Rotenone, a natural insecticide and piscicide, was shown to have an extremely small margin between no lethality (5.0 microg/L) and 100% mortality (6.6 microg/L) for static-renewal 96-hour toxicity tests with juvenile rainbow trout (Oncorhynchus mykiss). Dissolved organic carbon (DOC) at concentrations of 3.0 and 4.0 mg/L significantly increased the rotenone 96-hour LC(50) (median lethal concentration) from 5.80 microg/L (confidence interval (CI) 5.51 to 6.10) to 6.55 microg/L (CI 6.28 to 6.83) and 7.75 microg/L (CI 7.29 to 8.24), respectively, probably as a result of rotenone adsorption onto DOC, which decreased its bioavailability. Using concentrations of 0, 3.0, 4.0, and 5.0 microg/L rotenone and exposure periods of 2, 4, 6, 12, 16, 24, and 48 hours, the threshold concentration of rotenone for impairment of critical swimming performance (Ucrit) was 3.0 microg/L (P = 0.029), with no further impairment at higher concentrations and no time-dependent effect on Ucrit. Using continuous measures of oxygen uptake for 48 hours before and 48 hours during rotenone exposure (0, 1.5, 2.5, 3.0, and 3.5 microg/L), rotenone significantly decreased peak active oxygen uptake at all rotenone concentrations tested without affecting routine oxygen uptake. Fish were individually chased and then placed in rotenone concentrations of 0, 1.0, 3.0, 4.0, 5.0, and 6.0 microg/L to monitor initial postexercise oxygen uptake (Mo2Max) and excess postexercise oxygen consumption (EPOC) during a 40-minute recovery period. Rotenone significantly decreased Mo2Max (P = 0.002) after exposures to 4.0 and 5.0 microg/L, but not 6.0 microg/L, without affecting EPOC.

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A comprehensive data set for the acute toxicity of monochloramine to juvenile chinook salmon, Oncorhynchus tshawytscha, and the aquatic invertebrate Ceriodaphnia dubia are presented. For exposures up to 10 days, the equation LC50 = 7244t-0.4525 (where LC50 = monochloramine concentration in μg/L for 50% lethality and t = time in minutes) can predict the LC50 value for monochloramine in juvenile chinook salmon and accounts for 94.4% of the variability in the experimental data. Predictions of acute toxicity were less reliable for concentrations in the range 0.5 mg/L to 0.8 mg/L since the time to 50% mortality (LT50) value varied substantially in this range. Post-exposure mortality occurred only with exposures of >0.67 mg/L monochloramine. Feeding fish immediately before and during acute monochloramine exposure created a large chloramine demand in test chambers. In all tests where fish were fed, measured monochloramine concentrations were below detectable levels (<10 μg/L) and no fish mortality occurred. Monochloramine toxicity to the freshwater invertebrate Ceriodaphnia dubia was studied with time-to-lethality tests at 26 different concentrations. The equation LC50 = 61600t-1.0748 predicted the LC50 value for monochloramine in C. dubia and accounted for 94.8% of the variability in the experimental data. The mathematical equations that describe the LC50 for juvenile chinook salmon and C. dubia were used as reference lines for the evaluation of relative monochloramine toxicity. Both juvenile chinook salmon and C. dubia were among the most sensitive fish and aquatic invertebrate species, respectively, C. dubia being more sensitive than juvenile chinook salmon for exposure durations >30 minutes.

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