Quinoid redox cycling as a mechanism for sustained free radical generationby inhaled airborne particulate matter

The health effects of airborne fine particles are the subject of government regulation and scientific debate. ne aerodynamics of airborne particulate matter, the deposition patterns in the human lung, and the available experi mental and epidemiological data on health effects lead us to focus on airbo rne particulate matter with an aerodynamic mean diameter less than 2.5 mum (PM2.5) as the fraction of the particles with the largest impact in health. In this article we present a novel hypothesis to explain the continuous pr oduction of reactive oxygen species produced by PM2.5 when it is deposited in the lung. We find PM2.5 contains abundant persistent free radicals, typi cally 10(16) to 10(17) unpaired spins/gram, and that these radicals are sta ble for several months. These radicals are consistent with the stability an d electron paramagnetic resonance spectral characteristics of semiquinone r adicals. Catalytic redox cycling by semiquinone radicals is well documented in the literature and we had studied in detail its role on the health effe cts of cigarette smoke particulate matter. We believe that we have for the first time shown that the same, or similar radicals, are not confined to ci garette smoke particulate matter but are also present in PM2.5. We hypothes ize that these semiquinone radicals undergo redox cycling, thereby reducing oxygen and generating reactive oxygen species while consuming tissue-reduc ing equivalents, such as NAD(P)H and ascorbate. These reactive oxygen speci es generated by particles cause oxidative stress at sites of deposition and produce deleterious effects observed in the lung. (C) 2001 Elsevier Scienc e Inc.