Autophagy　was　involved　in　vascular　endothelial　injury　caused　by　PM2.5,　which　aggravated　the　pathogenesis　of　cardiovascular　diseases.　However,　major　toxic　components　and　underlying　mechanism　responsible　for　PM2.5-　induced　autophagy　remain　unclear.　In　this　study,　the　effects　of　water-extracted　PM2.5　(WE-PM2.5)　on　autophagy　in　human　umbilical　vein　endothelial　cells　(HUVEC)　were　studied.　Our　results　showed　WE-PM2.5　promoted　autophagosome　initiation　and　formation,　meanwhile,　lysosomal　function　was　impaired,　which　further　caused　autophagic　flux　blockage　in　HUVEC　cells.　Furthermore,　removal　of　metals　alleviated　WE-PM2.5-induced　auto-phagic　flux　blockage,　while　the　artificial　metal　mixture　reproduced　the　WE-PM2.5　response.　Mechanistically,　ROS　regulated　autophagy-related　proteins　evidenced　by　BECN1,　LC3B　and　p62　expression　reversed　by　NAC　pre-treatment　in　WE-PM2.5-exposed　cells.　WE-PM2.5　also　increased　TXNIP　expression　mediated　by　ROS;　moreover,　knockdown　of　TXNIP　in　WE-PM2.5-exposed　cells　decreased　BECN1　and　LC3B　expression,　but　had　little　effects　on　the　expression　of　p62,　CTSB,　and　CTSD,　indicating　WE-PM2.5-induced　TXNIP　was　involved　in　autophagosome　initiation　and　formation　rather　than　autophagic　degradation.　Collectively,　WE-PM2.5-induced　ROS　not　only　promoted　autophagosome　initiation　and　formation,　but　also　inhibited　autophagic　degradation.　However,　as　the　downstream　molecule　of　ROS,　TXNIP　was　only　involved　in　autophagosome　initiation　and　formation.　Importantly,　WE-PM2.5-bound　metals　were　largely　responsible　for　autophagic　flux　blockage　in　HUVEC　cells.