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Seasonal Variations in PM2.5-induced Oxidative Stress and Up-regulation of Pro-inflammatory Mediators

Category: Air Pollution and Health Effects

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DOI: 10.4209/aaqr.2019.06.0288
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To 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., doi: 10.4209/aaqr.2019.06.0288.

Juan Li, Yingying Liu, Zhen An, Wen Li, Xiang Zeng, Huijun Li, Jing Jiang, Jie Song, Weidong Wu

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

Highlights

  • 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.

Abstract

Inhaled particulate matter with an aerodynamic diameter ≤ 2.5 μm (PM2.5) has been demonstrated to induce season-dependent adverse health effects. Given the critical role that inflammation and oxidative stress play in PM2.5-induced health effects, this study investigated whether PM2.5-induced oxidative stress and pro-inflammatory response varied with season using a human monocytic cell line, THP-1. PM2.5 was collected in April (spring), July (summer), September (fall) and December (winter) of 2014. Cytotoxicity was assessed by 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. Reactive oxygen species (ROS) were determined with flow cytometry. Sulforaphane (SFN), an antioxidant, was used to determine whether ROS regulated PM2.5-induced expression of pro-inflammatory mediators. It was shown that winter PM2.5 was more potent in inducing cytotoxicity than the PM2.5 from other seasons. Similarly, winter PM2.5 induced more production of TNF-α and IL-1β from THP-1 cells than other PM2.5 at the same dose. The same was true of ROS production. Further studies demonstrated that pretreatment of THP-1 cells with SFN markedly blunted the winter PM2.5-induced release of TNF-α and IL-1β. Composition analysis revealed that summer and winter PM2.5 contained higher levels of anion (NO3- and SO42-) and water-soluble metals (Al, Ca, Mg, Zn and Cr) than the PM2.5 from other seasons. In summary, PM2.5-induced oxidative stress and subsequent production of pro-inflammatory mediators varies with season.

Keywords

PM2.5 THP-1 cells Cytotoxicity Oxidative stress Inflammation


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