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Evidence for cytotoxicity and mitochondrial dysfunction in human lung cells exposed to biomass burning aerosol constituents: Levoglucosan and 4-nitrocatechol.

Authors :
Khan F
Kwapiszewska K
Romero AM
Rudzinski K
Gil-Casanova D
Surratt JD
Szmigielski R
Source :
Environmental pollution (Barking, Essex : 1987) [Environ Pollut] 2024 Oct 21; Vol. 363 (Pt 2), pp. 125173. Date of Electronic Publication: 2024 Oct 21.
Publication Year :
2024
Publisher :
Ahead of Print

Abstract

Biomass burning (BB) emissions are one of the largest sources of carbonaceous aerosol, posing a significant risk as an airway irritant. Important BB markers include wood pyrolysis emissions, such as levoglucosan (LG) that is an anhydrous sugar bearing a six-carbon ring structure (i.e., 1,6-anhydro-β-D-glucopyranose). Atmospheric chemical aging of BB-derived aerosol (BBA) in the presence of nitrogen oxides (NO <subscript>x</subscript> ) can yield nitro-aromatic compounds, including 4-nitrocatechol (4NC). There is building evidence that NO <subscript>x</subscript> -mediated chemical aging of BBA poses a more serious exposure effect than primary pyrolysis emissions. This study provides a comparative toxicological assessment following the exposure to important BBA marker compounds in human lung cells (i.e., A549 and BEAS-2B) to determine whether aromatic 4NC is more toxic than BBA-bound anhydrous carbohydrate (i.e., LG). We determined inhibitory concentration-50 (IC <subscript>50</subscript> ) and examined reactive oxygen species (ROS) changes, mitochondrial dysfunction, and apoptosis induction in the two cell lines following exposure to LG and 4NC in a dose-response manner. In the BEAS-2B cells, estimated IC <subscript>50</subscript> values for 4NC were 33 and 8.8 μg mL <superscript>-1</superscript> , and for LG were 2546 and ∼3 × 10 <superscript>7</superscript>  μg mL <superscript>-1</superscript> at 24 h and 48 h of exposure, respectively. A549 cells exhibited a much higher IC <subscript>50</subscript> value than BEAS-2B cells. LG exposures resulted in mitochondrial stress with viability inhibition, but cells recovered with increasing exposure time. 4NC exposures at 200 μg mL <superscript>-1</superscript> resulted in the induction of apoptosis at 6 h. Mitochondrial dysfunction and ROS imbalance induced the intrinsic apoptotic pathway induction following 4NC exposures. While increased ROS is caused by LG exposure in lung cells, 4NC is a marker of concern during BB emissions, as we observed apoptosis and high mitochondrial ROS in both lung cells at atmospherically-relevant aerosol concentrations. It may be associated with higher airway or inhalation pathologies in higher BBA emissions, such as wildfires or during wood combustion.<br />Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.<br /> (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Details

Language :
English
ISSN :
1873-6424
Volume :
363
Issue :
Pt 2
Database :
MEDLINE
Journal :
Environmental pollution (Barking, Essex : 1987)
Publication Type :
Academic Journal
Accession number :
39442609
Full Text :
https://doi.org/10.1016/j.envpol.2024.125173