TOWARD A BETTER UNDERSTANDING OF THE BIOAVAILABILITY, PHYSIOLOGY AND TOXICITY OF SILVER IN FISH - IMPLICATIONS FOR WATER-QUALITY CRITERIA

In its ionic form, silver (Ag+) is highly toxic to fish (96-h 50% leth al concentration [LC50]: low mu g/L range). However, concentrations of Ag+ in aquatic environments are extremely low and other more common f orms of silver show only low to moderat(e) toxicities (e.g., 96-h LC50 : silver thiosulfate > 100,000 mu g Ag/L; silver chlorides > 100 mu g Ag/L). In bioassays with freshwater fish, acute toxicity appears to be derived exclusively from the Ag+ ion concentration of the water. Some other forms of silver are bioavailable but do not show obvious contri bution to acute toxicity. Complexation of Ag+ by chloride, dissolved o rganic carbon, and sulfide are important in reducing silver toxicity. The protective action of hardness (i.e. calcium) is modest. When added as the readily dissociating silver nitrate salt, the toxicity of silv er is considerably lower in seawater (96-h LC50 range: 330-2,700 mu g Ag/L) than in freshwater (96-h LC50 range: 5-70 mu g Ag/L). Acute silv er toxicity to fish is caused by failure of the organism to maintain c onstant Na+ and Cl- concentrations in the blood plasma. In freshwater fish, Agi exerts its toxic effects on the Na+ and Cl- transport across the gills, whereas the intestine has been indicated as the site of to xicity in seawater fish. Although there are still many gaps in our und erstanding of silver effects on fish, it can be concluded that present regulatory standards for silver can be much improved by taking into a ccount the important geochemical modifiers of silver toxicity.