Characterization of elements, PAHs, AhR-activity and pro-inflammatory responses of road tunnel-derived particulate matter in human hepatocyte-like and bronchial epithelial cells
Jazyk angličtina Země Velká Británie, Anglie Médium print-electronic
Typ dokumentu časopisecké články
PubMed
37164185
DOI
10.1016/j.tiv.2023.105611
PII: S0887-2333(23)00060-7
Knihovny.cz E-zdroje
- Klíčová slova
- Air pollution, Airway epithelial cells, Aryl hydrocarbon receptor (AhR), Diesel exhaust particles, Inflammation, Metals, Polyaromatic compounds,
- MeSH
- cytokiny MeSH
- epitelové buňky MeSH
- hepatocyty MeSH
- látky znečišťující vzduch * toxicita analýza MeSH
- lidé MeSH
- organické látky MeSH
- pevné částice toxicita analýza MeSH
- polycyklické aromatické uhlovodíky * toxicita analýza MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- cytokiny MeSH
- látky znečišťující vzduch * MeSH
- organické látky MeSH
- pevné částice MeSH
- polycyklické aromatické uhlovodíky * MeSH
The aims were to characterize the content of elements and polycyclic aromatic hydrocarbons (PAHs) in size-separated particulate matter (PM) sampled in a road tunnel, estimate the contribution of PAHs to the toxic potential, and measure the pro-inflammatory potential of PM samples and extracts with increasing polarity. Several elements/metals previously associated with cytokine responses were found. Based on PAHs levels and published PAHs potency, the calculated mutagenic and carcinogenic activities of size-separated samples were somewhat lower for coarse than fine and ultrafine PM. The AhR-activity of the corresponding PM extracts measured in an AhR-luciferase reporter model (human hepatocytes) were more similar. The highest AhR-activity was found in the neutral (parent and alkylated PAHs) and polar (oxy-PAHs) fractions, while the semi-polar fractions (mono-nitrated-PAHs) had only weak activity. The neutral and polar aromatic fractions from coarse and fine PM were also found to induce higher pro-inflammatory responses and CYP1A1 expression in human bronchial epithelial cells (HBEC3-KT) than the semi-polar fractions. Fine PM induced higher pro-inflammatory responses than coarse PM. AhR-inhibition reduced cytokine responses induced by parent PM and extracts of both size fractions. Contributors to the toxic potentials include PAHs and oxy-PAHs, but substantial contributions from other organic compounds and/or metals are likely.
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