Abstract
Residential wood combustion (RWC) contributes significantly to urban air pollution; however, the influence of atmospheric aging on adverse health effects of RWC emissions remains uncertain. We exposed C57BL/6J mice in parallel with different in vitro models of first-line of defense cells (macrophages: RAW264.7 and lung epithelial cells: A549) at the air–liquid interface to either fresh or aged RWC emissions generated from an oxidation flow reactor. Both in vivo and in vitro cellular and molecular outcomes show that photochemically aged emissions play a key role in triggering lung inflammation and the polarization of macrophages into an M2 phenotype, bridging the gap between epidemiology and toxicology on inflammatory lung responses. Furthermore, evidence of protumorigenic activity in lung epithelial cells is detected after exposure to both emissions, but more pronounced after exposure to aged RWC emissions. This study highlights the importance of considering atmospheric aging in the assessment of air-pollution-related health effects.
| Original language | English |
|---|---|
| Pages (from-to) | 16029-16043 |
| Number of pages | 15 |
| Journal | Environmental Science and Technology |
| Volume | 60 |
| Issue number | 22 |
| DOIs | |
| Publication status | Published - 9 Jun 2026 |
Keywords
- biomass burning
- genotoxicity
- inflammation
- macrophage polarization
- oxidation flow reactor
- secondary organic aerosol
- transcriptome
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