Airborne environmentally persistent free radicals (EPFRs) in PM2.5 from combustion sources: Abundance, cytotoxicity and potential exposure risks
As an emerging atmospheric pollutant, airborne environmentally persistent free radicals (EPFRs) are formed during many combustion processes and pose various adverse health effects. In health-oriented air pollution control, it is vital to evaluate the health effects of atmospheric fine particulate ma...
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Veröffentlicht in: | The Science of the total environment 2024-06, Vol.927, p.172202-172202, Article 172202 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | As an emerging atmospheric pollutant, airborne environmentally persistent free radicals (EPFRs) are formed during many combustion processes and pose various adverse health effects. In health-oriented air pollution control, it is vital to evaluate the health effects of atmospheric fine particulate matter (PM2.5) from different emission sources. In this study, various types of combustion-derived PM2.5 were collected on filters in a partial-flow dilution tunnel sampling system from three typical emission sources: coal combustion, biomass burning, and automobile exhaust. Substantial concentrations of EPFRs were determined in PM2.5 samples and associated with significant potential exposure risks. Results from in vitro cytotoxicity and oxidative potential assays suggest that EPFRs may cause substantial generation of reactive oxygen species (ROS) upon inhalation exposure to PM2.5 from anthropogenic combustion sources, especially from automobile exhaust. This study provides important evidence for the source- and concentration-dependent health effects of EPFRs in PM2.5 and motivates further assessments to advance public health-oriented PM2.5 emission control.
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•Abundant EPFRs in PM2.5 from three anthropogenic combustion sources•EPFRs from combustion are carbon centered radicals with an adjacent oxygen atom.•Potential health effects of inhaling PM2.5 contained EPFRs from automobile exhaust•PM2.5 contained EPFRs facilitates the substantial generation of ROS in human lung. |
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ISSN: | 0048-9697 1879-1026 |
DOI: | 10.1016/j.scitotenv.2024.172202 |