Vitamin C attenuates low-level PM_2.5 exposure-induced lung inflammation and mitochondrial loss

Prolonged exposure to PM_2.5 is recognised as a significant risk factor for the development of chronic pulmonary diseases, and was first recognised in countries with high levels of air pollution (e.g. as occurs in Asia). However, it is important to note that there is no safe level of PM_2.5. As such, the detrimental effects on the lungs caused by low levels of PM_2.5, as found in Europe and North America, are often overlooked. The objective of this study was to determine how a low level of PM_2.5 exposure affects lung integrity. Male mice (Balb/c, 6 weeks of age) were subjected to daily exposure to 5 μg/ml PM_2.5 (nasal installation) with or without the supplement of vitamin C (VC) in drinking water (1.5 g/L), while those in the sham group received saline exposure. The addition of VC effectively prevented the elevation of total reactive oxygen species (ROS), mitochondrial ROS, and inflammation induced by PM_2.5 exposure. Furthermore, in-vitro studies showed that PM_2.5 reduced the cell viability of human epithelial cells (BEAS-2B cells), while increasing their susceptibility to oxidative stress-induced cell injury and inflammatory responses. The pre-treatment with VC significantly mitigated the adverse effects of PM_2.5 exposure on cell viability, inflammatory response, mitochondrial ROS levels, and mitochondrial loss in BEAS-2B cells. These findings suggest that daily exposure to a low level of PM_2.5 possesses adverse effects on lung health through inflammatory response and oxidative stress-induced mitochondrial loss. VC supplement can effectively protect the lungs from the adverse effects of low-level PM_2.5 exposure.