Article

Importance of exposure to gaseous and particulate phase components of tobacco smoke in active and passive smokers

Analytisch-biologisches Forschungslabor Prof. Dr. F. Adlkofer, München, Federal Republic of Germany.
International Archives of Occupational and Environmental Health (Impact Factor: 2.2). 02/1990; 62(6):459-66. DOI: 10.1007/BF00379064
Source: PubMed

ABSTRACT

The uptake of tobacco smoke constituents from gaseous and particulate phases of mainstream smoke (MS), inhaled by smokers, and of environmental tobacco smoke (ETS), breathed in by non-smokers, was investigated in two experimental studies. Tobacco smoke uptake was quantified by measuring carboxyhemoglobin (COHb), nicotine and cotinine in plasma and urine and the data obtained were correlated with urinary excretion of thioethers and of mutagenic activity. An increase in all biochemical parameters was observed in smokers inhaling the complete MS of 24 cigarettes during 8 h, whereas only an increase in COHb and, to a minor degree, in urinary thioethers was found after smoking the gas phase of MS under similar conditions. Exposure of non-smokers to the gaseous phase of ETS or to whole ETS at similar high concentrations for 8 h led to identical increases in COHb, plasma nicotine and cotinine as well as urinary excretion of nicotine and thioethers which were much lower than in smokers. Urinary mutagenicity was not found to be elevated under either ETS exposure condition. As shown by our results, the biomarkers most frequently used for uptake of tobacco smoke (nicotine and cotinine) indicate on the one hand the exposure to particulate phase constituents in smoking but on the other hand the exposure to gaseous phase constituents in passive smoking. Particle exposure during passive smoking seems to be low and a biomarker which indicates ETS particle exposure is as yet not available. These findings emphasize that risk extrapolations from active smoking to passive smoking which are based on cigarette equivalents or the use of one biomarker (e.g. cotinine) might be misleading.

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Available from: Franz Adlkofer, Jun 22, 2015
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    • "Some studies have also reported elevated COHb levels in non-smokers exposed to environmental tobacco smoke (Scherer et al., 1990). CO is considered a toxic chemical at high concentrations , leading to a severe hypoxic condition by displacing oxygen from haemoglobin (Hb), leftward shift of the oxyhaemoglobin dissociation curve, and binding to intracellular enzymes. "
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    ABSTRACT: Carbon monoxide (CO) is a dangerous poison in high concentrations, but the long-term effects of low doses of CO, as in the gaseous component of tobacco smoke, are not well known. The aims of our study were to evaluate the long-term effects of inhaled CO on the respiratory and cardiovascular system at doses corresponding to tobacco smoking and its effect on tumourigenesis and pulmonary neuroendocrine (NE) cells. Female Wistar rats were exposed to either CO (200 ppm) for 20 h/day (n=51) or air (n=26) for 72 weeks. Carboxyhaemoglobin was 14.7+/-0.3% in CO exposed animals and 0.3+/-0.1% in controls. In the lungs, no signs of pathology similar to that associated with cigarette smoking were observed, and no differences in number of pulmonary NE cells were observed between the groups. Chronic CO inhalation induced a 20% weight increase of the right ventricle (p=0.001) and a 14% weight increase of the left ventricle and interventricular septum (p<0.001). Histological examination of the myocardium did not reveal any signs of scarring. In the aorta and femoral artery, no signs of atherosclerosis were observed in CO exposed rats. No exposure related carcinogenic effects were observed. Spontaneous tumours were identified in 29% of CO exposed animals and in 28% of the controls. Our results suggest that low dose CO exposure is probably not responsible for the respiratory pathology associated with tobacco smoking. The effects on the cardiovascular system seem to involve myocardial hypertrophy, but not atherogenesis.
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    • "Exposure of the platelet to epinephrine increases the tendency toward aggregation in the presence of agonists, e.g., ADP, collagen , thrombin, PAF, etc. (Smith et al., 1998). How much exposure to nicotine do nonsmokers receive from ETS? Serum nicotine concentrations between 0.9 and 2.8 ng/ml have been reported following ETS exposure (Biber et al., 1987; Davis et al., 1989; Jarvis et al., 1983; Scherer et al., 1990). Baseline serum nicotine concentration for controls not exposed to ETS is approximately 1 ng/ml. "
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    ABSTRACT: Two recent government reports have focused attention on the hypothesis that environmental tobacco smoke (ETS) exposure increases the risk of cardiovascular disease (CVD) in nonsmokers. The first report was published by the California Environmental Protection Agency (CAEPA) in 1997. The second report was issued in 1998 by the Scientific Committee on Tobacco and Health (SCOTH) in the United Kingdom. A meta-analysis of five large prospective epidemiology studies reports that the relative risk for actively smoking 20 cigarettes per day is 1.78. Active smoking exposes the smoker to approximately 16 times the ETS concentration, and 100- to 300-fold the total smoke dose experienced by a nonsmoker (Smith and Ogden, 1998, JAMA 280, 32-33.). Despite the much lower smoke exposure, these government reports estimate the relative risk for ischemic heart disease in ETS-exposed nonsmokers at 1.30 (CAEPA) and 1.23 (SCOTH). As an explanation for this nonlinear dose-response anomaly, platelet aggregation is proposed to be a plausible and quantitatively consistent mechanism. Herein, evidence is presented suggesting that this low-dose hypothesis is inconsistent with the biochemistry and physiology of platelets and with the literature on the cardiovascular pathology of active smoking. In addition, several important biases and confounders are ignored. These epidemiologic biases and confounders include the following: misclassification of smokers as nonsmokers; improper use of death certificates as surrogates for mortality statistics; underreporting of diabetes and hypertension in the relatives of smokers; and additional atherogenic risk factors in smoking households. Future field studies on ETS and CVD should emphasize proximal markers of risk for thrombosis in exposed nonsmokers. Proximal thrombogenic risk markers identified in field studies should be mechanistically examined under controlled exposure conditions.
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