title: Oxidative potential and inflammatory impacts of source apportioned ambient air pollution in Beijing.
abstract: Air pollution exposure is associated with a range of adverse health impacts. Knowledge of the chemical components and sources of air pollution most responsible for these health effects could lead to an improved understanding of the mechanisms of such effects and more targeted risk reduction strategies. We measured daily ambient fine particulate matter (<2.5 μm in aerodynamic diameter; PM2.5) for 2 months in peri-urban and central Beijing, and assessed the contribution of its chemical components to the oxidative potential of ambient air pollution using the dithiothreitol (DTT) assay. The composition data were applied to a multivariate source apportionment model to determine the PM contributions of six sources or factors: a zinc factor, an aluminum factor, a lead point factor, a secondary source (e.g., SO4(2-), NO3(2-)), an iron source, and a soil dust source. Finally, we assessed the relationship between reactive oxygen species (ROS) activity-related PM sources and inflammatory responses in human bronchial epithelial cells. In peri-urban Beijing, the soil dust source accounted for the largest fraction (47%) of measured ROS variability. In central Beijing, a secondary source explained the greatest fraction (29%) of measured ROS variability. The ROS activities of PM collected in central Beijing were exponentially associated with in vivo inflammatory responses in epithelial cells (R2=0.65-0.89). We also observed a high correlation between three ROS-related PM sources (a lead point factor, a zinc factor, and a secondary source) and expression of an inflammatory marker (r=0.45-0.80). Our results suggest large differences in the contribution of different PM sources to ROS variability at the central versus peri-urban study sites in Beijing and that secondary sources may play an important role in PM2.5-related oxidative potential and inflammatory health impacts.
authors.affiliation: College of Resources and Environment, University of Chinese Academy of Sciences , Beijing 100049, China.
authors.forename: Qingyang
authors.initials: Q
authors.lastname: Liu
authors.forename: Jill
authors.initials: J
authors.lastname: Baumgartner
authors.forename: Yuanxun
authors.initials: Y
authors.lastname: Zhang
authors.forename: Yanju
authors.initials: Y
authors.lastname: Liu
authors.forename: Yongjun
authors.initials: Y
authors.lastname: Sun
authors.forename: Meigen
authors.initials: M
authors.lastname: Zhang
mesh_terms: D000393:Air Pollutants / Q000032:analysis* / Q000633:toxicity; D000397:Air Pollution / Q000009:adverse effects / Q000032:analysis*; D000535:Aluminum / Q000032:analysis; D001681:Biological Assay; D015415:Biomarkers / Q000032:analysis; D002478:Cells, Cultured / Q000187:drug effects; D002681:China; D002947:Cities; D004391:Dust / Q000032:analysis; D004847:Epithelial Cells / Q000187:drug effects; D006801:Humans; D007249:Inflammation / Q000139:chemically induced* / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007854:Lead / Q000032:analysis; D008168:Lung / Q000166:cytology / Q000187:drug effects; D016877:Oxidants / Q000633:toxicity; D052638:Particulate Matter / Q000032:analysis*; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000393:Air Pollutants; D015415:Biomarkers; D004391:Dust; C508600:IL6 protein, human; D015850:Interleukin-6; D016877:Oxidants; D052638:Particulate Matter; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D007854:Lead; D000535:Aluminum