Proinflammatory and Cytotoxic Effects of Mexico City Air Pollution Particulate Matter in Vitro Are Dependent on Particle Size and Composition

Exposure to urban airborne particulate matter (PM) is associated with adverse health effects. We previously reported that the cytotoxic and proinflammatory effects of Mexico City PM10(≤ 10 μm mean aerodynamic diameter) are determined by transition metals and endotoxins associated with these particles. However, PM2.5(≤ 2.5 μm mean aerodynamic diameter) could be more important as a human health risk because this smaller PM has the potential to reach the distal lung after inhalation. In this study, we compared the cytotoxic and proinflammatory effects of Mexico City PM10with those of PM2.5using the murine monocytic J774A.1 cell line in vitro. PMs were collected from the northern zone or the southeastern zone of Mexico City. Elemental composition and bacterial endotoxin on PMs were measured. Tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) production by J774A.1 cells was measured in the presence or absence of recombinant endotoxin-neutralizing protein (rENP). Both northern and southeastern PMs contained endotoxin and a variety of transition metals. Southeastern PM10contained the highest endotoxin levels, 2-fold higher than that in northern PM10. Northern and southeastern PM2.5contained the lowest endotoxin levels. Accordingly, southeastern PM10was the most potent in causing secretion of the proinflammatory cytokines TNF-α and IL-6. All PM2.5and PM10samples caused cytotoxicity, but northern PMs were the most toxic, Cytokine secretion induced by southeastern PM10was reduced 50-75% by rENP. These results indicate major differences in PM10and PM2.5. PM2.5induces cytotoxicity in vitro through an endotoxin-independent mechanism that is likely mediated by transition metals. In contrast, PM10with relatively high levels of endotoxin induces proinflammatory cytokine release via an endotoxin-dependent mechanism.