No study was available that was designed specifically to investigate the carcinogenicity of passive smoking to experimental animals. Exposure to these complex mixtures results in mutagenic urine in smokers and in increased chromosomal damage in the somatic cells of smokers compared to nonsmokers. Cigarette-smoke condensate induces neoplastic transformation in mammalian cells in vitro. Certain biochemical markers of smoke intake, e.g., cotinine in plasma, urine or saliva, are sufficiently sensitive and specific to identify passive smokers. The precise quantitative relationship between the measured levels of these markers and the intake of carcinogenic compounds in tobacco smoke is not known.
Wide variation is found, however, among individuals.
Lung cancer patients with a history of smoking are more often extensive metabolizers of the drug debrisoquine or have high induced levels of aryl hydrocarbon hydroxylase than smokers without lung cancer. It remains to be established whether this association implies that individuals with such genotypes are at increased risk of tobacco smoke-associated cancer. Lung cancer is believed to be the most important cause of death from cancer in the world, with estimated total deaths in excess of one million annually. The major cause of the disease is tobacco smoking, primarily of cigarettes. Further, the longer the time period during which a major proportion of adults in a population have smoked, the greater the incidence and mortality from the disease in that population.