The toxicity of ambient fine particulate matter (PM2.5) to vascular endothelial cells

Several epidemiologic and toxicological studies have widely regarded ambient fine particulate matter (PM2.5), the particles with an aerodynamic diameter less than 2.5 mu m, as a strong potential threat to human health. PM2.5 exposure is mainly through the respiratory tract where it can permeate the lung alveoli and enter the blood circulation. After going into the circulation, PM2.5 directly confronts the vascular endothelial cells (VECs). The VECs, which are lined up in the innermost layer of the blood vessels, are essential in the homeostasis of physiological processes. Thus, the damage and dysfunction of VECs is a common cause of various diseases. In this review, we summarize the toxicity of PM2.5 to VECs including the pathophysiological mechanism and the effects of VEC-mediated physiological functions. The review has discussed the association of impaired VEC function by PM2.5 with various diseases, indicating that the VECs may be an effective assessment of public health recommendations under PM2.5 exposure. Therefore, reducing the adverse effect of PM2.5 on VECs will prevent the potential occurrence and fatality of the relevant diseases in the future.

Automated summary

The environmental fine particulate matter PM2.5 is considered a significant threat to human health, particularly through its impact on vascular endothelial cells (VECs). Understanding and reducing the toxic effects of PM2.5 on VECs could help prevent the occurrence and fatality of various diseases.