Toward a better understanding of the bioavailability, physiology, and toxicity of silver in fish: Implications for water quality criteria

Abstract

Abstract In its ionic form, silver (Ag+) is highly toxic to fish (96-h 50% lethal concentration [LC50]: low μg/L range). However, concentrations of Ag+ in aquatic environments are extremely low and other more common forms of silver show only low to moderate toxicities (e.g., 96-h LC50: silver thiosulfate >100,000 μg Ag/L; silver chlorides >100 μg 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 contribution to acute toxicity. Complexation of Ag+ by chloride, dissolved organic 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 silver is considerably lower in seawater (96-h LC50 range: 330–2,700 μg Ag/L) than in freshwater (96-h LC50 range: 5–70 μg Ag/L). Acute silver toxicity to fish is caused by failure of the organism to maintain constant Na+ and Cl− concentrations in the blood plasma. In freshwater fish, Ag+ exerts its toxic effects on the Na+ and Cl− transport across the gills, whereas the intestine has been indicated as the site of toxicity in seawater fish. Although there are still many gaps in our understanding of silver effects on fish, it can be concluded that present regulatory standards for silver can be much improved by taking into account the important geochemical modifiers of silver toxicity.