The　purpose　of　this　study　was　to　examine　the　direct　toxicity　of　PM2.5　collected　from　Beijing　on　human　umbilical　vein　endothelial　cells　(HUVEC).　A　Cell　Counting　Kit　8　(CCK8)　assay　demonstrated　that　PM2.5　exposure　decreased　the　proliferation　of　HUVECs　in　a　dose-dependent　manner.　We　also　found　that　PM2.5　exposure　induced　autophagy　in　HUVECs,　as　evidenced　by:　(1)　an　increased　number　of　double-membrane　vesicles;　(2)　enhanced　conversion　and　punctuation　of　the　microtubule-associated　protein　light　chain　3　(LC3);　and　(3)　decreased　levels　of　the　selective　autophagy　substrate　p62　in　a　time-dependent　manner.　Furthermore,　promoting　autophagy　in　PM2.5-exposed　HUVECs　with　rapamycin　increased　the　cell　survival　rate,　whereas　inhibiting　autophagy　via　3-methyladenine　significantly　decreased　cell　survival.　These　results　demonstrate　that　PM2.5　exposure　can　induce　cytotoxicity　and　autophagy　in　HUVECs　and　that　autophagy　play　a　protective　role　against　PM2.5-induced　cytotoxicity.　The　findings　of　the　present　study　imply　a　direct　toxic　effect　of　PM2.5　on　HUVECs　and　provide　novel　insight　into　the　mechanism　of　cardiovascular　diseases　caused　by　PM2.5　exposure.　(C)　2017　The　Research　Center　for　Eco-Environmental　Sciences,　Chinese　Academy　of　Sciences.　Published　by　Elsevier　B.V.