Photochemical ultrafine particles pose potential inflammatory risk despite low PM_2.5 mass

Air quality improvements have reduced PM2.5 mass, but particle surface area, which primarily contributes to inflammatory responses, may not follow the same trend, potentially creating health-relevant exposure.

To investigate this potential decoupling, we analyzed three years of observations in Fuzhou, China. Potential inflammatory responses were estimated from the lung-deposited surface area (LDSA) exceeding PM_2.5-based expectations, using an animal-derived dose-response relationship that relates particle surface area to pulmonary inflammation.

We identified that 6.6% of PM_2.5 attainment hours (<35 μg m^-3) exhibited elevated LDSA, with surface area exposure 7.5-fold greater than expected from the LDSA/PM_2.5 ratio during other attainment hours, and 82% of potential inflammatory risk was undetected by mass-based assessment. During these periods, despite median PM_2.5 mass concentrations of only 3.0 μg m^-3 (well below air quality standards), toxicological dose-response assessment predicts potentially clinically relevant inflammatory responses (27% lung neutrophil infiltration). Machine learning reveals that photochemical oxidation (elevated O₃ and secondary organic carbon importance) contributes to these periods by producing abundant 50-100 nm particles during summer-autumn afternoons under warm, high-radiation conditions.

These photochemical ultrafine particle events represent a mechanistically distinct pollution regime where mass-based frameworks may underestimate potential inflammatory effects, a gap that may widen as emission controls reduce primary sources and climate warming enhances photochemistry.