International archives of occupational and environmental health
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The question of whether asbestos workers with or without asbestosis have the same risk of lung cancer has not been adequately addressed in the literature. Studies of asbestos workers indicate that clinical symptoms and abnormal lung X-rays are more frequent among smokers than non-smokers, and some studies show that workers with asbestosis compared to those without asbestosis are more likely to be smokers or ex-smokers. Since smoking has a large affect on the risks of lung cancer, smoking habits should be considered when evaluating the risk of lung cancer among persons with and without asbestosis. ⋯ It is unlikely that the higher risk of lung cancer to persons with asbestosis is only due to their higher prevalence of smoking. Some studies have suggested that asbestos workers with asbestosis may have a higher risk of lung cancer, but no definite conclusions can be drawn since dose-response relations were not evaluated. Further studies are needed to evaluate the interrelationships of smoking, asbestosis and the risk of lung cancer.
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Int Arch Occup Environ Health · Jan 1990
ReviewImportance of exposure to gaseous and particulate phase components of tobacco smoke in active and passive smokers.
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. ⋯ 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.