Carcinogenesis, Vol 18, 575-586, Copyright © 1997 by Oxford University Press
H Witschi, I Espiritu, JL Peake, K Wu, RR Maronpot and KE Pinkerton
Male strain A/J mice were exposed for 6 h a day, 5 days a week to
environmental tobacco smoke (ETS) generated from Kentucky 1R4F reference
cigarettes. Chamber concentrations were 87 mg/m3 of total suspended
particulate matter (TSP), 246 p.p.m. of CO and 16 mg/m3 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 significant. A
second group of animals exposed for 5 months to ETS was allowed to recover
for another 4 months in filtered air. When they were killed, 85% of the ETS
animals had lung tumors (average number per lung: 1.4 +/- 0.2), whereas in
the control group 38% had lung tumors (average number of lung tumors in all
animals 0.5 +/- 0.2). The differences 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 multiplicity was lower in the ETS exposed animals after 5 months
compared with controls injected with a carcinogen and kept in air. However,
after an additional 4 month recovery period in air, lung tumor
multiplicities were the same in ETS plus carcinogen exposed mice as in
carcinogen-treated 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,
immunohistochemistry revealed increased staining for CYP1A1 in airway
epithelia and lung parenchyma; following recovery in air, the staining
disappeared again. Analysis of cell kinetics showed an initial burst of
increased DNA synthesis in the epithelial cells of the airways and a
smaller early positive response in the parenchyma. Feeding of butylated
hydroxytoluene during ETS exposure did not modulate lung tumor development.
It was concluded that ETS is a pulmonary carcinogen in strain A/J mice.
ARTICLES
The carcinogenicity of environmental tobacco smoke
University of California, Davis, Department of Molecular Biosciences, School of Veterinary Medicine, USA.
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