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Cobalt Poisoning

Cobalt Toxicity

Cobalt poisoning is a medical state caused by the excessive accumulation of cobalt in the body. Cobalt can enter the human organism via the respiratory tract or via ingestion.


Cobalt poisoning can manifest with symptoms of varying degrees of severity and can even cause death. An individual is exposed to this chemical element via inhalation, ingestion, or dermal exposure and, in general, chronic exposure is required for most of the adverse effects to develop.

The manifestations originating from the respiratory tract are traditionally linked to toxicity due to cobalt inhalation and comprise asthma, fibrosis, pneumonia, decreased lung function, and bronchospasm [1] [2] [3]. Cardiovascular manifestations are generally limited to cardiomyopathy accompanied with cardiomegaly and cardiac failure, while anemia with an approximate 5% decrease in hemoglobin has also been reported [4] [5] [6] [7]. Also documented are the effects of cobalt poisoning on the endocrine system, and specifically on the thyroid gland: even though reports evince a certain dissent, increased serum thyroxine (T4) or decreased concentrations of triiodothyronine (T3) have been observed [8]. In addition to the aforementioned symptomatology, persisting occupational exposure to cobalt may also lead to conjunctival congestion, weight loss in patients with the cobalt-associated pulmonary disease, and neurological sequelae which include nerve deafness, as well as memory and visual acuity impairment [9] [10] [11].

Ingesting cobalt is an important way of exposure to the element's toxic effects, with lethal cardiomyopathy having been reported as the most detrimental manifestation [12]. It develops abruptly with a clinical picture that resembles beriberi or alcoholic cardiomyopathy. Sinus tachycardia, left ventricular failure, and cardiogenic shock are some of the main manifestations, which may be preceded by nausea, diarrhea, and vomiting [13]. Ingestion of cobalt has also shown to result in polycythemia, increased hemoglobin levels, goiter, and histological changes of the thyroid gland [14].

Cobalt is known to cause dermatitis, should it come into contact with an individual's skin [15] [16].

An additional way in which cobalt poisoning is induced is metal-on-metal hip arthroplasty (MoM) [17]. The phenomenon is known as prosthetic hip-associated cobalt toxicity (PHACT) and leads to some of the manifestations that inhaled and ingested cobalt does, including cardiac, neurologic, and thyroid impairment [18]. Depression, lack of orientation and concentration, as well as aphasia, are also results of PHACT-related cobalt poisoning [19].

  • Cardiovascular manifestations are generally limited to cardiomyopathy accompanied with cardiomegaly and cardiac failure, while anemia with an approximate 5% decrease in hemoglobin has also been reported.[symptoma.com]
  • Haug Browse recently published Learning/CME Learning/CME View all learning/CME CME Case 3-2019: A 70-Year-Old Woman with Fever, Headache, and Progressive Encephalopathy Caplacizumab Treatment for Acquired Thrombotic Thrombocytopenic Purpura Randomized[nejm.org]
  • Depression, lack of orientation and concentration, as well as aphasia, are also results of PHACT-related cobalt poisoning.[symptoma.com]
  • When speaking to your doctor, we have a medical crib sheet that may be prove useful if you are uncertain what to ask about or worried you may forget important questions.[moriarty.com]


The diagnosis of cobalt poisoning initially requires a thorough medical history, including a history of potential exposure to toxic metals. This chemical element can be detected in the blood or urine [20] [21]. On average, an individual that has not been exposed to an excessive amount of cobalt is expected to exhibit values of the element less than 0.19 μg/dL and 2 μg/dL in the serum and urine, respectively [22]. A patient believed to have been exposed to a dangerous amount of cobalt should undergo laboratory evaluation of cobalt concentration in the urine and blood as soon as possible upon presentation, as the excretion rate is maximized within 24 hours after an occasion of exposure. Cobalt-associated allergic reactions can lead to elevated levels of IgE and IgA in the serum, which can be used both for diagnostic and monitoring purposes [23].


  • Treatment for skin contact : Since these rashes are rarely serious, very little will be done. The area may be washed and a skin cream may be prescribed. Treatment for lung involvement : Breathing problems will be treated based on your symptoms.[nlm.nih.gov]
  • In the first month, patients receive between five and 30 treatments (with 30 being most common), and are often advised to continue preventive treatment once a month. Individuals must pay for the treatment themselves.[sullolaw.com]
  • […] this review is to examine the use of cobalt alloys in total hip arthroplasty, to review the methods of measuring circulating cobalt levels, to define a level of cobalt which is considered pathological and to review the pathophysiology, risk factors and treatment[ncbi.nlm.nih.gov]
  • "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 .[ipfs.io]


  • 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[en.wikipedia.org]
  • Related: Cobalt Toxicity in Two Hip Replacement Patients (pdf) State of Alaska Epidemiology Bulletin, May 28, 2010 Out of joint: The story of the ASR BMJ 2011; 342:d2905 doi: 10.1136/bmj.d2905 (Published 14 May 2011) Cite this as: BMJ 2011; 342:d2905[nursinghomelawcenter.org]
  • Epidemiology A. Cobalt Toxicity in Two Hip Replacement Patients. State of Alaska Epidemiology Bulletin. May 28, 2010 2010(Bulletin No. 14). 19. Tower SS.[orthopaedicprinciples.com]
  • Tower, wrote about two cases of metallosis in the 2010 State of Alaska Epidemiology Bulletin. Both patients were fit, healthy 49-year-old men who received metal-on-metal implants.[drugwatch.com]
Sex distribution
Age distribution


  • The purpose of this review is to examine the use of cobalt alloys in total hip arthroplasty, to review the methods of measuring circulating cobalt levels, to define a level of cobalt which is considered pathological and to review the pathophysiology,[ncbi.nlm.nih.gov]
  • Useful For Suggests clinical disorders or settings where the test may be helpful Detecting cobalt toxicity Monitoring metallic prosthetic implant wear Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate[mayomedicallaboratories.com]


  • They bind to heavy metals in the body and prevent them from binding to other agents, creating a compound that can then be excreted from the body.[sullolaw.com]
  • You should call if you have any questions about poisoning or poison prevention. You can call 24 hours a day, 7 days a week.[nlm.nih.gov]
  • Elevated cobalt levels could prevent the body from repairing DNA while elevated chromium levels can result in DNA mutation.[depuyhiprecallattorney.wordpress.com]
  • The body’s goal is to “trap” the metals in the inflamed area and prevent them from spreading to other parts of the body.[sullolaw.com]



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  6. Jarvis JQ, Hammond E, Meier R, et al. Cobalt cardiomyopathy: A report of two cases from mineral assay laboratories and a review of the literature. J Occup Med.1992;34(6):620-626.
  7. Swennen B, Buchet J-P, Stanescu D, et al. Epidemiological survey of workers exposed to cobalt oxides, cobalt salts, and cobalt metal. Br J Ind Med.1993;50:835-842.
  8. Prescott E, Netterstrom B, Faber J, et al. Effect of occupational exposure to cobalt blue dyes on the thyroid volume and function of female plate painters. Scand J Work Environ Health.1992;18:101-104.
  9. Demedts M, Gheysens B, Nagels J, et al.Cobalt lung in diamond polishers. Am Rev Respir Dis.1984;130:130-135.
  10. Jordan C, Whitman RD, Harbut M, et al. Memory deficits in workers suffering from hard metal disease. Toxicol Lett. 1990;54:241-243.
  11. Meecham HM, Humphrey P. Industrial exposure to cobalt causing optic atrophy and nerve deafness: A case report. J Neurol Neurosurg Psychiatry. 1991;54(4):374-375.
  12. Bonenfant JL, Auger C, Miller G, et al. Quebec beer-drinkers' myocardosis: pathological
    aspects. Ann N Y Acad Sci 1969;156(1):577-582.
  13. Morin Y, Tetu A, Mercier G. Cobalt cardiomyopathy: Clinical Aspects. Br Heart J. 1971;33:175-178.
  14. Kriss JP, Carnes WH, Ross RT. Hypothyroidism and thyroid hypoplasia in patients treated with cobalt. JAMA.1955;157(2):117-121.
  15. Goossens A, Bedert R, Zimerson E.Allergic contact dermatitis caused by nickel and cobalt in
    green plastic shoes. Contact Dermatitis.2001;45(3):172.
  16. Minamoto K, Nagano M, Inaoka T, et al. Occupational dermatoses among fibreglass-reinforced plastics factory workers. Ind Health. 2002;40(1):42-50.
  17. Jones DA, Lucas HK, O’Driscoll M, Price CH, Wibberley B. Cobalt toxicity after McKee hip arthroplasty. J Bone Joint Surg. 1975;57(3):289–296.
  18. Devlin JJ, Pomerleau AC, Brent J, et al. Clinical Features, Testing, and Management of Patients with Suspected Prosthetic Hip-Associated Cobalt Toxicity: a Systematic Review of Cases. J Med Toxicol. 2013;9(4):405–415.
  19. Beck AT, Steer RA, Ball R, Ranieri WF. Comparison of beck depression inventories-IA and-II in psychiatric outpatients. J Pers Assess. 1996;67(3):588–597
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  21. Nemery B, Casier P, Roosels D, et al.Survey of cobalt exposure and respiratory health in diamond polishers. Am Rev Respir Dis.1992;145:610-616.
  22. Alexandersson R. Blood and urinary concentrations as estimators of cobalt exposure. Arch Env Health. 1988;43(4):299-303.
  23. Bencko V, Wagner V, Wagnerova M, et al. Immuno-biochemical findings in groups of individuals occupationally and non-occupationally exposed to emissions containing nickel and cobalt. J Hyg Epidemiol Microbiol Immunol.1983;27(4):387-394.

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Last updated: 2018-06-22 07:47