https://doi.org/10.3389/ftox.2025.1722968
Justine Fredoc-Louison 1, Maëva Cherrière 1,2, Bastien Rival 1, Suzanne De Araujo 1 , Sabine François 1, Samir Dekali 1
1 Biomedical Research Institute of the Armed Forces (IRBA), EBR Department, Emerging Technological Risks Unit (U.RTE), Brétigny-sur-Orge, France
2 National Institute for Industrial Environment and Risks (Ineris), MIV Department, Experimental Toxicology and Modelling Unit (TEAM), Verneuil-en-Halatte, France
This study shows how repeated, sub-lethal co-exposures to aluminum oxide nanoparticles (Al₂O₃ NPs) and hydrogen chloride (HCl) which is a realistic pollutant mixture in industrial accidents and military settings.
Using a physiologically relevant human air–liquid interface co-culture model combining alveolar epithelial cells and fibroblasts, the researchers show that although these exposures did not disrupt cell viability, barrier integrity, or trigger classic inflammatory/fibrotic mediators, they did lead to non-canonical paracrine signaling that activated fibroblast proliferation and migration.
These findings suggest that “silent” early epithelial stress from mixed airborne pollutants may initiate remodeling processes through unconventional epithelial-mesenchymal crosstalk, offering new insight into mechanisms relevant for hazard assessment and respiratory risk in complex exposure scenarios.
