Oxygen/nitrogen radicals and silica-induced diseases.
Oxygen/nitrogen radicals: lung injury and disease (Lung biology in health and disease). Vallyathan V, Castranova V, Shi X, eds. New York: Marcel Dekker, 2004 Apr; 187:161-177
Inhalation of crystalline silica has long been associated with lung disease. The rate of disease progression, i.e., acute, accelerated, or chronic silicosis, appears to depend on the rate in which crystalline silica is deposited in the lung. Acute silicosis results from exposure to high levels of freshly fractured dust associated with sand blasting, rock drilling, and silica flour milling. Acute silicosis is characterized by a rapid onset (a few years) of alveolar lipoproteinosis, edema, and inflammation, which result in a decrease in gas exchange. Accelerated silicosis develops more slowly and IS characterized by alveolar lipoproteinosis, chronic inflammation, and fibrotic granulomas. Chronic silicosis has an onset of 20-40 years and is characterized by silicotic nodules, which are fibrotic lesions with collagen Olaterial arranged in a spiral pattern. It has been proposed that silicosis results from a cycle of cell damage, inflammation, oxidant generation, scarring, and fibrosis (3,4). This scheme involves direct cytotoxicity of crystalline silica on lung cells due to the unique surface properties of quartz. In addition, alveolar macrophages (AMs) and/or alveolar epithelial cells are stimulated to produce inflammatory chemokines and cytokines
Silica-dusts; Silicates; Lung-function; Lung-disease; Inhalants; Dust-exposure; Dust-inhalation; Dust-particles; Cell-damage; Quartz-dust; Fibrosis; Respiratory-system-disorders; Pulmonary-system-disorders
Vallyathan-V; Castranova-V; Shi-X
Research Tools and Approaches: Cancer Research Methods
Oxygen/nitrogen radicals: lung injury and disease (Lung biology in health and disease)