Significance This report reveals a mechanism by which cigarette smoke (CS) could exacerbate local inflammatory disease. CS is a key environmental pollutant affecting millions of people globally and continues to be of considerable interest to the biomedical communities. We found that CS activates the AhR on Th17 cells, leading to the up-regulation of miR-132 , which is then packaged into extracellular vesicles that induce osteoclastogenesis via the suppression of Cox2 that catalyzes prostaglandins. Clinically, rheumatoid arthritis (RA) patients who smoke express a higher level of miRNA-132 compared to nonsmoking RA patients. This finding not only reveals a mechanism of CS signaling but also may provide a potential target for therapeutic intervention for inflammatory disease in general and RA in particular.