NOTE: Although the toxicity values presented in these toxicity profiles were correct at the time they were produced, these values are subject to change. Users should always refer to the Toxicity Value Database for the current toxicity values.
DECEMBER 1992Prepared by: Rosmarie A. Faust, Ph.D., Chemical Hazard Evaluation and Communication Group, Biomedical and Environmental Information Analysis Section, Health and Safety Research Division, *, Oak Ridge, Tennessee.
Prepared for: Oak Ridge Reservation Environmental Restoration Program.
*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400.
Silver is a relatively rare metal that occurs naturally in the earth's crust and is released to the environment from various industrial sources. Human exposure to silver and silver compounds can occur orally, dermally, or by inhalation. Silver is found in most tissues, but has no known physiologic function.
In humans, accidental or intentional ingestion of large doses of silver nitrate has produced corrosive damage of the gastrointestinal tract, abdominal pain, diarrhea, vomiting, shock, convulsions, and death (U.S. EPA, 1985). Respiratory irritation was noted following acute inhalation exposure to silver or silver compounds. Silver nitrate solutions are highly irritating to the skin, mucous membranes, and eyes (Stokinger, 1981).
Ingestion, inhalation, or dermal absorption of silver may cause argyria, the most common indicator of long-term exposure to silver or silver compounds in humans. Argyria is a gray or blue-gray, permanent discoloration of the skin and mucous membranes that is not a toxic effect per se, but is considered cosmetically disfiguring. Chronic inhalation exposure of workers to silver oxide and silver nitrate dusts resulted in upper and lower respiratory irritation, deposition of granular silver-containing deposits in the eyes, impaired night vision, and abdominal pain (Rosenman et al., 1979). Mild allergic responses have been attributed to dermal contact with silver (ATSDR, 1990).
In long-term oral studies with experimental animals, silver compounds have produced slight thickening of the basement membranes of the renal glomeruli, growth depression, shortened lifespan, and granular silver-containing deposits in skin, eyes, and internal organs (Matuk et al., 1981; Olcott, 1948, 1950). Hypoactivity was seen in rats subchronically exposed to silver nitrate in drinking water (Rungby and Danscher, 1984).
A Reference Dose (RfD) of 0.005 mg/kg/day for subchronic and chronic exposure was calculated from a lowest-observed-adverse-effect level (LOAEL) of 0.014 mg/kg/day for argyria observed in patients receiving i.v. injections of silver arsphenamine (U.S. EPA, 1992a,b). Data are presently insufficient to derive a Reference Concentration (RfC) for silver (U.S. EPA, 1992a).
Data adequate for evaluating the carcinogenicity of silver to humans or animals by ingestion, inhalation, or other routes of exposure were not found. Based on U.S. EPA guidelines, silver is placed in weight-of-evidence group D, not classifiable as to human carcinogenicity (U.S. EPA, 1992a).Retrieve Toxicity Profiles Formal Version
Last Updated 2/13/98