Search

Cobalt is regarded as being responsible for a form of myocardiopathy whose pathogenesis and clinical description must still find a specific place in the range of congestive myocardiopathies. In spite of this, epidemiological studies are not sufficient to prove the role of cobalt in inducing myocardiopathy in hard metal workers. This critical review intends to evaluate if hard metal exposure may induce toxic effects on the heart. In this context, the literature considered ranges from pioneer reports on 'beer drinkers' to the more recent papers concerning cases of patients occupationally exposed; subjects who, after a surgical operation died of fulminant heart failure and, lastly, hard metal workers who were examined for their cardiac function. Various pathogenetic mechanisms related to possible cardiac effects in hard metal workers have been analyzed. The most likely should be the inhibition of cellular respiration due to inhibition of the mitochondrial dehydrogenase.

This article summarizes the present state of the art and some recommendations for solutions to problems identified by the European Congress on Cobalt and Hard Metal Disease on the basis of the papers and posters presented, as well as a round table discussion which produced several dominant questions and revealed areas of weakness and uncertainty. The round table discussion (chairman, Professor E. Capodaglio) focussed on the following aspects: (i) Monitoring (opinion leaders: R. Lauwerys, E. Sabbioni). (ii) Mechanisms of toxicity (opinion leaders: B. Nemery, N.L. Sprince, G. Scansetti). (iii) Health effects (opinion leaders: G. Nordberg, I.B. Andersen). (iv) Diagnosis/health surveillance (opinion leaders: G. Chiappino, S. Hernberg, S. Brown).

A study was carried out on cobalt (Co) excretion in the urine of 12 workers exposed to known cobalt concentrations in the stone cutting diamond wheel production and in six volunteers: four of these were exposed in the same work environment for a whole workshift and the other two were exposed to cobalt in a cabin under experimental conditions. The kinetics of the urinary excretion was multiphase: (i) a first stage of rapid elimination (T 1/2' = 43.9 h); (ii) a second phase of slower elimination (T 1/2'' = 10 days); (iii) a longer period of retention, of the order of years, in subjects with higher exposure. In the control group (4 subjects), the excretion proved to be much faster in the first stage (T 1/2' = 20 h). The different behaviour of the two groups could be related to the different body burden, of cobalt and/or to the possibility of different kinetics induced by continuous exposure to the metal. Moreover, 3 weeks after the removal of the workers from exposure the urinary cobalt concentrations were not within the normal limits of CoU for the general population, (even for workers exposed to cobalt levels of the same order as the TLV). The increase of CoU concentrations in the first 3 h after the end of exposure, stresses the problem of when urine samples for biological monitoring of the workers should be collected. The present study confirms the utility of CoU in discriminating between exposed and non-exposed subjects as well as in assessing high and low level exposure.

A method for the determination of inorganic and organically-bound cobalt in human urine has been developed and applied to the urine of hard metal workers. The development was based on the use of the radionuclides 57Co, 58Co and 60Co-labelled Co compounds such as Co-Vitamin B12 and CO2+ ions which allowed the study of their biotransformations in human and rat urine. The proposed procedure is based on the use of Chelex 100 resin which retains quantitatively the inorganic Co from the urine while the organic complexed form of the element is eluted. Cobalt is detected in both column and eluate by neutron activation analysis (NAA). The method has been applied to speciate inorganic and organically-bound Co in the urine of hard metal workers. There is a significant increase (P0.02) of the ratio inorganic/organic Co (2.3) in the urine of workers compared with controls (1.01), showing an increase of the inorganic fraction of Co in the urine of workers. The ratio was constant for the wide range of urinary Co analyzed (from 180 micrograms to 1254 micrograms Co/l). Therefore, the discrimination between inorganic and organic Co in urine should not represent progress in the biological monitoring of Co compared with the determination of total urinary Co. However, a large amount of organically-complexed Co is formed in the body of hard metal workers and excreted in urine, thus, investigations of the nature of the organo-cobalt compounds are of fundamental importance in establishing their possible clinical significance.