Alveolar macrophage reaction to PM2.5 of hazy day in vitro: Evaluation methods and mitochondrial screening to determine mechanisms of biological effect

Hazy weather in China has recently become a major public health concern due to high levels of atmospheric fine particulate matter (PM2.5) with a large amount of polycyclic aromatic hydrocarbon (PAHs). In this study, the mass concentration of PAHs in hazy PM2.5 in urban Taiyuan city, China was determined and toxicities of different dosage of the hazy PM2.5 on rat alveolar macrophages (AMs) were examined. It was found that the hazy PM2.5, bounded with many species of PAHs (CHR, BbF, BaP, BaA, and etc.), significantly increased cellular malondialdehyde (MDA) content followed by the decreasing in superoxide (SOD) and glutathione peroxidase (GPx) in AMs. They induced mitochondrial changes in ultrastructure as evidenced by mitochondrial swelling and cristae disorganization, and a dose-dependent decrease in mitochondrial profile density. Also, the mRNA expression levels of mitochondrial fusion-related genes were modified. The Mfn1 and Mfn2 which are essential for mitochondrial fusion increased significantly in hazy PM2.5-treated group compared to the control in a dose dependent manner, OPAL was significantly increased at the highest PM2.5 dose delivered. These findings suggested that exposure to hazy PM2.5 could activate oxidative stress pathways in AMs, resulting in abnormal mitochondrial morphology and fusion/fission frequency. Possibly, the toxic effects were mostly attributed to the high burden of varied PAHs in hazy PM2.5.