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CURRENT DIGEST ( of Scientific Papers Relating to Tobacco Use (Compiled and Described for Ilnformational Purposes Only for The Council for Tobacco Research-U.S:A., Inc. The Summaries Are Not Internded to be Complete Scientific Abstracts.)I Vol. 28, No. 10. Contents October 1983 Page 1. Heart and Circulation 1 2. Respiratory Conditions 2 3. Pregnancy 5 4. Other Systemic Conditions 7 5. Statistics 9_ 6. Nicotine 10 7. Smoke Condensate and Constituents 14 8. Smoking Habits 18 9. Briefs from Meetings 20. 10. Additional References 31 C 1. HEART & CIRCULATION PETITTI, D.B., & KLATSKY, A.L., Kaiser-Permanente Medical Care Program, Oakland, California "Malignant hypertension in women aged!15 to 44 years and its relation to cigarette smoking and oral contraceptives." (American Journal of Cardiology 52/3: 297-8, August 1983) "To study the factors associated with malignant hypertension in young women~, we reviewed the medical records of all women aged 15 to 44 years who were hospitalized in any of 15 affiliated hospitals from 1971 to 1980 with malignant hypertension. There were 15 new patients in this period!, an inci- dence of 0.5 per 100,000 women of these ages per year. Four women~had under- lying renal disease. All of the remaining 11 use&oral contraceptives, smoked cigarettes, or both. Nine were white, and16 women had normal blood'.pressure in the 24 months before hospitalization. These findings support a relation of oral contraceptive use and cigarette smoking to an~increasedlrisk of malignant hypertension in young women." C FRIEDMAN, Cs.D., FIREMAN, B.H., RETITTI, D.B., SIEGELAUiB, A.B., URY, H.K. & KLATSKY, A.L., Kaiser-Permanente Medical Care Program, Oakland, California "Psychological questionnaire score, cigarette smoking, and myocardial in, farction: A continuing enigma." (Preventive Medicine 12/4: 533-40, July 1983) ~ "The ability of a group of 94 psychological questions to discrim- inate between men in whom cigarette smoking was associated with increased risk of myocardial infarction and men in whom~smoking was not so associated remains C.W ~ W IN W~+ 'J

2. d puzzling. Further anal!yses, controlling for reported alcohol consumption and for a questionnaire item that might reflect physical activity, failed to alter this finding. This interaction of the questionnaire responses with smoking was not found with two other major coronary risk factors, serum cholesterol and systolic bloodipressure. Believing that these observations may provide (a) a clue to how cigarette smoking affects risk of myocardial infarction, or (b) some means.of identifying greater or lesser susceptibility to the effects of smoking, we invite other investigators to join in the pursuit of this matter. A list of ten selected yes-or-no questions with strong interaction with smoking is provided!to assist others in studying this phenomenon~; these are similar to ten items on the Minnesota Multiphasic Personality Inventory." DOWNEY, H.F., CRYSTAL, G.J. & BASHOUR, F.A., University of Texas Health Science Center, Dallas (CTR-grant) "Regional myocardial blood flow during nicotine infusion after chronic coronary artery occlusion: Effect of :-adrenergic blockade."' (Journal of Cardlo- vascular Pharmacology 5/4: 685-90, 1983) "In eight dogs a portion of the left ventricular free wall (LVFW) was rendered collateral-dependent (CD) by gradual occlusion of the left anterior descending coronary artery with a surgically implante&Ameroid~con- strictor. Six to 8 weeks later, the dogs were anesthetized an6regi.onal myo- cardial blood flow was measured with 7-10-..,-.m radioactive microspheres during (a) control conditions, (b) nicotine alone (24 ctg/kg/min i.v.), and (c) nic- otine (24 ug/kg/min i.v.) after 5 -adrenergir blockade with propranolol. During control conditions, mean transmural flow was similar in CD, border, and normal regions of the LVFW. Nicotine alone increased flow in all regions of the LVFW, with normal (+ 104%) greater than CD (+ 56%). These changes in flow were accompanied by increases in mean arterial pressure (+ 34%) and mean aortic flow (+ 54%). Nicotine after ,-,-adrenergic blockade appreciably raise& mean arterial pressure (+ 83%) and mean left atrial pressure (+ 307%), but caused no increase in flow to any region of the LVFW. The results indicate (a) that the nicotine-induced increase in flow is blunted in a CD region, and that (b).;-adrenergic blockade unmasks coronary vasoconstrictor mechanisms during nicotine infusion which prevent increases in flow to either normal or CD regions despite increased perfusion pressure and augmented myocardial oxygen demands." 2. RESPIRATORY CONDITIONS CORREA, P., PICKLE, L.W., FONTHAM, E., LIN, Y. & HAENSZEL, W., Louisiana State University Medical Center, New Orleans "Passive smoking and lung cancer." (Lancet I'I: 595-7, September 10, 1983) "Questions about the smoking habits of parents and spouses were askedi in~a case-control study involving 1338 lung cancer patients and 1393 com- parison subjects in Louisiana, USA. Non-smokers marriedito heavy smokers had an increased risk of lung cancer, and so did subjects whose motherfi smokedl. There was no associationibetweenilung cancer risk and paternal smoking. The association with maternal smoking was found only in smokers and persisted, after controlling for variables indicative of active smoking.... C ( c

3. C < "Our findings indicate that maternal smoking,results in a slight in- crease in lung,cancer risk but do not indicate whether the effect is due to enhanced active smoking of the offspring or to enhanced susceptibility to lung cancer inductiion after the challenge of active smoking,later in life. "Our findings point to the need for more research on the subject of passive smoking,and cancer. Since large numbers of cases may be needed for adequate epidemiological analysis, multi-institutional collaboration may be indicated!." STONE, P.J., CALORE, J.D., McGOWAN, S.E., BERNARDO, J., SNIDER, G.L. & FRANZBLAU!, C., Boston University S'chool of Medicine, Massachusetts "Functional _-•,`1-protease inhibitor in the lower respiratory tract of cig- arette smokers is not decreased." (Science 221: 1187-9, September 16, 1983) "Cigarette smoking is the major risk factor for the development of pulmonary emphysema, a disorder that may result from an imbalance between the elastase and antielastase levels in the lungs. Decreased functional "~l-pro- tease inhibitor, an inhibitor of neutrophil elastase, might render smokers susceptible to elastase-catalyzed destruction of pulmonary elastic fibers and'the development of emphysema. Binding and inactivation of isotopically labeled porcine pancreatic elastase and human neutrophil elastase by •'1-pro- tease inhibitor were measured in fluid obtained by bronchoalveolar lavage of volunteers. The inhibition of elastase-catalyzed solubilization of elastin and'a tripeptide substrate were also determined. The mean~level of functional ~1-protease inhibitor in the bronchoalveolar lavage fluid of smokers was found to be equal to or greater than that of nonsmokers, contradicting reports by other investigators. Increased elastase derived'from~pulmonary neutro- phils, rather than decreased functional ~1-protease inhibitor, appears to be the main factor in the genesis of emphysema in smokers." [N = 21 smokers, 16 nonsmokers] ABBOUD, R.T., JOHNSON, A.J., RICHTER, A.M. & ELWOOD, R.K., Vancouver General Hospital, Canada "C'omparison~of in vitro neutrophil elastase release in nonsmokers and smokers." (American R'eview of Respiratory Disease 128/3: 507-10, September 1983) "Protease-antiprotease imbalance in the lung is considered.a likely pathogenetic mechanism in the development of emphysema. To assess whether differences in enzyme release from~stimulatedlneutrophils could be a factor leading to increased elastase release in the lung, we compared the in vitro release of elastase and a lysosomal enzyme, 1"-gllucosaminidase, from neutro- phils of nonsmokers and smokers. Neutrophils were stimulated in vitro by zymosan as a phagocytic stimulus, and the synthetic polypeptide, N-formyl- methionyl-lieucyl-phenyl-alanine (FMLP) as chemotactic factor. We studied 54 male subjects, 24 nonsmokers (mean age, 39.5 + SD 14.4!yr) and 30 smokers (mean age, 45.4!+ SD 8.2 yr). Smokers were divided into 2 groups according to results of their lung function, 17 with normal and 13 with abnormal lung function. Smokers with abnormal lung function were older (59.8 + SD 11.8 yr) i

4. and had smoked more (45.6 + SD 18.2 pack-years), than smokers withinormal lung function (mean age, 39.8 + SD 11.0 yr; smoking, 22.1 + SD 19'.4 pack- years). There were no differences in either -glucosamimidase or elastase release after either zymosan or FMLP stimulation among the 3 groups of subjects; there were also no significant differences in the content of these enzymes in whole cell neutrophil lysates. Our data indicate that chronic smoking did not affect neutrophil elastase release inivitro, and that among smokers there was no significant relationship betweenin vitro neutrophil elastase release and abnormalities in lung function, suggesting that in- herent differences in elastase release from stimulated'.neutsophils are not likely to be of pathogenetic importance in leading to abnormal lung,function in smokers.'° DAVIES, S.F., OFFORD, K.P., BROWN, M.G., CAMPE', H. & NIEWOEHNER, D., U'niversity of Minnesota Medical School, Minneapolis "Urine desmosine is unrelated to cigarette smoking or to spirometric function." (American Review of Respiratory Disease 128/3: 473-5, September 1983) "We measured urine desmosine by radioimmunoassay in 157 subjects. Desmosine excretion (expressed as desmosine/creatinine ratio) did not cor- relate with ventilatory function (assessed by spirometry) or with current smoking status or total lifetime cigarette consumption. We conclude that measurement of urine desmosine may not be useful as an indirect measure- ment of elastolysis in cigarette smokers." HUNTER, E., SLONEKER, S.D. & KOSTENBAUDER, H.B., University of Kentucky "Influence of chronic cigarette smoke exposure on the uptake and efflux of imipramine in the isolated perfused rat lung." (Drug Metabolism and Disposition 11/4: 361-5, 1983) "The pulmonary uptake and efflux of imipramine was determined in lungs removed from cigarette smoke-exposed and~nonexposed rats. Using an isolated perfused lung preparation, the lung was perfused for 220 sec with medium containing 2.5 x 10-7 M imipramine, followed by a 28-min drug-free perfusion. There was no significant difference (P ,~0.05) between either the rate or the amount of imipramine accumulated in the smoke-expose6and nonexposed animals. During the drug-free perfusion, the previously accu- mulated'.imipramine was released'.from~two distinct pools (El and E2). Cal- culation~of the total amount of effluxable imipramine indicated!that in the nonexposed animals approximately 30% of the amount taken up did not efflux at a measurable rate but formed a 'noneffluxable' pool. In the smoke-exposed animals, however, all of the accumulated imipramine appeared to be effluxable. These d'ata demonstrate that there may be components of cigarette smoke which are sequestered by lung tissue at the binding sites associatediwith the noneffluxable pool of imipramine. The presence in arette smoke of components possessing such high pulmonary affinity may a factor in discussed." cigarette smoke-mediated lung damage; this:possibility is C ~

5. ( TAGER, I.B., WEISS, S.T., MUNOZ, A., ROSNER, B. & SPEIZER, F.E., Channing Laboratory, Boston, Massachusetts "Longitudinal study of the effects of maternal smoking on pulmonary function in children." (New England Journal of Medicine 309/12: 699-703, September 22, 1983) "We investigated the effects of maternal cigarette smoking on pul- monary function in a cohort of children and adolescents observed prospectively for seven years. A multivariate analysis revealed that after correction for previous forced expiratory volume in one second (FEV1), age, height, change in height, and cigarette smoking in the child or adolescent, maternal cig- arette smoking significantly lowered the expected average annual increase in FEV1 (P = 0.015). On the basis of this analysis, it is estimated that if two children have the same initial FEV1, age, height, increase in height, and personal cigarette-smoking history, but the mother of one has smoked through- out the child"s life whereas the mother of the other has not, the difference in the change in FEV1 over time in the exposed child, as compared with that in the unexposed child, will be approximately 28, 51, and 101 ml after one, two, and five years, respectively, or a reduction of 10.7, 9.5, and 7.0 per cent, respectively, in the expected increase. These results suggest that passive exposure to maternal cigarette smoke may have important effects on the development of pulmonary function~ in child'ren." [N = 2,860] ( 3. PREGNANCY FORSS, M., LEHTOVIRTA, P., RAURAMO, I. & I:ARINIEMI, V., Helsinki, Finland "Midtrimester fetal heart rate variability and maternal hemodynamics in association with smoking." (American Journal of Obstetrics and Gynecology 146/6: 693-5, July 15, 1983) "Maternal heart rate (MHR), blood pressure (BP), the differential index (DI) describing the short-term component of fetal heart rate (FHR) variability, and the interval index (II) describing the long-term component were measure&in eight subjects in the midtrimester before, during, and after the mothers smoked a standard cigarette. The analyses of FHR variability were performed by an 'on-line' method with an abdominal fetal electro- cardiogram used as a triggering signal and with~alsample time of 1 minute. An increase of MHR, FHR', and BP with a concomitant decrease of II was ob- served. Unlike our findings regarding the third trimester, no significant change of DI was observed. A correlation analysis reveale&fetomaternal hemodynamic relationships different from~those in the third trimester: There was a negative correlation between DI and FHR:(pc 0.01) and between DI and MHR' (p < 0.01). There was a positive correlation between FHR and bLHR (p < 0.001). Unlike our findings regarding the third trimester, no cor- relation was found between DI and BP or between II and MHR. We suggest that the midtrimester fetus shows the narcotic effect (decrease of II) of one ~ cigarette, as does the term~fetus, but fails to show the hypoxic effect ~ (decrease of DI), which has been observed in the term fetus." ~j w ~ ~ ,

6. BUREAU, M.A., SHAPCOTT, D., BERTHIAU*'IE, Y., MONETTE, J~., BLOUIN, D~., BLANCHARD, P. & BEGIN'., R., University of Sherbrooke, Montreal, Canada. "Maternal cigarette smoking andifetal oxygen transport: A study of P50, 2,3-diphosphoglycerate, total hemoglobin, hematocrit, and type F hemoglobin in fetal blood." (Pediatrics 72/1: 22-6, July 1983) "The current study was undertaken to determine whether the 02 carrying capacity of newborns born to mothers who smoke can accommodate to carbon monoxide poisoning to compensate for the potential tissue hypoxia induced by CO. From a cohort of 1,222 women and newborn infants the total hemoglobin concentration, hematocrit, and carboxyhemoglobin (HbCO) were measured and analyzed with regard to the maternal HbCO level and the number of cigarettes smoked per d'ay. Also, for 100 pairs of mothers, of whom 50 were smokers and 50 nonsmokers, and their newborns, measurements were made of the intraerythrocyte concentration of 2,3-diphosphoglycerate (2,3'-DPG), the hemoglobin concentration, and the affinity of hemoglobin for oxygen by determination of 02 tension~for 50% of Hb-02 saturation (P50). The results showed no significant relationship between smoking,habits of mothers and their levels of hemoglobin, P50, and'2,3-DPG; only the hematocrit was slightly increased in smoking mothers. However, in fetal blood a signif- icant correlation was found between the number of cigarettes smoked per day and levels of hemoglobin, hematocrit, and P50. The P50 decreased in re- lationship to the increase inimaternal HbCO1. The P50,change was brought about by an increase in hemoglobin F found in the fetuses of mothers who smoked. Although al!l these changes were statistically significant, these mechanisms of acclimatization to CO poisoning appeared trivial in magnitude. It is concluded'that the human fetus does not have a biologic capacity to accommodlate to maternal cigarette smoking, and therefore the fetus is particularly susceptible to the adverse effects of cigarette smoking." GOLDING, J. & BUTLER, N.R., Royal Hospital for Sick Children, Bristol, England "Maternal smoking and anencephaly." (British Medical Journal 287: 533-4, August 201, 1983)~ "In 1979 Evans, Newcombe, and Campbell published a valuable analysis of the Cardiff Birth Survey, showing little association between maternal smoking in pregnancy and most types of those congenital defects which are recognized neonatally. They did, however, find a weak associ- ation with anencephaly (132 cases ) and spina bifida. (178 cases), even after controlling for social class. We present an analysis of 4:91 preg- nancies resulting in the birth of a singleton anencephalic.... "From the information~collected we calculated'the anencephalic incidence per 1000 births if the mother smoked~at the start of pregnancy as 2.89 (SE 01.19), which was significantly greater than that found if the mother did not smoke (2.18 (SE 0.13); p-,0.05). The table shows that there was some evidence for a trend with dose. C C

. 7. ( ( "As in other studies, however, the incidence of anencephaly in this survey rose sharply as social class fell, being 1.42 in classes I and II, 2.39 in social class III, and 3.16 in classes IV and V. The pro- portion of the control population of mothers smoking,in early pregnancy also exhibited a trend with social class (32% in I and II, 41% in III, and 47% in IV and V). Indirect standardization for each of the five sociall classes (table) resulted'lin no significant differences between the observed and expected numbers in each smoking group." TACHI, N:. & AOYAMA, M., Nagoya City University Medical School, Japan "Effect of cigarette smoke and carbon monoxide inhalation by gravid rats on the conceptus weight." (Bulletin of Environmental Contaminationiand Toxicology 31/1: 85-92, July 1983) "In summary, both continuous inhalation by [rat] mothers of cig- arette smoke and carbon monoxide lowered the weight of the conceptus on Days 14 and 21 of pregnancy, and the effect was more conspicuous in the group expose&to cigarette smoke than that to carbommonoxide alone. Therefore, the present study suggests that carbon monoxide is an important but not sole factor responsible for the adverse influence of cigarette smoke on the fetus. In addition, inhalation affected the fetus most deleteriously when performed during the last third of pregnancy, i.e. the phase of rapid fetal growth." 4. OTHER SYSTEMIC'CONDITIONS AMES, B.N., University of California, Berkeley "Dietary carcinogens and anticarcinogens. Oxygen radicals and degenerative d'iseases."' (Science 221: 1256-64, September 23, 1983) "The human diet contains a great variety of natural mutagens and carcinogens, as well as many natural antimutagens and anticarci~nogens. Many of these mutagens and carcinogens may act through the generation of oxygen radicals. Oxygen radicals:may also play a major role as endogenous initiators:of degenerative processes, such~as DNA damage and'mutation (and promotion), that may be related to cancer, heart disease, and aging. Di- etary intake of natural antioxidants could be an important aspect of the body's defense mechanism against these agents. Many antioxidants are being identified as anticarcinogens. Characterizing and optimizing such defense systems may be an important part of a.strategy of minimizi,ng cancer and other age-related diseases." KOST, N., PACAKOVA, E. & ZOZULYA, A., Moscow, USSR "A comparative study of the morphine effect on the level of cyclic AMP in C lymphocytes of smokers and nonsmokers." (Biologicali Psychiatry 18/7: 763-9, July 1983) (.J ~ ~ "A study of the effect of morphine on the level of cAMP in the ~ W lymphocytes of peripheral blood in smokers and nonsmokers was carried out. N rA C~

8'. It was shown that morphine enhances the activity of ad'enylate cyclase, and that this effect can~be abolished by naloxone. The dependence of the enzyme activity on the concentration of morphine is complex. The maximal effect of the investigate&opiate on the level of cAMP in lymphocytess occurs among smokers at a tenfoldiconcentration comparediwith nonsmokers. On the basis of our data two suggestions are made: (i) there are opiate receptors on lymphocytes with a mechanism of action connected with the regulation of adenylate cyclase activity; (ii) smoking develops tolerance to morphine at the level of the opiate-dependent adenyliate cyciase of lymphocytes." [N = six smokers, six nonsmokers] MITTLER, J.C., POGACH; L. & ERTEL, N.H., Veterans Adtninistration Medical Center, East Orange, New Jersey "Effects of chronic smoking on testosterone metabolism in dogs." (Journal of Steroid!Biochemistry 18/6: 759-63, June 1983) "The effects of long-term cigarette smoking on androgen hydroxy- lases and peripheral hormones were studied in male beagles. In the testis, chronic smoking of high nicotine/tar cigarettes was associated'with decreased~ activity of the 7~>-hydroxylase active on testosterone (68% of control, P'< 0.05) . Testicular 6,~-,and 16='. -hydro::ylases were not altered. The hepatic androgen 6-hy.droxylase activity in control animals was approximately 6 times the testis levels and was stimulatedimarkedly by smoking. This increase ranged from 221% imthe low nicotine/tar group (P < 0.02) to 304% in the high~nicotirne/'tar group (P ,;~0.006). Serum testosterone levels were reduced to 54% of control (P ,1'0.02) and prostate size to 44% (P,, 0.001)' of control withiheavy smoking. Serum~LH levels were elevated with smoking. These re- sults suggest that chronic cigarette smoking increased hepatic metabolism of testosterone. In addition~, serum testosterone levels and prostate size decreased and LH levels increased. Whether the hepatic and'the endocrine effects are causally related cannot be determined from this preliminary study." FRITHIOF, L., ANNEROTH, G., LASSON, Ui. & SEDERHOL.^1, C., Karolinska Hospital, Stockholm, Sweden "The snuff-inducedilesion. A clinical and morphological study of a Swedish material." (Act&Odontological Scandinavica 41/3: 53-64, 1983) "Snuff-ind'2iced oral lesions were studied clinically, histologically and'by electron miczvscopy. The material was collected from 21 male snuff users. The lesions had a characteristic whitish appearance with a wrinkled swollen texture and'the most common localization was in the vestibular area of the upper jaw. In two cases gingival retraction was observed!. The light- microscopical examination showed a mild epitheliial dysplasia in five cases. No carcinoma in situ or invasive carcinom&was recognized'. In some of the cases ultrastructural changes irn the basement lamina region, such~as defects of the basement lamin&and the occurrence of basal cell processes in the connective tissue, were observed. Odland bodies were seen in the epithelium. C C e t

9. C C In the connective tissue filamentous material of unknown nature was found. The ultrastructure of the filamentous material suggested that it might be amyloid. In summary, snuff-induced lesions should be diagnosedl, patients should be informed and made to quit the habit, and remaining,lesions should be foll!owe&up regularly." McCREDIE, Mi., STEWART, J.H. & FORD, J.M., Westmead Hospital, New South Wales, Australia "Analgesics and tobacco as risk factors for cancer of the ureter and renal pelvis." (Journal of Urology 130/1: 28-30, July 1983) "In alcase-control study of 36 men with~cancer of the ureter and 307 male controls withithe same age distribution tobacco smoking conferred a relative risk for this cancer of 2.9, whereas consumption of analgesics of any kind didinot increase the risk. The relative risk for cancer of the renal pelvis, determined for 29 men, was 2.4 for tobacco and 6.O for phenacetin-contalining analgesics. Analgesics containing no phenacetin con- ferred no increased risk for cancer at this site. Data for 13 women,with ureteral cancer, 5 of whom had taken phenacetin, are presented but not analyzed." IVES, T.J., University of North Carolina, Chapel Hill "Use of dimenhydrinate in the treatment of green tobacco sickness." (Drug Intelligence and Clinical Pharmacy 17/7-8: 548-9, July/August 1983) "A case of green tobacco sickness (GTS)~ in a 37-year-old male migrant worker and~the use of dimenhydrinate in its treatment/prophylaxis is presented. A brief discussion of the etiology and';symptomatology of CTS is included. Dimenhydrinate is a useful over-the-counter product for the treatment of this occupational illness in the tobacco-growing states of the Southeast." 5. STATISTICS MILLER, G.H'. & GERSTEIN, D.R., Edinboro, Pennsylvania "The life expectancy of nonsmoking mem and women." (Public Health Reports 98/4: 343-49, July/August 1983). "Survey data.were collected on the lifetime smoking habits of adults in Erie County, Pa., as of 1972-74. In the survey interviews, 0 careful distinctions were made between respondents who had formerly smoked w and respondents who had never smoked. The survey data were combined withi ~ data:collected fromisurviving relatives about the smoking habits of people ~ who had died in Erie County during the years 1972-74. After deaths attrib- w utable to traumatic causes ~ (accidents, suicides, and homicides) were removed, ~ life tables were calculated for male and female nonsmokers over age 30. The resulting life expectancy figures for nonsmoking men an&women of parallel age were virtually identical. Thus, differential rates of cigarette smoking are apparently the overwhelming cause for the male-female longevity difference.

10. Actuarial tables should be divided by smoking behavior to reflect this finding. The results of the study suggest that the present longevity difference between men and women will disappear." [N = 2195] 6. NICOTINE HENNINGFIELD, J.E., & JASINSKI, D.R., NIDA, Addiction Research Center, Baltimore, Maryland "Humanipharmacology of nicotine." (Psychopharmacology Bulletin 19/3: 413-5, 1983) "Subjects were male cigarette smokers between 18 and!50 years of age, who resided for 4 to 12'weeks at the clinical pharmacology re- search unit of the Addiction Research Center in Baltimore. Except as noted, subjects had histories of use andiabuse of a variety of drugs including opioids, stimulants, and alcohol. In some studies, nicotine doses were given by the controlled inhalation of smoke from research cigarettes, which delivered a range of nicotine doses from about 0.4 to 2.9 mg (Federal Trade Commission Method), while in other studies nicotine was given by 10-second intravenous injections of nicotine tartrate in doses from 0.75 to 4.5 mg (calculated'as the free base). In certain studies, subjects were pretreated with the nicotinic antagonist, mecamylamine, in orally given doses ranging from 2.5 to 10 mg. Drugs were given under double-blind conditions, with each dose presented~on several occasions to each subject (crossover design) according,to randomized block or Latin-square sequences. For each study, deprivation of cigarette smoking and other substances such as food and caffeine was held constant.... "Nicotine, in doses comparable to~those delivered by cigarette smoking, is psychoactive, is a euphoriant, and serves as a reinforcer. These are salient properties of drugs of abuse, such as morphine, cocaine, and alcohol. These findings provide direct evidence that nicotine is a diepen- dence-producing drug. Furthermore, these findings support the hypothesis that the role of nicotine in cigarette smoking is similar to the role of opium in morphine or heroin use, coca in cocaine use, and ethanol in~alco- holic beverage consumption." WESNES, K., WARBURTON, D.M. & MATZ, B., University of Reading, England "Effects of nicotine on stimulus sensitivity andlresponse bias in a visual vigilance task." (Neuropsychobiology 9/1: 41-4, January/February 1983) "Signal detection~analysis was used to~examine the effects of nic- ~ otine on a visual vigilance task. Groups of light, heavy and non-smokers performed the 80-min task on three separate occasions, and received dif- ~ ferent doses of nicotine each time. For all three types of smoker, nicotine ~ significantly counteracted the decrement in stimulus sensitivity which ~ occurred over time in the placebo condition, while having no effect on (p response bias. We argue that nicotine prod'uced this effect by acting on the central, cholinergic pathways controlling electrocortical arousal, and therefore that these pathways play a role in the control of human information processing.... ( ( c ~