8.

28
Tobacco Smoking
MARTIN 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 647
8.28.3.2 Smoking in Pregnancy 648
8.28.3.3 Health Effects of Passive Smoking 648
8.28.3.4 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 651
8.28.5.2 Adult Smoking: Disadvantage and Dependence 652
8.28.5.3 Factors Associated with Smoking Cessation 652
8.28.5.4 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 657
8.28.7.2 Assessing Nicotine Dependence 658
8.28.7.3 Questionnaire Measures of Dependence 658
8.28.7.4 Biochemical Measures of Dependence 660
8.28.8 TREATMENT APPROACHES 661
8.28.8.1 Behavioral and Public Health Approaches 661
8.28.8.2 Pharmacological Approaches to Smoking Cessation 663
8.28.8.2.1 Nicotine replacement therapy 663
8.28.8.2.2 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 of
drug dependence in the world, for years
cigarette smoking was regarded as no more
than a social habit and there was little awareness
of its psychoactive component, nicotine. Nico-
tine is in many ways an invisible drug, which
lacks obvious effects on users' cognitive per-
formance, mood, or social functioning. Yet it is
now regarded by many as the purest pharma-
cological dependence, the very paradigm of
drug addiction. Nicotine is a stimulant drug
which users say calms them down and sedates.
Smoking is often viewed as a form of self-
medication to cope with stress, but there is little
evidence that nicotine possesses any anxiolytic
or anti-depressant properties. Despite nicotine's
lack of euphoriant or other obvious mood
altering effects, smoking is remarkably recalci-
trant to change. Most smokers want to give up
smoking, and make numerous attempts to do
so. But even those with severe smoking-related
disease often fail to quit, and even in developed
countries with a strong antismoking ethos,
fewer than half of all those who have ever
smoked regularly succeed in stopping before the
age of 65. It is this feature above all which has
made smoking a focus of interest for psychol-
ogists. It has long been an area of active research
into methods of achieving behavior change, as
well as for understanding the complex interplay
between pharmacological, psychological, and
social determinants of behavior. After years
when progress was very limited, there have
recently been genuine advances in developing
effective, and cost-effective, treatment methods
for smoking cessation. But failure to succeed in
quit attempts, or relapse following initial
success, are still the norm, and young people
continue to be recruited to smoking in large
numbers. The smoking problem shows no sign
of going away.
8.28.2 PATTERNS OF SMOKING
PREVALENCE WORLDWIDE
While tobacco use has a long history, with
forms such as pipe and cigar smoking, chewing
tobacco, and nasal snuff predominating in
earlier periods, the manufactured cigarette,
and with it the epidemic of smoking worldwide,
is essentially a phenomenon of the twentieth
century. Annual per capita consumption of
cigarettes in adults in developed countries rose
steadily from 600 in 1920 to a peak of over 3000
in the mid-1970s, since when there has been a
modest decline of some 16% (Collishaw &
Lopez, 1996). In developing countries, on the
other hand, cigarette consumption increased
sharply in the 1970s and 1980s, so that the gap in
per capita cigarette consumption between
developed and developing countries is narrow-
ing. On current trends, per adult consumption in
developing countries will exceed that of devel-
oped countries shortly after the turn of the
century.
Table 1 shows WHO estimates of smoking
prevalence in men and women in various regions
in the world in the early 1990s, and also trends in
per 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 the
former socialist countries of Eastern Europe.
Globally, women's smoking is at much lower
levels than that of men (12%), with relatively
high prevalence being seen in developed coun-
tries and low rates in Africa, India, China, and
other parts of Asia where cultural traditions still
frown on female smoking. In terms of the total
world market, the decline since 1970 of 1.5%per
annum in per capita consumption in the
American region and of 0.6% in Western
European countries has been more than offset
by rapid growth in China (4.8%per annum) and
other less developed countries, with the result
that overall the size of the market continues to
increase.
8.28.3 SMOKING AS A CAUSE OF DEATH
Because the magnitude of the risk to health
rises with increased duration of the habit,
increases in deaths from smoking show a time
lag of about 3040 years from the onset of
regular smoking. As a result, differing patterns
of smoking related deaths are currently seen in
men and women. In the UK, although male
smoking declined from the 1960s onward,
smoking deaths have only recently begun to
decline; while in women death rates are rapidly
increasing and will continue to do so for some
years, despite prevalence peaking in the early
1970s (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, mostly
among men. Since that time smoking-attribut-
able deaths have risen dramatically and by 1995
almost 2 million people (1.5 million men and
500 000 women) in developed countries were
dying each year from tobacco. The rate of
increase is now slowing somewhat among men,
but continues to increase rapidly in women. In
the mid 1990s about 25%of all male deaths, and
Tobacco Smoking 646
9% of female deaths, in developed countries
were due to smoking. The proportion of deaths
in middle age (3569) caused by smoking is
considerably higher, at 36% in men and 13% in
women. Estimates of smoking related deaths in
the developing world are more uncertain, but it
is already clear that the increases in smoking
prevalence that have occurred in the developing
world since the 1970s will lead inexorably to
massive increases in deaths. The current world-
wide annual figure for deaths caused by
smoking of 3 million (made up of 2 million in
developed and 1 million in developing coun-
tries) is estimated to increase to 10 million per
year by about 2020 or 2030. The great bulk of
these deaths will be in the developing world
(Peto, Lopez, Boreham, Thun, & Heath, 1994).
8.28.3.1 Diseases Caused by Smoking
The link of smoking with lung cancer was first
reported in prewar Germany (Smith, Strobele,
& Egger, 1994), but this work was largely
forgotten, 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 the
foundations of our understanding of smoking
as a cause of disease. Based on the 20 year
follow-up of the British doctors cohort, it was
concluded that a young man who persists in
smoking will run a 1 in 4 chance of being killed
prematurely by tobacco (Royal College of
Physicians, 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 the
American Cancer Society (CPS II) (Thun,
Day-Lally, Calle, Flanders, & Heath, 1995)
have extended this understanding and forced a
re-evaluation of the extent of the risk. It is now
apparent that persistent smokers run a 1 in 2
risk of being killed by cigarettes, losing on
average eight years of life.
Table 3 summarizes data from the American
Cancer Society study of over 1 million men and
women aged 35 and over, giving mortality in
cigarette smokers and life-long nonsmokers for
the main fatal smoking-related diseases. The
relative risk and absolute excess risk is given for
each disease, together with the attributable
proportionthe proportion of all deaths for
each specified disease that is due to smoking.
Smoking is recognized to cause 80% or more of
all lung cancers with a relative risk in men of 22
andwomenof 12. Inadditionit is responsible for
most cancers of the upper respiratory tract (lip,
tongue, mouth, pharynx, and larynx) and for a
smaller fraction of cancers of the bladder,
pancreas, esophagus, and kidney. Among both
men 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 19701972
to 19901992 per capita
cigarette consumption
WHO regions
African region 29 4 1.2
American region 35 22 71.5
Eastern Mediterranean region 35 4 1.4
European region 46 26 0.0
Southeast Asia region 44 4 1.8
Western Pacific region 60 8 3.0
More developed countries 42 24 70.5
Established market economies 37 23 70.6
Formerly socialist economies of Europe 60 28 0.6
Less developed countries 48 7 2.5
China (1984) 61 7 4.8
India (1980s) 40 3 1.5
Other Asia and islands 54 7 2.1
Middle Eastern crescent 41 8 1.2
Sub-Saharan Africa 25 3 1.0
Latin 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 heart
disease, aortic aneurysm, andstroke) outnumber
those from all other causes, including lung
cancer. Over 70% of chronic obstructive lung
disease is attributable tosmoking, with a relative
riskinbothmaleandfemalesmokers of about 10.
Findings from the 40 year follow-up of the
British doctors' study are in general very similar,
but additionally indicate a causal effect of
smoking on stomach cancer and leukemia.
Associations between smoking and cirrhosis of
the liver, suicide, poisoning, and cancer of the
liver have been regarded as being due to
confounding (Doll et al., 1994). Similarly, there
is uncertainty whether the association of smok-
ing with cervical cancer is causal or attributable
to confounding (Phillips & Smith, 1994).
As well as being the single largest cause of
preventable premature death, cigarette smoking
is a cause of a number of disabling but generally
nonfatal conditions (Wald & Hackshaw, 1996).
These include peripheral vascular disease,
cataracts, Crohn's disease, gastric and duodenal
ulcers, 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 ectopic
pregnancy (Poswillo &Alberman, 1992). Babies
of smoking mothers weigh on average 150250
grams less at birth than babies of nonsmoking
mothers. This association has been shown to be
causal, since randomized trials of smoking
cessation in pregnancy have shown that birth
weight can be increased (Sexton &Habel, 1984).
Smoking by mothers has consistently been
found to be associated with sudden infant death
syndrome, although it is uncertain whether pre-
natal exposure, or passive exposure to mother's
and father's smoking postnatally, is more
important (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 on
health are not limited to active smoking. Since
the early 1980s there has been an explosion of
research into the effects on nonsmokers of
breathing in other people's smoke, and this
work has had a decisive impact on the debate
about the social acceptability of smoking.
Studies of the uptake of smoke constituents
by nonsmokers have shown doseresponse
relationships with the extent of exposure to
passive smoking (Jarvis, 1989). Cotinine con-
centrations in exposed individuals have been
found to average about 0.71.0% of those in
heavy smokers (Jarvis, Tunstall-Pedoe, Feyer-
abend, Vesey, & Saloojee, 1984; Jarvis et al.,
1985). A number of reports by independent
scientists have reviewed the evidence linking
passive smoking with lung cancer in nonsmok-
ing spouses exposed to their partners' smoke.
All have concluded that passive smoking causes
lung cancer in otherwise healthy nonsmokers,
with an estimated number of deaths each year of
3000 in the USA (US Environmental Protection
Agency [USEPA], 1992) and about 300 in the
UK(Froggatt, 1988). The USEPAhas classified
environmental tobacco smoke as a known
human carcinogen. The association of heart
disease with passive smoking is of similar
magnitude to that observed for lung cancer,
with exposed spouses having about a 30%
increase in risk. On a causal interpretation of
this association, passive smoking may kill far
more people through heart disease than through
lung cancerup to 60 000 deaths each year in
Table 2 Estimated deaths caused by smoking in developed countries, 19502000.
Men Women
Mid-decade year
No. of
deaths per
year
% of all
deaths
% of
deaths age
3569
No. of
deaths per
year
% of all
deaths
% of deaths
age 3569
1955 447 000 10 20 26 000 51 2
1965 793 000 17 28 70 000 2 4
1975 1 119 000 21 31 165 000 3 7
1985 1 369 000 24 35 317 000 6 11
1995 1 442 000 25 36 476 000 9 13
Total all deaths caused by
smoking 19502000
52 million 20 30 10.5 million 4 7
Source: Peto et al. (1994).
Tobacco Smoking 648
the USA (Wells, 1994; Steenland, 1992). How-
ever, because of the difficulty in making
appropriate allowance for confounders such
as diet, uncertainty remains about how much of
the observed association is truly causal.
Although the debate about the effects of
passive smoking has largely centered on lung
cancer in adults, the main public health burden
is borne by children with smoking parents.
Numerous studies have shown that babies from
smoking households are at increased risk for
admission to hospital with bronchitis and
pneumonia (USEPA, 1992). In later childhood
there is strong evidence of impairments in lung
function (Strachan, Jarvis, &Feyerabend, 1990;
Cook et al., 1993) and of increased risk of
middle ear effusion when parents smoke
(Strachan, Jarvis, & Feyerabend, 1989).
8.28.3.4 The Health Benefits of Smoking
Cessation
Stopping smoking benefits health at any age,
the more so the younger the smoker stops (US
Department of Health and Human Services,
1989). In the British doctors' study, those who
gave up by their mid-30s had a life expectancy
indistinguishable from never smokers, and even
those who gave up in their late 60s lived
significantly longer than continuing smokers
(Doll et al., 1994). Benefits have been observed
for a variety of conditions. The Lung Health
Study, a randomized trial of smoking cessation
in people at increased risk of chronic respiratory
disease, showed that on stopping smoking the
rate of loss of ventilatory capacity reverts from
the accelerated rate characteristic of smokers to
the slower age-related decline of nonsmokers
(Anthonisen et al., 1994; Jarvis, 1995). With
lung cancer a somewhat different picture is seen.
The extra risk incurred froma smoking career of
a given duration is never lost, but remains at the
level determined by the duration of smoking at
the time of quitting (Halpern, Gillespie, &
Warner, 1993). Since that risk would have
escalated exponentially with continued smok-
ing, a marked reduction in risk is observed by
comparison with persisting smoking. For heart
disease the risk in ex-smokers declines toward
that of never-smokers, although there is some
uncertainty as to how rapidly the excess risk is
lost, 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 women
aged 35+.
Standardized mortality per 100 000 per year
Life-long
nonsmoker
Current cigarette
smoker
Relative
risk
Absolute excess risk
per 100 000 per year
Attributable
(%)
Cancer
Lung M 24 537 22.4 513 87
F 18 213 11.9 195 77
Upper respiratory M 1 27 24.5 26 89
F 2 10 5.6 8 58
Bladder M 18 53 2.9 35 36
F 8 21 2.6 13 32
Pancreas M 18 38 2.1 20 25
F 16 37 2.3 21 29
Esophagus M 9 68 7.6 59 66
F 4 41 10.3 37 74
Kidney M 8 23 3.0 15 37
F 6 8 1.4 2 11
Ischemic heart M 500 970 1.9 470 22
F 386 688 1.8 302 19
Aortic aneurysm M 24 98 4.1 74 48
F 11 52 4.6 41 52
Stroke M 147 328 2.2 181 27
F 236 434 1.8 198 20
Chronic obstructive
lung disease
M 39 378 9.7 339 72
F 21 216 10.5 195 74
All diseases M 788 2520 3.2 1732 40
F 708 1720 2.4 1012 30
Smoking as a Cause of Death 649
8.28.4 CIGARETTE SMOKING AND
NICOTINE DEPENDENCE
Drug taking aspects of cigarette smoking were
largely ignored until the 1970s, but since then an
accumulation of research findings froma variety
of disciplines and from both human and animal
work has led to a consensus that cigarette
smoking is essentially a form of addiction to
nicotine. This was enshrined in the landmark
1988 report of the US Surgeon General which
concluded that the processes underlying addic-
tion to nicotine are similar to those of other
addictive drugs such as alcohol, heroin, and
cocaine (US Department of Health and Human
Services, 1988). Since then clear evidence has
emerged that this view is shared, privately if not
publicly, by the tobacco industry, which actually
reached it considerably earlier (Slade, Bero,
Hanauer, Barnes, &Glantz, 1995). The USFood
and Drug Administration has based its assertion
of jurisdiction over cigarettes and other tobacco
products on the evidence of nicotine's addictive
properties and the tobacco industry's exploita-
tion of them (Kessler et al., 1996, 1997).
Understanding of nicotine's role is fundamental
to an appreciation of smoking uptake, main-
tenance, and cessation. It does not follow, of
course, that cigarette smokingis explicable solely
in terms of pharmacological factors. Nicotine
effects provide a rich substrate for conditioning
and social learning mechanisms, and for broad
social, economic, and societal influences. In this
respect it is no different from other drug
dependencies.
The evidence relevant to nicotine's properties
as an addictive drug comes from a number of
areas (Henningfield &Keenan, 1993; Stolerman
& Jarvis, 1995). Some of the main lines are
briefly summarized here.
(i) Brain neurochemistry. Both animal and
human studies have shown that chronic nicotine
administration leads to an increase in the
expression of specific nicotine receptors on
neurons. Even prenatal exposure can produce
such nicotine receptor up-regulation (Slotkin,
Orband-Miller, & Queen, 1987). Postmortem
studies have revealed raised concentrations of
nicotine receptors in the brains of human
smokers (Benwell, Balfour, & Anderson,
1988). Investigations of dopaminergic systems
thought to be important in reward mechanisms
have shown effects of nicotine similar to those
of 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 a
variety of animal species. Early difficulties in
demonstrating nicotine's reinforcing effect seem
to have stemmed from the narrow range of
rewarding blood concentrations and the ease of
provoking aversive overdose.
(iii) Pharmacokinetics. Nicotine is readily
absorbed through the skin, and through the
lining of the mouth and nose, the rate of
absorption being enhanced in an alkaline en-
vironment and reduced in an acidic environ-
ment. Because of the large surface area of the
lungs the mildly acidic smoke of cigarettes is
absorbed almost immediately and completely
on inhalation, giving rise to high concentration
arterial nicotine boli which reach the brain in
less than 10 seconds (Henningfield, London, &
Benowitz, 1990; Russell, 1980). Nicotine has a
distributional half-life of about 15 minutes and
a terminal half-life in blood of about two hours
(Benowitz, 1988). This means that blood levels
decline overnight to nonsmoking levels, and
regular cigarettes are required over the course of
the day to maintain elevated blood nicotine
concentrations.
(iv) Regulation of blood nicotine intake from
different tobacco products and from cigarettes
with differing deliveries (titration). Levels of
blood nicotine maintained by cigarette smokers
and by dependent users of either oral (Holm,
Jarvis, Russell, & Feyerabend, 1992) or nasal
(Russell, Jarvis, Devitt, & Feyerabend, 1981)
snuff are remarkably similar, averaging in each
case about 35 ng/ml. Given the very different
sensory characteristics of burnt and noncom-
bustible tobacco, the different routes of absorp-
tion, and the absence from snuff of components
such as tar, this similarity points strongly to
nicotine as the factor controlling the behavior.
Manufactured cigarettes contain about
1014 mg of nicotine, an amount that does
not vary greatly between different brands. But
by techniques such as filtration and ventilation,
yields of nicotine when smoked by a machine in
a standardized way range fromas little as 0.1 mg
to over 1 mg, with concomitant tar yields being
closely correlated and ranging from 1 to 15 mg
or more. The relevance of these machine
smoked yields to human smoking is open to
serious question (US Department of Health and
Human Services, 1996), since smokers extract a
similar amount of nicotine (about 1 mg on
average) from cigarettes of widely differing
yields (Benowitz et al., 1983). Naturalistic
studies of smokers smoking their own self-
selected brands (Russell, Jarvis, Iyer, & Feyer-
abend, 1980; Gori & Lynch, 1985) and of
smokers experimentally switched to lower yield-
ing brands (Frost et al., 1995; Withey et al.,
1992) have both shown that the slope relating
machine-smoked yield and nicotine intake is
either flat or very shallow, so that smokers can
Tobacco Smoking 650
and do adjust the way they smoke so as to
maintain similar nicotine intakes from cigar-
ettes with widely differing deliveries. Similar up-
regulation of nicotine intake has been shown
when smokers temporarily reduce the number
of cigarettes smoked (Ho-Yen, Spence, Moody,
& Walker, 1982). This pervasive phenomenon
which is characteristic of human smoking is
termed nicotine compensation or titration
(Russell, 1980). A boundary model of nicotine
regulation has been proposed, whereby chronic
users seek to avoid the adverse effects of either
too little (withdrawal) or too much (overdose)
nicotine (Kozlowski, 1984).
(v) Acquisition of nicotine inhalation in novice
smokers. It is well established that children take
upsmokingfor mainlypsychosocial reasons, but
studies have shown that pharmacological mo-
tives take on importance very early in the
smoking career (Lynch & Bonnie, 1994;
McNeill, 1991). Already by the time they are
smoking on a daily basis, children take in as
much nicotine from each cigarette as dependent
adult smokers (McNeill, Jarvis, Stapleton, West,
&Bryant, 1989), and they report similar craving
(Goddard, 1990) and withdrawal symptoms on
trying tostop(McNeill, West, Jarvis, Jackson, &
Bryant, 1986). The FDA has aptly described
nicotine addiction as a pediatric disease.
(vi) Compulsive use. Although long-term oc-
casional smokers (so called chippers) are
found (Evans et al., 1992; Shiffman, 1989), they
are rare, and the typical smoker smokes much
the same number of cigarettes each day, aver-
agingabout 17inthe UK. Eventhose withsevere
smoking-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 at
least as difficult as their problemdrug (Kozlows-
ki et al., 1989). Compulsive use is the key feature
characterizing nicotine dependence.
(vii) Nicotine withdrawal syndrome. Cessa-
tion of smoking reliably leads to a variety of
signs and symptoms, with an onset within
12 hours or less of last tobacco use, and a
duration of three weeks or longer. The mani-
festations are predominantly affective in nature,
with subjects reporting irritability, difficulty
concentrating, anxiety, restlessness, increased
hunger and depressed mood, as well as craving
for tobacco. These findings have been observed
innumerous experimental studies (Hughes et al.,
1984; West, Jarvis, Russell, Carruthers, &
Feyerabend, 1984) and have been thoroughly
reviewed (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 tobacco
withdrawal syndrome is due to loss of nicotine
rather than behavioral aspects of use is shown
by the consistent finding that it is relieved by
nicotine 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 an
aid to smoking cessation. Numerous randomized
controlled trials have shown that nicotine
replacement, whether by patch, gum, nasal
spray, or inhaler, reliably enhances the chances
of success in an attempt at cessation, roughly
doubling success rates over placebo (Fiore et al.,
1996; Silagy, Mant, Fowler, & Lodge, 1994).
8.28.5 THE SMOKING CAREER:
PATTERNS OF UPTAKE,
MAINTENANCE, AND CESSATION
OF SMOKING
8.28.5.1 Recruitment of Young People to
Cigarette Smoking
Uptake of smoking typically occurs in
adolescence, with few people starting to smoke
after the age of 20 (Kessler, 1995; Kessler et al.,
1997). In the UK, from a prevalence of about
1% at age 11, there is a rapid increase over the
following few years, so that by age 15 about
25% of teenagers smoke, with some evidence
that at this age (although not among young
adults of 16 and above) girls are more likely to
smoke than boys (Diamond & Goddard, 1995).
Rates of smoking in young people have shown
no decline since the early 1980s in the UK, and
there is evidence that they are currently
increasing 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, and
personal factors all play a part (Goddard, 1990;
Lynch & Bonnie, 1994). Environmental influ-
ences include parental smoking (approximately
doubling the likelihood of a child starting to
smoke), and smoking by siblings and friends.
Tobacco advertising and promotions effectively
target young people with images of smoking as
trendy, 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 more
likely to become smokers, an association which
becomes 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 with
poor school performance, truancy, low aspira-
tions for future success, and early school leaving
or drop out (Lynch & Bonnie, 1994). Cigarette
smoking in adolescents is frequently associated
with other problembehaviors, including alcohol
and other drug use and other risk taking or
rebellious behaviors.
Personal characteristics consistently linked
with adolescent smoking include low self-
esteem, low knowledge of smoking's adverse
effects, 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-
signedtoequipchildrentoresist social influences
to smoke have shown some initial success, with a
number of randomized trials reporting lower
rates of recruitment in intervention than control
groups (Bruvold, 1993; Flay, 1985). Unfortu-
nately, longer term follow-up has found that
these effects dissipate (Flay et al., 1989;
Nutbeam, Macaskill, Smith, Simpson, & Cat-
ford, 1993), leading researchers to advocate
approaches involving the creation of a wider
social environment supportive of nonsmoking
(Flay, 1985). Bothinthe USAandthe UK, where
rates of teenage smoking are on the increase,
there is a recognition that preventing the uptake
of smoking by young people is an area where up
until now little has been achieved. If progress is
to be made, it will require a far better research
understanding than there is at present of the
factors influencing experimental smoking and
the development of nicotine dependence.
8.28.5.2 Adult Smoking: Disadvantage and
Dependence
In developed Western countries rates of
cigarette smoking have peaked and are now
declining, albeit slowly. In the USA and UK
about 2530% of adults smoke, with little
difference in prevalence between men and
women, except in the oldest age groups contain-
ing a cohort of women for whomnever-smoking
was the norm. The most striking feature of the
evolution of smoking since the late 1970s has
been the increasing association of cigarettes
with markers of disadvantage, whether it be
socioeconomic position, or a range of factors
indicating stressful living circumstances (Jarvis,
1994b). High rates of smoking are seen in the
unemployed (Lee, Crombie, Smith, & Tunstall-
Pedoe, 1991), lone parents (Marsh & McKay,
1994), people who are divorced or separated, the
homeless (Gill, Meltzer, Hinds, & Pettigrew,
1996), heavy drinkers (Jarvis, 1994b), drug users
(Meltzer, Gill, Pettigrew, & Hinds, 1995), and
prisoners (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 variety
of other neurotic disorders (Meltzer et al., 1995).
The association of cigarettes with lowered levels
of psychological well-being is not confined to
those with a formal psychiatric diagnosis, but
also extends into the general population of
smokers (Anda et al., 1990; Schoenborn &
Horm, 1993). In the general population there is
an increasingly strong association between
cigarette smoking prevalence and indicators
of deprivation (Pierce, Fiore, Novotny, Hat-
ziandreu, &Davis, 1989a, 1989b). Between 1973
and 1994, rates of smoking among affluent
people halved in the UK, but among the poorest
groups prevalence remained unchanged at close
to 70% (Bennett, Jarvis, Rowlands, Singleton,
& Haselden, 1996; Jarvis, 1997).
Cigarette smoking is unusual among drug
dependencies in that high levels of dependence
are typical of most users, rather than being
found only in a minority (Stolerman & Jarvis,
1995). At least 80% of cigarette smokers meet
the Diagnostic and statistical manual of mental
disorders (4th ed.; DSM-IV) criteria for
dependence (Cottler et al., 1995). Smokers'
dependence is manifested in a variety of ways,
which all point to a pattern of behavior that has
become highly stereotyped. The average smo-
ker smokes every day, at a rate of over one
cigarette for every waking hour. Survey data
indicate that almost one-third of smokers have
never stopped for as long as a week (US
Department of Health and Human Services,
1990). There is increasing consensus that time
to first cigarette of the day is the strongest
behavioral indicator of cigarette dependence.
Figure 1 shows the distribution of time to first
cigarette in a general population sample of
smokers, and also the corresponding levels of
nicotine intake as indexed by saliva cotinine
concentrations. Some 17% of smokers light up
within five minutes of waking, and over 50%
within half an hour. Overall levels of nicotine
intake are closely correlated.
8.28.5.3 Factors Associated with Smoking
Cessation
At any one time, about two-thirds of cigarette
smokers say that they would like to give up, but
most lack confidence that they would succeed if
Tobacco Smoking 652
30
25
20
15
10
5
0
How soon after waking do you smoke your first cigarette of the day?
Less than 515 1530 30 minutes 12 More than
5 minutes minutes minutes to 1 hour hours 2 hours
P
e
r
c
e
n
t
a
g
e

o
f

s
m
o
k
e
r
s
17
21
14 14
12
22
450
400
350
300
250
200
150
100
50
Time to first cigarette of the day
Less than 515 1530 30 minutes 12 More than
5 minutes minutes minutes to 1 hour hours 2 hours
n = 260 n = 322 n = 205 n = 214 n = 182 n = 307
S
a
l
i
v
a

c
o
t
i
n
i
n
e

(
n
g
/
m
l
)
Mean + 95% CI
Figure 1 Distribution of time to first cigarette of the day among smokers surveyed in primary care, and
corresponding 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 of
cessation (defined as the proportion of ex-
smokers among ever-regular cigarette smokers)
rise steadily with age, from about 18% in young
people in their early 20s to 60% among those
aged 60 and above (Bennett et al., 1996). Across
all age groups combined less than half of ever
smokers in the UK and the USA have quit
(Bennett et al., 1996; US Department of Health
and Human Services, 1990). Overall, rates of
cessation show little difference by gender, with
young women significantly more likely to quit
than men, and middle-aged women significantly
less 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 pharmacological
dependence (Jarvis, 1997). Influences within the
family are shown both by the association of
cessation in parents with number of children
(Jarvis, 1996) and by the strong concordance in
smoking habits among spouses and their
partners. Spouse smoking has consistently
emerged as one of the most powerful predictors
of cessation (Murray, Johnston, Dolce, Wondra
Wong, & Ohara, 1995; Nafstad, Botten, &
Hagen, 1996; Severson, Andrews, Lichtenstein,
Wall, & Zoref, 1995; Wakefield, Gillies, Gra-
ham, Madeley, & Symonds, 1993). Poverty has
become increasingly associated with lowrates of
cessation, indicating that those who can least
afford to smoke are the least likely to quit
(Jarvis, 1997; Marsh & Mackay, 1994). Figure 2
shows rates of cessation by level of deprivation
over the past 20 years in the UK. Among both
affluent men and women cessation rates have
more than doubled, but among the poorest only
10%or less of ever-smokers have quit, and there
has been no improvement since the 1970s.
Depressive illness (Glassman et al., 1990b)
and stressful life circumstances are associated
with low rates of cessation, although interest-
ingly there is evidence that successful cessation
leads to lower, rather than higher, levels of
perceived stress (Cohen & Lichtenstein, 1990).
8.28.5.4 Rates of Spontaneous Cessation in
Smokers
The concept of spontaneous or unaided
quitting is a difficult one. There are a multi-
plicity of influences, both those that are
explicitly recognized by smokers, and others
which, while unrecognized, may nevertheless be
present and influence behavior. In a US survey
of ex-smokers, respondents acknowledged little
assistance in giving up smoking (Fiore et al.,
1990). Over 90% said that they gave up without
any help at all, either fromfamily, physicians, or
more formal services. Only 4% said that they
had had any involvement with specialized
treatment agencies.
One way to estimate rates of successful
unaided quitting in the population is to look
at the rate at which prevalence declines year by
year, or, more specifically, the increase over time
in the cessation rate. By this yardstick, there has
been an approximate 1.5% increase in cessation
each year in the UK since the 1970s. However,
given that no information is available on the
number of cessation attempts smokers make in
any given year (even if it were possible to reach a
satisfactory definition of what constitutes a
serious attempt at cessation), this cannot easily
be translated into what the chances of success-
fully quitting are from any one attempt. The
figure of 1.5%represents the cumulative success
rate from all quit attempts made each year,
averaged across smokers. If smokers on average
make several attempts to quit each year, it
implies a success rate per quit attempt of under
1%; alternatively, if serious quit attempts occur
at a rate of less than once per year, the implied
success rate per quit attempt may be higher.
Two studies have explicitly recruited smokers
planning to make an unaided attempt at quitting
and have followed them up to establish success
rates. In the first, only one-third abstained
successfully for two days, one-quarter for one
week, and at six months 3% remained abstinent
(Hughes et al., 1992). Similar findings emerged
in the second study, with 4.9% not smoking at
six months (Cohen et al., 1989). Since some
further relapse to smoking would be anticipated
after six months, these percentages give an
overestimate of the long-term success rate.
There is a reasonable degree of agreement
between estimates from population cessation
rates and from the studies of self-quitters. Both
indicate a low rate of successful long-term
quitting from any given quit attempt. It would
appear that the chances of successfully quitting
on a particular attempt range between about 0.5
and 3%. Such low figures point once again to
the difficulty of the task faced by smokers who
wish to give up, and suggest that treatments
achieving modest success rates of only 510%
would have a valuable part to play in lowering
smoking prevalence, if they could be delivered
cost-effectively to the bulk of the smoking
population.
8.28.6 PSYCHOLOGICAL SYMPTOMS
Although the act of smoking does not in itself
cause any discernible mental or functional
impairment, this is not to say that there are no
negative psychological sequelae. For many
Tobacco Smoking 654
individuals there will be concern about current
or future illness, the effect of passive smoking on
children, and the financial burden. There is also
likely to be pressure to abstain from non-
smoking family and friends, and a dislike of
being dependent on a drug. However, the
clearest psychological impact of smoking arises
when an individual tries to stop. Most, but not
all, smokers experience some psychological and
physical signs and symptoms when they stop
smoking or significantly reduce the amount they
smoke. There has been much research both
prospectively andretrospectively onthe nicotine
withdrawal syndrome, most studies using simple
self-report questionnaires scored on likert or
visual analogue scales. The three most widely
reportedquestionnaires are the ShiffmanJarvik
Smoking Withdrawal Questionnaire (Shiffman
& Jarvik, 1976), the Smoker Complaints Scale
(Schneider, Jarvik, & Forsythe, 1984), and the
Minnesota Nicotine Withdrawal Questionnaire
(Hughes & Hatsukami, 1986).
60
50
40
30
20
10
0
Deprivation score
0 1 2 3 4 5
P
e
r
c
e
n
t
a
g
e

c
e
s
s
a
t
i
o
n

r
a
t
e
1973
1982
1994
Smoking cessation by deprivation GHS 1973, 1982, and 1994
60
50
40
30
20
10
0
Deprivation score
0 1 2 3 4 5
P
e
r
c
e
n
t
a
g
e

c
e
s
s
a
t
i
o
n

r
a
t
e
1973
1982
1994
(a)
(b)
Figure 2 Trends in rates of smoking cessation by deprivation in (a) men and (b) women in the UK, 1973, 1982,
and 1994. Deprivation was measured 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 subjective
nicotine withdrawal symptoms are craving for
cigarettes, 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 varies
considerably fromperson to person, withdrawal
symptoms are experienced by about 80% of ex-
smokers, three-quarters of whom may exhibit a
pattern that could be described as severe (Gritz,
Carr, & Marcus, 1991). Craving cigarettes,
which can be intermittent or more or less
continuous, is probably the most troublesome
and fundamental symptomand is a major factor
in triggering relapse in the first few weeks of an
attempt to quit. Self-reports of withdrawal
symptoms have been verified by observer
ratings (Hughes & Hatsukami, 1986).
Withdrawal symptoms occur abruptly on
cessation and changes in mood and ability to
concentrate can be detected within two hours of
the last cigarette. Symptoms peak in the first few
days of cessation and, with the exception of
craving, hunger, and weight gain which have a
longer time course, gradually subside to baseline
levels within a few days or weeks, with an
average duration of about 34 weeks (Snyder,
Davis, & Henningfield, 1989; West, Hajek, &
Belcher, 1987). Bouts of craving can persist for
months, however, and it is not uncommon for
ex-smokers to experience a strong urge to smoke
in certain situations or mood states associated
with prior smoking even some years after giving-
up. Increased appetite and weight gain continue
for at least 10 weeks after quitting and ex-
smokers typically gain about 610 lb in the first
year of cessation, though there is great variation
from one person to another, with the heaviest
smokers tending to gain the most weight.
Other physical and objective changes that
accompany tobacco withdrawal include de-
creases in catecholamine excretion, metabolic
rate, heart rate (1215 bpm) (West & Russell,
1987) blood pressure, and tremor, increases in
skin 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 on
tasks requiring vigilance or sustained attention
and memory is also impaired (Snyder et al.,
1989). Many of these subjective and objective
withdrawal effects are the opposite of the effects
that occur following nicotine use and can be
reversed by smoking or giving nicotine by
another route (e.g., nicotine gum, skin patch, or
injection) but not by a placebo or nicotine-free
cigarettes. Severity of withdrawal symptoms
have been found to correlate with baseline
smoking nicotine levels and also to predict
treatment outcome (West, Hajek, & Belcher,
1989; West & Russell, 1985b).
The DSM-IV (American Psychiatric Associa-
tion, 1994) diagnostic criteria for nicotine
withdrawal are shown in Table 4. Of particular
interest is the inclusion of depressed mood
which had not been listed in DSM-III-R. A
number of epidemiological studies have recently
focused attention on the relationship between
depression and smoking. Glassman et al.
(1990a) found that smoking was more prevalent
in individuals who had had a major depressive
disorder at some time in their lives and also that
they were less likely to succeed in quitting
smoking than those without such a history.
Mood changes, such as anxiety and depression
have 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 unfortunately
the case that while many have face validity they
have limited clinical utility. Clinically assess-
ments are most useful when the results can be
used to determine, for instance, which of a
number of treatments to apply in order to
maximize efficacy. This is rarely the case in
smoking cessation, however, since much of the
information gathered at assessment will at best
have prognostic value in predicting a smoker's
likelihood of succeeding but will have little to
offer in the way of indicating specific procedures
to improve the outcome. Empirical research
into matching smokers to particular treatments
is still in its infancy and has only recently started
to highlight some useful leads. The thorough-
ness and depth of assessment will be determined
by the treatment setting. In a specialized
smokers clinic offering intensive treatment,
for instance, a systematic assessment of in-
dividual patient characteristics is feasible and is
likely 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 previous
attempts 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 Smoking 656
Assessments in briefer community interven-
tions and primary care are likely to be con-
siderably less detailed and time consuming and
might only include questions about motivation
to stop smoking and severity of nicotine de-
pendence since these are the two patient char-
acteristics most likely to influence the course of
subsequent treatment and outcome.
8.28.7.1 Assessing Motivation and Intention to
Quit
There are very few smokers who are able to
quit smoking permanently without first being
highly motivated and believing that they can do
so. Regardless of the method employed to stop
smoking, a major factor will be the psycholo-
gical resources available to an individual when it
comes to changing a strongly conditioned
behavior and resisting withdrawal symptoms
and craving. A number of studies have shown
that without strong motivation to quit the
likelihood of succeeding is extremely low in all
but the most minimally dependent smokers
(Jackson, Stapleton, Russell, & Merriman,
1986). In brief intervention studies, motivation
to quit has been assessed by simple question-
naire items such as: How much do you want to
stop smoking altogether? (not at all, slightly,
moderately, quite strongly, very strongly), and
Would you give up smoking altogether, if you
could do so easily? (yes definitely, yes
probably, possibly, probably not, definitely
not). Only those scoring in the highest cate-
gories are likely to be sufficiently motivated to
persist in a serious quit attempt. The number of
previous attempts to stop smoking is also a
useful indicator of motivation.
The concepts of motivation and intention to
change behavior have been extended into a
theoretical model by Prochaska, DiClemente
and colleagues (Prochaska &DiClemente, 1986;
Prochaska, DiClemente, & Norcross, 1992).
Their Stages of Change model is based on
recognition of the fact that giving up smoking is
a dynamic process, rather than a discrete event,
often extending over many years, and char-
acterized by repeated cycles of attempts to stop
and relapses back to smoking. The model
identifies five main stages through which
smokers cycle:
(i) Precontemplation. Not seriously thinking
about quitting.
(ii) Contemplation. Staring to think seriously
about stopping within the next 6 months but not
within the next 30 days.
(iii) Preparation. Intending to quit within the
next 30 days.
(iv) Action. Stopped smoking within past
6 months.
(v) Maintenance. Stopped smoking for over
6 months.
Relapse leads to re-entry into the cycle at an
earlier stage. Three simple questions have been
identified 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 positive
behavior 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 impairment
in social, occupational, or other important areas of functioning
D. The symptoms are not due to a general medical condition and are not better
accounted for by another mental disorder
Assessment 657
individual's progression from one stage to the
next. They suggest that interventions which
encourage the use of the behavior change
processes most relevant to a smoker's current
stage, will be most effective. So, for instance,
precontemplators would be targeted with
information about the health risks of smoking
and benefits of stopping in the hope of raising
their motivation and thus moving them to the
contemplator stage, whereas individuals in the
action stage might receive training in strategies
aimed to prevent relapse. Although there has
been some empirical support for the notion of
stage-matched interventions, critics have ex-
posed inconsistencies and theoretical problems
with the model (Sutton, 1996). Perhaps the most
important contribution made by the Stages of
Change to date has been to encourage therapists
to assist smokers to stop over repeated attempts,
rather than using a one shot approach. The
model has also focused attention on alternative
measures of outcome besides total abstinence,
that is, in terms of moving smokers along a stage
(see also Chapter 8.01, this volume).
8.28.7.2 Assessing Nicotine Dependence
Nicotine dependence is now recognized as a
psychoactive substance dependence disorder
(DSM-IV, ICD-10). Under the DSM-IVcriteria
smokers are classified as dependent if they
exhibit impaired control and continue to smoke
despite awareness that it exacerbates a medical
condition, and if they experience withdrawal
symptoms when abstaining from smoking, or if
they have a history of unsuccessful attempts at
quitting. However the practical value of using
this all-or-nothing dichotomous classification
when assessing an individual smoker is limited
since it has been estimated that about 90% of
smokers are dependent (Woody, Cottler, &
Cacciola, 1993). It is therefore, more useful to
viewsmokers as lying onacontinuumof nicotine
dependence. When measured in this way
dependence has proved to be the strongest and
most consistent predictor of the success or failure
of an attempt toquit smoking (see Figure 3) such
that the likelihoodof stoppingsmokingis several
times greater at low, rather than high, levels of
dependence (Stapleton et al., 1995).
Although this would seem to suggest con-
siderable potential for tailoring cessation treat-
ment according to dependence level in order to
maximize overall cessation rates, little progress
has been made in this area. There are not as yet
any established behavioral treatments based on
the differing dependence level of the smoker.
One fundamental problemis that cessation rates
are modest even among smokers at the lower
end of the dependence range and special
attention and effort is only likely to be invested
in the more highly dependent smokers when
treatment programs are more successful gen-
erally. Not surprisingly, given that tobacco
dependence is largely a dependence on nicotine,
certain forms of nicotine replacement therapy
have been shown to be more effective at higher
levels of dependence and it is in this area that
most progress towards matching treatments is
likely to be made in the future (Sutherland &
Stapleton, 1994). This does not mean, however,
that an assessment of a smoker's level of
dependence has no clinical value, since it serves
to alert therapists to cases where withdrawal
symptoms are likely to be particularly severe
and the prognosis poor, indicating that more
intensive 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-reported
behavioral and subjective symptoms, and (ii)
objective biochemical markers of nicotine
intake. The simplest indicator of degree of
dependence is daily cigarette consumption
which can be obtained by self-report or by
self-monitoring diary records over a period of
time. Since smokers tend to report consumption
in multiples of 5 or 10, self-monitoring diaries
tend to be more accurate than self-report,
especially if the cigarette is recorded at the time
it is smoked, although the monitoring itself can
be a reactive measure and result in a decrease in
smoking (Frederiksen, Epstein, & Kosevsky,
1975; McFall, 1978). Consumption is only a
rough indicator of dependence, however, as
smoke intake per cigarette can vary a great deal
fromone individual to another. The most widely
used paper and pencil test of dependence is the
Fagerstro m Tolerance Questionnaire (FTQ),
consisting of an eight-item inventory designed
to assess: daily nicotine intake, smoking in the
morning (when nicotine levels are low); and
perceived difficulty in refraining from smoking
(Fagerstro m, 1978). More recently a shorter,
six-item, version of the FTQ, the Fagerstro m
Test for Nicotine Dependence (FTND), has
been developed to address some of the psycho-
metric weaknesses of the original and has
improved internal consistency and predictive
validity (Heatherton, Kozlowski, Frecker, &
Fagerstro m, 1991). Scores range from 0 (low
dependence) to 10 (high dependence).
An even shorter version, the Heaviness of
Smoking Inventory, is based on the two items
which together account for 60% of the FTND
score, namely, daily cigarette consumption, and
Tobacco Smoking 658
0.3
0.2
0.1
0.0
Saliva cotinine while smoking
(ng/ml)
100 200 300 400 500 600
P
r
o
b
a
b
i
l
i
t
y

o
f

s
t
o
p
p
i
n
g

s
m
o
k
i
n
g
Bars give 90% Cls
Relation between successful quitting
and nicotine dependence
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 is
smoked (Heatherton, Kozlowski, Frecker,
Rickert, & Robinson, 1989). Cut-off points
have been proposed for the FTND score (e.g.,
score greater than seven equals severe depen-
dence) inorder toprovide a simple classification.
Although theoretically there may be some
circumstances where such a classification is
desirable the rationale for the precise levels of
cut-off are weak and all the evidence points to
there being a continuum of dependence in the
population with no well defined clusters of
smokers at the different levels.
A further questionnaire measure in use is the
Overall Dependence Scale (ODS), a subset of
nine items taken from the HornRussell
Smoking Motivation Questionnaire. The ODS
(score 027) assesses perceived and experienced
difficulty in refraining from or quitting smok-
ing, craving for cigarettes when unable to
smoke, and degree of habitual or automatic
smoking (West & Russell, 1985b).
8.28.7.4 Biochemical Measures of Dependence
In addition to the questionnaire measures,
there are now also a number of objective
measures which can be used to provide quanti-
tative measures of smoke inhalationandnicotine
intake (Jarvis, Tunstall-Pedoe, Feyerabend,
Vesey, & Saloojee, 1987). These measures
provide a more accurate estimate of the extent
of smoking, and hence degree of dependence,
thancanbe gainedbyknowingsimplyhowmany
cigarettes an individual smokes. They also have
an invaluable role in validating self-reports of
abstinence. There are four main biochemical
indicators: (i) carbon monoxide in expired air or
blood; (ii) cotinine in saliva, blood, or urine; (iii)
nicotine in blood; and (iv) thiocyanate (SCN) in
saliva, blood, or urine.
In clinical settings the most useful and widely
applied method is a measure of the concentra-
tion of carbon monoxide (CO) in the expired-air
of the smoker which correlates highly with
blood (plasma) nicotine and with carboxyhae-
moglobin (COHb) (Jarvis, Russell, & Saloojee,
1980; Wald, Idle, Boreham, & Bailey, 1981).
Obtaining a breath sample and a reading takes
less than a minute, requires minimal training
of both therapist and patient, and has the
advantage over plasma nicotine of being
noninvasive. The main disadvantage of this
method is the relatively short half-life of COHb
(45 hours), less in very physically active
individuals, which means it is only possible to
detect smoking which has occurred over the past
few hours. Ideally, testing should be in the
afternoon of a normal smoking day by which
time CO levels have reached a stable level.
Though rarely a problem in practice, low level
exposure to CO from car exhausts and fires, for
instance, can produce CO levels in nonsmokers
equivalent 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). As
measures of smoke intake, nicotine, and
cotinine have the advantage over CO of being
highly specific to tobacco users. However,
unlike nicotine, cotinine can be measured
reliably in saliva which is considerably easier
to collect than a blood sample. Cotinine also has
the advantage over nicotine in having a longer
half-life of 1520 hours (compared to nicotine's
12 hours) which means sampling time is less
critical. Cotinine assays can reliably detect
regular smokers who typically have levels
between 200 and 400 ng/ml, as well as light
smokers. Nonsmokers have levels below
10 ng/ml. The drawback of both nicotine and
cotinine measures over CO is that they require
a laboratory assay which is expensive, time
consuming to collect, and cannot provide
immediate feedback of results. Very recently a
simple dipstick method for assessing total
urinary nicotine metabolites has become avail-
able (Cope, Nayyar, Holde, Gibbons, & Bunce,
1996). Although it does not produce as accurate
a measure as a laboratory assay, it will enable
health professionals to assess nicotine depen-
dence quickly and conveniently.
Thiocyanate (SCN) has also been used to
determine smoke intake and to corroborate
patients' self-reports but has a number of
drawbacks and in recent years has increasingly
been overtaken by cotinine as the marker of
choice. Its use stems fromthe fact that hydrogen
cyanide gas is present in high concentrations in
tobacco smoke and is metabolized to SCN by
the liver. It has a long half-life of between 10 and
14 days which is useful for validating smoking
abstinence but in comparison to cotinine its
sensitivity and specificity are low and it is
affected by naturally occurring SCN in the diet
(e.g., almonds, beer, and broccoli) resulting
in some overlap between smokers and non-
smokers.
The questionnaire measures of dependence
correlate moderately with the biochemical
markers of intake (West & Russell, 1985), and
with severity of withdrawal symptoms, but no
single measure has been shown to be consis-
tently superior to the others in predicting the
success of a quit attempt. The choice of which
measure to use will depend on both the purpose
for which the measure is taken and the setting.
For instance, the paper-and-pencil measures
have the advantage of low cost and simplicity
Tobacco Smoking 660
whereas salivary cotinine provides the most
stable measure of the actual nicotine intake
from cigarettes.
8.28.8 TREATMENT APPROACHES
There are four main approaches for reducing
the health consequences of tobacco smoking: (i)
treatment interventions aimed at encouraging
and assisting adult smokers to stop; (ii)
preventive interventions to reduce the uptake
of smoking by children; (iii) modifications to
cigarettes to make smoking less harmful; and
(iv) fiscal measures, legislation, and restrictions
on smoking in public places designed to reduce
active smoking as well as nonsmokers' exposure
to environmental tobacco smoke. This chapter
will focus primarily on treatment approaches.
8.28.8.1 Behavioral and Public Health
Approaches
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 these
approaches has not been adequately evaluated
in controlled clinical trials. This has been the
case particularly with behavioral treatments,
where inadequate statistical power through
insufficient sample sizes has been a particular
problem. Other methodological limitations
include: very short-term or unspecified length
of follow-up; absence of biochemical validation
of abstinence; lack of a control group; and
failure to present outcome on a strict intent to
treat basis whereby nonattenders are classified
as smokers. As a result there is little evidence
that one behavioral technique is more effective
than any other (Lichtenstein & Glasgow, 1992),
although there is consensus that multiple
component programs tend to be the most
successful (Schwartz, 1987). Little attention
has been paid to teasing out the specific
therapeutic ingredients of the multimodal
psychological packages which have been used
with smokers. A broad array of behavioral/
psychological/cognitive techniques have been
tried either individually or in combination, in
many settings, from brief self-help programs to
inpatient treatment units (Hurt et al., 1992). The
interventions have included: rapid smoking and
other aversion therapies; smoke dilution; nico-
tine fading; self-management approaches; for
example, contingency contracting and stimulus
control, skills training, relapse prevention,
cognitive, motivational, and educational inter-
ventions, cue exposure, hypnosis and individual
or group counselling (Hajek, 1996).
In the 1950s the field was dominated by
educational approaches, followed in the 1960s
by conditioning procedures such as rapid
smoking and satiation. The 1970s saw the
introduction of intensive multicomponent cog-
nitive self-management approaches which have
promising success rates but are severely limited
by the fact that most smokers will not attend
formal clinic programs (Lichtenstein, 1992).
This factor, together with a recognition of the
sheer scale of the problem (approximately 12
million smokers in the UK), prompted a move
away from these intensive clinical approaches
towards a broader community wide public
health perspective involving self-help and
advice in a wide variety of settings from health
care to the workplace. The current consensus is
that a stepped-care treatment model is likely to
be the most cost-effective approach in smoking
cessation. Similar models have been advocated
for other preventive medical interventions.
Stepped-care involves initially offering the least
intensive and least costly approaches to the
greatest number of smokers, and saving the
intensive and expensive second-line approaches
for those who fail to respond. Though the
absolute success rates of the brief interventions
are lower they tend to be more cost effective as
they have the potential to reach a far greater
number of smokers. Typical one year success
rates range from about 5% for brief advice in
primary care to 10% when NRT is added, and
up to 2030% for specialized smokers clinics
offering intensive multisession behavioral ap-
proaches combined with NRT.
Recently, after an extensive literature review,
the US Agency for Health Care Policy and
Research (AHCPR) published their influential
guidelines on smoking cessation (Fiore, Bailey,
et al., 1996). This targets three main audiences:
primary care clinicians; smoking cessation
specialists; and health care administrators.
The strategies they recommend for those work-
ing in primary care, or for whom smoking
cessation is just one of their many clinical
activities, are shown in Table 5. As part of the
assistance offered, the guidelines advise clin-
icians toprovide basic informationonthe nature
and time course of withdrawal and the addic-
tiveness of smoking, for example, that any
smoking increases the likelihood of full relapse.
Smokers should be helped to develop problem-
solving and coping skills by identifying events,
moodstates andactivities whichincrease the risk
of relapse, and identifying and practising skills
intended to cope with these high-risk situations.
The AHCPR guidelines for smoking cessa-
tion specialists overlap with those for health
professionals in primary care but involve
collecting more information at assessment on
Treatment Approaches 661
stress and psychiatric comorbidity, for instance,
as these variables are known to negatively affect
outcome. As there is a strong relationship
between the intensity of counseling or contact
with the patient and treatment success, the
recommendation is for treatment programs,
whether group or individual, to span a period of
at least two weeks, though preferably more than
eight weeks. This factor appears more impor-
tant than the specific behavioral techniques
employed. The optimal number of sessions is
47, with each session lasting for 2030 minutes.
Training in relapse prevention, thought by
many in the addictions field to be critical to
long-term success, has not been shown to be
cost-effective in smoking cessation. This has led
some to conclude that it is more beneficial to
encourage relapsers to wait and have another
attempt 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 the
importance of developing supportive systems
within the clinical setting to facilitate systematic
and repeated interventions with smokers. To
achieve this, environmental prompts (e.g.,
computerized systems) to remind staff to ask
about smoking are likely to be required, in
addition to policy changes to include smoking
Table 5 Recommendations for smoking intervention from AHCPR Clinical Practice
Guidelines.
Action Strategies for implementation
ASK about smoking status at
every visit and document
Include in vital signs, use stickers on patients
notes, or implement computerized reminder
system
ADVISE all smokers to quit, in a
clear, strong, and personalized
manner
for example, Quitting smoking is the most
important thing you can do to protect your
health
Tie smoking to current illness or impact on
children and family
IDENTIFY smokers willing to
make a quit attempt at this time
If willingprovide assistance (see below).
If patient prefers more intensive help or if it is
indicated, refer to specialist.
If unwillingprovide motivational intervention
A. ASSIST smoker with a quit
plan
Set a quit date
Help prepare smoker for quitting:
inform family and friends;
prepare the environment (discard cigarettes);
review previous quit attempts;
anticipate challenges
B. NICOTINE
REPLACEMENT (NRT)
Encourage use of NRT unless contraindicated
C. GIVE KEY ADVICE Total abstinence: Not a single puff
Avoid alcohol
Other smokers in household: consider quitting
with others or make specific plans for
maintaining abstinence among smokers
D. PROVIDE
SUPPLEMENTARY
MATERIALS
Booklets, etc., culturally, educationally, and age
appropriate for the smoker.
ARRANGE follow-up in person
or by telephone
First follow-up within 1 week of quit date,
second within a month
At follow-up, congratulate success, or use lapses
for constructive learning, elicit recommitment to
total abstinence, identify problems, anticipate
challenges, assess use of NRT
Adapted from AHCPR Smoking Cessation Guideline. Source: Fiore, Bailey et al. (1996).
Tobacco Smoking 662
assessment and cessation in the performance
expectations of clinicians. The basic thrust of
the recommendations is to greatly increase the
number of clinicians who intervene with
patients who smoke and to ensure that clinicians
accept smoking cessation as a vital part of their
role in health care provision.
In addition to brief physician-delivered and
intensive multicomponent behavioral smoking
interventions, workplace programs have also
been investigated. These provide the opportu-
nity to reach a large number of smokers, in a
convenient location and may therefore be more
acceptable to smokers than attending specialist
clinics. A meta-analysis of 20 controlled work-
place studies concluded that smokers were 58%
more likely to quit in the intervention condition
than in the control group (Fisher, Glasgow, &
Terborg, 1990).
8.28.8.2 Pharmacological Approaches to
Smoking Cessation
8.28.8.2.1 Nicotine replacement therapy
A number of nicotine and non-nicotine
pharmacological aids to smoking cessation have
been investigated. By far the most well re-
searched is nicotine replacement therapy (NRT)
which was designed to be used in conjunction
with a behavioral program, however brief. The
rationale for nicotine replacement is to tem-
porarily provide smokers with a safer, more
slowly delivered and lower dose of nicotine via a
different route, to reduce the severity of the
withdrawal symptoms and desire to smoke. The
process of quitting is effectively broken down
into two-stages. Initially the patient gives up the
behavioral act of smoking (i.e., it is decoupled
from the rewarding effects of nicotine) while
starting unlearning the many nondrug elements
of the habit and developing strategies to cope
without cigarettes. Once the ex-smoker has
gained confidence in their ability to stay off
cigarettes they are weaned off nicotine comple-
tely, usually over aperiodof 34months. NRTis
the most rigorously and thoroughly evaluated
treatment for smokers, and though success rates
are modest, varying according to the setting and
psychological support withwhichit is combined,
it marked a breakthrough in smoking cessation.
There are currently four different forms of NRT
which have been approved for clinical use on
prescription or are available over-the-counter
(OTC), althoughnot all have yet beenlicensedin
every country. One very important difference
between NRT products and inhaled tobacco
smoke is the speed with which nicotine is
absorbed. None can mimic the extremely rapid,
high but transient nicotine peaks in arterial
blood which characterize inhalation, so they do
not provide the same positive satisfaction as
smoking and therefore have less potential for
sustaining dependence.
(i) Nicotine gum
The first formulation to be developed and
thus the most extensively researched was
nicotine gum, which is available in two strengths
(2 or 4 mg per piece). Nicotine from the gum is
absorbed slowly through the lining of the mouth
(buccal mucosa) and blood levels reach a flat
peak after about 30 minutes chewing. Typically,
smokers obtain blood nicotine levels around
1015 ng/mg, about one-third of usual smoking
levels, when using the 2 mg gumad libitum(West
et al., 1984) and about two-thirds smoking levels
with the 4 mg gum (Fagerstro m, 1988). At these
levels, adverse mood effects and difficulty
concentrating associated with withdrawal are
partially relieved, though craving for cigarettes
is not reliably decreased. This is probably
because satisfaction from nicotine depends at
least in part on a rapid boost in nicotine levels. If
absorption rate is crucial nothing is gained by
using more gum. This may explain why in
routine clinical use smokers tend to chew only
seven to eight pieces per day rather than the
recommended 1215 pieces (Russell, 1988).
Despite relatively modest effects on withdrawal,
the efficacy of the gum in smoking cessation is
well established. Nearly 50 randomized con-
trolled trials have now been conducted, and a
recent metal-analysis concluded that the gum
was more 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 is
contraindicated in patients with peptic ulcers
and poses problems for denture wearers, tastes
unpleasant and gives rise to a number of minor
side effects and requires some effort and
perseverance in order to learn the correct
chewing technique.
(ii) Nicotine patches
The patch has the advantage over gum of
providing therapeutic levels of nicotine fromthe
first day of treatment with minimal effort and
instruction. They are available in three doses
(sizes) and most smokers start on the highest
dose for 48 weeks, followed by a systematic
weaning period of 28 weeks using progressively
smaller size patches. Two different types are
available; one worn during waking hours only,
with the highest dose patch delivering 15 mg
nicotine over 16 hours, and the other worn
Treatment Approaches 663
throughout the day and night delivering 21 mg
over 24 hours. Both appear to be equally
effective (Fiore, Smith, Jorenby, & Baker,
1994). After applying a patch, venous blood
nicotine levels build up slowly over several
hours to a plateau of around 1020 ng/ml,
roughly equivalent to 50% of mean plasma
nicotine levels produced by smoking. Levels
remain reasonably constant for much of the
waking day before declining during the evening.
Since nicotine absorption is very slow, patch
users are unlikely to experience any of the
positive subjective effects associated with ra-
pidly administered nicotine which suggests they
may be more helpful to individuals who smoke
to relieve or avoid withdrawal (negative re-
inforcement) than to smokers seeking positive
reinforcement. Other potentially important
differences between the patch and the other
forms of NRT include the fact that the patch
does not allow patients to self-titrate their dose
according to need, and does not provide a
behavioral or sensory component to substitute
for lighting-up. However, these factors together
with the lack of positive effects suggest the
dependence potential and abuse liability of the
patch will be very low, which is supported by
clinical experience. The most common side
effect is mild skin irritation but only about 5%
of patients have to stop treatment as a result of
adverse 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 absolute
success rates (2025% at 6 month follow-up)
tending to occur when the patch is combined
withan intensive behavioral treatment program.
The broad consensus from several reviews and
meta-analyses is that compared to a placebo, the
nicotine patch increases success rates two to
threefold irrespective of the intensity of the
adjunctive behavioral treatment (Fiore et al.,
1994; Silagyet al., 1994). It reduces the severityof
withdrawal, and perhaps surprisingly, appears
to reduce craving for cigarettes more consis-
tently than the nicotine gum, but its main
advantage over the latter is undoubtably the
improved patient compliance.
(iii) Nicotine nasal spray
The development of nicotine nasal spray
(NNS) stemmed from work showing the rapid
rate of nicotine absorption from nasal snuff
(Russell et al., 1981). Nicotine taken intrana-
sally is very swiftly absorbed into the systemic
circulation and peak venous levels are reached
within 510 minutes of taking a dose of NNS,
which is considerably faster than with the patch
or gum(Sutherland et al., 1992), although not as
rapid as inhaled cigarette smoke. Unlike
smoking however, NNS does not deliver arterial
bolus doses of nicotine, although the rate of
nicotine absorption is sufficiently rapid to
produce the positive stimulant subjective effects
(often described as a buzz) which many
smokers experience while smoking their first
cigarette of the day. Such effects are usually
considered rewarding and satisfying by smokers
and are not produced when nicotine is absorbed
more slowly. The spray delivers 1 mg of nicotine
per dose (0.5 mg to each nostril), and with
repeated dosing has the potential to provide
blood nicotine levels similar to those obtained
while smoking, although results from clinical
trials indicate smokers attain levels only about
3050% of baseline smoking levels when using
ad libitum.
The efficacy of NNS has been demonstrated
in three randomized placebo-controlled trials in
which it was combined with behavioral support
and produced remarkably similar success rates
at 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, NNS
reduces the severity of the affective symptoms of
withdrawal compared to placebo, but also has
the advantage of substantially relieving craving
for cigarettes. At times of acute craving not only
can the user obtain pharmacological relief in
minutes 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 of
view, is that the spray appears to be of greatest
benefit to the most highly dependent smokers, in
contrast to findings with the patch (see Figure 4)
which is equally effective across the full range of
dependence.
Studies are currently underway to determine
whether these initial but promising findings will
be replicated when the spray is used with less
intensive adjunctive treatment, such as in
general practice. It takes a few days to learn
the correct spraying technique and to acclima-
tize to the initial irritant side effects (to nose/
throat), which may pose problems in settings
where less time is available to support and
encourage new users.
Another issue concerns the greater depen-
dence potential of the spray compared to the
slower-actingnicotine deliverysystems (Hughes,
1988). In the two smoking cessation studies
which allowed the spray to be used for up to a
year, 43% and 29% of those who succeeded in
stopping smoking used it for this time, repre-
senting approximately 12% of all those origin-
ally assigned active spray. This figure is
somewhat higher than for the gum. However,
Tobacco Smoking 664
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
P
r
o
b
a
b
i
l
i
t
y

o
f

a
b
s
t
i
n
e
n
c
e
Relation between baseline nicotine levels
and abstinence at three months
Figure 4 Relationship between nicotine dependence (indexed by plasma nicotine concentration fromsmoking)
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 of
charge is likely to have encouraged longer term
and higher usage since cost has been shown to
influence these parameters for nicotine gum
(Hughes, Wadland, Fenwick, Lewis, & Bickel,
1991). Not surprisingly, the long-term users had
higher pretreatment nicotine levels (more de-
pendent) than those who stopped the spray
earlier on.
(iv) Nicotine inhaler
The inhaler, the newest form of NRT, is an
oral puffing device that consists of a hollow
plastic mouthpiece, roughly the size of a
cigarette, which contains a nicotine impreg-
nated porous plug. It evolved from an earlier
smoke-free product called Favor
1
, which in
preliminary studies was shown to have some
therapeutic potential (Hajek, Jarvis, Belcher,
Sutherland, & Feyerabend, 1989; Russell,
Jarvis, Sutherland, & Feyerabend, 1987). De-
spite its name, absorption of nicotine vapor
from the inhaler is not very rapid and does not
give an arterial peak, since most of it is deposited
in the mouth and upper airways rather than the
lungs. The pharmacokinetic profile resembles
the gum rather than cigarettes (Bergstrom,
Nordberg, Lunell, Antoni, &Langstrom, 1995).
Per puff, the nicotine delivered by the inhaler is
about one-tenth of that from a cigarette and is
both temperature and effort related, but even
with very frequent and intensive puffing, the
levels achieved are modest. However, the
regular handmouth activity involved offers
more habit replacement than other forms of
NRTand it provides sensory characteristics that
resemble smoking, which may have a role in
alleviating cigarette cravings (Rose, Behm, &
Levin, 1993).
The results of two randomized controlled
trials of the inhaler have been published and
report one year success rates of 15% active
inhaler vs. 5% placebo, and 13% vs. 8%,
respectively (Schneider et al., 1996b; Tnnesen,
Nrregaard, Mikkelsen, Jrgensen, & Nilsson,
1993).
Research is being undertaken to see whether
combining different types of NRT is more
effective than using each individually and
whether tailoring NRT to achieve 100%
replacement (i.e., up to smoking levels) is
warranted. Preliminary reports indicate that
higher nicotine replacement is associated with
better withdrawal relief and higher short- and
long-term success rates (Dale et al., 1995;
Fagerstro m, Schneider, & Lunell, 1993; Kor-
nitzer, Boutsen, Dramaix, Thijs, & Gustavsson,
1995). From a theoretical point of view, the best
combinations are likely to involve the patch,
which provides a steady background level of
nicotine, supplemented by one of the other
faster-acting delivery systems which enable the
patient to self-titrate dose as needed and provide
an alternative coping response. Despite the vast
literature on NRT many questions remain to be
answered, such as the optimal duration of
treatment and dosage, how it should be
discontinued (abruptly or gradually), and with
which psychological treatment it should be
combined for maximum efficacy. What does
seem clear at the present time is that NRT
combined with supportive treatment, however
brief, produces higher success rates than NRT
or behavioral treatment alone. This might be
because the two treatments affect different
aspects of nicotine dependence, for example,
NRT reduces withdrawal discomfort and
behavioral treatment enhances coping skills
(Hughes, 1995) or because each treatment
increases adherence to the other (Klesges,
Ward, & Debon, 1996).
8.28.8.2.2 Non-nicotine pharmacotherapy
A variety of non-nicotine pharmacological
treatments or agents have also been examined
including 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; Schneider
et al., 1996c; West, Hajek, & McNeill, 1991),
anorectics (Spring et al., 1995), citric acid
inhaler (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 unacceptable
side effects, or have not yet been evaluated
thoroughly enough with adequate sample sizes
to recommend their use at present. The only
exception to this concerns the antidepressant,
bupropion, which was approved for use in
smoking cessation by the US Food and Drug
Administration in 1997, though it has not yet
been licensed in the UK. Bupropion (Zyban
1
) is
an aminoketone antidepressant which is
thought to act primarily via a noradrenergic
mechanism but which also has some dopami-
nergic activity. Anecdotal reports of depressed
patients quitting smoking spontaneously while
Tobacco Smoking 666
taking bupropion, its generally favorable side
effect profile, and its low dependence potential,
stimulated interest in the drug for smoking
cessation. Although the results of the controlled
clinical trials have not yet been published the
data are convincing and provided that it is
licensed more widely, bupropion could, like
NRT, make a significant contribution to future
cessation rates.
8.28.9 APPROACHES TO REDUCE
SMOKING-RELATED DISABILITY
Although in developed countries studies
consistently show the majority of smokers are
aware that smoking carries significant health
risks, albeit grossly underestimating the real
risks to their own health, reducing smoking
prevalence has been a slow and hard fought
process. Despite their best efforts a number of
smokers cannot manage to give up and some
others simply do not want to stop, and unlike
other drug dependencies smokers do not seem
to mature out of it. Until more effective
interventions have been developed there is a
strong case for exploring approaches designed
to make smoking less dangerous. One way of
achieving this is by modifying the constituents
or design of cigarettes to reduce their toxicity.
Such strategies are akin to those adopted in the
drug dependence field under the umbrella of
harm minimization. This is an area that has
highlighted a number of ethical issues in
addition to having political implications, and
which has divided opinion among researchers in
the smoking cessation field.
In 1973 the Independent Scientific Commit-
tee on Smoking and Health (ISCSH) was
established in the UK to formulate national
policies on smoking and health. The main thrust
of the program has concerned product mod-
ification. Initially the Committee were involved
in a radical move examining the potential
advantages of substituting tobacco in cigarettes
with a less toxic synthetic substance based on
modified cellulose. Although 11 new cigarette
brands based on substitute tobacco (New
Smoking Material and Cytrel) were launched
in the UK in 1977 they were not adequately
acceptable to smokers and were soon with-
drawn from sale. Following this disappointing
outcome the ISCSH turned its attention instead
to the gradual reduction of tar yields of
cigarettes which has been a far more successful
strategy. Since 1972 the sales-weighted average
tar yield of cigarettes has declined from 20.8 mg
to around 11.0 mg per cigarette. This reduction
has been achieved by improving cigarette filters,
introducing ventilation holes, and increasing
the porosity of the paper in order to dilute the
smoke, as well as through changes to the
tobacco itself. Determination of the yields of
cigarettes are made using smoking machines
using internationally agreed puff parameters
(volume of smoke in puff, frequency of puffing,
etc.). Since tar and nicotine yields are highly
correlated (about 0.9) reductions in tar have
also been accompanied by reductions in
nicotine. Unfortunately when smokers switch
to cigarettes which have lower nicotine levels,
they tend to alter, often unconsciously, the way
in which they smoke in an attempt to maintain
adequate levels of nicotine. They may for
instance take more puffs, hold the smoke in
their lungs for longer, take larger puffs, smoke
to a shorter butt length, or even hold the
cigarette in a way that causes the ventilation
holes to be covered. This compensatory
smoking behavior, or upregulation of smoking,
has meant that the percentage reduction in tar
intake that would be expected when smokers
transfer froma mediumor high tar cigarette to a
low tar brand is not as great as predicted by the
smoking machine figures. Mainly as a result of
the lower nicotine levels, low-tar cigarettes tend
to be less acceptable to smokers which explains
why, despite the health advantages and the
selective advertising encouraging smokers to
switch, 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 offset
by the tendency to compensate by increasing
inhalation, and since consumer acceptability is
limited, there have been recommendations for
the development of low-tar cigarettes with
slightly enhanced nicotine yields (up to 1 mg).
Although the case for slightly higher nicotine
cigarettes is compelling, one must not under-
estimate the significance of the reductions in the
tar intake per cigarette over the last 25 years
which have contributed to a decline in mortality
from lung cancer (Peto, 1986) and also been
beneficial in chronic obstructive lung disease
(Darby, Doll, &Stratton, 1989). No matter how
intensively modern cigarettes are smoked it is
virtually impossible to obtain tar levels as high
as those delivered by the old high-tar brands.
The flip-side of this strategy, and one which is
far more radical, is the approach being
considered in the USA linked to the unprece-
dented proposed settlement with the tobacco
industry. In addition to the financial penalties
and other controls being imposed on tobacco
companies, the settlement stipulates that the
FDA will in future have the power to regulate
nicotine as a drug and gives them authority to
remove it fromcigarettes in 12 years, subject to a
number of provisions such as showing that this
Approaches to Reduce Smoking-related Disability 667
would not lead to a significant demand for black
market cigarettes. The thinking behind this plan
is that nicotine yields in cigarettes could be
lowered slowly over a number of years until the
maximum level a smoker could obtain from
cigarettes would be insufficient to create or
sustain nicotine dependence (Benowitz & Hen-
ningfield, 1994; Kessler et al., 1996, 1997;
Kozlowski & Henningfield, 1995; Slade,
1995). In future children might still experiment
with cigarettes but could not get a large enough
dose of nicotine to become pharmacologically
dependent and so would be unlikely to progress
to regular daily smoking. Although intuitively
appealing and plausible, a number of critical
questions remain unanswered. What will hap-
pen to existing smokers? It would be reasonable
to expect them to smoke more aggressively in an
attempt to obtain more nicotine and maintain
satisfaction, and in the process become exposed
to greater amounts of the more dangerous
components (CO and tar) than would otherwise
have been the case. What is the critical threshold
for creating dependence and what role does
tolerance play? By reducing nicotine yields very
slowly over several years, might neuronal
readaptation and sensitization occur so that
current smokers remain dependent albeit on
lower nicotine levels?
Another innovative but highly controversial
approach to safer smoking has come from
tobacco companies themselves. In 1987 the R. J.
Reynolds Tobacco Company spent $1 billion
developing and market-testing a novel virtually
tar free cigarette-like device (brand name
Premier) which heated rather than burned
tobacco (R. J. Reynolds Tobacco Co., 1988).
The smoke particles in which the nicotine was
transported were comprised mainly of glycerol
and water rather than tar. Glycerol is harmless
and metabolized as a source of energy and was
added simply to produce smoke. The yields of
all major carcinogens and many other poten-
tially harmful components were far lower than
those of conventional cigarettes and the biolo-
gical activity of its condensate was greatly
reduced. The tar yield was about 0.7 mg per
cigarette and the nicotine and carbon monoxide
yields about 0.3 and 12.0 mg, respectively. It was
estimated that the risks of tobacco-related
cancers and chronic obstructive lung disease
would be substantially reduced, possibly by as
much as 90%, for an average smoker switching
from a regular brand to Premier (Sutherland,
Russell, Stapleton, & Feyerabend, 1993). Pre-
mier was never marketed, however, due to lack
of acceptability (especially poor taste), and
strong protests frompublic health organizations
in the USA who petitioned the FDA to classify
and 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 its
predecessor, is virtually tar free but which is
claimed to have a more acceptable taste. It is
likely that in the USA this product will receive
near unanimous opposition once again on the
grounds that it might encourage smokers who
would otherwise stop to switch to the newsafe
cigarette instead, and that it may encourage
children to take up smoking.
8.28.10 PROSPECTS FOR THE FUTURE
Like all drug dependencies, cigarette smoking
is a multifaceted problem, whose understanding
requires attention to a range of factors,
from drug pharmacokinetics and pharmaco-
dynamics, genetics, individuals and their social
milieu, to broader economic and political
influences. No single policy response can hope
to address the range of issues which determine
smoking uptake, maintenance, and cessation.
Future progress will depend on developing a
better understanding of the processes operating
at each stage of the smoking career, and clinical
psychology will continue to have an important
contribution to make in furthering understand-
ing of individual liability to dependence, the
process of recruitment, the role of nicotine in
maintaining the habit, and in developing and
disseminating effective cessation interventions.
If there is one lesson which can be taken from
the past, it is that future progress is likely to be
equally slow and hard won.
8.28.11 REFERENCES
Altman, D. G., Levine, D. W., Coeytaux, R., Slade, J., &
Jaffe, R. (1996). Tobacco promotion and susceptibility
to tobacco use among adolescents aged 12 through 17
years in a nationally representative sample. American
Journal of Public Health, 86(11), 15901593.
American Psychiatric Association. (1994). Diagnostic and
statistical manual of mental disorders (4th ed.). Washing-
ton, DC: Author.
Anda, R. F., Williamson, D. F., Escobedo, L. G., Mast, E.
E., Giovino, G. A., & Remington, P. L. (1990).
Depression and the dynamics of smoking: A national
perspective. Journal of the American Medical Association
264(12), 15411545.
Anthonisen, N. R., Connett, J. E., Kiley, J. P., Altose, M.
D., Bailey, W. C., Buist, A. S., Conway W., Jr., Enright,
P. L., Kanner, R. E., Ohara, P., Owens, G. R., Scanlon,
P. D., Tashkin, D. P., & Wise, R. A. (1994). Effects of
smoking intervention and the use of an inhaled anti-
cholinergic bronchodilator on the rate of decline of
FEV 1: The lung health study. Journal of the American
Medical Association 272(19), 14971505.
Behm, F. M., Schur, C., Levin, E. D., Tashkin, D. P., &
Rose, J. E. (1993). Clinical evaluation of a citric acid
inhaler for smoking cessation. Drug & Alcohol Depen-
dence, 31(2), 131138.
Bennett, N., Jarvis, L., Rowlands, O., Singleton, N., &
Tobacco Smoking 668
Haselden, L. (1996). Living in Britain: Results from the
1994 General Household Survey. London: HMSO.
Benowitz, N. L. (1988). Pharmacologic aspects of cigarette
smoking and nicotine addiction. New England Journal of
Medicine 319(20), 13181330.
Benowitz, N. L., Hall, S. M., Herning, R. I., Jacob, P.,
Jones, R. T., & Osman, A. L. (1983). Smokers of low-
yield cigarettes do not consume less nicotine. New
England Journal of Medicine 309(3), 139142.
Benowitz, N. L., & Henningfield, J. E. (1994). Establishing
a nicotine threshold for addiction: The implications for
tobacco regulation. New England Journal of Medicine
331(2), 123125.
Benowitz, N. L., Kuyt, F., Jacob, P. I., Jones, R. T., &
Osman, A. L. (1983). Cotinine disposition and effects.
Clinical Pharmacology & Therapeutics, 34(5), 604611.
Benwell, M. E. M., Balfour, D. J. K., & Anderson, J. M.
(1988). Evidence that tobacco smoking increases the
density of (7)-(3H)nicotine binding sites in human
brain. Journal of Neurochemistry, 50(4), 12431247.
Bergstrom, M., Nordberg, A., Lunell, E., Antoni, G., &
Langstrom, B. (1995). Regional deposition of inhaled
c-11 nicotine vapor in the human airway as visualized by
positron emission tomography. Clinical Pharmacology &
Therapeutics, 57(3), 309317.
Berlin, I., Said, S., Spreux-Varoquaux, O., Launay, J. M.,
Olivares, R., Millet, V., Lecrubier, Y., & Puech, A. J.
(1995). A reversible monoamine-oxidase-a inhibitor
(moclobemide) facilitates smoking cessation and absti-
nence in heavy, dependent smokers. Clinical Pharmacol-
ogy & Therapeutics, 58(4), 444452.
Bigelow, G. E., Rand, C. S., Gross, J., Burling, T. A., &
Gottlieb, S. H. (1986). Smoking cessation and relapse
among cardiac patients. (NIDA Research Monograph
Series 72, pp. 167171). Rockville, MD: US Department
of Health and Human Services.
Blair, P. S., Fleming, P. J., Bensley, D., Smith, I., Bacon,
C., Taylor, E., Berry, J., & Tripp, J. (1996). Smoking and
the sudden infant death syndrome: results from 19935
case-control study for confidential inquiry into stillbirths
and deaths in infancy. British Medical Journal, 313,
195198.
Breslau, N., Kilbey, M. M., & Andreski, P. (1993).
Nicotine dependence and major depression: New evi-
dence from a prospective investigation. Archives of
General Psychiatry, 50(1), 3135.
Bridgwood, A., & Malbon, G. (1995). Survey of the
physical health of prisoners. London: HMSO.
Bruvold, W. H. (1993). A meta-analysis of adolescent
smoking prevention programs. American Journal of
Public Health, 83(6), 872880.
Cinciripini, P. M., Lapitsky, L., Seay, S., Wallfisch, A.,
Meyer, W. J., & Van Vunakis, H. (1995). A placebo-
controlled evaluation of the effects of buspirone on
smoking cessation: Differences between high-anxiety and
low-anxiety smokers. Journal of Clinical Psychopharma-
cology, 15(3), 182191.
Cohen, S., & Lichtenstein, E. (1990). Perceived stress,
quitting smoking, and smoking relapse. Health Psychol-
ogy, 9(4), 466478.
Cohen, S., Lichtenstein, E., Prochaska, J. O., Rossi, J. S.,
Gritz, E. R., Carr, C. R., Orleans, C. T., Schoenbach, V.
J., Biener, L., Abrams, D., DiClemente, C., Curry, S.,
Marlatt, G. A., Cummings, K. M., Emont, S. L.,
Giovino, G., & Ossipktein, D. (1989). Debunking myths
about self-quitting. Evidence from 10 prospective studies
of persons who attempt to quit smoking by themselves.
American Psychologist, 44(11), 13551365.
Collishaw, N. E., & Lopez, A. D. (1996, May). The
tobacco epidemic: a public health emergency. WHO
Tobacco Alert. Geneva, Switzerland: World Health
Organization.
Cook, D. G., Shaper, A. G., Pocock, S. J., & Kussick, S. J.
(1986). Giving up smoking and the risk of heart attack:
A report from the British Regional Heart Study. Lancet,
2, 13761379.
Cook, D. G., Whincup, P. H., Papacosta, O., Strachan, D.
P., Jarvis, M. J., & Bryant, A. (1993). Relation of passive
smoking as assessed by salivary cotinine concentration
and questionnaire to spirometric indices in children.
Thorax, 48(1), 1420.
Cope, G., Nayyar, P., Holder, R., Gibbons, J., & Bunce, R.
(1996). A simple near-patient test for nicotine and its
metabolites in urine to assess smoking habit. Clinica
Chimica Acta, 256(2), 135149.
Corrigall, W. A., & Coen, K. M. (1989). Nicotine
maintains robust self-administration in rats on a limited-
access schedule. Psychopharmacology, 99(4), 473478.
Cottler, L. B., Schuckit, M. A., Helzer, J. E., Crowley, T.,
Woody, G., Nathan, P., & Hughes, J. (1995). The DSM-
IV field trial for substance use disorders: Major results.
Drug and Alcohol Dependence, 38(1), 5969.
Covey, L. S., & Glassman, A. H. (1991). A meta-analysis of
double-blind placebo-trials of clonidine for smoking
cessation. British Journal of Addiction, 86(8), 991998.
Dale, L. C., Hurt, R. D., Offord, K. P., Lawson, G. M.,
Croghan, I. T., & Schroeder, D. R. (1995). High-dose
nicotine patch therapy: Percentage of replacement and
smoking cessation. Journal of the American Medical
Association, 274(17), 13531358.
Darby, S. C., Doll, R., & Stratton, I. M. (1989). Trends in
mortality from smoking related diseases in England and
Wales. In N. Wald & P. Froggatt (Eds.), Nicotine,
smoking, & the low tar program (pp. 7082). Oxford, UK:
Oxford University Press.
Davison, G., & Duffy, M. (1982). Smoking habits of long-
term survivors of surgery for lung cancer. Thorax, 37(5),
331333.
DeLeon, J., Dadvand, M., Canuso, C., White, A. O.,
Stanilla, J. K., & Simpson, G. M. (1995). Schizophrenia
and smoking: An epidemiological survey in a state
hospital. American Journal of Psychiatry, 152(3),
453455.
Diamond, A., & Goddard, E. (1995). Smoking among
secondary schoolchildren in 1994. London: HMSO.
DiFranza, J. R., Richards J. Jr., Paulman, P. M.,
WolfGillespie, N., Fletcher, C., Jaffe, R. D., & Murray,
D. (1991). RJR Nabisco's cartoon camel promotes
Camel cigarettes to children. Journal of the American
Medical Association, 266(22), 31493153.
Dobson, A. J., Alexander, H. M., Heller, R. F., & Lloyd,
D. M. (1991). How soon after quitting smoking does risk
of heart attack decline? Journal of Clinical Epidemiology,
44(11), 12471253.
Doll, R., & Hill, A. B. (1950). Smoking and carcinoma of
the lung. Preliminary report. British Medical Journal, ii,
739748.
Doll, R., Peto, R., Wheatley, K., Gray, R., & Sutherland, I.
(1994). Mortality in relation to smoking: 40 years'
observations on male British doctors. British Medical
Journal, 309(6959), 901911.
Edwards, N. B., Murphy, J. K., Downs, A. D., Ackerman,
B. J., & Rosenthal, T. L. (1989). Doxepin as an adjunct
to smoking cessation: A double-blind pilot study.
American Journal of Psychiatry, 146(3), 373376.
Evans, N. J., Gilpin, E., Pierce, J. P., Burns, D. M.,
Borland, R., Johnson, M., & Bal, D. (1992). Occasional
smoking among adults: evidence from the California
Tobacco Survey. Tobacco Control, 1, 169175.
Fagerstro m, K. O. (1978). Measuring degree of physical
dependence to tobacco smoking with reference to
individualization of treatment. Addictive Behaviors, 3,
235241.
Fagerstro m, K. O. (1988). Efficacy of nicotine chewing
gum: A review. In O. F. Pomerleau & C. S. Pomerleau
(Eds.), Nicotine replacement: A critical evaluation
References 669
(pp. 109128). New York: Alan R. Liss.
Fagerstro m, K. O., Schneider, N. G., & Lunell, E. (1993).
Effectiveness of nicotine patch and nicotine gum as
individual versus combined treatments for tobacco
withdrawal symptoms. Psychopharmacology, 111(3),
271277.
Fiore, M. C., Bailey, W. C., Cohen, S. J., Dorfman, S. F.,
Goldstein, M. G., Gritz, E. R., Heyman, R. B.,
Hobrook, J., Jaen, C. R., Kottbe, T. E., Lando, H. A.,
Mecklenburg, R., Mullen, P. D., Nett, L. M., Robinson,
L., Stitzer, M. L., Tommasello, A. C., Nillejo, L., &
Newers, M. E. (1996). Smoking cessation: Clinical
Practice Guideline No. 18 (AHCPR Publication No. 96-
0692). Rockville, MD: US Department of Health and
Human Services, Agency for Health Care Policy and
Research.
Fiore, M. C., Novotny, T. E., Pierce, J. P., Giovino, G. A.,
Hatziandreu, E. J., Newcomb, P. A., Surawicz T. S., &
Davis, R. M. (1990). Methods used to quit smoking in
the United States. Do cessation programs help? Journal
of the American Medical Association, 263(20), 27602765.
Fiore, M. C., Smith, S. S., Jorenby, D. E., & Baker, T. B.
(1994). The effectiveness of the nicotine patch for
smoking cessation: A meta-analysis. Journal of the
American Medical Association, 271(24), 19401947.
Fiore, M. C., Wetter, D. W., Bailey, W. C., Bennett, G.,
Cohen, S. J., Dorfman, S. F., Goldstein, M. G., Gritz, E.
R., Hasselblad, V., Henningfield, J. E., Heyman, R. B.,
Holbrook, J., Husten, C., Jaen, C. R., Kohler, C.,
Kottke, T. E., Lando, H. A., Manley, M., Mecklenburg,
R., Melvin, C., Mullen, P. D., Nett, L. M., Piasecki, T.
M., Robinson, L., Rothstein, D., Schriger, D. L., Stitzer,
M. L., Stachenko, S., Tommasello, A., Villejo, L.,
Wewers, M. E., & Baker, T. B. (1996). The agency for
health-care policy and research smoking cessation
clinical-practice guideline. Journal of the American
Medical Association, 275(16), 12701280.
Fisher, K. J., Glasgow, R. E., & Terborg, J. R. (1990).
Work site smoking cessation: A meta-analysis of long-
term quit rates from controlled studies. Journal of
Occupational Medicine, 32(5), 429439.
Flay, B. R. (1985). What we know about the social
influences approach to smoking prevention: Review and
recommendations. NIDA Research Monograph Series
(63), 67112.
Flay, B. R., Koepke, D., Thomson, S. J., Santi, S., Best, J.
A., & Brown, K. S. (1989). Six-year follow-up of the first
Waterloo school smoking prevention trial. American
Journal of Public Health, 79(10), 13711376.
Frederiksen, L. W., Epstein, L. H., & Kosevsky, B. P.
(1975). Reliability and controlling effects of three
procedures for self-monitoring smoking. Psychological
Record, 25, 255264.
Froggatt, P. (1988). Fourth report of the Independent
Scientific Committee on Smoking and Health. London:
HMSO.
Frost, C., Fullerton, F. M., Stephen, A. M., Stone, R.,
Nicolaides-Bouman, A., Densem, J., Wald, N. J., &
Semmence, A. (1995). The tar reduction study: Rando-
mised trial of the effect of cigarette tar yield reduction on
compensatory smoking. Thorax, 50(10), 10381043.
Gill, B., Meltzer, H., Hinds, K., & Pettigrew, M. (1996).
Psychiatric morbidity among homeless people. London:
HMSO.
Giovino, G. A., Henningfield, J. E., Tomar, S. L.,
Escobedo, L. G., & Slade, J. (1995). Epidemiology of
tobacco use and dependence. Epidemiologic Reviews,
17(1), 4865.
Glassman, A. H. (1993). Cigarette smoking: Implications
for psychiatric illness. American Journal of Psychiatry,
150(4), 546553.
Glassman, A. H., Helzer, J. E., Covey, L. S., Cottler, L. B.,
Stetner, F., Tipp, J. E., & Johnson, J. (1990a). Smoking,
smoking cessation, and major depression. Journal of the
American Medical Association, 264, 15461549.
Glassman, A. H., Helzer, J. E., Covey, L. S., Cottler, L. B.,
Stetner, F., Tipp, J. E., & Johnson, J. (1990b). Smoking,
smoking cessation, and major depression. Journal of the
American Medical Association, 264(12), 15461549.
Glendinning, A., Shucksmith, J., & Hendry, L. (1994).
Social class and adolescent smoking behavior. Social
Science and Medicine, 38, 14491460.
Glynn, T. J., Greenwald, P., Mills, S. M., & Manley, M. W.
(1993). Youth tobacco use in the United States
Problem, progress, goals, and potential solutions. Pre-
ventive Medicine, 22(4), 568575.
Goddard, E. (1990). Why children start smoking. London:
HMSO.
Gori, G. B., & Lynch, C. J. (1985). Analytical cigarette
yields as predictors of smoke bioavailability. Regulatory
Toxicology and Pharmacology, 5(3), 314326.
Gourlay, S. G., Stead, L. F., & Benowitz, N. L. (1997). A
meta-analysis of clonidine for smoking cessation. In
T. Lancaster, C. Silagy, & D. Fullerton (Eds.), Tobacco
addiction module of the Cochrane database of systematic
reviews (Vol. Issue 2). Oxford, UK: The Cochrane
Library, The Cochrane Collaboration, Update Software.
Gross, J., & Stitzer, M. L. (1989). Nicotine replacement:
ten-week effects on tobacco withdrawal symptoms.
Psychopharmacology, 98(3), 334341.
Gritz, E. R., Carr, C. R., & Marcus, A. C. (1991). The
tobacco withdrawal syndrome in unaided quitters.
British Journal of Addiction, 86(1), 5769.
Haglund, B., & Cnattingius, S. (1990). Cigarette smoking
as a risk factor for sudden infant death syndrome: A
population-based study. American Journal of Public
Health, 80(1), 2932.
Hajek, P. (1996). Current issues in behavioral and
pharmacological approaches to smoking cessation.
Addictive Behaviors, 21(6), 699707.
Hajek, P., Jarvis, M. J., Belcher, M., Sutherland, G., &
Feyerabend, C. (1989). Effect of smoke-free cigarettes
on 24h cigarettes withdrawal: A double-blind
placebo-controlled study. Psychopharmacology, 97(1),
99102.
Halpern, M. T., Gillespie, B. W., & Warner, K. E. (1993).
Patterns of absolute risk of lung cancer mortality in
former smokers. Journal of the National Cancer Institute,
85(6), 457464.
Hatsukami, D. K., Gust, W. G., & Keenan, R. M. (1987).
Physiologic and subjective changes from smokeless
tobacco withdrawal. Clinical Pharmacology and Ther-
apeutics, 41(1), 103107.
Heatherton, T. F., Kozlowski, L. T., Frecker, R. C., &
Fagerstro m, K. O. (1991). The Fagerstro m Test for
Nicotine Dependence: A revision of the Fagerstro m
Tolerance Questionnaire. British Journal of Addiction,
86(9), 11191127.
Heatherton, T. F., Kozlowski, L. T., Frecker, R. C.,
Rickert, W. S., & Robinson, J. (1989). Measuring the
heaviness of smoking: Using self-reported time to the
first cigarette of the day and number of cigarettes
smoked per day. British Journal of Addiction, 84,
791799.
Hilleman, D. E., Mohiuddin, S. M., Core, M. G., & Sketch,
M. H. (1992). Effect of buspirone on withdrawal
symptoms associated with smoking cessation. Archives
of Internal Medicine, 152(2), 350352.
Hjalmarson, A., Franzon, M., Westin, A., & Wiklund, O.
(1994). Effect of nicotine nasal spray on smoking
cessation: A randomized, placebo-controlled, double
blind study. Archives of Internal Medicine, 154(22),
25672572.
Henningfield, J. E., & Keenan, R. M. (1993). The anatomy
of nicotine addiction. Health Values, 17, 1219.
Henningfield, J. E., London, E. D., & Benowitz, N. L.
Tobacco Smoking 670
(1990). Arterial-venous differences in plasma concentra-
tions of nicotine after cigarette smoking. Journal of the
American Medical Association, 263(15), 20492050.
Himbury, S., & West, R. (1985). Smoking habits after
laryngectomy. British Medical Journal, 291(6494),
514515.
Holm, H., Jarvis, M. J., Russell, M. A. H., & Feyerabend,
C. (1992). Nicotine intake and dependence in Swedish
snuff takers. Psychopharmacology, 108(4), 507511.
Ho-Yen, D. O., Spence, V. A., Moody, J. P., & Walker, W.
F. (1982). Why smoke fewer cigarettes? British Medical
Journal, 284(6333), 19051907.
Hughes, J. R. (1988). Dependence potential and abuse
liability of nicotine replacement therapies. In O. F.
Pomerleau, & C. S. Pomerleau (Eds.), Nicotine replace-
ment: A critical evaluation (1st ed., pp. 261277). New
York: Alan R. Liss.
Hughes, J. R. (1992). Tobacco withdrawal in self-quitters.
Journal of Consulting and Clinical Psychology, 60(5),
689697.
Hughes, J. R. (1993). Non-nicotine pharmacotherapies for
smoking cessation. Journal of Drug Development, 6(4),
197203.
Hughes, J. R. (1995). Combining behavioral therapy and
pharmacotherapy for smoking cessation: An update.
NIDA Research Monograph Series (150), 92109.
Hughes, J. R., & Glaser, M. (1993). Transdermal nicotine
for smoking cessation. Health Values 17(2), 2531.
Hughes, J. R., Gulliver, S. B., Fenwick, J. W., Valliere, W.
A., Cruser, K., Pepper, S., Shea, P., Solomon, L. J., &
Flynn, B. S. (1992). Smoking cessation among self-
quitters. Health Psychology, 11(5), 331334.
Hughes, J. R., Gust, S. W., Skoog, K., Keenan, R. M., &
Fenwick, J. W. (1991). Symptoms of tobacco with-
drawal. A replication and extension. Archives of General
Psychiatry, 48(1), 5259.
Hughes, J. R., & Hatsukami, D. K. (1986). Signs and
symptoms of tobacco withdrawal. Archives of General
Psychiatry 43(3), 289294.
Hughes, J. R., Hatsukami, D. K., Pickens, R. W., Krahn,
D., Malin, S., & Luknic, A. (1984). Effect of nicotine on
the tobacco withdrawal syndrome. Psychopharmacology
83(1), 8287.
Hugnes, J. R., Wadland, W. C., Fenwick, J. W., Lewis, J.,
& Bickel, W. K. (1991). Effect of cost on the self-
administration and efficacy of nicotine gum: A pre-
liminary study. Preventive Medicine, 20(4), 486496.
Hurt, R. D., Dale, L. C., Offord, K. P., Bruce, B. K.,
McClain, F. L., & Eberman, K. M. (1992). Inpatient
treatment of severe nicotine dependence. Mayo Clinic
Proceedings, 67(9), 823828.
Jackson, P. H., Stapleton, J. A., Russell, M. A. H., &
Merriman, R. J. (1986). Predictors of outcome in a
general practitioner intervention against smoking. Pre-
ventive Medicine, 15(3), 244253.
Jarvis, M. J. (1989). Application of biochemical intake
markers to passive smoking measurement and risk
estimation. Mutation Research, 222(2), 101110.
Jarvis, M. J. (1994a). Gender differences in smoking
cessation: real or myth? Tobacco Control, 3, 324328.
Jarvis, M. J. (1994b). A profile of tobacco smoking.
Addiction, 89(11), 13711376.
Jarvis, M. J. (1995). Smoking cessation: Time for action.
Thorax, 50(S1), S22S24.
Jarvis, M. J. (1996). The association between having
children, family size and smoking cessation in adults.
Addiction, 91(3), 427434.
Jarvis, M. J. (1997). Patterns and predictors of smoking
cessation in the general population. In C. T. Bolliger, &
K. O. Fagerstro m, (Eds.), The tobacco epidemic. Progress
in respiratory research (Vol. 28, pp. 151164). Basel,
Switzerland: Karger.
Jarvis, M. J., Raw, M., Russell, M. A. H., & Feyerabend,
C. (1982). Randomised controlled trial of nicotine
chewing-gum. British Medical Journal, 285(6341),
537540.
Jarvis, M. J., Russell, M. A. H., Feyerabend, C., Eiser, J.
R., Morgan, M., Gammage, P., & Gray, E. M. (1985).
Passive exposure to tobacco smoke: Saliva cotinine
concentrations in a representative population sample of
non-smoking schoolchildren. British Medical Journal,
291(6500), 927929.
Jarvis, M. J., Russell, M. A. H., & Saloojee, Y. (1980).
Expired air carbon monoxide: A simple breath test of
tobacco smoke intake. British Medical Journal,
281(6238), 484485.
Jarvis, M. J., Tunstall-Pedoe, H., Feyerabend, C., Vesey,
C. J., & Saloojee, Y. (1984). Biochemical markers of
smoke absorption and self reported exposure to passive
smoking. Journal of Epidemiology and Community
Health, 38(4), 335339.
Jarvis, M. J., Tunstall-Pedoe, H., Feyerabend, C., Vesey,
C., & Saloojee, Y. (1987). Comparison of tests used to
distinguish smokers from nonsmokers. American Journal
of Public Health, 77(11), 14351438.
Kessler, D. A. (1995). Nicotine addiction in young people.
New England Journal of Medicine, 333(3), 186189.
Kessler, D. A., Barnett, P. S., Witt, A., Zeller, M. R.,
Mande, J. R., & Schultz, W. B. (1997). The legal and
scientific basis for FDA's assertion of jurisdiction over
cigarettes and smokeless tobacco. Journal of the Amer-
ican Medical Association, 277(5), 405409.
Kessler, D. A., Witt, A. M., Barnett, P. S., Zeller, M. R.,
Natanblut, S. L., Wilkenfeld, J. P., Lorraine, C. C.,
Thompson, L. J., & Schultz, W. B. (1996). The Food and
Drug Administration's regulation of tobacco products.
New England Journal of Medicine, 335(13), 988994.
Klesges, R. C., Ward, K. D., & Debon, M. (1996).
Smoking cessation: A successful behavioral/pharmaco-
logic interface. Clinical Psychology Review, 16(6),
479496.
Klonoff-Cohen, H. S., Edelstein, S. L., Lefkowitz, E. S.,
Srinivasan, I. P., Kaegi, D., Jae Chun, C., & Wiley, K. J.
(1995). The effect of passive smoking and tobacco
exposure through breast milk on sudden infant death
syndrome. Journal of the American Medical Association,
273(10), 796798.
Knott, V. J., & Venables, P. H. (1977). EEG alpha
correlates of non-smokers, smokers, smoking, and
smoking deprivation. Psychophysiology, 14(2), 150156.
Kornitzer, M., Boutsen, M., Dramaix, M., Thijs, J., &
Gustavsson, G. (1995). Combined use of nicotine patch
and gum in smoking cessation: A placebo-controlled
clinical trial. Preventive Medicine, 24(1), 4147.
Kozlowski, L. T., & Henningfield, J. E. (1995). Thinking
the unthinkable: The prospect of regulation of nicotine
in cigarettes by the United States government. Addiction,
90(2), 165167.
Kozlowski, L. T., Wilkinson, A., Skinner, W., Kent, C.,
Franklin, T., & Pope, M. (1989). Comparing tobacco
cigarette dependence with other drug dependencies.
Greater or equal difficulty quitting and urges to
use, but less pleasure from cigarettes. Journal of the
American Medical Association, 261(6), 898901.
Kozlowski, L. T. (1984). The interaction of psychosocial
and biological determinants of tobacco use: More on the
boundary model. Journal of Applied Social Psychology,
14(3) 244256.
Lee, A. J., Crombie, I. K., Smith, W. C. S., & Tunstall-
Pedoe, H. D. (1991). Cigarette smoking and employment
status. Social Science and Medicine, 33(11), 13091312.
Lichtenstein, E., & Glasgow, R. E. (1992). Smoking
cessation: What have we learned over the past decade?
Journal of Consulting & Clinical Psychology, 60(4),
518527.
Lichtenstein, E., & Hollis, J. (1992). Patient referral to a
References 671
smoking cessation program: Who follows through?
Journal of Family Practice, 34(6), 739744.
Lynch, B. S., & Bonnie, R. J. (Eds.) (1994). Growing up
tobacco free: Preventing nicotine addiction in children and
youths. Washington, DC: National Academy Press.
Marsh, A., & McKay, S. (1994). Poor smokers. London:
Policy Studies Institute.
McFall, R. M. (1978). Smoking cessation research. Journal
of Consulting & Clinical Psychology, 46(4), 703712.
McNeill, A. D. (1991). The development of dependence on
smoking in children. British Journal of Addiction, 86(5),
589592.
McNeill, A. D., Jarvis, M. J., Stapleton, J. A., West, R. J.,
& Bryant, A. (1989). Nicotine intake in young smokers:
Longitudinal study of saliva cotinine concentrations.
American Journal of Public Health, 79(2), 172175.
McNeill, A. D., West, R. J., Jarvis, M., Jackson, P., &
Bryant, A. (1986). Cigarette withdrawal symptoms in
adolescent smokers. Psychopharmacology, 90(4),
533536.
Meltzer, H., Gill, B., Pettigrew, M., & Hinds, K. (1995).
The prevalence of psychiatric morbidity among adults
living in private households (Vol. Report 1). London:
HMSO.
Murray, R. P., Johnston, J. J., Dolce, J. J., Lee, W. W., &
Ohara, P. (1995). Social support for smoking cessation
and abstinence: The Lung Health Study. Addictive
Behaviors, 20(2), 159170.
Nafstad, P., Botten, G., & Hagen, J. (1996). Partner's
smoking: A major determinant for changes in women's
smoking behavior during and after pregnancy. Public
Health, 110, 379385.
Nutbeam, D., Macaskill, P., Smith, C., Simpson, J. M., &
Catford, J. (1993). Evaluation of two school smoking
education programs under normal classroom conditions.
British Medical Journal, 306(6870), 102107.
Peto, R. (1986). Overview of cancer time-trend studies in
relation to changes in cigarette manufacture. In D. G.
Zaridze, & R. Peto (Eds.), Tobacco: A major interna-
tional health hazard (IARC Scientific Publications No.
74, pp. 211226). Lyon, France: IARC.
Peto, R., Lopez, A. D., Boreham, J., Thun, M., & Heath,
C. (1994). Mortality from smoking in developed countries
19502000: Indirect estimates from national vital statis-
tics. Oxford, UK: Oxford University Press.
Peto, R., Lopez, A. D., Boreham, J., Thun, M., Heath, C.,
& Doll, R. (1996). Mortality from smoking worldwide.
British Medical Bulletin, 52(1), 1221.
Phillips, A. N., & Smith, G. D. (1994). Cigarette smoking
as a potential cause of cervical cancer: Has confounding
been controlled? International Journal of Epidemiology,
23(1), 4249.
Pich, E. M., Pagliusi, S. R., Tessari, M., Talabot-Ayer, D.,
Hooft van Huisduijnen, R., & Chiamulera, C. (1997).
Common neural substrates for the addictive properties of
nicotine and cocaine. Science, 275(5296), 8386.
Pierce, J. P., Fiore, M. C., Novotny, T. E., Hatziandreu, E.
J., & Davis, R. M. (1989a). Trends in cigarette smoking
in the United States. Educational differences are
increasing. Journal of the American Medical Association,
261(1), 5660.
Pierce, J. P., Fiore, M. C., Novotny, T. E., Hatziandreu, E.
J., & Davis, R. M. (1989b). Trends in cigarette smoking
in the United States. Projections to the year 2000.
Journal of the American Medical Association, 261(1),
6165.
Pollay, R. W., Siddarth, S., Siegel, M., Haddix, A., Merritt,
R. K., Giovino, G. A., & Eriksen, M. P. (1996). The last
strawcigarette advertising and realized market shares
among youths and adults, 19791993. Journal of Market-
ing, 60(2), 116.
Pontieri, F. E., Tanda, G., Orzi, F., & Dichiara, G. (1996).
Effects of nicotine on the nucleus accumbens and
similarity to those of addictive drugs. Nature, 382,
255257.
Poswillo, D., & Alberman, E. (1992). Effects of smoking on
the fetus, neonate, and child. Oxford, UK: Oxford
University Press.
Prochaska, J. O., & DiClemente, C. C. (1986). Towards a
comprehensive model of change. In W. E. Miller, & N.
Heather (Eds.), Treating addictive behaviors: Processes of
change (pp. 327). New York: Plenum.
Prochaska, J. O., DiClemente, C. C., & Norcross, J. C.
(1992). In search of how people change: Applications to
addictive behaviors. American Psychologist, 47(9),
11021114.
Prochaska, J. O., & Goldstein, M. G. (1991). Process of
smoking cessation: Implications for clinician. Clinics In
Chest Medicine, 12(4), 727735.
R. J. Reynolds Tobacco Company (1988). Chemical and
biological studies on new cigarette prototypes that heat
instead of burn tobacco. Winston-Salem, NC: Author.
Rose, J. E., & Behm, F. M. (1994). Inhalation of vapor
from black pepper extract reduces smoking withdrawal
symptoms. Drug & Alcohol Dependence, 34(3), 225229.
Rose, J. E., Behm, F. M., & Levin, E. D. (1993). Role of
nicotine dose and sensory cues in the regulation of smoke
intake. Pharmacology Biochemistry & Behavior, 44(4),
891900.
Rose, J. E., Behm, F. M., Westman, E. C., Levin, E. D.,
Stein, R. M., & Ripka, G. V. (1994). Mecamylamine
combined with nicotine skin patch facilitates smoking
cessation beyond nicotine skin patch treatment alone.
Clinical Pharmacology & Therapeutics, 56(1), 8699.
Rose, J. E., & Hickman, C. S. (1987). Citric acid aerosol as
a potential cessation aid. Chest, 92(6), 10051008.
Rosenberg, L., Kaufman, D. W., Helmrish, S. P., &
Shapiro, S. (1985). The risk of myocardial infarction
after quitting smoking in men under 55 years of age. New
England Journal of Medicine, 313(24), 15111514.
Royal College of Physicians (1971). Smoking and Health
Now. London: Pitman Medical and Scientific Publishing.
Russell, M. A. H. (1980). Nicotine intake and its
regulation. Journal of Psychosomatic Research, 24(5),
253264.
Russell, M. A. H. (1988). Nicotine replacement: The role of
blood nicotine levels, their rate of change, and nicotine
tolerance. In O. F. Pomerleau, & C. S. Pomerleau (Eds.),
Nicotine replacement: A critical evaluation (1st ed.,
pp. 6394). New York: Alan R. Liss.
Russell, M. A. H., Jarvis, M. J., Devitt, G., & Feyerabend,
C. (1981). Nicotine intake by snuff users. British Medical
Journal, 283(6295), 814817.
Russell, M. A. H., Jarvis, M., Iyer, R., & Feyerabend, C.
(1980). Relation of nicotine yield of cigarettes to blood
nicotine concentrations in smokers. British Medical
Journal, 280(6219), 972976.
Russell, M. A. H., Jarvis, M. J., Sutherland, G., &
Feyerabend, C. (1987). Nicotine replacement in smoking
cessation: Absorption of nicotine vapor from smoke-free
cigarettes. Journal of the American Medical Association,
257(23), 32623265.
Russell, M. A. H., Stapleton, J. A., Feyerabend, C.,
Wiseman, S. M., Gustavsson, G., Sawe, U., & Connor,
P. (1993). Targeting heavy smokers in general practice:
Randomised controlled trial of transdermal nicotine
patches. British Medical Journal, 306(6888), 13081312.
Schneider, F. H., Mione, P. J., Raheman, F. S., Phillips, B.
M., & Quiring, J. N. (1996a). Reduction of tobacco
withdrawal symptoms by sublingual lobeline sulfate.
American Journal of Health Behavior, 20(5), 346363.
Schneider, N. G., Jarvik, M. E., & Forsythe, A. B. (1984).
Nicotine vs. placebo gum in the alleviation of withdrawal
during smoking cessation. Addictive Behaviors, 9(2),
149156.
Schneider, N. G., Olmstead, R., Mody, F. V., Doan, K.,
Tobacco Smoking 672
Franzon, M., Jarvik, M. E., & Steinberg, C. (1995).
Efficacy of a nicotine nasal spray in smoking cessation:
A placebo-controlled, double-blind trial. Addiction,
90(12), 16711682.
Schneider, N. G., Olmstead, R., Nilsson, F., Mody, F. V.,
Franzon, M., & Doan, K. (1996b). Efficacy of a nicotine
inhaler in smoking cessation: A double-blind, placebo-
controlled trial. Addiction, 91(9), 12931306.
Schneider, N. G., Olmstead, R. E., Steinberg, C., Sloan,
K., Daims, R. M., & Brown, H. V. (1996c). Efficacy of
buspirone in smoking cessation: A placebo-controlled
trial. Clinical Pharmacology & Therapeutics, 60(5),
568575.
Schoenborn, C. A., & Horm, J. (1993). Negative moods as
correlates of smoking and heavier drinking: Implications
for health promotion. Hyattsville, MD: National Center
for Health Statistics.
Schwartz, J. (1987). Review and evaluation of smoking
cessation methods: The United States and Canada,
19781985 (National Institute Health Publication
No. 872940). Bethesda, MD: National Cancer
Institute.
Severson, H. H., Andrews, J. A., Lichtenstein, E., Wall,
M., & Zoref, L. (1995). Predictors of smoking during
and after pregnancy: A survey of mothers of newborns.
Preventive Medicine, 24(1), 2328.
Sexton, M., & Hebel, J. R. (1984). A clinical trial of change
in maternal smoking and its effect on birth weight.
Journal of the American Medical Association, 251(7),
911915.
Shiffman, S. (1989). Tobacco chippers. Individual
differences in tobacco dependence. Psychopharmacology,
97(4), 539547.
Shiffman, S. M., & Jarvik, M. E. (1976). Smoking
withdrawal symptoms in two weeks of abstinence.
Psychopharmacology, 50(1), 3539.
Silagy, C., Mant, D., Fowler, G., & Lodge, M. (1994).
Meta-analysis on efficacy of nicotine replacement
therapies in smoking cessation. Lancet, 343(8890),
139142.
Slade, J. (1995). Are tobacco products drugs? Evidence
from US tobacco (Editorial). Tobacco Control, 4, 12.
Slade, J., Bero, L. A., Hanauer, P., Barnes, D. E., &
Glantz, S. A. (1995). Nicotine and addiction: The Brown
and Williamson documents. Journal of the American
Medical Association, 274(3), 225233.
Slotkin, T. A., Orband-Miller, L., & Queen, K. L. (1987).
Development of (3H)nicotine binding sites in brain
regions of rats exposed to nicotine prenatally via maternal
injections or infusions. Journal of Pharmacology and
Experimental Therapeutics, 242(1), 232237.
Smith, G. D., Strobele, S. A., & Egger, M. (1994). Smoking
and health promotion in Nazi Germany. Journal of
Epidemiology and Community Health, 48(3), 220223.
Snyder, F., Davis, F., & Henningfield, J, (1989). The
tobacco withdrawal syndrome: Performance decrements
assessed on a computerised test battery. Drug & Alcohol
Dependence, 23(3), 259266.
Spealman, R. D., & Goldberg, S. R. (1982). Maintenance
of schedule-controlled behavior by intravenous injec-
tions of nicotine in squirrel monkeys. Journal of
Pharmacology and Experimental Therapeutics, 223(2),
402408.
Spring, B., Wurtman, J., Wurtman, R., El-Khoury, A.,
Goldberg, H., McDermott, J., & Pingitore, R. (1995).
Efficacies of dexfenfluramine and fluoxetine in prevent-
ing weight gain after smoking cessation. American
Journal of Clinical Nutrition, 62(6), 11811187.
Stapleton, J. A., Russell, M. A. H., Feyerabend, C.,
Wiseman, S. M., Gustavsson, G., & Sa we, U. (1995).
Dose effects and predictors of outcome in a randomized
trial of transdermal nicotine patches in general practice.
Addiction, 90(1), 3142.
Steenland, K. (1992). Passive smoking and the risk of heart
disease. Journal of the American Medical Association,
267(1), 9499.
Stolerman, I. P., & Jarvis, M. J. (1995). The scientific case
that nicotine is addictive. Psychopharmacology, 117(1),
210.
Strachan, D. P., Jarvis, M. J., & Feyerabend, C. (1989).
Passive smoking, salivary cotinine concentrations, and
middle ear effusion in 7 year old children. British
Medical Journal, 298(6687), 15491552.
Strachan, D. P., Jarvis, M. J., & Feyerabend, C. (1990).
The relationship of salivary cotinine to respiratory
symptoms, spirometry, and exercise-induced broncho-
spasm in seven-year-old children. American Review of
Respiratory Disease, 142(1), 147151.
Sutherland, G., Russell, M. A. H., Stapleton, J. A., &
Feyerabend, C. (1993). Glycerol particle cigarettes: A
less harmful option for chronic smokers. Thorax, 48(4),
385387.
Sutherland, G., Russell, M. A. H., Stapleton, J., Feyer-
abend, C., & Ferno, O. (1992). Nasal nicotine spray: A
rapid nicotine delivery system. Psychopharmacology,
108(4), 512518.
Sutherland, G., & Stapleton, J. A. (1994). Nasal nicotine
spray for dependent smokers. Journal of Smoking
Related Disorders, 5(Suppl. 1), 195201.
Sutherland, G., Stapleton, J., Russell, M. A. H., &
Feyerabend, C. (1995). Naltrexone, smoking behavior
and cigarette withdrawal. Psychopharmacology, 120(4),
418425.
Sutherland, G., Stapleton, J. A., Russell, M. A. H., Jarvis,
M. J., Hajek, P., Belcher, M., & Feyerabend, C. (1992).
Randomised controlled trial of nasal nicotine spray in
smoking cessation. Lancet, 340(8815), 324329.
Sutton, S. R. (1996). Can stages of change provide
guidance in the treatment of addictions? A critical
examination of Prochaska and DiClemente's model.
In G. Edwards & C. Dare (Eds.), Psychotherapy,
psychol ogi cal t reatments, and the addi cti ons
(pp. 189205). Cambridge, UK: Cambridge University
Press.
Thun, M. J., Day-Lally, C. A., Calle, E. E., Flanders, W.
D., & Heath, C. W. (1995). Excess mortality among
cigarette smokers: Changes in a 20-year interval.
American Journal of Public Health, 85(9), 12231230.
Tnnesen, P., Nrregaard, J., Mikkelsen, K., Jrgensen, S.,
& Nilsson, F. (1993). A double-blind trial of a nicotine
inhaler for smoking cessation. Journal of the American
Medical Association, 269(10), 12681271.
US Department of Health and Human Services (1988). The
health consequences of smoking: Nicotine addiction. A
report of the Surgeon General (DHSS Publ. No. (CDC)
88-8406). Washington, DC: US Government Printing
Office.
US Department of Health and Human Services (1989).
Reducing the health consequences of smoking: 25 years of
progress. A report of the Surgeon General. Washington,
DC: US Government Printing Office.
US Department of Health and Human Services (1990). The
health benefits of smoking cessation: a report of the
Surgeon General. Washington, DC: US Department of
Health and Human Services, Public Health Service,
Centers for Disease Control, Center for Chronic Disease
Prevention and Health Promotion, Office on Smoking
and Health.
US Department of Health and Human Services (1996). The
FTC cigarette test method for determining tar, nicotine
and carbon monoxide yields of US cigarettes (NIH
Publication No. 96-4028). Bethesda, MD: National
Cancer Institute.
US Environmental Protection Agency (1992). Respiratory
health effects of passive smoking: Lung cancer and other
disorders. Washington, DC: Author.
References 673
Wakefield, M., Gillies, P., Graham, H., Madeley, R., &
Symonds, M. (1993). Characteristics associated with
smoking cessation during pregnancy among working-
class women. Addiction, 88(10), 14231430.
Wald, N. J., & Hacksaw, A. K. (1996). Cigarette smoking:
An epidemiological overview. British Medical Bulletin,
52(1), 311.
Wald, N. J., Idle, M., Boreham, J., & Bailey, A. (1981).
Carbon monoxide in breath in relation to smoking
and carboxyhaemoglobin levels. Thorax, 36(5), 366369.
Wells, A. J. (1994). Passive smoking as a cause of heart
disease. Journal of the American College of Cardiology,
24(2), 546554.
West, R. J., Hajek, P., & Belcher, M. (1987). Time course
of cigarette withdrawal symptoms during four weeks of
treatment with nicotine chewing gum. Addictive Beha-
viors, 12(2), 199203.
West, R. J., Hajek, P., & Belcher, M. (1989). Severity of
withdrawal symptoms as a predictor of outcome of an
attempt to quit smoking. Psychological Medicine, 19(4),
981985.
West, R. J., Hajek, P., & Burrows, S. (1990). Effect of
glucose tablets on craving for cigarettes. Psychopharma-
cology, 101(4), 555559.
West, R. J., Hajek, P., & McNeill, A. (1991). Effect of
buspirone on cigarette withdrawal symptoms and short-
term abstinence rates in a smokers clinic. Psychophar-
macology, 104(1), 9196.
West, R. J., Jarvis, M. J., Russell, M. A. H., Carruthers, M.
E., & Feyerabend, C. (1984). Effect of nicotine replace-
ment on the cigarette withdrawal syndrome. British
Journal of Addiction, 79(2), 215219.
West, R. J., & Russell, M. A. H. (1985a). Effects of
withdrawal from long-term nicotine gum use. Psycholo-
gical Medicine, 15(4), 891893.
West, R. J., & Russell, M. A. H. (1985b). Pre-abstinence
smoke intake and smoking motivation as predictors of
severity of cigarette withdrawal symptoms. Psychophar-
macology, 87(3), 334336.
West, R. J., & Russell, M. A. H. (1987). Cardiovascular
and subjective effects of smoking before and after 24 h of
abstinence from cigarettes. Psychopharmacology, 92(1),
118121.
Wills, T. A., Pierce, J. P., & Evans, R. I. (1996). Large-scale
environmental risk-factors for substance use. American
Behavioral Scientist, 39(7), 808822.
Withey, C. H., Papacosta, A. O., Swan, A. V., Fitzsimons,
B. A., Ellard, G. A., Burney, P. G. J., Colley, J. R. T., &
Holland, W. W. (1992). Respiratory effects of lowering
tar and nicotine levels of cigarettes smoked by young
male middle tar smokers: II. Results of a randomized
controlled trial. Journal of Epidemiology and Community
Health, 46(3), 281285.
Woody, G. E., Cottler, L. B., & Cacciola, J. (1993).
Severity of dependence: Data from the DSM-IV field
trials. Addiction, 88(11), 15731579.
World Health Organization (1992). The ICD-10 classifica-
tion of mental and behavioral disorders. Clinical descrip-
tions and diagnostic guidelines. Geneva, Switzerland:
Author.
Wynder, E. L., & Graham, E. A. (1950). Tobacco smoking
as a possible etiologic factor in bronchogenic carcinoma:
A study of 684 proved cases. Journal of the American
Medical Association, 143, 329336.
Tobacco Smoking 674