Pro-inflammatory responses to PM$_{0.25}$ from airport and urban traffic emissions

Airport particulate matter (PM) emissions are the known source of air pollution in the proximity of an airport. Often large airports are located near metropolises, and airport emissions may have a potentially considerable impact on public health in the surrounding urban areas. However, little is known about the sources that are relevant to air quality and health in the vicinity of airports. Therefore, the effect of the chemical composition of airport-related PM on adverse health risks was investigated in comparison to urban traffic emissions. PM0.25 were collected at the Los Angeles International Airport (LAX) and at a central Los Angeles site (USC campus), along with PM2.5 collected directly from turbine and diesel engines. The chemical composition, oxidative potential (OP) of particles as well as the reactive oxygen species (ROS) activity, inflammatory potential (IL 6, IL 8 and TNF–α) release and cytotoxicity on human bronchial epithelial (16HBE) cells were assessed. Chemical composition measurements confirmed that aircraft emissions were the major source to LAX PM0.25, while the sources of USC samples were more complex, including traffic emissions, suspended road and soil dust, and secondary sulfate. The traffic-related transition metals (Fe and Cu) in LAX and USC samples mainly affected OP values of particles, while multiple factors such as compositions, size distribution and internalized amount of particles contributed to the promotion of ROS generation in 16HBE cells during 4 h exposure. Internalized particles in cells might also play an important role in activating inflammatory responses during 20 h recovery period, with LAX particles being more potent. Our results demonstrate considerable toxicity of airport-related particles, even at low exposure concentrations, which suggests that airport emission as source of PM0.25 may also contribute to the adverse effects on public health attributable to PM.