Toxicity and toxicokinetics of fenvalerate in fish
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The influence of emulsifiers and toxicokinetics on the lethality of pyrethroid insecticides to fish was examined using fenvalerate as a model compound;Flow-through acute toxicity testing with technical grade and a 30% active ingredient emulsifiable concentrate (EC) formulation of the insecticide was conducted. Initially, technical fenvalerate was more toxic to fathead minnows; the 96-h LC(,50)s for technical fenvalerate and the EC were 0.69 and 0.99 (mu)g/L, respectively. By 168 h, an LC(,50) of 0.75 (mu)g/L was determined for the EC, indicating that the incipient lethalities of the two formulations were similar. Fenvalerate residues in fish and concentration factors, at the completion of each test, showed no significant difference between formulation; however, a significantly slower fenvalerate uptake was noted with the EC. Reduced fenvalerate uptake in the presence of emulsifiers was probably responsible for the initially lower toxicity of the EC formulation;An in vivo rainbow trout preparation was used to evaluate the gill uptake and toxicokinetics of ('3)H fenvalerate. Fish were exposed to technical fenvalerate (0.28 or 23 ng/L) or an EC formulation (16 ng/L) for 36 or 48 h. No significant effect of emulsifiers or fenvalerate concentration on uptake was observed, and an overall mean gill uptake efficiency of 28.6 (+OR-) 4.4% was determined. Effects of emulsifiers on fenvalerate uptake may only occur at concentrations near the insecticide's water solubility limit. Following a depuration period (8 to 48 h), carcass and bile contained 80-90 and 10-20% of the gill-absorbed doses, respectively. Significant excretion and blood transport of fenvalerate equivalents was completed within 8 to 12 h after exposure termination. Specific tissues from trout exposed to 0.28 ng/L fenvalerate were analyzed for fenvalerate equivalents after a 48 h depuration period. Bile contained the highest concentration of fenvalerate equivalents (7000 pg/g), followed by fat (200 pg/g). Analysis of biliary metabolites indicated the glucuronide of 4'-HO-fenvalerate to be the only significant degradation product. Results from this study suggest that efficient gill uptake is not a contributing factor in fenvalerate's toxicity to rainbow trout. Rather, a low rate of biotransformation and excretion does seem to play a significant role in the susceptibility of this species to the synthetic pyrethroids.