Atmospheric aging alters the toxicity mechanisms of residential wood combustion aerosol: a parallel in vivo and in vitro study
Authors
- Svenja Offer
- Hendryk Czech
- Sebastiano Di Bucchianico
- Anni Hartikainen
- Mika Ihalainen
- Henri Hakkarainen
- Mikko S. Happo
- Kati Huttunen
- Tuukka Ihantola
- Heikki Suhonen
- Oskari Uski
- Maria-Viola Martikainen
- Marco Dilger
- Christoph Schlager
- Joana Candeias
- Martin Irmler
- Johannes Beckers
- Gert Jakobi
- Tamara Kanashova
- Miika Kortelainen
- Kari Kuuspalo
- Heikki Lamberg
- Ari Leskinen
- Bernhard Michalke
- Sebastian Oeder
- Jürgen Orasche
- Johannes Passig
- Pasi Yli-Pirilä
- Teemu Rönkkö
- Jürgen Schnelle-Kreis
- Martin Sklorz
- Thorsten Streibel
- Jarkko Tissari
- Jeroen Buters
- Sonja Mülhopt
- Carsten Weiss
- Gunnar Dittmar
- Jorma Jokiniemi
- Maija-Riitta Hirvonen
- Pasi Jalava
- Olli Sippula
- Ralf Zimmermann
Journal
- Environmental Science and Technology
Citation
- Environ Sci Technol 60 (22): 16029-16043
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.