The impact of extractable organic matter from gasoline and alternative fuel emissions on bronchial cell models (BEAS-2B, MucilAir™)
Language English Country Great Britain, England Media print-electronic
Document type Journal Article
PubMed
35066112
DOI
10.1016/j.tiv.2022.105316
PII: S0887-2333(22)00013-3
Knihovny.cz E-resources
- Keywords
- BEAS-2B, Ethanol blend fuels, Exposure, Extractable organic matter, MucilAir™,
- MeSH
- Gasoline * MeSH
- Bronchi cytology MeSH
- Cell Line MeSH
- Cytochrome P-450 CYP1A1 genetics MeSH
- Epithelial Cells drug effects metabolism MeSH
- Histones metabolism MeSH
- Interleukin-1alpha genetics MeSH
- Air Pollutants toxicity MeSH
- Humans MeSH
- Oxygenases genetics MeSH
- Particulate Matter toxicity MeSH
- Reactive Oxygen Species metabolism MeSH
- Gene Expression Regulation drug effects MeSH
- Tumor Necrosis Factor-alpha genetics MeSH
- Vehicle Emissions toxicity MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Gasoline * MeSH
- Cytochrome P-450 CYP1A1 MeSH
- dimethylaniline monooxygenase (N-oxide forming) MeSH Browser
- Histones MeSH
- IL1A protein, human MeSH Browser
- Interleukin-1alpha MeSH
- Air Pollutants MeSH
- Oxygenases MeSH
- Particulate Matter MeSH
- Reactive Oxygen Species MeSH
- TNF protein, human MeSH Browser
- Tumor Necrosis Factor-alpha MeSH
- Vehicle Emissions MeSH
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.
Department of Chemistry and Toxicology Veterinary Research Institute 621 00 Brno Czech Republic
Department of Computer Science Czech Technical University Prague 121 35 Prague Czech Republic
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