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Title: Toxicity of polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans, and polychlorinated biphenyls during salmonid early development

Miscellaneous ·
OSTI ID:5138722

Experiments were conducted to evaluate the lethal potency and signs of toxicity of polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls (PCBs) during salmonid early development. Metabolism, elimination, and toxicity of 2,3,7,8tetrachlorodibenzo-p-dioxin (TCDD) during lake trout early life stage development was investigated following waterborne exposure of lake trout eggs to ({sup 3}H)TCDD. TCDD was not metabolized or eliminated by eggs or sac fry, but was rapidly eliminated from fry. TCDD toxicity was manifested by some hatching mortality, but predominantly by sac fry mortality associated with subcutaneous yolk sac edema and hemorrhages, resembling blue-sac disease. Based on the egg TCDD concentration, the no-observable-adverse-effect level for mortality was 34 pg TCDD/g egg and the lowest-observable-adverse-effect level for mortality was 40 pg/g. LD{sub 50} was 65 pg/g. An injection method was developed to administer graded doses of non-radiolabeled PCDD, PCDF, and PCB congeners to lake trout and rainbow trout eggs. Following TCDD egg injection, lake trout were more sensitive than rainbow trout to the lethal effect of TCDD with LD{sub 50}S of 47 and 402 pg/g, respectively; however, TCDD toxicity in both species was manifested by sac fry mortality and blue-sac disease. Toxicity of TCDD was assessed during lake trout early life stage development following TCDD maternal-deposition, TCDD egg injection, and TCDD waterborne egg exposure. The lethal potency of TCDD and signs of toxicity during lake trout early development following all three routes of egg exposure were essentially the same.

Research Organization:
Wisconsin Univ., Madison, WI (United States)
OSTI ID:
5138722
Resource Relation:
Other Information: Thesis (Ph.D.)
Country of Publication:
United States
Language:
English