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Commun Biol. 2019 Mar 5;2:90. doi: 10.1038/s42003-019-0332-7. eCollection 2019.

Non-volatile particle emissions from aircraft turbine engines at ground-idle induce oxidative stress in bronchial cells.

Author information

1
1Institute of Anatomy, University of Bern, 3012 Bern, Switzerland.
2
2Institute of Aerosol and Sensor Technology, Swiss University of Applied Sciences and Arts Northwestern Switzerland, 5210 Windisch, Switzerland.
3
Empa, Swiss Federal Laboratories for Materials Science and Technology, Laboratory for Advanced Analytical Technologies, 8600 Dübendorf, Switzerland.
4
6Present Address: Laboratory of Atmospheric Chemistry, Paul Scherrer Institute, 5232 Villigen, Switzerland.
5
SR Technics, 8302 Kloten, Switzerland.
6
7Present Address: Centre for Aviation, School of Engineering, Zurich University of Applied Sciences, 8401 Winterthur, Switzerland.
7
Present Address: Empa, Swiss Federal Laboratories for Materials Science and Technology, Automotive Powertrain Technologies Laboratory, 8600 Dübendorf, Switzerland.
8
Empa, Swiss Federal Laboratories for Materials Science and Technology, Automotive Powertrain Technologies Laboratory, 8600 Dübendorf, Switzerland.

Abstract

Aircraft emissions contribute to local and global air pollution. Health effects of particulate matter (PM) from aircraft engines are largely unknown, since controlled cell exposures at relevant conditions are challenging. We examined the toxicity of non-volatile PM (nvPM) emissions from a CFM56-7B26 turbofan, the world's most used aircraft turbine using an unprecedented exposure setup. We combined direct turbine-exhaust sampling under realistic engine operating conditions and the Nano-Aerosol Chamber for In vitro Toxicity to deposit particles onto air-liquid-interface cultures of human bronchial epithelial cells (BEAS-2B) at physiological conditions. We evaluated acute cellular responses after 1-h exposures to diluted exhaust from conventional or alternative fuel combustion. We show that single, short-term exposures to nvPM impair bronchial epithelial cells, and PM from conventional fuel at ground-idle conditions is the most hazardous. Electron microscopy of soot reveals varying reactivity matching the observed cellular responses. Stronger responses at lower mass concentrations suggest that additional metrics are necessary to evaluate health risks of this increasingly important emission source.

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