Understanding tobacco related cancer etiology requires the knowledge of cigarette smoke particle (CSP) deposition. Measurements of CSP deposition are inconsistent with typical deposition data. A deposition model that accounts for hygroscopic growth, coagulation, particle charge, and cloud behavior of CSP has not yet been presented. Nor have smoking patterns been accounted for in either deposition measurements or computer models. The dosimetry of Benzo[a]pyrene (BaP), which would add critical information to the relationship between anatomic site preferences of tumors and their histology, is currently unknown.The deposition model presented in this study is the rst to accurately account for the dynamic behavior of CSP. Using the model results, the effects of each dynamic behavior on deposition is examined along with the effect of smoking patterns. The dosimetry of BaP is also calculated. The results indicate that coagulation, hygroscopicity, and particle charge increase the total deposition by 16% over the stable charge-neutral case, which predicts 46%. Cloud behavior increases total deposition ef ciency by 36% over the simple case. Increasing exhalation time increases the deposition fraction by 3.9%/s. BaP concentrations are found to be as large as 1.8E-4 ng/cm 2 for the cloud model and 2.4E-5 ng/cm 2 for single particle behavior. Mass deposition occurs preferentially in the pulmonary region for all cases. However, signi cant increases in the tracheobronchial region are found if cloud behavior is considered. The model results indicate that cloud behavior, and not particle charge, coagulation, and hygroscopic growth, has a predominant effect on deposition. More data is required on cloud behavior in the airways to improve the accuracy of the model.

The deposition of inhaled aerosol particles in the human respiratory tract is due to the mechanisms of inertia impaction, Brownian diffusion, and gravitational settling. A theory is developed to predict the particle deposition and its distribution in human respiratory tract for any breathing condition. A convection-diffusion equation for the particle concentration with a loss term is used to describe the transport and deposition of particles. In this equation, an apparent diffusion coefficient due to the velocity dispersion in the lung is present and found to be the dominant diffusion mechanism for the cases considered here. Expressions for deposition by various mechanisms are also derived. The governing equation is solved numerically with Weibel's lung model A. The particle concentration at the mouth is calculated during washin and washout and compared favorably with experimental recordings for 0.5-mum diameter di(2-ethylhexyl) sebacate particles. The total deposition in the lung for particle size ranging from 0.05 to 5 mum is also computed for a 500-cm-3 tidal volume and 15 breaths/min. The results in general agree with recent measurements of Heyder et al. However, a particle size of minimum deposition is found to exist theoretically near 0.3 mum.

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