Gl. Squadrito et al., Quinoid redox cycling as a mechanism for sustained free radical generationby inhaled airborne particulate matter, FREE RAD B, 31(9), 2001, pp. 1132-1138
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.