Eicosanoid Production In The Alveolar Macrophage Exposed To Mineral Dust In Vitro Is Dependent On Surface Chemical Characteristics Of The Dust

It has been suggested that radicals on the surface of dust particles are key chemical factors in the pathophysiology which results from the occupational inhalation of coal and silica dust. In addition, oxygenated derivatives of arachidonic acid (eicosanoids) have been implicated as important biochemical mediators of mineral dust-induced lung disease through their role in bronchial and vascular smooth muscle reactivity, inflammation, and fibrosis. Therefore, we assessed eicosanoid production by the rat alveolar macrophage (AM) exposed in vitro to mineral dusts with varying surface chemical characteristics in order to determine if radicals associated with the mineral dub1 could influence the production of pro-inflammatory mediators in the lung environment. Rat AM were exposed to freshly fractured or "stale" bituminous coal dust, as well as untreated silica or silica calcined to 500°C and 1100°C. Prostaglandin E2 (PGE2) and thromboxane B2 (TxB2) levels in incubation medium were determined by specific radioimmunoassay. When AM were exposed to freshly fractured coal dust, PGE2 and TxB2 production were markedly increased. In contrast, exposure of AM to "stale" dust significantly reduced PGE2 and TxB2 production. In vitro exposure of AM to untreated silica resulted in a significant increase in PGE2 and TxB2 production compared to control. However, exposure of AM to silica calcined to 1100°C resulted in eicosanoid levels which were not significantly different from control. These findings suggest that radicals associated with respirable coal and silica particles may play a key role in the ability of mineral dust to activate AM eicosanoid production.