Road tunnel air pollution induces bronchoalveolar inflammation in healthy subjects
Road tunnel air pollution induces bronchoalveolar inflammation in healthy subjects
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DOI：
10.1183/09031936.00035706
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发表时间：
2007-04-01
影响因子：
24.3
通讯作者：
Svartengren, M.
中科院分区：
文献类型：
--
作者：
Larsson, B-M.;Sehlstedt, M.;Svartengren, M.
与农药有关的空气污染与有害的呼吸系统影响有关。本研究的目的是探讨暴露于公路隧道内的空气污染是否会引起气道炎症和凝血反应。共有16名健康受试者接受了两次支气管镜检查，包括支气管粘膜活检和支气管肺泡灌洗（BAL），随机顺序为：一次在忙碌公路隧道中暴露于空气污染2小时后的14小时，一次在正常活动期间暴露于城市空气的受试者的对照日之后。在支气管镜检查前采集外周血样本。公路隧道暴露包括50%截止空气动力学直径为2.5 μ m的颗粒物、50%截止空气动力学直径为10 μ m的颗粒物和二氧化氮，其中位浓度分别为64、176和230 μ g.m（-3）。与对照组相比，公路隧道暴露后BAL液总细胞数、淋巴细胞和肺泡巨噬细胞的数量显著增加。显着较高的核表达的转录因子组分c-Jun被发现在支气管上皮暴露后。没有上调的粘附分子或细胞浸润和凝血因子是unaffected.In的结论，健康受试者暴露于交通相关的空气污染导致在较低的气道炎症反应与细胞迁移，连同迹象的启动信号转导在支气管上皮细胞。
Traffic-related air pollution is associated with adverse respiratory effects. The aim of the present study was to investigate whether exposure to air pollution in a road tunnel causes airway inflammatory and blood coagulation responses.A total of 16 healthy subjects underwent bronchoscopy with bronchial mucosal biopsies and bronchoalveolar lavage (BAL) on two occasions, in random order: once at 14 h after a 2-h exposure to air pollution in a busy road tunnel, and once after a control day with subjects exposed to urban air during normal activities. Peripheral blood was sampled prior to bronchoscopy.The road tunnel exposures included particulate matter with a 50% cut-off aerodynamic diameter of 2.5 mu m, particulate matter with a 50% cut-off aerodynamic diameter of 10 mu m and nitrogen dioxide which had median concentrations of 64, 176 and 230 mu g.m(-3), respectively. Significantly higher numbers of BAL fluid total cell number, lymphocytes and alveolar macrophages were present after road tunnel exposure versus control. Significantly higher nuclear expression of the transcription factor component c-Jun was found in the bronchial epithelium after exposure. No upregulation of adhesion molecules or cellular infiltration was present and blood coagulation factors were unaffected.In conclusion, exposure of healthy subjects to traffic-related air pollution resulted in a lower airway inflammatory response with cell migration, together with signs of an initiated signal transduction in the bronchial epithelium.