A growing number of epidemiological surveys show that PM2.5 is an important promoter for the cardiovascular dysfunction induced by atmospheric pollution. PM2.5 is a complex mixture of solid and liquid airborne particles and its components determine the health risk of PM2.5to a great extent. However, the individual cardiotoxicities of different PM2.5 fractions are still unclear, especially in the cellular level. Here we used the neonatal rat cardiomyocytes (NRCMs) to evaluate the cardiac toxicity of PM2.5 exposure. The cytotoxicities of Total-PM2.5, water soluble components of PM2.5 (WS-PM2.5) and water insoluble components of PM2.5 (WIS-PM2.5), which include the cell viability, cell membrane damage, reactive oxygen species (ROS) generation, were examined with NRCMs in vitro. The results indicated that Total-PM2.5 or WIS-PM2.5 exposure significantly decreased the cell viability, induced the cell membrane damage and increased the ROS level in NRCMs at concentrations above 50 µg/mL. However, WS-PM2.5 exposure could induce the cytotoxicity on NRCMs until the concentration of WS-PM2.5 was raised to a higher concentration (75 µg/mL). Furthermore, the DNA damage was detected in NRCMs after 48 h of exposure with Total-PM2.5, WS-PM2.5 or WIS-PM2.5 (75 µg/mL) and the adverse effects on mitochondrial function and action potentials of NRCMs were detected only both in the Total-PM2.5 and WIS-PM2.5 treatment group. In summary, our project not only estimates the risk of PM2.5 on cardiac cells but also reveal that Total-PM2.5 and WIS-PM2.5 exposure were predominantly associated with the functional cardiotoxicities in NRCMs.
Keywords: Cardiac cell; Cardiotoxicity; Chemical composition; Mitochondria; PM(2.5).
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