McFadden D, Wright J, Wiggs B, Churg A
Am J Pathol. 1986 Apr;123(1):95-9.
For study of the penetration of asbestos fibers into airway walls, guinea pigs were given amosite asbestos by intratracheal instillation. Half of the animals were also exposed to cigarette smoke. Animals were sacrificed at 1 week and 1 month, and numbers of fibers in airway walls were counted in histologic sections. In both smoke-exposed and nonexposed groups, numbers of fibers per square millimeter of airway wall increased from 1 week to 1 month in the respiratory bronchioles. At each time period, smoke-exposed animals had significantly higher numbers of fibers in the airway walls, compared with nonexposed animals. It is concluded that 1) continued transport of fibers into interstitial tissues may be the reason that asbestosis can progress after cessation of exposure; 2) cigarette smoke increases the penetration of fibers into airway walls. This effect may play a role in the increased incidence of disease seen in smoking, compared with nonsmoking, asbestos workers.
为了研究石棉纤维向气道壁的渗透情况,通过气管内滴注的方式给豚鼠注入铁石棉。其中一半动物还暴露于香烟烟雾中。在1周和1个月时处死动物,并在组织学切片中计数气道壁中的纤维数量。在呼吸性细支气管中,无论暴露于烟雾与否的组,每平方毫米气道壁中的纤维数量从1周增加到1个月。在每个时间段,与未暴露动物相比,暴露于烟雾的动物气道壁中的纤维数量显著更高。得出以下结论:1)纤维持续向间质组织转运可能是石棉沉着病在接触停止后仍会进展的原因;2)香烟烟雾会增加纤维向气道壁的渗透。与不吸烟的石棉工人相比,这种效应可能在吸烟人群中疾病发病率增加方面起作用。