Inhalation Of Tobacco Smoke Research Articles

Smoking pattern of smokers with and without tobacco-smoke-related lung diseases.

The number of cigarettes smoked, the duration of the smoking habit, and the tar content of the smoke influence the occurrence of tobacco-smoke-related lung diseases, as may also patterns of smoke inhalation. We therefore determined the smoking pattern, especially the time relation between cigarette puff and inhalation, in smokers with and without tobacco-smoke-related lung diseases. On the basis of clinical and radiologic findings as well as pulmonary function tests, 91 smokers were classified as smokers without lung disease, with small airway disease, with simple chronic bronchitis, with obstructive bronchitis, with pulmonary emphysema, and with lung cancer. Smoking and breathing patterns were recorded, using a smoke-flow machine and a strain-gauge belt while the subject smoked a cigarette. Blood levels of COHb were determined before and after smoking. Of the smoking characteristics assessed, puff-inhalation time, puff peak pressure, and the venous difference in COHb level before and after smoking varied significantly among the smoker groups. Puff-inhalation time, reflecting the duration of smoke retention in the mouth, was only 0.08 s (i.e., practically zero) in smokers with pulmonary emphysema and differed significantly from the time in the other groups. This puffing characteristic may be the consequence or the cause of emphysema. If the latter is true, smokers with emphysema may perhaps lack the acute airway response to smoke inhalation that normally protects most smokers from immediately inhaling tobacco smoke.

Tobacco smoking: impairment of experimental flap survival.

The survival rate of experimental flaps as affected by exposure to inhaled tobacco smoke has been investigated in rats subjected to different smoking regimens. A distally based dorsal flap was raised and reattached in each animal. Evaluation of the flaps on postoperative day 8 showed a mean rate of necrosis of 28.5% in 25 control animals, 32.2% in 21 rats postoperatively smoking for 7 days, 41.3% in 18 rats preoperatively smoking for 7 days, and 45.7% in 21 rats smoking for 7 days both before and after the surgical procedure. Histological sections from the lungs of the smoking animals revealed a pattern compatible with mild smoke inhalation injury. Arterial oxygen tensions were lower in the tobacco smoking animals. It is assumed that the multiple effects of tobacco smoking contributed to the impairment of experimental flap survival.

The influence of passive smoking on pulmonary function—A study of 1,351 office workers

Until now it has been difficult to ascertain how much passive inhalation of tobacco smoke affects bronchopulmonary function. To answer this question, an investigation involving 1,351 white collar workers was carried out. Information about active and passive tobacco smoke exposure was obtained by a standardized questionnaire. This made it possible to subdivide the overall group into five subgroups: Never smokers, passive smokers, ex-smokers, current smokers, and other smokers. Forced expiratory vital capacity (FVC) and maximal expiratory flow-volume (MEFV) curves were used for lung function analysis. From these curves FVC, forced mid-expiratory flow (FEF 25/75), forced end-expiratory flow (FEF 75/85), and maximal mid-expiratory flow (MEF 25/75) were determined and standardized for sex, age, height, and body weight. Passive smokers evaluated by this method showed essentially no decrease in parameters describing ventilatory function. It is concluded from the dose-and time-effect relationships obtained in active smokers between the lung function parameters and the duration of tobacco smoke exposure on the one hand and the daily consumption of cigarettes on the other that passive smoking in small doses may have no essential effect on pulmonary function.

Toward a Global Strategy to Combat Smoking: The 5th World Conference on Smoking and Health

The World Conference on Smoking and Health meeting during July 1983 to discuss the scientific social and political aspects of smoking and its control around the world focused on 3 main themes: the problems of smoking and women smoking and children and smoking in developing countries. To examine the various aspects of these and other themes sessions were organized under 5 categories: the health consequences of smoking smoking cessation public information and public education the economic consequences of tobacco and legislation and political action. Overviews of the main themes and the 5 topic categories were presented in plenary sessions. The popularity of smoking has grown enormously among women worldwide. In the US the percentage of adult males who smoke exceeds that of adult females by fewer than 10 percentage points. 3 decades ago the gap was close to 30 percentage points. In the 1980s in the US lung cancer has overtaken breast cancer as the leading cancer cause of mortality in women. This results not from improvements in the treatment of breast cancers but rather from the epidemic of lung cancer in women. The average age of initiating smoking in the US is now about 16 years. There is general agreement that an individual is highly unlikely to start smoking after age 21. The concept of "immunizing" youngsters against smoking lies at the heart of this most primary of smoking disease. Several alternative approaches to preventing the onset of smoking by children were discussed at the Conference with greatest interest centering around the use of youths to influence their peers not to smoke. Smoking rates have leveled off or are falling in the developed world but they are increasing rapidly in developing countries. Cigarette companies have directed much of their marketing effort at this potentially substantial growth market and the profitability of tobacco farming in many developing countries is causing tobacco to compete successfully with staple food crops. Several Conference delegates reported that people in developing countries have little awareness of the health consequences of smoking. Other concerns discussed at the conference include passive smoking i.e. the nonsmokers inhalation of tobacco smoke in the air nonsmokers rights movement and civil disobedience. 20 recommendations were adopted by the Conference delegates. An additional 15 action oriented and somewhat bolder recommendations were also made and endorsed by the International Liaison Committee on Smoking and Health.

CIGARETTE SMOKING INHIBITS PROSTACYCLIN FORMATION

Urinary prostacyclin (PGI 2) was measured in 12 chronic smokers and 12 non-smokers after inhalation of smoke from nicotine-containing and nicotine-free cigarettes. In a separate study a pressor dose of noradrenaline, which increases PGI 2, was given to smokers and non-smokers. PGI 2 was measured as the stable metabolite, 6-keto-PGF 1α in 4 h urine samples by radioimmunoassay after chromatography on LH-20 'Sephadex'. Smoking of nicotine-free cigarettes had no effect on PGI 2 release in either smokers or non-smokers. In non-smokers inhalation of nicotine-containing tobacco smoke increased heart-rate, blood-pressure, and urine osmolality, but did not affect urinary 6-keto-PGF 1α. In contrast, when chronic smokers used nicotine-containing cigarettes there was a highly significant reduction in excretion of 6-keto-PGF 1α (192±20 to 138±17 ng/g creatinine). Noradrenaline increased PGI 2 in non-smokers (181±16 to 348±56) but not in smokers. Smoking of nicotine-containing tobacco abolished the PGI 2 response to noradrenaline. These observations suggest that inhalation of nicotine-containing tobacco smoke reduces vascular PGI 2 production; this may be a factor in the development of accelerated cardiovascular disease.

コレステロール負荷ウサギの血中脂質ならびに副腎機能に及ぼすたばこ煙吸入の影響

Rabbits were given cholesterol (CH) (1.5% CH supplemented diet ad libitum) and tobacco smoke (inhalation of smoke from 5mm length cigarette with or without glass fiber filter, two times a day), separately or in combination, for 4 weeks.Plasma HDL-CH levels in CH fed rabbits elevated in first two weeks then lowered gradually, while total CH, TG, and FFA increased significantly towards the end of experiment. Those increases in blood lipids by CH diet were inhibited by tobacco smoke inhalation, and especially by filtered smoke increase in atherogenic index (A. I) was only slight. Inhalations of both kinds of smoke induced a significant decrease in HDL after 2 weeks and increases in CH and A. I after 4 weeks.Corticoids (CD) in blood increased in CH fed rabbits either with or without tobacco smoke inhalation but showed no change in rabbits given tobacco smoke alone. As the adrenal weight increased by the CH diet, adrenal CS level per weight was lower in CH fed group, but total CS content in adrenals was not affected by CH diet.Adrenaline content increased both in blood and adrenals by both kinds of tobacco smoke seemed to be lowered. CH diet inhibited the increment of adrenaline (A) in adrenals. Noradrenaline (NA) increased only in adrenals of rabbits inhalated tobacco smoke.In summary, increases in blood lipids, blood and adrenal (A). and adrenal (NA) were resulted by tobacco smoke inhalation. Simultaneous application of CH diet inhibited the increase in blood lipids, however the mechanism of this combined effect was left for further researches.

ウサギにおけるコレステロール摂取およびたばこ煙吸入による実験的動脈硬化発生初期の生体顕微鏡的皮膚微小循環系変化所見

ウサギにおけるコレステロール摂取およびたばこ煙吸入による実験的動脈硬化発生初期の生体顕微鏡的皮膚微小循環系変化所見

Neoplastic Development in Airway Epithelium

Bronchogenic carcinoma is the most common fatal neoplastic disease in many parts of the world. The etiology of bronchogenic carcinoma is more firmly established than that of most other cancers. The evidence is overwhelming that most lung cancers are caused by tobacco smoke inhalation, the incidence depending on the duration of exposure and dose rate. Bronchogenic carcinoma is one of the few types of cancers with a well-defined etiology. However, factors, other than carcinogen exposure, which are important determinants of lung cancer induction are not certain. With the recent introduction of in vivo and in vitro approaches for the study of neoplastic development and the advances in culture systems that can be used for investigating the transformation of airway epithelial cells, the cellular analysis of the biologic potential of dysplastic airway lesions and the progression of initiated cells is now feasible. The chapter summarizes and critically analyzes primarily the information relevant to the induction and development of those cells and tissue changes that may progress to invasive cancer. Future investigations will no doubt lead to the discovery of new markers of neoplastic transformation and to a more complete understanding of the multiphasic process of neoplastic development as it occurs in the epithelial lining of the airways.

Bronchial hypersecretion, chronic airflow limitation, and peptic ulcer.

Men with and men without a history of peptic ulcers were compared using respiratory symptoms and spirographic measurements taken from data recorded in an epidemiologic study. Among the 1,049 men examined, 7% reported a history of peptic ulcer. A clear relationship appeared between bronchial hypersecretion and peptic ulcers. It persisted after adjustment for age, smoking habits, social class, and country of origin. Men with ulcers inhaled tobacco smoke more often. Ulcers, smoking, and chronic phlegm were independently related to a lower body build index. It seems that the relationship between smoking and ulcers was greater among men with chronic phlegm, and it is postulated that peptic ulcers and "chronic bronchitis" might be related to a "common secretory disorder." After adjustment for age, men with a history of peptic ulcers had, not a lower FEV1, but a higher vital capacity. A slightly lower FEV1/VC ratio cannot in such cases be considered as an index of chronic airflow limitation.

Effect of acute tobacco smoke inhalation on the mechanical responses of isolated rat cardiac muscle

To evaluate the effects of acute inhalation of tobacco smoke upon the intrinsic properties of cardiac muscle, rats were exposed to cigarette smoke from 2R1 Kentucky reference cigarettes in special smoking chambers for periods of 10Min/hr for 5 hr. Animals were sacrificed, and the mechanical properties of isolated left ventricular papillary and columnar carneae preparations were studied. Mean COHb concentration of animals exposed to tobacco smoke was 13.2 ± 0.9 vol%. No significant difference was found in rats exposed to tobacco smoke when compared to shams in (1) cardiac chamber weight or chamber wet-to-dry weight ratios, (2) cardiac muscle performance in oxygenated Krebs-Henseleit solution (95% O 2, 5% CO 2), (3) muscle performance during 60 min of hypoxia (95% N 2, 5% CO 2) followed by 30 min of reoxygenation, (4) muscle performance during graded hypoxia with and without glycolytic blockade (iodoacetic acid 10 −4 m), or (5) sensitivity of myocardial performance to isoproterenol. Thus, after acute exposure to tobacco smoke, no effects on the intrinsic mechanical properties of rat cardiac muscle were demonstrable.

Airways response to inhaled tobacco smoke: time course, dose dependence and effect of volume history.

We have measured puff by puff the effect of smoking three brands of cigarettes with different composition on airways resistance (Raw) thoracic gas volume (TGV) and the maximal expiratory flow volume (MEFV) curve. Raw increased significantly with all three brands of cigarettes after one puff. The maximum effect was reached after three puffs. Instantaneous flow at 50% of vital capacity (FEF50) decreased significantly with cigarettes high in nicotine content, but not so after smoking a low nicotine (0.31 mg) cigarette. Instantaneous flow at 75% of vital capacity out (FEF75) increased significantly 30 min after the low nicotine cigarette was smoked. A deep inspiration prior to Raw determination reduced by approximately one third the bronchoconstrictor effect of cigarette smoke. All effects were reversible within 30 min, except the delayed effect of the low nicotine cigarette on the FEF75. We conclude that the probable site of action of tobacco smoke is in the large and central airways. The bronchoconstrictor effect rapidly reaches a plateau. A delayed bronchodilation of the small airways observed after smoking the low nicotine cigarette might represent a response usually masked by other long-acting components in smoke. We suggest that the airway response to tobacco smoke is complex and probably a result of several components present in smoke which still have to be identified.

Small-airways dysfunction in nonsmokers chronically exposed to tobacco smoke.

We evaluated the effect of long-term passive smoking (involuntary inhalation of tobacco smoke by nonsmokers) and long-term voluntary smoking on specific indexes of pulmonary function in 2100 middle-aged subjects. Regardless of sex, nonsmokers chronically exposed to tobacco smoke had a lower forced mid-expiratory flow rate (FEF 25 to 75 per cent) and forced end-expiratory flow rate (FEF 75 to 85 per cent) than nonsmokers not exposed (P less than 0.005). In addition, values in passive smokers were not significantly different from those in light smokers and smokers who did not inhale (P less than 0.005). When we looked at the extent to which smoke exposure is related to graded abnormality, we found that nonsmokers in smoke-free working environments have the highest scores on the spirometric tests; passive smokers, smokers who do not inhale, and light smokers score similarly and significantly lower; and heavy smokers score the lowest (P less than 0.005). We conclude that chronic exposure to tobacco smoke in the work environment is deleterious to the nonsmoker and significantly reduces small-airways function.

Sucrose aversions in mice as a result of injected nicotine or passive tobacco smoke inhalation

Two studies using Swiss-Webster mice demonstrated that a delayed nicotine injection or passive tobacco smoking are effective treatments for conditioning sucrose aversions. The results are discussed in relation to future research as well as possible implications for human health.

Cigarette smoking and HDL cholesterol the Framingham offspring study

High density lipoproteins were measured on fasting blood samples from 4107 men and women. Control for reported alcohol consumption and subscapular skinfold thickness using multiple regression analysis allowed an examination of the relationship between cigarette smoking and HDL cholesterol. Cigarette smoking was found to be associated with an average difference in HDL cholesterol of about 4 mg/dl in men and 6 mg/dl in women. Furthermore, when heavy alcohol drinkers were eliminated a significant negative association between number of cigarettes smoked and HDL cholesterol was demonstrable in both men and women. There was no evidence that former cigarette smokers, with the exception of those who switched to cigars or pipes or had quit less than one year, had lower HDL levels. Cigar or pipe smokers who had never smoked cigarettes had alcohol- and skinfold-adjusted HDL cholesterol comparable to the non-smoker. These observations indicate another possible link between inhaled tobacco smoke and the atherosclerotic process and suggest the need for further studies and experiments that might clarify the mutual relationship of HDL cholesterol, cigarette smoking and the atherosclerotic process.

A tobacco smoke inhalation exposure device for rodents.

A system which utilizes a piston pump to generate cigarette smoke under standard conditions, and expose rodents to the inhalation of diluted smoke for controlled periods of time is described. Variations of the basic system have been employed to exposure groups of ten to twenty hamsters or rats, and should allow exposures of up to forty mice. The system has been in use for approximately 24 months in routine chronic exposures of rats. Data are presented to define the operating characteristics and typical dosimetry. Animal containment peculiar to this apparatus is described.

Activation of 2-aminoanthracene to mutagenic intermediates by guinea pig kidney microsomal enzymes following tobacco smoke inhalation

Male guinea pigs and male rats were exposed to the smoke of five cigarettes and killed at various time intervals up to 48 hr later. The activity of aryl hydrocarbon hydroxylase in kidney of both species was significantly higher than in controls at 3, 6, 12, and 24 hr after the end of smoke exposure. The 9000 g supernatant from guinea pig kidney homogenates activated 2-aminoanthracene into a compound(s) mutagenic for Salmonella typhimurium strain TA 98; the 9000 g supernatant from smoke-exposed animals had a greater activating capacity than preparations from control animals. Preparations from rat kidneys were much less active and no difference was seen between smoke-exposed and control animals.

The differential effects of exposure to tobacco smoke on the secretion of luteinizing hormone and prolactin in the proestrous rat.

The acute effects of tobacco smoke inhalation on the spontaneous proestrous rise in serum luteinizing hormone and prolactin have been investigated in the female Wistar rat. It was found that the surge of LH normally seen throughout the afternoon of proestrus was delayed by inhalation of tobacco smoke and that the delay was dose-related to the nicotine content of the cigarettes used in the experiment. In the case of prolactin neither the timing nor the magnitude of the surge was altered when compared with controls. These results suggest that under certain well-defined conditions inhalation of tobacco smoke of known nicotine content is capable of exerting profound influences on the hypothalamic-pituitary-gonadal axis.

Environmentally induced changes in immunological function: acute and chronic effects of inhalation of tobacco smoke and other atmospheric contaminants in man and experimental animals

Attention is drawn to the long-term effects of atmospheric contaminants in general (and cigarette smoke in particular) on immunological control mechanisms that are accepted as playing a vital role in the maintenance of health. The review argues that a hostile environment within the respiratory tract created by inhalation of air contaminants compromises local immunological function in the short term, and ultimately depresses systemic immunological function. Whether such a decline in immunological homeostasis is due directly to toxicity, or indirectly to accelerated aging of susceptible elements of the immune system, is speculative. The changes observed in both man and experimental animals exposed for long periods to air contaminants in many respects parallel those associated with normal aging and may represent an acceleration of the process of senescence. Specific biological effects of smoking, air pollution and immune functions in man and animal models are reviewed. The precise mechanism(s) by which air contaminants affect immunological function remains speculative, but the relative resistance of specified-pathogen-free animals to these agents infers a central role for the hosts' normal bacterial flora in the process.

Airway Response to Short-Term Inhalation of Tobacco Smoke: Lack of Racial Differences

Airway Response to Short-Term Inhalation of Tobacco Smoke: Lack of Racial Differences

Environmentally induced changes in immunological function: acute and chronic effects of inhalation of tobacco smoke and other atmospheric contaminants in man and experimental animals.

Attention is drawn to the long-term effects of atmospheric contaminants in general (and cigarette smoke in particular) on immunological control mechanisms that are accepted as playing a vital role in the maintenance of health. The review argues that a hostile environment within the respiratory tract created by inhalation of air contaminants compromises local immunological function in the short term, and ultimately depresses systemic immunological function. Whether such a decline in immunological homeostasis is due directly to toxicity, or indirectly to accelerated aging of susceptible elements of the immune system, is speculative. The changes observed in both man and experimental animals exposed for long periods to air contaminants in many respects parallel those associated with normal aging and may represent an acceleration of the process of senescence. Specific biological effects of smoking, air pollution and immune functions in man and animal models are reviewed. The precise mechanism(s) by which air contaminants affect immunological function remains speculative, but the relative resistance of specified-pathogen-free animals to these agents infers a central role for the hosts' normal bacterial flora in the process.