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A series of 12 littoral enclosures constructed within a 2 ha, mesotrophic pond near Duluth, Minnesota were used to determine if sublethal concentrations of the insecticide chlorpyrifos [0,0,-diethyl 0-(3,5,6-trichloro-2-pyridyl) phosphorothioate] could lead to changes in the diet and growth of fathead minnow larvae. Chlorpyrifos was added to the enclosures at nominal concentrations of 0.0, 0.5, 5.0, and 20.0 μg/L in a single application on June 16, 1986. Growth rates of larvae were significantly reduced in the treated enclosures during the 32-d study period. The most dramatic differences in the mean size of larvae from the four treatment groups were observed 15 d posttreatment. These differences corresponded to the most significant reductions in cladoceran, copepod, rotifer, and chironomid populations in the treated enclosures. These results indicate that toxicity to chlorpyrifos-sensitive invertebrate forage species forced dietary changes that led to reduced growth of native fathead minnow larvae in the treated enclosures.

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The source of acute toxicity of an aged gold mill effluent to juvenile mysid shrimp (Mysidopsis bahia [Americamysis bahia]) was identified. Effluent osmolality was equivalent to that of 12 ppt seawater. At five effluent concentrations ranging from 4 to 100% (v/v), using 12 ppt seawater for dilution, the onset of responses was most rapid at 37% effluent. Simulated effluent was created by adding Na+, Ca2+, Mg2+, K+, Cl−, and SO42− to distilled water at concentrations equal to those measured in the effluent. The unusual finding of a more rapid onset of responses at 37% than at 100% effluent was duplicated with simulated effluent, demonstrating that responses of M. bahia to effluent were attributable to one or more of the six ions that were included in simulated effluent. Proportionally, excess Ca2+ and Na+ deficiency were among the greatest differences in the ionic composition of effluent relative to seawater. Manipulation of Ca2+ and Na+ concentrations in effluent and in simulated effluent, along with the results of the previous experiments, demonstrated that excess Ca2+ was the sole source of effluent toxicity and that Na+ deficiency, relative to the proportion in seawater, reduced Ca2+ toxicity.