Transcriptional response to organic compounds from diverse gasoline and biogasoline fuel emissions in human lung cells

Toxicol In Vitro. 2018 Apr:48:329-341. doi: 10.1016/j.tiv.2018.02.002. Epub 2018 Feb 9.


Modern vehicles equipped with Gasoline Direct Injection (GDI) engine have emerged as an important source of particulate emissions potentially harmful to human health. We collected and characterized gasoline exhaust particles (GEPs) produced by neat gasoline fuel (E0) and its blends with 15% ethanol (E15), 25% n-butanol (n-But25) and 25% isobutanol (i-But25). To study the toxic effects of organic compounds extracted from GEPs, we analyzed gene expression profiles in human lung BEAS-2B cells. Despite the lowest GEP mass, n-But25 extract contained the highest concentration of polycyclic aromatic hydrocarbons (PAHs), while i-But25 extract the lowest. Gene expression analysis identified activation of the DNA damage response and other subsequent events (cell cycle arrest, modulation of extracellular matrix, cell adhesion, inhibition of cholesterol biosynthesis) following 4 h exposure to all GEP extracts. The i-But25 extract induced the most distinctive gene expression pattern particularly after 24 h exposure. Whereas E0, E15 and n-But25 extract treatments resulted in persistent stress signaling including DNA damage response, MAPK signaling, oxidative stress, metabolism of PAHs or pro-inflammatory response, i-But25 induced changes related to the metabolism of the cellular nutrients required for cell recovery. Our results indicate that i-But25 extract possessed the weakest genotoxic potency possibly due to the low PAH content.

Keywords: Alternative fuels; DNA damage response; Gasoline exhaust particles; Gene expression profiling; Organic extracts.

MeSH terms

  • Air Pollutants / analysis
  • Air Pollutants / toxicity*
  • Biofuels / analysis
  • Biofuels / toxicity*
  • Butanols / analysis
  • Butanols / toxicity
  • Cell Line
  • DNA Damage
  • Ethanol / chemistry
  • Gasoline / analysis
  • Gasoline / toxicity*
  • Gene Expression Profiling
  • Humans
  • Inflammation / chemically induced
  • Inflammation / pathology
  • Lung / drug effects*
  • Lung / pathology
  • MAP Kinase Signaling System / drug effects
  • Organic Chemicals / chemistry
  • Organic Chemicals / toxicity*
  • Oxidative Stress / drug effects
  • Particulate Matter / toxicity
  • Polycyclic Aromatic Hydrocarbons / analysis
  • Polycyclic Aromatic Hydrocarbons / toxicity
  • Transcription, Genetic / drug effects*
  • Vehicle Emissions / analysis
  • Vehicle Emissions / toxicity*


  • Air Pollutants
  • Biofuels
  • Butanols
  • Gasoline
  • Organic Chemicals
  • Particulate Matter
  • Polycyclic Aromatic Hydrocarbons
  • Vehicle Emissions
  • Ethanol