The impact of extractable organic matter from gasoline and alternative fuel emissions on bronchial cell models (BEAS-2B, MucilAir™)

Toxicol In Vitro. 2022 Apr:80:105316. doi: 10.1016/j.tiv.2022.105316. Epub 2022 Jan 21.

Abstract

Air pollution caused by road traffic has an unfavorable impact on the environment and also on human health. It has previously been shown, that complete gasoline emissions lead to toxic effects in cell models originating from human airways. Here we focused on extractable organic matter (EOM) from particulate matter, collected from gasoline emissions from fuels with different ethanol content. We performed cytotoxicity evaluation, quantification of mucin and extracellular reactive oxygen species (ROS) production, DNA breaks detection, and selected gene deregulation analysis, after one and five days of exposure of human bronchial epithelial model (BEAS-2B) and a 3D model of the human airway (MucilAir™). Our data suggest that the longer exposure had more pronounced effects on the parameters of cytotoxicity and mucin production, while the impacts on ROS generation and DNA integrity were limited. In both cell models the expression of CYP1A1 was induced, regardless of the exposure period or EOM tested. Several other genes, including FMO2, IL1A, or TNF, were deregulated depending on the exposure time. In conclusion, ethanol content in the fuels did not significantly impact the toxicity of EOM. Biological effects were mostly linked to xenobiotics metabolism and inflammatory response. BEAS-2B cells were more sensitive to the treatment.

Keywords: BEAS-2B; Ethanol blend fuels; Exposure; Extractable organic matter; MucilAir™.

MeSH terms

  • Air Pollutants / toxicity*
  • Bronchi / cytology*
  • Cell Line
  • Cytochrome P-450 CYP1A1 / genetics
  • Epithelial Cells / drug effects*
  • Epithelial Cells / metabolism
  • Gasoline*
  • Gene Expression Regulation / drug effects
  • Histones / metabolism
  • Humans
  • Interleukin-1alpha / genetics
  • Oxygenases / genetics
  • Particulate Matter / toxicity*
  • Reactive Oxygen Species / metabolism
  • Tumor Necrosis Factor-alpha / genetics
  • Vehicle Emissions / toxicity*

Substances

  • Air Pollutants
  • Gasoline
  • Histones
  • IL1A protein, human
  • Interleukin-1alpha
  • Particulate Matter
  • Reactive Oxygen Species
  • TNF protein, human
  • Tumor Necrosis Factor-alpha
  • Vehicle Emissions
  • Oxygenases
  • dimethylaniline monooxygenase (N-oxide forming)
  • Cytochrome P-450 CYP1A1