Reversible lung lesions in rats due to short-term exposure to ultrafine cobalt particles

Using an ultrasonic nebulizer, cobalt aerosols (MMAD = 0.76 microns, sigma g = 2.1) were generated from an aqueous suspension of ultrafine metallic cobalt particles (Uf-Co) with a primary diameter of 20 nm. Rats were exposed to Uf-Co aerosols at 2.72 +/- 0.44 mg/m3 for 5 hours (Exp. 1) or at 2.12 +/- 0.55 mg/m3 for 4 days at 5 hours/day (Exp. 2). Only minimum histopathological changes were observed in the lungs in Exp. 1. In Exp. 2, evidence of slight injury was noted, including focal hypertrophy or proliferation of the epithelium in the lower airways, damages of macrophages, intracellular edema of the type I alveolar epithelium, interstitial edema, and proliferation of the type II alveolar epithelium. A new finding in this study was the morphological transformation of some damaged type I cells to the juvenile form, which appeared to indicate the capability of self-repair of this cell type. The return to a juvenile form seemed to be a key response of type I cells during the early process of repair without cell division following non-lethal injury. Cobalt accumulated in the lungs after inhalation and was transferred rapidly to the blood. In conclusion, inhaled Uf-Co induced reversible pulmonary injury even after short-term exposure.