Rights statement: This document is the Accepted Manuscript version of a Published Work that appeared in final form in Environmental Science and Technology, copyright © American Chemical Society after peer review and technical editing by the publisher. To access the final edited and published work see https://pubs.acs.org/doi/10.1021/acs.est.8b05814
Accepted author manuscript, 703 KB, PDF document
Available under license: CC BY-NC: Creative Commons Attribution-NonCommercial 4.0 International License
Final published version
Research output: Contribution to Journal/Magazine › Journal article › peer-review
| <mark>Journal publication date</mark> | 2/04/2019 |
|---|---|
| <mark>Journal</mark> | Environmental Science and Technology |
| Issue number | 7 |
| Volume | 53 |
| Number of pages | 9 |
| Pages (from-to) | 3782-3790 |
| Publication Status | Published |
| Early online date | 4/03/19 |
| <mark>Original language</mark> | English |
Spatiotemporal trends in pro-inflammatory (interleukin (IL)-6 and IL-8) release after exposure to the water-soluble fractions of PM2.5 sampled in 10 large Chinese cities over 1 year were investigated. Chemical components (water-soluble ions, metal(loid) elements, water-soluble organic carbon (WSOC), humic-like substances (HULIS), and endotoxins) in PM2.5 samples were measured, and the molecular structure of WSOC was also analyzed by nuclear magnetic resonance. Changes in DNA methylation and gene expression of candidate genes were also evaluated to explore the potential mechanisms. PM2.5 from southern cities induced lower pro-inflammatory responses compared to those from northern cities. Seasonal differences in toxicity were noted among the cities. IL-6 was significantly correlated with HULIS (as the main fraction of WSOC with oxygenated carbohydrate structures characteristic), Pb, and endotoxin. Furthermore, DNA methylation and gene expression changes in RASSF2 and CYPIB1 were related to pro inflammatory secretion. Certain components of PM25, rather than PM2.5 mass itself, determine the pro-inflammatory release. In particular, HULIS, which originated from primary biomass burning and residual coal combustion, and secondary organic aerosols, appear to be the key component in PM2.5 to induce human health risk.