In this study, we demonstrated that indeno[1,2,3-cd]pyrene (IP) was the major component of ambient PAHs in Kaohsiung City in Taiwan, and that IP exposure exacerbated antigen-induced pulmonary inflammation in a mouse model of asthma and the IP’s effect was, at least in part, mediated by its impact on DC’s function in an AhR-dependent manner. This evidence concerns the gene AHR and asthma.