EPIDEMIOLOGIC SURVEY OF WORKERS EXPOSED TO COBALT OXIDES, COBALT SALTS, AND COBALT METAL

Several organs (lung, skin, thyroid, heart, bone marrow) are potential targets of cobalt (Co). Whereas there is no doubt that inhalation of Co alone may cause bronchial asthma, its role in the occurrence of har d metal disease is still controversial because most cases were reporte d in workers exposed not only to Co but also to other substances such as tungsten carbide, titanium carbide, iron, silica and diamond. To as sess whether exposure to pure Co dust (metal, oxides, or salts) may le ad to adverse health effects a cross sectional study was carried out a mong 82 workers in a Co refinery. The results were compared with those in a sex and age matched control group. The Co group had been exposed for 8-0 years on average (range 0.3-39.4). The geometric mean time we ighted average exposure assessed with personal samplers (n = 82) was a bout 125 mug/m3 and 25% of the values were higher than 500 mug/ml. The concentrations of Co in blood and in urine after the shift were signi ficantly correlated with those in air. Concentration of Co in urine in creased during the workweek. A slight interference with thyroid metabo lism (decreased T3, T4, and increased TSH), a slight reduction of some erythropoietic variables (red blood cells, haemoglobin, packed cell v olume) and increased white cell count were found in the exposed worker s. The exposed workers complained more often of dyspnoea and wheezing and had significantly more skin lesions (eczema, erythema) than contro l workers. Within the exposed group a dose-effect relation was found b etween the reduction of the forced expiratory volume in one second/vit al capacity and the intensity of current exposure to Co assessed by th e measurement of Co in air or in urine. The prevalence of dyspnoea was related to the dustiness of the workplace as reflected by a statistic ally significant logistic regression between this symptom and the curr ent levels of Co in air and in urine. No difference between lung volum es, ventilatory performances, carbon monoxide diffusing capacity, and serum myocardial creatine kinase and procollagen III peptide was found between the Co and control groups and no lung abnormalities were dete cted on the chest radiographs in both groups. The results suggest that exposure to high airborne concentrations of Co alone is not sufficien t to cause pulmonary fibrosis. This finding is compatible with experim ental studies indicating that interaction of other airborne pollutants with Co particles play a part in the pathogenesis of parenchymal lung lesions.