Abstract
The association between PM2.5 (particulate matter ≤ 2.5 µm) short-term exposure and its health effect is non-linear from the epidemiological studies. And this nonlinearity is suggested to be related with the PM2.5 heterogeneity, however, the underlying biological mechanism is still unclear. Here, a total of 38 PM2.5 filters were collected continuously for three weeks in winter Beijing, with the ambient PM2.5 varying between 10 and 270 µg/m3. Human monocytes-derived macrophages (THP-1) were treated with PM2.5 water-soluble elutes at 10 µg/mL to investigate the PM2.5 short-term exposure effect from a proinflammatory perspective. The proinflammatory cytokine tumor necrosis factor (TNF) induced by the PM2.5 elutes at equal concentrations were unequal, showing the heterogeneity of PM2.5 proinflammatory potentials. Of the various chemical and biological components, lipopolysaccharide (LPS) showed a strong positive association with the TNF heterogeneity. However, some outliers were observed among the TNF-LPS association. Specifically, for PM2.5 from relatively clean air episodes, the higher LPS amount corresponded to relatively low TNF levels. And this phenomenon was also observed in the promotion tests by treating macrophages with PM2.5 elutes dosed with additional trace LPS. Gene expression analysis indicated the involvement of oxidative-stress related genes in the LPS signaling pathway. Therefore, a potential oxidative-stress-mediated suppression on the PM2.5-borne LPS proinflammatory effect was proposed to be accounted for the outliers. Overall, the results showed the differential role of LPS in the heterogeneity of PM2.5 proinflammatory effects from a component-based perspective. Future experimental studies are needed to elucidate the signaling pathway of LPS attached on PM2.5 from different air quality episodes.
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