Cobalt is an essential oligoelement which enters in the composition of vitamin B₁₂. For the general population, food and beverages represent the main source of cobalt exposure. Traces of cobalt are also present in cement and various household products. In industry, the potential for exposure to cobalt is particularly important during the production of cobalt powder, the production, processing and use of hard metals, the polishing of diamonds with cobalt containing disks and the processing of cobalt alloys. Except in the production of cobalt powders, these activities involve exposure not only to cobalt but also to other substances such as tungsten carbide, iron and diamond which may modulate the biological reactivity of cobalt. Cobalt salts are used for the preparation of enamels and pigments. Cobalt is mainly absorbed from the pulmonary and the gastrointestinal tracts. Absorption through the skin can occur but is low. Concomitant exposure to tungsten carbide increases the pulmonary absorption rate of cobalt metal. Cobalt is not a cumulative toxin and is mainly excreted in urine and to a lesser extent via faeces. Cobalt in blood and urine mainly reflects recent exposure. In the past, outbreaks of cardiomyopathy occurred among heavy consumers of cobalt fortified beer. It is likely that poor nutrition and ethanol had played a synergistic role. Toxic manifestations, however, have mainly been reported following inhalation of cobalt containing dusts in industry. The two main target organs are the skin and the respiratory tract. Cobalt itself may cause allergic dermatitis, rhinitis and asthma. Specific IgE against a complex of cobalt with albumin can sometimes be shown and a bronchial provocation test with a cobalt salt may be positive. Inhalation of cobalt containing dust has also lead to pathologic reactions in the lung parenchyma. The lesions, called ‘hard metal disease’, have ranged from intense alveolitis resembling desquamative or giant-cell interstitial pneumonitis to end-stage pulmonary fibrosis. Epidemiological and experimental data suggest that parenchymal lesions are rarely if ever induced by pure cobalt dust alone, but require the concomitant exposure to other compounds such as tungsten carbide. At the present time, there is inadequate evidence to indicate whether cobalt alone can increase the risk of lung cancer in workers. Concomitant exposure to cobalt and other substances such as in hard metal industry might increase the risk of lung cancer, but this requires confirmation.