| View Larger Image | Quantitative measurements of the generation of hydroxyl radicals by soot particles in a surrogate lung fluid [An article from: Atmospheric Environment] | Digitalby H. Jung (Author), B. Guo (Author), C. Anastasio (Author), I.M. Kennedy (Author)
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| | Binding: | Digital | | Publisher: | Elsevier |
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This digital document is a journal article from Atmospheric Environment, published by Elsevier in . The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.Description: Epidemiological and toxicological studies have shown a relation between the inhalation of atmospheric particles and adverse cardiopulmonary health effects. The generation of reactive oxygen species (ROS) by particles is one current hypothesis for their toxic effects. Thus a quantitative measurement of ROS is important since that will be an index to assess the oxidative stress that particles may cause in the lung. We have developed a technique to quantitatively and specifically measure ^?OH (the strongest biological ROS) in an aqueous, buffered extract solution as a surrogate lung fluid (SLF). Using this technique we quantitatively measured ^?OH formation in SLF containing hydrogen peroxide (HOOH) for samples of flame soot particles, carbon black, and ambient fine particles (PM2.5). We have found that ^?OH is formed by flame soot, independent of transition metals, with a dose-dependent linear response that depends upon HOOH concentration. Experiments with carbon black revealed that its mass-normalized ^?OH generation was ~10 times lower than that of flame soot, suggesting that carbon black is not a good surrogate for soot particles in health effect studies, at least in terms of oxidative stress. Mass-normalized ^?OH generation by ambient PM2.5 was 6-30 times larger than that of flame soot. While much of the PM2.5 reactivity was suppressed by pretreating samples with a transition metal chelator, there was a significant fraction of reactivity which was not affected. Our results suggest that the in vivo generation of free radicals, specifically ^?OH, by inhalation of PM2.5 is partially due to carbonaceous soot as well as transition metals. |
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