Comparative reproductive and developmental toxicology of PCBs in birds

Abstract

The acute toxicity of PCBs to adult birds increases with increasing chlorination of the PCB mixture, and brain residues greater than 300 mg/kg are associated with mortality. Sublethal effects in adults include reduced parental attentiveness and abnormal reproductive behavior. PCBs cause a suite of developmental effects, including endocrine disruption, immunotoxicity and teratogenesis, rather than a specific etiology such as egg shell thinning. Possible polychlorinated dibenzofuran (PCDF) contamination in PCB mixtures may have been responsible for some of the reported toxic effects attributed to PCBs, such as edema. PCB concentrations causing embryo mortality range from 3.1 μg/kg for 3,3′,4,4′,5-pentachlorobiphenyl in chicken eggs to 30 mg/kg for total PCBs in double crested cormorant eggs. Dietary no adverse effect concentrations range from 0.5 ppm in the American kestrel to 50 ppm in the Japanese quail. Genetic differences related to expression of the aryl hydrocarbon (Ah) receptor, rather than toxicokinetics, may be the dominant factor determining reproductive toxicity of PCBs in birds. The assessment of potential injury to bird populations from PCBs is confounded by the presence of multiple contaminants in field-collected biota and environmental media.