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Planar halogenated hydrocarbons (PHHs) are known to be present in the Great Lakes ecosystem in sufficient concentrations to potentially cause adverse effects on reproduction in certain species of fish. Previously, we demonstrated the toxicity of a PHH mixture to newly fertilized rainbow trout eggs. The current study investigates the embryotoxicity of the same mixture on developing lake trout embryos. This study had four objectives: 1) to determine the accuracy of predictions about lake trout egg 2,3,7,8-TCDD equivalent concentrations (TEQ) made from the previous studies on rainbow trout; 2) to determine the relative potency (REP) of 2,3,7,8TCDF in early life stage lake trout; 3) to examine the chemical composition of the Lake Michigan lake trout extract in relation to an additive model of toxicity; and 4) to estimate the hazard these chemicals may represent to Great Lakes lake trout populations. The extract was made from whole adult lake trout collected from Lake Michigan in 1988. Graded doses of the final extract were injected into eggs of hatchery reared lake trout. The doses used for the injections were quantified as TEQs based on the concentrations of dioxins, furans and non-ortho-PCBs in the extract, and as equivalent amounts found in the eggs of the original lake trout (eggEQ). The LD50 of 2,3,7,8-TCDD in lake trout was 81 pg/g egg. Additionally, we determined the LD50 for 2,3,7,8-TCDF in lake trout to be 2.5 ng/g egg. Total TEQs in the Lake Michigan lake trout sample were 14.7 pg TEQ/g. The extract of the Lake Michigan lake trout was embryotoxic to lake trout embryos with an LD50 value of 7 eggEQ (4-11, 95% F.L.). The LD50 of the extract in terms of TEQs was 103 TEQs/g of lake trout egg. The estimated lowest observable adverse effect levels (LOAEL) for sublethal responses were: 29 pg TEQ/g for craniofacial anomalies, 15 pg TEQ/g for yolksac edema , and 2 pg TEQ/g for hemorrhage in the lake trout embryos. The mixture of chemicals present in lake trout from Lake Michigan acted to cause embryotoxicity in an approximately additive fashion. The composition of the extract was portioned equally on a TEQ basis among non-ortho-substituted PCBs, dioxins, and furans. This study confirms our earlier conclusions that PHHs in lake trout from Lake Michigan are above a threshold for adverse effects on mortality, but that these compounds may have implications for the lack of recruitment in certain Great Lakes lake trout populations. Introduction Lake trout (Salvelinus namaycush) were historically native to the lower Great Lakes. However, the lake trout fishery in the Great Lakes is currently hatchery-stocked: no natural reproduction occurs in Lake Michigan and few signs of natural reproduction are seen in northern Lake Huron and Lake Ontario (Marsden et al. 1988; Holey et al. 1995; Hansen et al. 1995; Manny et al. 1995). The exact cause of the lack of recruitment observed in Great Lakes lake trout populations is not known at this time; however, it is known that lake trout are particularly sensitive to the effects of planar halogenated hydrocarbons (Walker et al. 1991; Walker et al. 1994).

Great Lakes lake trout early mortality syndrome (EMS) : contaminants, thiamin status, and their possible interaction