Background: Chronic exposure to ambient polycyclic aromatic hydrocarbons (PAHs) is associated with asthma.
Objectives: We aimed to identify the main component of ambient PAHs in southern Taiwan and elucidate their role in allergic asthma.
Methods: One-year air samplings with measurement of 16 PAHs were performed. A mouse model of pulmonary allergic inflammation and its associated parameters were analyzed by established methods.
Results: Indeno[1,2,3-cd]pyrene (IP) was found to be a prominent PAH associated with ambient PM2.5 in a subtropical industrial city in Taiwan. IP exposure at the concentration ranging from 0.4 to 2 μM significantly enhanced antigen-induced allergic inflammation, including increased eosinophil infiltration, IL-4/IL-5 production and antigen-specific IgE level, which could be blocked by the addition of an AhR antagonist, CH223191, and was absent in dendritic cell (DC)-specific AhR-null mice. Mechanistically, IP treatment significantly altered DC’s function in vitro, including increased level of pro-inflammatory IL-6 secretion and decreased generation of anti-inflammatory IL-10. The IP’s effect was lost in DCs from mice carrying an AhR-mutant allele (AhRd).
Conclusion: Chronic exposure to IP, a prominent ambient PAH in southern Taiwan, enhanced the severity of allergic lung inflammation in mice through, at least in part, its ability in modulating the DC’s function in an AhR-dependent manner.