Potential Role of Silicon-Oxygen Radicals in Acute Lung Injury

Abstract

This paper summarizes our recent investigations of the potential role of silicon-oxygen based free radical species in the biochemical mechanism of the lung injury caused by the inhalation of freshly fractured silica. The impetus for this study came from the following observations. Inhalation of crystalline silica is associated with the development of acute and chronic silicosis. Chronic silicosis is characterized by the development of sharply marked concentric fibrotic nodules in the lung. This occurs over a period of several decades with the development of progressive respiratory impairment. In contrast, acute silicosis is manifested by the filling of the alveoli with an amorphous lipoproteinaceous exudate within a short period after exposure, and rapid development of respiratory disability often leading to fatality. Most studies on the pathogenesis of silicosis have focused on the elucidation of cellular mechanisms of cell injury and the development of chronic silicosis. Because pulmonary responses to crystalline silica are distinctly different for the acute and chronic silicosis, we hypothesized that the acute response is associated with some unique properties of freshly formed silica particle surfaces, due to the formation of some reactive chemical species caused by the rupturing of the silicon-oxygen bonds. In occupations involving drilling, tunneling and sandblasting operations acute silicosis can be correlated with this unique surf ace reactivity of silica.