Abstract
Air pollution affects the majority of the world's population and has been linked to over 7 million premature deaths per year. Exposure to particulate matter (PM) contained within air pollution is associated with cardiovascular, respiratory, and neurological ill health. There is increasing evidence that exposure to air pollution in utero and in early childhood is associated with altered brain development. However, the underlying mechanisms for impaired brain development are not clear. While oxidative stress and neuroinflammation are documented consequences of PM exposure, cell-specific mechanisms that may be triggered in response to air pollution exposure are less well defined. Here, we assess the effect of urban PM exposure on two different cell types, microglial-like BV2 cells and neural stem/precursor-like C17.2 cells. We found that, contrary to expectations, immature C17.2 cells were more resistant to PM-mediated oxidative stress and cell death than BV2 cells. PM exposure resulted in decreased mitochondrial health and increased mitochondrial ROS in BV2 cells which could be prevented by MitoTEMPO antioxidant treatment. Our data suggest that not only is mitochondrial dysfunction a key trigger in PM-mediated cytotoxicity but that such deleterious effects may also depend on cell type and maturity.