Cobalt poisoning

Cobalt poisoning is intoxication caused by excessive levels of cobalt in the body. Cobalt is an essential element for health in animals in minute amounts as a component of Vitamin B12. A deficiency of cobalt, which is very rare, is also potentially lethal, leading to pernicious anemia.[1]

Cobalt poisoning

Exposure to cobalt metal dust is most common in the fabrication of tungsten carbide. Another source is from wear and tear of certain metal-on-metal hip prostheses.[2]

Cobalt salts

The LD50 value for soluble cobalt salts has been estimated to be between 150 and 500 mg/kg. Thus, for a 100 kg person the LD50 would be about 20 grams.[1]

Beer drinker's cardiomyopathy

In August 1965, a patient presented to a hospital in Quebec City with symptoms suggestive of alcoholic cardiomyopathy. Over the next eight months, fifty more cases with similar findings appeared in the same area with twenty of these being fatal. It was noted that all patients were heavy drinkers who mostly drank beer and preferred the Dow brand, thirty out of those consuming more than 6 litres (12 pints) of beer per day.[3] Epidemiological studies found that Dow had been adding cobalt sulfate to the beer for foam stability since July 1965 and that the concentration added in the Quebec city brewery was ten times that of the same beer brewed in Montreal where there were no reported cases.[4][5]

Cobalt in the environment

Plants, animals, and humans can all be affected by high cobalt concentrations in the environment. For plants, the uptake and distribution of cobalt is entirely species-specific.[6] In some species of plants, the over accumulation of cobalt can lead to an iron deficiency. This in turn leads to poor growth of the plant as well as leaf loss which overall decreases the amount of oxygen produced by plants during photosynthesis. Eventually the deficiency would lead to plant death.[7] One such example was seen in an experiment involving the effects of increased cobalt concentration on tomato plants. As the dosage of cobalt in the soil surrounding the plants increased, so too did the rate of necrosis of the leaves of the tomato plant. Over time this led to an inability of the plant to produce fruit and eventually the plant died.[8]


  1. John D. Donaldson; Detmar Beyersmann (2005). "Cobalt and Cobalt Compounds". Ullmann's Encyclopedia of Industrial Chemistry. Weinheim: Wiley-VCH. doi:10.1002/14356007.a07_281.pub2.
  2. Zywiel, MG; Cherian, JJ; Banerjee, S; Cheung, AC; Wong, F; Butany, J; Gilbert, C; Overgaard, C; Syed, K; Jacobs, JJ; Mont, MA (January 2016). "Systemic cobalt toxicity from total hip arthroplasties: review of a rare condition Part 2. measurement, risk factors, and step-wise approach to treatment". The Bone & Joint Journal. 98-B (1): 14–20. doi:10.1302/0301-620X.98B1.36712. PMID 26733510.
  3. Y. L. Morin; A. R. Foley; G. Martineau; J. Roussel (1967). "Quebec beer-drinkers' cardiomyopathy: forty-eight cases". Canadian Medical Association Journal. 97: 881–883. PMC 1923396. PMID 6051256.
  4. Morin Y, Têtu A, Mercier G (1969). "Quebec beer-drinkers' cardiomyopathy: Clinical and hemodynamic aspects]". Ann N Y Acad Sci. 156: 566–576. doi:10.1111/j.1749-6632.1969.tb16751.x. PMID 5291148.
  5. "How Quebec beer and TV's Dr. House solved a medical mystery". CBC News. February 6, 2014. Retrieved February 7, 2014.
  6. The Botanical Review 60(2):149-181 · April 1994 DOI: 10.1007/BF02856575
  7. Palit, S., Sharma, A. & Talukder, G. Bot. Rev (1994) 60: 149. doi:10.1007/BF02856575
  8. Rajeev Gopal, B. K. Dube, Pratima Sinha & C. Chatterjee Pages 619-628 | Published online: 05 Feb 2007
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