Exposure　to　ambient　fine　particulate　matter　(＜2.5　mu　m;　PM2.5)　increases　the　risk　of　the　physiopathology　of　vascular　diseases.　However,　the　underlying　mechanism,　particularly　the　mitochondrial　damage　mechanism,　of　PM2.5-induced　vascular　dysfunction　is　still　unclear.　In　this　study,　we　examined　PM2.5-induced　alterations　of　mitochondrial　morphology,　and　further　demonstrated　the　adverse　effects　on　mitochondrial　dynamics　and　function　in　vascular　endothelial　cells.　Consequently,　cultured　EA.hy926　cells　were　subjected　to　PM2.5　collected　from　Beijing.　A　Cell　Counting　Assay　Kit-8　demonstrated　that　PM2.5　exposure　decreased　the　proliferation　of　EA.hy926　cells　in　a　dose-dependent　manner.　The　exposure　caused　an　increment　of　abnormal　mitochondria　coupled　with　the　decrease　of　fusion　protein　MFN2　and　the　increase　of　fission　protein　FIS1,　suggesting　that　PM2.5　inhibits　mitochondrial　fusion.　Further　analyses　revealed　PM2.5　decreased　the　mitochondrial　membrane　potential　(Delta　psi　m)　and　increased　the　mitochondrial　permeability　transport　pore　opening,　eventually　resulting　in　impairments　in　adenosine　triphosphate　synthesis.　Therefore,　it　is　clearly　shown　that　PM2.5　triggered　endothelial　toxicity　through　mitochondria　as　the　target,　including　the　damage　of　mitochondrial　homeostasis.