Nodular accumulation of type II cells and inflammatory lesions caused by inhalation of low cobalt concentrations.

Eight rabbits were exposed to 2 mg/m3 and eight to 0.4 mg/m3 of cobalt as CoCl2 for 14-16 weeks (5 days/week, 6 hr/day). Eight rabbits were used as controls. Light microscopic examination of the lungs showed nodular accumulation of alveolar type II cells in all cobalt-exposed rabbits. Abnormal macrophage reaction was observed in all eight rabbits exposed to the high dose and in five of the eight exposed to the low dose. Interstitial inflammation was present in all the rabbits exposed to the high dose and in half of the rabbits exposed to the low dose. Ultrastructural morphometric examination revealed no significant increase in the volume density of type II cells in the cobalt-exposed animals, as the nodular accumulation of these cells was balanced by an increased number of interjacent fields devoid of type II cells. In cobalt-exposed lungs, there was focal swelling of both type I and type II cells, and some of the latter lacked microvilli. The effect pattern after CoCl2 exposure was thus clearly different from those patterns seen after exposure to other toxic metals. We speculate that nodular accumulation of type II cells represents the primary lesion in CoCl2-exposed lungs and that the proliferation of such cells in interjacent areas might be suppressed by a feedback mechanism regulating surfactant production in the terminal airspaces.