Pathologic alterations in early life stages of lake trout, Salvelinus namaycush, exposed to 2,3,7,8-tetrachlorodibenzo- p-dioxin as

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Fertilized lake trout eggs exposed to vehicle or graded concentrations of [ 3H]-2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) in water for 48 h accumulated 0, < 15, 40, or 400 ppt (parts per trillion) [ 3H]-TCDD. The exposed eggs were then transferred to flowing [ 3H]-TCDD free water where they remained throughout early development. Lake trout embryos developed normally in all groups until one week prior to hatch. At this time retrobulbar, meningeal and subcutaneous hemorrhages were evident in many embryos and sac fry that were derived from eggs containing 400 ppt [ 3H]-TCDD. High mortality prior to or during hatching accompanied these lesions. All sac fry which survived hatching in the 400 ppt TCDD group developed severe subcutaneous edema, with cessation of blood circulation in the yolk sac and body. Necrosis of the retina, brain, and spinal cord occurred in morbid embryos and sac fry. All sac fry in the 400 ppt TCDD group showed arrested development from the time of hatching and all died prior to swim-up. One percent of sac fry in the vehicle control and < 15 ppt TCDD groups, and 2% in the 40 ppt TCDD group, exhibited blue-sac disease, an edematous syndrome identical grossly and nearly identical microscopically to that observed in the 400 ppt TCDD group. Thus, the cardiovascular system appears to be the initial tissue affected in both the TCDD toxicity syndrome and in blue-sac disease of developing lake trout. Lesions in other organs including brain, retina and liver develop as a result of circulatory derangements, anemia and hypoxia.