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Helen M. Crane,^1,2 Daniel B. Pickford,²* Thomas H. Hutchinson,² and J. Anne Brown¹

¹School of Biological Sciences, Hatherly Laboratories, University of Exeter, Exeter, United Kingdom; ²AstraZeneca, Global Safety, Health and Environment, Brixham Environmental Laboratory, Brixham, Devon, United Kingdom

Abstract
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. Key words: development, endocrine disruption, fathead minnow, perchlorate, thyroid, thyroxine, triiodothyronine. Environ Health Perspect 113:396-401 (2005) . doi:10.1289/ehp.7333 available via http://dx.doi.org/ [Online 10 January 2005]

Address correspondence to H. Crane, Environment Agency, Chemical Assessment Unit, Ecosystems and Human Health, Evenlode House, Howbery Park, Wallingford, Oxon, OX10 8DB UK. Telephone: 1491-828189. Fax: 1491-828556. E-mail: helen.jordinson@environment-agency.gov.uk

*Current address: Institute for the Environment, Brunel University, Uxbridge, Middlesex, UK.

We thank M. Field and M. Canty at Brixham Environmental Laboratory and S. Frankling at Exeter University for technical help.

This work was supported by AstraZenca and a Natural Environment Research Council Studentship (NER/S/C/1999/0453) awarded to H.M.C.

T.H.H. is employed by AstraZeneca, and H.M.C. and D.B.P. were employed by AstraZeneca during this study. J.A.B. declares she has no competing financial interests.

Received 17 June 2003 ; accepted 10 January 2005.