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A detailed description is given of the design and operation of a new smoking machine built for inhalation toxicity studies with small laboratory animals. Brief details are given of smoke monitoring carried out to determine the extent of loss of particulated matter along the smoke path through the machine.
We tested 20 different smoke inhalation machines and determined that 60% of the gas phase and 40% of the total paritulate matter reached the inhalation chamber; the remainder was lost in the exhaust gases. After determining these concentration percentages, we were able to calculate precisely the dosage of each puff of smoke administered to Syrian hamsters in our smoking machine. We also determined that the CO-Hb content in the blood of the hamsters rose to 60%; this CO-Hb value was a limiting factor for time of exposure to smoke, since too-high concentrations of CO-Hb would have killed the animals. On the basis of these results, we concluded that the animals should be exposed as long as possible to attain a high dose of smoke, but because of toxic effects the exposure time should not exceed 20 minutes, and the CO-Hb content should not exceed 60%.
The effects of cigarette smoking on phenacetin metabolism in the rat and in man have been investigated. Exposure of rats to cigarette smoke or pretreatment with the polycyclic hydrocarbon, 3,4-benzpyrene (benzo[a]pyrene), resulted in a more rapid disappearance of phenacetin in vivo. Additional studies demonstrated that hydrocarbon and smoking pretreatment of rats enhanced the 0-dealkylation of phenacetin to N-acetyl-p-aminophenol (APAP) by the intestinal mucosa. Cigarette smoking also increased the metabolism of phenacetin in man. The plasma concentration of phenacetin in cigarette smokers was lower than that in nonsmokers, whereas the ratio of the concentration of APAP to that of phenacetin was increased severalfold in the smokers. No difference in plasma half-life of elimination of phenacetin or in the amount of APAP excreted was found between smokers and nonsmokers. The lower blood levels of phenacetin in cigarette smokers could be the result of increased intestinal metabolism of the drug and/or first-pass metabolism in the liver.
Data derived from four major prospective epidemiological studies in the U.S. and Britain indicate that persistent cigarette smoking in later life carries an appreciable hazard. In two of these studies men aged over 65 years who smoked cigarettes had a significantly higher mortality from coronary heart disease than men who had ceased to smoke cigarettes, and in all four studies their overall mortality was significantly higher than that of ex-smokers. At 65-74 years the overall mortality of men still smoking cigarettes was higher by 24 percent or more than that of ex-smokers, and at 75-84 years it was higher by 12 to 18 percent. The absolute difference in overall mortality was 9 to 13/1000 per person-years in both age-groups. A comparison of data on men who had given up smoking at different ages suggests that while the benefit is greater if smoking is stopped earlier in life, men in their sixties and (especially in the case of heavy smokers) their early seventies may still increase their longevity by giving up smoking cigarettes.
Twenty normal subjects and 25 patients with coronary artery disease underwent systolic time interval analysis before and after rapidly smoking two cigarettes. A slight increase in heart rate and arterial pressure was seen in both groups. In patients with coronary artery disease, preejection period/left ventricular ejection time ratio increased; in normal subjects it decreased. Left ventricular performance is diminished after cigarette smoking among subjects who have preexisting significant coronary artery disease.
Cigarette smoking is a major risk factor of coronary artery disease. Frequent repetition of an acute effect on the heart caused by cigarette smoking has been suggested as the etiology because of the increased incidence of myocardial infarction in cigarette smokers which drops to the incidence in non-smokers after cessation of smoking. This study of cardiac patients during cardiac catheterization evaluates the acute effect of the ordinary cigarette, smoked in the individuals own manner, on parameters of cardiac pump and muscle performance. The accuracy of measurements was enhanced by employing high-fidelity pressure signals, signal averaging, and computer analysis of the data. The results of the present study suggest that when cardiac patients smoke 1 cigarette of their own brand in their accustomed manner, no deleterious effects on pump performance, ventricular contraction or relaxation and blood pressure are evident.
Chemiluminescence from cigarette smoke (aerosol) and smoke "extracts" (suspensoids) are described. The emissons from aqueous and organic suspensoids persist for hours, are proportional to oxygen solubilities, possess energy of at least 1.8 electron volts, and display characteristics which suggest that the emissions may be partially sensitized by singlet oxygen.
Volatile nitrosamines from the smoke of different cigarettes were enriched by manifold clean-up procedures. Amines obtained after acid catalyzed denitrosation were transformed to fluorescent derivates of 7-chloro-4-nitrobenzofuranzane (NBD-Cl). These NBD-amines separated on polyamid sheets were fluorimetrically determined with a chromatogram-spectrophotometer. Recovery rates of 60--80% were found for the different nitrosamines in cigarette smoke condensate. The following nitrosamines were quantitatively determined: N-nitrosodimethylamine, N-nitrosodiethylamine, N-nitrosopiperidine, N-nitrosopyrrolidine, N-nitrosoethylmethylamine, N-nitroso-ethyln-propylamine and N-nitroso-methyl-n-propylamine, N-nitroso-ethyl-n-propylamine and N-nitroso-methyl-n-propylamine. The last mentioned nitrosamine was proved for the first time in cigarette smoke. At the same time correlations between the nitrosamine content of the corresponding tobacco or condensate and the content of nitrate, total nitrogen, nicotine, volatile bases and ammonia were investigated. The nitrate content as well as the content of volatile bases showed an influence on the nitrosamine yield. The content of the different nitrosamines varied cosiderably depending on tobacco origin, so that a NNO-determination is recommended as index.
The influence of cigarette smoke on the numbers and viability of alveolar macrophages in the lungs of mice was determined by utilizing techniques for quantitating lung deposition of bacteria and alveolar macrophage harvest. Alveolar macrophages were obtained by pulmonary lavage. The studies were performed under basal conditions, after the inhalation of cigarette smoke and after exposure to bacterial aerosols and cigarette smoke in sequence. Macrophage yields were increased 1.1, 1.2, and 1.5 times basal levels by exposure to cigarette smoke alone for 1, 2, and 4 hours, repectively. The inhalation of Staphylococcus aureus for 30 minutes induced a 2.4-fold increase in macrophage numbers. Within 15 minutes after bacterial deposition, macrophage yields dropped 33 percent, but elevated levels were restored at 30 minutes and then maintained for the remainder of the 4 hour test period. Cigarette smoke introduced immediately after bacterial challenge and maintained for up to 4 hours did not alter the macrophage response provoked by pulmonary deposition of staphylococci. In addition, smoke inhalation had no effect on the cellular characteristics of lung harvests and the viability of alveolar macrophages. These data demonstrate that cigarette smoke provoked an increase in alveolar macrophage numbers and did not have a deleterious effect on the mobilization of alveolar macrophages; namely, the maintenance of a macrophage response in relation to an airborne bacterial challenge.
Mice were exposed to fresh cigarette smoke for 1,17, and 38 weeks. After each period the primary and secondary humoral immune response to intraperitoneal inoculation of sheep erythrocytes was studied. Direct and indirect plaque forming cell responses in the spleen and in a pool of cervical and mediastinal lymph nodes, as well as serum hemolytic and hemagglutinating antibodies were examined. Primary plaque forming cell and antibody response to sheep erythrocytes was first enhanced and then depressed by continual cigarette smoke exposure, while the secondary response was unaffected. Serum antibody response to polyvinylpyrrolidone, an immunogen independent of thymus-derived lymphocytes, was not impaired by 41 weeks of cigarette smoke exposure.
Mutagenic activities of cigarette smoke condensate were assayed in the presence of S-9 Mix using Salmonella typhimurium TA 98. The results were examined in relation to chemical data of tobacco leaves. Among the nitrogenous constituents examined, the contents of total nitrogen and protein nitrogen and the soluble nitrogenous fraction were positively and significantly related to an increase in mutagenic activity of the smoke condensate, whereas nicotine and nitrate were not important in contributing to mutagenic potency of such condensates. The age of tobacco leaves influenced the mutagenic potency of the condensate, which was lowest in leaves from the lower stalk position and increased with ascending leaf position on the stalk. Smoke condensate from tobacco with higher sugar content resulted in lower mutagenic activity. The present results, together with the previous study on the mutagenicity of the amino acid pyrolyzates, suggest that potent mutagens in cigarette smoke condensate are nitrogen-containing compounds, which may be formed from proteins and amino acids during the burning of a cigarette.
Mice were chronically exposed to cigarette smoke for various time periods up to 4 weeks. As a consequence of the exposure, there was an increase in the number of alveolar macrophages obtained from the lungs of these mice. Light microscopic examination of cultured cells revealed increased numbers of highly pleomorphic cells filled with pigmented residues of cigarette smoke. These cells were more mitotically active, with a five fold increase in the number of alveolar colony-forming cells compared to the controls. When macrophages derived from mice exposed to cigarette smoke were cultured at high density in the absence of serum, they secreted significantly greater amounts of elastase than did the same number of control macrophages. At concentrations as low as 0.50 micrograms/ml, cycloheximide reversibly inhibited elastase secretion from both the control and experimental cultures. The effects of cigarette smoke inhalation on elastase secretion by alveolar macrophages do not appear to be a direct effect of cigarette smoke on these cells. Exposure of normal mouse macrophages in vitro to pulses of aqueous extracts of cigarette smoke, while significantly increasing secretion of elastase by peritoneal exudative macrophages, did not augment that of resident or exudative alveolar macrophages. These results suggest that the increased elastase secretion observed with the use of cultured macrophages derived from mice exposed to cigarette smoke is the result of either indirect activation of resident macrophages or the recruitment of a highly activated exudative population into the lungs of the exposed animals.
Cigarette smoking is a major cause of illness and premature death in our society. Secondhand smoke is a definite irritant to nonsmokers and can, under certain conditions, have potentially serious effects on the nonsmoker's health. Despite the facts, millions of persons continue to smoke. Although no single health professional reaches all smokers, the dentist has a particularly good opportunity to reach his patients who smoke. By advising and couseling, providing helpful literature, creating an environment in which smoking is prohibited, and setting a good example, the dentist can have a singificant part in his patients' education on cigarette smoking. If the dentist's efforts are even partially successful in modifying behavior of the patient who smokes, much illness will be avoided and many lives saved.
Cigarette smoking was found to have no effect on the steady-state plasma levels of nortriptyline in a group of 22 smokers and 31 nonsmokers. Smokers achieved a mean steady-state nortriptyline concentration of 191.2 +/- 141.3 ng/ml; nonsmokers had a level of 169.3 +/- 92.4 ng/ml. Age, sex, and number of cigarettes smoked had no effect on the plasma concentrations achieved.
Aversive cigarette smoking that consisted of rapid smoking, warm smoky air, and handling of cigarette litter was investigated. Prior to treatment, all Ss were screened to minimize risks inherent in rapid smoking. Tree male and 9 female Ss completed 6 weeks of treatment. After treatment the mean smoking rate was 16% of baseline. At 3-,6-, and 9-month follow-ups, the mean average was 38%, 50% and 50% of baseline, respectively. Aversive smoking appears to be a promising behavioral approach to smoking cessation.
In order to evaluate a possible relation between cigarette smoking and prevalence of diabetic microangiopathy, a series of 180 consecutive patients suffering from insulin-dependent juvenile-onset diabetes mellitus with different durations of disease (60 patients each with diabetes for 10 to 19 years, 20 to 29 years, and 30 to 39 years, respectively) were examined for clinical signs of retinopathy, nephropathy, and peripheral neuropathy. The results were compared with the patients' previous and actual smoking habits. Cigarette smoking was defined as daily smoking of at least ten cigarettes for one year or more. Smoking habits of the total diabetic sample were not significantly different from those of a nondiabetic control sample. However, a decline in the number of cigarette smokers and a rising number of ex-smokers were noted with increasing duration of diabetes. In comparing smokers and nonsmokers, no difference was found in the prevalence of peripheral neuropathy, background retinopathy, and proliferative retinopathy. However, the prevalence of nephropathy (persistent proteinuria) was significantly higher (p less than 0.05) among these patients who were or had been cigarette smokers. Thus, cigarette smoking might be considered a risk factor for the development of diabetic nephropathy.
The hypothesis was investigated that cigarette smoking obstructs the blood flow response that develops as a protection against tissue damage in an organ subjected to ischemia (reactive hyperemia). Forearm blood flow was recorded at rest and following forearm ischemia before and after cigarette smoking in healthy male and female volunteers. The experiments were also repeated after pre-treatment of the subjects with indomethacin, a prostaglandin synthesis inhibitor. Before pre-treatment with indomethacin, ischemia induced a reactive hyperemia amounting to 20 +/- 4 ml/100 ml tissue. This hyperemia was significantly (p less than 0.01) reduced by cigarette smoking, to 12 +/- 3 ml/100 ml tissue. After indomethacin, which in itself lowered the reactive hyperemia to 8 +/- 2 ml/100 ml tissue, smoking did not elicit any effect. It is suggested that smoking counteracts reactive hyperemia in tissues by interfering with the same physiological mechanism as indomethacin, i.e. with the vascular formation of PG. The possible significance of this observation in relation to cigarette smoking and ischemic heart disease is stressed.
Some ciliostatic components of cigarette smoke were studied as inhibitors of in vitro chemotaxis of human polymorphonuclear leukocytes (PMNs). In comparison to their concentration in an inhibitory level of cigarette smoke, the unsaturated aldehydes acrolein and crotonaldehyde were the most potent inhibitors, whereas nicotine, cyanide, acetaldehyde, and furfural were the next strongest inhibitors. In contrast, sulfide, propionaldehyde, butyraldehyde, and the phenols (phenol and o-, m-, and p-cresol) were relatively weak inhibitors of PMN chemotaxis. Acrolein and crotonaldehyde mimicked whole cigarette smoke in their effects on PMNs by not causing loss of PMN viability, yet their effects were prevented by the addition of cysteine. On the other hand, addition of nicotine, cyanide, acetaldehyde, and furfural to PMN suspensions resulted in a limited loss of cellular viabilities, and their effects on PMNs were not prevented by cysteine. Of the tested components, only cyanide significantly altered PMN glucose metabolism by increasing carbon flow via the glycolytic and hexose monophosphate pathways in a manner similar to that observed with whole cigarette smoke. The results of this study suggest that the unsaturated aldehydes, including acrolein and crotonaldehyde, are major contributors to the inhibitory properties of cigarette smoke. The inhibitory effects of these unsaturated aldehydes are probably due to a direct interaction of these oxidants and/or thiol-alkylating agents with PMNs, yet the glucose metabolism of these cells is unaffected. One interpretation of these data is that PMN chemotaxis is dependent upon particular cellular proteins containing one or more essential thiol group(s) but that these proteins are unrelated to glucose metabolism.