Bald eagle mortality and chlorinated hydrocarbon contaminants in livers from British Columbia, Canada, 1989-1994.
Bald eagle mortality and chlorinated hydrocarbon contaminants in livers from British Columbia, Canada, 1989-1994.
复制标题
1989-1994 年加拿大不列颠哥伦比亚省秃鹰死亡率和肝脏中氯化烃污染物。
DOI:
10.1016/s0269-7491(96)00106-6
复制
发表时间:
1996
影响因子:
8.9
通讯作者:
R. Norstrom
中科院分区:
文献类型:
--
作者:
J. Elliott;L. Wilson;K. Langelier;R. Norstrom
Between 1989 and 1994, we obtained 278 carcasses of bald eagles (Haliaeetus leucocephalus) found dead or dying in British Columbia, Canada. All specimens were necropsied and the cause of death determined wherever possible. Livers from a subset of 75 birds were analyzed for polychlorinated biphenyl (PCB) and organochlorine (OC) pesticide residues. A further subset of 19 eagles found dead around the Strait of Georgia, an area of known pulp mill pollution, in summer, and therefore presumably resident birds, were analyzed for polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) and non-ortho PCBs. Liver concentrations ranged from less than 1 to 190 mg/kg for DDE, and up to 72 mg/kg for total PCBs. Concentrations of other OCs were generally less than 1 mg/kg, with the exception of chlordane-related compounds which were occasionally over 2 mg/kg. All birds analyzed for PCDDs and PCDFs contained detectable concentrations of the major 2,3,7,8-substituted isomers. Some birds were very contaminated; one eagle found near a kraft pulp mill site in 1990 contained: 400 ng/kg 2,3,7,8-TCDD, 1400 ng/kg 1,2,3,7,8-PnCDD and 4400 ng/kg 1,2,3,6,7,8-HxCDD. Birds with higher PCB and dichlorodiphenyldichloroethane (DDE) concentrations appeared to weigh less, and there was a significant negative relationship between both PCBs and DDE and numeric scoring of body condition, reflecting the well known process of starvation-induced mobilization of body lipids and contaminants. Birds with higher 2,3,7,8-TCDD concentrations tended to have unusually low concentrations of 2,3,7,8-TCDF, interpreted to indicate hepatic cytochrome P4501A-type induction by TCDD and subsequent metabolism of TCDF.