Pro-inflammatory effects of road wear particles and diesel exhaust particles in bronchial epithelial cells and macrophages.

Comparative studies on traffic-derived particulate matter (PM) from fuel combustion and non-exhaust sources are scarce. This study compares cytokine release (CXCL8, IL-1α, IL-1β, TNFα) and expression of genes linked to inflammation (CXCL8, IL1A, IL1B, COX2, IL6), xenobiotic metabolism (CYP1A1) and redox responses (HMOX1) in human bronchial epithelial cells (HBEC3-KT) and THP-1-derived macrophages after exposure to samples of tire and road wear particles (TRWP) and diesel exhaust particles (DEP). CH223191 was used to assess the involvement of the aryl hydrocarbon receptor (AhR) in the cytokine responses. The results show that TRWP and DEP induced pro-inflammatory responses in both cell types. Moreover, exposure to TRWP and DEP in combination enhanced the pro-inflammatory responses in HBEC3-KT. While the relative potency of TRWP differed between the cell types and endpoints, pro-inflammatory responses of similar or greater magnitude than DEP were observed. The AhR inhibitor CH223191 attenuated the particle-induced cytokine release in HBEC3-KT, but not in the THP-1-derived macrophages. In conclusion, TRWP and DEP induced pro-inflammatory responses in human bronchial epithelial cells and macrophage-like cells, acting through different mechanisms. Responses of a similar magnitude as DEP were observed after exposure to TRWP, showing that TRWP constitutes a potential health hazard. Moreover, the enhanced responses following exposure to TRWP and DEP in combination suggest that the interplay between PM components could be a contributing factor in PM-induced health effects.