 asbestos and silica are well - known fibrogenic dusts . however , there is no comprehensive understanding of the molecular and cellular events that lead to fibrosis as a consequence of asbestos or silica inhalation . 
 previous studies have shown that asbestos stimulates superoxide anion production in alveolar macrophages through the phospholipase c / protein kinase c pathway . 
 in contrast , silica does not appear to activate this pathway nor stimulate superoxide anion production , but silica does stimulate cytokine release by some undetermined pathway . 
 therefore , using human alveolar macrophages isolated from normal healthy volunteers , we evaluated the potential involvement of intracellular calcium and tyrosine kinases as potential signal transduction pathways . in the absence of serum , crystalline silica , and to a lesser extent amorphous silica , caused a rapid and dose - dependent elevation of intracellular calcium coming from the extracellular space . 
 however , in the presence of serum , which is required for silica - stimulated cytokine release , neither form of silica caused noticeable elevation of intracellular calcium . 
 silica , however , did increase the extent of tyrosine phosphorylation , most notably of proteins at approximately 46 and 50 kda , suggesting activation of a tyrosine kinase pathway . 
 preincubation of alveolar macrophages for 24 hr with silica - primed human alveolar macrophages for enhanced interleukin-1 beta ( il-1 beta ) release stimulated by endotoxin ( lps ) that was dose dependent . the enhanced lps - stimulated release of il-1 beta correlated with enhanced mitogen - activated protein kinase activity . taken together , 
 these results indicate that a tyrosine kinase pathway is activated during silica stimulation of human alveolar macrophages.imagesfigure 4 . 
 afigure 4 . 
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