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TOXICITY OF AHR AGONISTS TO FISH EARLY LIFE STAGES
Citation:
Hornung, M. W. AND P. M. Cook. TOXICITY OF AHR AGONISTS TO FISH EARLY LIFE STAGES. Presented at 2002 SETAC Annual Meeting, Salt Lake City, UT, November 16, 2002.
Description:
Fish early life stages are exceptionally sensitive to the lethal toxicity of chemicals that act as arylhydrocarbon receptor (AhR) agonists. Toxicity characterizations based on 2,3,7,8-tetrachlorodibenzo-p-dioxin, generally the most potent AhR agonist, support the toxicity equivalent model for fish. Toxicity manifested during embryo and larval stages is characterized by cardiovascular related effects including edema and hemorrhage, and craniofacial malformations. The occurrence and severity of the toxicity is dose-related with a wide range in sensitivities across species to the lethal toxicity. The most sensitive species tested to date is bull trout (Salvelinus confluentus) with estimated LD50egg value of 22 pg TCDD/g egg, and the least sensitive species is zebrafish (Danio rerio), with an LD50egg value of 2500 pg TCDD/g egg. The cause for this wide range in sensitivity to the lethal potency of AhR agonists and the decreasing sensitivity as exposure occurs later during development remains unknown. Although a range of lethal toxicity values for AhR agonists have been well established, there is far less information on the sublethal effects of AhR agonists in fish. Sublethal exposures to AhR agonists during early life stage development could have adverse effects on long term survival through behavioral effects. The post swim-up persistence of craniofacial malformations may also indicate that sub-embryolethal concentrations may lead to adverse effects later in life. Effects from acute exposures have suggested potential mechanisms for chronic toxicity by AhR agonists, but there is a paucity of dose-response data as well as definition of the precise mechanism of action. Since exposures of sensitive fish species near the threshold for early life stage mortality are occurring, the uncertainty for chronic toxicity can limit ecological risk assessments.
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