Biomonitoring Summary
Cobalt
CAS No. 7440-48-4
General Information
Cobalt is a magnetic element that occurs in nature either as a steel-gray, shiny, hard metal or in combination with other elements. The cobalt used in U.S. industry is imported or obtained by recycling scrap metal that contains cobalt. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines, hard metal (alloys of cobalt and tungsten carbide), blue-colored pigments, and fertilizers. Cobalt is used as a drying agent in paints, varnishes, and inks. It is also a component of porcelain enamel applied to steel bathroom fixtures, large appliances, and kitchenware. Cobalt compounds are used as catalysts in producing oil and gas, and in synthesizing polyester and other materials. Cobalt compounds are also used in manufacturing battery electrodes, steel-belted radial tires, automobile airbags, diamond-polishing wheels, and magnetic recording media. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.
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 for external air exposure to cobalt and several of its compounds 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. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week, but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al., 1994; Smith et al., 1972). 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 (Dickel et al., 2001; Lisi, 2003; Thomassen et al., 2001). Occupational exposure to cobalt-containing dusts has caused occupational asthma (Pisati and Zedda, 1994; Shirakawa et al., 1989). “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 (Cugell et al., 1990). The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al., 2003; Swennen et al., 1993).
Cobalt was once added as a foaming agent to beer, and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al., 1972). Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al., 1992). Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al., 1988). Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al., 1955). A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al., 1993).
Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al., 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al., 1999). An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al., 1998). IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans. Information about external exposure (i.e., environmental levels) and health effects is available from ATSDR at https://www.atsdr.cdc.gov/toxprofiles/index.asp.
Biomonitoring Information
Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al., 1988). 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 (CDC, 2012; Kristiansen et al., 1997; White and Sabbioni, 1998). 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 U.S. population (CDC, 2012; Daniel et al., 2006; Dunstan et al., 2005; Iavicoli et al., 2006; MacDonald et al, 2003).
Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 ?g/L. Information about the BEI is provided here for comparison, not to imply that the BEI is a safe level for general population exposure. For workers exposed to cobalt in the air, a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen, 1994; Lison et al., 1994). Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better. Correlations between air-exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al., 1985; Krause et al., 2001; Lauwerys and Hoet, 2001; Linnainmaa and Kiilunen, 1997).
Finding a measurable amount of cobalt in the urine does not imply that the levels of cobalt cause an adverse health effect. Biomonitoring studies on levels of cobalt provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of cobalt than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.
References
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