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Cobalt is an essential trace element. It occurs in vitamin B12, which is required by all mammals for hemoglobin synthesis. In humans and all other monogastric species, B12is the only bioavailable form of cobalt, since these organisms are unable to synthesize the vitamin from dietary cobalt. Uptake of cobalt from the diet, therefore, must be in the form of vitamin B12 (1), which is also suspected to exacerbate, if not induce, cobalt allergy (2).

Cobalt compounds can pose significant dermal and respiratory toxicity problems, primarily in industry, due to their allergenic potential (3,4) and as causative factors for hard metal disease, a particular form of pneumoconiosis (5). Occurrence of the latter, ranging in form from intense alveolitis to end-stage pulmonary fibrosis, appears to require concomitant exposure to other agents, including tungsten metal dust (6,7). It is prevalent among workers exposed to metal-containing, respirable dust generated in the production and use of hard metal cutting tools. Evidence of cobalt carcinogenicity in humans is inadequate and cannot be evaluated quantitatively (7).


The human stratum corneum appears to be an effective barrier to cobalt penetra- s tion. In guinea pigs, in vivo, on the other hand, percutaneous toxicity of cobalt J

was considerable, based on the observation that 11 of 20 animals died within 2 o weeks of continuous dermal exposure (8). Skin absorption of the metal also de- |

pends on the respective counterion with chloride > tartrate > hydroxide (9). |

Hair analysis is seen as a suitable method for biological monitoring of exposure to the metal in the work environment, as atomic absorption analysis revealed geometrical mean values for cobalt in exposed workers to be signifi- <->

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