Short-term in vivo exposure to the water contaminant triclosan: Evidence for disruption of thyroxine

Kevin M Crofton; Katie B Paul; Michael J Devito; Joan M Hedge

doi:10.1016/j.etap.2007.04.008

Short-term in vivo exposure to the water contaminant triclosan: Evidence for disruption of thyroxine

Environ Toxicol Pharmacol. 2007 Sep;24(2):194-7. doi: 10.1016/j.etap.2007.04.008. Epub 2007 Apr 27.

Authors

Kevin M Crofton¹, Katie B Paul, Michael J Devito, Joan M Hedge

Affiliation

¹ Neurotoxicology Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. EPA, Research Triangle Park, NC, United States.

PMID: 21783810
DOI: 10.1016/j.etap.2007.04.008

Abstract

Triclosan (5-chloro-2-(2,4-dichlorophenoxy)phenol) is a chlorinated phenolic antibacterial compound found as an active ingredient in many personal care and household products. The structural similarity of triclosan to thyroid hormones and recent studies demonstrating activation of the human pregnane X receptor (PXR) and inhibition of diiodothyronine (T(2)) sulfotransferases, have raised concerns about adverse effects on thyroid homeostasis. The current research tested the hypothesis that triclosan alters circulating concentrations of thyroxine. The hypothesis was tested using a 4-day oral triclosan exposure (0-1000mg/kg/day) in weanling female Long-Evans rats, followed by measurement of circulating levels of serum total thyroxine (T(4)). Dose-dependent decreases in total T(4) were observed. The benchmark dose (BMD) and lower bound on the BMD (BMDL) for the effects on T(4) were 69.7 and 35.6mg/kg/day, respectively. These data demonstrate that triclosan disrupts thyroid hormone homeostasis in rats.