Etiology and pathogenesis of hard metal disease

Workers exposed to cobalt by inhalation are at risk from interstitial lung disease (hard metal disease) and occupational asthma. Exposed groups include tungsten carbide (TC) producers, diamond polishers, grinders and sharpeners of TC tools, and metal coaters using powdered hard metal. Cobalt, the binding agent for TC, is believed to be the casual agent. Information available to date suggests that cobalt in the absence of tungsten or TC can cause interstitial lung disease (ILD) and occupational asthma, while tungsten or TC does not. Questions for further investigation are whether cobalt toxicity is enhanced in the presence of TC or other metals and whether pure cobalt in the absence of any other metals can cause ILD. Prevalence and exposure-response information is available for ILD in workers exposed to cobalt. The prevalence of interstitial lung disease among studies on TC production workers range from 0 to 13%. Because of subject selection for active employed workers, these are probably underestimates of the true prevalence in the industry. Our study of 1039 US TC workers showed that 2.6% had abnormal chest radiographs ( profusion ≥ 1 0 ). We found that the relative odds of an abnormal chest radiograph were increased fivefold when lifetime average cobalt levels exceeded 100 μg/m 3 , among those with at least 10 years latency. On the other hand, we found three workers with ILD whose exposures had never exceeded 50 μg/m 3 and whose latencies where less than 10 years. This study and supporting data from the literature suggests that a subgroup of workers exposed to cobalt is at risk for hard metal disease. Among the subgroup at risk, individual susceptibility to cobalt varies. This may explain why some exposed workers will develop hard metal disease after brief, low cobalt exposures (below the current US standard of 50 μg/m 3 ), while others will develop the disease only after higher cobalt exposures of longer duration.