Alveolitis progressing to lung
fibrosis has been reported in workers exposed to
cobalt containing dust (e.g.,
tungsten carbide-
cobalt mixture as produced by the
hard metal industry) but rarely following exposure to pure
cobalt dust (e.g., in
cobalt-producing factories). We have previously demonstrated that
tungsten carbide-
cobalt mixture is more toxic toward rat alveolar macrophages in vitro than pure
cobalt metal powder. The present study was undertaken to compare in female rats the acute pulmonary response (lung weight, lung histology, cellular and biochemical analyses of bronchoalveolar lavage fluid, and mortality) following the intratracheal instillation of pure
cobalt (Co) particles (median particle size, d50:4 microns), pure
tungsten carbide (WC) particles (d50:2 microns),
tungsten carbide-
cobalt (WC-Co)
powder (d50:2 microns;
cobalt 6.3%,
tungsten 84%,
carbon 5.4%) and crystalline
silica (d50 less than 5 micron) used as pneumotoxic reference material. WC alone (15.67 mg/100 g body wt) behaves as an inert dust producing only a mild accumulation of macrophages in the alveolar duct walls. Co alone (1.0 mg/100 g) only causes a moderate inflammatory response. An identical amount of Co given as WC-Co mixture (16.67 mg/100 g; corresponding to 1.0 mg Co/100 g) produces a severe alveolitis and fatal
pulmonary edema. Cellular and biochemical characteristics of bronchoalveolar lavage fluid collected 24 hr after the intratracheal instillation of WC (1.0 mg/100 g) or Co (0.06 mg/100 g) are not significantly different from those of control animals instilled with sterile saline. On the contrary, bronchoalveolar lavage fluid changes following administration of the WC-Co mixture (1.0 mg/100 g; corresponding to 0.06 mg Co/100 g) are very similar to those induced by crystalline
silica (1.0 mg/100 g). The amount of
cobalt excreted in urine is significantly higher when the animals are exposed to WC-Co
powder as compared to an equivalent amount of pure
cobalt particles, suggesting an increased bioavailability of
cobalt metal when combined with
tungsten carbide. This study demonstrates that the acute lung toxicity of
tungsten carbide-
cobalt mixture is much higher than that of each individual component and may explain why lung
fibrosis is rarely if ever induced by exposure to pure
cobalt dust.