  Could the microdroplets formed by viscoelastic stretching and break-up of
mucosal liquids in the upper respiratory tract (URT), when inhaled further
downwind, explain the brisk pace at which deep lung infections emerge following
onset of initial infection at the URT? While it is well-established that
particulates inhaled from outside can possibly penetrate to the lower airway
only if they are < 5 microns, the fate of particulates (many > 5-microns in
diameter) sheared away from the intra-URT mucosa during inhalation remains an
open question. These particulates predominantly originate at the nasopharynx,
oropharynx, and laryngeal chamber with the vocal folds. To resolve the posed
question, this study considers a CT-based 3D anatomical airway reconstruction
and isolates the tract from the laryngeal vocal fold region, mapping the entire
tracheal cavity and concluding at generation 2 of the tracheobronchial tree.
Through the delineated geometry, airflow simulation is conducted using the LES
scheme to replicate relaxed inhalation at 15 L/min. Against the ambient air
flux, numerical experiments have been performed to monitor the transport of
liquid particulates with diameters 1-30 microns, bearing physical properties
akin to aerosolized mucus with embedded virions. The full-scale numerical
transmission trends to the lower airway were found consistent with the findings
from a reduced-order mathematical model that conceptualized the impact of
intra-airway vortex instabilities on local particle transport through point
vortex idealization in an anatomy-guided 2D potential flow domain. The results
collectively demonstrate markedly elevated trends of deep lung penetration by
the URT-derived particulates, even if they are as large as 10- and 15 microns.
The high viral load carried by such droplets to the bronchial spaces could
mechanistically explain the accelerated seeding of infection in the lungs.
