Accurate predictions of the droplet transport, evolution, and deposition in human airways are critical for the quantitative analysis of the health risks due to the exposure to the airborne pollutant or virus transmission. The droplet/particle-vapor interaction, i.e., the evaporation or condensation of the multi-component droplet/particle, is one of the key mechanisms that need to be precisely modeled. Using a validated computational model, the transport, evaporation, hygroscopic growth, and deposition of multi-component droplets were simulated in a simplified airway geometry. A mucus-tissue layer is explicitly modeled in the airway geometry to describe mucus evaporation and heat transfer. Pulmonary flow and aerosol dynamics patterns associated with different inhalation flow rates are visualized and compared. Investigated variables include temperature distributions, relative humidity (RH) distributions, deposition efficiencies, droplet/particle distributions, and droplet growth ratio distributions. Numerical results indicate that the droplet/particle-vapor interaction and the heat and mass transfer of the mucus-tissue layer must be considered in the computational lung aerosol dynamics study, since they can significantly influence the precise predictions of the aerosol transport and deposition. Furthermore, the modeling framework in this study is ready to be expanded to predict transport dynamics of cough/sneeze droplets starting from their generation and transmission in the indoor environment to the deposition in the human respiratory system.
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.
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