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  • Title: Monitoring biological effects of polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls in great blue heron chicks (Ardea herodias) in British Columbia.
    Author: Sanderson JT, Elliott JE, Norstrom RJ, Whitehead PE, Hart LE, Cheng KM, Bellward GD.
    Journal: J Toxicol Environ Health; 1994 Apr; 41(4):435-50. PubMed ID: 8145284.
    Abstract:
    The Canadian Wildlife Service monitors levels of polychlorinated aromatic hydrocarbons in great blue heron (Ardea herodias) eggs in British Columbia as indicators of environmental contamination. The present project assessed the temporal effects of environmental contamination with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls (PCBs) on hepatic microsomal ethoxyresorufin O-deethylase (EROD) activities and several morphological parameters in heron hatchlings. Between 1990 and 1992, eggs were collected from two great blue heron colonies in British Columbia that had elevated levels of contamination in 1988: Vancouver in 1990 and 1992, and Crofton in 1991. Biological parameters in the hatchlings and chemical contaminant levels in matched eggs from the same clutch were measured and compared with the findings from the same colonies studied in 1988. Levels of TCDD and other PCDDs and PCDFs had decreased significantly in both colonies since 1988. A concomitant decrease in EROD activity and incidence of chick edema, increase in body weight, and improvement of the reproductive success of the Crofton colony was observed. Body, yolk-free body, stomach, and intestine weights, tibia wet, dry, and ash weights, and tibia length regressed negatively on TCDD level (p < .01; n = 54). Hepatic EROD activity regressed positively on TCDD level (r2 = .49; p = .00005; n = 54). Regression of these parameters on the sum of TCDD toxic equivalents (TEQ) resulted in similar relationships. The reduction in severity of the effects observed in the contaminated colonies in the recent collections, accompanied by the declines in levels of PCDDs and PCDFs, was consistent with the dose-response relationships determined in 1988.
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