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: Robert A. Young, Ph.D., D.A.B.T., Chemical Hazard Evaluation and Communication Group, Biomedical and Environmental Information Analysis Section, Health and Safety Research Division, *.
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.
Cadmium is a naturally occurring metal that is used in various chemical forms in metallurgical and other industrial processes, and in the production of pigments. Environmental exposure can occur via the diet and drinking water (ATSDR, 1989).
Cadmium is absorbed more efficiently by the lungs (30 to 60%) than by the gastrointestinal tract, the latter being a saturable process (Nordberg et al., 1985). Cadmium is transported in the blood and widely distributed in the body but accumulates primarily in the liver and kidneys (Goyer, 1991). Cadmium burden (especially in the kidneys and liver) tends to increase in a linear fashion up to about 50 or 60 years of age after which the body burden remains somewhat constant. Metabolic transformations of cadmium are limited to its binding to protein and nonprotein sulfhydryl groups, and various macromolecules, such as metallothionein, which is especially important in the kidneys and liver (ATSDR, 1989). Cadmium is excreted primarily in the urine.
Acute oral exposure to 20-30 g have caused fatalities in humans. Exposure to lower amounts may cause gastrointestinal irritation, vomiting, abdominal pain, and diarrhea (ATSDR, 1989). An asymptomatic period of one-half to one hour may precede the onset of clinical signs. Oral LD50 values in animals range from 63 to 1125 mg/kg, depending on the cadmium compound (USAF, 1990). Longer term exposure to cadmium primarily affects the kidneys, resulting in tubular proteinosis although other conditions such as "itai-itai" disease may involve the skeletal system. Cadmium involvement in hypertension is not fully understood (Goyer, 1991).
Inhalation exposure to cadmium and cadmium compounds may result in effects including headache, chest pains, muscular weakness, pulmonary edema, and death (USAF, 1990). The 1-minute and 10-minute lethal concentration of cadmium for humans has been estimated to be about 2,500 and 250 mg/m3, respectively (Barrett et al., 1947; Beton et al., 1966). An 8-hour TWA (time-weighted-average) exposure level of 5 mg/m3 has been estimated for lethal effects of inhalation exposure to cadmium, and exposure to 1 mg/m3 is considered to be immediately dangerous to human health (Friberg, 1950). Renal toxicity (tubular proteinosis) may also result from inhalation exposure to cadmium (Goyer, 1991).
Chronic oral RfDs of 5E-4 and 1E-3 mg/kg/day have been established for cadmium exposure via drinking water and food, respectively (U.S. EPA, 1991). Both values reflect incorporation of an uncertainty factor of 10. The RfDs are based on an extensive data base regarding toxicokinetics and toxicity in both human and animals, the critical effect being renal tubular proteinuria. Confidence in the RfD and data base is high.
Inhalation RfC values are currently not available.
The target organ for cadmium toxicity via oral exposure is the kidney (Goyer, 1991). For inhalation exposure, both the lungs and kidneys are target organs for cadmium-induced toxicity (ATSDR, 1989; Goyer, 1991).
There is limited evidence from epidemiologic studies for cadmium-related respiratory tract cancer (ATSDR, 1989). An inhalation unit risk of 1.8E-3 (µg/m3)-1 and an inhalation slope factor of 6.1E+0 (mg/kg/day)-1 are based on respiratory tract cancer associated with occupational exposure (U.S. EPA, 1985). Based on limited evidence from multiple occupational exposure studies and adequate animal data, cadmium is placed in weight-of-evidence group B1 - probable human carcinogen. Retrieve Toxicity Profiles Formal Version
Last Updated 8/29/97