Abstract-The upper Clark Fork River, above Flathead River, is contaminated with large amounts of As, Cd, Cu, Pb, Mn, and Zn ores from past mining activities. The contaminated area extends from the Butte and Anaconda area to at least 230 km downstream to Milltown Reservoir. Both the upper Clark Fork River and Milltown Reservoir have been designated as U.S. Environmental Protection Agency Superfund sites because of metal-contaminated bottom sediments. We evaluated the impacts of past mining activities on the Clark Fork River ecosystem using benthic invertebrate community assessment, residue chemistry, and toxicity testing. Oligochaeta and Chironomidae generally accounted for over 90% of the benthic invertebrate community in the soft sediment depositional areas. Taxa of Oligochaeta and Chironomidae were predominantly pollution tolerant. Higher numbers of Chironomidae genera were present at stations with higher concentrations of metals in sediment identified as toxic by the amphipod Hyalella azteca in 28-d exposures. Frequency of mouthpart deformities in genera of Chironomidae was low and did not correspond to concentrations of metals in sediment. Total abundance of organisms/m2 did not correspond to concentrations of metals in the sediment samples. Chemical analyses, laboratory toxicity tests, and benthic community evaluations all provide evidence of metal-Induced degradation to aquatic communities in both the reservoir and the river. Using a weightof-evidence approach -the Sediment Quality Triad -provided good concurrence among measures of benthic community structure, sediment chemistry, and laboratory toxicity.
Juvenile bluegill (Lepornis macrochirus) were exposed to the pyrethroid insecticide esfenvalerate [(S)-ol-cyano-3-phenoxybenzyl-(S)-2-(4-chlorophenyl)-3-methyl butyrate], continuously for 90 d and for six 11-h pulses. No bluegill survived continuous exposure to esfenvalerate at 0.200 pg/L for 30 d or 0.100 pg/L for 60 d. The lowest-observable-effect concentration (LOEC) for survival in a 90-d continuous exposure of esfenvalerate was 0.025 pg/L. In comparison, no mortality occurred among fish exposed to pulsed doses of up to 0.200 pg/L. Behavioral responses, including gross body tremors, were highly sensitive indicators of totticity among pulse-exposed fish, with symptoms appearing within 4 h of exposure to concentrations as low as 0.025 pg/L. Similar behavioral responses were observed after continuous exposure to 0.025 pg/L esfenvalerate. Behavioral responses were observed at concentrations an order of magnitude less than concentrations impacting growth or survival in simulated field studies. These results provide encouraging evidence that laboratory studies designed to simulate field exposure conditions can be predictive of concentrations causing mortality and other adverse effects.
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