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Several halogenated chemicals are found in an array of products that can cause endocrine disruption. Human studies have shown that endocrine responses are sex specific, with females more likely to develop hypothyroidism and males more likely to have reproductive impairment. The objective of this study was to assess sex differences on thyroid and estrogenic effects after exposure of Japanese medaka (Oryzias latipes, SK2MC) to halogenated compounds. This strain is an excellent model for these studies as sex can be determined non-destructively a few hours postfertilization. Medaka embryos were exposed to sublethal concentrations of Tris(1,3-dichloro-2-propyl) phosphate (TDCPP, 0.019 mg/L), perfluorooctanoic acid (PFOA, 4.7 mg/L) and its next generation alternative, perfluorobutyric acid (PFBA, 137 mg/L). Methimazole (inhibits thyroid hormone synthesis) and the thyroid hormone triiodothyronine served as reference controls. Fish were exposed throughout embryo development until 10 days postfertilization. Females displayed significantly larger swim bladders (which are under thyroid hormone control) after exposure to all chemicals with the exception of triiodothyronine, which caused the opposite effect. Females exposed to TDCPP and PFOA had increased expression of vitellogenin and exposure to PFOA upregulated expression of multiple thyroidrelated genes. Upregulation of estrogenic-regulated genes after exposure to TDCPP, PFOA and methimazole was only observed in males. Overall, our results suggest that females and males show an estrogenic response when exposed to these halogenated chemicals and that females appear more susceptible to thyroid-induced swim bladder dysfunction compared with males. These results further confirm the importance of considering sex effects when assessing the toxicity of endocrine-disrupting compounds.

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Offspring survival, cohort performance, and ultimately population dynamics are strongly influenced by maternal characteristics (e.g., fecundity), whereas paternal contribution is often considered limited to genetic-driven fitness of males through sexual selection. However, male contribution to reproductive success can be particularly influential in species exhibiting paternal offspring care. Polychlorinated biphenyls (PCBs) are widespread, persistent contaminants that can disrupt maternal reproductive processes and negatively affect offspring. In contrast, how PCBs affect paternal reproductive success is largely unknown, but could ultimately affect population dynamics. We examined the effects of lifelong PCB exposure on the reproductive processes of male fathead minnows (Pimephales promelas), a species exhibiting sole paternal offspring care, by examining endocrine-associated gene expression, testes histology, secondary sexual characteristics, courtship ability, offspring care, and offspring survival. PCBs minimized male secondary sexual characteristics, but did not affect gonadal end points or inhibit ability to court females. Fathers exposed to high concentrations of dioxin-like PCBs had changes in gene expression, reduced offspring care behavior, and higher embryo mortality, possibly due to fathers spending less time within nests and less frequently tending to embryos. Through complex interactions among gene expression, physical characteristics, and behavior, PCBs inhibit paternal reproductive success and have the potential to suppress population size.