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The effects of Tordon 202c exposure on urethan-induced lung adenoma formation in female CD-1 mice

S L Adams1, S T Horvat, A E Irwin

  • 1Department of Veterinary Physiological Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Canada.

Veterinary and Human Toxicology
|June 1, 1991
PubMed

Insights

Exposure to the herbicide Tordon 202c, containing 2,4-dichlorophenoxyacetic acid and picloram, increased pulmonary adenoma formation in mice. This suggests Tordon 202c influences tumor development through immunological mechanisms.

Area of Science:

  • Toxicology
  • Carcinogenesis
  • Environmental Health

Background:

  • The herbicide Tordon 202c contains 2,4-dichlorophenoxyacetic acid and picloram.
  • Understanding the carcinogenic potential of herbicides is crucial for public health.
  • Previous studies have not fully elucidated the mechanisms by which Tordon 202c may affect tumor development.

Purpose of the Study:

  • To investigate the effect of Tordon 202c exposure on pulmonary adenoma production in mice.
  • To explore the potential mechanisms, including immunological effects and alterations in chemical metabolism, underlying Tordon 202c's influence on tumor formation.

Main Methods:

  • Female CD-1 mice were administered Tordon 202c in drinking water for 15 weeks.
  • Urethane was administered intraperitoneally at 3 weeks.
  • Pulmonary adenoma incidence and size were evaluated 12 weeks after urethane administration.
  • Urethane-induced sleeping times were measured to assess metabolism/excretion rates.

Main Results:

  • Tordon 202c exposure resulted in a dose-dependent increase in the number of pulmonary adenomas.
  • Tumor size was not significantly affected by Tordon 202c exposure.
  • While urethane-induced sleeping times were altered, no clear dose-related correlation with tumor production was observed.

Conclusions:

  • Tordon 202c exposure promotes pulmonary adenoma formation in a dose-dependent manner.
  • The findings suggest that Tordon 202c influences adenoma development primarily through immunological mechanisms.
  • The herbicide's effect is unlikely to be mediated by significant alterations in urethane metabolism or excretion.

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