Diseases caused by silica: mechanisms of injury and disease development.
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.
Ding
Min
M
Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA.
Chen
Fei
F
Shi
Xianglin
X
Yucesoy
Berran
B
Mossman
Brooke
B
Vallyathan
Val
V
D000208:Acute Disease; D000818:Animals; D002283:Carcinoma, Bronchogenic / Q000209:etiology; D002908:Chronic Disease; D006801:Humans; D008175:Lung Neoplasms / Q000209:etiology; D012822:Silicon Dioxide / Q000009:adverse effects*; D012829:Silicosis / Q000209:etiology* / Q000235:genetics; D014376:Tuberculosis / Q000209:etiology
D012822:Silicon Dioxide