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In 1978-81, 293 bald eagles (Haliaeetus leucocephalus) from 32 states were necropsied and analyzed for organochlorine pesticides, polychlorinated biphenyls (PCB), and lead residues. DDE was found in all carcasses; PCB, DDD, trans-nonachlor, dieldrin and oxychlordane were next in order of percent frequency of detection. The median levels of DDE and PCB have declined when compared with previous collections. Five specimens contained high levels of dieldrin in their brains which may have contributed to their deaths. Seventeen eagles contained liver lead residues greater than 10 ppm and probably died of lead poisoning. Trauma and shooting are the most common causes of death.

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Twenty-two female big brown bats (Eptesicus fuscus) were collected in a house attic in Montgomery County, Maryland. Seventeen were fed mealworms (Tenebrio molitor larvae) that contained 166 ppm DDE; the other five were fed uncontaminated mealworms. After 54 days of feeding, six dosed bats were frozen and the remaining 16 were starved to death. In a second experiment, 21 female big brown bats were collected in a house attic in Prince Georges County, Maryland. Sixteen were fed mealworms that contained 9.4 ppm Aroclor 1254 (PCB). After 37 days, two bats had died, four dosed bats were frozen, ant the remaining 15 were starved to death. Starvation caused mobilization of stored residues. After the feeding periods, average weights of all four groups (DDE-dosed, DDE control, PCB-dosed, PCB control) had increased. However, weights of DDE-dosed bats had increased significantly more than those of their contols, whereas weights of PCB-dosed bats had increased significantly less than those of their controls. During starvation, PCB-dosed bats lost weight significantly more slowly than controls. Because PCB levels in dosed bats resembled levels found in some free-living big brown bats, PCBs may be slowing metabolic rates of some free-living bats. It is not known how various common organochlorine residues may affect metabolism in hibernating bats. DDE and PCB increased in brains of starving bats as carcass fat was metabolized. Because the tremors and/or convulsions characteristic of neurotoxicity were not observed, we think even the maximum brain levels attained (132 ppm DDE, 20 ppm PCB) were sublethal. However, extrapolation of our DDE data predicted lethal brain levels when fat reserves declined sufficiently. PCB-dosed bats were probably in no danger of neurotoxic poisoning. However, PCB can kill by a nonneurotoxic mode, and this could explain the deaths of two bats on PCB dosage.

No abstract