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墨西哥下加利福尼亚州墨西卡利的混合粉尘实验性诱导的肺细胞毒性。

Lung cell toxicity experimentally induced by a mixed dust from Mexicali, Baja California, Mexico.

作者信息

Osornio-Vargas A R, Hernández-Rodríguez N A, Yáñez-Buruel A G, Ussler W, Overby L H, Brody A R

机构信息

Department of Biochemistry, Instituto Nacional de Cardiología Ignacio Chávez, México, D.F.

出版信息

Environ Res. 1991 Oct;56(1):31-47. doi: 10.1016/s0013-9351(05)80107-0.

DOI:10.1016/s0013-9351(05)80107-0
PMID:1655401
Abstract

Lung disease caused by nonoccupational exposures to inorganic particles from the soil has been reported in several areas of the world. We tested the toxic potential of dust samples from a Mexican city (Mexicali) that is frequently affected by dust storms and is geographically related to the area of San Diego, CA, where constituents of the soil have been reported to be fibrogenic. We found that samples of Mexicali dust are a mixture of approximately 75% potassium aluminum silicates (illite) and approximately 20% silica. Respirable size particles were highly hemolytic and induced lactic dehydrogenase release from alveolar macrophages exposed in vitro. Animals instilled intratracheally with the dust developed a multifocal interstitial lung disease associated with deposits of the aluminum silicates, which were identified by X-ray microanalysis. Inhalation studies in rats demonstrated that the majority of particles were deposited preferentially at the first alveolar duct bifurcations. Twenty-four hours later, numerous particles had been ingested by alveolar macrophages that had migrated to those sites of deposition. It is proposed that alveolar macrophages are attracted to the deposited particles by complement fragments since Mexicali dust is capable of activating complement proteins from both serum and bronchoalveolar lavage. Activation resulted in alveolar macrophage chemotaxis. Mexicali dust induced biological activities and lung changes similar to those of asbestos and silica, suggesting that this material could be an etiologic agent of pulmonary fibrosis in exposed individuals.

摘要

世界上多个地区都报道过因非职业性接触土壤中的无机颗粒而导致的肺部疾病。我们对来自墨西哥城市墨西卡利的沙尘样本的潜在毒性进行了测试,该城市经常受到沙尘暴影响,并且在地理位置上与加利福尼亚州圣地亚哥地区相关,据报道圣地亚哥地区土壤成分具有致纤维化作用。我们发现,墨西卡利沙尘样本约75%为钾铝硅酸盐(伊利石)和约20%为二氧化硅的混合物。可吸入粒径的颗粒具有高度溶血作用,并能在体外诱导肺泡巨噬细胞释放乳酸脱氢酶。经气管内注入沙尘的动物出现了多灶性间质性肺病,与铝硅酸盐沉积物有关,通过X射线微量分析得以确定。对大鼠的吸入研究表明,大多数颗粒优先沉积在第一级肺泡管分支处。24小时后,大量颗粒被迁移至这些沉积部位的肺泡巨噬细胞吞噬。有人提出,肺泡巨噬细胞被沉积颗粒吸引是由于补体片段,因为墨西卡利沙尘能够激活血清和支气管肺泡灌洗中的补体蛋白。激活导致肺泡巨噬细胞趋化。墨西卡利沙尘诱导的生物活性和肺部变化与石棉和二氧化硅相似,表明这种物质可能是接触者肺纤维化的病因。

相似文献

1
Lung cell toxicity experimentally induced by a mixed dust from Mexicali, Baja California, Mexico.墨西哥下加利福尼亚州墨西卡利的混合粉尘实验性诱导的肺细胞毒性。
Environ Res. 1991 Oct;56(1):31-47. doi: 10.1016/s0013-9351(05)80107-0.
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Pulmonary macrophages are attracted to inhaled particles through complement activation.肺巨噬细胞通过补体激活被吸引至吸入颗粒处。
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Inhalation of high concentrations of low toxicity dusts in rats results in impaired pulmonary clearance mechanisms and persistent inflammation.在大鼠中吸入高浓度低毒性粉尘会导致肺部清除机制受损和持续性炎症。
Toxicol Appl Pharmacol. 1997 Jul;145(1):10-22. doi: 10.1006/taap.1997.8102.
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Electron microscopic microanalysis of bronchoalveolar lavage: a way to identify exposure to silica and silicate dust.支气管肺泡灌洗的电子显微镜微量分析:一种识别二氧化硅和硅酸盐粉尘暴露的方法。
Occup Environ Med. 1997 Aug;54(8):560-5. doi: 10.1136/oem.54.8.560.
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Initiating the risk assessment process for inhaled particulate materials: development of short term inhalation bioassays.启动吸入颗粒物材料的风险评估过程:短期吸入生物测定法的开发。
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Pulmonary response to inhaled silica or titanium dioxide.肺部对吸入二氧化硅或二氧化钛的反应。
Toxicol Appl Pharmacol. 1991 Nov;111(2):201-10. doi: 10.1016/0041-008x(91)90024-9.
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In vitro induction of abnormal anaphases by contaminating atmospheric dust from the City of Mexicali, Baja California, Mexico.墨西哥下加利福尼亚州墨西卡利市大气尘埃污染导致体外异常后期的诱导。
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Silica-exposed macrophages release a growth-promoting activity for type II pneumocytes.接触二氧化硅的巨噬细胞释放促进II型肺细胞生长的活性物质。
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The comparison of a fibrogenic and two nonfibrogenic dusts by bronchoalveolar lavage.
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Complement facilitates macrophage phagocytosis of inhaled iron particles but has little effect in mediating silica-induced lung inflammatory and clearance responses.补体促进巨噬细胞对吸入铁颗粒的吞噬作用,但在介导二氧化硅诱导的肺部炎症和清除反应方面作用甚微。
Environ Res. 1991 Dec;56(2):186-203. doi: 10.1016/s0013-9351(05)80008-8.

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