THE CARCINOGENIC POTENTIAL OF THE GAS-PHASE OF ENVIRONMENTAL TOBACCO-SMOKE

Female strain A/J mice were exposed to unfiltered or HEPA-filtered env ironmental tobacco smoke (ETS), Total suspended particulates (TSP) in the full smoke exposure chamber was 78.5 mg/m(3) and in the filtered s moke chamber 0.1 mg/m(3); nicotine concentrations in the full and filt ered smoke chamber were 13.4 and 3.1 mg/m(3), respectively. Animals ex posed to filtered ETS (6 h a day, 5 days a week) and killed after 5 mo nths had a higher lung tumor incidence and multiplicity than controls maintained in filtered air, although the differences were not statisti cally significant, Animals exposed to filtered and full ETS and allowe d to recover in air for 4, months had an average of 1.2 +/- 0.3 tumors per lung and 1.3 +/- 0.3 tumors per lung, respectively, Air exposed c ontrol animals had an average tumor multiplicity 0.5 +/- 0.1 tumors pe r lung. Increased immunstaining for CYP 1A1 was not evident in the lun g of animals exposed to filtered smoke. Based on the chamber concentra tions of selected nitrosamines and polycyclic aromatic hydrocarbons, t he possible maximum uptakes by the mice of NNK, NNN and benzo[a]pyrene during the 5 months exposure period were three to six orders of magni tude below doses reported in the literature to produce 1 lung tumor in strain A/J mice, It was concluded that the gas phase of ETS is as car cinogenic as is full ETS, The carcinogenicity of the gas phase may be due to some as yet unidentified, yet highly potent carcinogens or by p lacing a substantial, possibly free radical-mediated oxidative stress on the lung.