Oxidative Potential of Particulate Matter and Generation of Reactive Oxygen Species in Epithelial Lining Fluid

活性氧 氧化应激 化学 环境化学 抗坏血酸 微粒 抗氧化剂 氧化磷酸化 沉积(地质) 生物化学 生物 有机化学 沉积物 食品科学 古生物学
作者
Ting Fang,Pascale S. J. Lakey,Rodney J. Weber,Manabu Shiraiwa
出处
期刊:Environmental Science & Technology [American Chemical Society]
卷期号:53 (21): 12784-12792 被引量:119
标识
DOI:10.1021/acs.est.9b03823
摘要

Reactive oxygen species (ROS) play a central role in adverse health effects of atmospheric particulate matter (PM). Respiratory deposition can lead to the formation of ROS in the epithelial lining fluid due to redox reactions of PM components with lung antioxidants. As direct quantification of ROS is challenging, PM oxidative potential is more commonly measured using antioxidant surrogates including dithiothreitol and ascorbic acid, assuming that the decay of surrogates corresponds to ROS formation. However, this assumption has not yet been validated and the lack of ROS quantification in the respiratory tract causes major limitations in evaluating PM impacts on oxidative stress. By combining field measurements of size-segregated chemical composition, a human respiratory tract model, and kinetic modeling, we quantified production rates and concentrations of different types of ROS in different regions of the epithelial lining fluid by considering particle-size-dependent respiratory deposition. The extrathoracic region is found to have higher ROS concentrations compared to the bronchial and alveolar regions. Although H2O2 and O2- production is governed by Fe and Cu ions, OH radicals are mainly generated by organic compounds and Fenton-like reactions of metal ions. In winter when affected by biomass burning, model comparisons suggest that humic-like substances (HULIS) contribute to ROS formation substantially. We found that PM oxidative potential is a good indicator of the chemical production of H2O2 and O2- but does not represent OH generation. These results provide rationale and limitations of the use of oxidative potential as an indicator of PM toxicity in epidemiological and toxicological studies.
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