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雪松和松木成分对肺上皮的毒性。

The toxicity of constituents of cedar and pine woods to pulmonary epithelium.

作者信息

Ayars G H, Altman L C, Frazier C E, Chi E Y

机构信息

Department of Internal Medicine, University of Washington, Seattle 98195.

出版信息

J Allergy Clin Immunol. 1989 Mar;83(3):610-8. doi: 10.1016/0091-6749(89)90073-0.

DOI:10.1016/0091-6749(89)90073-0
PMID:2926083
Abstract

Occupational exposure to cedar and pine woods and pine resin (colophony) can cause asthma and chronic lung disease. Prior studies suggest that plicatic and abietic acids are responsible for the asthmatic reactions that occur in cedar-wood and colophony workers; however, the etiologic mechanism(s) of the chronic lung disease is unknown. To determine if plicatic acid from cedar wood and abietic acid from pine resin could directly damage lung cells, we exposed monolayers of rat type II and human A549 alveolar epithelial cells, intact rat lungs, and rat tracheal explants to solutions of plicatic and abietic acids. As indices of injury, we measured lysis of alveolar epithelial cells with a 51Cr technique, quantitative desquamation of epithelial cells from tracheal explants, and histologic alterations in tracheal explants and intact lungs. Plicatic and abietic acids both caused dose- and time-dependent lysis of alveolar epithelial cells. Instillation of plicatic and abietic acids into rat lungs produced bronchial epithelial sloughing. Abietic acid also caused destruction of the alveolar epithelium. The addition of either acid to rat tracheal explants caused epithelial desquamation that was dose- and time-dependent. Our results suggest that plicatic acid, a unique constituent of cedar wood, and abietic acid, the major constituent in pine resin, can produce lytic damage to alveolar, tracheal, and bronchial epithelial cells. We hypothesize that repeated occupational exposure to these substances might promote the chronic lung damage observed in some cedar- and pine-wood workers and in electronic workers exposed to colophony.

摘要

职业性接触雪松、松木和松脂(松香)可导致哮喘和慢性肺病。先前的研究表明,plicatic酸和松香酸是导致雪松木材和松香工人出现哮喘反应的原因;然而,慢性肺病的病因机制尚不清楚。为了确定来自雪松木材的plicatic酸和来自松脂的松香酸是否会直接损伤肺细胞,我们将大鼠II型和人A549肺泡上皮细胞单层、完整的大鼠肺和大鼠气管外植体暴露于plicatic酸和松香酸溶液中。作为损伤指标,我们用51Cr技术测量肺泡上皮细胞的裂解、气管外植体上皮细胞的定量脱落以及气管外植体和完整肺的组织学改变。plicatic酸和松香酸均导致肺泡上皮细胞出现剂量和时间依赖性裂解。向大鼠肺中滴注plicatic酸和松香酸会导致支气管上皮脱落。松香酸还会导致肺泡上皮破坏。向大鼠气管外植体中添加任何一种酸都会导致上皮脱落,且呈剂量和时间依赖性。我们的结果表明,雪松木材的独特成分plicatic酸和松脂中的主要成分松香酸可对肺泡、气管和支气管上皮细胞产生裂解损伤。我们推测,职业性反复接触这些物质可能会促使在一些雪松和松木工人以及接触松香的电子工人中观察到的慢性肺损伤。

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The toxicity of constituents of cedar and pine woods to pulmonary epithelium.雪松和松木成分对肺上皮的毒性。
J Allergy Clin Immunol. 1989 Mar;83(3):610-8. doi: 10.1016/0091-6749(89)90073-0.
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