The　chemical　and　bioreactivity　properties　of　fine　particulate　matter　(PM2.5)　in　indoor　and　outdoor　environments　in　Xi＇an　were　characterized,　and　the　lung　function　of　various　participants　was　investigated.　The　concentrations　of　polycyclic　aromatic　hydrocarbons　(PAHs),　oxygenated　polycyclic　aromatic　hydrocarbons,　and　nitrated　polycyclic　aromatic　hydrocarbons　were　higher　in　outdoor　environments　than　in　indoor　environments;　in　addition,　urban　areas　had　higher　concentrations　of　these　compounds　than　did　suburban　areas,　with　fossil　fuel　combustion　likely　being　the　primary　source.　Moreover,　PM2.5-induced　inflammation　was　higher　in　urban　areas　than　in　suburban　areas.　Indoor　environments　with　coal　combustion　emissions　showed　relatively　higher　oxidative　potential　and　inflammation.　Moderate　(phenanthrene)　to　strong　(acenaphthylene　and　benzo(a)pyrene)　correlations　were　observed　between　selected　PAHs　against　interleukin　6　(IL-6),　8-hydroxy-desoxyguanosine　(8-OHdG),　and　necrosis　factor-α　(TNF-α).　Moreover,　9-fluorenone,　9,10-anthraquinone,　and　5,12-naphthacenequinone　exhibited　higher　oxidative　stress　and　inflammation　than　did　their　parent　PAHs.　Forced　vital　capacity　(FVC)　and　forced　expiratory　volume　in　1　s　(FEV1)　were　negatively　correlated　with　8-OHdG,　and　FEV1/FVC　was　negatively　correlated　with　TNF-α　and　IL-6.　These　findings—which　integrates　PM2.5　with　lung　function　and　bioreactivity　analyses—suggest　that　coal　burning,　especially　indoors,　could　elevate　the　cytotoxicity　of　PM2.5　to　the　occupants　and　that　chronic　exposure　may　lead　to　a　decline　in　lung　function.　©　2019　Elsevier　Ltd