Toxic responses in human lung epithelial cells (BEAS-2B) exposed to particulate matter exhaust emissions from gasoline and biogasoline

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68407700%3A21220%2F21%3A00350163" target="_blank" >RIV/68407700:21220/21:00350163 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68407700:21230/21:00350163 RIV/60460709:41310/20:85808 RIV/68378041:_____/21:00560412

Výsledek na webu

<a href="https://doi.org/10.37904/nanocon.2020.3763" target="_blank" >https://doi.org/10.37904/nanocon.2020.3763</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.37904/nanocon.2020.3763" target="_blank" >10.37904/nanocon.2020.3763</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Toxic responses in human lung epithelial cells (BEAS-2B) exposed to particulate matter exhaust emissions from gasoline and biogasoline

Popis výsledku v původním jazyce

Motor vehicle emissions substantially contribute to air pollution worldwide and cause serious health problems. While the deleterious effects of diesel exhaust particulate matter (PM) have been widely studied, much less attention is paid to toxicity of PM emitted by gasoline engines although they also produce considerable amount of PM. The primary objective of this research was to assess toxic potencies of exhaust PM released by conventional gasoline engine fueled with neat gasoline (E0) or gasoline-ethanol blend (15% ethanol, v/v, E15). Despite a similar particle mass (μg PM/kg fuel) produced by both fuels, PM emitted by E15 contained higher amount of harmful polycyclic aromatic hydrocarbons (PAH) as suggested by chemical analysis. To examine the toxicity of organic PM constituents, human lung BEAS-2B cells were exposed for 4h and 24h to a subtoxic dose of E0 and E15 PM organic extracts. We used genome scale transcriptomic analysis to characterize the toxic response and to identify modulated biological process and pathways. Whereas 4h exposure to both PM extracts resulted in modulation of similar genes and pathways related to lipid and steroid metabolism, activation of PPARa, oxidative stress and immune response, 24h exposure was more specific for each extract; although both induced expression of PAH-metabolic enzymes, modulated metabolism of lipids or activated PPARa, E15 additionally deregulated variety of other pathways. Overall, the PM mass produced by both fuels was similar, however, higher PAH content in E15 PM organic extract may have contributed to more extensive toxic response particularly after 24h exposure in BEAS-2B cells.

Název v anglickém jazyce

Toxic responses in human lung epithelial cells (BEAS-2B) exposed to particulate matter exhaust emissions from gasoline and biogasoline

Popis výsledku anglicky

Motor vehicle emissions substantially contribute to air pollution worldwide and cause serious health problems. While the deleterious effects of diesel exhaust particulate matter (PM) have been widely studied, much less attention is paid to toxicity of PM emitted by gasoline engines although they also produce considerable amount of PM. The primary objective of this research was to assess toxic potencies of exhaust PM released by conventional gasoline engine fueled with neat gasoline (E0) or gasoline-ethanol blend (15% ethanol, v/v, E15). Despite a similar particle mass (μg PM/kg fuel) produced by both fuels, PM emitted by E15 contained higher amount of harmful polycyclic aromatic hydrocarbons (PAH) as suggested by chemical analysis. To examine the toxicity of organic PM constituents, human lung BEAS-2B cells were exposed for 4h and 24h to a subtoxic dose of E0 and E15 PM organic extracts. We used genome scale transcriptomic analysis to characterize the toxic response and to identify modulated biological process and pathways. Whereas 4h exposure to both PM extracts resulted in modulation of similar genes and pathways related to lipid and steroid metabolism, activation of PPARa, oxidative stress and immune response, 24h exposure was more specific for each extract; although both induced expression of PAH-metabolic enzymes, modulated metabolism of lipids or activated PPARa, E15 additionally deregulated variety of other pathways. Overall, the PM mass produced by both fuels was similar, however, higher PAH content in E15 PM organic extract may have contributed to more extensive toxic response particularly after 24h exposure in BEAS-2B cells.

Druh

D - Stať ve sborníku

CEP obor

—

OECD FORD obor

30108 - Toxicology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2021

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název statě ve sborníku

NANOCON Conference Proceedings - International Conference on Nanomaterials

ISBN

978-80-87294-98-7

ISSN

—

e-ISSN

2694-930X

Počet stran výsledku

6

Strana od-do

453-458

Název nakladatele

TANGER

Místo vydání

Ostrava

Místo konání akce

Brno

Datum konání akce

21. 10. 2020

Typ akce podle státní příslušnosti

WRD - Celosvětová akce

Kód UT WoS článku

000664505500077