Blue-sac disease

By far the most comprehensive research into AHR-related effects of PCDD/Fs on fish was a retrospective analysis of Lake Ontario lake trout reproductive impairment due to AHR-mediated early life stage mortality [16]. This includes blue sac disease as well as sublethal effects, which may increase susceptibility of sac fry and alevins to increased mortality and predation during swim-up. Lake trout are more susceptible to AHR-mediated toxic effects than any other Great Lakes species, with the possible exception of mink. WHO TEFs for fish were used to calculate the 2378-TCDD equivalent (TECegg or TEQ) concentrations in lake trout eggs. The validity of the additive toxicity equivalence model was established through early life stage trout toxicity tests. The WHO fish TEFs are likely to be fairly robust for lake trout, since they were determined primarily from relative potency values for effects in embryos of a related salmonid, rainbow trout, even if the relative sensitivity of the species to 2378-TeCDD toxicity may be different. 

Toxicity of non-ortho- and mono-orfho-PCDEs to fish has recently been studied with early life stages of Japanese medaka [84], PCDEs 77, 105, and 118 were shown to be embryotoxic to medaka, but the potencies relative to 2,3,7,8-TCDD were low the toxic equivalency factors (TEF) were 0.00001-0.00056. The PCDE fraction isolated from a Lake Ontario lake trout was also embryotoxic and PCDEs in trout were suggested to have the potential to induce toxic effects in early life stages of fish, although not blue-sac disease. 

---