Dioxin, polychlorinated biphenyls (PCBs), and pesticides impact neural systems in birds due to interference with sexual differentiation. Early endocrine disrupting chemical (EDC) effects may delay maturation and have long-term effects on lifetime reproduction, especially in precocial birds that complete sexual differentiation prior to hatch. Semi-altricial and altricial species appear more resilient to EDC effects and show a gradient in sensitivity, especially in the neuroplastic song system. Embryonic steroid exposure occurs via maternally deposited steroids followed by embryo produced hormones; EDCs potentially affect these developing systems. As such, EDCs can impact lifelong fitness by acting on neural systems that regulate reproduction, metabolism, and behavior.

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The Japanese quail (Coturnix japonica) egg bioassay was used to directly compare the toxicity of 3,3’,4,4’,5‐pentachlorobiphenyl (PCB 126), 3,3’,4,4’‐tetrachlorobiphenyl (PCB 77), and 2 environmentally relevant polychlorinated biphenyl (PCB) mixtures over specified dose ranges relative to vehicle and uninjected controls. Measures included lethality and deformities. Results showed clear dose‐response relationships for PCB 126 and the 2 PCB mixtures by logistic analysis of covariance using a varying threshold model because there was a low but significant slope for mortality of vehicle controls over incubation. No dose‐dependent increase in mortality was observed with PCB 77 treatment. Mortality increased above baseline for PCB 126 and the 2 mixtures after embryonic day 7 (ED07) to a stable slope from ED10. Median lethal doses and thresholds for response differed for PCB 126 and the 2 PCB mixtures, with the mixtures having lower initial toxicity and all showing progressively greater toxicity over the course of development. Further, the lethality of the PCB mixtures appeared to involve both aryl hydrocarbon receptor (AhR) and non‐AhR mechanisms. Incidence of deformities was unrelated to treatments. In summary, complex mixtures of PCBs were lethal in a dose‐related manner, with sublethal effects from exposure to PCB 77. Environ Toxicol Chem 2019;38:2637–2650. © 2019 SETAC

The avian embryo is an excellent model for testing adverse developmental effects of environmental chemicals as well as uptake and movement of xenobiotics within the egg compartments. Before incubation at embryonic day 0, 14 C 3,3 0 ,4, 4 0 -tetrachlorobiphenyl ( 14 C PCB 77) was injected into Japanese quail eggs either onto the air cell or into the albumen. All egg components were collected on embryonic day 1, 5, or 10, and concentrations of 14 C PCB 77 were measured in various egg components (shell, membrane, yolk, albumen, and embryo). The results showed measurable 14 C PCB 77 in all egg components, with changing concentrations in each egg component over the course of embryonic development. Specifically, concentrations in the shell content decreased between embryonic days 1 and 10, increased in albumen from embryonic days 1 to 5 and then decreased at embryonic day 10, and increased in both yolk and embryo from embryonic days 1 to 10. Vehicle and injection site both influenced 14 C PCB 77 allantoic fluid concentrations, with little effect on other egg components except for the inner shell membrane. The fatty acid vehicle injected into the albumen yielded the highest 14 C PCB 77 recovery. These findings demonstrate dynamic movement of toxicants throughout the egg components during avian embryonic development and a steady increase of relatively low levels of 14 C PCB 77 in the embryo compared with the yolk, albumen, and shell, suggesting that embryonic uptake (i.e., exposure) mirrors utilization of egg components for nutrition and growth during development. Environ Toxicol Chem 2018;37:126-135. C 2017 SETAC