Churg A, Wright J L, Hobson J, Stevens B
Department of Pathology, University of British Columbia, Vancouver, Canada.
Int J Exp Pathol. 1992 Jun;73(3):287-97.
Long asbestos fibres are generally considered to have greater disease-producing potential than short asbestos fibres. However, recent reports have suggested that short fibre asbestos appears to be as effective an inducer of macrophage growth factors and toxic oxygen species as long fibre asbestos, but that short fibres are readily removed from lung and do not gain access to tissues. Because smoke is believed to impair the clearance of asbestos fibres from lung, we examined the clearance of a short (geometric mean length 1.3 microns) amosite preparation administered by intratracheal instillation to guinea-pigs. Half the animals in each group were exposed to the smoke of 10 cigarettes daily. Animals were sacrificed 1 day, 1 week, or 1 month later, the macrophages recovered by lavage, and fibre concentrations and sizes determined by analytical electron microscopy in macrophages and lung tissue. A 30-fold increase was seen in total numbers of fibres retained in macrophages in smokers compared to non-smokers by 1 month, and there was an eightfold increase in retention of short fibres in the lung tissue by 1 month. By contrast, a long fibre amosite preparation (geometric mean length 8.9 microns) showed approximately the same increase in fibre retention in macrophages, but only a twofold increase in tissue retention. We conclude that (1) cigarette smoke markedly impairs the clearance of short amosite fibres from the lung with enhanced retention of fibres in both macrophages and tissue; (2) the effects of smoke on short fibre tissue retention appear to be greater than those on long fibre retention; (3) with the long fibre preparation, smoke causes increased tissue retention of relatively shorter fibres; (4) for both fibre size experiments, the increase in total fibres in macrophages in smoke-exposed animals reflects an increase in the total number of fibre-containing macrophages, rather than an increase in the number of fibres phagocytized per macrophage; (5) enhanced short fibre retention markedly increases total fibre surface area, a parameter which has been suggested as a measure of fibre toxicity, to the point where short fibres might under some circumstances have roughly the same potential toxicity as long fibres. These observations suggest that short asbestos fibres could play an important role in the pathogenesis of some types of asbestos-related disease in cigarette smokers.
一般认为,长石棉纤维比短石棉纤维具有更大的致病潜力。然而,最近的报告表明,短纤维石棉似乎与长纤维石棉一样,是巨噬细胞生长因子和有毒氧物种的有效诱导剂,但短纤维很容易从肺部清除,无法进入组织。由于人们认为烟雾会损害石棉纤维从肺部的清除,我们研究了通过气管内滴注给予豚鼠的短(几何平均长度1.3微米)铁石棉制剂的清除情况。每组动物中有一半每天暴露于10支香烟的烟雾中。在1天、1周或1个月后处死动物,通过灌洗回收巨噬细胞,并通过分析电子显微镜测定巨噬细胞和肺组织中的纤维浓度和大小。到1个月时,与非吸烟者相比,吸烟者巨噬细胞中保留的纤维总数增加了30倍,到1个月时,肺组织中短纤维的保留量增加了8倍。相比之下,长纤维铁石棉制剂(几何平均长度8.9微米)在巨噬细胞中的纤维保留量增加大致相同,但组织保留量仅增加了两倍。我们得出以下结论:(1)香烟烟雾明显损害短铁石棉纤维从肺部的清除,导致纤维在巨噬细胞和组织中的保留增加;(2)烟雾对短纤维组织保留的影响似乎大于对长纤维保留的影响;(3)对于长纤维制剂,烟雾会导致相对较短纤维在组织中的保留增加;(4)对于两种纤维尺寸实验,暴露于烟雾的动物巨噬细胞中总纤维的增加反映了含纤维巨噬细胞总数的增加,而不是每个巨噬细胞吞噬的纤维数量的增加;(5)短纤维保留的增加显著增加了总纤维表面积,这一参数被认为是衡量纤维毒性的指标,以至于在某些情况下短纤维可能具有与长纤维大致相同的潜在毒性。这些观察结果表明,短石棉纤维可能在吸烟者某些类型的石棉相关疾病的发病机制中起重要作用。