Skip directly to search Skip directly to A to Z list Skip directly to site content
CDC Home

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 http://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

Alexander CS. Cobalt-beer cardiomyopathy. A clinical and pathological study of twenty-eight cases. Am J Med 1972;53:395-417.

Alexandersson R. Blood and urinary concentrations as estimators of cobalt exposure. Arch Environ Health 1988;43(4):299-303.

Bucher JR, Hailey JR, Roycroft JR, Haseman JK, Sills RC, Grumbein SL, et al., Inhalation toxicity and carcinogenicity studies of cobalt sulfate. Toxicol Sci 1999;49:56-67.

Centers for Disease Control and Prevention (CDC). Fourth National Report on Human Exposure to Environmental Chemicals. Updated Tables, 2012. [online] Available at URL: http://www.cdc.gov/exposurereport/. 10/26/12

Christensen JM, Poulsen OM. A 1982-1992 surveillance programme on Danish pottery painters. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. Sci Total Environ 1994;50(1-3):95-104.

Cugell DW, Morgan WKC, Perkins DG, Rubin A. The respiratory effects of cobalt. Arch Intern Med 1990;150:177-183.

Daniel J, Ziaee H, Salama A, Pradhan C, McMinn DJ. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. J Bone Joint Surg Br 2006;88(4):443-448.

De Boeck M, Kirsch-Volders M, Lison D. Cobalt and antimony: genotoxicity and carcinogenicity. Mutat Res 2003;533:135-152.

Dickel H, Radulescu M, Weyher I, Diepgen TL. Occupationally-induced "isolated cobalt sensitization." Contact Dermatitis 2001;45:246-247.

Dunstan E, Sanghrajka AP, Tilley S, Unwin P, Blunn G, Cannon SR, et al. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. J Bone Joint Surg Br 2005;87(5):628-631.

Goldberg MA, Dunning SP, Bunn HF. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Science 1988;242:1412-1415.

Hedge AG, Thakker DM, Ghat IS. Long-term clearance of inhaled 60Co. Health Phys 1979;36:732-734.

Iavicoli I, Falcone G, Alessandrelli M, Cresti R, DeSantis V, Salvatori S, et al. The release of metals from metal-on-metal surface arthroplasty of the hip. J Trace Elem Med Biol 2006;20(1):25-31.

Ichikawa Y, Kuska Y, Goto S. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Int Arch Occup Environ Health. 1985;55(4):269-276.

Jarvis JQ, Hammon E, Meier R, Robinson C. Cobalt cardiomyopathy. A report of two cases from mineral assay laboratories and a review of the literature. J Occup Med 1992;34:620-626.

Kraus T, Schramel P, Schaller KH, Zobelein P, Weber A, Angerer J. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Occup Environ Med 2001;58(10):631-634.

Kriss JP, Carnes WH, Gross RT. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955;157:117-121.

Kristiansen J, Christensen JM, Iversen BS, Sabbioni E. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Sci Total Environ 1997;204:147-160.

Lauwerys RB, Hoet P. Industrial Chemical Exposure: Guidelines for Biological Monitoring. 3rd ed. Boca Raton (FL): Lewis Publishers, 2001.

Lhotka C, Szekeres T, Steffan I, Zhuber K, Zweymuller K. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. J Orthop Res 2003;21(2):189-195.

Linna A, Oksa P, Palmroos P, Roto P, Laippala P, Uitti J. Respiratory health of cobalt production workers. Am J Ind Med 2003;44:124-132.

Linnainmaa M, Kiilunen M. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Int Arch Occup Environ Health 1997;69(3):193-200.

Lisi P. Co-sensitivity between cobalt and other transition metals. Contact Dermatitis 2003;48:172-173.

Lison D, Buchet JP, Swennen B, Molders J, Lauwerys R. Biological monitoring of workers exposed to cobalt metal, salt, oxides, and hard metal dust. Occup Environ Med 1994;51(7):447-450.

MacDonald SJ, McCalden RW, Chess DG, Bourne RB, Rorabeck CH, Cleland D, et al. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Clin Orthop Relat Res 2003;406:282-296.

Mosconi G, Bacis M, Vitali MT, Leghissa P, Sabbioni E. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Sci Total Environ 1994;150;(1-3):133-139.

Moulin JJ, Wild P, Romazini S, Lasfargues G, Peltier A, Bozec C, et al. Lung cancer risk in hard-metal workers. Am J Epidemiol 1998;148:241-248.

Pisati G, Zedda S. Outcome of occupational asthma due to cobalt hypersensitivity. Sci Total Environ 1994;150(1-3):167-171.

Shirakawa T, Kusaka Y, Fujimura N, Goto S, Kato M, Heki S, et al. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Chest 1989;95:29-37.

Smith T, Edmonds CJ, Barnaby CF. Absorption and retention of cobalt in man by whole-body counting. Health Phys 1972;22:359-367.

Swennen B, Buchet JP, Stanescu D, Lison D, Lauwerys R. Epidemiological survey of workers exposed to cobalt oxides, cobalt salts, and cobalt metals. Br J Ind Med 1993;50(9):835-842.

Thomassen H, HoffmannB, Schank M, Hoher T, Thabe H. Meyer zum Buschenfelde K-H, et al. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. J Rheumatol 2001;28(5):1121-1128.

White MA, Sabbioni E. Trace element reference values in tissues from inhabitants of the European Union. X. a study of 13 elements in blood and urine of a United Kingdom population. Sci Total Environ 1998;216:253-270.


 
USA.gov: The U.S. Government's Official Web PortalDepartment of Health and Human Services
Centers for Disease Control and Prevention   1600 Clifton Rd. Atlanta, GA 30333, USA
800-CDC-INFO (800-232-4636) TTY: (888) 232-6348 - Contact CDC–INFO
A-Z Index
  1. A
  2. B
  3. C
  4. D
  5. E
  6. F
  7. G
  8. H
  9. I
  10. J
  11. K
  12. L
  13. M
  14. N
  15. O
  16. P
  17. Q
  18. R
  19. S
  20. T
  21. U
  22. V
  23. W
  24. X
  25. Y
  26. Z
  27. #