Jump to:

RJ Reynolds

Current Digest of Scientific Papers Relating to Tobacco Use.

Date: Dec 1981
Length: 67 pages
501530422-501530488
Jump To Images
snapshot_rjr 501530422-501530488

Fields

Type
PUBLISHED DOC
Site
R&D
R&D Tech Svcs-R&D Library
Copied
I, N.S.
Request
Blanchard
1rfp1
1rfp72
1rfp76
1rfp77
1rfp88
Minnesota
1rfp71
Cordova
1rfp29
Texas
Initial
Disclosure
Castano
Burton
2rfp16
Ohioironworkers
by
Agreement
2rfp20
Referenced Document
List of Abstracts.
Date Loaded
27 Feb 1998
Named Person
Ctr
Rjr
Box
Rjr1129
Author
Current Digest
Characteristic
Marginalia
UCSF Legacy ID
bzs39d00

Document Images

Text Control

Highlight Text:

OCR Text Alignment:

Image Control

Image Rotation:

Image Size:

Page 1: bzs39d00
CURRENT DIGEST of Scientific Papers Relating to Tobacco Use (Compiled and Described for Informational Purposes Only for The Council for Tobacco Research-U.S.A., Inc. The Summaries Are Not Intended to be Complete Scientific Abstracts.) Vol. 26, No. 12 December 1981 Contents RJR RESEARCH LIBRA[:Y age 1. Heart and Circulation 1 2. Respiratory Conditions 1981 6 3. Occupational Studies 10 4. Other Systemic Conditions 12 5. Statistics is 6. Nicotine 16 7. Smoke Condensate & Constituents 17 8. Smoking Habits 19 9. Smokeless Tobacco 22 10. Briefs from Meetings 23 11. Additional References 40 1. HEART AND CIRCULATION WALD, N.J., IDLE, M., BOREHAM, J., BAILEY, A. $ VAN VUNAKIS, H., Radcliffe Infirmary, Oxford, England $ Brandeis University, Waltham, Massachusetts "Serum cotinine levels in pipe smokers: evidence against nicotine as cause of coronary heart disease." (Lancet II: 775-7, October 10, 1981) "Serum levels of cotinine (a principal metabolite of nicotine) were studied in men who did not smoke (28), and in men who smoked cigarettes only (150), cigars only (70), and pipes only (56). The mean cotinine level for pipe smokers was 389 ng/ml, significantly higher than the mean level for the cigarette and cigar smokers (306 and 121 ng/ml, respectively); no cotinine was detected in the serum from any of the nonsmokers. Large prospective studies have shown that pipe smokers have no material excess risk of coronary heart disease but cigarette smokers do, so that our observations indicate that nicotine is unlikely to be the major cause of the excess coronary heart disease mortality in cigarette smokers.... "The chewing of nicotine gum is a proposed method of helping people to stop smoking. While we have not studied nicotine gum in relation to all diseases, our results indicate that it is unlikely to cause an excess risk of coronary heart disease, since the method of absorption of nicotine from the gum is likely to be similar to that associated with pipe smoking. "The observation that COHb levels, in pipe and cigar smokers, fall between those in cigarette smokers and nonsmokers is consistent with CO being responsible for the excess risk of coronary heart disease in smokers. However, it is not strong evidence in favor of this hypothesis; it is possible that some other constituent of cigarette smoke which is corre- lated with the CO yield might be the principal etiological agent."
Page 2: bzs39d00
2. JARVIS, M.J. F, RUSSELL, M.A.H., Institute of Psychiatry, London "Nicotine, carbon monoxide and heart disease." (Letter: Lancet II: 1045, November 7, 1981) "Dr. Wald and his colleagues report higher cotinine levels in pipe smokers than in cigarette smokers. Epidemiological evidence indicates that the risk of coronary heart disease is little raised in pipe smokers but considerably raised in cigarette smokers. They combine these findings to argue that nicotine is unlikely to be the major cause of the excess coronary heart disease mortality in cigarette smokers. Those who have espoused a nicotine model of smoking would like to be able to welcome this conclusion, but caution is necessary before accepting it.... "The data on blood carboxyhemoglobin as reported do not permit a valid comparison of CO intake from cigarette and cigar smoking, since 89% of the cigarette smokers but only 47% of the cigar smokers had smoked already on the day of attendance. Noninhaling, mainly primary cigar smokers absorb little CO, but those who switch from cigarettes often continue to inhale. Did those cigar smokers who were ex-cigarette smokers and who had already smoked on the day of their visit to the clinic have COHb (and, indeed, cotinine) levels substantially different from those of the cigarette smokers? "This paper does not advance our understanding of whether nicotine, CO, or some other constituent of cigarette smoke is responsible for the excess risk of coronary heart disease in smokers." SALOOJEE, Y. F, COLE, P.V., St. Bartholomew's Hospital, London "Nicotine, carbon monoxide, and heart disease." (Letter: Lancet II: 1044, November 7, 1981) "Dr. Wald and his colleagues report some interesting data on cotinine levels in pipe, cigar, and cigarette smokers. The suggestion that their findings absolve nicotine as a cause of coronary heart disease (CHD) is, however, contentious. Alternative explanations for the lower risk of CHD associated with pipe or cigar smoking may be offered. "The rapid absorption of nicotine through the lungs makes each inhaled puff of cigarette smoke equivalent to an intravenous bolus in- jection of nicotine. Cigarette smokers are, therefore, exposed to an in- termittent series of high-nicotine boli, associated with each puff. The absorption of nicotine from pipe and cigar smoke through the buccal mucosa is slower and does not produce puff-by-puff nicotine peaks in blood. The pattern of exposure to nicotine in inhaling and non-inhaling smokers is thus very different, and nicotine delivery to the heart or c other organs cannot easily be predicted. (r LA) "Wald et al. also fail to consider the possibility of a synergistic o relation between nicotine and carbon monoxide. The higher mortality from ~ CHD in cigarette smokers may be related to an increased myocardial oxygen w demand caused by nicotine and a decreased myocardial oxygen supply produced by carboxyhemoglobin (COHb). Furthermore, during an episode of myocardial ischemia, both nicotine and COHb can reduce the threshold for ventricular fibrillation. Cigarette smokers are, therefore, subjected to dual stresses while primary pipe or cigar smokers, who have low COHb concentrations, are not."
Page 3: bzs39d00
3. CLYNE, C. F, ARCH, P.J., Southampton General Hospital, England "Nicotine, carbon monoxide, and heart disease." (Letter: Lancet II: 1044-5, November 7, 1981) "We support the contention of Dr. Wald and his colleagues that carboxyhemoglobin (COHb) levels in the blood of smokers may correlate well with their risk of acquiring vascular disease. We studied 43 male cigarette smoking patients with arteriographic evidence of peri- pheral vascular disease (PVD) and compared their COHb levels with 25 age, sex, and weight matched smokers without PVD, and a control group of 25 similarly matched nonsmokers without PVD. There was no significant difference in overall cigarette consumption between the two smoking groups ()(2=0.23, not significant), but those smokers with PVD had significantly greater COHb levels (5.1%) than those smokers without PVD (3. 4 0) (t=3. 37, p< 0. 00l) . "These data, with Wald's findings, do suggest that COHb or a substance as yet unmeasured but with similar blood levels, does provide a sensitive index for the risk of development of vascular disease." CRIQUI, M.H., WALLACE, R.B., MISHKEL, M., BARRETT-CONNOR, E. 4 HEISS, G., University of California, San Diego, La Jolla "Alcohol consumption and blood pressure. The Lipid Research Clinics Prevalence Study." (Hypertension 3/5: 557-65, September/October 1981) "The relationship between alcohol consumption and systolic and diastolic blood pressure (BP) was examined in 2482 men and 2301 women 20 years of age or older in nine North American populations. Men at the highest level of alcohol consumption (.~k 30 ml alcohol per day) had the highest BP, while women either at the highest level of alcohol consump- tion or consuming no alcohol had the highest BP. Men aged -'b _ 35 years of age consuming , 30 ml alcohol per day were 1.5 to 2 times more likely to be hypertensive than nondrinkers. Multivariate analysis showed systolic and diastolic BP in both men and women to be positively and significantly (p< 0.05) related to alcohol consumption, and this relationship was inde- pendent of the potential confounding effects of age, obesity, cigarette smoking, regular exercise, education, and gonadal hormone use in women. The regression coefficients indicated that an average of 30 ml of alcohol per day would produce a 2 to 6 mm Hg increase in systolic BP. Analyses suggested the univariate U-shaped alcohol-BP association in women was confounded by differences in obesity and cigarette smoking in nondrinking women, and by very low alcohol consumption in hypertensive women using medication. Additional analyses indicated that alcohol con- sumed in the 24 hours prior to the study was much more strongly associated with elevated BP than alcohol consumed in the week prior to the study excluding the previous 24 hours. We conclude that alcohol appears to have a modest but consistent and independent effect on systolic and diastolic BP.... "Cigarettes show a negative relationship to BP, such that smoking a pack of cigarettes a day is associated with a systolic BP reduction of 2 to 3 mm Hg. Cigarettes have been inconsistently related to BP in previous studies, but the most common finding is a weak, negative relationship in studies that have controlled for the effect of obesity simultaneously.
Page 4: bzs39d00
However, a recent report indicated small and inconsistent changes in BP in persons quitting smoking. Smoking increases BP acutely, and it has been suggested that smokers not smoking before or during a health study examination might experience a downward rebound in BP. Another possi- bility is that the known negative association between smoking and obesity has somehow been inadequately controlled in our analysis, and smoking is serving as a surrogate variable for additional unquantified 'thinness.' A behavioral bias might also be true for cigarettes. If hypertensive men and women are less likely to smoke due to medical or other influences, or are less likely to report smoking if they do smoke, at least part of the negative association of smoking with BP might be spurious. However, the data for smoking in table 3 do not support this hypothesis." GREENHALGH, R.M., LAING, S.P., COLE, P.V. & TAYLOR, G.W., Charing Cross Hospital & St. Bartholomew's Hospital, London "Smoking and arterial reconstruction." (British Journal of Surgery 68/9: 605-7, September 1981) "Fasting levels of serum triglyceride, serum cholesterol, lipoprotein, uric acid, fibrinogen and carboxyhemoglobin (COHb) were measured in 64 patients with stenosing arterial disease before reconstructive surgery, and were compared with those for normal, age- and sex-matched controls. All except fibrinogen were significantly higher in the patients with arterial disease than in the controls. The outcome of arterial recon- struction, assessed both clinically and by Doppler pressure measurements, was compared in terms of these risk factors. "The reconstructions of 12 patients failed between 3 months and 5 years, leaving 52 patients with patent reconstructions at the end of the follow-up period. There was no difference between the two groups in terms of any of the risk factors, excEpt for COHb. The COHb level (associated with inhalation of cigarette smoke) was significantly higher in the reconstruction failure group than in the reconstruction success group. We believe that patients should stop smoking cigarettes before reconstructive arterial surgery is undertaken." RABKIN, S.W., BOYKO, E. & STREJA, D.A., University of Manitoba, Winnipeg, Canada "Relationship of weight loss and cigarette smoking to changes in high-density lipoprotein cholesterol." (American Journal of Clinical Nutrition 34/9: 1764-8, September 1981) "To determine the effect of weight loss on serum high-density lipoprotein cholesterol (HDL-C), we measured serum HDL-C as well as total cholesterol and triglycerides in 65 subjects (56 women and 9 men, mean age 41.1 + 1.5 (+ SEM yr) before and after a weight reduction program. At entry into the program there was a significant correlation between HDL-C and several indices of overweight -- relative weight, body mass =ndex and sum of skinfold thickness. For all subjects, despite a significant weight loss of 4.5 kg or 5.8% of initial body weight and significant decrease in sum of skinfold thickness, there was no signi- ficant increase in HDL-C or correlation between changes in HDL-C and change in body weight or skinfold thickness. For women, but not men,
Page 5: bzs39d00
5. a weak negative correlation between change in HDL-C and change in weight or percentage change in weight was observed. However, in the subset of women who were current cigarette smokers a significant (p ( 0.01) correlation was observed between change in HDL-C and change in weight (r = -0.876) and percentage change in weight (r = -0.881). Thus a modest weight loss is not usually associated with a significant increase in serum HDL-C concentration except in cigarette smoking women." LANDGRAF, H. & EHRLY, A.M., Johann-Wolfgang-Goethe University, Frankfurt, West Germany "'Chronic' cigarette smoking and flow properties of blood." (Clinical Hemorheology 1/3: 241-9, 1981) "The flow properties of blood of 60 healthy young smokers (30 female and 30 male, average 24.4 years and 25.6 years resp.) have been compared with the flow properties of blood obtained from 60 healthy non- smokers (30 female, average age 23.7 years and 30 male, average age 27.2 years). Statistically significant differences were found for the hema- tocrit values in both sexes and for the relative whole blood viscosity in the men's group; relative whole blood viscosity in the women's group and the other rheological parameters as relative plasma viscosity, RBC filtration rate and RBC aggregation, showed some discrepancy but not statistically significant differences. The cause for the differences between the results presented and those of other authors might be seen in different measuring devices as well as in different selection criteria for the investigated volunteers." HUGOD, C., Copenhagen, Denmark "Myocardial morphology in rabbits exposed to various gas-phase constituents of tobacco smoke." (Atherosclerosis 40/2: 181-90, October 1981) "Rabbits were continuously exposed to 200 ppm carbon monoxide. Using the same criteria as applied by earlier investigators for morpho- logical myocardial damage, no histotoxic effect on myocardial morphology could be demonstrated when electron-microscopic investigations were per- formed blindly. Similarly, exposure to 0.5 ppm hydrogen cyanide, 0.5 ppm hydrogen cyanide + 200 ppm carbon nionoxide, 0.5 ppm hydrogen cyanide + 200 ppm carbon monoxide + 5 ppm nitric oxide and to 50 ppm carbonyl sulphide for 1-7 weeks had no significant effect on myocardial ultra- structure." BOOYSE, F.M., OSIKOWICZ, G. & RADEK, J., Michael Reese Research Foundation, Chicago, Illinois (CTR-grant) "Effect on nicotine on cultured bovine aortic endothelial cells." (Thrombosis Research 23/1-2: 169-85, July 15, 1981) "The short (1-4 days) and long-term (10 passages, 12-14 weeks) effect of nicotine tartrate (NT) has been examined on the following cultured bovine aortic endothelial cell properties and functions: growth properties, morphology, total protein and collagen synthesis and turnover, fibrinolysis, lactate production and platelet-subendothelial
Page 6: bzs39d00
6. interaction/adhesion. Low concentrations of NT (<10-4M) had no apparent effect on endothelial cells proliferation, morphology, DNA synthesis (thymidine incorporation), overall protein synthesis (leucine and proline incorporation), fibrinolysis, lactate production and platelet-subendothelial interaction/adhesion. However, NT (10-5 and 10-6M) did increase the net accumulation of collagen in these cultures. In addition, high concentrations of NT (> 10-4M) caused rapid and extensive vacuolation of these cultured bovine endothelial cells and also increased lactate production 2-fold." OCHSNER, A., New Orleans, Louisiana "Abstinence from tobacco in peripheral vascular disease called essential." (Letter: Geriatrics 36/6: 158, 1981) "I was astounded when I read Dr. Nathan P. Couch's article 'How to establish a diagnosis in peripheral vascular disease' in the February 1981 issue of GERIATRICS which, incidentally, is a very good issue. There was no mention made in the discussion on treatment that it is necessary for the individual to completely abstain from the use of tobacco in any form. Many persons feel that in peripheral arterial disease in the elderly, because it is largely due to arteriosclerotic obliteration, vasospasm plays no role. "This is far from the truth. In an individual who uses tobacco in any form, whether it be smoking, chewing, or inhaling as snuff, vaso- spasm is caused by nicotine in the tobacco. The first obligation the patient has is to completely discontinue the use of tobacco in any form." COUCH, N.P., Boston, Massachusetts "Abstinence from tobacco in peripheral vascular disease called essential." (Letter: Geriatrics 36/6: 158, 1981) "I agree wholeheartedly with Dr. Ochsner that all patients should abstain from tobacco. In fact, I spend a great deal of my time delivering sermons on that very topic. "The only reason why I did not happen to mention it in the article was simply that my charge was to discuss the diagnosis of peripheral vascular disease, and I therefore deemphasized the causation." 2. RESPIRATORY CONDITIONS VILLIGER, B., BROEKELMANN, T., KELLEY, D., HEYMACH, G.J. III $ McDONALD, J.A., liashington University School of Medicine at the Jewish Hospital of St. Louis, Missouri "Bronchoalveolar fibronectin in smokers and nonsmokers." (American Review of c* Respiratory Disease 124/5: 652-4, November 1981) 0 .. tr "Fibronectin (FN) is an important nonimmune plasma opsonin for binding of fibrin, gelatin (denatured collagen), and staphylococci by 0 phagocytic cells. Alveolar macrophages play a key role in the clearance r N of particles and microorganisms in the terminal airways, but they lack -4
Page 7: bzs39d00
7. ready access to high molecular weight plasma proteins such as FN. Therefore, to determine if FN is present in the terminal respiratory tract, we used a sensitive radioimmunoassay to measure FN concentrations in broncho- alveolar lavage (BAL) fluid from 13 nonsmoking and 16 smoking volunteers. Fibronectin was present in the BAL fluid of all subjects, and was immuno- logically similar to human plasma FN. The mean FN content in BAL fluid from nonsmokers was 7.3 + 2.9 (SD),,~cg/mg albumin or 2.7 + 1.1,qg/mg total protein. In smokers, the mean FN content was 11.3 + 3.9,tcg/mg albumin or 3.9 + 1.4 k g/mg total protein, values significantly higher than those of nonsmokers (p ( 0.01 and p< 0.02, respectively, for FN/albumin and FN/total protein in smokers versus nonsmokers). The similar (nonsmokers) or elevated (smokers) ratio of FN/albumin in BAL fluid and plasma suggest local production of FN in the lower respiratory tract of humans. One likely source of this FN is the alveolar macrophage because FN is a major secreted protein in vitro. However, there was a poor correlation between the number of recovered macrophages and BAL FN concentrations. Our study demonstrates that: (1) FN is uniformly present in BAL fluid from normal persons, (2) mean FN concentrations in BAL fluid are signi- ficantly higher in smokers than in nonsmokers, (3) BAL fluid FN is probably in part produced in the lower respiratory tract. We concluded that FN may serve as an important nonimmune opsonin for macrophage function in the lower respiratory tract of humans." ELLIS, D.A., THORNLEY, P.E., WIGHTMAN, A.J., WALKER, M., CHALMERS, J. ~, CROFTON, J.W., ltniversity of Edinburgh $ City Hospital, Scotland "Present outlook in bronchiectasis: clinical and social study and review of factors influencing prognosis." (Thorax 36/9: 559-64, September 1981) "One hundred and sixteen patients with proven bxonchiectasis diagnosed at least five years previously were studied to determine the clinical outcome, change in pulmonary function, and degree of social disability. Twenty-two patients had died and the mean duration of follow-up in the survivors was 14 years. The patients who died were characterized by a poorer initial ventilatory capacity than the survivors and cor pulmonale was present in 37% at the time of death. The survivors showed a tendency for improvement in symptoms whether treated surgically or medically. Thirty per cent were better than at diagnosis while only 11% were worse. Measurements of FEV1 and FVC were made at diagnosis and at review, mild airways obstruction being the predominant abnormality. The change in pulmonary function was expressed as the decline in FE1'1 in ml/yr. The decline in FEV1 was no greater than expected in 80% of patients and in a further 15% was of the order seen in cigarette smokers with mild airways obstruction. Poor ventilatory capacity was therefore not an important limitation in these patients. Of the survivors 77% had a good work record with less than two weeks loss of work annually from chest illness. The spouses of all married patients were interviewed at home by a trained social worker. Fifty per cent reported no social problem but 46% of spouses found the patient's cough distasteful and 29% of couples had experienced difficulties with normal sexual life. Seven per cent of the patients were severely disabled. While the overall prog- nosis of our patients was good a minority still have severe physical and social problems as a result of bronchiectasis.... "The proportion of smokers at diagnosis was similar in each category of severity though there were more ex-smokers in the severe group. Overall only 30% of patients were smokers at diagnosis."
Page 8: bzs39d00
8. ROTH, C., ARNOUX, A., HUCHON, G., LACRONIQUE, J., MARSAC, J. f, CHRETIEN, J., Paris, France "Effet du tabagisme sur les cellules broncho-alveolaires chez 1'homme." (Effects of tobacco smoke on bronchoalveolar cells in man) (Bulletin European de Physiopathologie Respiratoire/International Journal of Respiratory Physiopathology 17/5: 767-73, September/October 1981: authors' English abstract) "To evaluate the effects of tobacco smoking on the bronchoalveolar cells, a bronchoalveolar lavage was done in 23 healthy subjects with no signs of pulmonary disease. Two groups of subjects were compared: group S composed of 13 smokers and group NS composed of 10 nonsmokers. In group_S, the total cell count in the recovered lavage fluid (50.9 + 34.2 106; x + SD) was greater (p < 0.05) than in group NS (27.7 + 14.4 106): this difference was due to the greater number of macrophages recovered in group S (49.3 + 34.2 106) compared to group NS (25.3 + 13.9 106). The number of recovered lymphocytes was the same in group S (1.3 + 1.8 106) and in group NS (1.9 + 1.3 106). The number of recovered neutrophils was also the same in group S(32 + 48 104) and in group NS (30 + 30 104). The conclusion of the study is that tobacco smoke increases the number of alveolar macrophages in healthy subjects with no signs of pulmonary infection, but has no effect on the number of lymphocytes or neutrophils." van der LENDE, R., KOK, T.J., REIG, R.P., QUANJER, Ph.H., SCHOUTEN, J.P. $ ORIE, N.G.M., University Hospital, Groningen, The Netherlands "Decreases in VC and FEV1 with time: indicators for effects of smoking and air pollution." (Bulletin European de Physiopathologie Respiratoire/Inter- national Journal of Respiratory Physiopathology 17/5: 775-92, September/ October 1981) "In longitudinal epidemiological investigations in Vlagtwedde and Vlaardingen in the Netherlands, the inhabitants of the moderately polluted town of Vlaardingen showed a greater disease in VC and FEV1 with time than did the inhabitants of the rural community of Vlagtwedde. Furthermore, smokers compared with nonsmokers and heavy smokers with those who smoked less also showed a greater decline in VC and FEV1. Although in previous cross-sectional studies in the same populations we found no systematic relationship between air pollution (S02, standard smoke, and oxidants) and decreased mean VC and FEV1 values, there are now indications that the air pollution in Vlaardingen indeed has a significant effect on the decrease in VC and FEV1 with time. The results of the studies therefore indicate that it is not advisable to increase the present air pollution standards for S02 and standard smoke on the basis of the fact that previous cross-sectional epidemiological studies did not show evident hazardous effects of moderate levels of air pollution on VC and FEV1. Such an increase would be permissible only after longitudinal studies are carried out to prove that no harm is done to the inhabitants in the polluted area."
Page 9: bzs39d00
9. DOBRE, V., Baia Mare, Roumania "Der Widerwille gegcn das Rauchen -- ein subjektive-paradoxales Symptom bei Zigarettenrauchern mit zentralem Lungenkrebs." (Repulsion against smoking - a paradoxical subjective clinical symptom in smokers' pulmonary cancer with central localization)(Zeitschrift fur Erkrankungen der Atmungsorgane 1S6/3: 267-71, 1981: author's English summary) "The paper insists on a paradoxical clinical symptom in smokers' pulmonary cancer: the degust for smoking. A group of 79 smokers (men), of which 68 had smoked an average of over 200,000 cigarettes, among 71 had smoked more than 20 cigarettes per day, presenting a centrally localized pulmonary cancer, were interrogated with the aid of a simple questionary, about the changes that had appeared in their smoking habits during the last 24 months. The consultation revealed that 70 patients (88.6%) complained about a repulsion against smoking which had appeared 2-4 months before, making them stop smoking or reduce the number of cigarettes. This repulsion against smoking may be considered as a new sign in the diagnosis of the central pulmonary cancer in men smokers." GILNt0.N, M.J., SYLVESTER, J.T., KENNEDY, T.P., MENKES, H.A. F, TRAYSTMAN, R.J., Baltimore City Hospitals, Maryland "Vascular effects of cigarette smoke in isolated pig lungs." (American Review of Respiratory Disease 124/5: 549-53, November 1981) "To determine the local effects of cigarette smoke on the pulmonary vasculature, we measured pulmonary artery pressure -- flow curves in isolated, blood-perfused pig lungs before and after 4 exposures to cigar- ette smoke. During each exposure, smoke was administered into the trachea for 3 to 4 min at a rate of 20 to 25 puffs/min and a puff volume of 35 to 50 ml with a smoking machine. During hypoxia (inspired P02, 50 mmHg), when baseline vasomotor tone was high, cigarette smoke caused an acute transient vasodilation. During control (inspired P02, 200 mmHg), when baseline tone was low, no significant effect was observed. In addition to this acute effect, cigarette smoke caused a depression of the pulmonary pressor response to hypoxia, which developed gradually during the course of the experiment. Indomethacin, at perfusate concentrations of 20 and 100a g/ml, did not significantly alter the acute vasodilating effect of smoking, suggesting that prostaglandins synthesized by cyclooxygenase were not the mediators of this response. Indomethacin did, however, prevent the gradual depression of the pulmonary vasoconstrictor response to hypoxia.... "We do not know whether the pulmonary vascular responses to cigarette smoke observed in isolated pig lungs also occur in humans. If they do, they could be deleterious." BETTS, T.E., 0'SULLIVAN, J.P. $ ELSON, L.A., Brompton Hospital, London "Comparative lung pathology of rats after exposure to cigarette and cigar smoke." (British Journal of Experimental Pathology 62/4: 429-35, August 1981) "In a series of 3 experiments, rats bred and maintained under minimum disease conditions suffered much less lung damage after exposure to cigar
Page 10: bzs39d00
10. smoke than did similar animals exposed to the smoke of Virginia tobacco. "Rats exposed to cigar tobacco smoke also showed a greater weight gain and a lower acute-phase protein increase than did their Virginia tobacco counterparts. These differences in response were compounded by the results obtained from measuring changes in the epithelium of the intrapulmonary airways. "The smoke of air-cured but not fermented cigar tobacco had an effect similar to the smoke of Virginia tobacco." WEHNER, A.P., Battelle Pacific Northwest Laboratories, Richland, Washington "Effects of inhaled asbestos, asbestos plus cigarette smoke, asbestos- cement and talc baby powder in hamsters." (IARC Scientific Publication 1/30: 373-6, 1980) "Chronic exposure of hamsters to chrysotile asbestos resulted in severe asbestosis in all animals and in increased mortality; concomitant exposure to cigarette smoke did not affect type or severity of asbestotic lesions. Chronic exposure to asbestos-cement dust increased the number of macrophages and ferruginous bodies. Exposure to talc baby powder caused no significant changes. Deposition of talc particles in the lungs was demon- strated by x-ray fluorescence and x-ray diffraction and by a study with neutron-activated talc. No malignant tumors were observed in any of these studies." 3. OCCUPATIONAL STUDIES Mcr9ILLAN, G.H.G., Dockyard Medical Center, Gibraltar "The health of welders in naval dockyards: welding, tobacco smoking and absence attributed to respiratory diseases." (Journal of the Society of Occupational Medicine 31: 112-18, 1981) "The relationship between absence attributed to respiratory disease, exposure to welding and smoking habits of three groups of craftsmen [N 1888) in three naval dockyards has been examined over a 5-year period. The men studied were welders, shipwrights and boilermakers intermittently exposed to welding pollutants as neighborhood workers, and joiners, painters and electrical fitters rarely if ever so exposed. In comparison with the other two groups of men, a higher proportion of welders could be classi- fied as smokers and a lower proportion as nonsmokers. Welders who are or have been smokers are found to have higher absence indices. Welders who have never smoked have lower absence indices compared with nonsmokers in the other two groups. The presence of welding pollutants in the working environment may prompt welders with respiratory symptoms to take absence although the cause of these symptoms may be unrelated to work."

Text Control

Highlight Text:

OCR Text Alignment:

Image Control

Image Rotation:

Image Size: