Ohashi Y, Nakai Y, Sugiura Y, Ohno Y, Okamoto H
Department of Otolaryngology, Osaka City University Medical School, Japan.
ORL J Otorhinolaryngol Relat Spec. 1993;55(1):36-40. doi: 10.1159/000276350.
Nitrogen dioxide exposure-induced mucosal pathology of the guinea pig trachea was studied. Exposure to 3 or 9 ppm of nitrogen dioxide for 6 h a day, 6 times weekly for 2 weeks resulted in decreased ciliary activity as well as a dramatic eosinophil accumulation to the epithelium and submucosal layer. Especially exposure to 9 ppm of nitrogen dioxide induced epithelial injury through the activation of eosinophils accumulated in the tracheal mucosa. The epithelial damage induced by nitrogen dioxide could lead to hyperresponsiveness and prolonged allergic inflammation. Our study suggests that environmental nitrogen dioxide could contribute to the hyperresponsiveness and could most probably be involved in the development and chronicity of airway allergic disorders.
研究了二氧化氮暴露诱导的豚鼠气管黏膜病理学变化。每天暴露于3或9 ppm二氧化氮中，每周6次，每次6小时，持续2周，结果导致纤毛活性降低，以及上皮和黏膜下层出现大量嗜酸性粒细胞积聚。特别是暴露于9 ppm二氧化氮通过激活积聚在气管黏膜中的嗜酸性粒细胞诱导上皮损伤。二氧化氮诱导的上皮损伤可导致高反应性和持续性过敏性炎症。我们的研究表明，环境中的二氧化氮可能导致高反应性，很可能参与气道过敏性疾病的发生和慢性发展。
