Inhalation of subway fine particles induces murine extrapulmonary organs damage.

Because of its speed and convenience, the subway has become the first choice for travel by many residents. However, the concentration of fine particles (PM2.5) in the air of a subway platform is higher than that of the ground level or carriage. Moreover, the composition and source of subway PM2.5 differ from those of atmospheric PM2.5. Currently, there is insufficient research on the impact of subway PM2.5 on health. In this study, intratracheally subway PM2.5-inoculated wild type (WT) and Rag1-/- mice, lacking functional T cells and B cells, were used to investigate the potential of subway PM2.5 exposure to cause extrapulmonary organ injuries. Subway PM2.5 increased inflammatory cells infiltration, tumor necrosis factor (TNF)-α, interleukin (IL)-6, as well as monocyte chemotactic protein (MCP)-1 gene and protein expression, cyclooxygenase-2 (COX-2) induction, and Toll-like receptor (TLR)-2, TLR4, myeloid differentiation factor 88 (MyD88), and nuclear factor (NF)-κB levels in liver, kidney, spleen, and thymus in a dose-dependent fashion in WT mice. Subway PM2.5 exposure resulted in slight macrophage (F4/80+) and neutrophil (Ly6G+) infiltration and caused no increase in the protein levels of TNF-α, IL-6, MCP-1, or COX-2 in the liver, kidneys, spleen, and thymus of Rag1-/- mice. These results demonstrate a dose-response manner between subway PM2.5 exposure and inflammatory injuries of extrapulmonary organs, which could be related to the TLR/MyD88/NF-κB signaling pathway. Subway PM2.5-induced extrapulmonary organ damage was dependent on T cells and B cells; this finding may provide insight for research on the mechanisms responsible for the health hazards posed by air pollution.