Predictive models for deposition of inhaled diesel exhaust particles in humans and laboratory species.

Mathematical and computer models of the respiratory tracts of human beings and of laboratory animals (rats, hamsters, guinea pigs) were used to estimate the deposition patterns of inhaled diesel exhaust particles from automobile emissions. The accuracy of these models was tested by comparing the calculated depositions in laboratory animals with actual laboratory data. Our goal was to be able to predict the relation between exposure to diesel exhaust particles and the deposition of these particles in the lungs of humans of various ages. Diesel exhaust particles are aggregates with a mass median aerodynamic diameter of approximately 0.2 micron. Their actual size depends on the conditions under which they are generated. Using an appropriate particle model, we derived mathematical expressions that describe the effects of diffusion, sedimentation, impaction, and interception on the deposition of these particles. Because of their small size, we found that most diesel exhaust particles deposited through diffusion, and that the role of the other mechanisms was minor. Anatomical models of the human lung from birth to adulthood, as well as models of the lungs of laboratory species were formulated mathematically using available morphometric data. We used these lung models, together with the corresponding ventilation conditions of each species, to calculate deposition of diesel exhaust particles in the lungs. Under normal breathing conditions, we calculated that 7 to 13 percent (depending on particle size) of inhaled diesel exhaust particles deposit in the alveolar region of the adult human lung. Although the breathing mode (nose or mouth breathing) did not appear to affect alveolar deposition, increasing the minute ventilation (the number of breaths per minute multiplied by the tidal volume) increased alveolar deposition significantly. The calculated deposition patterns for diesel exhaust particles in younger humans (under age 25) were similar. However, with the exception of alveolar deposition in very young children (under age two), predicted deposition was greater in the lungs of younger humans than in the lungs of humans age 25 or older. For an equal exposure, the surface minute dose (particle mass deposited per minute per unit surface area) of unciliated airways appeared to change profoundly with age. Predicted dose was maximal in the lung models of two-year-old children. At this age, the calculated dose was approximately twice as high as in the mature adult lung. Deposition predictions for laboratory species compared favorably with existing data. Distribution of deposition was found to be similar among all species studied, although surface minute dose decreased with body weight.