THE CARCINOGENICITY OF ENVIRONMENTAL TOBACCO-SMOKE

Male strain A/J mice were exposed for 6 h a day, 5 days a week to envi ronmental tobacco smoke (ETS) generated from Kentucky 1R4F reference c igarettes, Chamber concentrations were 87 mg/m(3) of total suspended p articulate matter (TSP), 246 p.p.m. of CO and 16 mg/m(3) of nicotine, After 5 months, 33% of the ETS exposed and 11% of the control animals had one or several lung tumors; the difference was statistically not s ignificant, A second group of animals exposed for 5 months to ETS was allowed to recover for another 4 months in filtered air, When they wer e killed, 85% of the ETS animals had lung tumors (average number per l ung: 1.4 +/- 0.2), whereas in the control group 38% had lung tumors (a verage number of lung tumors in all animals 0.5 +/- 0.2), The differen ces in tumor incidence and multiplicity were statistically significant . More than 80% of all tumors were adenomas, the rest adenocarcinomas. When animals were pretreated with a carcinogen, lung tumor multiplici ty was lower in the ETS exposed animals after 5 months compared,vith c ontrols injected with a carcinogen and kept in air. However, after an additional 4 month recovery period in air, lung tumor multiplicities w ere the same in ETS plus carcinogen exposed mice as in carcinogen-trea ted air-exposed controls, Histopathologic and morphometric analysis of the lung tissue failed to reveal any differences between ETS exposed and control animals, However, immediately after ETS exposure, immunohi stochemistry revealed increased staining for CYP1A1 in airway epitheli a and lung parenchyma; following recovery in air, the staining disappe ared again, Analysis of cell kinetics showed an initial burst of incre ased DNA synthesis in the epithelial cells of the airways and a smalle r early positive response in the parenchyma, Feeding of butylated hydr oxytoluene during ETS exposure did not modulate lung tumor development , It was concluded that ETS is a pulmonary carcinogen in strain A/J mi ce.