Abstract
Environmental persistent free radicals (EPFRs) are a class of long-lived, redox-active species that persist on fine particulate matter (PM2.5) surfaces for days to months. Upon inhalation, EPFRs catalyze the generation of hydroxyl radicals through Fenton-like cycling, driving oxidative stress and inflammation at the site of deposition. Current air filtration technology focuses almost exclusively on physical interception of particulate matter, leaving the surface-bound radical activity of captured PM entirely unaddressed. This review advances a testable hypothesis rather than reporting a validated outcome: that cerium dioxide (CeO2)-based materials, whose Ce3+/Ce4+ redox cycling is well-established as a broad-spectrum antioxidant mechanism in biomedical contexts, can be functionally migrated to air filtration to chemically quench EPFRs on captured PM2.5. We first summarize the formation and health impacts of EPFRs, then introduce the mechanistic basis of CeO2 radical scavenging, emphasizing its self-regenerating valence cycling. We then examine the existing but functionally distinct use of CeO2 in air pollution control, including its role as an oxygen storage component in three-way catalysis and as an additive in filter media, and argue that these high-temperature oxidation applications do not constitute a functional precedent for ambient-temperature radical scavenging. The central gap is that no study has systematically tested whether CeO2 can chemically quench EPFRs on PM2.5 surfaces under filtration conditions. We articulate the key experimental questions that must be resolved—direct EPFR quenching versus ROS interception, the effects of humidity, airflow, and contact time, and the long-term fate of CeO2 under realistic filtration conditions—and argue that the demonstrated gaseous ROS scavenging of CeO2 in cigarette smoke, together with its self-recovery capability, provides sufficient mechanistic justification to pursue this direction experimentally.