Reactive Oxygen Species and Oxidative Potential of Outdoor and Indoor Particulate Matter in Wintertime Fairbanks, Alaska
SUKRITI KAPUR, Kasey Edwards, Ting Fang, Meredith Schervish, Pascale Lakey, Yuhan Yang, Ellis Robinson, Peter F. DeCarlo, William Simpson, Rodney J. Weber, Manabu Shiraiwa, University of California, Irvine
Abstract Number: 453
Working Group: Health-Related Aerosols
Abstract
Sub-arctic cities can face episodes of high air pollution during wintertime owing to extremely low temperatures and shallow surface-based inversion layer. During the ALPACA campaign in Fairbanks, Alaska in January – February 2022, we conducted sampling of outdoor fine particulate matter (PM2.5) using a high-volume sampler and of indoor PM using a size-segregated cascade impactor in a house during activities including cooking and residential heating using a pellet stove. We measured environmentally persistent free radicals (EPFRs), stable organic radicals contained in PM, using electron paramagnetic resonance (EPR) spectroscopy. We also quantified the formation of reactive oxygen species (ROS) in water by EPR with a spin-trapping technique as well as PM oxidative potential (OP) using the dithiothreitol (OP-DTT) and OP-OH assays. We found good correlations of EPFRs with combustion and vehicular markers, indicating that residential wood stoves and traffic emissions may be major sources of EPFRs in Fairbanks. Outdoor PM mainly generates •OH (67%) and carbon-centered radicals (33%), while indoor PM forms predominantly •OH in water. Indoor submicron PM shows higher ROS and OP-DTT values compared to coarse PM. Both indoor and outdoor ROS exhibit little correlations with OP-DTT, indicating the need for additional analysis for the link between ROS and oxidative potential. Outdoor •OH also correlates well with water-soluble iron (R2 = 0.51), indicating the role of Fenton or Fenton-like reactions in generating •OH in the aqueous phase. OP-OH correlates strongly with EPFRs and the modeled OH production rate in lung lining fluid correlates tightly with EPFRs, implying that EPFRs are redox active to generate •OH upon inhalation and respiratory deposition.