PM2.5-bound nitrated and oxygenated PAHs induced lipid metabolism disorder through different target organs.

Exposure to fine particulate matter (PM2.5) in the atmosphere associated with the onset and progression of cardiovascular and metabolic diseases in humans, with particular attention focused on the role of lipid metabolism. Research indicated that organic components of polycyclic aromatic hydrocarbons (PACs) attached to PM2.5 may significantly contribute to its toxicity, with nitrated and oxidized polycyclic aromatic hydrocarbons (NPAHs and OPAHs) representing two important derivative classes. The in vitro and in vivo experiments exposure to PM2.5-bound 3-nitrobenzoanthrone (3-NBA) and benzanthrone (BZO) were conducted to investigate the effects of NPAHs and OPAHs on lipid metabolism and the potential mechanisms. Key findings indicated that 3-NBA may induce vascular cell dysfunction, alter lipid levels in vivo, and cause oxidative damage, thereby participating in atherosclerotic plaque formation and potentially increasing cardiovascular disease risk. Conversely, BZO primarily caused liver damage by disrupting hepatocyte function. The accumulation of lipid peroxides and associated lipid metabolism disorders may promote fatty liver formation while also potentially increasing atherosclerosis risk. This study suggested that NPAHs and OPAHs may influence lipid metabolism through distinct molecular mechanisms acting on different target organs, thereby contributing to the development of related diseases. These findings provided scientific reference for comprehensively evaluating the health risks of polycyclic aromatic hydrocarbon pollutants.