Response of Alveolar Macrophages to in vitro Exposure to Freshly Fractured versus Aged Silica Dust: The Ability of Prosil 28, an Organosilane Material, to Coat Silica and Reduce Its Biological Reactivity

"We have reported previously that crushing or grinding crystalline silica results in the generation of silica-based radicals on the particulate surface and that these radicals can generate hydroxyl radicals in aqueous solution. Data in the present study indicate that freshly ground silica is more cytotoxic and is a more potent activator of alveolar macrophages than comparably sized aged silica. That is, compared to aged silica, fresh silica is 4.2-fold more potent in decreasing the membrane integrity of macro· phages; is 50% more potent in activating hydrogen peroxide secretion by macro· phages; and is 4.frfold more potent in stimulating cellular chemiluminescence. Prosil 28, an organosilane material, is an effective coating agent for fresh silica. It decreases the cytotoxicity of fresh silica by as much as 78% and decreases the ability of fresh silica to induce chemiluminescence from alveolar macrophages by 58%. The data suggest that surface radicals associated with freshly cleaved dust may be an important factor in the induction of pulmonary disease. Furthermore, treating dust with coating agents may substantially decrease toxicity. INTRODUCTIONThe U.S. Department of Labor estimates that over 1.25 million American workers may be exposed to crystalline silica and that nearly 60,000 may be at risk of developing some degree of occupational lung disease (Parkes, 1982; Peters, 1986). Occupations of concern include miners, stone quarry workers, sand and gravel workers, sandblasters, foundry workers, and glass workers. Acute silicosis is characterized by inflammation, alveolar lipoproteinosis, and the rapid development of respiratory disability (Banks, 1986). In contrast, chronic silicosis develops 20-40 yr after initial exposure and is characterized by the appearance of concentric hyalinized nodular lesions and the progressive development of dyspnea (Parkes, 1982; Ziskind et al., 1976)."