Toxicity of aircraft engine emissions in Calu-3 human cells in air-liquid interface condition

Particulate Matter (PM) emissions from aircraft engines adversely affect air quality around airports, contributing to public health concerns for airport workers and neighbouring communities. In this research, PM was collected from the exhaust of turbine engine after combustion of various types of aircraft fuels, including conventional fuel types Jet A and Jet A1, and more sustainable alternatives with relative low levels of aromatics. PM samples’ toxicity was studied in vitro by air-liquid interface (ALI) exposure of Calu-3 cells in monoculture and co-culture with macrophages (differentiated THP-1 cells). Cells were exposed to PM suspensions (250 µg/mL) using a cloud-based ALI exposure system and analysed 24-hours after exposure. DNA damage was detected through Comet assay in cells exposed to Jet A and Jet A1 samples in absence of cytotoxicity; co-incubation with endonucleases-III and formamidopyrimidine-DNA glycosylase showed that this was not associated with oxidation of DNA bases. Real-Time PCR was performed to investigate the expression profile of genes involved in oxidative stress and DNA repair pathways. Heme Oxygenase 1 gene, Mucin 5AC, and Angiotensin-Converting Enzyme 2 were modulated in the same samples where DNA damage was present. No differences were shown in the pro-inflammatory interleukine-8 secretion among the samples. Most of the PM samples generated using jet fuel with high content of aromatic compounds induced enhanced genotoxicity, suggesting that strategies lowering aromatic content may also result in less toxic PM emissions. Funded by Horizon2020 – Research of Aviation PM Technologies, mOdelling and Regulation (RAPTOR), grant number 863969.