In this study, a composite, biophysical mechanism-based microdosimetric model was developed for the assessment of the primary cellular consequences of radon inhalation. Based on the concentration of radio-aerosols in the inhaled air and the duration of exposure, this mathematical approach allows the computation of the distribution of cellular burdens and the resulting distribution of cellular inactivation and oncogenic transformation probabilities within the epithelium of the human central airways. The composite model is composed of three major parts. The first part is a lung-particle interaction model applying computational fluid and particle dynamics (CFPD) methods. The second part is a lung dosimetry model that quantifies the cellular distribution of radiation exposure within the bronchial epithelium. The third part of the composite model is the unit-track-length model, which allows the prediction of the biological outcome of the exposure at the cellular level. Computations were made for different exposure durations for a miner working in a New Mexico uranium mine. The spatial pattern of the exposed cell nuclei along the epithelium, the distributions of single and multiple alpha-particle hits, the distributions of cell nucleus doses, and cell inactivation and cell transformation probabilities as a function of the number of inhalations (length of exposure) were investigated and compared for up to 500 inhalations.