A Theoretical Approach to the Deposition of Cancer-Inducing Asbestos Fibers in the Human Respiratory Tract

R. Sturm
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引用次数: 10

Abstract

In the study presented here a stochastic model predicting the deposition of variably shaped asbestos fibers in the human respiratory tract is introduced. Deposition calculations are commonly based on the concept of the aerodynamic diameter. Besides Brownian diffusion, inertial impaction, and sedimentation, also interception representing the capture of particles at the carinal ridges of single airway bifurcations is considered as main deposition mechanism for the computa- tion of regional and local deposition fractions. Concerning total deposition in the human respiratory tract, fibers with a cy- lindrical diameter, termed dp, smaller than 0.1 � m exhibit lower deposition fractions than comparable spheres, whilst fi- bers with dp greater than 0.1 � m show higher deposition fractions than spheres. The fiber aspect ratiohas only an insig- nificant influence on total deposition, i.e. total deposition fractions of fibers with � = 10 and � = 100 differ by 2 to 10 %. Regarding regional deposition, the fiber diameter represents a controlling factor insofar, as fibrous particles with dp = 0.1 � m are preferably deposited in the bronchioles and alveoli, whereas fibers with dp = 10 � m are exclusively accumulated in the extrathoracic region. Only deposition behavior of fibers with dp = 1 � m is more complex, since valuable particle frac- tions deposit in all compartments of the lungs. Local (i.e. generation-by-generation) deposition of fibrous particles is char- acterized by a deposition peak at airway generation 19 in the case of fibers with dp = 0.1 � m. The deposition maximum is subject to a continuous dislocation towards more proximal airway generations with increasing dp. Therefore, particles with dp = 10 � m are chiefly deposited in the first three bronchial airway generations. Differences of fiber deposition between sitting and light-work breathing conditions may be evaluated is insignificant in most cases. Only fibrous particles with dp = 1 � m significantly change their deposition behavior with increasing inhalative flow rate in the way that proximal depo- sition is remarkably enhanced at the cost of bronchiolar and alveolar deposition. In general, any increase of the inhalative flow rate Q causes a successive dislocation of fiber deposition from distal to proximal compartments of the human respi- ratory tract. The results obtained from the theoretical approach lead to the conclusion that thin fibers with variable length tend to deposit in the pulmonary region of the lung, where they represent a remarkable hazard for mesothelioma. Thick fi- bers are preferentially accumulated in the proximal bronchi and therefore may induce bronchial lung cancer (adenocarci- noma).
致癌石棉纤维在人呼吸道沉积的理论探讨
本文介绍了一种预测变形石棉纤维在人呼吸道沉积的随机模型。沉积计算通常基于气动直径的概念。除布朗扩散、惯性冲击和沉积作用外,单气道分岔脊上颗粒的捕获截留也被认为是计算区域和局部沉积分数的主要沉积机制。关于人体呼吸道中的总沉积,直径小于0.1 μ m的纤维(称为dp)的沉积分数比类似的球体低,而直径大于0.1 μ m的纤维的沉积分数比球体高。纤维长径比对总沉积的影响不显著,即当纤维= 10和纤维= 100时,总沉积分数相差2 ~ 10%。关于局部沉积,纤维直径是一个控制因素,因为dp = 0.1 μ m的纤维颗粒最好沉积在细支气管和肺泡中,而dp = 10 μ m的纤维只积聚在胸外区域。只有dp = 1 μ m的纤维的沉积行为更复杂,因为有价值的颗粒碎片沉积在肺的所有隔室。在dp = 0.1 μ m的纤维中,纤维颗粒局部(即一代一代)沉积的特征是在气道第19代出现沉积峰。随着dp的增加,沉积最大值会向更近的气道几代持续错位。因此,dp = 10 μ m的颗粒主要沉积在前3代支气管气道。在大多数情况下,坐着和轻度呼吸条件下纤维沉积的差异可以评估为微不足道。只有dp = 1 μ m的纤维颗粒随着吸入流速的增加而显著改变其沉积行为,近端沉积显著增强,但以细支气管和肺泡沉积为代价。一般来说,吸入流速Q的任何增加都会引起人体呼吸道远端至近端纤维沉积的连续脱位。从理论方法得到的结果得出结论,长度可变的细纤维倾向于沉积在肺的肺区,在那里它们对间皮瘤具有显著的危害。厚纤维优先积聚在近端支气管,因此可能诱发支气管肺癌(腺癌-瘤)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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