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Sci Total Environ. 2018 Nov 1;640-641:997-1003. doi: 10.1016/j.scitotenv.2018.05.382. Epub 2018 Jun 5.

Pro-inflammatory responses to PM0.25 from airport and urban traffic emissions.

Author information

1
National Institute for Public Health and the Environment (RIVM), P.O. Box, 2720 BA Bilthoven, the Netherlands; Institute for Risk Assessment Sciences, Utrecht University, P.O. Box 80178, 3508 TD Utrecht, the Netherlands.
2
University of Southern California, Department of Civil and Environmental Engineering, 3620 S Vermont Ave, Los Angeles, CA 90089, USA.
3
National Institute for Public Health and the Environment (RIVM), P.O. Box, 2720 BA Bilthoven, the Netherlands.
4
National Institute for Public Health and the Environment (RIVM), P.O. Box, 2720 BA Bilthoven, the Netherlands; Institute for Risk Assessment Sciences, Utrecht University, P.O. Box 80178, 3508 TD Utrecht, the Netherlands. Electronic address: flemming.cassee@rivm.nl.

Abstract

Air traffic is rapidly growing, raising concerns about the air pollution in the surroundings of airports and its impact on public health. However, little is known about the impact of air pollution sources on air quality and health in the vicinity of airports. In this study, the sources and adverse health effects of airport-related particulate matter (PM) were investigated and compared to those of urban traffic emissions. Ambient 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 particle chemical composition, oxidative potential (OP) (ascorbic acid (AA), and electron spin resonance (ESR) assay) as well as their reactive oxygen species (ROS) activity, inflammatory potential (interleukin (IL) 6 and 8 and tumor necrosis factor (TNF)-α) 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 the USC samples were more complex, including traffic emissions, suspended road and soil dust, and secondary aerosols. The traffic-related transition metals (Fe and Cu) in LAX and USC samples mainly affected OP values of particles, while multiple factors such as composition, 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 cell recovery period, with LAX particles being more potent. Our results demonstrated considerable toxicity of airport-related particles, even at low exposure concentrations, suggesting that airport emission as source of PM0.25 may also contribute to the adverse effects on public health attributable to PM. The potency of such particles is in the same range as those collected at a site in urban area impacted heavily by traffic emissions.

KEYWORDS:

Aviation emission; Oxidative potential; PM(0.25); Pro-inflammation; Traffic emission

PMID:
30021333
DOI:
10.1016/j.scitotenv.2018.05.382
[Indexed for MEDLINE]

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