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Peer-reviewedCC BYEnvironmental science & technology

Aging of Urban Traffic Fine Particles Modulates Toxicity Mechanisms and Oxidative Stress Responses.

  • Michal Pardo1
  • Noga Kozer2
  • Carolina Molina3
  • Yanfang Chen4
  • Haim Barr2
  • Galit Cohen2
  • Damianos Pavlidis3,5
  • Christos Kaltsonoudis3
  • Katerina Seitanidi3
  • Georgia A Argyropoulou3,5
  • Christina N Vasilakopoulou3,6
  • Christina Christopoulou3,5
7 more authors
  • Angeliki Matrali3,5
  • Mingchen Wei7,8
  • Andre S H Prevot4
  • David M Bell4
  • Spyros N Pandis3,5
  • Athanasios Nenes3,5,7
  • Yinon Rudich1
8 affiliations
  1. 1Department of Earth and Planetary Sciences, Faculty of Chemistry, Weizmann Institute of Science, 234 Herzl Street, P.O.Box 26, Rehovot7610001, Israel.
  2. 2Maurice and Vivienne Wohl Institute for Drug Discovery, Nancy and Stephen Grand Israel National Center for Personalized Medicine, Weizmann Institute of Science, Rehovot7610001, Israel.
  3. 3Institute of Chemical Engineering Sciences (FORTH/ICE-HT), Patras26504, Greece.
  4. 4PSI Center for Energy and Environmental Sciences, Paul Scherrer Institute (PSI), Villigen5232, Switzerland.
  5. 5Department of Chemical Engineering, University of Patras, Patras26504, Greece.
  6. 6Université Paris Cité and Univ Paris Est Creteil, CNRS, LISA, F-75013Paris, France.
  7. 7School of Architecture, Civil & Environmental Engineering, École Polytechnique Fédérale de Lausanne, LausanneCH-1015, Switzerland.
  8. 8Aix-Marseille Université, Université de Toulon, CNRS, IRD, MIO, 13288Marseille Cedex 09, France.
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Abstract

Vehicular emissions are an important source of urban air pollution that can age through atmospheric processes, but how their health effects change during atmospheric aging remains poorly understood. To simulate realistic urban emissions, we sampled air in a parking garage where cold-start and urban emissions coexist. Following aging in an oxidation flow reactor (OFR), we studied the cellular and acellular effects of the fresh and aged aerosols. Photochemical aging in the OFR increased secondary organic aerosol (SOA) mass by up to 6.9-fold, the oxygen-to-carbon (O:C) ratio from 0.26 to 0.79, and both the intrinsic oxidative potential (OPm) and the volume-normalized oxidative potential (OPv). In contrast, the peroxide-sensitive DCF activity decreased following aging. Cellular exposure to aged aerosol extracts increased cellular reactive oxygen species (ROS) formation in lung (A549) and liver (HepG2) cells, whereas fresh extracts strongly reduced cellular respiration, particularly in HepG2 cells. Cell painting analysis showed distinct morphological profiles. Exposure to aged extracts showed greater oxidative stress and DNA damage responses than those of exposure to fresh extracts. These findings suggest that atmospheric aging shifts the toxicity of fresh emissions from suppression of mitochondrial respiration toward oxygenated organics that can drive intracellular oxidative stress and DNA damage phenotypes. In conclusion, atmospheric aging of cold-start and urban vehicular emissions contributes to enhanced SOA formation and leads to distinct biological outcomes that depend on the degree of oxidative aging.

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Cite

BibTeXRIS
BibTeX
@article{pardo2026aging,
  title = {{Aging of Urban Traffic Fine Particles Modulates Toxicity Mechanisms and Oxidative Stress Responses.}},
  author = {Michal Pardo and Noga Kozer and Carolina Molina and Yanfang Chen and Haim Barr and Galit Cohen and Damianos Pavlidis and Christos Kaltsonoudis and Katerina Seitanidi and Georgia A Argyropoulou and Christina N Vasilakopoulou and Christina Christopoulou and Angeliki Matrali and Mingchen Wei and Andre S H Prevot and David M Bell and Spyros N Pandis and Athanasios Nenes and Yinon Rudich},
  journal = {Environmental science \& technology},
  year = {2026},
  month = oct,
  doi = {10.1021/acs.est.6c06323},
  url = {https://europepmc.org/article/MED/42899670},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Aging of Urban Traffic Fine Particles Modulates Toxicity Mechanisms and Oxidative Stress Responses.
AU  - Michal Pardo
AU  - Noga Kozer
AU  - Carolina Molina
AU  - Yanfang Chen
AU  - Haim Barr
AU  - Galit Cohen
AU  - Damianos Pavlidis
AU  - Christos Kaltsonoudis
AU  - Katerina Seitanidi
AU  - Georgia A Argyropoulou
AU  - Christina N Vasilakopoulou
AU  - Christina Christopoulou
AU  - Angeliki Matrali
AU  - Mingchen Wei
AU  - Andre S H Prevot
AU  - David M Bell
AU  - Spyros N Pandis
AU  - Athanasios Nenes
AU  - Yinon Rudich
PY  - 2026
DA  - 2026/10/01
JO  - Environmental science & technology
DO  - 10.1021/acs.est.6c06323
UR  - https://europepmc.org/article/MED/42899670
AB  - Vehicular emissions are an important source of urban air pollution that can age through atmospheric processes, but how their health effects change during atmospheric aging remains poorly understood. To simulate realistic urban emissions, we sampled air in a parking garage where cold-start and urban emissions coexist. Following aging in an oxidation flow reactor (OFR), we studied the cellular and acellular effects of the fresh and aged aerosols. Photochemical aging in the OFR increased secondary organic aerosol (SOA) mass by up to 6.9-fold, the oxygen-to-carbon (O:C) ratio from 0.26 to 0.79, and both the intrinsic oxidative potential (OPm) and the volume-normalized oxidative potential (OPv). In contrast, the peroxide-sensitive DCF activity decreased following aging. Cellular exposure to aged aerosol extracts increased cellular reactive oxygen species (ROS) formation in lung (A549) and liver (HepG2) cells, whereas fresh extracts strongly reduced cellular respiration, particularly in HepG2 cells. Cell painting analysis showed distinct morphological profiles. Exposure to aged extracts showed greater oxidative stress and DNA damage responses than those of exposure to fresh extracts. These findings suggest that atmospheric aging shifts the toxicity of fresh emissions from suppression of mitochondrial respiration toward oxygenated organics that can drive intracellular oxidative stress and DNA damage phenotypes. In conclusion, atmospheric aging of cold-start and urban vehicular emissions contributes to enhanced SOA formation and leads to distinct biological outcomes that depend on the degree of oxidative aging.
SN  - 0013-936X
SN  - 1520-5851
ER  -