Reference SummaryWitschi H, Carcinogenesis 1997 Mar;18(3):575-86

Title

 The carcinogenicity of environmental tobacco smoke.

Authors

 Witschi H; Espiritu I; Peake JL; Wu K; Maronpot RR; Pinkerton KE

Journal

 Carcinogenesis

Volume

 18

Issue

 3

Year

 1997

Pages

 575-86

Abstract

 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.

Links

 J:39409 – MGI References
9067559 – National Library of Medicine/PubMed

Models
Strain Model Name Treatment Agent(s) Organ Affected Frequency Model Details
A/J Lung tumor Lung

8.3 - 57
A/J Lung tumor
  • environmental tobacco smoke (ETS)
 Lung

25 - 83
A/J Lung tumor
  • urethane (ethyl carbamate)
 Lung

100
A/J Lung tumor
  • urethane (ethyl carbamate)
  • environmental tobacco smoke (ETS)
 Lung

100
A/J Lung tumor
  • 3-methylcholanthrene (MCA) (3-MC)
 Lung

100
A/J Lung tumor
  • 3-methylcholanthrene (MCA) (3-MC)
  • environmental tobacco smoke (ETS)
 Lung

100
A/J Lung tumor
  • butylated hydroxytoluene (BHT)
  • environmental tobacco smoke (ETS)
 Lung

76
A/J Lung tumor
  • butylated hydroxytoluene (BHT)
 Lung

56