Special Issue on Pulmonary and Neurological Health Impacts from Airborne Particulate Matte

Juan Li, Yingying Liu, Zhen An, Wen Li, Xiang Zeng, Huijun Li, Jing Jiang, Jie Song, Weidong Wu This email address is being protected from spambots. You need JavaScript enabled to view it.

International Collaborative Laboratory for Air Pollution Health Effects and Intervention, School of Public Health, Xinxiang Medical University, Xinxiang, Henan 453003, China


Received: August 5, 2019
Revised: November 18, 2019
Accepted: November 30, 2019

 Copyright The Author(s). This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are cited.

Download Citation: ||https://doi.org/10.4209/aaqr.2019.06.0288 

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Cite this article:

Li, J., Liu, Y., An, Z., Li, W., Zeng, X., Li, H., Jiang, J., Song, J. and Wu, W. (2020). Seasonal Variations in PM2.5-induced Oxidative Stress and Up-regulation of Pro-inflammatory Mediators. Aerosol Air Qual. Res. 20: 1686–1694. https://doi.org/10.4209/aaqr.2019.06.0288


  • PM2.5 from different seasons own distinct composition.
  • The water-soluble composition of PM2.5 showed seasonal variations.
  • PM2.5 -induced oxidative stress and subsequent production of pro-inflammatory mediators varies with season.


Inhaling particulate matter with an aerodynamic diameter of ≤ 2.5 µm (PM2.5) has been demonstrated to induce season-dependent adverse health effects. As inflammation and oxidative stress play a critical role in PM2.5-induced health effects, this study used a human monocytic cell line, THP-1, to investigate whether the PM2.5-induced oxidative stress and pro-inflammatory response varied by season. PM2.5 was collected during April (spring), July (summer), September (fall) and December (winter) of 2014. The cytotoxicity was assessed with a lactate dehydrogenase (LDH) release assay. The levels of pro-inflammatory mediators, including tumor necrosis factor (TNF-α) and interleukin-1β (IL-1β), were measured with ELISA, and the reactive oxygen species (ROS) were identified with flow cytometry. Sulforaphane (SFN), an antioxidant, was used to determine whether ROS regulated the PM2.5-induced expression of pro-inflammatory mediators. The PM2.5 from winter exhibited the highest potency in inducing cytotoxicity as well as the production of TNF-α and IL-1β from THP-1 cells; the same was true for ROS production. Further experiments demonstrated that pretreating THP-1 cells with SFN markedly mitigated the winter-PM2.5-induced release of TNF-α and IL-1β. Composition analysis revealed that the PM2.5 contained higher levels of anions (NO3 and SO42–) and water-soluble metals (Al, Ca, Mg, Zn and Cr) during summer and winter than spring and fall. In summary, PM2.5-induced oxidative stress and the subsequent production of pro-inflammatory mediators vary by season.

Keywords: PM2.5; THP-1 cells; Cytotoxicity; Oxidative stress; Inflammation.

Aerosol Air Qual. Res. 20:1686-1694. https://doi.org/10.4209/aaqr.2019.06.0288 

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