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Maki Tabuchi,^1,2 Nik Veldhoen,² Neil Dangerfield,¹ Steven Jeffries,³ Caren C. Helbing,² and Peter S. Ross¹

¹Institute of Ocean Sciences, Fisheries and Oceans Canada, Sidney, British Columbia, Canada; ²Department of Biochemistry and Microbiology, University of Victoria, Victoria, British Columbia, Canada; ³Washington Department of Fish and Wildlife, Tacoma, Washington, USA

Abstract
Persistent organic pollutants are environmental contaminants that, because of their lipophilic properties and long half-lives, bioaccumulate within aquatic food webs and often reach high concentrations in marine mammals, such as harbor seals (Phoca vitulina) . Exposure to these contaminants has been associated with developmental abnormalities, immunotoxicity, and reproductive impairment in marine mammals and other high-trophic-level wildlife, mediated via a disruption of endocrine processes. The highly conserved thyroid hormones (THs) represent one vulnerable endocrine end point that is critical for metabolism, growth, and development in vertebrates. We characterized the relationship between contaminants and specific TH receptor (TR) gene expression in skin/blubber biopsy samples, as well as serum THs, from free-ranging harbor seal pups (n = 39) in British Columbia, Canada, and Washington State, USA. We observed a contaminant-related increase in blubber TR- gene expression [total polychlorinated biphenyls (PCBs) ; r = 0.679 ; p < 0.001] and a concomitant decrease in circulating total thyroxine concentrations (PCBs ; r = –0.711 ; p < 0.001) . Consistent with results observed in carefully controlled laboratory and captive feeding studies, our findings suggest that the TH system in harbor seals is highly sensitive to disruption by environmental contaminants. Such a disruption not only may lead to adverse effects on growth and development but also could have important ramifications for lipid metabolism and energetics in marine mammals. Key words: endocrine disruption, gene expression, marine mammal, PCBs, persistent organic pollutant, polychlorinated biphenyls, POP, seal, thyroid, thyroid hormone receptor. Environ Health Perspect 114:1024–1031 (2006) . doi:10.1289/ehp.8661 available via http://dx.doi.org/ [Online 16 March 2006]

Address correspondence to P.S. Ross, Institute of Ocean Sciences, Fisheries and Oceans Canada, P.O. Box 6000, 9860 West Saanich Rd., Sidney, British Columbia, V8L 4B2 Canada. Telephone: (250) 363-6806. Fax: (250) 363-6807. E-mail: rosspe@pac.dfo-mpo.gc.ca

We thank D. Lambourn, C. Main, M. Wagner, D. Domanski, L. Ji, F. Zhang, M. Gunderson, L. Mos, D. Cullon, and J. Christensen for support.

This work was supported by grants from the Environmental Sciences Strategic Research Fund, Species at Risk Act Science Program, Toxic Substances Research Initiative, and the Washington Department of Fish and Wildlife to P.S.R. C.C.H. is recipient of a Society for Environmental Toxicology and Chemistry Early Career Award for Applied Ecological Research.

The authors declare they have no competing financial interests.

Received 14 September 2005 ; accepted 16 March 2006.