Air pollution might have a great impact on pulmonary health, but biological evidence in response to particulate matter less than 2.5μm in size (PM2.5) has been lacking. Physicochemical characterization of haze PM2.5 collected from Beijing, Xian and Hong Kong was performed. Biological pathways were identified by proteomic profiling in mouse lungs, suggesting that WNT/β-catenin is important in the response to haze PM2.5. Suppression of β-catenin levels, activation of caspase-3 and alveolar destruction, as well as IL-6, TNF-α and IFN-γ production, were observed in the lungs. The inhibition of β-catenin, TCF4 and cyclin D1 was observed invitro in response to haze PM2.5. The inhibition of WNT/β-catenin signaling, apoptosis-related results (caspase-3 and alveolar destruction), and inflammation, particularly including caspase-3 and alveolar destruction, were more highly associated with polycyclic aromatic hydrocarbons in haze PM2.5. In conclusion, decreased WNT/β-catenin expression modulated by haze PM2.5 could be involved in alveolar destruction and inflammation during haze episodes.

Original languageEnglish
Pages (from-to)118-129
Number of pages12
JournalAtmospheric Environment
Publication statusPublished - May 1 2015


  • Air pollution
  • Apoptosis
  • Metal
  • Particulate matter
  • Polycyclic aromatic hydrocarbons
  • β-catenin

ASJC Scopus subject areas

  • General Environmental Science
  • Atmospheric Science


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