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A B S T R A C T Pulmonary alveolar macrophages were obtained from healthy, volunteers by saline pulmonary lavage, and aryl hydrocarbon hydroxylase was measured in the cells. Enzyme activity was low in cells from five nonsmokers with a mean of 0.0080.004 U/106 cells. Cells obtained from nine cigarette smokers contained higher enzyme levels, with a mean of 0.0950.024 U/16 cells. A former cigarette smoker was lavaged on five occasions. Enzyme activity during two lavages 4 mo apart were 0.010 and 0.009 U/106 cells, respectively. 1 wk after smoking was resumed, the enzyme activity rose slightly to 0.013, and reached 0.041 U/106 cells by 1 mo. Upon cessation of smoking, the enzyme activity re- turned to control levels by the next lavage, 2 mo later. These data indicate that aryl hydrocarbon hydroxylase may be induced in pulmonary alveolar macrophages of subjects chronically exposed to cigarette smoke. ing and cancer are related have not been delineated. Cigarette smoke and constituent chemicals such as benzo apyrene (BP)' can induce tumors in a dose-related manner in experimental animals
Cantrell et al. (1973) studied this question.