Reproductive and Developmental Toxicity of a Pentabrominated Diphenyl Ether Mixture, DE-71, to Ranch Mink (Mustela vison) and Hazard Assessment for Wild Mink in the Great Lakes Region

• Published in: Toxicological sciences Vol. 110; no. 1; pp. 107 - 116
• Main Authors: Zhang, Si, Bursian, Steven J., Martin, Pamela A., Chan, Hing M., Tomy, Gregg, Palace, Vince P., Mayne, Greg J., Martin, Jonathan W.
• Format: Journal Article
• Language: English
• Published: United States Oxford University Press 01.07.2009
• Subjects: Animals; Animals, Domestic; Animals, Newborn; Animals, Wild; Cytochrome P-450 CYP1A1 - blood; development; Eating - drug effects; Female; Flame Retardants - toxicity; Great Lakes Region; Halogenated Diphenyl Ethers - toxicity; Liver - drug effects; Liver - enzymology; Liver - metabolism; Male; Mink - physiology; Organ Size - drug effects; polybrominated diphenyl ether; Pregnancy; reproduction; Reproduction - drug effects; Risk Assessment; Survival Analysis; Teratogens - toxicity; thyroid; Thyroid Diseases - chemically induced; Thyroid Diseases - pathology; Thyroid Hormones - blood; wildlife; development; thyroid; wildlife; polybrominated diphenyl ether; reproduction
• ISSN: 1096-6080; 1096-0929
• DOI: 10.1093/toxsci/kfp095

Polybrominated diphenyl ethers (PBDEs) are widespread persistent and bioaccumulative environmental contaminants. Recent scientific attention has focused on the developmental toxicity of PBDE commercial mixtures following perinatal exposure of rodents; however, these studies do not necessarily predict toxicity to highly exposed top predators, such as mink (Mustela vison). Here we assessed the effects of environmentally relevant doses (0, 0.1, 0.5, and 2.5 ppm [wt/wt] in feed) of a technical pentabrominated diphenyl ether mixture, DE-71, on reproductive performance of mink and on development of offspring exposed perinatally and post-weaning until 33 weeks. A dietary concentration that causes no effects on reproduction in rodents, 2.5-ppm DE-71, resulted in complete reproductive failure in these mink, while whelping rates were not affected at all lower does. Developmental effects in offspring were evident in 33-week-old juveniles, which were more sensitive to effects than their respective dams. Juvenile thyroid hormone homeostasis was also much more sensitive compared to rodents, and at 0.5-ppm DE-71, total triiodothyronine (T3) was significantly decreased in all males and females, even despite a compensatory increase of total thyroxine (T4) in females. T4-outer-ring deiodinase activity, mainly contributed by type II deiodinase, was not affected at any dose for any life stage, but thyroid follicular epithelium cell height was elevated in the 0.5-ppm–treated juveniles (p = 0.057). Ethoxyresorufin O-deethylase activity was significantly induced in all offspring at 33 weeks, most likely as a consequence of polybrominated dioxin, furan, or biphenyl impurities in DE-71. Biomonitoring of wild mink in the Great Lakes region indicated that most populations had lower concentrations than what are expected to affect thyroid hormone homeostasis, but margins of safety are small and mink around Hamilton Harbour exceeded the no observed adverse effect level for T3 disruption.