Source-dependent variation in hydroxyl radical production by airborne particulate matter

Epidemiological studies suggest exposure to airborne particles is responsible for a wide range of adverse health effects, potentially arising from particle-induced oxidative stress. A highly sensitive fluorescence method was employed to measure the production of hydroxyl radical by a broad range of particle types including urban dust, diesel particulate matter, coal fly ash, kaolinite, and silica. Little or no production of (OH)-O-center dot was observed in the absence of an added electron donor or H2O2. In the presence of a biological electron donor (NADPH, 3 mM), the rate of (OH)-O-center dot production (R-OH) for 3 mg/mL of these particles varied from 23 nM s(-1) for diesel particulate matter (SRM 2975) to 0.20 nM s(-1) for coal fly ash (SRM 2689). No detectable (OH)-O-center dot was produced by kaolinite or silica. Hydroxyl radical formation was eliminated under anaerobic conditions and in the presence of catalase, indicating that O-2 and H2O2 are required for its generation. Partial inhibition of (OH)-O-center dot formation by superoxide dismutase (SOD) was also observed in some cases, suggesting that superoxide (O-2(center dot-)) is also involved. The metal chelator deferoxamine mesylate (DFX) in most cases suppressed (OH)-O-center dot formation, but diethylenetriaminepentaacetic acid (DTPA) generally enhanced it, implicating metal ion reactions in (OH)-O-center dot generation as well. The dependence of R-OH on NADPH concentration further implicates particle surface reactions in (OH)-O-center dot formation. To our knowledge, these measurements provide the first quantitative estimate of R-OH for a broad range of particle types.