On the mechanics of inhaled bronchial transmission of pathogenic microdroplets generated from the upper respiratory tract, with implications for downwind infection onset.

Could the microdroplets formed by viscoelastic fragmentation of mucosal liquids within the upper respiratory tract (URT) explain the brisk onset of deep lung infection following initial URT infections? Generally, particulates, inhaled through the nostrils and therefore navigating the intricate topography of the anterior nasal cavity, can efficiently reach the lower airway only if they are small enough, typically [Formula: see text]. However, the fate of larger particulates, many exceeding 5-[Formula: see text] in diameter, that are sheared from the initial infection sites along the intra-URT mucosa during inhalation remains unresolved. These particulates originate primarily from the nasopharynx, oropharynx, and the laryngeal chamber containing the vocal folds. To investigate, this study employs a computed tomography-based three-dimensional anatomical airway reconstruction, isolating the tract from the larynx and mapping the tracheal cavity through to the third generation of the tracheobronchial tree; constituent transport across the distal bronchial outlets is also recorded to assess deep lung penetration. Within the defined geometry, airflow simulations are conducted with the Large Eddy Simulation scheme to replicate relaxed inhalation at 15 L/min flow rate. Against the ambient air flux, numerical experiments are performed to monitor the downwind transport of particulates (aerosols/droplets) with diameters [Formula: see text], bearing physical properties akin to aerosolized mucus with embedded virions. The full-scale numerical transmission trends, representatively validated against a small set of published experimental data, are consistent with findings from our reduced-order mathematical model that conceptualizes the influence of intra-airway vortex instabilities on local particle transport through point vortex idealization in an anatomy-guided two-dimensional potential flow domain. The results collectively demonstrate a markedly elevated lower airway penetration by URT-derived particulates, even by those as large as 10 and 15 [Formula: see text]. The high viral load, often exceeding the pathogen-specific infectious dose, carried by such droplets into the bronchial spaces of the sample airway, provides a plausible mechanistic explanation for the accelerated seeding of secondary lung infection.