Abstract

The aim of the present study was to investigate the effects of size-fractionated (i.e., <1; 1–2.5, and 2.5–10 µm in an aerodynamic diameter) ambient particulate matter (PM) on reactive oxygen species (ROS) activity and cell viability in human bronchial epithelial cells (BEAS-2B). The PM samples were collected from an urban site (uPM) in Beijing and a steel factory site (sPM) in Anshan, China, from March 2013 to December 2014. Metal elements, organic and elemental carbon, and water-soluble inorganic ions in the uPM and sPM were analyzed. The cell viability and ROS generation in PM-exposed BEAS-2B cells were measured by MTS and DCFH-DA. The results showed that both uPM and sPM caused a decrease in the cell viability and an increase in ROS generation. The level of ROS measured in sPM1.0 was approximately triple that in uPM1.0. The results of correlation analysis showed that the ROS activity and cytotoxicity were related to different PM composition. Moreover, deferoxamine (DFO) significantly prevented the increase of ROS generation and the decrease of cell viability. Taken together, our results suggest that the metals absorbed on PM induced oxidant radical generation in BEAS-2B cells that could lead to impairment of pulmonary function.

Highlights

  • In recent years, industrial emissions, urban construction, and increased vehicle exhausts led to poor air quality in many cities in China [1,2]

  • We found that different size-fractioned uPM and sPM caused a significant decrease in cell viability

  • We found that exposure to size-fractioned uPM and sPM led to a significant increase in intracellular reactive oxygen species (ROS) generation

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Summary

Introduction

Industrial emissions, urban construction, and increased vehicle exhausts led to poor air quality in many cities in China [1,2]. The adverse health effects of airborne particulate matters (PM) pollution have become a growing concern [1,3]. Numerous epidemiological studies have documented a positive correlation between exposure to ambient PM concentrations and increased respiratory and cardiovascular morbidity and mortality [4,5,6]. The size, shape, and chemical composition of PM play crucial roles in the adverse effects on human health. The penetration depth and deposition of PM in the lung are particle size dependent [10]. Particular attention has been paid to respirable fine particles. It has been reported that PM2.5–10 tend to deposit in the nasopharyngeal compartment, while PM2.5–1 and PM0.1 exhibit

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