to aquatic organisms, except for 2,3,7,8-TCDD and freshwater biota (Table 4); 

 2,3,7,8-TCDD and liver microsomal enzyme activities in two marine species: 

 winter flounder, Pseudopleuronectes americanus , and the little skate. Raja 

 erinacea (Pohl it aT 1976); an^ 1,3,6,8-TCDD uptake and elimination by 

 fathead minnows and rainbow trout (Corbet et al. 1983). 



Sensitive species of teleosts exhibited reduced growth and fin necrosis 

 at concentrations as low as 0.1 ppt of 2,3,7,8-TCDD after exposure for 24 to 

 96 hours. Concentrations of 1.0 ppt and higher were eventually fatal, and 

 exposure to lower concentrations of 0.01 ppt for 24 hours had no measurable 

 effect (Table 4). A typical 2,3,7,8-TCDD poisoning sequence in guppies 

 ( Poecilia reticulatus ) and coho salmon ( Oncorhynchus kisutch ) during a 

 postexposure observation period included: decl ining interest in feeding (5-8 

 days postexposure); skin discoloration and fin necrosis (30 days), with caudal 

 fin most severely affected; reduced resistance to fungal infestations; reduced 

 swimming; and, finally, death several weeks to months after exposure (Miller 

 et al. 1973). In general, older and larger fish die last, and smaller or 

 younger specimens succumb first (Norris and Miller 1974). 



Histopathologic and teratogenic effects were noted in fry of rainbow 

 trout ( Salmo gairdneri ) exposed to 10 ppt of 2,3,7,8-TCDD for 96 hours as 

 eggs, or as yolk-sac fry (Helder 1981). Some fry showed extensive 

 degeneration and necrosis of the liver, and subsequently developed edema prior 

 to death. The remaining fry showed a high incidence of teratogenic changes, 

 including opercular defects, and foreshortened maxillas. 



Invertebrates, plants, and amphibians were comparatively resistant to 

 2,3,7,8-TCDD. For example, there were no adverse effects on growth, 

 reproduction, or food consumption of algae, daphnids, and snails during 

 immersion for 32 days in solutions containing 2.4 to 4.2 ppt of 2,3,7,8-TCDD 

 (Yockim et al . 1978). 



Accumulation of 2,3,7,8-TCDD from the aquatic environment was evident for 

 all species examined (Table 4). The isomer 1,3,6,8-TCDD was also accumulated 

 from the environment by freshwater teleosts, but accumulations were much lower 

 than predicted when compared to 2,3,7,8-TCDD, and elimination was 10 to 15 

 times more rapid than 2,3,7,8-TCDD (Corbet et al. 1983). In outdoor pond 

 studies, a major portion of the added 2,3,7,8-TCDD concentrated in aquatic 

 plants and at the sediment-water interface (Tsushimoto et al. 1982); however, 

 most (85-99%) of the 2,3,7,8-TCDO originally added to the ecosystem remained 

 in the sediments at the end of the study (Isensee and Jones 1975). Among 

 teleosts, body burdens of 2,3,7,8-TCDO increased with increasing concentration 

 in the water column and with increasing duration of exposure; on removal to 

 uncontaminated water, less than 50% was lost in 109 days (Miller et al. 

 1979). The significance of 2,3,7,8-TCDD residues in aquatic organisms is not 

 clear, and loss-rate kinetics are not fully documented; both areas merit 

 additional research. 



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