Diseases caused by silica: mechanisms of injury and disease development.
Ding-M; Chen-F; Shi-X; Yucesoy-B; Mossman-B; Vallyathan-V
Int Immunopharmacol 2002 Feb; 2(2-3):173-182
While silica particles are considered to be fibrogenic and carcinogenic agents, the mechanisms responsible are not well understood. This article summarizes literature on silica-induced accelerated silicosis, chronic silicosis, silico-tuberculosis, bronchogenic carcinoma, and immune-mediated diseases. This article also discusses the generation of reactive oxygen species (ROS) that occurs directly from the interaction of silica with aqueous medium and from silica-stimulated cells, the molecular mechanisms of silica-induced lung injuries with focus on silica-induced NF-kappaB activation, including its mechanisms, possible attenuation and relationship to silica-induced generation of cyclooxygenase II and TNF-alpha. Silica-induced AP-1 activation, protooncogene expression, and the role of ROS in these processes are also briefly discussed.
Silica-dusts; Fibrogenesis; Carcinogenesis; Silicosis; Bronchial-cancer; Immune-system-disorders; Respiratory-system-disorders; Pharmacodynamics; Pulmonary-system-disorders; Physiopathology; Cell-alteration; Lung-cells; Lung-disease; Oncogenic-agents; Oxygen-uptake; Free-radical-generation; Free-radicals
Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, 1095 Willowdale Road, Morgantown, WV 26505, USA