Cobalt occurs naturally in airborne dust, seawater, and soil. It is emitted into the environment from burning coal and oil and car and truck exhaust. Usual human exposure is from food sources. Cobalt may be released into the systemic circulation of patients who receive joint prostheses that are fabricated from cobalt alloys (Lhotka et al., 2003). Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin), an essential human nutrient. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.
Exposure in the workplace may come from electroplating, refining or processing alloys, using hard metal cutting tools, or using diamond-polishing wheels that contain cobalt metal. Workplace standards and guidelines have been established by OSHA and ACGIH, respectively.
Cobalt is absorbed by oral and pulmonary routes. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al., 1972). Once absorbed and distributed in the body, cobalt is excreted predominantly in the urine, and to a lesser extent, in the feces. A portion of cobalt retained for long periods is concentrated in the liver. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged, with pulmonary clearance half-lives of from one to two years (Hedge et al., 1979). Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al., 1994).
Toxic effects of cobalt have been encountered in workplace settings. Cobalt compounds are a recognized cause of allergic contact dermatitis. Occupational exposure to cobalt-containing dusts has caused occupational asthma. “Hard metal” disease, an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis, has been associated with exposure to dusts that contain cobalt, usually in combination with tungsten carbide.
Cobalt was once added as a foaming agent to beer, and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy. A subclinical decrease in thyroid production was observed in a study of cobalt production workers.
Cobalt compounds elicited numerous genotoxic effects in both in vitro and ;in vivo assays. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans.
Finding a measurable amount of cobalt in the urine does not imply that the levels of cobalt cause an adverse health effect. Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases . Urinary measurements mainly reflect recent exposure, although substantial occupational exposures have produced elevated urinary levels for many weeks. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U.S. population results. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations, with mean levels that were about 15-20 times higher than in the general population.
More Information about external exposure (i.e., environmental levels) and health effects is available from ATSDR at https://www.atsdr.cdc.gov/toxprofiles/index.asp.