How silicosis and coal workers' pneumoconiosis develop - a cellular assessment.
Lapp NL; Castranova V
Occup Med: State of the Art Rev 1993 Jan; 8(1):35-56
The pathogenesis of silicosis and coal workers' pneumoconiosis (CWP) were reviewed from a cellular prospective. Topics included proposed mechanisms of lung damage, direct cytotoxicity of silica (7631869) or coal, release of toxic substances from alveolar macrophages, release of inflammatory factors from alveolar macrophages, effects of macrophage derived mediators on polymorphonuclear leukocytes, and the release of fibrogenic factors from macrophages. Evidence supporting proposed mechanisms for the development and progression of silicosis and coal workers' pneumoconiosis was presented including the results of in-vitro stimulation of toxic products from alveolar macrophages, in-vitro stimulation of inflammatory mediators from alveolar macrophages, in-vitro stimulation of fibrogenic factors from alveolar macrophages, in-vivo exposure of animals to coal dust, and in-vivo exposure of animals to silica (14808607). Human studies were discussed, including work on general lung fibrosis, asymptomatic coal miners, coal miners with CWP, asymptomatic silica workers, and workers with silicosis. The authors note that the present evidence supports the role of macrophage products in the development and progression of silicosis and CWP. Such products include enzymes and reactive oxygen species which may cause lung damage; cytokines which recruit and/or activate polymorphonuclear leukocytes and, thus, result in further oxidant damage to the lung; and fibrogenic factors which induce fibroblast proliferation and collagen synthesis.
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