Road tunnel air pollution induces bronchoalveolar inflammation in healthy subjects

被引:73
作者
Larsson, B-M. [1 ]
Sehlstedt, M.
Grunewald, J.
Skold, C. M.
Lundin, A.
Blomberg, A.
Sandstrom, T.
Eklund, A.
Svartengren, M.
机构
[1] Karolinska Inst, Dept Publ Hlth Sci, Div Occupat Med, SE-17176 Stockholm, Sweden
[2] Karolinska Inst, Dept Med, Div Resp Med, Stockholm, Sweden
[3] Stockholm Cty Council, Dept Environm & Occupat Hlth, Stockholm Ctr Publ Hlth, Stockholm, Sweden
[4] Univ Hosp, Dept Resp Med & Allergy, Umea, Sweden
关键词
air pollution; airway inflammation; bronchoalveolar lavage; cell count; particles;
D O I
10.1183/09031936.00035706
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
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.
引用
收藏
页码:699 / 705
页数:7
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