Adverse effects of metals on the alveolar part of the lung

Rabbits were exposed to low levels of metal dust or metal ions by inhalation for 1-8 months, 5 days/week and 6 h/day. Following exposure lung tissue was examined by light and electron microscopy, the lung content of phospholipid was analyzed and the morphology and function of alveolar macrophages were investigated. Metallic nickel dust as well as soluble nickel chloride produced accumulation of macrophages and laminated structures in alveoli and increased volume density of alveolar type II cells. The amount of phospholipids was elevated, mainly due to an increase in disaturated phosphatidylcholine. After one month exposure to metallic nickel dust or soluble nickel chloride, the alveolar macrophages contained surfactant inclusions and were functionally activated. After 3 and 6 months exposure to metallic nickel the macrophages were 'overfed' and inactive. A similar reaction is seen in the human disease pulmonary alveolar proteinosis. Exposure to cadmium chloride gave a similar reaction pattern as nickel did but in addition interstitial alveolitis. One month exposure to cobalt chloride affected the growth pattern of type II cells which formed nodules projecting into the alveolar lumen. Four months exposure to cobalt chloride resulted in further developed type II cell nodules, areas of hyperreactive type II cells, and interstitial inflammation. Copper chloride produced no effects apart from a slight increase in volume density of type II cells. Hexa- and trivalent chromium mainly affected the alveolar macrophages which showed enlarged lysosomes. Thus, different metal ions, in similar concentrations produced different pathological effects in the lung.