Oxidative stress and inflammation induced by air pollution-derived PM2.5 persist in the lungs of mice after cessation of their sub-chronic exposure

Oxidative stress and inflammation induced by air pollution-derived PM2.5 persist in the lungs of mice after cessation of their sub-chronic exposure

More than 7 million early deaths/year are attributable to air pollution. Current health concerns are especially focused on air pollution-derived particulate matter (PM). Although oxidative stress-induced airway inflammation is one of the main adverse outcome pathways triggered by air pollution-deriv...

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Published in:Environment international Vol. 181; p. 108248
Main Authors: Barbier, Emeline, Carpentier, Jessica, Simonin, Ophélie, Gosset, Pierre, Platel, Anne, Happillon, Mélanie, Alleman, Laurent Y., Perdrix, Esperanza, Riffault, Véronique, Chassat, Thierry, Lo Guidice, Jean-Marc, Anthérieu, Sébastien, Garçon, Guillaume
Format: Journal Article
Language:English
Published: Elsevier 01-11-2023
Subjects:
A/JOlaHsd mouse
Acute/Sub-chronic exposures
Air pollution-derived PM2.5
Analytical chemistry
Chemical Sciences
Life Sciences
Lung
Ocean, Atmosphere
Oxidative stress
Recovery period
Sciences of the Universe
Toxicology
Sub-chronic exposures
Oxidative stress
Inflammation
JOlaHsd mouse Lung Acute
Air pollution-derived PM 2.5 A
Recovery period
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Summary:More than 7 million early deaths/year are attributable to air pollution. Current health concerns are especially focused on air pollution-derived particulate matter (PM). Although oxidative stress-induced airway inflammation is one of the main adverse outcome pathways triggered by air pollution-derived PM, the persistence of both these underlying mechanisms, even after exposure cessation, remained poorly studied. In this study, A/JOlaHsd mice were also exposed acutely (24 h) or sub-chronically (4 weeks), with or without a recovery period (12 weeks), to two urban PM2.5 samples collected during contrasting seasons (i.e., autumn/winter, AW or spring/summer, SS). The distinct intrinsic oxidative potentials (OPs) of AW and SS PM2.5, as evaluated in acellular conditions, were closely related to their respective physicochemical characteristics and their respective ability to really generate ROS over-production in the mouse lungs. Despite the early activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) cell signaling pathway by AW and, in a lesser degree, SS PM2.5, in the murine lungs after acute and sub-chronic exposures, the critical redox homeostasis was not restored, even after the exposure cessation. Accordingly, an inflammatory response was reported through the activation of the nuclear factor-kappa B (NF-κB) cell signaling pathway activation, the secretion of cytokines, and the recruitment of inflammatory cells, in the murine lungs after the acute and sub-chronic exposures to AW and, in a lesser extent, to SS PM2.5, which persisted after the recovery period. Taken together, these original results provided, for the first time, new relevant insights that air pollution-derived PM2.5, with relatively high intrinsic OPs, induced oxidative stress and inflammation, which persisted admittedly at a lower level in the lungs after the exposure cessation, thereby contributing to the occurrence of molecular and cellular adverse events leading to the development and/or exacerbation of future chronic inflammatory lung diseases and even cancers.
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content type line 23
ISSN:0160-4120
1873-6750
DOI:10.1016/j.envint.2023.108248