Toxicity of pulse-exposed fenvalerate and esfenvalerate to larval Australian crimson-spotted rainbow fish (Melanotaenia fluviatilis)

The effects of pulse exposure with two synthetic pyrethroids, fenvalerate and esfenvalerate, on survival of larval Australian crimson-spotted rainbow fish (Melanotaenia fluviatilis) were studied. Fenvalerate and esfenvalerate were both highly toxic to larval rainbow fish with 1-h esfenvalerate pulse-exposure concentrations as low as 0.32 μg l^-1, and 1-min fenvalerate pulse-exposure concentrations of 4.5 μg l^-1, sufficient to cause significant mortality. Technical grades were significantly more toxic than emulsified grades of the pesticides. The 1-h pulse-exposure 96-h LC₅₀'s were 12.75, 30.25, 1.18, and 1.99 μg l^-1 for technical fenvalerate, emulsified fenvalerate, technical esfenvalerate, and emulsified esfenvalerate, respectively. Emulsified fenvalerate and esfenvalerate were also extremely toxic to adult crimson-spotted rainbow fish. The 96-h continuous exposure LC₅₀'s for adult fish using 50% daily partial replacement were 14.58 and 6.24 μg l^-1, respectively, comparable with results for holarctic species. Fenvalerate is a racemic mixture containing four optical isomers (2R, aR; 2R, aS; 2S, aR, 2S, aS), while esfenvalerate contains mainly the 2S isomers. Esfenvalerate contains approximately twice the quantity of 2S isomers as does fenvalerate on a weight basis. Pulse-exposure LC₅₀'s for esfenvalerate were 10 to 15 times lower than for fenvalerate, a much higher toxicity of esfenvalerate than the roughly two fold difference which would have been predicted solely on a weight basis. Thus the 2R isomers, which make up approximately 50% of the fenvalerate formulation and which previously were regarded as non-active, appear to have reduced the expected toxicity of fenvalerate relative to measured esfenvalerate toxicity, perhaps via the inhibition of sodium channel activation. There was a complex relationship between pesticide concentration and time to mortality. At low concentrations of pesticide, most mortality occurred within the first 24 h, while at higher concentrations, mortality continued for 96 h after exposure. This suggests that mortality within the first 24 h was due to direct physiological effects of the pesticide on the larvae, while subsequent mortality was primarily due to starvation of larvae unable to recover from the initial insult. Duration of exposure (0 to 120 min) to emulsified fenvalerate and esfenvalerate significantly affected the acute toxicity to larval rainbow fish. For esfenvalerate, there was a linear relationship between duration of exposure and acute toxicity, while for fenvalerate, exposures of longer than 20 min did not significantly increase 96-h mortality.