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A Pathological Study of Acute Pulmonary Toxicity Induced by Inhaled Kanto Loam Powder

机译:吸入关东壤土粉引起的急性肺毒性的病理学研究

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摘要

The frequency and volume of Asian sand dust (ASD) (Kosa) are increasing in Japan, and it has been reported that ASD may cause adverse respiratory effects. The pulmonary toxicity of ASD has been previously analyzed in mice exposed to ASD particles by intratracheal instillation. To study the pulmonary toxicity induced by inhalation of ASD, ICR mice were exposed by inhalation to 50 or 200 mg/m3 Kanto loam powder, which resembles ASD in elemental composition and particle size, for 6 h a day over 1, 3, 6, 9, or 15 consecutive days. Histological examination revealed that Kanto loam powder induced acute inflammation in the whole lung at all the time points examined. The lesions were characterized by infiltration of neutrophils and macrophages. The intensity of the inflammatory changes in the lung and number of neutrophils in both histological lesions and bronchoalveolar lavage fluid (BALF) appeared to increase over time. Immunohistochemical staining showed interleukin (IL)-6- and tumor necrosis factor (TNF)-α-positive macrophages and a decrease in laminin positivity in the inflammatory lesions of the lung tissues. Electron microscopy revealed vacuolar degeneration in the alveolar epithelial cells close to the Kanto loam particles. The nitric oxide level in the BALF increased over time. These results suggest that inhaled Kanto loam powder may induce diffuse and acute pulmonary inflammation, which is associated with increased expression of inflammatory cytokines and oxidative stress.
机译:在日本,亚洲沙尘(ASD)(Kosa)的发生频率和数量正在增加,据报道,ASD可能引起呼吸道不良反应。先前已经通过气管内滴注在暴露于ASD颗粒的小鼠中分析了ASD的肺毒性。为了研究吸入ASD引起的肺毒性,将ICR小鼠吸入50或200 mg / m 3 关东壤土粉,其元素组成和粒径类似于ASD,持续6天连续1、3、6、9或15天。组织学检查表明,关东壤土散剂在所有检查的时间点都引起整个肺部的急性炎症。病变的特征是嗜中性粒细胞和巨噬细胞浸润。随着时间的推移,组织学病变和支气管肺泡灌洗液(BALF)中肺部炎症变化的强度和中性粒细胞的数量似乎增加。免疫组织化学染色显示,白细胞介素(IL)-6和肿瘤坏死因子(TNF)-α阳性巨噬细胞,肺组织炎性病变中层粘连蛋白阳性率降低。电子显微镜检查显示,关东壤土颗粒附近的肺泡上皮细胞液泡变性。 BALF中的一氧化氮含量随时间增加。这些结果表明,吸入的关东壤土粉可能会引起弥漫性和急性肺部炎症,这与炎症性细胞因子的表达增加和氧化应激有关。

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