ABSTRACT
It is clear that inhaled particles have the capacity to cause acute lung damage and inflammation, and that transition metals play a major role in mediating this toxicity, particularly for occupationally derived substances, such as silica and asbestos. These compounds serve as solid-phase chelants for iron, and lung injury after silica and asbestos exposure is associated with the generation of oxygenbased free radicals, that is catalyzed by iron complexed to the dust. These oxidants can contribute to both cytotoxicity and release of mediators relevant to lung injury. The production of oxygen-based free radicals by mineral oxide particles can be observed after heating to high temperatures, grinding, dehydration, and coordination of transition metals (iron, copper, zinc, vanadium, and nickel) with two stable valence states at the solid-solution interface (1,2). Only the last of these can result in oxidant generation within a biological system.
