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Cobalt Poisoning

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.


Presentation

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].

Axillary Rash
  • At 3 months post-op, he complained of bilateral axillary rashes. At 8 months post-op, he reported unaccustomed shortness of breath. Pulmonary function tests and allergy testing for metals were normal.[earlsview.com]
Aphasia
  • Depression, lack of orientation and concentration, as well as aphasia, are also results of PHACT-related cobalt poisoning.[symptoma.com]

Workup

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].

Nodular Fibrosis
  • fibrosis 1 reference reference URL dermatitis 1 reference reference URL weight loss 1 reference reference URL decreased pulmonary function 1 reference reference URL wheeze 1 reference reference URL dyspnea 1 reference reference URL first aid measures[wikidata.org]
Hepatic Necrosis
  • Gastrointestinal PO 0.04 mgCo/kg/day [27,28] Nausea Vomiting Diarrhea Hepatic effects [26,27] PO 0.04 mgCo/kg/day Central hepatic necrosis Increased Serum Bilirubin Increase AST,ALT,LDH Increase Creatine Phosphokinase Increase Ornithine CarbamylTransferase[toxicology.imedpub.com]

Treatment

  • 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.[medlineplus.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]
  • Treatment Treatment for signs of cobalt toxicity from a metal on metal hip implants may include removing the implant and replacing it with a traditional hip implant.[thelawfirm.com]

Prognosis

  • The prognosis of Cobalt Poisoning is dependent on the amount of substance consumed, time between consumption and treatment, severity of the symptoms, as well as general health status of the patient.[dovemed.com]

Etiology

  • Morin Y,Daniel P (1967) Quebec beer-drinkers' cardiomyopathy: Etiological considerations. Can Med Assoc J 97: 926-928. Sullivan JF,Egan JD,George RP (1969) A distinctive myocardiopathy occurring in Omaha,Nebraska:Clinical aspects.[toxicology.imedpub.com]
  • Exclusion of other potential etiologies.[path.upmc.edu]
  • Quebec beer-drinkers’ cardiomyopathy: etiological considerations . Can Med Assoc J 1967 ; 97 : 926 – 8 . 24. A review of the health hazards posed by cobalt . Crit Rev Toxicol 2013 ; 43 : 316 – 62 . 25.[ajcn.nutrition.org]

Epidemiology

  • It was noted that all patients were heavy drinkers who mostly drank beer and preferred the Dow brand , 30 out of those consuming more than 6 liters (12 pints) of beer per day. [3] Epidemiological studies found that Dow had been adding cobalt sulfate to[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]
  • State of Alaska Epidemiology Bulletin . link May 28, 2010. Cohen, Deborah. "Tony Nargol." British Medical Journal . link . June 7, 2011.[gpwlaw.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

Pathophysiology

  • 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]

Prevention

  • Elevated cobalt levels could prevent the body from repairing DNA while elevated chromium levels can result in DNA mutation.[depuyhiprecallattorney.wordpress.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.[medlineplus.gov]
  • 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]
  • 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]

References

Article

  1. Davison AG, Haslam PL, Corrin B, et al. Interstitial lung disease and asthma in hard-metal
    wokers: bronchoalveolar lavage, ultrastructural, and analytical findings and results of bronchial
    provocation tests. Thorax.1983;38:119-128.
  2. Deng JF, Sinks T, Elliott L, et al.Characterization of respiratory health and exposures are a sintered permanent magnet manufacturer. Br J Ind Med.1991;48:609-615.
  3. Sundaram P, Agrawal K, Mandke JV, et al.Giant cell pneumonitis induced by cobalt. Indian J Chest Dis Allied Sci.2001;43 (1):47-49
  4. Horowitz SF, Fischbein A, Matza D, et al. Evaluation of right and left ventricle function in hard metal workers. Brit J Ind Med.1998;45:742-746
  5. Barborik M, Dusek J. Cardiomyopathy accompanying industrial cobalt exposure. Br Heart J.1972;34:113-116.
  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
  20. Lison D, Lauwerys R. Cobalt bioavailability from hard metal particles. Arch Toxicol.1994;68:528-531.
  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