Epidemiological　studies　have　associated　high　levels　of　airborne　particulate　matter　(PM)　with　increased　respiratory　diseases.　In　order　to　investigate　the　mechanisms　of　air　pollution-induced　lung　toxicity　in　humans,　human　bronchial　epithelial　cells　(16HBE)　were　exposed　to　various　concentrations　of　particles　smaller　than　2.5　mu　m　(PM2.5)　collected　from　Beijing,　China.　After　observing　that　PM2.5　decreased　cell　viability　in　a　dose-dependent　manner,　we　first　used　Illumina　RNA-seq　to　identify　genes　and　pathways　that　may　contribute　to　PM2.5-induced　toxicity　to　16HBE　cells.　A　total　of　539　genes,　283　up-regulated　and　256　down-regulated,　were　identified　to　be　significantly　differentially　expressed　after　exposure　to　25　mu　g/cm(2)　PM2.5.　PM2.5　induced　a　large　number　of　genes　involved　in　responses　to　xenobtiotic　stimuli,　metabolic　response,　and　inflammatory　and　immune　response　pathways　such　as　MAPK　signaling　and　cytokine-cytokine　receptor　interaction,　which　might　contribute　to　PM2.5-related　pulmonary　diseases.　We　then　confirmed　our　RNA-seq　results　by　qPCR　and　by　analysis　of　IL-6,　CYP1A1,　and　IL-8　protein　expression.　Finally,　ELISA　assay　demonstrated　a　significant　association　between　exposure　to　PM2.5　and　secretion　of　IL-6.　This　research　provides　a　new　insight　into　the　mechanisms　underlying　PM2.5-induced　respiratory　diseases　in　Beijing.