Yu C P, Xu G B
State University of New York at Buffalo, Amherst.
Res Rep Health Eff Inst. 1987(10):3-22.
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.
利用人类以及实验动物（大鼠、仓鼠、豚鼠）呼吸道的数学和计算机模型来估算汽车尾气排放中吸入的柴油废气颗粒的沉积模式。通过将实验动物体内计算出的沉积情况与实际实验数据进行比较，对这些模型的准确性进行了测试。我们的目标是能够预测接触柴油废气颗粒与这些颗粒在不同年龄段人类肺部沉积之间的关系。柴油废气颗粒是聚集体，质量中值空气动力学直径约为0.2微米。它们的实际大小取决于其产生时的条件。使用合适的颗粒模型，我们推导出了描述扩散、沉降、撞击和截留对这些颗粒沉积影响的数学表达式。由于其尺寸较小，我们发现大多数柴油废气颗粒通过扩散沉积，其他机制的作用较小。利用现有的形态测量数据，对从出生到成年的人类肺部以及实验物种的肺部进行了数学建模。我们将这些肺部模型与每个物种相应的通气条件相结合，来计算柴油废气颗粒在肺部的沉积情况。在正常呼吸条件下，我们计算出吸入的柴油废气颗粒中有7%至13%（取决于颗粒大小）沉积在成年人类肺部的肺泡区域。尽管呼吸方式（经鼻或经口呼吸）似乎不影响肺泡沉积，但增加分钟通气量（每分钟呼吸次数乘以潮气量）会显著增加肺泡沉积。较年轻人类（25岁以下）体内柴油废气颗粒的计算沉积模式相似。然而，除了两岁以下幼儿的肺泡沉积外，较年轻人类肺部的预测沉积量高于25岁及以上人类肺部。对于相同的暴露情况，无纤毛气道的表面分钟剂量（每分钟每单位表面积沉积的颗粒质量）似乎随年龄发生显著变化。预测剂量在两岁儿童的肺部模型中最大。在这个年龄，计算出的剂量约为成熟成年肺部的两倍。对实验物种的沉积预测与现有数据相符。尽管表面分钟剂量随体重降低，但在所研究的所有物种中，沉积分布相似。
