Eggs, early life stages

Spitsbergen, J.M., M.K. Walker, J.R. Olson, and R.E. Peterson. 1991. Pathologic alterations in early life stages of lake trout, Salvelinus namaycush, exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin as fertilized eggs. Aquat. Toxicol. 19 41-72. 

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. 

The non-chlorinated skeleton compound of C4-PCPHs, retene, occurs at high levels in pulp mill effluents and in recipient sediments up to 2 mg g 1 dw.Retene causes MFO induction in fish and is toxic to early life-stages of zebrafish at LOEL of 16 pg 1 h TEF of egg mortality related to 2,3,7,8-tetrachlorodibenzo-p-dioxin is on average about 0.007 [59]. Accordingly, chlorinated retenes are of concern as possible dioxin-type of persistent xenobiotics. 

It has been difficult to assess the ecotoxicology of dioxin in the field because of the presence of other chemicals that cause similar effects and are present at higher concentrations. However, it appears that the early life stages of fish are most susceptible to the effects of dioxin and that birds may exhibit decreased egg production, embryotox-icity, and fetal malformations as a result of dioxin exposure. 

Walker, M.K., L.C. Hufnagle, M.K. Clayton, and R.E. Peterson. 1992. An egg injection method for assessing early life stage mortality of polychlorinated dibenzo-p-dioxins, dibenzofurans, and biphenyls in rainbow trout (Oncorhynchus mykiss). Aquat. Toxicol. 22 15-38. 

Tier 2 Testing Enhanced early-life stage toxicity test (OECD 210) = Partial life-cycle test Pertilized egg —> 60 dph Hatching success, growth, VTG, secondary sexual characteristics, gonadal histology... 

Marked differences in the effect of temperature on the toxicity of pentachlorophenol to rainbow trout have been observed (Hodson and Blunt 1981), and early life-cycle stages were more adversely affected in fish exposed to a cold-water regime (6°C) than with those exposed to a warm-water regime (10°C). These results could have serious implications for natural populations exposed to pentachlorophenol during low temperatures when spring egg development occurs. 

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