Freshly fractured quartz inhalation leads to enhanced lung injury and inflammation. Potential role of free radicals.

Abstract

Silicosis is a devastating pulmonary disease that continues to occur in industrial workplaces. Its pathogenesis is under critical evaluation, and this report provides new concepts on the possible early events that occur in lungs resulting from the inhalation of freshly fractured versus aged quartz in the development of two diverse disease entities. In this study, we evaluated the biochemical and pathologic changes in the lavagate and lungs of rats exposed to freshly fractured quartz (generated by jet milling), aged quartz (milled then aged for 2 mo prior to use), or clean air 5 h a day for 10 d over a 2-wk period. The concentration of crystalline quartz in the chambers averaged 20 mg/m3. Particle concentrations and particle size were similar for the freshly milled and aged quartz exposures. However, free radical concentrations associated with the freshly milled quartz samples were significantly higher than those for aged quartz. After a 2-wk exposure, animals were killed and studied by bronchoalveolar lavage and pulmonary histopathology. Inhalation of aged quartz increased the number of bronchoalveolar lavage cells, demonstrated histopathologic evidence of increased pulmonary infiltrates, showed enhanced concentrations of biochemical markers of lung injury, increased lipid peroxidation, and the ability of pulmonary phagocytes to produce more oxygen radicals. In general, all these pulmonary responses were significantly more pronounced after inhalation of freshly fractured quartz compared with aged quartz. In contrast, antioxidant enzymes showed decreased concentrations in the freshly fractured quartz-exposed group compared with the aged quartz-exposed animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Silicosis and coal workers' pneumoconiosis.

“…There appears to be a direct relationship between the ability of silica particles to generate hydroxyl radicals and the potential to cause lipid peroxidation and cytotoxicity in vitro (17,91). A similar relationship has been demonstrated in vivo as well (18,86). Surface iron plays an important role in augmenting silica-induced hydroxyl radical production and cytotoxicity both in vitro and in vivo (17,92).…”

“…Negatively charged silica particles would react strongly with scavenger receptors on alveolar macrophages and would activate the generation of reactive oxygen species (ROS) and inflammatory cytokines (9,10). A third theory is that deavage of the silica crystal, as would occur in silica flour milling, rock drilling, and sandblasting, results in the generation of Si and SiO' radicals on the fracture planes, which can induce oxidant damage (9,17,18). Stishovite is another polymorph of pure crystalline silica that is distinguished by its octahedral structure.…”

“…They develop cyanosis and respiratory failure, often complicated by mycobacterial infections. It has been proposed that acute silicosis occurs in workers exposed to freshly fractured silica dust and that surface Si' and SiO' radicals generated during fracturing play an important role in the rapid onset of this disease (17,18).…”

“…In studies of silica exposure of rats, the recruitment of PMNs from the pulmonary capillaries to the alveolar airspaces is a hallmark of the initiation and progression of silica-induced lung disease (83,85,86,103). As with cytotoxic responses, the degree of pulmonary inflammation is related to the ability of the silica particles to generate radicals, i.e., freshly fractured silica exhibits more surface radicals and causes more PMN recruitment than aged silica (18,86). PMN recruitment has also been demonstrated as a hallmark of acute silicosis in humans (97).…”

Modelling the health risks of exposure to respirable crystalline silica from hydraulic fracturing operations in the USA shale plays

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