Perchlorate is a known environmental contaminant, largely due to widespread military use as a propellant.
Perchlorate acts pharmacologically as a competitive inhibitor of thyroidal
iodide uptake in mammals, but the impacts of
perchlorate contamination in aquatic ecosystems and, in particular, the effects on fish are unclear. Our studies aimed to investigate the effects of concentrations of
ammonium perchlorate that can occur in the environment (1, 10, and 100 mg/L) on the development of fathead minnows, Pimephales promelas. For these studies, exposures started with embryos of < 24-hr postfertilization and were terminated after 28 days. Serial sectioning of thyroid follicles showed thyroid
hyperplasia with increased follicular epithelial cell height and reduced
colloid in all groups of fish that had been exposed to
perchlorate for 28 days, compared with control fish. Whole-body
thyroxine (T4) content (a measure of total circulating T4 in fish exposed to 100 mg/L
perchlorate was elevated compared with the T4 content of control fish, but 3,5,3-
triiodothyronine (T3) content was not significantly affected in any exposure group. Despite the apparent regulation of T3, after 28 days of exposure to
ammonium perchlorate, fish exposed to the two higher levels (10 and 100 mg/L) were developmentally retarded, with a lack of scales and poor pigmentation, and significantly lower wet weight and standard length than were control fish. Our study indicates that environmental levels of
ammonium perchlorate affect thyroid function in fish and that in the early life stages these effects may be associated with developmental retardation.