Governed by the conservation laws of nature, the Computational Fluid-Particle Dynamics (CFPD) and Physiologically Based
Toxicokinetic (PBTK) model is a promising tool to assess the chronic exposure risks of EC aerosols and provide informative and
high-resolution data promptly. The schematic of the CFPD-PBTK modeling framework is shown inFigure
1 . Integrating the multiscale model validations and optimizations, the CFPD-PBTK model provides local information about how
different levels of puffing may affect the deposition and translocation of toxicants in both lung and systemic regions. The CFPD model
is developed based on Euler-Lagrange scheme (Feng, Kleinstreuer, Castro, & Rostami, 2016 )
specifically for multi-component EC aerosol dynamics in an idealized human upper airway model from mouth to Generation 3 (G3). The
existence of the dominant chemicals of the nicotine, acrolein, formaldehyde, vegetable glycerin (VG), and propylene glycol (PG) are
tracked both in the particle and vapor forms. Also, the wall of the respiratory system is considered as a sink with fractional to
complete absorption for the uptake of the chemicals into the systemic region. The PBTK model for inhaled toxicants is developed and
validated. It is assumed that the toxicant`s distribution through blood flow with the biological structure of tissues which are
homogeneous rate-limited diffusion (Robinson, Balter, & Schwartz, 1992 (link)). The important
mechanisms including absorption, distribution, metabolism, and excretion in each organ for each toxicant are considered. Physiologic
parameters (cardiac output, ventilation rate, blood flow rate to the organs and organ volumes) are obtained and optimized accordingly.
The system of governing equations and boundary conditions are provided in theSupplemental Information (SI) .
Toxicokinetic (PBTK) model is a promising tool to assess the chronic exposure risks of EC aerosols and provide informative and
high-resolution data promptly. The schematic of the CFPD-PBTK modeling framework is shown in
1
different levels of puffing may affect the deposition and translocation of toxicants in both lung and systemic regions. The CFPD model
is developed based on Euler-Lagrange scheme (Feng, Kleinstreuer, Castro, & Rostami, 2016 )
specifically for multi-component EC aerosol dynamics in an idealized human upper airway model from mouth to Generation 3 (G3). The
existence of the dominant chemicals of the nicotine, acrolein, formaldehyde, vegetable glycerin (VG), and propylene glycol (PG) are
tracked both in the particle and vapor forms. Also, the wall of the respiratory system is considered as a sink with fractional to
complete absorption for the uptake of the chemicals into the systemic region. The PBTK model for inhaled toxicants is developed and
validated. It is assumed that the toxicant`s distribution through blood flow with the biological structure of tissues which are
homogeneous rate-limited diffusion (Robinson, Balter, & Schwartz, 1992 (link)). The important
mechanisms including absorption, distribution, metabolism, and excretion in each organ for each toxicant are considered. Physiologic
parameters (cardiac output, ventilation rate, blood flow rate to the organs and organ volumes) are obtained and optimized accordingly.
The system of governing equations and boundary conditions are provided in the
