Ecological risk assessment (ERA) of inorganic metals and metalloids (metals) must be specific to these substances and cannot be generic because most metals are naturally occurring, some are essential, speciation affects bioavailability, and bioavailability is determined by both external environmental conditions and organism physiological/biological characteristics. Key information required for ERA of metals includes: emissions, pathways, and movements in the environment (Do metals accumulate in biota above background concentrations?); the relationship between internal dose and/or external concentration (Are these metals bioreactive?); and the incidence and severity of any effects (Are bioreactive metals likely to result in adverse or, in the case of essential metals, beneficial effects?) -ground-truthed in contaminated areas by field observations. Specific requirements for metals ERA are delineated for each ERA component (Hazard Identification, Exposure Analysis, Effects Analysis, Risk Characterization), updating Chapman and Wang (2000). In addition, key specific information required for ERA is delineated by major information category (conceptual diagrams, bioavailability, predicted environmental concentration [PEC], predicted no effect concentration [PNEC], tolerance, application [uncertainty] factors, risk characterization) relative to three different tiered, iterative levels of ERA: Problem Formulation, Screening Level ERA (SLERA), and Detailed Level ERA (DLERA). Although data gaps remain, a great deal of progress has been made in the last three years, forming the basis for substantial improvements to ERA for metals.

Juvenile rainbow trout (Oncorhynchus mykiss) were exposed to waterborne Cu (22 microg/l) in moderately hard water for up to 28 days. Relative to control fish kept at background Cu levels (2 microg/l), Cu-preexposed fish displayed decreased uptake rates of waterborne Cu via the gills but not of dietary Cu via the gut during 48-h exposures to (64)Cu-radiolabeled water and diet, respectively. At normal dietary and waterborne Cu levels, the uptake rates of dietary Cu into the whole body without the gut were 0.40-0.90 ng. g(-1). h(-1), >10-fold higher than uptake rates of waterborne Cu into the whole body without the gills, which were 0.02-0.07 ng. g(-1). h(-1). Previously Cu-exposed fish showed decreased new Cu accumulation in the gills, liver, and carcass during waterborne (64)Cu exposures and in the liver during dietary (64)Cu exposures. A 3-h gill Cu-binding assay showed downregulation of the putative high-affinity, low-capacity Cu transporters and upregulation of the low-affinity, high-capacity Cu transporters at the gills in Cu-preexposed fish. Exchangeable Cu pools in all the tissues were higher during dietary than during waterborne (64)Cu exposures, and previous Cu exposure reduced waterborne exchangeable Cu pools in gill, liver, and carcass. Overall, these results suggest a quantitatively greater role for the dietary than for the waterborne route of Cu uptake, a key role for the gill in Cu homeostasis, and important roles for the liver and gut in the normal metabolism of Cu in fish.

SUMMARYOurs is the first study to demonstrate an influence of dietary sodium on waterborne copper uptake in fish. We examined possible interactions between dietary sodium and the response of freshwater rainbow trout (Oncorhynchus mykiss) to waterborne copper in light of recent evidence of interactions between sodium and copper metabolism in the gills. Trout were maintained for 6 days on one of four diets of increasing sodium concentration (0.25 mmol g-1, 0.51 mmol g-1, 0.76 mmol g-1 and 1.27 mmol g-1, which corresponds to 0.6%, 1.2%, 1.8% and 3% sodium by mass, respectively). At the end of 7 days, fish were exposed for 6 h to waterborne copper spiked with 64Cu to determine if the dietary sodium affected responses to a subsequent short-term waterborne copper exposure. The radiotracer allowed us to distinguish between Cu occurring in fish tissues before the experiment and `newly accumulated' Cu arising from the experimental exposure. Dietary sodium concentrations of 1.8% or 3% reduced newly accumulated copper concentrations in gill (from 93.9 ng g-1in control to 38.9 ng g-1 and 20.0 ng g-1 in fish fed 1.8% or 3% Na+-supplemented diets, respectively), liver (from 64.3 ng g-1 to 23.1 ng g-1 and 7.5 ng g-1,respectively), kidney (from 29.3 ng g-1 to 11.7 ng g-1and 7.8 ng g-1, respectively), plasma (from 64.7 ng g-1to 21.5 ng g-1 and 10.7 ng g-1, respectively) and gut(from 6.8 ng g-1 to 3.4 ng g-1 and 2.2 ng g-1, respectively) by 50.0-88.2%. The 3%Na+-supplemented diets also increased plasma and gut sodium concentrations by 38.1% (from 137.1 μmol g-1 to 189.3 μmol g-1) and 104.3% (from 56.5 μmol g-1 to 115.4 μmol g-1), respectively, relative to fish maintained on untreated diets. Whole body uptake rates of both sodium and copper were significantly reduced,and highly correlated (r=0.97) with one another, in fish fed high-sodium diets relative to controls. Moreover, sodium efflux was 12% and 38% higher in fish fed 1.8% and 3% sodium-enriched diets, respectively. Fish fed high-sodium diets also drank more water, but the contribution of drinking to waterborne copper uptake was negligible. From these results, we speculate that, at least in part, aqueous sodium and copper share a common branchial uptake route, probably through an apical sodium channel. According to this hypothesis, as the channel is downregulated with increasing internal sodium concentrations, both sodium and copper uptake from the water are inhibited.

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Juvenile rainbow trout (Oncorhynchus mykiss) were exposed to 11 (control), 300 (medium), and 1000 µg Cu·g–1 (high) (as CuSO4·5H2O) in the diet for 28 days at a daily ration of 4% wet body weight, with a background waterborne Cu concentration of 3 µg·L–1. There was no effect of dietary Cu on growth, condition factor, or food conversion efficiency. Whole-body Cu content increased continuously over the exposure period in all groups and was twofold and fourfold higher than controls at day 28 for the medium- and high-Cu diets, respectively. Copper accumulated mainly in liver and gut tissue, with the latter stabilizing by day 14. Accumulation also occurred in gill, kidney, and carcass. Plasma Cu concentration was not different from the controls whereas Cu in bile was greatly elevated, an indication of increased hepatobiliary excretion. Dietary Cu pre-exposure decreased the uptake of waterborne Cu across the gills, providing the first evidence of homeostatic interaction between the two routes of uptake. Electron microscopic observations of the midintestine revealed numerous mitochondria, lysosomes, lamellated bodies, and extensive lamellar processes in the enterocytes. Apoptosis, mitosis, and eosinophilic granule cells were more apparent in Cu-exposed fish.