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15-40

16. BEHAVIORAL FACTORS IN THE
ESTABLISHMENT, MAINTENANCE, AND
CESSATION OF SMOKING.
National Institute on Drug Abuse

CONTENTS
Introduction .............................................................. 5
The Social Learning Model.. ........................................ 5
The Nicotine Addiction Model . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
A Context for Behavioral Research on Smoking.. ............ 9
The Establishment of Smoking .................................... 12
The Maintenance of Smoking ...................................... 13
The Cessation of Smoking.. ........................................ 14
Conclusions ............................................................... 18
References ............................................................... 21
16-3

introduction
Smoking is a behavior-a highly complex act which is accompanied by
certain cog&ions and hedonic states and based on various biochemical
and physiological processes. In that sense, research on smoking
behavior is at the interface between psychosocial and biological
investigations of smoking. While behavioral research has contributed
greatly to the technology of smoking cessation, relatively few
behavioral investigations have been carried out to elucidate the
mechanisms underlying smoking. Because of this, the present chapter
will focus on social learning theory and nicotine regulation as general
considerations to provide a context for a behavioral analysis of
smoking. An evaluation of the contributions from the experimental
analysis of behavior to the treatment of cigarette smoking and
recommendations for further research will be made. Behavioral
research findings on the establishment, maintenance, and cessation of
smoking will be summarized. Emphasis will be on those stages (16) of
smoking which follow initiation and during which the processes that
contribute to the tenacity of the habit and its resistance to change are
set in motion.
The Social Learning Model
Social learning theory has functioned less as a formal explanatory
model of smoking and more as a methodological approach with an
associated intervention technology (35). The impetus for using
behavior modification techniques has been provided by the belief that
research procedures which operationalize definitions, emphasize well-
controlled empirical research, and are derived from concepts from the
experimental laboratory will provide valuable practical and theoretical
knowledge-a belief justified by the previous contributions of the
behavioral approach toward the understanding of other difficult
problems in human behavior. Behavior modification is derived from
basic research on animal learning by Pavlov and Skinner. It
emphasizes the control of antecedent and consequent environmental
events (stimuli) in determining behavior (4). Social learning theory
represents an extension of behavior modification to situations which
involve interpersonal activity, but it incorporates the added explanati
ry concept of modeling, based on imitation and social reinforcement.
In brief, a social learning explanation of smoking proceeds along the
following general lines (35): The habit is acquired under conditions of
social reinforcement, typically those of peer pressure. Initially the
inhalation of smoke is aversive, but after sufficient practice, habitua-
tion (or tolerance) occurs, and the behavior begins to produce sufficient
positive reinforcement in its own right to be sustained independently
of social reinforcement. Smoking now generalizes to situations other
than the one in which it was originally acquired. It is important to note
16-5

that, from the perspective of social learning theory, smoking is seen as
a learned behavior from the onset.
The analysis continues as follows: Discriminations between situa-
tions in which smoking is punished socially and those in which it is
either ignored or favorably received are formed, and various circum-
stances (both external and internal) begin to control smoking. Insofar
as they are associated with smoking, some situations, such as an empty
cigarette pack or an annoying telephone call, may serve as conditional
stimuli (Cs's) which elicit covert responses. These responses (i.e.,
physiological changes or discomfort, perceived as craving) increase the
likelihood of smoking. In turn, they can serve as discriminative stimuli
(SD's), setting the occasion for the reinforcement provided by smoking.
Moreover, stimuli which are preparatory to the act of smoking, such as
the sight of a cigarette, can function as secondary reinforcers for
behaviors preceding them (for example, purchasing a full cigarette
pack). These cues can also serve as discriminative stimuli for behaviors
which follow them, such as lighting the cigarette, thus forming a
linked chain of responses (a smoking ritual). For successful termination
of the overt act of smoking to occur, the extinction of most or all of the
conditional stimuli, secondary reinforcers, and discriminative stimuli
which make up the habit is required. The way in which these ideas
have been put to specific use in therapy will be discussed in some detail
later in this chapter.
The number of emotional events which can influence smoking are
potentially quite great. If smoking is seen, in part, as an avoid-
ance/escape response to aversive withdrawal states, then, hypotheti-
cally, by a process of stimulus generalization, other dysphoric states
(for example, anger, tension, boredom) might also serve as discrimina-
tive stimuli for smoking. Also, response generalization may occur. In
this case, the smoking ritual serves as a temporary escape (coping
response) from various aversive situations (that is, smoking as a
response which provides relief). Smoking can be seen, therefore, as a
generalized primary and secondary reinforcer providing both positive
and negative reinforcement over a remarkably wide array of life
situations.
From a social learning theory perspective, smoking is difficult to
modify because of its ability to provide immediate reinforcement-
nicotine from an inhaled cigarette reaches the brain in seven seconds
(twice as fast as intravenous administration from the arm). Further-
more, the habit is tremendously overlearned: at ten puffs per cigarette,
the pack-aday smoker gets more than `70,000 nicotine "shots" in a
year-a frequency which is unmatched by any other form of drug
taking (40). While most smokers recognize that sustained smoking can
lead to a variety of unpleasant events, ranging from bronchitis to lung
cancer, the ultimate aversive consequences of smoking-though
potentially of great magnitude-are delayed and therefore have less
16-6

influence over ongoing smoking behavior than immediate conse-
quences. This is a situation common to a number of self-management
problems (37). Unlike alcohol and many other drugs of dependence,
there are few immediately noticeable negative consequences (40).
To a large extent, behavioral researchers have assumed relationships
between environmental events and smoking. Treatment practices have
been based on general theory rather than on research or a functional
analysis of smoking behavior as such. Thus, though part of the promise
of social learning theory has been fulfilled, and behavioral concepts
may have generated new standards of effectiveness in the treatment
of smoking, there has not been a comparable contribution to the
understanding of smoking per se.
The Nicotine Addiction Model
A physiologically based model of smoking, emphasizing the key role of
nicotine as a reinforcer, has evolved from the work of Schachter (.&?,
43) and others like Jarvik (19) and Russell (40). The main focus is on
explaining the maintenance of the smoking habit following acquisition.
Under this formulation, smoking is viewed as an escape/avoidance
response to aversive stimulation provided by periodic nicotine with-
drawal in the addicted smoker. An internal regulatory mechanism is
implied which detects the level of nicotine and maintains it within
characteristic upper and lower limits by regulating the frequency of
smoking (and possibly other intake parameters).
Much of the evidence in support of smoking as negatively reinforced
behavior comes from a series of innovative experiments conducted by
Schachter and his associates over a lo-year span. In one study, Nesbitt
(30) used the amount of shock a subject was willing to tolerate as a
behavioral measure of anxiety. They found that heavy smokers
tolerated a higher shock intensity (were less "anxious") when allowed
to smoke than when not allowed to smoke; nonsmokers tolerated an
intermediate shock intensity. The design did not allow a differentiation
between the possibility that smokers tolerated higher shock intensity
because of a "sedative" effect of smoking (positive reinforcement) or
because smoking constituted escape from withdrawal symptoms
perceived as "anxiety" (negative reinforcement). To test for this,
Silverstein (46) varied the amount of nicotine in cigarettes given prior
to shock presentation. He found that smokers given a high-nicotine
cigarette tolerated more shock than smokers given low-nicotine
cigarettes and that there was no significant difference between
smokers given low-nicotine cigarettes and deprived smokers. He
concluded that the sensory-motor and oral positive reinforcement
provided by low-nicotine cigarettes played a negligible role in
increasing shock tolerance compared with the negative reinforcement
provided by escape from withdrawal symptoms using high-nicotine
16-7

cigarettes. Further support came from the observation that nonsmok-
ers exhibited higher endurance thresholds (lower "anxiety"} than
deprived or low-nicotine smokers. This suggests that "smoking doesn't
reduce anxiety or calm the nerves [but rather that] not smoking
increases anxiety by throwing the smoker into withdrawal" (54. Thus,
a nicotine deficit seems to exacerbate the distress induced by aversive
shock. Heimstra, et al. (1.5) found the same effect for psychomotor
performance on a simulated driving test.
The next problem was to account for why smokers smoke more when
stressed. According to Schachter (M), the debilitating effects of no or
low nicotine are the result of withdrawal, and the effect of stress is to
put the smoker into withdrawal by depleting the available supply of
nicotine. This hypothesis was strengthened and new leads were
generated by biochemical studies showing that, while some nicotine is
catabolized (mainly in the liver, at a constant rate determined in part
by the duration of the habit), a fraction of the nicotine escapes
detoxification and is eliminated directly in the urine. Furthermore, the
rate of urinary excretion is rapid, increases linearly with dosage, and
increases as the pH of the urine becomes more acid. The hypothesis was
confirmed by direct manipulation of urinary acidity through the
administration of mild acidifying agents like ascorbic acid or glutamic
acid hydrochloride or alkalizers like sodium bicarbonate (4.3). In
addition, stressful events associated with heavier smoking increased
urinary acidity and nicotine excretion in the expected direction (4.2). To
test whether stress or urinary pH or both were the independent
variable, Schachter et al. (4.3) independently manipulated stress and
pH and reported that smoking seemed to be under the control of
urinary acidity rather than stress as such.
Schachter's model posits that nicotine is the primary reinforcer
because of its role in reducing tension and distress associated with
nicotine deprivation. If this is true, secondary reinforcers should be
relatively unimportant. For example, smokers should not smoke
nicotine-free cigarettes, and supplying alternative sources of nicotine
should eliminate the desire to smoke. According to Jarvik (19), much of
the evidence for the role of nicotine as the primary reinforcer in
cigarette smoke is circumstantial. Smokers evidently prefer cigarettes
with, rather than without, nicotine; but they will smoke nicotine-free
cigarettes for a while if no others are available. The fact that smoking
such cigarettes is not sustained despite the usual cues for smoking
suggests that the other variables are secondary reinforcers that
extinguish when nicotine-the primary reinforcer-is not present.
Attempts to investigate the role of nicotine as the sufficient condition
for smoking, however, have produced conflicting results. F'reloading
nicotine, by having subjects smoke or chew gum containing nicotine
before testing, did reduce subsequent puffing (20, 21, 25). And
administration of the drug mecamylamine, which functioned as a
16-8

nicotine "antagonist," increased the smoking rate (52). But Kumar, et
al. (21) were unable to demonstrate a dose-response effect on
subsequent smoking when nicotine preloading was administered
intravenously. The fact that lettuce cigarettes reinforced with nicotine
were as unacceptable as non-nicotine cigarettes also seems to
undermine the nicotine-only hypothesis (19). Jarvik (19) concluded that
nicotine may be a necessary but not sufficient condition for smoking
behavior to occur and to be sustained and that more research is clearly
needed to settle the issue of whether nicotine functions as the primary
reinforcer or as a "reinforcing co-factor."
The nicotine addiction model suggests that the smoker regulates
nicotine levels under widely varying conditions. It implies a mechanism
which senses nicotine and provides the impetus for directed behavior-
possibly a central "nicostat" or the integration of the various
peripheral drug effects of nicotine. While the model is plausible and
straightforward, critical tests have yet to be performed. Particularly,
direct measurements of changes in nicotine titer and of the withdrawal
state have not been attempted. Finally, among variables not adequate-
ly explained by the model are the role of environmental stimuli in the
control of the habit, the nature of individual differences in smoking
behavior (for example, light versus heavy smokers and occasional
versus chronic smokers), and the mechanism(s) by which relapse occurs
following withdrawal (35).
A Context for Behavioral Research on Smoking
Clearly, neither social learning theory nor the nicotine addiction model
alone can provide a complete understanding of smoking at present. A
recent model, the opponent process theory (47,48,49,53) does attempt
to link psychological and physiological factors involved in the
maintenance of smoking in a more comprehensive fashion. The
principal features of the opponent process model as it applies to
smoking are as follows: (1) the reaction to cigarette smoke is biphasic,
with a brief pleasurable component (a process) followed by a more
sustained dysphoric component (6 process); (2) the hedonic tone-
pleasurable A state or dysphoric B state-is determined by the
algebraic sum of the two opponent processes at a given point in time;
and (3) stimuli associated with a given state can elicit this state as a
conditioned response after repeated pairings.
The opponent process model assumes that cigarettes contain
substances which provide pleasure (initiate the a process) during early
use. While there may be some unpleasant effects on the first few
occasions, these should be offset by the drug effect or by other
reinforcers such as peer pressure; if not, the act of smoking will not
continue. As cigarette smoking becomes established, the opponent
16-9

process grows in strength: the pleasurable A state weakens and the
withdrawal B state intensifies correspondingly.
Because the b process is the opponent of the a process, the best way
of attenuating the B state is to ingest the substance that produces the
A state. As an operant behavior, smoking is both positively reinforced
by a pleasurable consequence and negatively reinforced by terminating
aversive withdrawal, thus setting up an addictive cycle. As the b
process is further strengthened, still larger amounts of tobacco have to
be smoked to produce a pleasurable A state, resulting in tolerance.
Stimuli associated with smoking (CSa's), such as a pack of cigarettes
or the sight of matches, should elicit a brief conditioned (pleasurable) A
state at stimulus onset and a conditioned withdrawal (unpleasant) B
state at stimulus offset. Furthermore, stimuli associated with the B
state (CSB'S)-SUCh as an empty cigarette pack, empty pockets, no
stores, or "no smoking" signs-should elicit conditioned craving or
withdrawal. The concept of conditioned A and B state elicitors leads to
the important implication that, as the smoking habit becomes well
established and the b process becomes stronger, CSa's elicit a brief
conditioned state which is pleasant but then is followed by a more
extended conditioned craving which intensifies the preexisting
withdrawal B state. Similarly, CSB'S directly elicit conditioned craving,
which also adds to the discomfort of the withdrawal state. An
additional implication (derived from Pavlovian conditioning theory) is
that as CSB'S become stronger, they may become more anticipatory,
leading to shorter redosage and restimulation intervals until an
asymptote is reached. If the smoker quits, the CSB'S and the b process
should weaken eventually through disuse, but the CSa's and the
a process should intensify correspondingly. Thus, if a cigarette is
smoked after a period of abstinence, the pleasurable component has
increased to its original level and the resumption of the addictive cycle
is facilitated. The smoker is clearly locked into the pattern of smoking
and, in that sense, once established, the habit seems to be overdeter-
mined.
The opponent process model has not been tested in formal research
on cigarette smoking, though recent experiments in the area of opiate
addiction do provide general support (31,44, 56). The demonstration of
conditionability, in particular, has important implications for the
understanding of smoking recidivism. Wikler (55) has observed that
environmental stimuli associated with withdrawal may precipitate
conditioned craving (or withdrawal) even after an extended abstinence
period has ended physical dependence in heroin addicts. The opponent
process model predicts a biphasic response by smokers (A state
followed by B state) to the presentation and removal of stimuli
associated with cigarettes during acquisition. Later on in the addiction
process, when tolerance is large, the dominant conditioned effects
should be those of craving or withdrawal (B state predominates). The
16-10

implication for treatment is that unless conditioned craving is
extinguished or modified as a part of therapy, the probability of
relapse will remain high.
There are a number of different issues that need to be resolved
among the current behavioral formulations of smoking before an
adequate understanding is achieved. For example, the nicotine
addiction model suggests that the day-to-day regulation of smoking is
more under the control of pharmacological variables than of environ-
mental stimuli, though their relative contribution remains to be
determined. Moreover, the issue of whether smoking reduces anxiety is
not settled. For example, Hutchinson and Emley (18) have suggested
that nicotine can be classified as a tranquilizer since it decreases
aggression as well as the conditioned emotional response (CER). They
have speculated that difficulty in training animals to smoke under
ordinary conditions may have been because a background of aversive
stimulation is needed to provide motivation to use smoking to relieve
anxiety. Also, as has been mentioned, the pharmacological primacy of
nicotine implied by the nicotine addiction model has yet to be
established unequivocally.
The opponent process model encounters similar problems. For
example, Wikler (55) has argued that certain responses associated with
chronic drug use, such as tolerance or conditioned withdrawal, are
counteradaptations, serving to protect the organism by acting in a
direction opposite to the normal drug effect. The opponent process
model is stated in sufficiently general terms to incorporate these
observations if certain (untested) assumptions are made: Wikler's
observations emphasize the dominant drug-negative B state; in
opponent process theory, the initial drug-positive a process (and thus
the pleasurable A state) is still operative but may be so brief and
attenuated that it goes undetected. Only closer examination of the
time course for the response to drugs at different states of acquisition
will settle this issue. An additional complication has been raised by
Siegel (.&.5), who has shown that the stimuli which constitute the ritual
of (repeated) drug injection can elicit conditioned reactions which
increase tolerance to the drug; extinction of these conditioned
reactions, using a series of saline injections, results in decreased
tolerance. Siegel proposes that tolerance is the result of compensatory
associative processes and is not simply a pharmacological, nonassocia-
tive phenomenon. While opponent process theory can be modified to
accommodate these findings, by defining them as the manifestations of
stimuli which serve as conditioned B state elicitors, the relative
contribution of associative and nonassociative factors cannot be
specified at present. Furthermore, if tolerance is basically an
associative process, the problem of explaining why certain substances,
such as nicotine, produce tolerance while others do not will also have to
be dealt with (3.5).
16-11

The remainder of the present discussion will reexamine some of the
phenomena of acquisition, perpeluation, and termination of smoking
from the point of view of the three models. Special attention will be
given to implications for further research.
The Establishment of Smoking
The establishment of smoking can be seen as the result of initial
experimentation with cigarettes repeated sufficiently often for
acquisition of a habit and/or for addictive processes to take hold.
Among the major variables contributing to initiation are social
pressure and imitation of peers or family members who smoke (1, 11).
The following variables influence the decision to smoke: peer pressure,
best friends who are smokers, parents who smoke, adolescent rebellion,
imitation of adult behavior, and misconceptions concerning the risks of
smoking. A recommendation to conduct longitudinal comprehensive
studies on the acquisition of smoking in the natural environment, and
to determine the conditions under which smoking does or does not
begin, would seem especially appropriate.
Once the smoking habit is acquired, the stage is set for addictive
processes to contribute to the maintenance of the habit and to its
overdetermination under the influence of the variables alluded to in
the several smoking models. Additional physiological variables and
explanatory variables from personality theory and typology studies
(both types described elsewhere in the present report) are clearly
relevant. These two sets of variables suggest a number of possible
mechanisms by which acquisition might take place, although, as
Leventhal and Clear-y (22) point out, they are not necessarily the same
mechanisms which contribute to onset. The need for careful, directed
research in this area is evident to achieve a better understanding of
onset and acquisition which may lead to more effective methods for
prevention and treatment.
A promising approach to the investigation of physiological and
behavioral, as well as psychosocial, factors in acquisition comes from
animal research. Some studies have shown that nicotine facilitates
conditioned-avoidance behavior as well as positively reinforced behav-
ior in rats (51) and that it reduces social or pain-induced aggression in
both animals and humans (18). Analogues of addiction might also be
explored in the laboratory. While the laboratory approach might seem
artificial to some, increasing experimental control by restricting
extraneous variables has been useful in other difficult areas, such as
alcoholism (e.g., Nathan and O'Brien (29)) and heroin addiction (e.g.,
O'Brien, et al. (32)). If such explorations are successful, subsequent
research could be conducted under increasingly complex and more
"natural" conditions. Finally, studies of different methods for
deterring smoking in children (e.g., Evans (7) and Piper (34)) should
16-12

increase understanding of the conditions under which smoking begins
and allow us to identify those environmental patterns which facilitate
the movement from "experimental" smoking to addiction.
The Maintenance of Smoking
Once smoking is established as a habit, a number of factors contribute
to its persistence and resistance to change. Each of the formulations
described above devotes considerable attention to the phenomenon of
maintenance, and a large body of research has been carried out from
various points of view. In a sense, maintenance can be seen as a stage
of smoking characterized by steady-state behavior. Pattern consistency
is provided by environmental influences through stimulus control as
well as by underlying physiological processes regulating consumption
within characteristic limits. As an acquired motivation, smoking
constitutes a behavioral pattern with powerful reinforcing value,
overdetermined to a remarkable degree by its generating mechanisms.
A better understanding of these processes is needed.
With a few exceptions, the determination of environmental influ-
ences on smoking has received relatively little direct attention
experimentally, despite the fact that treatment techniques based on
social learning theory have been used extensively. Among the better
examples of a functional analysis of behavior is a study by Griffiths, et
al. (12). Following detoxification, alcoholics in a residential laboratory
were allowed to consume ethanol at certain times, and the amount of
tobacco smoked was measured under various conditions. Cigarette
smoking was shown to increase from 26 to 117 percent when the
solutions consumed contained ethanol. The effect was robust, was
observed in each of the five subjects, and was replicated 15 times
employing a within-subject design. Control procedures indicated that
the effect did not depend on: (1) the pattern of ethanol ingestion, (2)
adjunctive maintenance through social interactions, (3) the pattern of
days in which the ethanol or ethanol-free vehicle was scheduled, (4)
alterations in the portion of cigarette smoked or the number of puffs
taken, or (5) knowledge that a given drink did or did not contain
ethanol. The study constitutes a good demonstration of the potential of
the experimental analysis of smoking behavior, and the method should
be extended to other problems of interest.
Smoking as an avoidance/escape response to withdrawal implies an
internal regulatory mechanism by which the levels of nicotine (or other
substances) are maintained within limits characteristic for each
smoker. To get at these processes in research, measures should be
taken of smoking behavior (specifying variables such as puff frequency
and duration, depth of inhalation, amount of nicotine drawn from a
standard cigarette), of major physiological variables (for example,
cardiovascular changes, relevant biochemical activity including cholin-
16-13

ergic, catecholamine, and nicotine changes), and of cognitive variables
(for example, hedonic states and the subjective desire to smoke at
different points in time). As in investigations on the establishment of
smoking, a laboratory approach may provide a good initial strategy, if
supported by adequately controlled studies in the natural environment.
As a preliminary step, the variables involved in nicotine regulation
should be explored directly in habitual smokers by studying the
relationships between the act of smoking, subjective desire, and plasma
nicotine levels. Also, nicotine excretion rates could be shifted using
techniques identified by Schachter, such as drugs or psychological
stress, to provide further modulation of physiological, behavioral, and
subjective responses, thus replicating and extending previous work in
this area. The demonstration of the contribution of nicotine by direct
measurement might stimulate further explorations of the relationship
between smoking behavior and other important biochemical variables
such as catecholamines.
The Cessation of Smoking
Both initiation and cessation can be conceptualized as the result of
decisions (evidenced by stated intention or other overt behavior) to
start or to stop smoking. Thus, cognitive variables may play a major
explanatory role, and the subjective utility of the change under
consideration may provide important clues for predicting its outcome
or success (33). (The cognitive aspects of initiation and quitting are
extensively reviewed in a separate context elsewhere in this report.)
Once the decision to start or stop smoking has been made, however,
behavioral variables and the models described above come into play.
When habitual smokers stop smoking, they may experience a wide
variety of unpleasant side effects, including craving for tobacco,
irritability, restlessness, dullness, sleep disturbances, gastrointestinal
disturbances, anxiety, and impairment of concentration, judgment,
and psychomotor performance (19). The onset of symptoms may occur
within hours or days after quitting and may persist from a few days to
several months. Additional objective signs include a decrease in heart
rate and blood pressure, increased rapid eye movement (REM) sleep,
and slower rhythms in the EEG (35). Spontaneous jaw clenching
(increased masseter potentials) lasting several weeks has been
correlated with verbal reports of irritability (18).
After the ex-smoker successfully overcomes withdrawal symptoms,
further problems may persist. In terms of the opponent process model,
one can construct the following account: Subjectively, the pleasure of
smoking in the addicted smoker is masked by the discomfort of craving
from not smoking. After abstaining for a few weeks, however, craving
decreases. If smoking is resumed, the first few cigarettes seem very
strong and are highly pleasurable. Thus, the stage for re-addiction is
16-14

set. Moreover, various internal and external stimuli may serve as
conditioned elicitors of craving or withdrawal. Particularly trouble-
some may be events too infrequent to extinguish quickly (e.g.,
attending a reunion where former classmates smoke) or emotional
situations which resemble withdrawal (e.g., anticipation of an unpleas-
ant or challenging social event).
A major contribution of the behavioral approach has been the
development of new techniques in smoking cessation-procedures
which seem to be more effective than those that preceded them. In
most nonbehavioral clinics, fewer than half the smokers quit (e.g.,
Guilford (13)), and of those who quit only 25 to 30 percent are still
abstinent 9 to 18 months later (17); the estimated long-term abstinence
rate in nonbehavioral treatment is about 13 percent (27). The three
main lines of behavioral treatment have involved punishment and
aversive conditioning, stimulus control and contingency management,
and controlled smoking procedures. While a thorough review of the
modification of smoking is provided elsewhere in this report, the
contribution of social learning to therapy is of sufficient importance to
warrant a brief review here.
Aversive conditioning techniques are the oldest and most widely
utilized behavioral procedures for smoking cessation. Among the
aversive stimuli used have been electric shock (e.g., Best and Steffy
(a)), covert or imagined aversive events, and cigarette smoke (e.g.,
Resnick (39)). The typical procedure has involved contingent punish-
ment for overt smoking behavior in the laboratory or in the natural
environment (e.g., Powell and Azrin (38)). Some investigators have
attempted to punish motoric and cognitive components as well (e.g.,
Steffy, et al. (50)). With the exception of aversive smoking procedures,
aversive conditioning techniques have not produced outstanding
results (Bernstein and Glasgow (2)).
Aversive smoking combines the principles of extinction, negative
practice, and aversive conditioning, using stimuli from the cigarettes
themselves as the aversive component. The procedure assumes that the
positive reinforcing aspects of a stimulus are reduced and become
aversive if that stimulus is presented at an artificially elevated
frequency or intensity. A further assumption is that aversion based on
stimuli intrinsic to the maladaptive behavior is more salient and
generalizable than that from artificial sources such as shock (Bernstein
and Glasgow (2)). The most successful use of aversive smoking can be
found in the recent work of Lichtenstein, et al. (24, using a technique
called rapid smoking. The procedure calls for smoking cigarettes at a
rapid rate (inhaling smoke about 6 seconds after each exhalation) until
no more can be tolerated. Sessions are repeated on a daily basis until
the smoker no longer reports a desire to smoke; booster sessions are
provided if the desire returns. In a recent review of several studies
using the procedure, the abstinence rate was 54 percent in short-term
16-15

follow-up and 36 percent in long-term follow-up (2 to 6 years after
treatment). Though the method was a clear improvement over
previous approaches, there are a number of problems which may make
it less than the optimal procedure for the elimination of smoking. In
particular, individuals with cardiopulmonary diseases-those who most
need help-are the least likely to tolerate intense exposure to tobacco
smoke without ill effect (35). Moreover, rapid smoking may be
dangerous even to seemingly healthy people (28).
Another social learning approach to the modification of smoking
behavior is represented by stimulus control tactics. The basic assump
tion is that smoking is associated with or controlled by environmental
cues and that these cues (discriminative or conditional stimuli)
contribute to the persistence of the habit (2). Treatment involves
gradual elimination of smoking through programmed restriction of the
range of stimuli that lead to smoking. Typically, self-monitoring is
used to increase awareness of smoking along with designated daily
quotas to provide targets for reduction (36). In general, stimulus
control procedures have not been very effective in isolation (e.g.,
Levinson, et al. (23)). When used in combination with contingency
contracting, in which deposited money is reimbursed for reaching
specified goals (e.g., Elliott and Tighe (6)), and with other techniques,
however, considerably better results are achieved (Bernstein and
Glasgow (2)).
Recent research on multicomponent treatment procedures (employ-
ing techniques such as stimulus analysis, interference with situational
control or environmental stimuli, social and monetary reinforcement of
incompatible behavior, group support, and follow-up sessions, present-
ed in an integrated sequence) has produced results as favorable as that
reported for rapid smoking, with 61 percent of the first 100
participants quitting smoking after eight sessions of treatment and 32
percent not smoking a year after the onset of treatment (36). These
data account for all smokers who entered treatment (including the 15
percent of the sample who could not be reached and were classified as
smoking) and were based on self-reported smoking status corroborated
by urinary nicotine analysis. The recidivism rate of 49 percent also
compares favorably with the `70 to 75 percent recidivism reported for
nonbehavioral clinics by Hunt and Bespalec (17'). These positive
findings are qualified somewhat by the observation that not all
multicomponent treatment combinations are successful (e.g., Danaher
(5)) and by a controlled multivariate study by Flaxman (8) indicating
that the variables responsible for a successful outcome are poorly
understood.
Smoking practices have changed considerably in recent years as
smokers have attempted to reduce health risks on their own
(Hammond, et al. (14)) by switching to filtered and low tar/nicotine
cigarettes (Russell (41)). These natural trends provide a context for
16-16

recent research by Frederiksen and associates (9, IO), demonstrating
that behavioral technology can be used to control not only the rate and
strength of cigarettes consumed but also to modify the topography of
the habit. Additional impetus for the research comes from the fact that
many smokers report difficulty reducing their smoking rate below 10
to 12 cigarettes per day (Levinson, et al. (23)). While it has been
suggested that the reason for this is that the positive reinforcing value
of each cigarette increases when fewer are smoked (Mausner (26)),
according to opponent process theory there should be a corresponding
lessening of the negative reinforcing effect resulting from withdrawal
from nicotine over time. Clearly more research is needed to settle this
issue. The technology developed by Fredericksen is still in the clinical
development stage, and the long-term stability of the changes has yet
to be determined. However, because some smokers are motivated to
reduce their health risk even though they are unable to quit, controlled
smoking technology may provide a useful alternative to the more
traditional abstinence-oriented treatment and deserves further explo-
ration.
While recent behavioral treatment seems more effective than
previous approaches, 50 percent recidivism and 33 percent long-term
abstinence leave considerable room for improvement. What is needed
at present is outcome research directed at demonstrating the relative
effectiveness of complete treatment packages in long-term randomized
clinical trials. Subsequently, when a given procedure is shown to be
superior in independent replications, components can be partitioned
out and tested in order to produce clinical procedures that are both
effective and efficient. Research designs should take into account the
fact that recent improvements in outcome statistics for smoking-
cessation clinics may reflect changing social attitudes toward smoking
and higher levels of motivation rather than better treatment as such
(2-59.
In an important sense, current treatment efforts-especially
behavioral treatment-have been devoted primarily toward the
modification of the overt act of smoking (an operant behavior). Less
formal attention has been given to the cognitive and physiological
re;pondents that constitute precursors of smoking (e.g., craving and
withdrawal) and that are under the control of both environmental
(exteroceptive) and emotional (interoceptive) stimuli. Moreover, the
increased success of multiwmponent programs may well be the result
of more effective handling of these variables, using integrated
sequences, than has been possible with unicomponent approaches. The
fact that various previously neutral stimuli have been shown to elicit
conditioned craving or withdrawal after being paired or associated
with these states in various addictions has important implications for
smoking treatment.
                                         16-17

Treatment can be seen as extinguishing the act of smoking but not
necessarily the concomitant conditioned cognitive or physiological
respondents. As a result, the ex-smoker may continue to be exposed to
various stimuli which have been associated with smoking, and the
probability of relapse will remain great (for example, in the "negative
affect" smoker (36)). Demonstrations that continued autonomic or
cognitive reactivity persist after standard smoking-cessation therapy
might lead to an entirely new approach to the old problem of relapse.
Studies comparing a standard smoking-cessation treatment with
"deconditioning" therapy, in which autonomic responses are extin-
guished in a simulated environment or modified directly using
biofeedback, might lead to a demonstrably lower rate of recidivism for
those smokers exposed to augmented therapy. The above suggests that
basic research which leads to a better understanding of the mecha-
nisms underlying smoking may result in the eventual development of a
truly rational and more effective therapy for smoking.
Conclusions
The present chapter makes no claim to be exhaustive. Rather it has
surveyed selectively what is known and not known concerning
behavior in the establishment, maintenance, and cessation of smoking.
The object has been to develop a context for directing research, for
improving treatment, and for guiding social policy. In closing, a few
specific recommendations seem appropriate.
While it is difficult to pinpoint accurately which of many research
possibilities will be most fruitful on an a @ori basis, certain themes
seem particularly important for current behavioral research. They are
the phenomenon of withdrawal, the reinforcing effects of nicotine, the
role of nicotine antagonists or blockers, and the behavioral pharmawl-
ogy of cigarette smoking.
1. Withdrawal symptoms of varying severity following cessation are
among the principal reasons cited for relapse to smoking. Little
scientific information is available on the sequelae to abstinence,
however, and at present it is difficult to assess accurately their
contribution to recidivism.
2. As discussed at some length, the problem of analyzing the
reinforcing effects of nicotine is of great importance in understanding
smoking. The role of nicotine as a positive and negative reinforcer
should be examined in animals using various routes of administration
as well as explored systematically in humans in laboratory and natural
settings.
3. A related theme is derived from recent research suggesting that
specific CNS receptor sites for nicotine can be blocked in a fashion
analogous to the opiate antagonists. This phenomenon has implications
16-B

for understanding the effect of nicotine on the body as well as in
helping smokers who have stopped to maintain abstinence.
4. The behavioral pharmacology of smoking deserves further
emphasis. A more precise definition of smoking behaviors, involving
psychometric analyses by puff volume, inter-puff interval, total
amount smoked, and rate of smoking may have important implications
for the understanding of stimulus control as well as of the relationship
between blood nicotine levels and cigarette self-administration.
Similarly, the development of objective criteria for validating depen-
dent measures (such as self-reported smoking behavior using various
biological assays) seems worthwhile.
In the treatment area, further improvement is clearly needed.
Multicomponent procedures have provided sequences for handling
different aspects of the smoking-cessation process; and components
dealing specifically with problems in measuring baseline smoking,
facilitating reduction, inducing abstinence, and managing side effects
have been developed. Among the major current deficits for all
approaches and programs, however, is maintenance of nonsmoking.
Several suggestions have been made from a behavioral point of view.
These include: (1) dealing promptly and effectively with the potential
side effects of quitting (such as obesity and tension); (2) developing
alternative activities to replace smoking (such as regular physical
exercise or formal relaxation techniques); (3) providing a cognitive
focus on mastery, self-help, and individual responsibility; and (4)
adding "booster" sessions and continued interpersonal support in
extended follow-up. Much more remains to be done-especially on the
utilization of techniques derived from basic research, such as the
extinction of conditioned craving described above.
Behavioral research may also make contributions to social policy. For
example, the suggestion that nicotine plays a major or dominant role in
the self-regulation of smoking raises the issue of the appropriateness
of trying to persuade people to smoke low-tar, low-nicotine cigarettes.
As Schachter (4.2) puts it, low-tar, high-nicotine cigarettes might be
safer because fewer cigarettes would be smoked, thereby minimizing
exposure to the products of incomplete combustion known to enhance
the atherosclerotic process and to increase the risk of myocardial
infarction (19). This problem could be investigated further, using a
careful description of the number of cigarettes smoked and the number
of puffs per cigarette (backed up with quantitative determinations of
nicotine, carbon monoxide, tars, and other smoke products), to provide
more exact information than is currently available from surveys of
smoking in the natural environment. Finally, a greater understanding
of the stimulus control of smoking and its limits may be very valuable.
From a behavioral perspective, the current growing emphasis on the
social unattractiveness of smoking (for example, the nonsmoker's
rights movement) is helpful, because it provides a method which
16-19

administers more immediate social reinforcement for quitting and
staying off cigarettes than has been possible when the focus was
strictly on the health consequences of the habit. It should be noted that
the effects of these social processes on the decision to quit smoking are
still relatively underexplored.
Much work remains to be done in the behavioral research area.
Sufficient progress has been made, however, to indicate that the
development of a rational therapy for smoking based on a scientific
understanding of smoking behavior and its underlying mechanisms
constitutes a worthy objective.
16-20

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17. SMOKING IN CHILDREN AND
ADOLESCENTS: PSYCHOSOCIAL
DETERMINANTS AND PREVENTION
STRATEGIES.
National Institute of Child Health and Human
        Development

CONTENTS
Introduction .............................................................. 5
Current Smoking Patterns and Beliefs.. ......................... `7
Relevant Conceptual Models in Developmental and Social
Psychology ............................................................. 9
Typical Psychosocial Influences on
the Smoking Decision ............................................. .12
  Changing Sex Roles.. ........................................... 13
  Parental Smoking Habits ...................................... 13
Parental Acceptance of Children's Smoking ............. 13
  Siblings Who Smoke.. .......................................... 14
  Rebellion Against Family Authority ...................... .14
  Peer Pressures .................................................... 14
  School Environment.. ........................................... 15
  Mass Media.. ..................................................... .15
  Individual Characteristics ..................................... .16
  Perceptions of Dangers of Smoking.. ...................... 17
Critical Evaluations Of Some Current
Prevention Programs ............................................. .17
  Public Information Campaigns ............................... 1'7
  School Programs ................................................ .18
  General Comments.. ............................................ .21
Some Recommendations for Future Research and
Prevention Programs ............................................. .22
References .............................................................. .26
17-3