Residential Wood Burning and Vehicle Emissions as Major Sources of Environmentally Persistent Free Radicals in Fairbanks, Alaska.

Environmentally persistent free radicals (EPFRs) play an important role in aerosol effects on air quality and public health, but their atmospheric abundance and sources are poorly understood. We measured EPFRs contained in PM2.5 collected in Fairbanks, Alaska, in winter 2022. We find that EPFR conce...

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Bibliographic Details
Published in:Environmental Science & Technology
Main Authors: Edwards, Kasey, Kapur, Sukriti, Fang, Ting, Cesler-Maloney, Meeta, Yang, Yuhan, Holen, Andrew, Wu, Judy, Robinson, Ellis, DeCarlo, Peter, Pratt, Kerri, Weber, Rodney, Simpson, William, Shiraiwa, Manabu
Format: Article in Journal/Newspaper
Language:unknown
Published: eScholarship, University of California 2024
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Online Access:https://escholarship.org/uc/item/2qc603mg
https://escholarship.org/content/qt2qc603mg/qt2qc603mg.pdf
https://doi.org/10.1021/acs.est.4c01206
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Summary:Environmentally persistent free radicals (EPFRs) play an important role in aerosol effects on air quality and public health, but their atmospheric abundance and sources are poorly understood. We measured EPFRs contained in PM2.5 collected in Fairbanks, Alaska, in winter 2022. We find that EPFR concentrations were enhanced during surface-based inversion and correlate strongly with incomplete combustion markers, including carbon monoxide and elemental carbon (R2 > 0.75). EPFRs exhibit moderately good correlations with PAHs, biomass burning organic aerosols, and potassium (R2 > 0.4). We also observe strong correlations of EPFRs with hydrocarbon-like organic aerosols, Fe and Ti (R2 > 0.6), and single-particle mass spectrometry measurements reveal internal mixing of PAHs, with potassium and iron. These results suggest that residential wood burning and vehicle tailpipes are major sources of EPFRs and nontailpipe emissions, such as brake wear and road dust, may contribute to the stabilization of EPFRs. Exposure to the observed EPFR concentrations (18 ± 12 pmol m-3) would be equivalent to smoking ∼0.4-1 cigarette daily. Very strong correlations (R2 > 0.8) of EPFR with hydroxyl radical formation in surrogate lung fluid indicate that exposure to EPFRs may induce oxidative stress in the human respiratory tract.