Ultrafine particle libraries for exploring mechanisms of PM2.5-induced toxicity in human cells

• Published in: Ecotoxicology and environmental safety 2018-08, Vol.157, p.380-387
• Main Authors: Bai, Xue, Liu, Yin, Wang, Shenqing, Liu, Chang, Liu, Fang, Su, Gaoxing, Peng, Xiaowu, Yuan, Chungang, Jiang, Yiguo, Yan, Bing
• Format: Article
• Language: English
• Subjects: Haze particle; Lung disease; Smog; Toxicity mechanism; Ultrafine particle library
• ISSN: 0147-6513; 1090-2414
• DOI: 10.1016/j.ecoenv.2018.03.095

Air pollution worldwide, especially in China and India, has caused serious health issues. Because PM2.5 particles consist of solid particles of diverse properties with payloads of inorganic, organic and biological pollutants, it is still not known what the major toxic components are and how these components induce toxicities. To explore this complex issue, we apply reductionism principle and an ultrafine particle library approach in this work. From investigation of 63 diversely functionalized ultrafine particles (FUPs) with adsorbed key pollutants, our findings indicate that 1) only certain pollutants in the payloads of PM2.5 are responsible for causing cellular oxidative stress, cell apoptosis, and cytotoxicity while the particle carriers are much less toxic; 2) pollutant-induced cellular oxidative stress and oxidative stress-triggered apoptosis are identified as one of the dominant mechanisms for PM2.5-induced cytotoxicity; 3) each specific toxic component on PM2.5 (such as As, Pb, Cr or BaP) mainly affects its specific target organ(s) and, adding together, these pollutants may cause synergistic or just additive effects. Our findings demonstrate that reductionism concept and model PM2.5 particle library approach are very effective in our endeavor to search for a better understanding of PM2.5-induced health effects. •Payloads of PM2.5 particles are responsible for cytotoxicity.•Pollutants on PM2.5 cause synergistic toxicity.•Pollutants on PM2.5 induce cytotoxicity in an organ-dependent manner.•A major toxicity mechanism from PM2.5 is ROS-induced cell apoptosis.