The variability of quartz hazard is related to the characteristics of particulate toxicants. Although these have the same chemical composition, they exist in various forms and surface states, each one eliciting different biological responses. On the basis of data from the literature, surface chemical properties are associated to the subsequent stages reported by Donaldson and Borm, 1998 in the mechanistic model proposed for quartz carcinogenicity. Surface radicals and iron-derived reactive oxygen species (ROS) are implicated in oxidative stress, considered to be the key event in the development of fibrosis and lung cancer. Other chemical functionalities related to cytotoxicity, however, modulate the overall pathogenicity by regulating transport and clearance. The chemical features deriving from the intrinsic characteristics of a silica dust—e.g. its origin—as well as those generated by external factors—e.g. contaminants, associated minerals—are discussed in relation to their possible role in the pathogenic mechanism.

Surface chemistry and quartz hazard

Inflammatory effects of respirable quartz collected in workplaces versus standard DQ12 quartz: particle surface correlates.

Aluminium Lactate Treatment of DQ12 Quartz Inhibits Its Ability to Cause Inflammation, Chemokine Expression, and Nuclear Factor-κB Activation

Fracturing quartz produces silica-based radicals on the fracture planes and generates hydroxyl radicals (.OH) in aqueous media. .OH production has been shown to be directly associated with quartz-induced cell damage and phagocyte activation in vitro. This .OH production in vitro is inhibited by desferrioxamine mesylate, an Fe chelator, indicating involvement of a Fenton-like reaction. Our objective was to determine if Fe contamination increased the ability of inhaled quartz to cause inflammation and lung injury. Male Fischer 344 rats were exposed 5 hr/day for 10 days to filtered air, 20 mg/m3 freshly milled quartz (57 ppm Fe), or 20 mg/m3 freshly milled quartz contaminated with Fe (430 ppm Fe). High Fe contamination of quartz produced approximately 57% more reactive species in water than quartz with low Fe contamination. Compared to inhalation of quartz with low Fe contamination, high Fe contamination of quartz resulted in increases in the following responses: leukocyte recruitment (537%), lavageable red blood cells (157%), macrophage production of oxygen radicals measured by electron spin resonance or chemiluminescence (32 or 90%, respectively), nitric oxide production by macrophages (71%), and lipid peroxidation of lung tissue (38%). These results suggest that inhalation of freshly fractured quartz contaminated with trace levels of Fe may be more pathogenic than inhalation of quartz alone.

/pdf/augmentation-of-pulmonary-reactions-to-quartz-inhalation-by-4sjxd1e067.pdf

Augmentation of pulmonary reactions to quartz inhalation by trace amounts of iron-containing particles.

Variation of biological responses to different respirable quartz flours determined by a vector model.

/pdf/protection-by-iron-against-the-toxic-effects-of-quartz-4cg6t3bbct.pdf

S. Hagen

Papers

Protection by iron against the toxic effects of quartz