title: Triclosan exposure modulates estrogen-dependent responses in the female wistar rat.
abstract: Triclosan is an antimicrobial found in personal care and sanitizing products, such as soaps, toothpaste, and hair products. There have been recent concerns for the possible effects on human health, as triclosan has been detected in human breast milk, blood, and urine samples. In a previous study, we found that triclosan alters serum thyroid hormone and testosterone concentrations in male rats. In the current study, we evaluated the effects of triclosan in the female Wistar rat following exposure for 21 days in the Endocrine Disruptor Screening Program pubertal protocol and the weanling uterotrophic assay (3-day exposure). In the pubertal study, triclosan advanced the age of onset of vaginal opening and increased uterine weight at 150 mg/kg, indicative of an estrogenic effect. In the uterotrophic assay, rats received oral doses of triclosan (1.18, 2.35, 4.69, 9.37, 18.75, 37.5, 75, 150, and 300 mg/kg) alone, 3 microg/kg ethinyl estradiol (EE), or triclosan (same doses as above) plus 3 microg/kg EE. Uterine weight was increased in the EE group (positive control) as compared with the control but was not affected by triclosan alone. However, there was a significant dose-dependent increase in the group cotreated with EE and triclosan (>or= 4.69 mg/kg) as compared with EE alone, indicating a potentiation of the estrogen response on uterine weight. This result was well correlated with potentiated estrogen-induced changes in uterine histology. Serum thyroid hormone concentrations were also suppressed by triclosan in this study, similar to other studies in the male and female rat. In conclusion, triclosan affected estrogen-mediated responses in the pubertal and weanling female rat and also suppressed thyroid hormone in both studies. The lowest effective concentrations in the rodent model are approximately 10 (for estrogen) and 40 (for thyroid hormone) times higher than the highest concentrations reported in human plasma.
authors.affiliation: Endocrine Toxicology Branch, Toxicity Assessment Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711, USA. stoker.tammy@epa.gov
authors.forename: Tammy E
authors.initials: TE
authors.lastname: Stoker
authors.forename: Emily K
authors.initials: EK
authors.lastname: Gibson
authors.forename: Leah M
authors.initials: LM
authors.lastname: Zorrilla
mesh_terms: D000818:Animals; D004305:Dose-Response Relationship, Drug; D052244:Endocrine Disruptors / Q000633:toxicity*; D004967:Estrogens / Q000502:physiology*; D005260:Female; D007986:Luteinizing Hormone / Q000097:blood; D009929:Organ Size / Q000187:drug effects; D011247:Pregnancy; D011388:Prolactin / Q000097:blood; D011863:Radioimmunoassay; D051381:Rats; D017208:Rats, Wistar; D012741:Sexual Maturation / Q000187:drug effects; D013963:Thyroid Hormones / Q000097:blood; D014260:Triclosan / Q000633:toxicity*
chemical_list: D052244:Endocrine Disruptors; D004967:Estrogens; D013963:Thyroid Hormones; D014260:Triclosan; D011388:Prolactin; D007986:Luteinizing Hormone