Abstract
Because metals such as Cu inhibit ionoregulation, the increased energy requirement to counter passive diffusive losses in soft water may translate into increased sensitivity to metal exposure. We developed a method to determine whole-body Na concentrations of larval fathead minnows (Pimephales promelas) as a physiological indicator of health. This method was used to characterize net rates of Na flux from fish exposed to Cu in the presence of varying levels of hardness and alkalinity. In extremely soft waters (hardness, < or = 10 mg/L as CaCO(3)), larval fish experienced rates of net whole-body Na loss greater than what has been observed in juvenile and adult fish when exposed to Cu at concentrations near the median lethal concentration. Elevating hardness (>10 mg/L as CaCO(3)), however, decreased the apparent kinetics of Na loss caused by Cu exposure, which suggests the process was related to uncompetitive inhibition of Cu by hardness cations. Although the percentage of Na loss associated with mortality in larval fish was similar to that in juvenile and adult fish (30% loss of exchangeable Na pool), larvae reached this level within 12 h of exposure, and it was not representative of the onset of mortality. These results suggested that ionoregulatory measures by themselves are not a conclusive metric for Cu regulation using larval fish. To account for increased sensitivity in low-hardness waters in the development of biotic ligand models, the critical amount of Cu associated with the gill to cause mortality (i.e., the median lethal accumulation value) should be characterized more appropriately as a function of hardness below 20 mg/L as CaCO(3).
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