Tobacco Documents Online

PHAIL1tACOi.O6ICAIL A'NDPSYCHIDLfJCICAL: DETERMINANTS OF SMOKING 217 in smoking with even a strongly effective acidifying manipulation which~ours was not. It seems dear t'harof the body's two chief mechanisms for disposing of nicotine, enzymatic breakdbwn and, urinary excretion, of unchanged nicwtine,,tlte urinary excretion route plays by far the lesser role in the confirmed smoker. Nevertheless acidification does affect smoking,behaviour and this finding raises the possibility that it may be usefiallto invoke this bit of pharmacological machinery in order to understand some of the presumed psychological and situational determinants of srnoking rate. Conceivably, events that stimulate smoking may do so:via their action on urinary pH. To learn~ if this guess had' any merit as a possible explanation of the stress-smoking relationship, Schachter et: al (115'Z7b) examined the effects of a variety of academic stressors on pH. In one study, subjects urinated immediately before an obviously stressfui event suehl as d'el'ivering a Coilbquiumlecture or taking Ph.D, examinatimns. And, for control purposes, these same subjects urinated ac precisely the same time on routine, non-stressful'days. The results are presented in Table 17:3 where it cann be seen t'hat for nine of ten subjects, the urine,is considerably more acid'ac on stress than: on control days. Precisely the same pattern is manifest in another study of the effects of stress (Schachter, er a1, 1977b). Nine of the twenty members of an undergraduate seminar Table 117.1 The effects of academic stresuon urinary pH Subject pH' on: Stress Day Control Day Stress-Control E.G. A. CollioquiumiTalk 5.50 6.35: -0.8'5 H:T. 5.70 5.93 -0.2'5 M.C. 6.70 6.90 -0.2b H.K- 5.50 6.20 -0.70 ~ S.S. 5.40 6.4I5 -1.05 Q. E.D. B. Ph.D. Oral Defense 5.40 7.10, -1.7 0 CA 0 A.L. 6.00: 6.2®, -0:20 CA' W C: Ph.D. Comprehensive Examination 0 B.S. 5.85 5:80 +0.05 IV . I /~~ ~1 LS 5.2D 5.70 -0.50. D:P. 5.40 5.70 -0_3.0 All subjpcts(mean) S'.67 6.24! - .57 were assigned to read highly technical material and prepare 1045 minute oral reports for class. The remaining students were simply expected'to listen to the reports. Alll' of the students urinated shortly before class. For the reporters pH'.averaged 6.01 and for the listeners 6.67 (p .OS): Before a control class, pH was identica1for the two

2'1'8' SMOK1NG B'EF+fi#VIOUR groups of students. It does appear that stress, at least of the sort'endernic to~academiC 't<-' .., J however, considerably calmerthangroups of smokers who are prevented from ~ smoking, or: permitted to smoke only low nicotine cigarettes: This fact'can be interpreted as h=,' ' life, acidifies the urine,- a f nding which at least encourages the exploratlom of a pharmacological interpretation: of smoking behaviour, 'fo review the line of argument so far: it has been widely reported that'smoking increases with stress and that smoking is zalming. These observations appear to go hand in hand and to supporr the assert2on that nicotine or tar or some component of the act of smoking is anxiety reducing. The experimental facts are peculiarly at'variance with this interpretation. Smoking dbes.inerease wi th~stressbut smokingg smokers are no more or less calm than a control!group of non-srnokers. They are, indicating that smoking isn't anxiety reducing but'that' not smoking or insuflicient nicotine is anxiety, increasing: In effect, the smoker smokes more during stress because ~-~ of budding withdrawal symptoms andl not because of any psychological property of nicotine or of the act of smoking. Such an interpretation is plausible.if one assumes f>w::., that the smoker smokes in order to keep nicotine atsome constantlevel and that there is something about the state of'stress that depletes the body's supply of nicotine. A variety of studies have been described which, via the:effects of urinary pH' on the rate!of'nicotine excretion, suggest'a biochemical mechanism that couldiaccountfior this set of facts. Though this elegant juxtaposition of facts makes altnost irresistable the conclusior~ that the smoker's tnind is in the bladder, obviously we are hardly yet in a, position to rule out psychological explanations of'smoking. Though'anxiety reduction'' seems, by now, a particularly unsatisfactory explanation of the stress-smoking, relationship, innumerable other purely psychological explana'tions are still conceivable. Ferster ('1970), for example, has attempted to explain the relationship in theseterttas: 'With the increase in emotional syrnptoms there is frequentlya major cessation in rnost of theongo•rng,repertoire the person might engage in. With such a temporary decrease in the frequency in most of the items in al person's repertoue; the relative importance of even the minor reinforcers increases enormously. Thus the relative posit6on of smoking in the entire repertoire is increased considerably whenother, major it'etns of the repertoire are depressed: Sm,oking,becomes something to do when no other behaviour is'appropriate': (page 99). In short, though the effect of pH oni nicotine elimination is a well established pharma- cological fact, it may have little, if anything, to do with the effects of stress on smoking, for it is certainly conceivable that, stress, with or without acrompanyirlg,pH changes, wilI~ affect smoking rate. In order: to learn if pH changes are a necessary and suflficient' explanation of the stress-smoking,relationship, it is clear that we must experimentally pit the:mind against the bladder and this Schachter,,Silverstein and Perlick (1977) - attempted!to do in an experiment, which independent'liy manipulated stress and the pH of the urine. If it is correct that pH changprare a necessary parn of the machinery, we should expect rnore smoking in high, than in low stress conditions when pH is uncontrolled and no difference between the two conditions when pH is experimentally stabilised. If, on the other hand, pH changes are irrelevant to the smoking-stress relationship, therrshoulti be more smoking in high than in low stress conditions no matter what the state of the urine.

PHARMACOLOGICAL AND PSYCHOLOGICAL IDETERMiINANTS OF SMOKING 219 9 In this study, too,, stress was manipulated by use of electric shock. The experimentt alteady describ ed on the effects of stress on smoking,('Schachter et a4 1'977b) was replicated with one majpr modification - in one pair of conditions the high or low stress manipulation began ffity minutes after the subjects took alplacebo; in the other condition, it'began fifty minutes after subjects had taken 3g. of bicarbonate of soda - azr agpnt virtually guaranteed to quickly elevate urinary pH' and for a time to stab- t7ise it at highI}r alkaline levels. In Table 17.4, we note fust the effects of the man- ipulation on uriirary pH. Examining first the two placebo conditions, it will be noted1that pH decreases inithe High Stress condition (p =.02),and tends to increase. Table 17.4 The effects of themanipulartions oin~urinary pH Nfean piH: No. of'subjects whose pH: Condition N Pre- stress Post- stress Pre- post Decreased Stayed same Increased High Stress- Placebo 12 6.00, 5.83: -0.17' 8 3' 1 Low Stress- Placebo 12 5.99 &13 +0:114 4 1 7 High Stress- Bicarbonate 1'2' 6.08' 7.44, +i.36' 0 0 12 Low Stress- Bicarbonate 12' 6.20, 7.01 +0.81 2 1 9 in.the Low Stress condition. In the two bicarbonate conditions, in sharp contrast, pH inereases markedly from the beginning to the end of the experiment and the, stress manipulation has had absolutely no effect on pH. Next we note that on alvariety of seDf•report measures, the manipulation of stress was highly successful in both the placebo and bicarbonate conditions. Obviously, then, the conditions necessary tolpit the psychological against the pharmacological explanatibnof the effects of stress on smoking have been established. Subjects in, High Stress conditions are considerably more tiense than are subjects in Low Stress conditions, whether they have taken a placebo or bicarbonate. In the placebo conditions, however, where pH is uncontrolled„stress aeidi'fies whereas in the bicarbonate conditions, it does not. The effeets of these manipulations on smoking are presenrted in Figure 17.3 which plots the mean number of'puffs taken by subjects once the stress manipulation had begNn. It, is clear that with placebo, there is considerably more smoking in high than in low stress conditions while with bicarbunate, stress has absolutely no:effect on smoking,(interaction p<.01)i It does appear, then, that smoking under stress has nothing to do with psychological, sensory or manipulative needs that are presumably actiivated by the state of stress but is explained! by the effects of stress on the nane of excretion of nicotine. The smoker under stress smokes to replenish nicotine supply. not to relieve anxiety. Obviously, the research presented is an openly reductionist attempt to explain uenu

220' SMOKING BEH,PIVIOUR THE EFFEGTS OF SODIUM BIIIGARBONAT'E AND PLACEBO ON, SMOKING UNDER STRESS NUiMB'ER OF PUFFS 30t . 20 10' T LOM/ DEGR'EE OIF STRESS' HIGH! Fig. 1'7:3

PHARMACOLOGICAL AND PSYCHOLOGICAL DETERMINANTS OF SMOKING 221 of the effects of psychological variables without making,use of the conceptual equipment of psychology. I believe that in the case of stress; the attempt has been successful'for given the facts outlined, attempts to formulate the : stress•smoking relationship in psychological terms (Ferster, 1970;,Hunt, 1970; Marcovitz, 1969; Nesbitt, 1973; Schachter, 1973) seen unnecessary ad hoc constructions. In addition to stress, there is evidence suggesting that this may also~be the case forr the widely reported effects of party-going on smoking. In two studies„Silverstein, Kozlowski and Schachter (1977) have found that party-going does increase smoking and have also toun(V that parties markedly increase unnary acidity. This is true tor non+smokers' s as well as smokers-a finding,which indicates that'it is not'smoking which is the cause -! " of acidity and which rnakes'somewhat more plausible the guess that the urinary pH -• mechanismimay also be responsibie:for the party smoking relationship. I suspect that many of the presumed'psychological and situational determinants of'smoking behaviour may prove reducible tio, these elementary biochemical terms. It must be admitted, however, that satisfactory though this mechanistic view of smoking may be for understanding the behaviour of many, perhaps mosty smokers, the apparent exceptions to this model are maddeningly various. There are smokers (Schachter, 1973) who do: not track nicotine content. Though it is known (Isaacc and Rand, 1972) that plasma nicotine level is zero on awakening, there are smokers who4ind cigarettes distasteful in the morning and do not light up their first cigarette before lunchtime. Though withdrawal is a necessary component of virtuaily any model of addiction, some orthodox Jewish smokers, forbidden to smoke on the Sabbath, report that they can do so without a qualm. And so on. Just how to cope with such blatant exceptions is problematic. Perhaps it is necessary to invent psychologicai'typologies (McKennell, 1'973; Russell, 1974b; Tomkins, 1968) toaccommodate the distressing,apparent variety of smokers, but I find'this'an unsatis• f~ing scientlfc stratagem. As a working hypot'hesis, I propose instead'that virtually " all'Iong-titnesmokers areaddicted and, suggest that, many, perhaps all; exceptions to, an addiction model can b'e understood'in terms of such notions as self-control, cioncera with health, restraints etc. Certainly alI smokers are aware of the dangers andI expense of'smoking: To the extent that such concerns are prominent, the smoker probably inhibits his smoking by such devices as imposing an u!pper, limit on his daily consumption, scheduling his smoking, and so on -devices intended to lower consumption and' which would tend to masksuch behavioural''manifestations of addiction as~tracking nicotine content. If thi's is correct, we should' expect to find other, less obwious indications'of addictionn and, of these, I would'suB8est that withdrawaliis the key. Obviously anyone can give up smoking, limit his daily intake or restrict smoking,to particular times or occasions if he is willing and ablrto put up with the withdrasval syndrome. If it is correct , tharvirtually alliIong,titne smokers are addicted, it should be anticipated'that smokers who don't smoke in the morning wi11, be more irritable at that time of day than in, the afternoon; that smokers who restrain their sm'oking will be more volatile people than heavy smokers, and so on. To: test such expectations, Perlick ('1'977) in the experimentdescribed'e'arlier, compared a group of'heavy, unrestrained'i smokers~ to a, matched group ofhighly restrained smokers, mostly former heavy smokers who on a variety of indices indicated that'they were deliberately and'successfully attempting to cut down, though not eliminate, smoking by a combination of devices . 1DOS0a~~~~8

222' SI+iOKITlG BEEdAV!IbUR' such as smoking cigarettes only halfway, smoking,very low nicotine cigarett~es, counting daily intake and the h7te. On the average these~restrained, srrtokers reported smoking,at a rate less t;han, half of their former level. As described earlier, all subjects rated how annoying they found the noise of each of a series of simulnted aircraft over-flights while, depending on condition, they were either prevented from smoking, or permitted ad lt7iismoking,of'high or of'low nicotine cigarettes. It should be noted first that inithe conditions where they were permitted to smmke, restrained former heavy smokers smoked'oniy half as muclvas did current hearryy smokers. They behaved in the laboratory, then, as they report they do in life. The effects of these manipulations on the two groups of smokers are presented in, Figure 17.4. As noted earlier, the extent to whichiheavy, unrestrained smokers were annoyed depends on the nicotine manipulation. When they did not smoke or smoked very low nicotine cigarettes they THE EFFECTS OF N1COTiNE DEPRIVATION ON THE IRRITABILITY OF' HEAVY S'11OKERS~:NO'N-5M0KER5, AND RESTRAINED SMOKERS ANNOYANCE RATING :-~, :. (MA'GNITUDE ESTIMATION) 3001 A HEAVY 'SM0KER5 5 C NON I SMt)KE'RS' 61f.5TftAIPJED' SMtDKfiRS. 250 200 ~ 150 so 0: lDW NIGM 0 0 LOW MIG ._ NO (0.3 m9) (('3 nn9)' NO N0: (Oa3 i^9)(1'3 ng)' SMit)KJNG NI4 NIG 51MOKUiIG' ' 5A'10KIMG, fiUC NIG NICDTINE W1AN1PULATION Fig. 1 7.41 were markedly more annoyed than when they smoked high nicotine cigarettes. The restrained, former heavy smokers stand' in fascinating contrast for they were: chronically annoyed - as they should be evenlin the high nicotine condition where they were still getting,considerabl.y less nicotine than in former days was their want. In other tests of't'he same hy,pothesis, Perliek (1977) dernonstrates that such, restraiited smokers eat more than do heavy smokers whenigiven free access teicandyand alsu do worse at a proofreading task requiring concentration. Restrained sniokcrs appear to be chronir:a'lly more irascible, to nibble more and to have poprerctonccntratiim than 1005053029

0 PfiAR'hfACOLOGICAL AT;tD!PSYCHOt.OG1CAL DETER%f INANTS 0'(i S~'lID1:IMG' 223' unrestrained smokers. It is possible to control and restrict smoking;bu2 at ai price - and the price appeamto be a chronic state ofwithdrawal.' It does appear that one of the exceptions to a purely addictive view of'smoking is no exception. I suspect that this shalPbe the case with most of these exceptionst and that by'taking,account of withdtanwal we can understand those studies (Finnegan erQl,' 1'945) (Goldfarbb et A 1'970) which fail to demonsurate nicotine regulation. I:et us review our conclusions so far. For the confirmed smoker: 1!. The psychological andi probably the sensory and manipulative gratifcations of smok'ing,are illusory. Serious'smokers smoke to prevent'withdrawal. 2. Smokers regulate nicotine intake. 3, Variations in smoking rate which customarily have:been interpreted in psychological terms seem better understood as an attempt to regulate nicotine. 4. Apparent exceptions to a regulatory model of'smroking,seem understan'dable in terms of'withdrawal.'Ihe smoker who fails to regulate suffers withdrawal. Given this array of factra formidable case can be made:for a predominantly pharmacolbgical„addictive view of cigarettie smoking and it wouldy certain9y seemm that the campaign for low nicotine cigarettes is misguided and rests onia set of fallacious premises. It must be noted: however„that with the exception of the Perlick (1977) study these conclusions are all based on stud'aes in which the state of nicotine deprivation or'lowered nicotine intake is maintained from an hour or so to, at most, a few days as inithe Schachter (1977) study. Can we expect that, in real l'ife„shiffing to a low nicotine cigarette will, lead to a permanent increase in amounts smoked or is there some sort of adaptation process so that eventually the smoker returns to former levels of consumption? ' The question is crucial and particularly so in light of ('a) Hammond et aCs (1976) demonstration th'at heavy smokers of low nicotine cigarettes are in: considerably more danger than light smokers of highh nicotine cigarettes even when tar'and nicotine intake, by'my ealculation from their data, are probab'Iy, roughly equivalent and (b) Ross's ('1'976a, I'9'7'6b) evidence that carbon monoxide, hy,drogen cyanide and nitrogen oxide delivery is:considerably greater inimost of the popul'ar, brands of low nicotine„Filter cigarettes than in high nicotine,, non- filter ;cigzrettes. The!only evidence I know of on the long-time effects of switching brands derivess from a major study conducted by the American Cancer Society (Hammond and Garfinkel, 1964) and a considerably smaller scale version of the same study sponsored by the Public Health Service (Waingrow and Horn, 1968). In both studies subjects were interviewed about their smoking habits'twice over a two-year period. Since • One alternative interpretation of these data must be considered. It is conceivable that naturally irascible:people are most 1Diely to restrain their smoking. If so, thesrresults could bcattributable to self=seleetion ratherthan,withdtawaL Acutely aware of this possibiliry; Perlick (1977)lcompared these groups on numbers of personality and dtmographic variables and found~no diffcrences betwcen, the two groupL t With one exception- therrare a small number of long-time, light smokers who give no cvidence of nicotine reeulation Schachter (I1977) and no indication ofwithdrawal when dcprivedof nicotine; Perlick (1977). What to make of such cases is, at this time, equivocal but by any of the standard criteria of 3ddictionthey appear to be genuinely non•addictedsmokers. 1005053030 _ .,,

224 SMmKPNG BEHAVIOUR over this period many subjects switched brands of cigarettes, it is possiblt to evaluate the effects of changing,brands ow the number of cigarettes smoked. On the basis of such analysis, these investigators conclude that switching to a cigarette with lower nicotine content does not increase the amount'smoked'and on this basis Hammond `" er a4 (1976) justsfy the campaign for low nicotine cigarettes. 11 It shall be my contention that'the particular mode of'analysis employed inithese studies unfortunately obscures the relationship of shift in nicotine level to amount smoked and in fact what, trends exist in these data suggest, for many smokers aa conclusion that is opposite to that drawn by these authors: Though both studies are similar, I shall restrict my discussion to theRammond and' Garfinkel'(1964)) paper for inthe:Wautgrow and Horn (196g) study the number of subjects who switch to lower nicotine brands is so small (I+J = 161) and the data are presented in such a way that it'is impossible from the published material! to make the kindlof analysis requiredl Hammond and Garfinkeli(1'954) divide their group of 98,632 male smokerss into fiour categories - those who in 1959-6b'smoked'less than tien cigarettes a day, 1i0.19 cigarettes a day; 20-39 cigarettes a day; and forty or more cigarettes a day. An interviewee is categorised as changing,the amount smoked only if in 1961-62 his answer to the qtrestion'how many cigarettes do you usually smoke a day?' moves him from one category to another. Thus if a 195'9 pack-a-day smoker were in1'961to report that he smoked 35 cigarettes a, day, he would not be classified as inereasing,ift smoking; only if in 1961' he reported smoking forty or more cigarettes a:day would be be so classified. To understand'the problems created by this particular mode of'categorisat2oniit is necessary to examine a frequency distribution of smoking behaviour. Since Hammond & Garffutkel present only grouped data, I have plotted in Figure 17.5 the distributionn of answers to a question about' daily cigarette smoking included in some of'my own surveys. It is immediately evident first, that most smokers answer such a question in round nurnbers, that is, they say they srnoke twenty, thirty or forty cigarettes a day and second, that in each of the Hammmond'>Garfinkel categories by far the . heaviest concentration of smokers fall at thclower end of the category. Thus in the 20139 cigarettes a day category, 669'o of the subjects report that they smoke twenty ©garettes and 77% report that they smoke fewer than thirty cigarettes a day. Givew this distribution it can be simply calculated that i'f every subject in the 20-39 cigarette category were to increase smoking by 25`h, the liiarnmond-Garfnkel criteria would permit us to classify only 3.5%of t'hese subjects as increasing. Similarly, if every subjeet inthis category were to increase~his smoking by 50% only 24% of all of the subjects wouldibe classif~ied as increasers. Though not as extreme thesame unfortunate dreulmstance!obtainsinitachofthese categories except the 4~0+cigarettes category where, by definition, no one cart: increase smoking, for 40+ is the maximum category. It can scarcelybe considered surprising,that these investigators find relatively few people who increase smoking with time and fand'that changing brands has no effect on t'he amount smoked. Even more perversely a breakdown of the Hammon-Garfnkel data indicates in Table 17.5 a significant tendency for a shift to a lower nicotine cigarette to result in.an increase in amount smokedlin those categories (1-9') and (10-1'9) where, as indicated in Figure t'7.5; because a larger proportion of subjects are at the upper end of the category, the distributions are swchlas to make it more likely that changes will

® PHARMACOLOGICAL AND PSYC1t0LOIGICAL DETERSfINnNTS'OF SMOKING 225 FREQUENCY 01STRIBUIfION OF NUMBER OF GiC,ARETTES_ SMOKED PER DAY' NUMB'E?. OF GhSES 140 T n 120t ' II00t 80t 60} 410 t n wf 1-4 6-9 10 I I-!4 15' I6i9 120 2t24 25 26*?9'30 35 40 45 50 5D l NUN1OEFl OF ClGARJ:TTES 5190KED P[R' DAY 5 Fig. 17.5 be detected. Though these differences are small, they are highly significant and do at' least suggest that an analysis based on a less stringent criterion of change might very well reveal that switching to low nicotine cigarettes has a marked effect on amounts smoked. Ihough~ the results of my own work obviously bias me to this expectation, it is clear that this point is hardly yet proven within the context of a large scale, long time flield study. It is also clear, however, that the majpr body of data that has been used to justify the campaign for low nicotine cigarettes dioesnothung, of the sort. Table 17.5 Changes in number of cigarettes smokedper day in relation to decrease in in nicotine content per cigarette (Adipted from Hammond and Garfinkel, 1964, Table 8) 1961-62 cigarette smoking,of men who smoked: 1- 9 cigarettes a 10-19 cigarettes a 20-39 cigarettes a dny in 1959•60 day in 195I9L60 day in 1959-6i01 Changss ut nicotine content of cigarettes smoked in 1961- 62 vs: 1959-60 Total N % who increase to 10+ Tot'al % who increase to 20+ Total °S who . increase to 40+ 5136 3'9.9' 14047 42.4 51456I 9.3 5132 47.4 13'33 47.3' 4648 9.1. 11.17 12.12 0.2 .001 .001 na. ;:,

226 SMOKING BEHAVIOUR Acknowledgements . . I antindeb'ted'.tt7lDr. Jeremiah Barondess and Dr. Danrid' Rush for their critical reading of this paper. The permission of the editor of Annals of Internal liiedicine to reproduce this article is gratefully acknowledged. References Ashton, H. & Watsonl(1970) Puffing frequency and nicotine intake in cigarette smokers. Brdti.rh hledlcallournal, 3; 679-6811. ~Beckett!, A.H., Rowland, M; & Tiiggs, E.G. (1965), Significance of smoking in investigations of urinary excretion rates of amines in man. Narure. London, 207, 200-201. Beckett, A.H. & Triggs; E.G. (1967) Enzyme induction in man caused by smoking. Nature. London, 216, 587. Domino, E.F. (1973) Neur~opsychopharrnacology of nicotine and'tobacco smoking. In Smoking Behaviour: Motives and Lncemtives, ed. Dunn, W.L. pp.S-3'1, Washington: V.Hi Winston4 Sons. Ferster, C:B. (1970) Cornments on paper by Hunt and'Matarazzo. In Learning Mechanisms in Smoking, ed: Hunt, W.A. Chicagp: Aldine. Finrtegan, J'.K., Larson, P.S. & Haag, H.B: (1'945) The role of'nicotine in the cigarette habit: Science, N. Y., 102, 94-96. Fri 'Uli, C:D: (1!97'i') The!effeet of varying the nicotine content of cigarettes on human smoking behaviour. Psychopharrnacologia; 19, 18'8'-192: Goldfarb4 T.L., Jarvak, M.F. & Glick, S.D.(1970) Cigarette nicotine content asa determinant of'human smoking behaviour. Plychopharmacologi4 17, 39-93: Goodman, L.S. & Gil'rnan, A. (1!9'58) The Pharrrtacological Basis of Tlcerapeutics, New York: MacMillan. . Hammond~ E.C. & Garfinkel, L. (1964) Changes in cigarette smoking: Journal of the Narional Cancer Institute, 27, 4119-4!42. ' Hammond~ E.C., Garfinkel, L., Szidm'an, H. & Lew, E.A. (1976) Some recent fitnd.ings aoncerning cigarette smoking. Paper presented at a meeting on, "The Origins of HumaniCancer."'at ColdiSprings Harbor Laboratory on September, 14; 1976. Heimstra4 N. (1973) The effects of smoking,on mood change. ln Smoking Behaviour: Motives and Incentives ed. Dunn, W:L., pp. 197-207. Washington, V.H. Winston & Sons. Heimstra, Ni W., Bancroft, N.P. & DeKock, A.R. (1967) Effects of smoking upon sustained performance in alsimulated driving task. Aiurals of theNew York Academy of Sciences, 142, 295.307. Herman, C.P. (1974) Externat!and internal cues as determinants of thesmoking behavior of lighr and heavy smokers. Jounral'of Personality and'Social Ps,vchulogy.. 30;664-672.Hunt, W.A. (1970) (ed) Learning hrechanisms in Smoking Chicagu: Aldine. Isaac, P.F. & Rand, MJ. (1972) Cigarette smoking and plasrrta levcls of nicotine. Nature, London, 236, 3081 Jarvik, M.E., Glick„SM. & Nakamura, R.K. (1970) lnhibitioniofcigarctte smoking, by'orally administered nicotine. Clinical Plrarniacolnsy and Tlrrra,herrtics„ 11, 574-576. . 1005053033