Aerosol properties and lung deposition.

important experiments on total and regional lung deposition for healthy subjects has recently been published by the International Commission on Radiation Protection (ICRP) [2]. The mean values of experimental deposition data are approximated by mathematical expressions, which are then implemented into a computer program [3] that is commercially available on diskette. Since this model is applicable to a wide population of healthy subjects, it is valuable for risk-assessment studies and may also benefit therapeutic aerosol lung deposition studies. A physical basis for the deposition of aerosol particles in the human lung became available when FINDEISEN [4] published the first lung deposition model. This model uses a lung structure comprised of different lung generations, equations for deposition by sedimentation, diffusion, impaction and interception, and a mathematical model that combines these elements to calculate particle deposition as a function of lung generation. Since Findeisen's initial work, a large number of deposition models have been developed which are based essentially on the same principal. Like FINDEISEN’S model, [4], the modern models use a lung structure such as Weibel's dichotomous symmetrical model "A" [5], or, an even more complicated lung structure. In addition, there are newly derived or improved deposition equations for particle sedimentation, diffusion and impaction, empirical equations for extrathoracic deposition, and theoretical equations to calculate the mean deposition in each lung generation. A recent model [6] closely approximates the mean experimental total and regional lung deposition data as collected by the ICRP [2]. Another model has incorporated the growth of hygroscopic particles [7]. Important parameters for lung deposition are: the particle distribution; the respiratory manoeuvre, such as inhalation and exhalation flow rates, tidal volume, pause between inhalation and exhalation; and the shape of the upper airways. The structure of the bronchial and alveolar regions in normal lungs is considered to be of minor influence. However, this is probably not the case for diseased lungs.