B. Swennen et al., EPIDEMIOLOGIC SURVEY OF WORKERS EXPOSED TO COBALT OXIDES, COBALT SALTS, AND COBALT METAL, British Journal of Industrial Medicine, 50(9), 1993, pp. 835-842
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.