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17. Pharmacological and Psychological Determinants of Smoking

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Schachter, S.
Thornton, R.E.
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Ashton
Bancroft
Barondess, J.
Beckett
Christ, J.
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Emley
Ferster
Finnegan
Frith
Garfinkel
Gilman
Glick
Goldfarb
Goodman
Gritz
Haag
Hammond
Heimstra
Herman
Horn
Hunt
Isaac
Jarvik
Johnston
Kozlowski
Larson
Lucchesi
Marcovitz
Mckennell
Nakamura
Nesbitt
Perlick
Rand
Ross
Rowland
Rush, D.
Russell
Schachter, S.
Schuster
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Tomkins
Triggs
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Annals of Internal Medicine
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Schachter, Si. Pharmacological and Psychological Determinants of Smoking,. In: -Thornton, R'.EI. (Editor). Smoking Behaviour. Physiological and, PSychological Ihfluences. Edinburgh, Churchill Livingstone, 1978, pp.20S-228'. The low nicotine and tar campaign is based on the notion that ci'garette smoking stems from a variety of psychological, sensory and manipulative needs which,can probably be as well satisfied with a low as with a high nicotine cigarette. If a smoker is smoking to keep nicotine or its meta- bolites at some optimal level, if he switches to low nicotine brands, he may smoke more cigarettes and take more puffs of each. In this case the concerned smoker should smoke high, not low, nicotine cigarettes. The recommendations for smoking low or high nicbtine cigarettes depends onn the relative importance of the pharmacological versus phychological needs satisfied by smoking. Studies on the effects of nicotine on shock tolerance, irritability, and stress and those that support aipharmacplooical basis for smoking behavior are reviewediwith the conclusions that: (1) The psychological and probably the sensory and manipulative gratifications of smoking are illusory. Serious smokers smoke to prevent withdrawal. (2) Smokers regulate nicotine intake. (3) Variations in smoking,rate which customarily have been interpreted inipsychological terms seem betterr understood'as an attempt ot regulate nicotine. (4) Apparent exceptions to a regulatory model of smoking seem understandable in terms of withdrawal. The smoker who fails to regulatp suffers withdrawal. Therefore, a serious case can be made for a pharmacological, addictive view of cigarette smoking, unless there is a long.-term effect of switching brands soithat smokers~ eventually return to their former level of consumption. Two such studies on long.-term effects of switching brands are reviewed. Overall conclusions are that switching to:low nicotine cigarettes results in an increase in amounts smoked so:that the campaign for low nicotine cigarettes is not ustified.
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17. Pharmacological and! psychological determinants of srmoking The gist of the anti+smoking campaign is simply ''Quit and! if you can't or won t quit, switch to~a low-nicotine, lotiv-tar cigarette'. With the backing of the American Cancer Society, the Royal College of Physicians and the Public Health Service, this message pervades the mass media and appears responsible for the tedious competition among,tobacco companies for the safest cigarette, thesearch for an acceptable tobacco -free cigarette stimulated by the British government and taxation policies such as that of New York' City which taxes cigarettes by nicotine and tar content in an apparent effort to use economic muscle in order to help the smoker help himself.' Though no one has bothered'to make explicit the premises on whichsucli policy is based, it appears reasonable to guess that, in part, the lovv nicotine and'tar corrtpaign is based on the notion that cigarette smoking stems from a variety of psychological, sensory and manipulative needs whirh~can probably be as well satisfied with~a low as with a high nicotine cigarette. The possibility that this campaign may perversely bc increasing the health~hazards of smoking has been raised by Dbmino (1973);, Russell (1974a) and others who point out that there is evidence, after all, that nicotine is addicting. To the extent that the smoker is an addict, he is probably smoking to keep nicotine or one of its actiWemetabolites at some optimal level. If„then, the heavy smoker does switch to low nicotine brands, he may very, well'end up smoking more cigarettes and taking more puffs of each. HewsTl in the process of regulating,nicotine probably gFt the same amounts of nicotine and'tar and unquestionably get more of the combustion products, such as carb=monoxide which appears to be at least as much of a medical villain as tar or nicotine:for it is implicated in the incieased risk to smokers of arterio, sclerosis, ischaemic heart disease,,fetal darnage and so oni(I;arson, Haag and!Silvette,. 1961; US Surgeon General's Report, 1'9°72). If'this shift in level of smoking is permanent, theinet effect of switching to low nicotine cigarettes shouldl beto inerease the dangers of smoking. From this point of view, the concerned smoker should smoke higli, not low, nicotine cigarettes. Since almost everyone would agree that cigarette: smoking involves both pharRna- cologicai and psychological determinants there does seem to be some support for either position. Whether rationality dictates the recommendation of a low or a, high nicotine cigarette depends, of course, on the relative importance of the pharmacological vetsus the psychological needs satisfied by smoking. I F 1005053015
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PEdARa'{ACOLOGICAL AND PSYCHOLOGICAL DETERMINANTS OF SbfOICIM6 209 On the gratificatio ns ofi smoking Altnost any smoker can convince you and himself that there are major psychologqcal' components to smoking. They will convince yoathat smoking calms them; that it' helps them work; that they smoke more at a party and so on. In short, smoking serves some psychological function; it, does something positive fon the smoker and *T this is the reason he smokes. This emphasis on the functional properties of smoking is at the heart of virtually every serious psychological attempt to understand, smoking. :' Presumably nicotine~or tar or some component of the act of smokingis so gratifying r.Vi4 that despite the well-publicised dangers the smoker is unwilling to give up the habit. :.:~~; Undoubted1v the ultimate eulogy of the act is hiarcovitz's suggestion (Marcovitz, 1969V that 'as a psyehologicall phenomenon, smoking is comparable to the ritual of the Eucharist. There the communicant incorporates bread and wine and iniso doing symbolically introjects the Lord Jesus Christ. This is a conscious process, with the hope of identification, of attaining some of the attributes of Jesus. Similarly, the l ;.;X, 'pcting in an unconscious fantasy some object smoker incor orates the smoke intro J P which wt11l confer on him its magic powers."(p. 11082). Among,these magic powers, smoking,serves to'detimit the body image in the quest torthe sense ot seu; to `relieve the unconscious fear of suffocation' and as 'proof of'iinmortality'. Though ;, ~% ?y no one has matched 14iarcovitz's panegyric, almost all'attempts to account for the habit have assumed that it does something positive for the smoker - an assumption that is shared by the smoker himself for n'umerous studies indicate that heavy smokers report that cigarettes relax them or stimulate them„put them at ease, give them some thirtg to do with their hands, and so on. In short, for both the psychologist and, the smoker, the act of smoking is functionalt it does something fprthe smoker' and this is the rea€onihe smokes. In this paper, I shall concentrate on one of the presumed!motivations for smoking. Smokers widely report that they smoke more _,fV when they are tense or anxious and'they also report that smoking calms them. Smoking, then serves a respectable psychological function and this presumably is one of the motivations for and explanations of smoking under stress. Before worrying through interpretiations of these facts, let us make sure that they are facts. Firstly„does smoking increase with stress?' The avat7able evidence indicates that indeed it does, if the stress is fairly intense: In, two almost'identical experiments (Schachter eral, 1977b;'Schachter, Silverstein and Perlick, 1'977), my associates and'I manipulatedistress within the context'of experiments presumably designed to measure tactile sensitimity: In high stress conditions, such sensitivity was measured by the administratio'n, sporadically over an experimental hour, of a series of intense, quite painful shocks. In!lohv stress conditions, the shocks were a barely percepttbbe'tingle. Between the!testing intervals, the subjects, all smokers; were free to smoke!or not as they pleased. In bothistudies, the subjects smoked'considerably more in higtnh than inilow stress conditions. Turning to the effects of smoking on stress, we ask next does smoking reduce stress? The answer appears to be that it depends upon how you look at it. Silverstein (1976) attempted to answer thequestiiomby measuring how much electric shock a subject was willing to take within the context of a study of tactile perception, The procedure required that electrodes be attachedi to a subject's fittgers, thar he be exposed to a series of shocks of gradually increasing voltag; and that he report when 1o05os301!s
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210, SMOKING BEI3AVIIDt1'It' - he could fust feei t'he shock, next when the shock first becarne.painful and finally when the shock became soipainful that he could no longer bear it. Silverstein assumed ` that,the more anxious the:subject, the less pain he would be willing to tolerate. There! were four experimental groups - smokers who smoked either high or low nicotine cigarettes during the experiment or who did not smoke at all during this time andia group of non-smokers who did not smoke. The results of this experiment are presented in, Figure 17.11. The ordinate plots the number of shocks the subjects endured before calling it quits. It is:clear that =3` smokers take more shocks when they are smoking high nicotine than when smoking low nicotine cigarettes than when not smoking. Given this pattern one has a choice ;., of interpretations: either nicotine decreases anxiety or lack of nicotine increases' anxiety. The choice of depends, of course, on the position of the group of non- smokers who, as can be seen in Figure.17.1 take virtually the same number of shocks. as smokers on high nicotine. It would appear then that, smoking is not anxiety reducing but, rather, that no smoking or insufficientnicotine.is for the heavy smoker, anxiety increasing. Precisely the same pattern of results emergerin~a study of irritability conducted1by Perlick ('1'977'). Within the context of a study of'aucraft noise, subjects„wat'chirtg a,television drama, rated how annoying they found'a series of sim'ulatedlover-flights. Daring,the experunent, heavy smding subjects were permitted ad,lib smoking of high nicotine cigarettes in one cond'ition; of low nicotine cigarettes in anotherr condition and were prevented from smoking in a, thit& condition. Finally, there was a, control group of'non-smokers. The results are presented irn Figure 17.2 where it can be seen that smokers onhigh, nicotine! cigarettes are markedly less irritated. • by this series of obnoxious noises'than are smokers restricted to low nicotine cigarettes or prevent'edl from smoking. However,,t'Iiese high nicotine smokers are neither less nor more irritated! than the group of non+smokers. Again, it would' appear that smoking I doesn't make the smoker less irritable or vulnerable tp annoyance„ not smoking or insufficient nicotine makes him more irritable. This same pattern~is characteristic of psychomotor as well as emotio'nal behaviour. Heimstra, Bancroft and DeKock ('1'967) exarnirted! the hypothesis that smoking facilitates driving performance by comparing ad la3 smokers, depriwed'smokers and non-smokers in a si;%-hour simulated driving test. On a variety of m'easures of'trarking and vigilance, ad lib smokers do neither better rlor worse than non-smokers but do markedly better than deprived smokers. Again and again, then, one finds the same pattern - smokiitr3,doesn't improve the mood or calm thesmoker or improve his performance when compared wsth!the non- smoker.' However not smoking or insufficient nicotine makerhirrticonsidkrably 'There is of course, an alternative interpretation of this consistent pattern. Rather than indicating withdrawal„it is conceivable that people who become smokers ue by nature more frig}itenedlof;shocltf more irritated by noise and worse drivers thanpeople:who never becomesmmkus, and that for sueh, people smoking is indeed calming and does improve psychomotor performance. Though nothing short of a longitudinal study could' unequivo+cally settle the matter, it shouldibe noted,that there have been a formid9ble number of studies that compared smokers and non-smokers onivirtually every personality dimension imaginable. Smith (1'97l)) in hisaeview of thisiliterature concludes'thatthe only variables which, with reasonable consistency, disctdrrtinate : between smokers and non-smokers are extravers'ion and anti-social tendencies: And evenion these variables the differences are quite small. 1005053017
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PHARtitA'Ct)LOGICAL A14D PSYCHGLOG1CAdi DE71SR.Ni[NANTS OT SM©K1NG 2111 THE EFFECTS OF NICOTINE ON TOLERANCE OF SHOCK NUN1B'ER OF SHOCKS 20 t c~.._ NON-SM0KERS 15 10 0-3 rrrg 1 I nrng LOW HIQ,H NICOTINE CONTENT Fig. 17.1 1005053018
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212 SMOKING BEHAVIIDUR' THE EFFEGT& OF NICOTIINE' ON' 1RRITABILl~TY~ A b' HEAVY SMOKERS NiOW S'M©KEP5 ANNOYANCE ftATIING (MAGNITUDE ESTIMATION). 300 t 250 t 200 } 100 ~ 50 f 0 LOW HIQH 0 NO (0-3n)(I-3'mg), NO SMOKING NIC NIC SMOKING Fig. 17.2 NICOTINE N'1ANIP'l1LAT10N, worse on all dimensions. Given this persistent fact, how then, to account L the fact that the smoker smokes more when he is stressed? One can, obsious:.; i*,.ounr fimr the generally debilitating,effecxs of no or low nicotine by assumir,g th_: ;he deprived smoked is in withdrawalibut this assumption alone cannot accou_ fo; the effects of sUress on smoking rate unless one assumes tharstress, in so-ie f~on; depletes the available supply of nicotiine. And this hypothesis, of coursr _: ic,Ount, for this pattern of data only if it is the case that the smoker, an addiz„is S=:rking to keep nicotine at a constant level. 1005053019
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PHARMACOLOGICAL AND PSV!CHO'LpGICAL D'ETERS6iI'NANTS OF SMOKING 213 Anotherway of phrasing this same conclusion is that the heavy smoker gets nothing out of smoking. He smokes only to prevent withdrawal. I' freely admit that this is a perverse conclusion to reach about a habit that is quite as costly and universally' pervasive as smoking but the existing data for humans don't encourage any other conclusion. Though my colleaguerand I have found occasional hirtts that smoking may do something,for the smoker when compared to the non-smoker (Silverstein, as subjects. It may be that in the early stages of the smoking habit, there are indeed ... .,: rnajorgrati'frcations and effects, that the smoker gradually adapts to these effects andi 1976) in general these differences ~ have been quite small. In addit6on; Heimstra (1973'). has presented tentative evidence that'smokers may have somewhat less mood fluctuation than non-smokers and there have been numerous studies (Larson er al, 1961) suggesting that smoking may affect one or another psychomotor or mental ability but inigeneral these have allibeenismall effects and inconsistent from study to study. It should be noted, however, that altnost all studies of the matter have used long-time, heavy smokers by the time smoking no longer does anything,for hirrt he is t'horoughiy addicted. or some nicotine metabolite as the active:agent, is addicting, the evidence in support of this assumption is puzzlingly inconsistent. On the assumption that one manifesti ation of addictionlis the regulationlof nicotine intake, studies of the matter have either pre.loaded subjjects with varying amounts of nicotine or have manipulated the nicotine content of t'he available cigarettes and measured the effects on smoking. There have been at leasc ten such studies on human subjects with results varying fromino indication of regulation to one study which appears to indicate exquisitely precise eontrol'of nicotine intake. At one extreme, Finnegan, Iarsoniand Haag (1945) and Goldfarb, Jarvik and Glick (1970) supplned subjects with severallweeks' worth of cigarettes of varying nicotine content, and checked daily cigarette consumption. 'I?hough bothh studies did find some subjects who regulated - i_e:, smoked substantially more low than high nicotine eigaret'tes - the groups of subjects as a whole failed to demonstrate regulation; In sharp contrast, Ashton and Watson (1970), observed subjects smoke high and low nicotine cigarettes under controllediconditions and' found evidence of . precise regulation in that theu subjects puflfed'considerably more at Iuw than athigh nicotine cigarettes and, via this mechanism, extracted almost the same amount of nicotine fromithe two kinds of cigarettes. Betweemthese extremes Frith (1971) and Russell et al (1973) find! reasonably gpod evidence of nicotine regulation and' at least five studies (Herman,1974; Jarvik, Glick and N,lkamura, 1970; Johnston, 1942;, Kozlowski, Jarvik'and Gritz, P975; Lucchesi; Schuster and Ernley, 1967),have found a tendency for smokers to regulate nicotine intake but, at best, crudely and impreciselly. Though there is probably no single, simple reconciliation of this spectrum of diverse results one suggestion may partially account for the general failure to find concltzsive evidence for the precise regulation that might be expected from the addictionhypothesis.. There are smokers who don't inhale; there are smokers who simply toy with the habit smoking an oceasional cigarette at parties and meetings and', most importantly„there are undoubtedly many smokers, sensitive to the health hazards, who deliberately itahibit: smoking by such devices as imposing an upper linut' on daily consumption, scheduling Nicotine as addiction Though almost everyone would probably agree that cigarette sntoking, with nicotine 1005053020
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T 214 SMOKING BEHAVIOUR smoking, restricitng,smoking to particular occasions and!so on- all deyiccs intcnd'ed .-= _: P to lower consumption and which would tend to mask such behavioural'mani'festations : ; of addiction as tracking nicotine content. To the extent that such pcople are subjects in studies of regulation, one should expect that the manipulationn of levc[of nicotine ~' would have weak effects on smoking behaviour. ~ In aniattemptto eliminate such, subjects, Schachter(i1977) deliberately selected!a : group of subjects who satisfied the:following criteria: a. By self-report, the subject currently smoked1 at least a pack a day and had'smoked • at this level for many years. b. By sellf-report, the subject was trying neither to cut down or limit his smoking. c. If the subject had every attempted to quit, he reported great difficulty and suffering. - d. By self-report, the subject exhibited 'regular' smoking behaviour, i.e. smoked about the same amount each day, began smoking in the rnorning,and continued' regularly throughout the day, etc. . The salient characteristics of each of these subjects are presented on the left side of Table 17.1 where it can be seen that they al1 had smoked a, pack or more a day for at least twenty years. Bor the course of the experiment these subjects agreeditp smoke onlythe:experimenter's cig4retrcies and on aiternating,weeks each subjectwas presentied with cartons of specially prepared and packaged cigarettes which delivered! either 1.3 mg of nicotine per cigarette or 0.3 mg of nicotine per cigarette. Art bedtime, the subjects noted the number of cigarettes smoked. Obviously, there was an inherent and deliberate circularity in the design of this study. I'was simply asking,do smokers who appear to be addicted by one set of criteria (behavioural selfdescription)„behave inianiaddictad fashion on a totally independent criterion (nicotine regulation)? The effects of'the nicotine manipulation are presentedion the right side of Table 17.1. Obviously, the manipulation had a strong Tabte 17.1 The effects of nicotine content on smoking Subject Characteristic_s Smoking Behaviour. Cgs/day on: Subject Age Sex No. yrs. a serious smoker No. cigs/day self-report Low (0.3 mg) Nic High (1.3 mg) Nic qo Increase High Nic to Low Nic J.A. 52 F 30, 30 31.25 21.S0 +45.3 S.S. 37 F 22 40 S5:0D, 40S0, +35.8' R.R. 38 F 19 40 42:50' 30.75 +38.2' R.S. 41 F 27 20 22.75 20.00 +113.8 QR 47. F 29 40-45: 70.75! 58.75i +20:4' R.a. 50 M 40 30 ' 30:25I 26.25 +15i2 1.E S2 M 33 33 48.00 44.25 + 8:5 Mean 45.6 28.6 33.6 42.93 34.57 +25:3
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PHARtitACOLOGICAL AND PSYCHOLOGICAL DETEMUINiAMmS'OF'SMOKING 2'1'S and consistent effect on these long-t2ine heavy smokers for each of them smoked more low than high nicotine cigarettes. One the average, there was a 2S% increase (pG.01) ~, of smoking accompanying the manipulations of nicotine content. that the manipulation involved a fiour-fold d'ifference in nicotine content wh9e smoking .... increased, only 25%„it would appear to be at best crude and imprecise regulation. There . ..~„ It does appear, then, that heavy, long-time : smokers do regulate nicotine. Given ; is,, however, reason to believe that nicotine regulation is considerably more precise than ; , these data suggest, First, several studies(Ashton and Watson, 1'970; Herman, 1974; cigarettes would have:to smoke almost nine packs a day of our low nicotine cigarettes to get his customary dose of nicotine. Under these circumstances, virtually any theory Schachter, et al, 1977b) report that smokers puff more at low than at high nicotine cigarettes - clearly a mechanism for increasing,nicotine intake. Second, given the range of nicotine content inithisstudy precise reaulation was virtually impossible. For example, a subject' who normally smoked two packs a day of 1.3 mg nicotine of addiction would, predict withdrawal for the subjects on low nicotine cigarettes. It does appear, then, that heavy smokers do adjust smoking rate so as to keep nicotine at a roughly constant level. To account for this fact, one may suppose that there is an internal machine of sorts -one which d'etects the level of nicotine and regulates smoking,accordingly. To beginconsideration of the nature of svch a regulator let us review some of the basic facts about the metabolic fate and excretion of nicotine. As summarisedby Goodman!and Giltnan (1958): 'Nicotine is chemically altered in the body, mainly in the liver buG also in the kidney and lung. The fraction of nicotine which escapes detioxicartion is completely eliminated as such in the urine along with the chemically altered forms. The rate of excretion of'the alkaloid is rapid, and increases linearly with the dose. Whentheurineisalk~aline, only one fourth as much nicotine is excreted as when the urine is acid; this is explainedd by the fact that nicotine base is reabsorbed from an alkaline urine: (page 622). The effects of the acidity of the urine on the rate of excretion of unchanged! nicotine suggests, given the fact that smokersregulate nicotine intake, that the pH', of the urine may affect the rate of'smoking. Whether an effKct' of any consequence is to be anticipated„however, depends on the proportion of unchanged nicotine which is excreted. One can make reasonably accurate estimates from the work of Beckett and hisassociatesi Beckett„Rowdand and Triggs (1965) have shown that subjects who smoke twenty cigarettes a day excrete anaverage of 1'.0pg nicotine per minuteunder normal cond'itions„ 5:0 1y g nicotine per minute when the urine was made acidic by the oral administration of ammonium chloride!and 0.1 p g/minafter oral administration of the alkaliser sodium bicarbonate. In another study, Beckett and Triggs (1!967) have dbmonstra!ted'that smokers whose urine has been maintained acidic excrete in unchanged form about 35%of known quantitics of nicotine that have been adm!in- Though unfortunately no systematic provision was made in this study to measure withdrawal, there is dramatic anecdotal evidence that the subjects who were the worstt regulators in this study were in states of marked irritability andl explosive emotimnality while on the low nicotirte cigarettes. Supporting this observation, Perlick (1977)iand Silverstein (1976) have both demonstrated experimentally that heavy smokers on low nicotine cigarettes are marked2y, more anxious and irritable than such smokers on high nicotine cigarettes. H• 10U5053022.
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216 SMOKINC BEHAVIOUR istered either by intravenous injiection, inhalat2onof nicotine vapour or smoking. Ptrtting,these facts tiogether, it appears reasonable to estimate that the proportion of nicotine which will be excreted in unchanged form will vary with the rnanipulated'. acidity of the urine as follows: urine is: ` % nicotine excreted acid 35 normal 7 alkaline <1 Obviously the exact proportions will vary with the precise pH of the urine. Howevery, one thing,seems clear: given the quite low proportion of unchanged nicotine which is excreted under normal or placebo conditions, increasing the alkalinity of'the urinee can at best have trivial effects on plasma level nicotine while increasing the acidity of' urine can potentially have substantial effects. If then, one assumerfirst, first,,that in urinary pH are reflected in circulating nicotine and second, that the amounts smoked vary with changes in plasma level nicotine, it should be expected that experimentally increasing the acidity of the unine will increase the amounts smoked. To test this guess, Schachter, Kozlowski and' Silverstein (1'977) manipulated urinary pH by, in alternate weeks, administering to a group of 131 smokers substantial daily doses of placebo or of the acidifying agents vitamin C'(ascorbic acid) and Aciditlin (glutamic acid hydrochloride). The subjects were given cartons of their favourite cigarettes and kept count of the amount they hadIsmoked each day of't'he study. The effects of these manipulations on smoking,are presented in Table 17.2'where it' can be seen that aeidiiicationis accompanied by increased smoking. During the period they were taking,either of two different acidifying agents, subjects smoked 700/'o more cigarettes than during,the time they were taking a corn starch placebo. - It should be specifically noted'that inkeeping with the magnitude of the phannacol- ogical effects this 20% increase is not a large experimental effect. On the basis of our estimation of nicotine excretionione would expect, at best, roughly a,30r1'o increase Table 17.2 Ttireffecta of vitaminC, Acidulin and'placebo on cigarette smoking, Condition Cigarettes smoked Mean % change per day Vitamin C 26.7' Placebo 2311 Acidulin Comparison Vitamin C vs Placebo Acidulin vs Placebo from placebo +19.8 +20.9 <.os !'nsI
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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
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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.
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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
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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
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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
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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
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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 _ .,,
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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
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® 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. ;:,
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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
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PHARMACOLOGICAL A'ND'PSYCHOLAGSCAL D'ET&RMTNANTS O'F SMOKING 227' Kozlowski, L.T.,,Jarvik,lr1.E: & Gritz, E.R. (1975) Nicotine regulation and cigarette smoking. ETutical Pharmacology and'Therapeutics; 17, 93-97. Larson, P.S.,,Haag; HLB.,& Silvette, Hi (1961) ; Tobacco. Experimental and Clunical. S•tudies. Baltimore: Williams & Wilkins. Lucchesi, B.R., Schuster, C.R. & Emley, G.S. (1i967) The role of'nicotine as a determinant of cigarette smoking in man with observations of'certain cardiovascular effects associated with the tobacco alkaloid. CTfnical Pharmacology and Therapeutics, 8, 789-796. . Marcovitz, E. (1969) On the nature of addiction to cigarettes. Jour>,ral'of the Aimerrcan Psychoanalytic Association, 17, 1074-1096 McKennell, A.C. (1'973) A Comparison of Two Smokbag Typologies Research Paper, 112. London: Tobacco Research Council. Nesbitt, P.D. (1973) Smoking, physiological arousal, and emotional response. Journal of Persortality arrd Social Ps3 cholngy, 25, 137 -145. Perlick„D: (1'977) The wit!hdrawal syndrome: Nicotine addiction and the effects of stopping,.smoking in heavy andilight smokers., (Unpublished doctoral d'issertation). Columbia University. Ros:s, W.S: (1'976a) Poison gases:in your cigarettes, Part 1: Carbon Monoxide. Reader's Digest, November, 1976. Ross„W.S: ('1976b) Poison gases in your cigarettes, Part II, Hydrogen Cyanide and Nitrogen Oxides. !*'eader'sDfgest, December, 1976. Russell, M.A.H. (1974a) Realistic goals for smoking,and health. Lancet, I; 254-258. Russell, M:A.H. (1974b) The smoking,habit and its classitiication.Practitiovrer, 212, 79'1.800: RusselI, MIA.H., Wilsoni C., Pate1, U.A.,,Cole, P.V. & Feyerabend, C: (1973) Comparison, of'effect on tobacco consumption and carbon:monoxide absorption of changing to high and lrow, nicotine, cigarettes. Bdtish Al edical Journal, 4, 5 112-5~16. Schachter, S. (1973)', Nesbitt's paradox. In Smoking, Behayiorur.• Nlotives and lncentives ed. Dunn; W.L. pp. 147-155. Washington: V.H. Winston & Sons. Schachter, S. (1977) Nicotine regulation in heavy and light smokers. Journal of Experimental'Psychology: General,' 1106, 5.12. Schachter, S., Kmzlbwski, L.T. & Silverstein, B. (1977a) Effecmof urinary pH on cigarette smoking. Journal of ExperimrntalPsychology: General. 106, 13-19. Schachter„S., Siiverstein, B:, Kozlowski: L, Herman, C.P. & Iiiebling; B. (1977b)i Effects of stress on cigarette smoking,and oniuritoary pH. JournaLof Experunental. PsyeAology: General, I06,,2430: Schachter, S., Silverstein, B'. & Perlick, D. (1977c) Psycholpgical and pharmacological! explanations of smoking under stress. Journal of ExperimentaLPsychology: General, 106, 31-4I01 SiH+erstein, B. (1976)i An addiction explanation of'ci¢arette«induced relaxation. ('Unpublished!doctoral dissertation). Columbia University. Siliverstein, B.,, Kozlowski, I..T. & Schacluer, S, (U977) Social life, cigarette smoking, andl urinary pH. Journai'of Experimental Psychology: Grnrra4' 106, 20123. Smith; G.M. (1970) Personality and smioking; A review oFl the empiricallitcrature. In Learning,rlfechanisms in Smoking, ed. Hunt, W:A., Chicago: Aldine. Surgeon General's Report (1972) The HcaltJi Cvnseqttenccs of Smoking, U.S. Departmenrof Health, Educationiand Welfare. 100S0S3034
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2281 SMOKING BEHAVIOUR Tomkins, S. (1968) A modified model of smoking beHaviour: In Smoking, Health and'Behavion ed, Borgatta, E.F. & Evans, P.R. Chicago: Aldine. ~= Waingrow; S. & Horn, D. (1968) Relationship of number of cigarettes smwkcd'to "tai' rating. National 'Cancer Institute Nlono,graph, 28, 29-33'. N ~. Q ~. 0 ~ W. 0 -, W U1 ~

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