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.
Prepared 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.
Copper occurs naturally in elemental form and as a component of many minerals. Because of its high electrical and thermal conductivity, it is widely used in the manufacture of electrical equipment. Common copper salts, such as the sulfate, carbonate, cyanide, oxide, and sulfide are used as fungicides, as components of ceramics and pyrotechnics, for electroplating, and for numerous other industrial applications (ACGIH, 1986). Copper can be absorbed by the oral, inhalation, and dermal routes of exposure. It is an essential nutrient that is normally present in a wide variety of tissues (ATSDR, 1990; U.S. EPA, 1987).
In humans, ingestion of gram quantities of copper salts may cause gastrointestinal, hepatic, and renal effects with symptoms such as severe abdominal pain, vomiting, diarrhea, hemolysis, hepatic necrosis, hematuria, proteinuria, hypotension, tachycardia, convulsions, coma, and death (U.S. AF, 1990). Gastrointestinal disturbances and liver toxicity have also resulted from long-term exposure to drinking water containing 2.2-7.8 mg Cu/L (Mueller-Hoecker et al., 1988; Spitalny et al., 1984). The chronic toxicity of copper has been characterized in patients with Wilson's disease, a genetic disorder causing copper accumulation in tissues. The clinical manifestations of Wilson's disease include cirrhosis of the liver, hemolytic anemia, neurologic abnormalities, and corneal opacities (Goyer, 1991; ATSDR, 1990; U.S. EPA, 1987). In animal studies, oral exposure to copper caused hepatic and renal accumulation of copper, liver and kidney necrosis at doses of >=100 mg/kg/day; and hematological effects at doses of 40 mg/kg/day (U.S. EPA, 1986; Haywood, 1985; 1980; Rana and Kumar, 1978; Gopinath et al., 1974; Kline et al., 1971).
Acute inhalation exposure to copper dust or fumes at concentrations of 0.075-0.12 mg Cu/m3 may cause metal fume fever with symptoms such as cough, chills and muscle ache (U.S. AF, 1990). Among the reported effects in workers exposed to copper dust are gastrointestinal disturbances, headache, vertigo, drowsiness, and hepatomegaly (Suciu et al., 1981). Vineyard workers chronically exposed to Bordeaux mixture (copper sulfate and lime) exhibit degenerative changes of the lungs and liver. Dermal exposure to copper may cause contact dermatitis in some individuals (ATSDR, 1990).
Oral or intravenous administration of copper sulfate increased fetal mortality and developmental abnormalities in experimental animals (Lecyk, 1980; Ferm and Hanlon, 1974). Evidence also indicates that copper compounds are spermicidal (ATSDR, 1990; Battersby et al., 1982).
A Reference Dose (RfD) for elemental copper is not available (U.S. EPA, 1992). However, EPA established an action level of 1300 ug/L for drinking water (56 FR 26460, June 7, 1991). Data were insufficient to derive a Reference concentration (RfC) for copper.
No suitable bioassays or epidemiological studies are available to assess the carcinogenicity of copper. Therefore, U.S. EPA (1991a) has placed copper in weight-of-evidence group D, not classifiable as to human carcinogenicity. Retrieve Toxicity Profiles Formal Version
Last Updated 8/29/97