Psychological Bulletin

1980, Vol. 88, No. 2, 370-405

The Smoking Problem: A Review of the Research and Theory

in Behavioral Risk Modification
Howard Leventhal Paul D, Cleary
University of WisconsinMadison School of Social Work, Rutgers University

This article reviews findings and examines theoretical implications of studies

concerned with initiation, maintenance, and therapy of cigarette smoking in chil-
dren and adults. The following conclusions are offered: (a) Recent increases in
success rates may be due to changes in the social environment that multiply the
action of previously unsuccessful procedures, (b) current interventions are based
on communication and behavioral models that ignore features unique to smoking,
(c) methodological refinements of current interventions are unlikely to signifi-
cantly increase success rates, (d) prevention studies should be directed toward
critical steps in the developmental history of smoking (e.g., preventing initial
attempts, facilitating negative interpretations of initial attempts, and retarding
regular usage), and (e) studies of cessation and withdrawal must consider find-
ings and theories of nicotine dependence. A hypothesis is presented to account
for the development of craving conditioned to internal and external cues, and
suggestions about how to eliminate the craving state are made.

Recent epidemiological and biomedical re-
search has clearly shown that smoking in-
creases risks of diseases such as lung cancer
(Cornfield et al., 19S9; Doll & Hill, 1964;
Hammond & Horn, 1954; Horn, 1968), coro-
nary heart disease (Doll & Hill, 1964; Doll &
Peto, 1976; Friedman, Dales, & Ury, 1979;
Gordon, Kannel, McGee, & Dawber, 1974;
Hammond & Horn, 1954; Horn, 1968), and
emphysema (Horn, 1968; U.S. Dept. of Health,
Education and Welfare, 1964, 1973); King
James's attacks on smoking over 3 centuries
ago (Eckholm, 1977) have been vindicated.
Despite the evidence, young people continue
to be recruited into the ranks of smokers, and
smokers continue to struggle with the problem
of quitting. This may seem all the more pe-
culiar, given that most smokers believe smok-
ing is hazardous; indeed, even in 1968 (Horn,
Note 1), 53% of smokers reported that they
would like to stop. That the antipathy does
not necessarily depend on scientific data is
Requests for reprints should be sent to Howard
Leventhal, Department of Psychology, W. J. Brogden
Psychology Building, University of Wisconsin, 1202
West Johnson Street, Madison, Wisconsin S3706.
evident from the response of Solomon Islanders
and Saharan Africans: Though uninformed of
the evidence on risks, they believe that smok-
ing is a health hazard and a practice unfit for
children (Damon, 1973). But they also stated
that they could not go without cigarettes even
for a day.
The clear demonstration of risk and the
desire of so many smokers to quit establish
the need for effective techniques to help people
stop smoking and to reduce the number of
persons who start. Despite the intensive re-
search efforts of epidemiologists, health edu-
cators, physicians, physiologists, psycholo-
gists, and sociologists on the origins and na-
ture of smoking and on ways of modifying it,
the procedures for bringing about smoking
reduction and cessation are still imperfect.
Indeed, it is unclear what mixture of social,
psychological, and pharmacological factors ac-
counts for the apparent strength of the smok-
er's dependence on his or her cigarettes
(Borgatta & Evans, 1968; Dunn, 1973; Frith,
1971b; Fuller, 1973, 1975; Fuller & Forrest,
1973; Hunt, 1970; Jaffe, 1976; Knapp, Bliss,
& Wells, 1963; McKennelL 1973; Peele, 1977;
Russell, 197la, 1971b; Schubert, 1965). What

Copyright 1980 by the American Psychological Association, Inc. 0033-2909/80/8802-0370500.75

370
 THE SMOKING PROBLEM
is clear is that it is now far more difficult to
control the behavioral risk factors that pre-
dict chronic disease (e.g., smoking, excessive
consumption of alcohol, or diets overly rich
in cholesterol) than it is to modify the risk
factors for infectious disease (Ebert, 1978);
there is no smoking swamp analogous to the
breeding ground of the anopheles mosquito
and no hypertension pump analogous to the
Broad Street pump in London that helped
identify contaminated water as the source of
cholera. Intervention aimed at risk factors
linked to behavior requires careful attention
not only to the intervention process but to the
processes involved in the targeted risk be-
havior (Leventhal, 1968, 1973; Leventhal &
Cleary, 1979) and to the fit between the two.
Lewin's statement that "there is nothing so
practical as a good theory!" (cited in Hovland,
Janis, & Kelley, 1953) appears to be an apt
summary of the need for a theoretical ap-
proach to the process of chronic disease risk
factor modification.
The present article has three goals. The
first is to review what we now know about the
intervention process. This entails briefly de-
scribing the basic approaches to intervention,
the assumptions they make about the smok-
ing response, and their successes and failures.
The second goal is to review what we now
know about the origins and maintenance of
smoking behavior, with particular attention
to the processes that underlie its initiation and
maintenance. The third and final goal is to
relate knowledge about the determinants of
smoking to theories of intervention and when
possible to suggest ideas for developing new
intervention procedures. The theoretical analy-
sis and integration of these areas may provide
important clues for resolutions to what now
seems an intractable problem. A touch, if not
a goodly dose, of chauvinism may well be re-
sponsible for the lack of theoretical develop-
ment in the area of smoking prevention and
cessation. People doing research on interven-
tion are usually unaware of findings from re-
search on initiation and maintenance. Indeed,
people doing research on one aspect of inter-
vention, such as community health programs,
are usually unaware of the findings from re-
search on smoking therapies, and those who
371
research therapies tend to be unaware of the
literature on community programs. Because
of such isolation, researchers have failed to
recognize the startling similarities between
findings from investigations of therapies,
small-scale communication programs, school
programs, and large community efforts. Thus
the results from a diverse set of research per-
spectives point to common issues in behavioral
risk factor intervention. We can profit from
the almost endless stream of smoking research
only if it addresses these key issues.
Intervention Studies
We review two classes of intervention study:
(a) those following a therapy or doctor-pa-
tient model for intervention and (b) those
following a public health, community, or pub-
lic opinion model. Therapy studies are time
and procedure intensive; thus it is often sup-
posed that they set an upper limit for the ef-
fectiveness of intervention. Public health stud-
ies provide insight into the possibility of
effective, publicly directed intervention efforts.
Both sets of studies need to be evaluated with
regard to both practical effectiveness (i.e., is
smoking reduced?) and theoretical significance
(i.e., do they provide insight into the inter-
vention process?). In our view the evidence
suggests that all methods have failed to pro-
duce sustained change; neither public health
programs nor face-to-face therapies have
proven effective in achieving long-term reduc-
tions in smoking when compared with control
cases or with the rates of spontaneous quitting
in the population at large. We also suggest
that these studies have added little to our
knowledge as to what is needed for a success-
ful intervention. The final section of our ar-
ticle addresses this issue in detail.
Therapy Model
In therapy studies smoker and therapist are
usually in direct dyadic interaction, though
group and self-treatment programs are also
used (Schwartz, 1969). In most therapy studies
the smoker assumes the role of a patient; he
or she is clearly motivated (at some level) and
has made a decision to stop smoking. In addi-
372 HOWARD LEVENTHAL AND PAUL D. CLEARY
tion, he or she anticipates some cost or un-
pleasantness to get to, stay in, and benefit
from treatment. Subjects in these samples
may be biased toward smokers who have tried
but failed to stop smoking on their own, but
they are also likely to be more motivated to
stop and more aware of the difficulty of chang-
ing their habit. There also is a strong passive
component to the patient role that may vitiate
efforts at effective self-control (Carlson, 197S).
Thus in comparison with public health stud-
ies, therapy studies are likely to deal with a
more homogeneous audience. Finally, the
"messages" used in many therapies involve
direct experience, for example, shock, inhala-
tion of warm smoke, or smoking on signal, as
opposed to the verbal-symbolic material to
which public health studies are generally
restricted.
Types of Therapies
Behavior therapies. The behavior therapies
treat the smoking response, not the smoker;
smoking is a habit that is to be modified.
Operand procedures are designed to detect the
environmental stimuli that control the smok-
ing response (Gutmann & Marston, 1967;
Levinson, Shapiro, Schwartz, & Tursky, 1971;
A. Miller & Gimpl, 1971; Ober, 1968) and
extinguish their control of the response. For
example, smokers are asked to carry a timer
that buzzes at random intervals and to smoke
whenever it signals. Smoking regularly to this
cue is supposed to attach the response to the
buzzer and detach it from environmental cues.
When the buzzer is discarded, so too is smok-
ing. In one study, subjects reduced smoking by
75% after 2 months of buzzer-controlled
smoking, but the success rate had declined to
43 % 6 weeks later (Shapiro, Tursky, Schwartz,
& Shnidman, 1971); there was no change in
untreated controls. Other procedures, such as
earning points toward a course grade or pro-
viding verbal rewards that one is doing well,
achieved roughly comparable effects31%
reduction after only 2 weeks (A. Miller &
Gimpl, 1971), a level of success that is repre-
sentative of other behavior therapies.
Sensitization and/or desensitization proce-
dures, the most commonly used of the be-
havior therapies, appear to focus on both con-
trolling the smoking response and eliminating
the urge to smoke that precedes it. In sensi-
tization therapies, a noxious stimulus, such as
an electric shock or the imagination of aver-
sive scenes (Barrett & Sachs, 1974; Conway,
1977), immediately follows the act of smoking
or the thought of a situation that induces
smoking (Berecz, 1971, 1972a, 1972b; Best &
Steffy, 1971; Carlin & Armstrong, 1968;
Steffy, Meichenbaum, & Best, 1970; von
Hilsheimer ; 1968; Whitman, 1972).
A common stimulus in smoking cessation
programs is, not surprisingly, cigarette smoke.
One technique is to induce aversion and/or
satiation by having a person smoke at two to
three times the normal rate (Best, Owen, &
Trentadue, 1978; Dawley, 197S; Lando, 1976;
Lando & Davison, 1975; Resnick, 1968;
Schmahl, Lichtenstein, & Harris, 1972; Wilde,
1964). Other research used artificially pro-
duced warm, stale, smoky air, sometimes in
combination with rapid smoking, to induce
aversion (Dawley, 1975; Lichtenstein, Harris,
Birchler, Wahl, & Schmahl, 1973; Wilde,
1964; see, also, the review by Pechacek, 1979).
The aim of these studies was to produce an
aversive state and to associate that state with
the act of smoking in the hope that the state
will generalize to the environmental cues that
stimulate smoking. The objective is identical
to that of programs that teach avoidance of
poisonous foods (Garcia, Hankins, & Rusiniak,
1974) and control of alcohol intake (Baker &
Cannon, 1979). Early studies using sensitiza-
tion therapies showed high initial rates of
success in quitting and smoking reduction
(60%-90% reductions in relation to base-
line) with reasonably good long-term effects
(e.g., 45%). More recent studies, however,
are less promising with respect to both the
short- and the long-term effectiveness of the
procedure (Elliott Si Denney, 1978; Glasgow,
1978; Lando, 1975, 1976; Sutherland, Amit,
Golden, & Roseberger, 1975); for example,
rapid smoking is not superior to other controls
and shows only 20% reductions at 6-month
follow-up.
Desensitization therapies attempt to elimi-
nate the distress and anxiety that stimulate
smoking by practiced relaxation in response
 THE SMOKING PROBLEM 373

to internal or situational cues that are stress- many of the investigations reported failed to
ful (Gerson & Lanyon, 1972; Hoenig & Reed, include control groups. The success rates in
1966; Kazdin & Wilcoxon, 1976; Koenig & these single-group studies range from 17%
Masters, 1965; Sutherland et al, 197S; Wag- to 38% quitting for 6 months or longer, sug-
ner & Bragg, 1970). gesting effects equal to those found with other
Other methods of behavior therapy include interventions (Burns, 1969; Burnum, 1974;
contracting, in which the subject pays a sum Handel, 1973; Pincherle & Wright, 1970;
of money to the experimenter and has it re- H. 0. Williams, 1969). Studies using controls
turned if he or she succeeds in cutting down, also show varying rates, for example, 33%
and self-monitoring procedures, in which the versus 9% quitting, as measured at a 6-month
subject keeps records of varying degrees of follow-up, in experimental and control groups,
complexity for each cigarette smoked (Karoly respectively (J. S. Mausner, Mausner, & Rial,
& Doyle, 197S; Leventhal & Avis, 1976; Mc- 1968) and 10.3% to 19.1% quitting, as mea-
Fall, 1970; McFall & Hammen, 1971). sured at 1 year, in control and maximal impact
Psychological therapies. Psychotherapy and experimental condition in a careful random-
counseling claim to focus on the total patient ized trial conducted by Russell, Wilson, Tay-
and use verbal procedures rather than direct lor, and Baker (1979), These studies also
experience. Controlled studies of traditional reported substantial differences between physi-
therapies (Schwartz & Dubitzky, 1967) are cians (Pincherle & Wright, 1970; Russell et
relatively rare, though a therapy group is al,, 1979) and between the sexes, males quit-
sometimes included as a condition in studies ting and cutting down more than did females
of behavior therapy (Gerson & Lanyon, 1972; (Burnum, 1974; Handel, 1973; H. 0. Wil-
Jenks, Schwartz, & Dubitzky, 1969; Ober, liams, 1969), as well as more difficulty with
1968). withdrawal symptoms in smokers scoring high
A possible disadvantage to the psychothera- on scales of neuroticism (Burns, 1969).
peutic approach is that the therapist (source) Unfortunately, there is little theoretical
can have an unpredictable effect on the out- analysis and perhaps even less empirical data
come (Kiesler, 1966; Locke, 1971). Jenks et to suggest how to strengthen these effects.
al. (1969) reported that patients failed to There is some reason to believe that inter-
stop smoking if their life situation contained vention may be more effective at critical junc-
factors the therapist regarded as insurmount- tures, such as, when a smoker is pregnant
able barriers to successful quitting; this oc- (Barec, MacArthur, & Sherwood, 1976) or
curred even though these factors were unim- symptomatic with chest disease (Burns, 1969;
portant for patients of other therapists. Thus H. 0. Williams, 1969). At least two factors
a fair evaluation of traditional therapy pro- make study in this area of critical importance.
cedures requires that therapists hold accurate First, the number of smokers that can be
beliefs about smoking as well as be masters reached is large, and the cumulative effect
of the therapy procedures (Kiesler, 1966; could be substantial (Russell et al,, 1979),
Koenig & Masters, 1965; Marston & McFall, Second, the interventions so far used have
1971). This problem seems less serious for been relatively weak, consisting of serious ad-
behavior therapies in which the therapist's vice and pamphlets, and the time per patient
behavior is more closely circumscribed. is typically brief, from a suggestion to stop to
Physician intervention. White, Williams, 7 minutes. Both the theoretical and practical
and Greenberg (1961) estimated that 750 out payoffs appear to be potentially great.
of 1,000 adults are ill during an average month Clinics. Clinics (Schwartz, 1969) have been
and that 2SO of them will visit a physician. used to provide relationship and group ther-
Given the potential coverage, it is of obvious apy with (Ejrup, 1964) or without a drug
importance to determine whether the primary component. Examples range from the 5-day
care physician or internist can be an effective treatment plan of the Seventh-day Adventists
agent for smoking reduction. Little research (combining educational material, threat films,
has been done on this problem, however, and buddy support systems, etc,) to clinics run
374 HOWARD LEVENTHAL AND PAUL D. CLEARY
in a wide variety of medical and community
settings (Bozzetti, 1972; Dubitzky & Schwartz,
1968, 1969; Jenks et al, 1969; Marrone,
Merksamer, & Salzberg, 1970; B. Mausner,
1966; Schwartz & Dubitzky, 1967; Tamerin,
1972; West, Graham, Swanson, & Wilkinson,
1977). Early studies of group therapy and
drug treatment reported success rates of 76%
of the smokers quitting for the short run and
31% for the long run. Later studies included
control conditions, and showed no advantage
of drug over placebo, implying that the ef-
fect was at a behavioral level (e.g., Bartlett &
Whitehead, 1957; Edwards, 1964). Recent
clinic studies promise no greater success than
earlier ones. Initial cessation rates are high,
but so is the rate of return to smoking (Jacobs,
1972; West et al., 1977).
Hypnosis and sensory deprivation. Finally,
there are numerous studies on procedures such
as hypnosis (M. M. Miller, 197S; Pederson,
Scrimgeour, & Lefcoe, 1975; Perry & Mullen,
1975). This technique has been used for smok-
ing modification, often incorporating aversion
and desensitization treatments, though some
hypnotic approaches simply have the smoker
repeat short health messages such as "My
body is a machine; I live in my body; I must
take care of my body; I must not smoke"
(Perry & Mullen, 1975). Investigators report
high success rates with hypnosis, such as 90%
abstention rates 1 month and 68% 1 year
after starting therapy (M. M. Miller, 1975).
Most of these studies are clinical reports, how-
ever, and do not give data on the number of
successes relative to patients treated, criteria
for success, and comparable results for un-
treated control groups (Johnston & Donoghue,
1971).
In sensory deprivation studies (Suedfeld &
Best, 1977; Suedfeld & Heard, 1974; Suedfeld,
Landon, Pargament, & Epstein, 1972), the
smoker may spend 24 hours in bed, in a dark,
sound-reducing chamber, with no objects avail-
able, and eat by sucking liquid through plastic
tubes. Suedfeld and Ikarcl reported an 88%
reduction in smoking postdeprivation, and 1
year later these subjects were smoking 48%
less than they had before the session.
Key findings. One must be careful, of
course, in making comparisons among therapies
using data from different studies, as they dif-
fer in procedures for subject selection, dropout
rates, criteria for success, and so forth. Ther-
apies can be compared only in those studies in
which investigators randomly assigned sub-
jects to different treatments; there is high
internal validity to comparisons of treatments
in these studies, even if the external validity
(generalization to other populations and set-
tings) is low (Campbell & Stanley, 1963).
Despite the limitations, we feel that four
findings stand out. First, whether the criterion
be quitting or significant reduction, there is
an impressive decrease in smoking during
treatment. The reviews of the pre-1970 litera-
ture (Bernstein, 1969, 1970; Keutzer, Lich-
tenstein, & Mees, 1968; Lichtenstein &
Keutzer, 1971; Schwartz, 1969), the report
by Hunt and Bespalec (1974) based on a
summary of all studies listed in Psychological
Abstracts and Cumulated Index Medicus from
1968 to 1973, and the more recent summaries
(Hunt & Matarazzo, 1973; Lichtenstein &
Danaher, 1975; Zane, Kunze, & Kunze, 1974)
all agree that initial results are impressive.
Second, there is a relatively high dropout
rate, often reaching 50% of those included in
the initial sample. Thus many outcome reports
are inflated, as dropouts from therapy are ex-
cluded from the denominator when success
rates are computed. For example, Schwartz
(1969) reported that in the Institute-Perma-
nente Smoking Control Research Project, the
end-of-treatment success rate would increase
from 47.2% to 70% if only those subjects
completing at least half of the treatment were
counted. The success rate at the 1-year fol-
low-up would change from 27.8% to 45%
with similar adjustments.
Third, therapy works well in helping people
to stop smoking but does less well in keeping
them stopped. Whereas most backsliding oc-
curs within 6 months, it continues with inex-
orable force for 12 months till there is a resid-
ual of quitters and smoking reducers of 10%
to 25% of the pretherapy base level although
figures of 35%. to 45% are occasionally
reported.
Fourth, success rates for different therapies
are not markedly different; it is simply better
to do something than nothing. The similar
 THE SMOKING PROBLEM
outcomes across therapies could occur because
each therapy affects a different group of smok-
ers. On the other hand, the therapies could
work about equally well with similar people in
each sample studied because they share com-
mon components such as motivated volunteer-
ing, behavioral structuring, and self-monitor-
ing (McFall & Hammen, 1971). At this point
no particular therapy stands out as vastly su-
perior to the others, and simple interventions
by medical practitioners may well match the
effectiveness of more complex therapies.
Given the poor long-term results, one might
ask whether the effects of different therapies
in combination are superior to the effects of
each used alone. Recent data suggests that
combinations of therapeutic procedures con-
taining both motivational and skill-training
components produce more favorable outcomes,
though the increments are not striking (Dela-
hunt & Curran, 1976; Elliott & Denney, 1978;
Lando, 1977; Pederson et al., 1975; Suther-
land et al., 197S). In some instances, however,
combinations produce no positive gain over
single therapies (Danaher, 1977) and may
even decrease effectiveness (Lamontagne, Gag-
non, & Gaudette, 1978). Best (197S) com-
bined aversion therapy with three other pro-
cedures: (a) focusing treatment on internal
or external cues; (b) punishment, by smoking
at double the normal rate on a clay following
an infraction; and (c) presenting an attitude
change communication either before or after
behavior change. None of the three procedures
produced main effects or interacted with aver-
sion therapy. Two of the factors (treatment
focus and timing of attitude change) inter-
acted significantly with client characteristics
in determining treatment outcome, but the
matching of the intervention factors to sub-
ject personality dispositions did not augment
the impact of the aversive treatment; rather,
it prevented the added components from re-
ducing the impact of treatment relative to an
aversive conditioning only control. Similarly,
in two studies of sensory deprivation (Sued-
feld & Ikard, 1974; Suedfeld et al., 1972),
there was no lasting increment in smoking re-
duction as a result of adding a procedure (ex-
plicit persuasive messages) to the basic treat-
ment. Several studies here found decreases in
375
the effectiveness of antismoking treatments
when they are followed by phone calls or
booster sessions to reinforce quitting (Best,
Bass, & Owen, 1977; Elliott & Denny, 1978;
Kapel, 1974).
The varied outcome of combined therapies
may seem discouraging, but it should not be
unexpected, as most of the studies compared
and combined treatments on an empirical basis
(e.g., Elliott & Denny, 1978); the theories
used to design these treatments are theories
of intervention, not theories of smoking. Al-
though all of the techniques attempt to in-
fluence the person's motivation to quit and
develop skills to break the habit, both moti-
vation and skills training are conceptualized
in an overly simplistic way. For example, mo-
tivation is usually seen as a combination of
undefined internal desires and various external
commitments and contracts as well as the de-
sire to control the impulse to smoke. Such
impulses are usually defined in vague and gen-
eral terms such as addiction, anxiety, or lack
of health concern. Rarely is any attention paid
to the complex psychological and physiologi-
cal processes underlying smoking and the tre-
mendous individual differences in these pro-
cesses. Skill training usually focuses on tech-
niques such as step-by-step self-management
programs (e.g., Conway, 1977), how to make
smoking inconvenient, attaching smoking to
some new stimulus such as a buzzer, counting,
and so forth and ignores or fails to identify
the multifaceted stimuli actually controlling
the behavior. Unless the range, frequency,
periodicity, and strength of the various stim-
uli controlling a person's smoking are identi-
fied and dealt with, the skills taught in any
intervention program will be only partially
relevant to the person's problems and may in
fact lure the person into a false sense of se-
curity about his or her ability to control the
habit. It could be counterproductive to teach
people skills to stop smoking if they learn
that even with professionally taught tech-
niques they are incapable of controlling their
urge to smoke. This need not happen if the
participant is appropriately prepared and so is
led to recognize the trial-and-error or experi-
mental aspects of the procedures.
376 HOWARD LEVENTHAL AND PAUL D. CLEARY
Public Health Model
The public health model is clearly a mass
communication model. The hope is to find a
cost-effective means of reducing the smoking
epidemic. The basic assumption appears to be
that repetition of the antismoking message
over multiple media will attract attention,
lead to its learning, change attitudes, and
change behavior. If advertising does not work
in this straightforward way, why then do
cigarette companies, auto manufacturers,
pharmaceutical houses, and others spend bil-
lions on advertising? Unfortunately, this
simple compliance model (Kelman, 1958) of
media effects does little more than hold out
false hope. Our review of the literature from
laboratory communication studies and school
and community studies shows how the model
has misdirected media efforts, making these
intervention efforts even less effective than
they should be.
Types of field study. Studies of antismok-
ing programs in this area fall into one of three
categories: (a) small-scale communication ex-
periments, (b) studies in schools, and (c)
studies in communities. These studies vary
greatly in the degree to which they provide
outcome statistics, for example, figures on
number of smokers quitting in experimental
versus control conditions, and/or insight into
the social and psychological processes under-
lying continuance and change in smoking
behavior.
Small-scale communication studies. The
majority of the studies carried out in a mass
communication framework on changing health
attitudes and behavior have examined two
kinds of message content: (a) information
that is fear arousing (scenes of lung surgery,
death from tetanus, etc.) and (b) informa-
tion that provokes a sense of personal vul-
nerability to the illness threat. Findings from
these studies show that the process of influ-
ence is far more complex than that pictured
by the compliance model. First, studies on
tetanus shot taking, X ray taking, and smok-
ing cessation conducted by our group in the
mid 1960s (Dabbs & Leventhal, 1966; Leven-
thal, Singer, & Jones, 196S; Leventhal &
Watts, 1966; Leventhal, Watts, & Pagano,
1967) indicate that vivid threat messages,
compared with milder messages, generate
stronger attitudes and intentions favorable to
stopping smoking. But although these atti-
tudes and behavioral intentions may be strong
immediately after the message, they are not
persistent; the attitudes and related inten-
tions dissipate as the emotion associated with
the message weakens (Leventhal & Niles,
1965).
It was also found that strong fear messages
might stimulate undesirable reactions such as
avoidance of threatening situations; for ex-
ample, not taking X rays (Leventhal & Watts,
1966) and not exposing oneself to health
information.
Messages conveying information on per-
sonal vulnerability to damage, a variable
identified by the health belief model as a
central mediator of health decisions (Hoch-
baum, 1965; Leventhal, Hochbaum, & Rosen-
stock, 1960; Maiman & Becker, 1974; Rosen-
stock, 1974), appear to be successful in stim-
ulating feelings of personal vulnerability, thus
strengthening antismoking attitudes and re-
ducing smoking (Horn, 1960; Janis & Mann,
1965; B. Mausner & Platt, 1971; Watts,
1968). But these messages can have unex-
pected effects when combined with informa-
tion on threat; whereas the independent ef-
fects of each factor are often favorable, their
joint effects may be less than that of either
alone (Leventhal, 1970; B. Mausner & Platt,
1971; Niles, 1964; Watts, 1968). Combining
these factors seems to stimulate the belief
that protective action is impossible (Selig-
man, 1975) by undercutting feelings of com-
petence.
Studies in our laboratory (Leventhal, 1974)
also showed that although vivid threat mes-
sages aroused more fear and stronger inten-
tions to stop smoking, these changes did not
lead to behavior change in the absence of
specific action plans. Action plans specified
the details of the recommended response;
for example, when, where, and how to get a
chest X ray or tetanus shot, including exact
streets, turns, and landmarks, how to control
the urge and how to regulate external induce-
ments to smoke. Subjects who received spe-
cific instructions on how to control the smok-
ing habit along with a high- or a low-fear
message showed significantly reduced smoking
 THE SMOKING PROBLEM
at a 3-month follow-up; the uninstructed
groups had reverted to baseline levels. When
presented without a fear message, the specific
action plans had no effects on attitudes or
behavior. Both motivation and action plans
are necessary for action. The specific action
plans apparently serve to insure the carry-over
of attitudes to action, developing feelings of
competence. Other factors that might be im-
portant in developing an action structure (D.
Cartwright, 1949) include the act's relevance
to the goal and reference group support for
the goal (Fishbein, 1967).
Small-scale communication studies have also
demonstrated that the impact of persuasive
health messages differs with the population
studied. For example, educational level alters
response to threat messages: Students in col-
lege-directed programs do not become more
persuaded of the need to take protective ac-
tion as messages become more fear provoking;
students in noncollege programs do (Haefner,
196S; Singer, 196S). Response to increasingly
threatening communications is also moderated
by self-esteem: Subjects low in esteem may
fail to act when made overly fearful (Korn-
zweig, 1968) though efforts to enhance the in-
dividual's sense of competence before exposing
him or her to threat can overcome this bar-
rier (T. J. Rosen, 1970). The esteem factor
may also be related to the helplessness phe-
nomenon discussed earlier. Individual dif-
ference variables may be more or less impor-
tant at different stages of the processing
sequence. Some individual differences may be
more important with regard to stimulating
motivation and decisions to quit smoking,
others may be more important with respect to
planning and action, and still others may be
more important with respect to establishing
sustained behavioral change.
Little research has been directed to other
types of information that might increase the
desire to stop smoking, such as economic fac-
tors (cost of cigarettes, of maintaining health,
and of treating diseases resulting from smok-
ing), positive emotions or humor (Evans,
Rozelle, Lasater, Dembroski, & Allen, 1970),
and messages that introduce special effects on
the self-image of the recipient (Evans, 1976).
B. Mausner (1973), for example, found that
377
one must integrate information about a wide
variety of perceived outcomes of smoking to
predict whether subjects will cut down or
quit. His data showed that people make the
decision to stop smoking not only because
they have a heightened fear of the conse-
quences of continuing to smoke but also
because they have an increased expectation of
the benefits of stopping.
Each type of appeal may have its own
specific pattern of effects on attitudes, inten-
tions, and behaviors, and each may interact
in interesting and sometimes unexpected ways
with other appeals, depending on the char-
acteristics of the source and audience. More
detailed and precise theoretical models are
needed to deal with these complexities (Lev-
enthal, 1974; Peak, 19SS; Rosenberg & Abel-
son, 1960).
School studies. The school studies are of
special interest because of the often expressed
hope that risk prevention will be more effec-
tive than risk reduction (Leventhal, 1973).
As early as 1968, a report by Merki, Creswell,
Stone, Huffman, and Newman mentioned that
over SO studies of antismoking programs had
been conducted in school systems. More re-
cently Thompson (1978) reviewed twice that
number (see, also, Green, 1979), Some used
simple posttest designs, with questionnaires
given to assess attitudes and behavior in
youngsters after an antismoking program
(Morison & Medovy, 1961; Morison, Me-
dovy, & MacDonell, 1964; Swinehart, 1966).
Others used complex experimental designs,
with programs varying on several factors,
either with a single school assigned to each
type of communication program and com-
pared with a control (nonprogram) school
(Monk, Tayback, & Gordon, 196S) or with
several schools or classes randomly assigned
to both experimental and control conditions
(Evans, 1976; Holland & Elliott, 1968; Horn,
1960; Merki et al, 1968; Piper, Jones, &
Matthews, 1970, 1971, 1974; Rabinowitz &
Zimmerli, 1974); the latter procedure per-
mitted an estimate of program effectiveness
independent of the particular classroom or
school.
The programs are varied. The most limited
might include lectures by the school principal
or a physician and posters displayed about the
378 HOWARD LEVENTHAL AND PAUL D. CLEARY
school. More intensive programs add threat
films, teacher participation (e.g., introducing
material on smoking into science and hygiene
classes; Morison et al., 1964), and student
participation (e.g., planning communication
content, poster construction, antismoking
essays, and group discussion).
These programs are generally successful in
teaching students about the hazards of smok-
ing; those participating in the programs
acquire more knowledge than do unexposed
students (Jefferys & Westaway, 1961; Monk
et al., 1965; Morison et al.. 1964; Piper et al.,
1974; Rabinowitz & Zimmerli, 1974). In
addition, antismoking attitudes are usually
stronger in the schools with the program than
in control schools. These differences, however,
are not always statistically reliable, and when
reliable they are often small.
Unfortunately, behavioral effects are usually
nonexistent, and when they do appear they are
usually of small magnitude. For example,
Horn (1960) reported roughly 10% less
smoking in a school given messages about the
potential future dangers of smoking. Piper et
al. (1971) reported 5% ( f o r females) to 1%
(for males) lower smoking rates in experi-
mental than in control schools, and Rabino-
witz and Zimmerli (1974) reported about an
\lc/c drop in the experimental and a 1% in-
crease in the control schools. In some studies
conducted with very young children, there are
indications of a drop in the rate of recruit-
ment to smoking (Evans, 1976; Merki et al.,
1968); the difference here is also roughly
lO^o fewer students recruited to smoking.
Perry, McAlister, and Farquhar (Note 2) also
reported that there were 5%&% fewer stu-
dents who smoked in treatment groups than in
control groups. The Evans (1976), Rabino-
witz and Zimmerli (1974), and Perry et al.
(Note 2) studies are of special interest, as
their programs were initiated with very young
children.
The outcomes of these studies are clearly
small in magnitude; indeed, Thompson
(1978) suggested that none of the programs
are effective. Is there reason to anticipate any
substantial increase in the effectiveness of
such programs in studies of higher quality?
The answer to this question is likely to be no,
if quality is equated with technical sophistica-
tion or higher cost. The issue is what type of
information or change in the social context
is necessary to achieve impact, not how to
package or present the information. The stud-
ies discussed attempted to build antismoking
motivation through an emphasis on health
risks and attempted to shape behavior using
models and role playing to develop action
plans for dealing with the motivation to
smoke. For example, Evans's (1976) inno-
vative school program is based on concepts
such as role playing specific action plans to
innoculate oneself against later peer pressures
(Leventhal et al., 1967; McGuire, 1964).
However, none of the programs reviewed deal
extensively with the motivations to smoke,
such as the need to be accepted (Hill, 1971),
achieve status and self-definition (Ferguson,
Freedman, & Ferguson, 1977; Newman,
1970b) or control anxiety and distress (Ikard
& Tomkins, 1973). Only recently has anyone
attempted to make vivid the immediate im-
pact of smoking on the body (Mitchell, 1978;
C. L. Williams, Arnold, & Wynder, 1977), and
rigorous tests of these procedures are lacking.
What is more, the programs fail to provide
ways of sustaining nonsmoking attitudes and
behaviors, by tying them either to more
fundamental self-concepts or to social and
group norms (Salber, Freeman, & Abelin,
1968).
It appears that teacher and student involve-
ment can enhance program effectiveness, but
nowhere to the degree hoped for (Morison et
al., 1964). Also, although many efforts in
schools are motivated by the belief that pre-
ventive efforts with children will be more
effective than intervention efforts with adults,
it is conceivable that prevention programs
merely delay the onset of smoking rather than
actually reduce the proportion of youngsters
who become smokers. We have little reason to
believe that children are more easily influ-
enced than adults or that the influence will
carry over to the later years (Leventhal,
1973). In fact, studies in Canada (Piper et
al., 1970) and Portland, Oregon (Horn,
1960), suggested that the effect of programs
in the Sth through 10th grades all but disap-
pear by the llth and 12th grades.
One important benefit of these studies is
that they have provided us with a good deal
 THE SMOKING PROBLEM
of descriptive information about the factors
associated with the initiation of smoking.
Examples of such variables are social class
(Borland & Rudolph, 1975; A, Cartwright,
Martin, & Thompson, 19S9; Leeder & Wool-
cock, 1973), use of other drugs (Kandel,
1973, 1975), the image of what a "smoker"
is (Bland, Bewley, & Day, 1975), and pa-
rental smoking (Baer & Katkin, 1971). They
have also provided information about the
process of becoming a heavy smoker (e.g.,
Salber et al, 1968; Salber, Goldman, Buka,
& Welsh, 1961; Salber, Reed, Harrison, &
Green, 1963). Unfortunately, the studies
lacked an adequate conceptual base, and thus
their contribution to a truly effective science
of prevention and intervention has been lim-
ited (Evans, Henderson, Hill, & Raines,
1979).
Community studies. Evaluations of a
number of community antismoking efforts in
Scotland (McKennell, 1968) show essentially
no change from pre- to postcampaign assess-
ments of attitudes and smoking behavior in
the program community (A. Cartwright et
al., 1959).
Perhaps the single largest community study
to date is the Stanford Heart Disease Preven-
tion Program (Maccoby & Farquhar, 1975;
Meyer, Nash, McAlister, Maccoby, & Far-
quhar, 1980; Stern, Farquhar, Maccoby, &
Russell, 1976) that studied three communities,
one of which served as a control, a second of
which was exposed to a mass media campaign
on heart disease risk factors including smok-
ing, and a third of which received a mass
media campaign and face-to-face instruction
for selected high-risk persons. Although the
study is classified as a community study, the
behavioral therapies in the intensive treat-
ment condition were traditional behavior
therapy interventions (Meyer & Henderson,
1974), and the intensive treatment results are
better compared with those of therapy studies
than with those of studies in which commu-
nity programs (media, use of existent groups,
etc.) were the vehicles for intervention.
At a 2-year follow-up, there was a 17%
reduction in the number of smokers (relative
to base levels) in the media plus face-to-face
instruction community, a 5% reduction in the
379
media-only community, and a 12% increase
in the control community. The difference be-
tween the intensive instruction and control
community was statistically significant, but
the difference between the mass media and
control community was not.
Among high-risk participants (risk defined
by a multiple logistic risk function), 20 out
of the 40 smokers quit for 2 years following
exposure to both media and intensive instruc-
tion, whereas only 15% of the smokers quit
in the control community (Meyer et al.,
1980). This 35% difference is large but not
substantially greater than that reported in
other therapy studies (Leventhal, Safer,
Cleary, & Gutrnann, 1980; Schwartz, 1969).
A recent study in Belgium (Kornitzer, De-
Backer, Dramaix, & Thilly, 1980) investi-
gated the impact of a health program on
smoking, blood pressure, serum cholesterol,
and so forth in randomly selected and high-
risk male factory workers. Thirty factories
were randomly assigned to intervention and
control conditions, and 16,222 male workers
were studiedthe men were about equally
distributed in the two groups. Among the
workers of high risk, 18.7% stopped smoking
in the intervention group, and 12.2% re-
ported stopping in the control group, a dif-
ference that is significant, given the large
sample. There were no differences between
experimental and control groups for the ran-
dom-sample (non-high-risk) participants. The
intervention material (TV, booklets, medical
advice) does not seem to have been designed
to achieve maximum behavior change, and it
is difficult to tell why this group achieved
effects for reductions in serum cholesterol
similar to those of the Stanford program
while doing so much more poorly for smoking.
It is important to compare the results of
community studies with prior expectations
lest we too quickly regard these efforts as
failures and overlook the lessons they teach.
We know from past research that the effect of
media on anything except minor decisions
among brands is likely to be small (Katz &
Lazarsfeld, 1955; Klapper, 1961; O'Keefe,
1971; Weiss, 1969). For most topics studied,
for example, changes in political attitudes
and behavior (Klapper, 1961), movie going,
380 HOWARD LEVENTHAL AND PAUL D. CLEARY
or prescribing of medications by physicians
(Katz & Lazarsfeld, 1955), media techniques
are less effective in changing beliefs or be-
havior than is face-to-face communication in a
laboratory setting. There are at least four
reasons why this is the case. First, exposure
to the message, assured in a face-to-face set-
ting, is uncontrollable in the field. Second,
media messages are usually symbolic and
abstract and do not focus on the concrete
experiences that are salient to the audience.
With few exceptions (e.g., Evans, 1976; Horn,
1960; Meyer et al., 1980), researchers have
failed to include specific action instructions to
ensure that motivational effects are carried
forward into performance. Third, messages
are often developed on the basis of hunches,
with minimal prior experimental assessment
or formative evaluation of actual interest in
and response to the message by the audience
of interest (Scriven, 1967). Fourth, the con-
text of communication is different for media
studies than for therapy or laboratory com-
munication studies. In media studies the audi-
ence may be alone at home, among friends,
or in school, and the context and groups may
interfere with or be supportive of message
acceptance. Social contexts, the individual's
reference, and face-to-face groups provide
important anchors for his or her beliefs and
action (Weiss, 1969). When those group
memberships and their associated norms are
salient, influence by media is usually weak
(Bauer & Bauer, 1960; Kelley, 1958; Kel-
ley & Volkart, 1952).
As could be expected, the community stud-
ies show that comrnunitywide campaigns have
had only a minor impact on smoking. The
most dramatic example of the limitations of
community programs is Ryan's (1973) report
of the cold turkey project in Greenfield, Iowa.
In association with United Artists's filming of
Cold Tiirkey on location in Greenfield, the
city council voted August 8th, 1969, Cold
Turkey Day, declared it a holiday, had smok-
ers sign pledges to quit, advertised the dangers
of smoking and virtues of quitting, installed
no smoking signs, removed tobacco from
stores, and had a 30-day follow-up honoring
the quitters. Seven months later Ryan inter-
viewed 1,385 respondents and found that only
3.9% of the active female smokers and 14.27c
of the active male smokers were abiding by
their nonsmoking pledge. As Leventhal et al.
(1980) noted, most community studies give
us little more than outcomes for smoking. It
is the rare study that tells us about the so-
cial-psychological factors associated with the
initiation and cessation of the habit (e.g., Mc-
Kennell, 1973).
Indeed, we know far more about the process
of media influence on individual opinion lead-
ers and the interactions among persons and
groups in establishing the stages that led
farmers to adopt new seed and forms of crop
rotation (Rogers & Shoemaker, 1971) than
we know about the impact of these same
processes on an individual's decision and abil-
ity to quit smoking.
Overall Evaluation of Intervention Efforts
From the practical point of view, when the
goal was to demonstrate the effectiveness of
techniques to discourage new smokers and
encourage quitting, the studies reviewed dem-
onstrated that specific, isolated programs must
be regarded largely as failures. What is needed
is innovative studies that provide more in-
sight into processes involved in the initiation
and cessation of smoking (see Leventhal et
al., 1980; Lichtenstein, 1971). Past studies
were conducted in a communication frame-
work, a communicator delivering a message
over a particular medium to a particular recip-
ient, and focused on outcome, that is, number
of people quitting or cigarettes reduced. As a
whole the studies make clear the incorrect-
ness of the common sense view of communica-
tion as a process in which a message is re-
peated by an authoritative source (TV star,
famous athlete, Nobel laureate, doctor) a
sufficient number of times (a) to capture at-
tention, (b) to produce learning of the con-
tent, (c) to change attitudes, and (d) to
change behavior. This compliance model of
the communication process (Kelman, 1958)
sees the steps from attending to behavior
change as an inexorable progression. It leaves
few degrees of freedom for complex processes
in message receivers or their social context
and does not accurately describe what we
know about these processes. Because this
 THE SMOKING PROBLEM
model focuses on the trappings of the act of
communication and not the process, it should
come as no surprise that major conceptual
and substantive problems concerning the
process of intervention and the processes
underlying smoking have, to a large extent,
been ignored.
There are several ways in which the com-
munication model is deficient in describing
the intervention process. First, nearly all in-
tervention efforts reviewed involved a single
effort or a series of efforts over a relatively
short span of time. Second, intervention ef-
forts have usually targeted the individual.
This is true for school and community studies
as well as for therapy studies. The involve-
ment of peers, groups, family, and so forth is
generally minimal, and little attention is paid
to the way these group and social factors are
associated with individual change. It is usually
assumed that intensive, individual therapy
can generate the most significant impact on
smoking, but the opposite may in fact be true.
Intensive efforts to alter societal, community,
and group values and norms might be more
effective in producing change in smoking be-
havior. Restricting smoking in public build-
ings, requiring nonsmoking sections in air-
planes and restaurants and changing attitudes
about trie rights of nonsmokers might do more
to change smoking habits than intensive pro-
cedures directed at individuals. The Stanford
investigation has taken a step toward looking
for interactions between media and intensive
therapy procedures (Meyer et al., 1980).
The available research tells us little about
the perception of community norms and val-
ues and how such perceptions affect the smok-
er's desire to smoke, motivation to stop, abil-
ity to stop, and ability to remain a nonsmoker.
The school and community studies should
have made a major contribution to our under-
standing of these normative and group pro-
cesses but they have not. Their failure to do
so reflects a focus on outcome as opposed to
process. The practical demands for solving the
problem build hopes for quick solutions
through media efforts and detracts from ef-
forts to trace the complex social processes
involved.
Two kinds of data support the contention
that investigators have been seriously negli-
381
gent in ignoring changes in community values
for smoking reduction and that these changes
may be the primary levers for initiating and
maintaining smoking cessation. The first is a
complex statistical analysis of cigarette con-
sumption over the years immediately preced-
ing and following the surgeon general's report.
The second is national survey data collected
by the National Clearinghouse for Smoking
Research (U.S. Dept. of Health, Education
and Welfare, 1973). Warner (1977) showed
that although major events in the campaign
against smoking, such as the surgeon general's
report (U.S. Dept. of Health, Education and
Welfare, 1964), may have caused only a 4%-
5% transitory decrease in annual per capita
consumption, the cumulative effects are more
dramatic. He estimated that in the absence
of the antisrnoking campaign, per capita con-
sumption would have exceeded its actual 1975
value by 20% or 30%. This is a conservative
estimate, as it ignores other behavior changes
such as the shift to low-tar and low-nicotine
cigarettes. The National Clearinghouse for
Smoking Research has reported findings from
a pair of U.S. national studies showing the
impact of the surgeon general's report on
smokers. Of a representative sample of smok-
ers first interviewed in 1964, 80% were rein-
terviewed about 20 months later. Of this
group, 52.9% considered quitting, 34.4%
tried, 15.5% achieved short-term success, and
7.1%) achieved long-term success (minimum
of 3 months). More recent data suggest short-
and long-term success rates roughly double
those reported earlier (Horn, Note 3; see,
also, Swinehart & Kirscht, 1966). Panel data
and the national survey data provided by the
National Clearinghouse for Smoking Research
suggest that the continuing antisrnoking ef-
fort could have both cumulative effects and
a number of unexpected indirect effects; for
example, these campaigns stimulated smokers
to switch to filter cigarettes, led to the lower-
ing of tar and nicotine levels (Gori, 1976),
perhaps making it easier for more recently
recruited smokers to quit, and stimulated the
militancy of nonsmokers for ordinances re-
quiring nonsmoking sections in aircraft, res-
taurants, and so forth. All of these factors may
intensify the pressures on smokers to quit or
382 HOWARD LEVENTRAL AND PAUL D. CLEARY
reduce their level of smoking (see Eisinger,
1971).
These historical changes may also have
important effects on the outcomes of specific
intervention experiments, as it may be easier
to induce and sustain smoking change now
than before. The usual experimental design,
for example, therapy versus control or experi-
mental versus control community, does not
allow the investigator to detect these effects,
as they may interact with the treatment.
Historical changes may be necessary but not
sufficient conditions for improved treatment
outcomes. The changes in attitude and knowl-
edge may also encourage smokers to experi-
ment more with quitting, and participants in
experimental treatments may be more likely
to try a variety of tactics when they experi-
ence difficulty in maintaining smoking reduc-
tions. Experimenting with different procedures
over a period of time may achieve quitting
rates better than those reported in the studies
reviewed. In summary, statements about the
effectiveness of specific treatment interven-
tions (of any kind) independent of the norms
and values of the social context are meaning-
less. Media and other specific interventions
may operate differently within a context of
values and beliefs that are supportive of their
messages than in the absence of such a con-
text (see Hovland, 19S4; Weiss, 1969).
Intervention efforts with school children
have also been severely limited by ignoring
the processes underlying smoking and by
treating smoking as a response like any other
response. Because of this set, the goal of inter-
vention has been to place a barrier between
the youngster and his or her first cigarette,
hence the focus on techniques for resisting
peer pressure. But as is demonstrated in the
following section, smoking has a long and
complex developmental history, beginning
well before the first cigarette is smoked and
extending sometimes over S or 10 years to
dependence. This history can be divided into
stages and processes, and preventive methods
should be designed to deal with the key
points of this history and should incorporate
different procedures to deter smoking at each
step in the process of becoming a dependent
smoker.
Investigators are acutely aware of the diffi-
culty of developing methods to sustain reduc-
tion and cessation of smoking (Lichtenstein,
1971). The situation contrasts with the suc-
cess of behavior therapy in treating phobias
(Lang, Lazovik, & Reynolds, 1965; Lang,
Melamed, & Hart, 1970). Results in this latter
area have been more lasting (e.g., G. M.
Rosen, Glasgow, & Barrera, 1976, 1977), and
the durability of therapy has been enhanced
by conducting therapy in real-life settings
(Sherman, 1972) or by using booster sessions
and by various forms of modeling with guided
participation (Bandura, Blanchard, & Ritter,
1969). However, there is doubt that impres-
sive short-term results of the smoking thera-
pies can be extended to the longer term simply
by adding on these extra methods. For ex-
ample, buddy systems and follow-up booster
sessions have been recommended (Hunt &
Matarazzo, 1973), but controlled studies of
booster sessions show no advantage over
standard treatments, such as rapid smoking,
for long-term follow-ups of 6 months (Best
et al., 1977; Elliott & Denney, 1978; Kapel,
1974).
To develop a more powerful therapy that
can sustain long-term change, it is necessary
to consider both the dependence process itself
and skills for self-regulation. As for depen-
dence, we need to better understand the
underlying process, the stimuli that trigger
the craving to smoke, the emotional desires
generated by these stimuli (their nature and
origin), and the links between these experi-
ences and pharmacological factors such as
nicotine (Schachter, Silverstein, & Perlick,
1977, p. 40). One can readily collect system-
atic data and incidental comments pointing
to a host of factors that make it difficult to
sustain quitting. These include a wide range
of physiological and subjective withdrawal
symptoms, some of which appear soon after
smoking cessation (e.g., decreases in heart
rate and systolic blood pressure, declines in
body temperature, increase in low-frequency
alpha, drops in adrenaline and norepine-
phrine) and others of which appear over
longer periods of time (e.g., weight gain, im-
paired psychomotor performance, nausea,
headache, constipation, drowsiness, fatigue,
sleep disturbances, and increases in anxiety,
 THE SMOKING PROBLEM
irritability, and hostility; Shiftman, Note 4).
Some of these signs, for example, images and
dreams of smoking (Knapp et al, 1963) and
craving (Shiftman, Note 4) may appear 5 or
more years after quitting. Many of these
symptoms appear to be more noticeable
among neurotic than nonneurotic quitters
(Burns, 1969). Current intervention methods
fail to take account of these effects and offer
no means of dealing with these phenomena.
The second issue, the longer term aspects
of developing skills for self-regulation, is
receiving more attention from social behavior
theorists (e.g., Bandura, 1977; Kanfer, 197S;
Meichenbaum, 1979) but needs much work in
the specifics of efforts to self-regulate smok-
ing. We know little about the effects of re-
peated attempts to quit, the consequences of
success followed by failure, or of overt success
(not smoking) and covert yearning, on belief
in one's ability to self-regulate and willingness
to exert effort to do so. We know less than we
should about the events surrounding success
and failure in smoking withdrawal (e.g.,
Pechacek, 1979; Schwartz & Dubitzky, 1968;
Shiftman, Note 4; Russell, Note S). Lack of
knowledge of the long-term aspects of the
dependence and coping process is clearly due
in part to the assumption that smoking is
treatable by methods applicable to any other
response. Ignoring the processes underlying
the behavior, its similarities and uniqueness
in the internal (affective and pharmacological)
and external domain (the stimuli provoking
pharmacological and affective changes),
greatly limits our ability to develop an inter-
vention capable of maintaining long-term
smoking withdrawal.
In the next section, we review and evaluate
several models of smoking behavior. Our goal
is to discuss what is known about the origin
and maintenance of smoking, to evaluate the
relevance of this information to past inter-
vention procedures, and to suggest new possi-
bilities for intervention.
Theories of Smoking
We have found that the model separating
motivational and skill factors is an improve-
ment on the simple compliance model of inter-
vention, but it is still inadequate to the task
383
of generating new and more powerful anti-
smoking programs. It is deficient because it
fails to fully take into account the many
complex social and individual processes medi-
ating intervention efforts and the functions
underlying smoking. It is naive to expect
remote threats of illness to serve as sufficient
motives for smoking prevention, cessation, or
abstinance. The research reviewed suggests
that the functions of smoking are extremely
important to the individual smoker, and if we
are to be at all successful in our bid to reduce
smoking, we must identify substitutes for
these functions and stimulate motivation to
adopt those substitutes by vivid and salient
illustrations of the actual impact of smoking
on an individual's health. In addition, we must
develop better techniques to induce cessation
that are based on the mechanism(s) control-
ling the habit. In B. Mausner's (1973) terms,
we must deal with the full range of factors
that determine the expected utility of
smoking.
In this section we present material basic to
the conceptual and empirical aspects of the
initiation, maintenance, and cessation of smok-
ing. We present our ideas in a developmental
framework, that is, in terms of stages leading
from anticipation and initial experimentation
with cigarettes to regular smoking and smok-
ing cessation. We relate our theory of the
stages of smoking to the intervention ap-
proaches reviewed and make suggestions for
new interventions.
Stages of Smoking
Smoking has a complex ontogeny (Hoch-
baum, 1965; Leventhal, 1968; B. Mausner &
Platt, 1971; McKennell, 1968; Tomkins,
1968; Horn, Note 1). The developmental
history for the individual smoker seems to
move in steps through the stages of prepara-
tion, initiation, becoming a smoker, and main-
tenance 0} smoking (Dunn, 1973; Salber et
al., 1968) to stages of dissatisfaction, decision
to stop, and adoption and maintenance of the
self-image of ex- or nonsmoker (B. Mausner
& Platt, 1971; Sarbin & Nucci, 1973). Our
discussion focuses on the first four of these
stages: preparation, initiation, becoming, and
maintenance.
384 HOWARD LEVENTHAL AND PAUL D. CLEARV
Preparation, Initiation, and Becoming:
First Three Stages oj Smoking
Social pressure is probably a prime initiator
of experimentation with cigarettes (Bergen &
Olesen, 1963; Hill, 1971); at the urging of
peers or perhaps an elder sibling (Gorsuch &
Butler, 1976), a youngster is encouraged to
try a cigarette. Smoking by family members,
parents in particular, seems to operate by
reducing the barriers to peer pressure (Bor-
land & Rudolph, 197S) and by increasing the
opportunities for obtaining cigarettes for
further experimentation (Baer & Katkin,
1971).
Initial experimentation is a critical step to
becoming a smoker; data show that 85$-
90$ of those who smoke four cigarettes
become regular smokers (Salber et al., 1968),
implying that adolescent experimentation with
smoking led to adult smoking whether or not
the young people had originally intended to
become smokers.
One consequence of these findings has been
the inclusion in antismoking programs of
educational material on the social pressures
that promote smoking. Evans (1976) and his
associates (Evans et al., 1978) are teaching
grade school students about peer and media
pressure and using films of models demon-
strating self-assertive techniques to avoid ac-
cepting cigarettes, and so on. This innovative
approach to action planning seems likely to
succeed with those who do not wish to experi-
ment with smoking, but it may be less effec-
tive with those who want to experiment or
take on the air of maturity, rebelliousness, and
sexual sophistication often attributed to the
smoker (Leventhal, 1973).
The limited successfulness of these well-
designed programs suggests that there is more
to the initiation of smoking than social pres-
sure. It is likely that "smoking" begins well
before a child tries a first cigarette. Children
develop attitudes about smoking and have
images of what smoking is like well before
they try it. These attitudes seem to be im-
portant in the development of the smoking
habit. In one study a statement of intention
to try cigarettes proved to be the best single
predictor of later smoking (Newman, Martin,
& Petersen, Note 6). Indeed, it is clear that
there is a preparatory stage that includes
perceptions of what smoking involves and
what the potential functions of smoking are.
Grade school students assign different person-
ality characteristics to smokers and nonsmok-
ers; they rate the smoker as foolish, careless,
tough, easygoing, lazy, more often in trouble,
and so forth (Bland et al., 197S; Bynner,
1970). Interestingly, few youngsters who
smoke see themselves as possessing these
characteristics. Why would this image serve
as a motive to smoke? One possibility is that
it suggests a toughness, an ability to express
impulses, an independence from authority,
and a state of being grown-up and successful
in areas that, though "bad," are exciting and
interesting. These inviting aspects of the
image may encourage experimentation with
smoking, and we believe they may form one
basis for becoming a smoker. Indeed, we
speculate that children who are less successful
in school (Bewley & Bland, 1977; Borland &
Rudolf, 197S; Horn, 1963; Jessor & Jessor,
1977; Newman, 1970b), more rebellious, and
doing less well in meeting expectations of
parents and traditional authorities (Newman,
1970a; Smith, 1970; Stewart & Livson, 1966)
are more likely to be attracted to smoking at
an early age and begin using cigarettes as a
means of defining themselves as tough, cool,
and independent of authority, as well as using
other drugs later on (Seltzer, Friedman, &
Siegelaub, 1974; Tennant & Detels, 1976).
It is unlikely that youngsters who define
themselves as independent of authority try
cigarettes to comply with peer pressures.
Youngsters who first try cigarettes at the
urging of friends may have a different pre-
paratory set. Some may feel anxious and in-
adequate and smoke to achieve social accep-
tance and be part of the gang. Others may
share a wide variety of experimental activities
with a close friend, and smoking may simply
be one of the experimental or risk-taking
actions. These two sets of factors, defining the
self as tough and seeking social approval, are
not likely to exhaust the attitudes that make
up the preparatory stage. It is probable that
some people begin smoking to control emo-
tions such as work anxiety. Smoking may be
seen as useful for enhancing performance on
examinations and increasing one's chances of
 THE SMOKING PROBLEM
achieving the rewards of high grades and
admission to top colleges. This orientation
may be important for individuals starting
smoking relatively late in adolescence or early
adulthood, the kind of smoking seen in college
and medical students (Borgatta & Evans,
1968; Smith, 1970; Thomas, 1960).
Whatever the reasons, preparation for trying
the first cigarette is only a beginning step:
The next is actually smoking one's first cig-
arette. Smoking the first cigarette is but one
additional step in the developmental process.
Although the Salber et al. (1968) data sug-
gested that smoking four cigarettes was suf-
ficient to lead to adult smoking and depen-
dence on cigarettes, it is also clear that many
youngsters never get to their fourth cigarette,
Studies show that &0%-9Qfo of youngsters
have tried at least one cigarette (Grant &
Weitman, 1968; Palmer, 1970; Wohlford &
Giammona, 1969), yet the proportion of
smokers in grade, junior, and high school
years rarely exceeds 50%'of those who try.
Something happens to move many of the ini-
tial triers off the experimental track.
Indeed, the data seem to support the hy-
pothesis that it takes upwards of two years
and possibly longer (A. Cartwright et al.,
1959) from initial tries and occasional experi-
mentation to arrive at heavy, consistent smok-
ing: This is the stage of becoming a smoker.
There are gradual increases in the percentage
of students smoking (1% in 7th grade to
46% in llth grade) and gradual increases in
the number of cigarettes smoked (1 per week
to 20 per day), with the big increase occurring
as females enter the 5-9 per day category and
as males enter the 10-19 per day category in
Grade 10 (Horn, Courts, Taylor, & Solomon,
1959; Salber et al., 1961). Unfortunately,
many of the data are cross-sectional, and those
that are not are retrospective (A. Cartwright
et al., 1959), so we do not know whether there
is a gradual change in the percentage of smok-
ing and the amount smoked by individual
smokers or if the average reflects an agglom-
eration with some students rapidly moving
from experimentation to pack-a-day smoking,
others gradually making the transition, and
some staying at low levels of consumption
that vary little over time. We believe that
385
good longitudinal data would reveal a variety
of patterns, but we also suspect that Salber
et al. (1968) are correct in estimating that 2
years pass between initial experimentation
and becoming a regular smoker.
What does this analysis suggest about the
intervention process? First, it is clear that dif-
ferent information is needed to deal with the
different stages, that is, with preparation and
the different readiness or sets within it, with
initial experiences, and with becoming a smoker
through repeated tries and regular usage. Sec-
ond, it is clear we need to understand more
about the mechanisms underlying these phe-
nomena to select content and to decide how
best to present this information. If prepara-
tory sets exist, that is, if young people do
start smoking to define themselves, to achieve
social acceptance, and to control affect, why
are these gains so clear and the losses so ob-
scure? Can we make salient the paradox that
young smokers do not apply the negative im-
age of "smoker" to themselves? In other
words, can we make young people see that
when they try smoking they are adopting a
habit they view negatively? Making explicit
the differences between the students' current
self-images and their view of a "smoker" may
lead some students to question their motiva-
tion to experiment. Also, it suggests that
efforts be made to show that the exciting as-
pects of the image are illusory and that good
health, attractive appearance, neat dress, and
not smoking are linked to greater success in
sex, greater strength and daring, and so forth.
Unfortunately, smoking is highly salient: It
presents a concretely visible action by an in-
dividual as he or she relates to others. It may
be difficult to make the behaviors leading to
economic and social success equally salient;
they may be less visible, and adults may be
less willing and less able to articulate the role
they play in these achievements.
It is also clear that the grade schooler's
picture of the smoker is incomplete. Young
people in the preparatory phase seem to be
unaware of the problem of addiction or de-
pendence. They believe they will be able to
stop smoking when they wish and seem un-
aware of the degree to which adults become
dependent on cigarettes (Brecher, 1972) and
386 HOWARD LEVENTHAL AND PAUL D. CLEARY
struggle and humiliate themselves for their
inability to control the habit. Elaborating the
presmoker's concept of the smoker as a per-
son lacking self-control, using cigarettes to
compensate for inadequate social skills, inabil-
ity to manage emotions, and inadequacy in
heterosexual relationships, might add sub-
stantially to the perceived unattractiveness of
the habit. It might also conflict more directly
with motivation to define oneself as strong
and "cool" and socially competent. The
thought of using smoking to regulate emotional
tension might even become aversive if it elicits
anxiety at loss of self-control. Thus informa-
tion on dependence could be tuned to each of
the preparatory views of smoking.
The second stage, the initial tries at smok-
ing, appears to be a time when many young-
sters decide not to continue with their experi-
mentation. Although the initial harshness of
smoking may be a critical factor in this de-
cision, it seems unlikely that individual dif-
ferences in physiological responsivity to smoke
and heat can fully account for who does and
who does not stop at this point. The mere
presence of pain is not sufficient to deter or
promote behavior; the way a pain is inter-
preted, for example, as a sign of illness and
danger to the self (Safer, Tharps, Jackson, &
Leventhal, 1979; Suchman, 1965; Zborowski,
19S2) is critical for motivating seeking medi-
cal advice and regarding oneself as at risk.
Interpreting noxious bodily sensations as be-
nign may actually facilitate getting used to and
ignoring them (Leventhal, Brown, Shacham,
& Engquist, 1979; Leventhal & Everhart,
1979) and may play an important role in
adapting to smoking.
With time there is clearly a development of
tolerance to the physiological effects of smok-
ing (Russell, Note 5 ) . The daily experience
of smoking and being alert, relaxed, and re-
freshed can then serve as powerful evidence
for its usefulness. The fading of harsh cues
that accompany initial smoking experiences,
for example, the burning, roughness, and bite
of the heat and smoke of the cigarette, may
then be interpreted as evidence that smoking
will not be harmful to oneself. Children's be-
lief that smoking is harmful for others and for
older people but not for themselves may arise
from the experience of adaptation. To counter
such beliefs, it may be necessary to alter the
school curriculum to increase understanding
of the human body and its reaction to insult.
This is a general issue in biological educa-
tion; it is not specific to smoking. Our con-
ceptions of pain are undifferentiated and un-
informed. Children can be taught about pain,
symptoms, and their adaptation and that not
all serious illness and harm are preceded by
pain (see Leventhal & Everhart, 1979). The
initial cigarette might also seem much more
dangerous if the various sensations have been
described and clearly labeled as cues to noxious
effects on sensory organs and tissues.
Finally, it is important to confront the is-
sue of becoming a regular smoker. The grad-
ual increase in frequency of smoking and the
increasing variety of situations in which cig-
arettes are used suggests that becoming a
smoker is not unlike the process involved in
concept formation, with the smoker going
through a lengthy stage of "correct respond-
ing," that is, smoking when it is appropriate
to do so, before he or she develops a schema
or self-image as a smoker (Hull, 1920; Posner,
1973). Several nonverbal motivational sys-
tems, iconic, kinesthetic, autonomic, and so
forth, may be involved in integrating smoking
with a variety of coping responses before the
individual fully develops this self-concept. Re-
stricting the situations in which smoking oc-
curs and developing a narrow definition of the
functions of smoking (e.g., as a social gesture)
may help prevent the development of heavy
addictive smoking.
Unfortunately, we know very little about
the processess involved in the stages of be-
coming a heavy smoker. Longitudinal descrip-
tive data on variables such as those mentioned
previously and on other aspects of the social
processes involved in smoking (B. Mausner
& Platt, 1971) would provide better ground
for the formulation of process models that
could guide educational programs.
Maintenance: Fourth Stage of Smoking
Once smoking is an integral part of self-
regulation in a variety of situations, the indi-
vidual is truly a smoker. Understanding the
 THE SMOKING PROBLEM
regulatory functions of the behavior is likely
to be critical for the development of interven-
tion techniques able to generate long-term
smoking cessation and reduction. The fac-
tors maintaining smoking have been investi-
gated at both a psychological and biological
level. Unfortunately, the two approaches are
often presented as antagonistic, as though the
description of psychological functions has in-
volved nothing more than investigating the
phenomenology of the smoking experience or
smokers' reports of the satisfactions of smok-
ing, whereas biological research has elucidated
only the physiological mechanisms underlying
smoking. Actually, the two approaches are
complementary ways of describing the same
problem (Graham, 1Q72). It is unlikely that
one can describe the mechanisms for smoking
at a biological level if one cannot first de-
scribe them at a psychological level: Biologi-
cal analysis often follows the contours of psy-
chological analysis. At the very least a psy-
chological analysis can lead to a more refined
view of the processes underlying the response
and assist in the defining of samples of per-
sons and situations in which smoking is likely
to reflect particular processes for which one
can locate particular biological mechanisms.
Psychological models. Psychological models
of smoking are based primarily on factor
analyses of self-report data. Tomkins's (1966)
model, the basis for the self-appraisal kit de-
veloped by the National Clearinghouse for
Smoking Research (Ikard, Green, & Horn,
1969; Horn, Note 7), suggests that smoking
is used to regulate internal emotional states,
producing positive emotional reactions and
minimizing negative emotional reactions in a
variety of situations. Factor analysis of smok-
ers' ratings of reasons for smoking generate
factors such as smoking for stimulation, smok-
ing for pleasure and relaxation (taste), smok-
ing to reduce anxiety or tension, smoking to
reduce social anxiety, smoking to reduce gen-
eral anxiety, smoking to reduce craving (psy-
chological addiction), smoking simply to
handle the cigarette, and smoking from habit.
The questions used to measure these factors
ask directly about the subjects' experience
with cigarettes.
387
Tomkins (1966, 1968) advanced the addi-
tional hypothesis that dependence (addiction)
develops by the sequential linking of emotional
states: A negative emotional state (e.g., anx-
iety) stimulates smoking, smoking produces a
positive affect or lift that reduces the nega-
tive emotion, and when the individual stops
smoking for a period of time, the negative af-
fect returns and becomes a powerful stimulus
to smoking. Thus the absence of cigarettes re-
instates smoking and the behavior becomes
part of a self-reinforcing system.
The factors described by Tomkins appear
to be reliable. Leventhal and Avis (1976) fac-
tor analyzed the responses of four samples of
college students on different questionnaires on
reasons for smoking and found virtually iden-
tical results from sample to sample, despite
changes in the items included in the analysis.
McKennell (1968) also reported virtually
identical factors from a set of independently
derived questions about the occasions on which
individuals smoked. Thus the reported func-
tions of smoking appear to be similar whether
smokers are asked about the satisfactions
they obtain while smoking or the occasions on
which they smoke (Kozlowski, 1979). A study
by Best and Hakstian (1978) that collected
reasons for smoking responses from com-
muters waiting for a ferry failed, however, to
replicate these findings.
Of course, consistency is not equivalent to
validity: Smokers may give similar descrip-
tions of their reasons for smoking when ques-
tioned in different ways and still be wrong in
the causal analysis of their behavior. Leventhal
and Avis (1976) and Ikard and Tomkins
(1973) examined the validity of these judg-
ments by having subjects complete a question-
naire on reasons for smoking, sorting them
into high and low scorers on particular scales,
and comparing the actual smoking behaviors
of these groups in response to experimentally
manipulated variables. When smokers were
given cigarettes adulterated with vinegar,
those high on the pleasure-taste factor showed
a sharp drop in the number of cigarettes
smoked; those low on the factor did not.
When smokers were assigned the task of moni-
toring their smoking (filling out a card for
each cigarette smoked), habit smokers signift-
388 HOWARD LEVENTHAL AND PAUL D. CLEARY
cantly reduced their smoking, pleasure-taste
smokers did not (Leventhal & Avis, 1976).
There was more smoking following a fear film
for smokers who used smoking for anxiety re-
duction (Ikard & Tomkins, 1973). Both of
the studies support earlier data (e.g., Schwartz
& Dubitzky, 1968) in finding that psycho-
logical addicts suffered the most during pe-
riods of deprivation, though Leventhal and
Avis could not document increased smoking by
addictive smokers following 18 hours of depri-
vation. A short deprivation (20 minutes) ap-
pears to have led to increased smoking by
addictive smokers in a study by Herman
(1974).
In summary, the data suggest that the func-
tions of smoking are reliably reported and that
some of these self-reports, addiction being an
exception, identify the conditions that stimu-
late smoking. It is also clear that the rela-
tionship between report and behavior is not
perfect. Many smokers have inaccurate per-
ceptions of the mechanisms that underly their
smoking, and smokers are more likely to see
much of their behavior as habitual after a
prolonged period of self-monitoring (Leven-
thal & Avis, 1976). This latter finding sug-
gests that systematic self-monitoring could be
an important precursor to smoking reduction
or withdrawal (Engeln, 1969; Lichtenstcin &
Keutzer, 1971; McFall & Hammen, 1971).
It is also clear that only a few of the inter-
ventions reviewed are relevant to the particu-
lar functions identified by the reasons for
smoking factors. Of the behavioral therapies,
the densensitization procedures appear to tar-
get anxiety-control smokers, and aversive pro-
cedures appear to target taste and positive-
affect smokers. There is little reason, however,
to argue that the investigators who used these
procedures considered the dynamics of the
underlying functions in any detail in designing
their intervention techniques, and virtually
none of the studies reviewed even bothered to
examine the impact of the intervention on
particular smoking subgroups. One might ar-
gue that sensory deprivation (removal of all
affect-arousing cues) was designed to deal with
particular smoking subtypes, but it appears
this method was simply tried, and no effort
was made to look at the impact for separate
smoking types: Time and cost tend to militate
against this. The group most clearly targetable
by current procedures, the anxiety-reducing
smoker, is the most intractable to treatment
(e.g., Burns, 1969), and the closest interven-
tionists come to dealing with the addictive
smoker is examining the impact of their pro-
cedure for light and heavy smokers.
It seems reasonable to conclude therefore
that intervention has proceeded by ignoring
what is known about the psychological func-
tions of smoking. The possible exception is
the National Clearinghouse for Smoking Re-
search manuals for quitting, which ask the
smoker to self-monitor and score himself or
herself on the factors, but it is unclear how
this is to effect subsequent quitting efforts.
Pharmacological models. Pharmacological
research is designed to locate specific chemi-
cal agents, which are either in the cigarette or
generated during combustion, that are re-
sponsible both for dependency and the harm-
fulness of smoking and to then develop anti-
dotes for them. The most likely candidate for
dependency is nicotine (Jarvik, 1970, 1973).
It is not clear precisely how nicotine generates
dependence. An examination of the literature
suggests, however, that three different models
are used to account for nicotine's effectiveness
in maintaining smoking: (a) the fixed-effect
model, (b) the nicotine regulation model,
and (c) the multiple regulation model. For
clarity of exposition we greatly oversimplify
each, recognizing that few if any investigators
would adopt these positions when they are
reduced to their bare essentials and not com-
bined with other, more psychological processes.
The nicotine fixed-effect model assumes that
smoking is reinforced because nicotine reliably
stimulates specific reward-inducing centers of
the nervous system. For example, nicotine
changes the levels of neuroamines (Essman,
1973), and alters nervous system activity
(Brown, 1973); for example, it lowers the.
strength of evoked cortical potentials produced
by external stimuli (Hall, Rappaport, Hop-
kins, & Griffin, 1973). Nicotine also speeds
heart rate (Armitage, 1973) and acts on the
inhibitory (Renshaw) cells in the dorsal col-
umn of the spinal cord to produce skeletal
muscle relaxation (Domino, 1973). Some of
 THE SMOKING PROBLEM
these effects are produced indirectly by nico-
tine's action on the level of circulating
catecholarnines.
It is still unknown how nicotine can simul-
taneously produce autonomic arousal and feel-
ings of mental alertness and relaxation (Gil-
bert, 1979). For present purposes, it is more
important to note that the described effects
are basically acute in nature; that is, they are
induced by nicotine and disappear when the
drug is withdrawn. These short-term effects
may account for the initial repeated use of
cigarettes, but they do not seem able to ac-
count for the extraordinary persistence of
smoking or the inability of most people to
avoid returning to smoking after they
have stopped (Russell, 1971a, 1971b). If
these effects are viewed as reinforcers, some
additional factors, such as conditioning, would
have to be responsible for maintaining the be-
havior. The inability to produce sustained
smoking withdrawal with behavioral therapies
based on operant and classical conditioning
models suggests, however, that a simplified
version of this model cannot fully describe
the mechanisms underlying and controlling
the behavior.
Nicotine regulation models argue that smok-
ing serves to regulate or titrate the level of
nicotine (or a related agent) in the internal
milieu; departures from the optimal level of
the agent stimulates smoking. This model
differs from a simple reinforcement model in
predicting that smoking is rewarded only when
the level of nicotine circulating in the body
is below a "set point" and suggests that sus-
taining the level of nicotine is a sufficient
mechanism for maintaining smoking.
Jarvik (1973) reviewed a considerable body
of evidence consistent with this model. First,
individuals who switched from high- to low-
nicotine cigarettes increased the number of
cigarettes smoked, smoked more of the ciga-
rette, and inhaled more deeply (Frith, 1971a;
Jarvik, 1973), apparently compensating for
the reduced nicotine levels of the new ciga-
rettes (Ashton & Watson, 1970). Second,
doses of nicotine led to drops in cigarette con-
sumption; for example, 5 mg of nicotine tar-
trate per day orally led to an average reduc-
tion of two cigarettes per day. Although these
389
reductions are statistically significant, they
are far smaller than one would expect on the
basis of a dose-dependent hypothesis (Jarvik,
1973). Russell and his associates (Russell,
1977; Russell, Feyerabend, & Cole, 1976;
Russell, Wilson, Feyerabend, & Cole, 1976)
had smokers chew nicotine-laden gum, and
smoking reductions were slight even with the
higher of the two dosage levels used. Russell
suggests the rate of oral nicotine absorption
may be too slow to affect smoking.
It may well be that the oral route is not
the best for evaluating the nicotine regulation
hypothesis. Absorption through the lungs
and/or other organs may be more effective
methods of regulating plasma nicotine levels
and testing the nicotine regulation model. In
a series of ingenious studies, Schachter (1977)
and his associates have generated the most
compelling evidence to date for the nicotine
regulation model. In their first study they
lowered the level of nicotine in cigarettes and
found an average increase in cigarettes smoked
of 25.3% for heavy smokers and 17.5% for
light smokers. Assuming this change reflected
the need to maintain an optimal plasma level
of nicotine, Schachter, Kozlowski, and Silver-
stein (1977) compared smoking levels in
groups of subjects who took vitamin C, Acidu-
lin, bicarbonate, or placebo pills on different
weeks. (Subjects were blind as to pill content.)
These pills varied the pH of the individual's
urine, which in turn varied the rate of excre-
tion of nicotine; when urinary pH is low
(acidic) nicotine (an alkaloid) is excreted,
and smoking should increase to compensate
for this loss. When urinary pH is high (alka-
line), nicotine is retained and smoking should
be at relatively low levels. Subjects taking
vitamin C or Acidulin increased an average of
about four cigarettes per day or roughly 15%-
20% from base levels.
The findings suggest that smokers, or at
least heavy smokers, smoke to regulate nico-
tine and not to regulate stress, anxiety, or
boredom. If so, why do both light and heavy
smokers smoke more at parties, during doc-
torate exams, colloquia, and stressful seminar
presentations (Schachter, Silverstein, Kozlow-
ski, Herman, & Liebling, 1977)? Schachter
suggests they do because stress leads to a
390 HOWARD LEVENTHAL AND PAUL D. CLEARY
drop in urinary pH, which increases smoking.
To show that stress-induced changes in smok-
ing were dependent on urinary pH change,
Schachter, Silverstein, and Perlick (1977) ex-
posed smokers to either a high- (painful elec-
tric shock) or a low-stress stimulus (barely
perceptible shock) and gave half the sub-
jects in each group three bicarbonate capsules
and the other half three placebo capsules.
High stress was expected to lead to more
smoking than low stress when subjects were
given placebo pills; high stress was not ex-
pected to increase smoking when subjects
were given bicarbonate pills, which block pH
drop and nicotine excretion. The results were
as expected and are consistent with the nico-
tine regulation model rather than with a
stress regulation model.
The nicotine regulation model paints a
pessimistic picture of intervention efforts. In-
deed, Schachter (1977) suggested that smokers
be left alone lest they be done harm by pro-
cedures such as lowering cigarette nicotine
levels, which will increase the number of
cigarettes smoked and expose the smokers to
more dangerous combustion products while
they are working to obtain their requisite level
of plasma nicotine. This warning seems reason-
able if the plasma regulation model was suffi-
cient to explain all smoking behavior. But we
must remember that regulation is not as tight
as Schachter would hope. Indeed, it is clear
that some smokers follow an addicted pattern
(e.g., difficulty quitting, withdrawal symp-
toms, etc.), even though they have zero
plasma nicotine levels (Russell, Note S ) . Evi-
dence also suggests that the availability of
low-tar, low-nicotine cigarettes has led to
substantial reductions in tar intake: Schach-
ter's fears do not seem to have been realized
in the population at large (Garfinkel, 1979).
The plasma regulation model also suggests
that work to discover a nicotine antagonist is
the most important avenue for achieving smok-
ing reduction. This direction would be no dif-
ferent from that unsuccessfully pursued to
overcome heroin addiction (Brecher, 1972).
Still, if we compare this diagnosis and pre-
scription with other interventions, we see it
is at least part of the picture. However, there
are other findings that pose serious threats
to the nicotine regulation model.
A consideration of the nicotine regulation
model's shortcomings leads us to the need
for multiple regulation model. The nicotine
regulation model suggests that "the brain is in
the bladder"; a phrase Schachter has used
for his colloquia. This statement has the ring
of truth, given that socially induced stress
affects urinary pH levels that, in turn, affect
the rate at which nicotine is excreted or taken
up in the blood stream. Unfortunately, neither
the parsimonj' of the model nor the brilliance
of the experiments compensates for the failure
to address several important problems. Per-
haps the most important of the problems ig-
nored by the model is how the nicotine set
point develops and how deviations from the
set point come to generate a craving for cig-
arettes. Schachter's model and studies appear
to assume a direct and automatic step from
changes in plasma nicotine level to craving and
smoking and say nothing about the mecha-
nisms and experience that give rise to either.
We believe that this omission makes it
impossible for the model to account for find-
ings such as the following: (a) High relapse
rates are observed in the 3 months to 1 year
following smoking cessation. Plasma nicotine
levels and some of the withdrawal symptoms
are at zero levels a few days after smoking
cessation (Jacobs, Knapp, Rosenthal, & Has-
kell, 1970); other factors are needed to ac-
count for the motivation to resume smoking.
In addition, many smokers report a rapid
return to heavy smoking (Jacobs et al., 1970;
Schwartz & Dubitzky, 1968). (b) Smokers
will smoke lettuce cigarettes that contain no
nicotine at all. (c) Smokers do not appear to
regulate their nicotine intake enough to com-
pensate for experimentally induced changes
in the nicotine content of cigarettes (Jarvik,
1970, 1973). Schachter (1977), for example,
found that a 77% reduction in nicotine level
produced only a 11%-25% increase in cig-
arette consumption, (d) The oral ingestion of
nicotine fails to produce substantial drops in
smoking, (e) Smoking is responsive to swiftly
changing emotional states (Nesbitt, 1973) and
minor changes in the salience of environ-
mental cues (Herman, 1974). (f) Individuals
have substantially more difficulty quitting
 THE SMOKING PROBLEM
smoking when under stress. White collar and
executive workers still seeking advancement
or workers facing job loss are much less likely
to quit than those'in less stressful job circum-
stances. By contrast, blue collar workers in
stable job situations often spontaneously re-
duce or stop smoking during middle age, when
life stresses appear to be at a minimum (Cap-
Ian, Cobb, & French, 1975). (g) Protected
environments such as sensory deprivation
chambers seem to make nonsmoking (not
reduced smoking) relatively effortless (Sued-
feld&Ikard, 1974). (h) Factor analyses show
that people smoke for different reasons, for
example, to regulate stress, for stimulation,
pleasure, and so forth (Ikard et al., 1969;
Tomkins, 1966). (i) It appears that smoking
has a long developmental history; in one study
half of the adult smokers reported taking 6
months to 2 years to develop the habit, the
other half still longer (A. Cartwright et al.,
1959). The rapidity of development may
depend on the reasons for initiation. It has
been speculated that emotionally motivated
smokers who need to control negative emo-
tion, distress due to failure, and so forth,
may become dependent more rapidly (Jacobs
et al., 1970). (j) Finally, smokers who are
nicotine deprived do worse in tracking tasks
such as the driving simulator (Heimstra, Ban-
croft, & DeKock, 1967) and show decreased
tolerance to shock when smoking low-nicotine
cigarettes, a finding that holds only for ex-
perienced smokers (Nesbitt, 1973). Nicotine
also reduces aggressive biting reactions in
monkeys (Hutchinson & Emley, 1973). Al-
though these last findings are not really incon-
sistent with Schachter's model, nowhere does
he give an explanation of the mechanisms that
link nicotine deprivation to them. Yet they all
suggest that some kind of emotional state is
active in connecting changes in plasma nico-
tine level to behavior.
Schachter (1977) and his colleagues appear
to deal with these problems by arguing that
individual differences account for many of
these phenomena, They suggest that nicotine
regulation applies to heavy smokers, whereas
the use of smoking for the regulation of emo-
tional states induced by multiple sources
applies to light smokers. For example, Her-
391
man (1974) found light smokers to be more
responsive to external cues than were heavy
smokers. This is an unsatisfactory resolution
to our question; The division between light
and heavy smokers reflects an arbitrary cutoff
point on a distribution of frequency of smoking,
and there is no clear evidence that the differ-
ences in level are associated with different
underlying mechanisms. Both Schachter and
Herman found light smokers responsive to
nicotine levels. In addition, many so-called
light smokers have enormous difficulty in
quitting. Besides, all smokers begin as light
smokers, implying some degree of continuity
and overlap in function rather than discrete
categories of underlying process.
We think that the answer to these problems
lies not in refining or elaborating Schachter's
model of pharmacological regulation but
rather in adopting a type of model which
assumes that the smoker is regulating emo-
tional states and that nicotine levels are
being regulated because certain emotional
states have become conditioned to them in a
variety of settings. We refer to this model,
which is an elaboration of similar models by
Tomkins (1968) and Solomon and Corbit
(1973), as the multiple regulation model.
The core of the model is that emotional
regulation is the key to smoking and that
departures from emotional or hedonic home-
ostasis stimulate smoking behavior. Heavy,
dependent smokers act to regulate nicotine
level because drops in plasma nicotine level
stimulate the dysphoric hedonic state of crav-
ing, but other external stimuli can also gen-
erate this affective reaction. The distress in-
duced by nicotine level drops can also combine
with the distress induced by various tasks
(e.g., shock tolerance, driving), and by smok-
ing to return nicotine to base levels, the
smoker can tolerate the same level of shock
(Nesbitt, 1973) and perform at the same
level of tracking (Heimstra, 1973; Heimstra
et al., 1967) as nonsmokers. Thus externally
and internally generated cues gain control
over fluctuation in emotional states.
As pointed out earlier, an adequate model
must explain how craving becomes linked to
drops in nicotine levels. We think that there
are two possible ways in which such a linkage
develops and is maintained. One possible
392 HOWARD LEVENTHAL AND PAUL D. CLEARY
source of craving is from the nicotine itself.
Following the assumptions of the opponent-
process theory of emotional motivation pre-
sented by Solomon and Corbit (1973, 1974),
it can be posited that nicotine gives rise to an
initial, positive, affective reaction, which in
turn automatically gives rise to a weaker,
slave, opponent (or homeostatic), negative,
hedonic response. The opponent, slave state
becomes stronger with the repeated activa-
tion of its initiating emotion; the more one
uses smoking to elicit positive affect, the more
one strengthens the opponent, negative state
(craving?). Second, the negative, opponent
state can be eliminated by reinstating the
initial positive emotion; that is, as Tomkins
(1968) argued, smoking will do away with its
opponent dysphoria. The catch, of course, is
that repeated smoking strengthens the nega-
tive state it is used to control or builds its
own craving.
External stimulation provides an alterna-
tive source for craving. The smoker probably
begins smoking as an experiment. Smoking is
initially seen as mature and exciting. Having
learned the techniques of smoking (e.g., how
to inhale, habituation to physiological effects),
the new smoker will likely begin to use smok-
ing in various stressful circumstances (i.e., in
the presence of social or work threats), and
these situations may themselves provide the
negative emotion that becomes conditioned to
declines in plasma nicotine level. Thus if a
youngster is socially anxious, high in need for
affiliation, and low in autonomy or self-confi-
dence (Hill, 1971), smoking can instill a
sense of security, temporarily screening social
anxiety. The anxiety will reappear when the
cigarette is withdrawn, and, at the very point
that plasma nicotine levels begin to decline, it
will be conditioned to or combined with the
bodily sensations generated by drops in nico-
tine level. As is discussed shortly, this model
does not treat as craving the sensations gen-
erated by drops in nicotine level. These sen-
sations become craving only after they are
conditioned to environmentally stimulated
negative affects.
Either of the above proposals provides a
source of negative emotion for the develop-
ment of the craving reaction, but they are
not sufficient to account for the phenomena
outlined earlier. We need to address the
question of why changes in life stress (in-
creases or decreases) can substantially affect
craving, why the presence of craving should
exaggerate inaccuracies in driving (Heimstra
et al., 1967) and changes in response to
shock (Nesbitt, 1973) and why craving can
be so rapidly stimulated by external cues.
A few simple assumptions expand the range
of the model. First, it is assumed that several
emotional processes may operate simultane-
ously. These may be from multiple exogenous
sources (thus one can feel threat from work
or social situations and positive affect from
smoking) or multiple opponent processes. One
can also feel threat from work stress followed
by a positive slave affect and a positive affect
from smoking followed by a negative slave
affect.
Second, we assume that emotional or he-
donic states from different sources combine
algebraically at any given point in time. For
example, the negative, exogenously induced
affect of social stressors can lead to a posi-
tive, slave response that can be strengthened
by the positive affective response induced by
smoking if the two overlap in time. The nega-
tive slave response that follows the positive
affect induced by smoking will then add to
any negative affect induced by the continuing
presence of stressors. Thus the negative af-
fective craving for a cigarette will be intensi-
fied by the summation of the slave response
to smoking and the negative affect induced
by social stress.
The third important assumption made in
the model is that changes in plasma nicotine
level generate a variety of bodily sensations
(such as heart rate deceleration) that can be
conditioned to these emotional states (Knapp
et al., 1963; Lucchesi, Schuster, & Emley,
1967; Shiftman & Jarvik, 1976; Shiffman,
Note 4). We emphasize the term sensations
to distinguish the experiences generated by
increases or decreases in nicotine from well-
formed emotional reactions. The various direct
effects of nicotine mentioned earlier and simi-
lar effects produced by nicotine decline do
not comprise a fully structured craving reac-
tion, and it is hypothesized that conditioning
of externally induced or opponent negative
emotional reactions to these sensations is the
 THE SMOKING PROBLEM 393

basis of such a response. This is clearly an This proposal of an emotional memory, our
area in need of study. fifth and final assumption, does more than
A fourth assumption is that smoking does restate the conditioning assumptions made by
far more than generate a positive hedonic Solomon and Corbit (1974). What it does is
state that can cancel the negative affect of provide a mechanism for integrating and sus-
stress or help to sum with the positive slave taining the combination of external stimulus
reactions elicited by such hedonically negative cues (social events, work, nothing to do,
situations. It also facilitates reactions that taste, etc.), internal stimulus cues (sensa-
can directly enhance adaptation to the specific tions from drops in plasma nicotine levels),
situation that is negatively hedonic. For ex- and a variety of reactions including sub-
ample, because smoking increases neural acti- jective emotional experience and expressive
vation, it can increase alertness, useful for motor and autonomic reactions associated with
coping with intellectually stressful situations. the hedonic experience and with smoking.
As a social gesture, it can reduce feelings of The elicitation of any of the components can
insecurity and the perceived threat in social provoke the remaining components of this
settings. By accelerating heart rate, it may memory schema. Hence, it is the schema that
help control anxiety when the arousal gen- makes possible the reexperiencing of craving
erated by external threats is misattributed to when one sees someone else smoke, and it is
the cigarette. Because smoking induces muscu- the schema through which nicotine loss stimu-
lar inhibition, it may enhance relaxation and lates craving because the sensory features of
help to control fear, anger, and level of dis- nicotine loss elicit the other affective com-
tress in a variety of threat situations (Gil- ponents of the schema.
bert, 1979; Malmo, 1975). In this model, differences between smokers,
If smoking can regulate the internal mileau that is, whether they label themselves as so-
by dampening or augmenting arousal induced cial, stimulation, anxiety reducing, addictive,
by external events and at the same time pro- or habitual, will depend on the elements
vide direct help in coping with these events, linked into the schema and on their relative
it is likely that the smoking experience will vividness. One strong possibility is that ex-
be strongly associated with memories of ternal cues such as taste or social settings are
these episodes, and so form emotional mem- more available or noticeable, and people are
ory schemata (Leventhal, 1979, 1980; Leven- likely to use them to label their "reason for
thal & Everhart, 1979). Schematic emotional smoking." The labeling is not totally spu-
memories should combine imagelike repre- rious: Light, social smokers are nicotine sensi-
sentations of situations with impressions of tive (see Herman, 1974), but their nicotine
motoric and physiological reactions in these sensations are linked to craving along with
situations, for example, the subjective emo- imagery of social situations. Anxious smokers
tions experienced in the situation and the are also nicotine sensitive, but their nicotine
autonomic, expressive motor and instrumental sensations are linked to craving along with
behaviors made in that setting. Schemata of imagery of threatening situations. Both re-
this sort will sustain the conditioning of a port the more salient component of the con-
range of memories experienced as craving to crete memory, both show some degree of se-
nicotine levels in a variety of situations. lective sensitivity, with craving elicited by
Leventhal and Everhart give examples of different external cues, and both show nico-
schematic memories such as phantom pain: a tine regulation.
long-lasting memory combining the sensations Heavy smokers are likely to "protect" their
of an amputated body part with the au- plasma levels of nicotine because declines in
tonomic, expressive, and subjective pain ex- nicotine level have been conditioned to emo-
perience associated with it. These phantom tional schemata and now elicit negative emo-
experiences show many of the characteristics tional states, This internal conditioning pro-
of smoking, such as a strong tendency to cess could take some time because the cues
reappear during times of life stress (see are less noticeable or because it takes a high
Melzack, 1973). rate of smoking across many situations before
394 HOWARD LEVENTHAL AND PAUL D. CLEARY
internal cues dominate the onset of craving.
This could account for the time lag in becom-
ing a heavy smoker and would also predict
that individuals who smoke to regulate strong
negative affects will experience internal crav-
ings more quickly and more strongly and have
more difficulty stopping, a common finding in
the literature (e.g., Coan, 1967). One impli-
cation of this model is that an abrupt altera-
tion of the emotional schema associated with
a drug would help break the pattern of
addiction.
Robins, Davis, and Goodwin (1974) re-
ported some fascinating results that are con-
sistent with this prediction. In studying the
archetype of pharmacological addiction
heroin dependencethey found that when
addicted U.S. soldiers returned from Vietnam,
they were surprisingly successful in giving up
their habit. The strongest predictor of con-
tinued addiction was preservice use. Those
who had integrated their drug-taking experi-
ences into everyday experiences continued to
be dependent. Those who had developed a
pattern of use in a different environment
(Vietnam) were able to quit when the environ-
ment was changed. (See also Peele, 1977, for
a detailed discussion of the inadequacies of
the pharmacological model of addiction.) The
use of nicotine across many life situations
prior to efforts at smoking withdrawal may
develop a broad emotional smoking schema
and may account for the difficulty in sustain-
ing quitting. Indeed, it has been claimed that
it is more difficult to quit nicotine than heroin
(Brecher, 1972, p. 2 1 7 ) .
If this model sounds more complicated and
therefore less plausible than a more physio-
logically oriented model of addiction, we
should point out that even the physiological
responses to certain drugs must be explained
with a learning model. For example, Siegel's
(1975, 1977) data convincingly demonstrate
that drug responses such as morphine toler-
ance are conditioned reactions. Repeated
injections of morphine are less successful in
pain reduction if the injections are given in
the same setting in which pain thresholds are
tested. If the injections are given in a very
different setting from that in which thresh-
olds are tested, there is no drug tolerance. In
addition, methadone withdrawal symptoms
have been conditioned to external cues (O'-
Brien, Testa, O'Brien, Brady, & Wells, 1977).
Finally, the model is similar to that devel-
oped by Marlatt (1976) to account for the
effects of alcohol and expectations on response
to drinking intoxicating beverages.
In summary, this interpretation suggests
that the mechanism underlying the change
from light to heavy smoking produces a shift
in the target of regulation; initially, smoking
regulates emotional responses elicited by en-
vironmentally induced stress, then regulates
craving conditioned to external cues, and
finally regulates craving and distress caused
by changes in the level of nicotine itself. In
all instances, however, emotional regulation
is central to the dependence process; that is,
the individual is not smoking just to sustain
plasma levels of nicotine but to suppress the
emotional distress induced by drops in plasma
nicotine levels. The analysis suggests the con-
nection between drops in plasma nicotine level
and craving is not automatic. It depends on a
special history of smoking experience, and it
may be altered by techniques that can dis-
sociate or change the link between affective
states and discrepancies in plasma nicotine
levels. It is likely that the dissociation occurs
naturally in cases in which there are major
reductions in life stress and there is no longer
a negative emotional background to summate
with the more temporary induced shifts of
decline in plasma nicotine levels.
Implications for intervention. The regula-
tion models illuminate the reasons for the
limited success of the last 20 years of inter-
vention research. As we have already made
clear, intervention models to date are based
on the development of a motive to quit
(usually an antismoking attitude related to
health concerns) and a management program
developed either through specific plans, mea-
sures to enhance self-esteem or what Bandura
(1977) calls "self-effectance," or one or an-
other form of behavioral therapy (e.g., con-
tracting, self-monitoring, or reinforcement of
nonsmoking). None of these techniques
clearly focus on changing motivational factors
such as the conditioned emotional schema,
with its sensory and opponent affective com-
ponents, that may underlie the maintenance of
smoking. The evolution of these structures
 THE SMOKING PROBLEM 395

from their origins in individual motivation or pulsion. Such a process may account for the
social pressures to try smoking a cigarette relatively high rate of successful abstention
has led some theorists to conclude these inde- when imagery is used with heavy smokers
pendent motivational systems must be pre- (Berecz, 1972a). When we use a stimulus such
vented, as they cannot be "cured" (Bejerot, as thinking noxious thoughts or an electric
1972). shock to avoid the pitfalls of reward associ-
The nature of the mechanism in the multi- ated with rapid smoking, we have to face the
ple regulatory model does indeed suggest that risk that the distress generated by the punish-
it will be extremely difficult to eliminate ment, whatever its nature, may add to the
craving (see Solomon & Corbit, 1973). The distress generated by being below plasma
key to the difficulty lies in breaking up the nicotine set point and so strengthen craving
emotional memory schema. In conditioning (see Solomon & Corbit, 1974).
terms, it is extremely difficult to produce the This brings us to the second set of alterna-
external and internal sensory (cue) com- tives, techniques for generating and attaching
ponents of the schema without recreating the positive emotion to the cues produced by
emotional reactions (subjective, expressive, drops in plasma nicotine levels. One possible
and autonomic) and thereby strengthening way of doing this is to expose subjects to sham
rather than disassembling the structure. This smoking and have them handle and light cig-
can be seen more clearly from two perspec- arettes but not smoke them. This procedure
tives: (a) the use of rapid smoking to elimi- would be analogous to that used by Siegel
nate craving and (b) the difficulty of produc- (1975, 1977) to extinguish morphine toler-
ing a positive affect to substitute for craving ance. How can strong positive affects be gen-
at the same time that declines in plasma nico- erated when nicotine plasma levels are de-
tine level generate their internal cues. clining? This may happen naturally when
In rapid smoking the smoker is told to puff there are major changes in life situations and
in time to a metronome and continue till he it may also occur in group support procedures
or she feels ill, in the expectation that the used to deal with alcoholism and drug addic-
feeling of illness will attach itself to the tion (Brecher, 1972; Sarbin & Nucci, 1973).
action. However, if therapy begins when the Devising a therapy to condition positive affect
plasma level of nicotine is low (e.g., in the to cues from drops in plasma nicotine level
morning or when the person is anxious), the would be abetted first by procedures designed
initial puffs will be reinforced. Thus the to more clearly identify the sensory com-
therapy provides a reward for smoking at the ponents associated with these drops and sec-
point at which the desire to smoke is highest ond by the generation of these cues by pre-
and does not generate disgust or aversion for cisely controlled alternative methods. Such
smoking until the desire to smoke is gone, methods could aid in pairing the cues with
that is, when the regulatory mechanism no other more positive expressive acts and emo-
longer signals a deficit. It is not at all remark- tional feelings. Agents that block nicotine
able that an individual will feel disgust if he receptor sites, such as pentolinium (Stolerman,
or she overeats or oversmokes, and it is not Goldfarb, Fink, & Jarvik, 1973), might serve
remarkable that aversive conditioning will this function. Positive imagery could be gen-
strengthen avoidance of smoking to cues of erated during these experiences, perhaps using
nicotine excess. imagery emphasizing feelings of health, vigor,
The analysis of aversive conditioning might and self-control. The therapy would also strive
suggest that we need to develop procedures to separate situational imagery (e.g., images
for generating negative affective reactions, of self smoking in social setting, during exam-
such as disgust and aversion, when nicotine inations, or when work loads are high) from
plasma levels are below set point. One might the affective craving and link-these images to
do this by using imagery to induce aversive positive affect clue to self-control.
feelings while one is experiencing the need to The result would be a new schematic struc-
smoke; that is, an image of self or of cig- ture linking situational imagery and body
arettes that converts an appetite into a re- cues to the positive emotion of self-control
396 HOWARD LEVENTHAL AND PAUL D. CLEARY
and to expressive actions and gestures other
than those associated with craving and smok-
ing. Removing the schematic structures for
craving might well produce the cure needed
to maintain long-term abstinence from smok-
ing and reduce the risk that a single cigarette
will reestablish the complete pattern of crav-
ing-based compulsive behavior. Major changes
in societal views of smoking and smokers
could help sustain these new structures, just
as they now establish an environment sug-
gesting connections between smoking and the
regulation of emotional experience in specific
situations. These sociocultural sets orient
smokers and help them find the associations
needed to establish addictive schemata.
Looking Ahead
We do not wish to give a negative view of
the research on intervention, for it has helped
us to define the essential elements in the inter-
vention process, including (a) the develop-
ment of a motive to quit and (b) the learning
of techniques for behavioral management when
quitting. The national survey data also sug-
gests a cumulative impact of antismoking
campaigns on community norms about smok-
ing that is reflected in the surprisingly large
percentage of smokers who regard smoking as
dangerous and have succeeded in quitting
smoking for short periods of time. The data
also suggest that antismoking information and
activity has had a variety of unexpected ef-
fects ranging from the switch to filter cig-
arettes to the passage of legislation protecting
the rights of nonsmokers. In addition, it is
clear that current methods for dealing with
smoking are probably no more effective than
those devised by smokers trying to manage
the problem on their own.
Our reading of the data suggests that anti-
smoking efforts directed at school children or
the community at large will lead to continued
declines in smoking but that the programs
could achieve a greater impact on smoking
reduction if they would make better use of
existing theoretical knowledge. We also be-
lieve these campaigns could benefit by adopt-
ing more flexible goals, such as urging smok-
ers to smoke less, to smoke low-tar and low-
nicotine cigarettes if they do not increase the
number of cigarettes smoked, and to avoid
smoking before retiring (which increases car-
diovascular risk). But we may be reaching the
limit of effectiveness of current intervention
methods, and it is clear that new approaches
are needed to discourage young people from
experimenting with cigarettes and developing
a dependence on them. The goal of preven-
tion will not be met simply with new tech-
niques of delivering information; we need
new kinds of information, information that
builds a more valid, concrete understanding of
the body, its strengths and weaknesses, and
the inadequacies and inaccuracies that exist in
our systems for self-monitoring and deciding
when we are ill or at risk. We need a new
approach to the perception of benefits and
costs of smoking to enhance self-esteem and
social adjustment. Indeed, it may well be
necessary to alter our conception of preven-
tion, to expand the current view of preventing
young people from ever smoking their first
cigarette (a one-chance-last-chance view of
prevention) to a more developmental view.
The developmental view would use knowledge
of the developmental history of smoking to
seek a series of specific junctures at which to
direct different antismoking efforts.
We also need to study smoking as a socio-
logical phenomena. The largest changes in
smoking behavior seem to be a result of his-
torical factors. Changing norms and values,
evolving definitions of the role of the indi-
vidual in society, and shifting perceptions of
the importance of self-regulation as opposed
to technological (i.e., drug) intervention are
all important in determining the extent and
meaning of smoking in our society. The socio-
logical or cultural view of smoking must also
be connected to the individual psychology of
the smoker. The individual's preparation, ex-
perimentation, becoming, regular use or main-
tenance, decision to quit or reduce, efforts to
do so, and success in maintaining quitting and
reduction all occur in a social context. The
norms and values of the context direct the
smoker's attention and provide interpreta-
tions or meaning for specific experiences, ac-
tions, and success and failure in reduction
efforts. Although this goal is ambitious and
possibly unrealistic, it is impossible to under-
 THE SMOKING PROBLEM
stand the meaning of chemical self-regulation
without understanding its context.
Finally, new approaches are needed to deal
with the emotional structures involved in the
maintenance of smoking. The development
and addition of these innovations to our al-
ready considerable armamentarium could re-
sult in a fairly dramatic increase in the prac-
tical success of antismoking efforts and a
substantial increase in the sophistication of
our theoretical models for educational inter-
vention in other risk-inducing life-style be-
haviors.
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