TY - JOUR
T1 - Hydrophobic Organic Components of Ambient Fine Particulate Matter (PM 2.5) Associated with Inflammatory Cellular Response.
AU - Jiang, Xing
AU - Xu, Fanfan
AU - Qiu, Xinghua
AU - Shi, Xiaodi
AU - Pardo, Michal
AU - Shang, Yu
AU - Wang, Junxia
AU - Rudich, Yinon
AU - Zhu, Tong
N1 - This research was supported by the National Natural Science Foundation of China grant (NSFC; 21876002), the Israel Science Foundation (ISF)-NSFC joint project (#2229/15 and 41561144007), the National Research Program for Key Issues in Air Pollution Control (DQGG0401-03), and the Ministry of Science and Technology of China Grant (973 program; 2015CB553401). YR acknowledges support by a research grant from the Herbert L. Janowsky Lung Cancer Research Fund, Adam Glickman, Eric Gordon, Alex Rotzang, the David M. Polen Charitable Trust, the Benoziyo Endowment Fund for the Advancement of Science, and the Midwest Electron Microscope Project. This work is part of AeroHEALTH Helmholtz International Lab.
PY - 2019/9/3
Y1 - 2019/9/3
N2 - Nowadays, knowledge regarding component-specific inflammatory effect of fine particulate matter (PM2.5) is limited. In this study, an omics approach based on time-of-flight mass spectrometry was established to identify the key hydrophobic components of PM2.5 associated with pro-inflammatory cytokines released by macrophages after in vitro exposure. Of 764 compounds, 62 components were robustly screened with firmly identified 37 specific chemicals. In addition to polycyclic aromatic hydrocarbons (PAHs) and their methylated congeners, novel oxygen- and nitrogen-containing PAHs and, especially, oxygenated PAHs (Oxy-PAHs) were identified. Interleukin (IL)-6 was associated with Oxy-PAHs of 1,8-naphthalic anhydride, xanthone, and benzo[ h]quinolone, especially, whereas IL-1β and tumor necrosis factor (TNF)-α were associated with most species. Most species were related to IL-1β, which was significantly higher in the heating season, with a monotonic dose-response pattern mainly for Oxy-PAHs and a U-shaped dose-response pattern for primary species. On the basis of the identified components, four sources of pollution (coal combustion, traffic emissions, biomass burning, and secondary formation, traced by Oxy-PAHs such as 1,8-naphthalic anhydride and quinones) were resolved by the positive matrix factorization model. TNF-α was associated with primary sources, whereas IL-1β and IL-6 were associated with both primary and secondary sources, suggesting different inflammatory effects between primary and secondary sources when assessing the toxicity-driven disparities of known and unknown PM2.5 components.
AB - Nowadays, knowledge regarding component-specific inflammatory effect of fine particulate matter (PM2.5) is limited. In this study, an omics approach based on time-of-flight mass spectrometry was established to identify the key hydrophobic components of PM2.5 associated with pro-inflammatory cytokines released by macrophages after in vitro exposure. Of 764 compounds, 62 components were robustly screened with firmly identified 37 specific chemicals. In addition to polycyclic aromatic hydrocarbons (PAHs) and their methylated congeners, novel oxygen- and nitrogen-containing PAHs and, especially, oxygenated PAHs (Oxy-PAHs) were identified. Interleukin (IL)-6 was associated with Oxy-PAHs of 1,8-naphthalic anhydride, xanthone, and benzo[ h]quinolone, especially, whereas IL-1β and tumor necrosis factor (TNF)-α were associated with most species. Most species were related to IL-1β, which was significantly higher in the heating season, with a monotonic dose-response pattern mainly for Oxy-PAHs and a U-shaped dose-response pattern for primary species. On the basis of the identified components, four sources of pollution (coal combustion, traffic emissions, biomass burning, and secondary formation, traced by Oxy-PAHs such as 1,8-naphthalic anhydride and quinones) were resolved by the positive matrix factorization model. TNF-α was associated with primary sources, whereas IL-1β and IL-6 were associated with both primary and secondary sources, suggesting different inflammatory effects between primary and secondary sources when assessing the toxicity-driven disparities of known and unknown PM2.5 components.
U2 - 10.1021/acs.est.9b02902
DO - 10.1021/acs.est.9b02902
M3 - مقالة
C2 - 31397158
SN - 0013-936X
VL - 53
SP - 10479
EP - 10486
JO - Environmental Science & Technology
JF - Environmental Science & Technology
IS - 17
ER -