Transcription profiles in BEAS-2B cells exposed to organic extracts from particulate emissions produced by a port-fuel injection vehicle, fueled with conventional fossil gasoline and gasoline-ethanol blend

https://doi.org/10.1016/j.mrgentox.2021.503414Get rights and content
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Highlights

  • Port-fuel injection engines are non-negligible sources of particulate matter (PM).

  • The PM organic extracts of gasoline (E0) and its ethanol blend (E15) were compared.

  • The level of polycyclic aromatic hydrocarbons (PAHs) was much higher in E15 extract.

  • Both extracts induced toxic effects in BEAS-2B cells associated with PAH exposure.

  • E15 extract modulated various genes and pathways related to cancer development.

Abstract

Emissions from road traffic are among the major contributors to air pollution worldwide and represent a serious environmental health risk. Although traffic-related pollution has been most commonly associated with diesel engines, increasing evidence suggests that gasoline engines also produce a considerable amount of potentially hazardous particulate matter (PM). The primary objective of this study was to compare the intrinsic toxic properties of the organic components of PM, generated by a conventional gasoline engine fueled with neat gasoline (E0), or gasoline-ethanol blend (15 % ethanol, v/v, E15). Our results showed that while E15 has produced, compared to gasoline and per kg of fuel, comparable particle mass (μg PM/kg fuel) and slightly more particles by number, the organic extract from the particulate matter produced by E15 contained a larger amount of harmful polycyclic aromatic hydrocarbons (PAHs), as determined by the chemical analysis. To examine the toxicity, we monitored genome-wide gene expression changes in human lung BEAS-2B cells, exposed for 4 h and 24 h to a subtoxic dose of each PM extract. After 4 h exposure, numerous dysregulated genes and processes such as oxidative stress, lipid and steroid metabolism, PPARα signaling and immune response, were found to be common for both extract treatments. On the other hand, 24 h exposure resulted in more distinctive gene expression patterns. Although we identified several common modulated processes indicating the metabolism of PAHs and activation of aryl hydrocarbon receptor (AhR), E15 specifically dysregulated a variety of other genes and pathways related to cancer promotion and progression. Overall, our findings suggest that the ethanol addition to gasoline changed the intrinsic properties of PM emissions and increased the PAH content in PM organic extract, thus contributing to a more extensive toxic response particularly after 24 h exposure in BEAS-2B cells.

Abbreviations

AhR
aryl hydrocarbon receptor
CVS
constant volume sampler
DEP
diesel exhaust particles
DMSO
dimethyl sulfoxide
E0
neat gasoline fuel
E15
blend of gasoline and 15 % ethanol
ECM
extracellular matrix
GDI
gasoline direct injection
HPLC/DAD
high-performance liquid chromatography with a diode-array detector
IARC
international agency for research on cancer
i-but25
blend of gasoline and 25 % isobutanol
LC/MS-MS
liquid chromatography with tandem mass spectrometry
log2FC
log2 transformation of fold change
n-but25
blend of gasoline and 25 % n-butanol
PAHs
polycyclic aromatic hydrocarbons)
PFI
port-fuel injection
PM
particulate matter
PN
particle number
qRT-PCR
quantitative reverse transcription polymerase chain reaction
UFP
ultrafine particles
WLTC
worldwide harmonized light vehicles test cycle

Keywords

Particulate matter emissions
Gasoline
Alternative fuels
Toxicity
Gene expression profiling

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