Epidemiological studies have shown a strong relationship between particulate matter (PM) pollution and adverse health effects. One of the proposed mechanisms of particle toxicity is the particle-induced formation of reactive oxygen species (ROS) such as hydrogen peroxide (H2O2) and hydroxyl (?OH) radicals in the lungs leading to oxidative stress and inflammatory responses. A number of studies have indicated that catalytic mechanisms involving quinones may be involved in oxidative stress induced by particulate matter. However, the origin of quinones (direct emission versus in-situ formation from the oxidation of polyaromatic hydrocarbons, PAHs) is uncertain.  In this study we report the results of field measurements in Claremont, CA and Fresno, CA. Gas- and particle-phase concentrations of quinones and PAHs, along with a set of organic markers used for source apportionment were measured. Samples were collected on Teflon filters with a Hi-Volume PM2.5 sampler and semivolatile organics were collected on Polyurethane Foam Plugs (PUF). Particles were extracted into a cell-free surrogate lung fluid (SLF) containing four antioxidants: ascorbate, citrate, glutathione, and uric acid at physiological relevant concentrations. Residual organics on the sampling media were then extracted into an organic solvent (dichloromethane or hexane).Quinones, polycyclic aromatic hydrocarbons, C20-C32 n-alkanes, levoglucosan, cholesterol, and hopanes were quantified by gas chromatography-mass spectrometry. The results were then used to evaluate the major sources of particulate-phase quinones at the two sites. Metals and ROS (OH and H2O2) production were measured in a parallel set of studies, and the organic measurements reported here will ultimately be combined with these results to evaluate the relative contribution of the quinones to ROS production by fine particulate matter.

Mass loadings and source apportionment of quinones in fine particulate matter air pollution

245th National Meeting (2013)

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