CIGARETTE-SMOKE MAKES AIRWAY AND EARLY PARENCHYMAL ASBESTOS-INDUCED LUNG-DISEASE WORSE IN THE GUINEA-PIG
CIGARETTE-SMOKE MAKES AIRWAY AND EARLY PARENCHYMAL ASBESTOS-INDUCED LUNG-DISEASE WORSE IN THE GUINEA-PIG
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DOI：
10.1164/ajrccm/136.2.271
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发表时间：
1987-08-01
期刊：
影响因子：
--
通讯作者：
CHURG, A
中科院分区：
文献类型：
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作者：
TRON, V;WRIGHT, JL;CHURG, A
为了评估香烟烟雾和石棉暴露的影响，我们将豚鼠分为4组：吸烟组和不吸烟组，石棉暴露组和不石棉暴露组。暴露于石棉的动物接受5 mg UICC amosite的单次气管内滴注，我们之前已经证明了这种剂量和给药方法会产生小气道的形态学变化以及最小的间质纤维化。动物每周吸烟5天，持续6个月。吸烟本身并不影响肺胶原含量、小气道壁厚度或气道周围组织的体积分数，但确实导致肺泡平均线性截距（Lm）显著增加。单独使用天冬氨酸可增加胶原含量、气道壁厚度和气道周围组织体积分数，后者用于评估间质纤维化。一个意想不到的发现是，石棉也增加了Lm。两种药物一起给药引起的所有类型的变化比任何一种药物单独给药引起的变化更严重，两种药物之间的相互作用通常是协同作用。暴露于烟雾的动物保留的石棉纤维负荷的3倍，那些没有暴露于烟雾中，保留的增加是更短的比长纤维。我们的结论是，香烟烟雾可以增强石棉引起的纤维化，可能是因为增加纤维潴留。同样，在这个模型中，石棉或石棉加上香烟烟雾会增加肺泡大小。纤维化的变化可能是吸烟石棉工人报告的非肿瘤性肺实质疾病发生率较高的原因;如果存在于人类，空气空间大小的变化可能与某些粉尘暴露工人组中观察到的气流阻塞有关。
In order to assess the effects of cigarette smoke and asbestos exposure, we divided guinea pigs into 4 groups: smoking or nonsmoking, and asbestos-exposed or not asbestos-exposed groups. Asbestos-exposed animals were given a single intratracheal instillation of 5 mg UICC amosite, a dose and method of administration that we have previously shown produces morphologic changes in the small airways as well as minimal interstitial fibrosis. Animals were smoked 5 days per week for 6 months. By itself, smoking did not affect lung collagen content, small airways wall thickness, or the volume fraction of tissue surrounding airways, but it did cause a significant increase in alveolar mean linear intercept (Lm). Asbestos alone increased collagen content, airway wallt thickness, and tissue volume fraction surrounding airways, the latter measure used to assess interstitial fibrosis. An unexpected finding was that asbestos also increased Lm. The two agents administered together caused more severe changes of all types than were produced by either agent alone, and the interaction between the 2 was generally synergistic. Smoke-exposed animals retained 3 times the asbestos fiber burden of those not smoke-exposed; the increase in retention was greater for short than for long fibers. We conclude that cigarette smoke can potentiate the fibrosis induced by asbestos, possibly because of increased fiber retention. As well, in this model, asbestos or asbestos plus cigarette smoke produces increases in alveolar size. The fibrotic changes may account for the greater incidences of non-neoplastic parenchymal lung disease reported in smoking asbestos workers; changes in air space size might, if present in humans, be related to the air-flow obstruction seen in some groups of dust-exposed workers.