Cobalt is a hard, steel-grey or silver-grey coloured, somewhat malleable, magnetic, ductile metal, which exists in two allotropic forms with the hexagonal (alpha) form more stable at ambient temperatures than the cubic (beta) form. It is usually available in the form of hard metal which is actually an alloy of cobalt (5 to 25%) and tungsten carbide (75 to 95%). Toxicity is due to the former while the latter is relatively inert and harmless. Cobalt has exceptional magnetic properties in alloys.
· Manufacture of extremely hard steel and cutting tools. Also used in cemented carbide cutting tools, jet engines, as a co-ordination and complexing agent.
· Together with nickel, aluminium, copper, beryllium, chro- mium and molybdenum, cobalt is utilised in the electrical, automobile, aircraft and other industries.
· Manufacture of chemicals (cobalt salts); in alloys; cobalt steels for permanent magnets (in telephones, magnetic tape, microphones, speakers, computers, and motors) and for soft magnets and high-speed tool steels; in nuclear technology; and as oxidising agent.
· Used in alloys (nickel-aluminium-cobalt alloys), heat resistant alloys (gas turbines, electrical heating elements,and aircraft engines), and high-strength alloys (specialised axles, space equipment, cobalt steels).
· Cobalt is found in lamp filaments, as a trace element in fertilisers, and as drying agent in printer inks, paints, and varnishes.
· Cobalt compounds are contained in enamels, glazes, glass, pottery and paints. They are also used in glass pottery, photog-raphy and electroplating processes.
· Cobalt chloride may be present in chemistry sets, and in crystal-growing sets sold in supermarkets and toy-stores.
· Cobalt is often added to beer to promote the formation of foam.
· A component of vitamin B12 (cyanocobalamin), cobalt plays an important role in human nutrition. Vitamin B12 is necessary for proper development of red blood cells; its absence causes pernicious anaemia. The recommended daily allowance of cobalt in the form of Vitamin B12 is 0.13 mcg/day. Cobalt is found naturally in foods, especially in fish, cocoa, bran, and molasses, and green leafy vegetables, such as lettuce, cabbage and spinach.
· The classic toxidrome of chronic cobalt poisoning is the tetrad of goitre, polycythaemia, cardiomyopathy, and metabolic acidosis.
· Chronic exposure to cobalt in the form of inhalation results in hard metal lung disease, characterised by pulmonary fibrosis and an obstructive airway syndrome. It can induce or exacerbate asthma.
· Regular consumption of beer to which cobalt chloride or sulfate has been added (to enhance foaming) over a period of time can result in cardiomyopathy, referred to as beerdrinker’s heart which carries a relatively high mortality ofnearly 50%.
· Dermal contact can cause “cobalt itch” or “carboloy-itch” (an allergic erythematous papular eruption). Chronic expo-sure can cause nerve deafness and optic atrophy.
· Ingestion of magnets can cause acute cobalt toxicity.
Cobalt exposure has also been linked to an increased risk of cancer.
· Cobalt in its ionised form readily reacts with proteins, and may act as a hapten to induce allergic dermatitis and reac-tive airway disease.
· A deleterious effect on myocardial mitochondria may be responsible for the development of cobalt-induced cardio-myopathy.
· Protein deficiency (especially of tryptophan, DL-methionine, and L-cysteine) may be one important factor in the develop-ment of cobalt-induced cardiomyopathy.
· Zinc and magnesium deficiencies may also play a part in the aetiology of cobalt-beer cardiomyopathy.
· Monitor haemoglobin, haematocrit, RBC counts, urinalysis, and thyroid function tests.
· Monitor chest x-ray, arterial blood gases, ECG, and possibly echocardiogram if cardiomyopathy is present.
· Monitor pulmonary function tests and chest x-ray if inhala-tion exposure or respiratory disease is present.
· If chronic ingestion has occurred, evaluate for the presence of cardiomyopathy, pericardial effusion, and polycythaemia. Chest x-ray, electrocardiogram, echocardiogram, arterial blood gases, and complete blood count should be obtained and monitored if abnormal.
· Intensive supportive care may be required if cardiomyopathy is present. Digitalis preparations, diuretics, thiamine, and potassium replacement when indicated have been beneficial in some cases.
· Nausea and vomiting may occur in acute ingestions from local gastrointestinal tract irritation. Maintain fluid and electrolyte balance as necessary.
· Monitor red blood cell count and urinalysis. Monitor thyroid function tests if goitre is present.
· Replacement of zinc and magnesium deficits, correction of metabolic acidosis with sodium bicarbonate, and adminis-tration of thiamine seemed to be beneficial in some cases of cobalt-beer cardiomyopathy.
· Treat severe acidosis (pH < 7.1) with intravenous sodium bicarbonate. Begin with 1 to 2 mEq/kg in adults and 1 mEq/kg in children. Repeat every 1 to 2 hours as required. Monitor arterial blood gases to adjust dose.
· Indications: BAL has been suggested for use in symp-tomatic cobalt poisoning although the indications for its use are not well defined. Chelation has not been reported to be effective therapy for cobalt-induced cardiomyopathy or respiratory disease.
· Dose: 4 mg/kg IM (not more than 300 mg per dose) every 4 hours for the first day; then every 6 hours for the second day; then 3 times daily for approxi-mately 7 days.
· Alternative regimen: 3 to 5 mg/kg per dose deep
· IM every 4 hours for the first 2 days; then 2.5 to 3 mg/kg per dose IM every 6 hours for 2 days; and finally 2.5 to 3 mg/kg per dose IM every 12 hours for one week.
· Calcium Disodium Edetate: Some animal data havesuggested that calcium EDTA may be useful in cobalt poisoning, although it has not been reported to be effi-cacious in treating either cobalt-induced myocardial or respiratory disease, and its indications for use are unclear.
· While systemic corticosteroid therapy has been used in patients with cobalt-induced interstitial lung disease, it has not been successful unless accompanied by removal from further cobalt exposure.
· Patients who develop hypersensitivity reactive airway disease should be precluded from further cobalt exposure.
· Acute bronchospasm resulting from cobalt hypersensi-tivity may require treatment with inhaled sympathomi-metic agents. If more severe, other treatments effective in bronchospastic airway disease such as theophylline or corticosteroids may be required.
· Some studies suggest that haemodialysis could be of some value in patients with renal failure, uraemic cardi-omyopathy, and elevated serum cobalt levels. There is no evidence that haemodialysis would be beneficial in any other cobalt-induced disease.