Road tunnel air pollution induces bronchoalveolar inflammation in healthy subjects.
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 microm, particulate matter with a 50% cut-off aerodynamic diameter of 10 mum and nitrogen dioxide which had median concentrations of 64, 176 and 230 microg.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.
Larsson
B-M
BM
Dept of Public Health Sciences, Division of Occupational Medicine, Karolinska Institutet, SE-171 76 Stockholm, Sweden. britt-marie.larsson@ki.se
Sehlstedt
M
M
Grunewald
J
J
Sköld
C M
CM
Lundin
A
A
Blomberg
A
A
Sandström
T
T
Eklund
A
A
Svartengren
M
M
D000328:Adult; D000393:Air Pollutants / Q000633:toxicity*; D000397:Air Pollution; D001980:Bronchi / Q000473:pathology*; D001992:Bronchoalveolar Lavage Fluid; D005260:Female; D006801:Humans; D007249:Inflammation / Q000139:chemically induced* / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D052638:Particulate Matter; D011650:Pulmonary Alveoli / Q000473:pathology*; D012130:Respiratory Hypersensitivity / Q000139:chemically induced*; D020545:Respiratory Mucosa / Q000473:pathology; D001335:Vehicle Emissions
D000393:Air Pollutants; D052638:Particulate Matter; D001335:Vehicle Emissions