Pocock, & Kussick, 1986).

Table 3 Fatal diseases associated with smoking: American Cancer Society (CPS II) men and womenaged 35+.

Standardized mortality per 100 000 per year

Life-longnonsmoker

Current cigarettesmoker

Relativerisk

Absolute excess riskper 100 000 per year

Attributable(%)

CancerLung M 24 537 22.4 513 87

F 18 213 11.9 195 77Upper respiratory M 1 27 24.5 26 89

F 2 10 5.6 8 58Bladder M 18 53 2.9 35 36

F 8 21 2.6 13 32Pancreas M 18 38 2.1 20 25

F 16 37 2.3 21 29Esophagus M 9 68 7.6 59 66

F 4 41 10.3 37 74Kidney M 8 23 3.0 15 37

F 6 8 1.4 2 11Ischemic heart M 500 970 1.9 470 22

F 386 688 1.8 302 19Aortic aneurysm M 24 98 4.1 74 48

F 11 52 4.6 41 52Stroke M 147 328 2.2 181 27

F 236 434 1.8 198 20Chronic obstructivelung disease

M 39 378 9.7 339 72F 21 216 10.5 195 74

All diseases M 788 2520 3.2 1732 40F 708 1720 2.4 1012 30

Smoking as a Cause of Death 649

8.28.4 CIGARETTE SMOKING ANDNICOTINE DEPENDENCE

Drug taking aspects of cigarette smokingwerelargely ignored until the 1970s, but since then anaccumulation of research findings froma varietyof disciplines and from both human and animalwork has led to a consensus that cigarettesmoking is essentially a form of addiction tonicotine. This was enshrined in the landmark1988 report of the US Surgeon General whichconcluded that the processes underlying addic-tion to nicotine are similar to those of otheraddictive drugs such as alcohol, heroin, andcocaine (US Department of Health and HumanServices, 1988). Since then clear evidence hasemerged that this view is shared, privately if notpublicly, by the tobacco industry, which actuallyreached it considerably earlier (Slade, Bero,Hanauer,Barnes,&Glantz, 1995).TheUSFoodandDrugAdministration has based its assertionof jurisdiction over cigarettes and other tobaccoproducts on the evidence of nicotine's addictiveproperties and the tobacco industry's exploita-tion of them (Kessler et al., 1996, 1997).Understanding of nicotine's role is fundamentalto an appreciation of smoking uptake, main-tenance, and cessation. It does not follow, ofcourse, that cigarette smoking is explicable solelyin terms of pharmacological factors. Nicotineeffects provide a rich substrate for conditioningand social learning mechanisms, and for broadsocial, economic, and societal influences. In thisrespect it is no different from other drugdependencies.The evidence relevant to nicotine's properties

as an addictive drug comes from a number ofareas (Henningfield &Keenan, 1993; Stolerman& Jarvis, 1995). Some of the main lines arebriefly summarized here.(i) Brain neurochemistry. Both animal and

human studies have shown that chronic nicotineadministration leads to an increase in theexpression of specific nicotine receptors onneurons. Even prenatal exposure can producesuch nicotine receptor up-regulation (Slotkin,Orband-Miller, & Queen, 1987). Postmortemstudies have revealed raised concentrations ofnicotine receptors in the brains of humansmokers (Benwell, Balfour, & Anderson,1988). Investigations of dopaminergic systemsthought to be important in reward mechanismshave shown effects of nicotine similar to thoseof cocaine (Pontieri, Tanda, Orzi, & Dichiara,1996; Pich et al., 1997).(ii) Animal self-administration. Under appro-

priate schedules of reinforcement nicotine func-tions as a robust primary reinforcer (Corrigall &Coen, 1989; Spealman & Goldberg, 1982) in avariety of animal species. Early difficulties in

demonstrating nicotine's reinforcing effect seemto have stemmed from the narrow range ofrewarding blood concentrations and the ease ofprovoking aversive overdose.(iii) Pharmacokinetics. Nicotine is readily

absorbed through the skin, and through thelining of the mouth and nose, the rate ofabsorption being enhanced in an alkaline en-vironment and reduced in an acidic environ-ment. Because of the large surface area of thelungs the mildly acidic smoke of cigarettes isabsorbed almost immediately and completelyon inhalation, giving rise to high concentrationarterial nicotine boli which reach the brain inless than 10 seconds (Henningfield, London, &Benowitz, 1990; Russell, 1980). Nicotine has adistributional half-life of about 15 minutes anda terminal half-life in blood of about two hours(Benowitz, 1988). This means that blood levelsdecline overnight to nonsmoking levels, andregular cigarettes are required over the course ofthe day to maintain elevated blood nicotineconcentrations.(iv) Regulation of blood nicotine intake from

different tobacco products and from cigaretteswith differing deliveries (titration). Levels ofblood nicotine maintained by cigarette smokersand by dependent users of either oral (Holm,Jarvis, Russell, & Feyerabend, 1992) or nasal(Russell, Jarvis, Devitt, & Feyerabend, 1981)snuff are remarkably similar, averaging in eachcase about 35 ng/ml. Given the very differentsensory characteristics of burnt and noncom-bustible tobacco, the different routes of absorp-tion, and the absence from snuff of componentssuch as tar, this similarity points strongly tonicotine as the factor controlling the behavior.Manufactured cigarettes contain about

10±14mg of nicotine, an amount that doesnot vary greatly between different brands. Butby techniques such as filtration and ventilation,yields of nicotine when smoked by a machine ina standardized way range from as little as 0.1mgto over 1mg, with concomitant tar yields beingclosely correlated and ranging from 1 to 15mgor more. The relevance of these machinesmoked yields to human smoking is open toserious question (USDepartment of Health andHuman Services, 1996), since smokers extract asimilar amount of nicotine (about 1mg onaverage) from cigarettes of widely differingyields (Benowitz et al., 1983). Naturalisticstudies of smokers smoking their own self-selected brands (Russell, Jarvis, Iyer, & Feyer-abend, 1980; Gori & Lynch, 1985) and ofsmokers experimentally switched to lower yield-ing brands (Frost et al., 1995; Withey et al.,1992) have both shown that the slope relatingmachine-smoked yield and nicotine intake iseither flat or very shallow, so that smokers can

Tobacco Smoking650

and do adjust the way they smoke so as tomaintain similar nicotine intakes from cigar-ettes with widely differing deliveries. Similar up-regulation of nicotine intake has been shownwhen smokers temporarily reduce the numberof cigarettes smoked (Ho-Yen, Spence, Moody,& Walker, 1982). This pervasive phenomenonwhich is characteristic of human smoking istermed nicotine compensation or titration(Russell, 1980). A boundary model of nicotineregulation has been proposed, whereby chronicusers seek to avoid the adverse effects of eithertoo little (withdrawal) or too much (overdose)nicotine (Kozlowski, 1984).(v) Acquisition of nicotine inhalation in novice

smokers. It is well established that children takeup smoking formainlypsychosocial reasons, butstudies have shown that pharmacological mo-tives take on importance very early in thesmoking career (Lynch & Bonnie, 1994;McNeill, 1991). Already by the time they aresmoking on a daily basis, children take in asmuch nicotine from each cigarette as dependentadult smokers (McNeill, Jarvis, Stapleton,West,& Bryant, 1989), and they report similar craving(Goddard, 1990) and withdrawal symptoms ontrying to stop (McNeill,West, Jarvis, Jackson,&Bryant, 1986). The FDA has aptly describednicotine addiction as a ªpediatric disease.º(vi) Compulsive use. Although long-term oc-

casional smokers (so called ªchippersº) arefound (Evans et al., 1992; Shiffman, 1989), theyare rare, and the typical smoker smokes muchthe same number of cigarettes each day, aver-aging about 17 in theUK.Even thosewith severesmoking-related disease persist in smoking,whether it be heart disease (Bigelow, Rand,Gross, Burling,&Gottlieb, 1986), laryngectomy(Himbury & West, 1985), or lung cancer (Davi-son&Duffy, 1982). Dependent users of alcohol,heroin, and cocaine rate giving up smoking as atleast as difficult as their problemdrug (Kozlows-ki et al., 1989). Compulsive use is the key featurecharacterizing nicotine dependence.(vii) Nicotine withdrawal syndrome. Cessa-

tion of smoking reliably leads to a variety ofsigns and symptoms, with an onset within12 hours or less of last tobacco use, and aduration of three weeks or longer. The mani-festations are predominantly affective in nature,with subjects reporting irritability, difficultyconcentrating, anxiety, restlessness, increasedhunger and depressed mood, as well as cravingfor tobacco. These findings have been observedinnumerous experimental studies (Hughes et al.,1984; West, Jarvis, Russell, Carruthers, &Feyerabend, 1984) and have been thoroughlyreviewed (Hughes, 1992; Hughes, Gust, Skoog,Keenan, & Fenwick, 1991; Hughes & Hatsu-kami, 1986). Similar effects are seen after

cessation of nicotine chewing gum (West &Russell, 1985) or of smokeless tobacco (Hatsu-kami, Gust, & Keenan, 1987). That the tobaccowithdrawal syndrome is due to loss of nicotinerather than behavioral aspects of use is shownby the consistent finding that it is relieved bynicotine replacement but not placebo (Gross &Stitzer, 1989; Jarvis, Raw, Russell, & Feyera-bend, 1982; Russell et al., 1993; Sutherland,Russell, Stapleton, Feyerabend, & Ferno, 1992;West et al., 1984).

(viii) Efficacy of nicotine replacement as anaid to smoking cessation. Numerous randomizedcontrolled trials have shown that nicotinereplacement, whether by patch, gum, nasalspray, or inhaler, reliably enhances the chancesof success in an attempt at cessation, roughlydoubling success rates over placebo (Fiore et al.,1996; Silagy, Mant, Fowler, & Lodge, 1994).

8.28.5 THE SMOKING CAREER:PATTERNS OF UPTAKE,MAINTENANCE, AND CESSATIONOF SMOKING

8.28.5.1 Recruitment of Young People toCigarette Smoking

Uptake of smoking typically occurs inadolescence, with few people starting to smokeafter the age of 20 (Kessler, 1995; Kessler et al.,1997). In the UK, from a prevalence of about1% at age 11, there is a rapid increase over thefollowing few years, so that by age 15 about25% of teenagers smoke, with some evidencethat at this age (although not among youngadults of 16 and above) girls are more likely tosmoke than boys (Diamond & Goddard, 1995).Rates of smoking in young people have shownno decline since the early 1980s in the UK, andthere is evidence that they are currentlyincreasing in the USA (Giovino, Henningfield,Tomar, Escobedo, & Slade, 1995; Glynn,Greenwald, Mills, & Manley, 1993).Initiation of smoking is subject to a number

of influences: environmental, behavioral, andpersonal factors all play a part (Goddard, 1990;Lynch & Bonnie, 1994). Environmental influ-ences include parental smoking (approximatelydoubling the likelihood of a child starting tosmoke), and smoking by siblings and friends.Tobacco advertising and promotions effectivelytarget young people with images of smoking astrendy, sporty, and successful (Altman, Levine,Coeytaux, Slade, & Jaffe, 1996; DiFranza et al.,1991; Pollay et al., 1996; Wills, Pierce, & Evans,1996). Young people from deprived back-grounds where smoking is the norm are morelikely to become smokers, an association whichbecomes accentuated in adulthood, implying

The Smoking Career 651

that smoking is a marker for social trajectory(Glendinning, Shucksmith, & Hendry, 1994).Cigarette smoking is often an early manifes-

tation of problem behavior. It is linked withpoor school performance, truancy, low aspira-tions for future success, and early school leavingor drop out (Lynch & Bonnie, 1994). Cigarettesmoking in adolescents is frequently associatedwith other problem behaviors, including alcoholand other drug use and other risk taking orrebellious behaviors.Personal characteristics consistently linked

with adolescent smoking include low self-esteem, low knowledge of smoking's adverseeffects, and anxiety and depression (Breslau,Kilbey, & Andreski, 1993).School-based interventions to reduce the

uptake of smoking by teenagers have been ex-tensively studied. Skills based approaches de-signed to equip children to resist social influencesto smoke have shown some initial success, with anumber of randomized trials reporting lowerrates of recruitment in intervention than controlgroups (Bruvold, 1993; Flay, 1985). Unfortu-nately, longer term follow-up has found thatthese effects dissipate (Flay et al., 1989;Nutbeam, Macaskill, Smith, Simpson, & Cat-ford, 1993), leading researchers to advocateapproaches involving the creation of a widersocial environment supportive of nonsmoking(Flay, 1985).Both in theUSAandtheUK,whererates of teenage smoking are on the increase,there is a recognition that preventing the uptakeof smoking by young people is an area where upuntil now little has been achieved. If progress isto be made, it will require a far better researchunderstanding than there is at present of thefactors influencing experimental smoking andthe development of nicotine dependence.

8.28.5.2 Adult Smoking: Disadvantage andDependence

In developed Western countries rates ofcigarette smoking have peaked and are nowdeclining, albeit slowly. In the USA and UKabout 25±30% of adults smoke, with littledifference in prevalence between men andwomen, except in the oldest age groups contain-ing a cohort of women for whom never-smokingwas the norm. The most striking feature of theevolution of smoking since the late 1970s hasbeen the increasing association of cigaretteswith markers of disadvantage, whether it besocioeconomic position, or a range of factorsindicating stressful living circumstances (Jarvis,1994b). High rates of smoking are seen in theunemployed (Lee, Crombie, Smith, & Tunstall-Pedoe, 1991), lone parents (Marsh & McKay,

1994), people who are divorced or separated, thehomeless (Gill, Meltzer, Hinds, & Pettigrew,1996), heavy drinkers (Jarvis, 1994b), drug users(Meltzer, Gill, Pettigrew, & Hinds, 1995), andprisoners (Bridgwood & Malbon, 1995). Cigar-ette smoking is strongly associated with psy-chiatric illness, whether it be schizophrenia(DeLeon et al., 1995; Hughes et al., 1991),depressive illness (Glassman, 1993), or a varietyof other neurotic disorders (Meltzer et al., 1995).The association of cigarettes with lowered levelsof psychological well-being is not confined tothose with a formal psychiatric diagnosis, butalso extends into the general population ofsmokers (Anda et al., 1990; Schoenborn &Horm, 1993). In the general population there isan increasingly strong association betweencigarette smoking prevalence and indicatorsof deprivation (Pierce, Fiore, Novotny, Hat-ziandreu, &Davis, 1989a, 1989b). Between 1973and 1994, rates of smoking among affluentpeople halved in the UK, but among the poorestgroups prevalence remained unchanged at closeto 70% (Bennett, Jarvis, Rowlands, Singleton,& Haselden, 1996; Jarvis, 1997).Cigarette smoking is unusual among drug

dependencies in that high levels of dependenceare typical of most users, rather than beingfound only in a minority (Stolerman & Jarvis,1995). At least 80% of cigarette smokers meetthe Diagnostic and statistical manual of mentaldisorders (4th ed.; DSM-IV) criteria fordependence (Cottler et al., 1995). Smokers'dependence is manifested in a variety of ways,which all point to a pattern of behavior that hasbecome highly stereotyped. The average smo-ker smokes every day, at a rate of over onecigarette for every waking hour. Survey dataindicate that almost one-third of smokers havenever stopped for as long as a week (USDepartment of Health and Human Services,1990). There is increasing consensus that timeto first cigarette of the day is the strongestbehavioral indicator of cigarette dependence.Figure 1 shows the distribution of time to firstcigarette in a general population sample ofsmokers, and also the corresponding levels ofnicotine intake as indexed by saliva cotinineconcentrations. Some 17% of smokers light upwithin five minutes of waking, and over 50%within half an hour. Overall levels of nicotineintake are closely correlated.

8.28.5.3 Factors Associated with SmokingCessation

At any one time, about two-thirds of cigarettesmokers say that they would like to give up, butmost lack confidence that they would succeed if

Tobacco Smoking652

30

25

20

15

10

5

0

“How soon after waking do you smoke your first cigarette of the day?”

Less than 5–15 15–30 30 minutes 1–2 More than5 minutes minutes minutes to 1 hour hours 2 hours

Per

cent

age

of s

mok

ers

17

21

14 1412

22

450

400

350

300

250

200

150

100

50

Time to first cigarette of the day

Less than 5–15 15–30 30 minutes 1–2 More than5 minutes minutes minutes to 1 hour hours 2 hours

n = 260 n = 322 n = 205 n = 214 n = 182 n = 307

Sal

iva

cotin

ine

(ng/

ml)

Mean + 95% CI

Figure 1 Distribution of time to first cigarette of the day among smokers surveyed in primary care, andcorresponding saliva cotinine concentrations. Time to first cigarette is the strongest available predictor of

nicotine dependence.

The Smoking Career 653

they tried (Bennett et al., 1996). Rates ofcessation (defined as the proportion of ex-smokers among ever-regular cigarette smokers)rise steadily with age, from about 18% in youngpeople in their early 20s to 60% among thoseaged 60 and above (Bennett et al., 1996). Acrossall age groups combined less than half of eversmokers in the UK and the USA have quit(Bennett et al., 1996; US Department of Healthand Human Services, 1990). Overall, rates ofcessation show little difference by gender, withyoung women significantly more likely to quitthanmen, andmiddle-aged women significantlyless likely (Jarvis, 1994a).Smoking cessation is influenced by a number

of factors, including immediate family circum-stances, the broader socioeconomic setting,psychological well-being, and pharmacologicaldependence (Jarvis, 1997). Influences within thefamily are shown both by the association ofcessation in parents with number of children(Jarvis, 1996) and by the strong concordance insmoking habits among spouses and theirpartners. Spouse smoking has consistentlyemerged as one of the most powerful predictorsof cessation (Murray, Johnston, Dolce,WondraWong, & Ohara, 1995; Nafstad, Botten, &Hagen, 1996; Severson, Andrews, Lichtenstein,Wall, & Zoref, 1995; Wakefield, Gillies, Gra-ham, Madeley, & Symonds, 1993). Poverty hasbecome increasingly associated with low rates ofcessation, indicating that those who can leastafford to smoke are the least likely to quit(Jarvis, 1997; Marsh &Mackay, 1994). Figure 2shows rates of cessation by level of deprivationover the past 20 years in the UK. Among bothaffluent men and women cessation rates havemore than doubled, but among the poorest only10%or less of ever-smokers have quit, and therehas been no improvement since the 1970s.Depressive illness (Glassman et al., 1990b)

and stressful life circumstances are associatedwith low rates of cessation, although interest-ingly there is evidence that successful cessationleads to lower, rather than higher, levels ofperceived stress (Cohen & Lichtenstein, 1990).

8.28.5.4 Rates of Spontaneous Cessation inSmokers

The concept of ªspontaneousº or unaidedquitting is a difficult one. There are a multi-plicity of influences, both those that areexplicitly recognized by smokers, and otherswhich, while unrecognized, may nevertheless bepresent and influence behavior. In a US surveyof ex-smokers, respondents acknowledged littleassistance in giving up smoking (Fiore et al.,1990). Over 90% said that they gave up withoutany help at all, either from family, physicians, or

more formal services. Only 4% said that theyhad had any involvement with specializedtreatment agencies.One way to estimate rates of successful

unaided quitting in the population is to lookat the rate at which prevalence declines year byyear, or, more specifically, the increase over timein the cessation rate. By this yardstick, there hasbeen an approximate 1.5% increase in cessationeach year in the UK since the 1970s. However,given that no information is available on thenumber of cessation attempts smokers make inany given year (even if it were possible to reach asatisfactory definition of what constitutes aserious attempt at cessation), this cannot easilybe translated into what the chances of success-fully quitting are from any one attempt. Thefigure of 1.5% represents the cumulative successrate from all quit attempts made each year,averaged across smokers. If smokers on averagemake several attempts to quit each year, itimplies a success rate per quit attempt of under1%; alternatively, if serious quit attempts occurat a rate of less than once per year, the impliedsuccess rate per quit attempt may be higher.Two studies have explicitly recruited smokers

planning tomake an unaided attempt at quittingand have followed them up to establish successrates. In the first, only one-third abstainedsuccessfully for two days, one-quarter for oneweek, and at six months 3% remained abstinent(Hughes et al., 1992). Similar findings emergedin the second study, with 4.9% not smoking atsix months (Cohen et al., 1989). Since somefurther relapse to smoking would be anticipatedafter six months, these percentages give anoverestimate of the long-term success rate.There is a reasonable degree of agreement

between estimates from population cessationrates and from the studies of self-quitters. Bothindicate a low rate of successful long-termquitting from any given quit attempt. It wouldappear that the chances of successfully quittingon a particular attempt range between about 0.5and 3%. Such low figures point once again tothe difficulty of the task faced by smokers whowish to give up, and suggest that treatmentsachieving modest success rates of only 5±10%would have a valuable part to play in loweringsmoking prevalence, if they could be deliveredcost-effectively to the bulk of the smokingpopulation.

8.28.6 PSYCHOLOGICAL SYMPTOMS

Although the act of smoking does not in itselfcause any discernible mental or functionalimpairment, this is not to say that there are nonegative psychological sequelae. For many

Tobacco Smoking654

individuals there will be concern about currentor future illness, the effect of passive smoking onchildren, and the financial burden. There is alsolikely to be pressure to abstain from non-smoking family and friends, and a dislike ofbeing dependent on a drug. However, theclearest psychological impact of smoking ariseswhen an individual tries to stop. Most, but notall, smokers experience some psychological andphysical signs and symptoms when they stopsmoking or significantly reduce the amount they

smoke. There has been much research bothprospectively and retrospectively on the nicotinewithdrawal syndrome,most studies using simpleself-report questionnaires scored on likert orvisual analogue scales. The three most widelyreportedquestionnaires are theShiffman±JarvikSmoking Withdrawal Questionnaire (Shiffman& Jarvik, 1976), the Smoker Complaints Scale(Schneider, Jarvik, & Forsythe, 1984), and theMinnesota Nicotine Withdrawal Questionnaire(Hughes & Hatsukami, 1986).

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Figure 2 Trends in rates of smoking cessation by deprivation in (a) men and (b) women in the UK, 1973, 1982,and 1994. Deprivation wasmeasured on a five-point scale, where respondents scored 1 for each of the following:manual occupation; rented housing; no access to a car; crowded accommodation; unemployment. From Jarvis

(1997).

Psychological Symptoms 655

The most commonly reported subjectivenicotine withdrawal symptoms are craving forcigarettes, depressed mood, irritability, rest-lessness, difficulty concentrating, anxiety/ten-sion, sleep disturbance, and increased appetite,particularly for sweet, high calorific foods.Although the number and intensity variesconsiderably from person to person, withdrawalsymptoms are experienced by about 80% of ex-smokers, three-quarters of whom may exhibit apattern that could be described as severe (Gritz,Carr, & Marcus, 1991). Craving cigarettes,which can be intermittent or more or lesscontinuous, is probably the most troublesomeand fundamental symptom and is amajor factorin triggering relapse in the first few weeks of anattempt to quit. Self-reports of withdrawalsymptoms have been verified by observerratings (Hughes & Hatsukami, 1986).Withdrawal symptoms occur abruptly on

cessation and changes in mood and ability toconcentrate can be detected within two hours ofthe last cigarette. Symptoms peak in the first fewdays of cessation and, with the exception ofcraving, hunger, and weight gain which have alonger time course, gradually subside to baselinelevels within a few days or weeks, with anaverage duration of about 3±4 weeks (Snyder,Davis, & Henningfield, 1989; West, Hajek, &Belcher, 1987). Bouts of craving can persist formonths, however, and it is not uncommon forex-smokers to experience a strong urge to smokein certain situations or mood states associatedwith prior smoking even some years after giving-up. Increased appetite and weight gain continuefor at least 10 weeks after quitting and ex-smokers typically gain about 6±10 lb in the firstyear of cessation, though there is great variationfrom one person to another, with the heaviestsmokers tending to gain the most weight.Other physical and objective changes that

accompany tobacco withdrawal include de-creases in catecholamine excretion, metabolicrate, heart rate (12±15 bpm) (West & Russell,1987) blood pressure, and tremor, increases inskin temperature, changes in REM sleep,decreases in peak alpha EEG frequency indicat-ing decreased cortical arousal (Knott & Ven-ables, 1977) and gastrointestinal disturbances(Hughes & Hatsukami, 1986). Performance ontasks requiring vigilance or sustained attentionand memory is also impaired (Snyder et al.,1989). Many of these subjective and objectivewithdrawal effects are the opposite of the effectsthat occur following nicotine use and can bereversed by smoking or giving nicotine byanother route (e.g., nicotine gum, skin patch, orinjection) but not by a placebo or nicotine-freecigarettes. Severity of withdrawal symptomshave been found to correlate with baseline

smoking nicotine levels and also to predicttreatment outcome (West, Hajek, & Belcher,1989; West & Russell, 1985b).TheDSM-IV (American Psychiatric Associa-

tion, 1994) diagnostic criteria for nicotinewithdrawal are shown in Table 4. Of particularinterest is the inclusion of depressed moodwhich had not been listed in DSM-III-R. Anumber of epidemiological studies have recentlyfocused attention on the relationship betweendepression and smoking. Glassman et al.(1990a) found that smoking was more prevalentin individuals who had had a major depressivedisorder at some time in their lives and also thatthey were less likely to succeed in quittingsmoking than those without such a history.Mood changes, such as anxiety and depressionhave been shown to predict relapse.

8.28.7 ASSESSMENT

Although there are a wide range of assess-ment procedures which have been, or could be,applied to smoking behavior it is unfortunatelythe case that while many have face validity theyhave limited clinical utility. Clinically assess-ments are most useful when the results can beused to determine, for instance, which of anumber of treatments to apply in order tomaximize efficacy. This is rarely the case insmoking cessation, however, since much of theinformation gathered at assessment will at besthave prognostic value in predicting a smoker'slikelihood of succeeding but will have little tooffer in the way of indicating specific proceduresto improve the outcome. Empirical researchinto matching smokers to particular treatmentsis still in its infancy and has only recently startedto highlight some useful leads. The thorough-ness and depth of assessment will be determinedby the treatment setting. In a specializedsmokers clinic offering intensive treatment,for instance, a systematic assessment of in-dividual patient characteristics is feasible and islikely to include measures of the following:(i) motivation, intention, or desire to stop

smoking;(ii) demographics and smoking history in-

cluding number and duration of previousattempts to quit and reasons for relapse;(iii) self-report and objective measures of

current tobacco consumption;(iv) severity of nicotine dependence;(v) suitability for nicotine replacement or

other pharmacological treatment;(vi) psychosocial factors such as degree of

social support, stress, coping skills, and pre-sence of psychiatric comorbidity.

Tobacco Smoking656

Assessments in briefer community interven-tions and primary care are likely to be con-siderably less detailed and time consuming andmight only include questions about motivationto stop smoking and severity of nicotine de-pendence since these are the two patient char-acteristics most likely to influence the course ofsubsequent treatment and outcome.

8.28.7.1 Assessing Motivation and Intention toQuit

There are very few smokers who are able toquit smoking permanently without first beinghighly motivated and believing that they can doso. Regardless of the method employed to stopsmoking, a major factor will be the psycholo-gical resources available to an individual when itcomes to changing a strongly conditionedbehavior and resisting withdrawal symptomsand craving. A number of studies have shownthat without strong motivation to quit thelikelihood of succeeding is extremely low in allbut the most minimally dependent smokers(Jackson, Stapleton, Russell, & Merriman,1986). In brief intervention studies, motivationto quit has been assessed by simple question-naire items such as: ªHowmuch do you want tostop smoking altogether?º (not at all, slightly,moderately, quite strongly, very strongly), andªWould you give up smoking altogether, if youcould do so easily?º (yes definitely, yesprobably, possibly, probably not, definitelynot). Only those scoring in the highest cate-gories are likely to be sufficiently motivated topersist in a serious quit attempt. The number ofprevious attempts to stop smoking is also auseful indicator of motivation.The concepts of motivation and intention to

change behavior have been extended into a

theoretical model by Prochaska, DiClementeand colleagues (Prochaska&DiClemente, 1986;Prochaska, DiClemente, & Norcross, 1992).Their ªStages of Changeº model is based onrecognition of the fact that giving up smoking isa dynamic process, rather than a discrete event,often extending over many years, and char-acterized by repeated cycles of attempts to stopand relapses back to smoking. The modelidentifies five main stages through whichsmokers cycle:(i) Precontemplation. Not seriously thinking

about quitting.(ii) Contemplation. Staring to think seriously

about stopping within the next 6months but notwithin the next 30 days.(iii) Preparation. Intending to quit within the

next 30 days.(iv) Action. Stopped smoking within past

6months.(v) Maintenance. Stopped smoking for over

6months.Relapse leads to re-entry into the cycle at an

earlier stage. Three simple questions have beenidentified to assess a smoker's current stage(Prochaska & Goldstein, 1991):(i) Are you intending to quit within the next 6

months? If no, the smoker is in the precontem-plation stage.(ii) Are you intending to quit smoking in the

next month? If no, but answered yes to question(i), they are in the contemplation stage.(iii) Did you try and quit smoking in the past

year? If yes, and answered yes to question (ii)they are in the preparation stage.In addition to these stages, Prochaska and

DiClemente have identified 10 different positivebehavior change processes or activities (e.g.,counterconditioning, reinforcement manage-ment, stimulus control) which facilitate an

Table 4 DSM-IV diagnostic criteria for nicotine withdrawal.

A. Daily use of nicotine for at least several weeks

B. Abrupt cessation of nicotine use, or reduction in the amount of nicotine used,followed within 24 hours by four (or more) of the following signs:

(1) dysphoric or depressed mood;(2) insomnia;(3) irritability, frustration, or anger;(4) anxiety;(5) difficulty concentrating;(6) restlessness;(7) decreased heart rate;(8) increased appetite or weight gain

C. The symptoms in criterion B cause clinically significant distress or impairmentin social, occupational, or other important areas of functioning

D. The symptoms are not due to a general medical condition and are not betteraccounted for by another mental disorder

Assessment 657

individual's progression from one stage to thenext. They suggest that interventions whichencourage the use of the behavior changeprocesses most relevant to a smoker's currentstage, will be most effective. So, for instance,precontemplators would be targeted withinformation about the health risks of smokingand benefits of stopping in the hope of raisingtheir motivation and thus moving them to thecontemplator stage, whereas individuals in theaction stage might receive training in strategiesaimed to prevent relapse. Although there hasbeen some empirical support for the notion ofstage-matched interventions, critics have ex-posed inconsistencies and theoretical problemswith the model (Sutton, 1996). Perhaps the mostimportant contribution made by the Stages ofChange to date has been to encourage therapiststo assist smokers to stop over repeated attempts,rather than using a ªone shotº approach. Themodel has also focused attention on alternativemeasures of outcome besides total abstinence,that is, in terms ofmoving smokers along a stage(see also Chapter 8.01, this volume).

8.28.7.2 Assessing Nicotine Dependence

Nicotine dependence is now recognized as apsychoactive substance dependence disorder(DSM-IV, ICD-10). Under theDSM-IV criteriasmokers are classified as dependent if theyexhibit impaired control and continue to smokedespite awareness that it exacerbates a medicalcondition, and if they experience withdrawalsymptoms when abstaining from smoking, or ifthey have a history of unsuccessful attempts atquitting. However the practical value of usingthis all-or-nothing dichotomous classificationwhen assessing an individual smoker is limitedsince it has been estimated that about 90% ofsmokers are dependent (Woody, Cottler, &Cacciola, 1993). It is therefore, more useful toview smokers as lyingona continuumofnicotinedependence. When measured in this waydependence has proved to be the strongest andmost consistentpredictorof the successor failureof an attempt to quit smoking (see Figure 3) suchthat the likelihoodof stopping smoking is severaltimes greater at low, rather than high, levels ofdependence (Stapleton et al., 1995).Although this would seem to suggest con-

siderable potential for tailoring cessation treat-ment according to dependence level in order tomaximize overall cessation rates, little progresshas been made in this area. There are not as yetany established behavioral treatments based onthe differing dependence level of the smoker.One fundamental problem is that cessation ratesare modest even among smokers at the lower

end of the dependence range and specialattention and effort is only likely to be investedin the more highly dependent smokers whentreatment programs are more successful gen-erally. Not surprisingly, given that tobaccodependence is largely a dependence on nicotine,certain forms of nicotine replacement therapyhave been shown to be more effective at higherlevels of dependence and it is in this area thatmost progress towards matching treatments islikely to be made in the future (Sutherland &Stapleton, 1994). This does not mean, however,that an assessment of a smoker's level ofdependence has no clinical value, since it servesto alert therapists to cases where withdrawalsymptoms are likely to be particularly severeand the prognosis poor, indicating that moreintensive help may be required.

8.28.7.3 Questionnaire Measures of Dependence

Measures of the severity of nicotine depen-dence fall into two categories: (i) self-reportedbehavioral and subjective symptoms, and (ii)objective biochemical markers of nicotineintake. The simplest indicator of degree ofdependence is daily cigarette consumptionwhich can be obtained by self-report or byself-monitoring diary records over a period oftime. Since smokers tend to report consumptionin multiples of 5 or 10, self-monitoring diariestend to be more accurate than self-report,especially if the cigarette is recorded at the timeit is smoked, although the monitoring itself canbe a reactive measure and result in a decrease insmoking (Frederiksen, Epstein, & Kosevsky,1975; McFall, 1978). Consumption is only arough indicator of dependence, however, assmoke intake per cigarette can vary a great dealfrom one individual to another. Themost widelyused paper and pencil test of dependence is theFagerstroÈ m Tolerance Questionnaire (FTQ),consisting of an eight-item inventory designedto assess: daily nicotine intake, smoking in themorning (when nicotine levels are low); andperceived difficulty in refraining from smoking(FagerstroÈ m, 1978). More recently a shorter,six-item, version of the FTQ, the FagerstroÈ mTest for Nicotine Dependence (FTND), hasbeen developed to address some of the psycho-metric weaknesses of the original and hasimproved internal consistency and predictivevalidity (Heatherton, Kozlowski, Frecker, &FagerstroÈ m, 1991). Scores range from 0 (lowdependence) to 10 (high dependence).An even shorter version, the Heaviness of

Smoking Inventory, is based on the two itemswhich together account for 60% of the FTNDscore, namely, daily cigarette consumption, and

Tobacco Smoking658

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as measured by saliva cotinine

Figure 3 Relationship between nicotine dependence (indexed by saliva cotinine concentrations while smoking)and the probability of succeeding in a cessation attempt. Adapted from Stapleton et al. (1995).

Assessment 659

how soon after waking the first cigarette issmoked (Heatherton, Kozlowski, Frecker,Rickert, & Robinson, 1989). Cut-off pointshave been proposed for the FTND score (e.g.,score greater than seven equals ªsevereº depen-dence) in order to provide a simple classification.Although theoretically there may be somecircumstances where such a classification isdesirable the rationale for the precise levels ofcut-off are weak and all the evidence points tothere being a continuum of dependence in thepopulation with no well defined clusters ofsmokers at the different levels.A further questionnaire measure in use is the

Overall Dependence Scale (ODS), a subset ofnine items taken from the Horn±RussellSmoking Motivation Questionnaire. The ODS(score 0±27) assesses perceived and experienceddifficulty in refraining from or quitting smok-ing, craving for cigarettes when unable tosmoke, and degree of habitual or automaticsmoking (West & Russell, 1985b).

8.28.7.4 Biochemical Measures of Dependence

In addition to the questionnaire measures,there are now also a number of objectivemeasures which can be used to provide quanti-tativemeasuresof smoke inhalationandnicotineintake (Jarvis, Tunstall-Pedoe, Feyerabend,Vesey, & Saloojee, 1987). These measuresprovide a more accurate estimate of the extentof smoking, and hence degree of dependence,thancanbegainedbyknowing simplyhowmanycigarettes an individual smokes. They also havean invaluable role in validating self-reports ofabstinence. There are four main biochemicalindicators: (i) carbonmonoxide in expired air orblood; (ii) cotinine in saliva, blood, or urine; (iii)nicotine in blood; and (iv) thiocyanate (SCN) insaliva, blood, or urine.In clinical settings the most useful and widely

applied method is a measure of the concentra-tion of carbonmonoxide (CO) in the expired-airof the smoker which correlates highly withblood (plasma) nicotine and with carboxyhae-moglobin (COHb) (Jarvis, Russell, & Saloojee,1980; Wald, Idle, Boreham, & Bailey, 1981).Obtaining a breath sample and a reading takesless than a minute, requires minimal trainingof both therapist and patient, and has theadvantage over plasma nicotine of beingnoninvasive. The main disadvantage of thismethod is the relatively short half-life of COHb(4±5 hours), less in very physically activeindividuals, which means it is only possible todetect smokingwhich has occurred over the pastfew hours. Ideally, testing should be in theafternoon of a normal smoking day by whichtime CO levels have reached a stable level.

Though rarely a problem in practice, low levelexposure to CO from car exhausts and fires, forinstance, can produce CO levels in nonsmokersequivalent to those found in very light smokers.Inhaled nicotine from cigarettes is rapidly

distributed throughout the body and about 90%is subsequently metabolized to cotinine (Beno-witz, Kuyt, Jacob, Jones, & Osman, 1983). Asmeasures of smoke intake, nicotine, andcotinine have the advantage over CO of beinghighly specific to tobacco users. However,unlike nicotine, cotinine can be measuredreliably in saliva which is considerably easierto collect than a blood sample. Cotinine also hasthe advantage over nicotine in having a longerhalf-life of 15±20 hours (compared to nicotine's1±2 hours) which means sampling time is lesscritical. Cotinine assays can reliably detectregular smokers who typically have levelsbetween 200 and 400 ng/ml, as well as lightsmokers. Nonsmokers have levels below10 ng/ml. The drawback of both nicotine andcotinine measures over CO is that they requirea laboratory assay which is expensive, timeconsuming to collect, and cannot provideimmediate feedback of results. Very recently asimple ªdipstickº method for assessing totalurinary nicotine metabolites has become avail-able (Cope, Nayyar, Holde, Gibbons, & Bunce,1996). Although it does not produce as accuratea measure as a laboratory assay, it will enablehealth professionals to assess nicotine depen-dence quickly and conveniently.Thiocyanate (SCN) has also been used to

determine smoke intake and to corroboratepatients' self-reports but has a number ofdrawbacks and in recent years has increasinglybeen overtaken by cotinine as the marker ofchoice. Its use stems from the fact that hydrogencyanide gas is present in high concentrations intobacco smoke and is metabolized to SCN bythe liver. It has a long half-life of between 10 and14 days which is useful for validating smokingabstinence but in comparison to cotinine itssensitivity and specificity are low and it isaffected by naturally occurring SCN in the diet(e.g., almonds, beer, and broccoli) resultingin some overlap between smokers and non-smokers.

The questionnaire measures of dependencecorrelate moderately with the biochemicalmarkers of intake (West & Russell, 1985), andwith severity of withdrawal symptoms, but nosingle measure has been shown to be consis-tently superior to the others in predicting thesuccess of a quit attempt. The choice of whichmeasure to use will depend on both the purposefor which the measure is taken and the setting.For instance, the paper-and-pencil measureshave the advantage of low cost and simplicity

Tobacco Smoking660

whereas salivary cotinine provides the moststable measure of the actual nicotine intakefrom cigarettes.

8.28.8 TREATMENT APPROACHES

There are four main approaches for reducingthe health consequences of tobacco smoking: (i)treatment interventions aimed at encouragingand assisting adult smokers to stop; (ii)preventive interventions to reduce the uptakeof smoking by children; (iii) modifications tocigarettes to make smoking less harmful; and(iv) fiscal measures, legislation, and restrictionson smoking in public places designed to reduceactive smoking as well as nonsmokers' exposureto environmental tobacco smoke. This chapterwill focus primarily on treatment approaches.

8.28.8.1 Behavioral and Public HealthApproaches

Since the 1950s a wide variety of interven-tions, both pharmacological and behavioral,have been developed to help smokers stop,although the efficacy of many of theseapproaches has not been adequately evaluatedin controlled clinical trials. This has been thecase particularly with behavioral treatments,where inadequate statistical power throughinsufficient sample sizes has been a particularproblem. Other methodological limitationsinclude: very short-term or unspecified lengthof follow-up; absence of biochemical validationof abstinence; lack of a control group; andfailure to present outcome on a strict ªintent totreatº basis whereby nonattenders are classifiedas smokers. As a result there is little evidencethat one behavioral technique is more effectivethan any other (Lichtenstein & Glasgow, 1992),although there is consensus that multiplecomponent programs tend to be the mostsuccessful (Schwartz, 1987). Little attentionhas been paid to teasing out the specifictherapeutic ingredients of the multimodalpsychological packages which have been usedwith smokers. A broad array of behavioral/psychological/cognitive techniques have beentried either individually or in combination, inmany settings, from brief self-help programs toinpatient treatment units (Hurt et al., 1992). Theinterventions have included: rapid smoking andother aversion therapies; smoke dilution; nico-tine fading; self-management approaches; forexample, contingency contracting and stimuluscontrol, skills training, relapse prevention,cognitive, motivational, and educational inter-ventions, cue exposure, hypnosis and individualor group counselling (Hajek, 1996).

In the 1950s the field was dominated byeducational approaches, followed in the 1960sby conditioning procedures such as rapidsmoking and satiation. The 1970s saw theintroduction of intensive multicomponent cog-nitive self-management approaches which havepromising success rates but are severely limitedby the fact that most smokers will not attendformal clinic programs (Lichtenstein, 1992).This factor, together with a recognition of thesheer scale of the problem (approximately 12million smokers in the UK), prompted a moveaway from these intensive clinical approachestowards a broader community wide publichealth perspective involving self-help andadvice in a wide variety of settings from healthcare to the workplace. The current consensus isthat a stepped-care treatment model is likely tobe the most cost-effective approach in smokingcessation. Similar models have been advocatedfor other preventive medical interventions.Stepped-care involves initially offering the leastintensive and least costly approaches to thegreatest number of smokers, and saving theintensive and expensive second-line approachesfor those who fail to respond. Though theabsolute success rates of the brief interventionsare lower they tend to be more cost effective asthey have the potential to reach a far greaternumber of smokers. Typical one year successrates range from about 5% for brief advice inprimary care to 10% when NRT is added, andup to 20±30% for specialized smokers clinicsoffering intensive multisession behavioral ap-proaches combined with NRT.Recently, after an extensive literature review,

the US Agency for Health Care Policy andResearch (AHCPR) published their influentialguidelines on smoking cessation (Fiore, Bailey,et al., 1996). This targets three main audiences:primary care clinicians; smoking cessationspecialists; and health care administrators.The strategies they recommend for those work-ing in primary care, or for whom smokingcessation is just one of their many clinicalactivities, are shown in Table 5. As part of theassistance offered, the guidelines advise clin-icians toprovide basic informationon thenatureand time course of withdrawal and the addic-tiveness of smoking, for example, that anysmoking increases the likelihood of full relapse.Smokers should be helped to develop problem-solving and coping skills by identifying events,mood states andactivitieswhich increase the riskof relapse, and identifying and practising skillsintended to cope with these high-risk situations.The AHCPR guidelines for smoking cessa-

tion specialists overlap with those for healthprofessionals in primary care but involvecollecting more information at assessment on

Treatment Approaches 661

stress and psychiatric comorbidity, for instance,as these variables are known to negatively affectoutcome. As there is a strong relationshipbetween the intensity of counseling or contactwith the patient and treatment success, therecommendation is for treatment programs,whether group or individual, to span a period ofat least two weeks, though preferably more thaneight weeks. This factor appears more impor-tant than the specific behavioral techniquesemployed. The optimal number of sessions is4±7, with each session lasting for 20±30minutes.Training in relapse prevention, thought bymany in the addictions field to be critical tolong-term success, has not been shown to be

cost-effective in smoking cessation. This has ledsome to conclude that it is more beneficial toencourage relapsers to wait and have anotherattempt at a later time rather than offering time-consuming training in relapse prevention (Lich-tenstein & Glasgow, 1992).The AHCPR guidelines for health care

administrators and purchasers focus on theimportance of developing supportive systemswithin the clinical setting to facilitate systematicand repeated interventions with smokers. Toachieve this, environmental prompts (e.g.,computerized systems) to remind staff to askabout smoking are likely to be required, inaddition to policy changes to include smoking

Table 5 Recommendations for smoking intervention from AHCPR Clinical PracticeGuidelines.

Action Strategies for implementation

ASK about smoking status atevery visit and document

Include in vital signs, use stickers on patientsnotes, or implement computerized remindersystem

ADVISE all smokers to quit, in aclear, strong, and personalizedmanner

for example, ªQuitting smoking is the mostimportant thing you can do to protect yourhealthºTie smoking to current illness or impact onchildren and family

IDENTIFY smokers willing tomake a quit attempt at this time

If willingÐprovide assistance (see below).If patient prefers more intensive help or if it isindicated, refer to specialist.If unwillingÐprovide motivational intervention

A. ASSIST smoker with a quitplan

Set a quit dateHelp prepare smoker for quitting:inform family and friends;prepare the environment (discard cigarettes);review previous quit attempts;anticipate challenges

B. NICOTINEREPLACEMENT (NRT)

Encourage use of NRT unless contraindicated

C. GIVE KEY ADVICE Total abstinence: ªNot a single puff ºAvoid alcoholOther smokers in household: consider quittingwith others or make specific plans formaintaining abstinence among smokers

D. PROVIDESUPPLEMENTARYMATERIALS

Booklets, etc., culturally, educationally, and ageappropriate for the smoker.

ARRANGE follow-up in personor by telephone

First follow-up within 1 week of quit date,second within a monthAt follow-up, congratulate success, or use lapsesfor constructive learning, elicit recommitment tototal abstinence, identify problems, anticipatechallenges, assess use of NRT

Adapted from AHCPR Smoking Cessation Guideline. Source: Fiore, Bailey et al. (1996).

Tobacco Smoking662

assessment and cessation in the performanceexpectations of clinicians. The basic thrust ofthe recommendations is to greatly increase thenumber of clinicians who intervene withpatients who smoke and to ensure that cliniciansaccept smoking cessation as a vital part of theirrole in health care provision.In addition to brief physician-delivered and

intensive multicomponent behavioral smokinginterventions, workplace programs have alsobeen investigated. These provide the opportu-nity to reach a large number of smokers, in aconvenient location and may therefore be moreacceptable to smokers than attending specialistclinics. A meta-analysis of 20 controlled work-place studies concluded that smokers were 58%more likely to quit in the intervention conditionthan in the control group (Fisher, Glasgow, &Terborg, 1990).

8.28.8.2 Pharmacological Approaches toSmoking Cessation

8.28.8.2.1 Nicotine replacement therapy

A number of nicotine and non-nicotinepharmacological aids to smoking cessation havebeen investigated. By far the most well re-searched is nicotine replacement therapy (NRT)which was designed to be used in conjunctionwith a behavioral program, however brief. Therationale for nicotine replacement is to tem-porarily provide smokers with a safer, moreslowly delivered and lower dose of nicotine via adifferent route, to reduce the severity of thewithdrawal symptoms and desire to smoke. Theprocess of quitting is effectively broken downinto two-stages. Initially the patient gives up thebehavioral act of smoking (i.e., it is decoupledfrom the rewarding effects of nicotine) whilestarting unlearning the many nondrug elementsof the habit and developing strategies to copewithout cigarettes. Once the ex-smoker hasgained confidence in their ability to stay offcigarettes they are weaned off nicotine comple-tely, usually over aperiodof 3±4months.NRT isthe most rigorously and thoroughly evaluatedtreatment for smokers, and though success ratesare modest, varying according to the setting andpsychological supportwithwhich it is combined,it marked a breakthrough in smoking cessation.There are currently four different forms of NRTwhich have been approved for clinical use onprescription or are available over-the-counter(OTC), althoughnot all have yet been licensed inevery country. One very important differencebetween NRT products and inhaled tobaccosmoke is the speed with which nicotine isabsorbed. None can mimic the extremely rapid,high but transient nicotine peaks in arterial

blood which characterize inhalation, so they donot provide the same positive satisfaction assmoking and therefore have less potential forsustaining dependence.

(i) Nicotine gum

The first formulation to be developed andthus the most extensively researched wasnicotine gum, which is available in two strengths(2 or 4mg per piece). Nicotine from the gum isabsorbed slowly through the lining of themouth(buccal mucosa) and blood levels reach a flatpeak after about 30minutes chewing. Typically,smokers obtain blood nicotine levels around10±15 ng/mg, about one-third of usual smokinglevels, when using the 2mg gum ad libitum (Westet al., 1984) and about two-thirds smoking levelswith the 4mg gum (FagerstroÈ m, 1988). At theselevels, adverse mood effects and difficultyconcentrating associated with withdrawal arepartially relieved, though craving for cigarettesis not reliably decreased. This is probablybecause satisfaction from nicotine depends atleast in part on a rapid boost in nicotine levels. Ifabsorption rate is crucial nothing is gained byusing more gum. This may explain why inroutine clinical use smokers tend to chew onlyseven to eight pieces per day rather than therecommended 12±15 pieces (Russell, 1988).Despite relatively modest effects on withdrawal,the efficacy of the gum in smoking cessation iswell established. Nearly 50 randomized con-trolled trials have now been conducted, and arecent metal-analysis concluded that the gumwasmore effective than placebo (odds ratio 1.6),regardless of the setting (Silagy et al., 1994).Although the gum undoubtedly marked a

breakthrough in the treatment of smokers,success rates have nevertheless been disappoint-ing and it has a number of other limitations. It iscontraindicated in patients with peptic ulcersand poses problems for denture wearers, tastesunpleasant and gives rise to a number of minorside effects and requires some effort andperseverance in order to learn the correctchewing technique.

(ii) Nicotine patches

The patch has the advantage over gum ofproviding therapeutic levels of nicotine from thefirst day of treatment with minimal effort andinstruction. They are available in three doses(sizes) and most smokers start on the highestdose for 4±8 weeks, followed by a systematicweaning period of 2±8weeks using progressivelysmaller size patches. Two different types areavailable; one worn during waking hours only,with the highest dose patch delivering 15mgnicotine over 16 hours, and the other worn

Treatment Approaches 663

throughout the day and night delivering 21mgover 24 hours. Both appear to be equallyeffective (Fiore, Smith, Jorenby, & Baker,1994). After applying a patch, venous bloodnicotine levels build up slowly over severalhours to a plateau of around 10±20 ng/ml,roughly equivalent to 50% of mean plasmanicotine levels produced by smoking. Levelsremain reasonably constant for much of thewaking day before declining during the evening.Since nicotine absorption is very slow, patchusers are unlikely to experience any of thepositive subjective effects associated with ra-pidly administered nicotine which suggests theymay be more helpful to individuals who smoketo relieve or avoid withdrawal (negative re-inforcement) than to smokers seeking positivereinforcement. Other potentially importantdifferences between the patch and the otherforms of NRT include the fact that the patchdoes not allow patients to self-titrate their doseaccording to need, and does not provide abehavioral or sensory component to substitutefor lighting-up. However, these factors togetherwith the lack of positive effects suggest thedependence potential and abuse liability of thepatch will be very low, which is supported byclinical experience. The most common sideeffect is mild skin irritation but only about 5%of patients have to stop treatment as a result ofadverse effects (Hughes & Glaser, 1993).Numerous controlled trials of the patch in a

variety of settings and populations have demon-strated its efficacy with the highest absolutesuccess rates (20±25% at 6 month follow-up)tending to occur when the patch is combinedwith an intensive behavioral treatment program.The broad consensus from several reviews andmeta-analyses is that compared to a placebo, thenicotine patch increases success rates two tothreefold irrespective of the intensity of theadjunctive behavioral treatment (Fiore et al.,1994;Silagyet al., 1994). It reduces the severityofwithdrawal, and perhaps surprisingly, appearsto reduce craving for cigarettes more consis-tently than the nicotine gum, but its mainadvantage over the latter is undoubtably theimproved patient compliance.

(iii) Nicotine nasal spray

The development of nicotine nasal spray(NNS) stemmed from work showing the rapidrate of nicotine absorption from nasal snuff(Russell et al., 1981). Nicotine taken intrana-sally is very swiftly absorbed into the systemiccirculation and peak venous levels are reachedwithin 5±10minutes of taking a dose of NNS,which is considerably faster than with the patchor gum (Sutherland et al., 1992), although not as

rapid as inhaled cigarette smoke. Unlikesmoking however, NNS does not deliver arterialbolus doses of nicotine, although the rate ofnicotine absorption is sufficiently rapid toproduce the positive stimulant subjective effects(often described as a ªbuzzº) which manysmokers experience while smoking their firstcigarette of the day. Such effects are usuallyconsidered rewarding and satisfying by smokersand are not produced when nicotine is absorbedmore slowly. The spray delivers 1mg of nicotineper dose (0.5mg to each nostril), and withrepeated dosing has the potential to provideblood nicotine levels similar to those obtainedwhile smoking, although results from clinicaltrials indicate smokers attain levels only about30±50% of baseline smoking levels when usingad libitum.The efficacy of NNS has been demonstrated

in three randomized placebo-controlled trials inwhich it was combined with behavioral supportand produced remarkably similar success ratesat one year, averaging 26% vs. 11% for placebo.(Hjalmarson, Franzon, Westin, & Wiklund,1994; Schneider et al., 1995; Sutherland et al.,1992). As with other forms of NRT, NNSreduces the severity of the affective symptoms ofwithdrawal compared to placebo, but also hasthe advantage of substantially relieving cravingfor cigarettes. At times of acute craving not onlycan the user obtain pharmacological relief inminutes but there is also a behavioral response(i.e., spraying) with a marked sensory impact.However, perhaps the most significant finding,both from a clinical and theoretical point ofview, is that the spray appears to be of greatestbenefit to themost highly dependent smokers, incontrast to findings with the patch (see Figure 4)which is equally effective across the full range ofdependence.Studies are currently underway to determine

whether these initial but promising findings willbe replicated when the spray is used with lessintensive adjunctive treatment, such as ingeneral practice. It takes a few days to learnthe correct spraying technique and to acclima-tize to the initial irritant side effects (to nose/throat), which may pose problems in settingswhere less time is available to support andencourage new users.Another issue concerns the greater depen-

dence potential of the spray compared to theslower-actingnicotinedelivery systems (Hughes,1988). In the two smoking cessation studieswhich allowed the spray to be used for up to ayear, 43% and 29% of those who succeeded instopping smoking used it for this time, repre-senting approximately 12% of all those origin-ally assigned active spray. This figure issomewhat higher than for the gum. However,

Tobacco Smoking664

Placebo

Active

Bars give 90% Cls

0.7

0.6

0.5

0.4

0.3

0.2

0.1

0.0

Baseline smoking nicotine (ng/ml)

5 15 25 35 45 55 65 75

Pro

babi

lity

of a

bstin

ence

Relation between baseline nicotine levelsand abstinence at three months

Figure 4 Relationship between nicotine dependence (indexed by plasma nicotine concentration from smoking)and the probability of successfully quitting on active or placebo nasal nicotine spray. Treatment with active

spray is especially helpful at high levels of dependence. From Sutherland et al. (1992).

Treatment Approaches 665

the fact that the spray was provided free ofcharge is likely to have encouraged longer termand higher usage since cost has been shown toinfluence these parameters for nicotine gum(Hughes, Wadland, Fenwick, Lewis, & Bickel,1991). Not surprisingly, the long-term users hadhigher pretreatment nicotine levels (more de-pendent) than those who stopped the sprayearlier on.

(iv) Nicotine inhaler

The inhaler, the newest form of NRT, is anoral puffing device that consists of a hollowplastic mouthpiece, roughly the size of acigarette, which contains a nicotine impreg-nated porous plug. It evolved from an earliersmoke-free product called Favor1, which inpreliminary studies was shown to have sometherapeutic potential (Hajek, Jarvis, Belcher,Sutherland, & Feyerabend, 1989; Russell,Jarvis, Sutherland, & Feyerabend, 1987). De-spite its name, absorption of nicotine vaporfrom the inhaler is not very rapid and does notgive an arterial peak, sincemost of it is depositedin the mouth and upper airways rather than thelungs. The pharmacokinetic profile resemblesthe gum rather than cigarettes (Bergstrom,Nordberg, Lunell, Antoni, & Langstrom, 1995).Per puff, the nicotine delivered by the inhaler isabout one-tenth of that from a cigarette and isboth temperature and effort related, but evenwith very frequent and intensive puffing, thelevels achieved are modest. However, theregular hand±mouth activity involved offersmore habit replacement than other forms ofNRT and it provides sensory characteristics thatresemble smoking, which may have a role inalleviating cigarette cravings (Rose, Behm, &Levin, 1993).The results of two randomized controlled

trials of the inhaler have been published andreport one year success rates of 15% activeinhaler vs. 5% placebo, and 13% vs. 8%,respectively (Schneider et al., 1996b; Tùnnesen,Nùrregaard, Mikkelsen, Jùrgensen, & Nilsson,1993).Research is being undertaken to see whether

combining different types of NRT is moreeffective than using each individually andwhether tailoring NRT to achieve 100%replacement (i.e., up to smoking levels) iswarranted. Preliminary reports indicate thathigher nicotine replacement is associated withbetter withdrawal relief and higher short- andlong-term success rates (Dale et al., 1995;FagerstroÈ m, Schneider, & Lunell, 1993; Kor-nitzer, Boutsen, Dramaix, Thijs, & Gustavsson,1995). From a theoretical point of view, the bestcombinations are likely to involve the patch,

which provides a steady background level ofnicotine, supplemented by one of the otherfaster-acting delivery systems which enable thepatient to self-titrate dose as needed and providean alternative coping response. Despite the vastliterature on NRT many questions remain to beanswered, such as the optimal duration oftreatment and dosage, how it should bediscontinued (abruptly or gradually), and withwhich psychological treatment it should becombined for maximum efficacy. What doesseem clear at the present time is that NRTcombined with supportive treatment, howeverbrief, produces higher success rates than NRTor behavioral treatment alone. This might bebecause the two treatments affect differentaspects of nicotine dependence, for example,NRT reduces withdrawal discomfort andbehavioral treatment enhances coping skills(Hughes, 1995) or because each treatmentincreases adherence to the other (Klesges,Ward, & Debon, 1996).

8.28.8.2.2 Non-nicotine pharmacotherapy

A variety of non-nicotine pharmacologicaltreatments or agents have also been examinedincluding lobeline (Schneider, Mione, Rahe-man, Phillips, & Quiring, 1996a), naltrexone(Sutherland, Stapleton, Russell, Feyerabend,1995), antidepressants (Berlin et al., 1995;Edwards, Murphy, Downs, Ackerman, &Rosenthal, 1989), mecamylamine (Rose et al.,1994), glucose (West, Hajek, & Burrows, 1990),the antihypertensive clonidine (Covey & Glass-man, 1991; Gourlay, Stead, & Benowitz, 1997),buspirone (Cinciripini et al., 1995; Hilleman,Mohiuddin, Core, & Sketch, 1992; Schneideret al., 1996c; West, Hajek, & McNeill, 1991),anorectics (Spring et al., 1995), citric acidinhaler (Behm et al., 1993; Rose & Hickman,1987), black pepper vapor inhaler (Rose &Behm, 1994), benzodiazepines, beta-blockers,anticholinergics, stimulants, ACTH, silver acet-ate, and sodium bicarbonate (Hughes, 1993).Although some show promise, most have not

been found to be effective, to have unacceptableside effects, or have not yet been evaluatedthoroughly enough with adequate sample sizesto recommend their use at present. The onlyexception to this concerns the antidepressant,bupropion, which was approved for use insmoking cessation by the US Food and DrugAdministration in 1997, though it has not yetbeen licensed in theUK. Bupropion (Zyban1) isan aminoketone antidepressant which isthought to act primarily via a noradrenergicmechanism but which also has some dopami-nergic activity. Anecdotal reports of depressedpatients quitting smoking spontaneously while

Tobacco Smoking666

taking bupropion, its generally favorable sideeffect profile, and its low dependence potential,stimulated interest in the drug for smokingcessation. Although the results of the controlledclinical trials have not yet been published thedata are convincing and provided that it islicensed more widely, bupropion could, likeNRT, make a significant contribution to futurecessation rates.

8.28.9 APPROACHES TO REDUCESMOKING-RELATED DISABILITY

Although in developed countries studiesconsistently show the majority of smokers areaware that smoking carries significant healthrisks, albeit grossly underestimating the realrisks to their own health, reducing smokingprevalence has been a slow and hard foughtprocess. Despite their best efforts a number ofsmokers cannot manage to give up and someothers simply do not want to stop, and unlikeother drug dependencies smokers do not seemto ªmatureº out of it. Until more effectiveinterventions have been developed there is astrong case for exploring approaches designedto make smoking less dangerous. One way ofachieving this is by modifying the constituentsor design of cigarettes to reduce their toxicity.Such strategies are akin to those adopted in thedrug dependence field under the umbrella ofªharm minimization.º This is an area that hashighlighted a number of ethical issues inaddition to having political implications, andwhich has divided opinion among researchers inthe smoking cessation field.In 1973 the Independent Scientific Commit-

tee on Smoking and Health (ISCSH) wasestablished in the UK to formulate nationalpolicies on smoking and health. Themain thrustof the program has concerned product mod-ification. Initially the Committee were involvedin a radical move examining the potentialadvantages of substituting tobacco in cigaretteswith a less toxic synthetic substance based onmodified cellulose. Although 11 new cigarettebrands based on substitute tobacco (NewSmoking Material and Cytrel) were launchedin the UK in 1977 they were not adequatelyacceptable to smokers and were soon with-drawn from sale. Following this disappointingoutcome the ISCSH turned its attention insteadto the gradual reduction of tar yields ofcigarettes which has been a far more successfulstrategy. Since 1972 the sales-weighted averagetar yield of cigarettes has declined from 20.8mgto around 11.0mg per cigarette. This reductionhas been achieved by improving cigarette filters,introducing ventilation holes, and increasing

the porosity of the paper in order to dilute thesmoke, as well as through changes to thetobacco itself. Determination of the yields ofcigarettes are made using smoking machinesusing internationally agreed puff parameters(volume of smoke in puff, frequency of puffing,etc.). Since tar and nicotine yields are highlycorrelated (about 0.9) reductions in tar havealso been accompanied by reductions innicotine. Unfortunately when smokers switchto cigarettes which have lower nicotine levels,they tend to alter, often unconsciously, the wayin which they smoke in an attempt to maintainadequate levels of nicotine. They may forinstance take more puffs, hold the smoke intheir lungs for longer, take larger puffs, smoketo a shorter butt length, or even hold thecigarette in a way that causes the ventilationholes to be covered. This ªcompensatoryºsmoking behavior, or upregulation of smoking,has meant that the percentage reduction in tarintake that would be expected when smokerstransfer from amedium or high tar cigarette to alow tar brand is not as great as predicted by thesmoking machine figures. Mainly as a result ofthe lower nicotine levels, low-tar cigarettes tendto be less acceptable to smokers which explainswhy, despite the health advantages and theselective advertising encouraging smokers toswitch, such brands still only account for 30%of the market (Bennett et al., 1996).Since some of the health advantage of

switching to lower-tar cigarettes may be offsetby the tendency to compensate by increasinginhalation, and since consumer acceptability islimited, there have been recommendations forthe development of low-tar cigarettes withslightly enhanced nicotine yields (up to 1mg).Although the case for slightly higher nicotinecigarettes is compelling, one must not under-estimate the significance of the reductions in thetar intake per cigarette over the last 25 yearswhich have contributed to a decline in mortalityfrom lung cancer (Peto, 1986) and also beenbeneficial in chronic obstructive lung disease(Darby, Doll, & Stratton, 1989). Nomatter howintensively modern cigarettes are smoked it isvirtually impossible to obtain tar levels as highas those delivered by the old high-tar brands.The flip-side of this strategy, and one which is

far more radical, is the approach beingconsidered in the USA linked to the unprece-dented proposed settlement with the tobaccoindustry. In addition to the financial penaltiesand other controls being imposed on tobaccocompanies, the settlement stipulates that theFDA will in future have the power to regulatenicotine as a drug and gives them authority toremove it from cigarettes in 12 years, subject to anumber of provisions such as showing that this

Approaches to Reduce Smoking-related Disability 667

would not lead to a significant demand for blackmarket cigarettes. The thinking behind this planis that nicotine yields in cigarettes could belowered slowly over a number of years until themaximum level a smoker could obtain fromcigarettes would be insufficient to create orsustain nicotine dependence (Benowitz & Hen-ningfield, 1994; Kessler et al., 1996, 1997;Kozlowski & Henningfield, 1995; Slade,1995). In future children might still experimentwith cigarettes but could not get a large enoughdose of nicotine to become pharmacologicallydependent and so would be unlikely to progressto regular daily smoking. Although intuitivelyappealing and plausible, a number of criticalquestions remain unanswered. What will hap-pen to existing smokers? It would be reasonableto expect them to smoke more aggressively in anattempt to obtain more nicotine and maintainsatisfaction, and in the process become exposedto greater amounts of the more dangerouscomponents (CO and tar) than would otherwisehave been the case.What is the critical thresholdfor creating dependence and what role doestolerance play? By reducing nicotine yields veryslowly over several years, might neuronalreadaptation and sensitization occur so thatcurrent smokers remain dependent albeit onlower nicotine levels?Another innovative but highly controversial

approach to safer smoking has come fromtobacco companies themselves. In 1987 the R. J.Reynolds Tobacco Company spent $1 billiondeveloping and market-testing a novel virtuallytar free cigarette-like device (brand namePremier) which heated rather than burnedtobacco (R. J. Reynolds Tobacco Co., 1988).The smoke particles in which the nicotine wastransported were comprised mainly of glyceroland water rather than tar. Glycerol is harmlessand metabolized as a source of energy and wasadded simply to produce ªsmoke.º The yields ofall major carcinogens and many other poten-tially harmful components were far lower thanthose of conventional cigarettes and the biolo-gical activity of its condensate was greatlyreduced. The tar yield was about 0.7mg percigarette and the nicotine and carbon monoxideyields about 0.3 and 12.0mg, respectively. It wasestimated that the risks of tobacco-relatedcancers and chronic obstructive lung diseasewould be substantially reduced, possibly by asmuch as 90%, for an average smoker switchingfrom a regular brand to Premier (Sutherland,Russell, Stapleton, & Feyerabend, 1993). Pre-mier was never marketed, however, due to lackof acceptability (especially poor taste), andstrong protests frompublic health organizationsin the USA who petitioned the FDA to classifyand therefore regulate Premier as a drug as

opposed to a cigarette. In the last year R. J.Reynolds have launched another new smoke-free cigarette called Eclipse which like itspredecessor, is virtually tar free but which isclaimed to have a more acceptable taste. It islikely that in the USA this product will receivenear unanimous opposition once again on thegrounds that it might encourage smokers whowould otherwise stop to switch to the new ªsafeºcigarette instead, and that it may encouragechildren to take up smoking.

8.28.10 PROSPECTS FOR THE FUTURE

Like all drug dependencies, cigarette smokingis a multifaceted problem, whose understandingrequires attention to a range of factors,from drug pharmacokinetics and pharmaco-dynamics, genetics, individuals and their socialmilieu, to broader economic and politicalinfluences. No single policy response can hopeto address the range of issues which determinesmoking uptake, maintenance, and cessation.Future progress will depend on developing abetter understanding of the processes operatingat each stage of the smoking career, and clinicalpsychology will continue to have an importantcontribution to make in furthering understand-ing of individual liability to dependence, theprocess of recruitment, the role of nicotine inmaintaining the habit, and in developing anddisseminating effective cessation interventions.If there is one lesson which can be taken fromthe past, it is that future progress is likely to beequally slow and hard won.

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