No abstract

Fine particulate matter is a leading air pollutant, and its composition profile relates to sources and health effects. The human respiratory tract hosts a warmer and more humid microenvironment in contrast with peripheral environments. However, how the human respiratory tract impacts the transformation of the composition of environmental PM2.5 once they are inhaled and consequently changes of source contribution and health effects are unknown. Here, we show that the respiratory tract can make these properties of PM2.5 reaching the lung different from environmental PM2.5. We found via an in vitro model that the warm and humid conditions drive the desorption of nitrate (about 60%) and ammonium (about 31%) out of PM2.5 during the inhalation process and consequently make source contribution profiles for respiratory tract-deposited PM2.5 different from that for environmental PM2.5 as suggested in 11 Chinese cities and 12 US cities. We also observed that oxidative potential, one of the main health risk causes of PM2.5, increases by 41% after PM2.5 travels through the respiratory tract model. Our results reveal that PM2.5 inhaled in the lung differs from environmental PM2.5. This work provides a starting point for more health-oriented source apportionment, physiology-based health evaluation, and cost-effective control of PM2.5 pollution.