Diesel exhaust enhances airway responsiveness in asthmatic subjects.
Particulate matter (PM) pollution has been associated with negative health effects, including exacerbations of asthma following exposure to PM peaks. The aim of the present study was to investigate the effects of short-term exposure to diesel exhaust (DE) in asthmatics, by specifically addressing the effects on airway hyperresponsiveness, lung function and airway inflammation. Fourteen nonsmoking, atopic asthmatics with stable disease, on continuous treatment with inhaled corticosteroids, were included. All were hyperresponsive to methacholine. Each subject was exposed to DE (particles with a 50% cut-off aerodynamic diameter of 10 microm (PM10) 300 microg x m(-3)) and air during 1 h on two separate occasions. Lung function was measured before and immediately after the exposures. Sputum induction was performed 6 h, and methacholine inhalation test 24 h, after each exposure. Exposure to DE was associated with a significant increase in the degree of hyperresponsiveness, as compared to after air, of 0.97 doubling concentrations at 24 h after exposure (p < 0.001). DE also induced a significant increase in airway resistance (p=0.004) and in sputum levels of interleukin (IL)-6 (p=0.048). No changes were detected in sputum levels of methyl-histamine, eosinophil cationic protein, myeloperoxidase and IL-8. This study indicated that short-term exposure to diesel exhaust, equal to high ambient levels of particulate matter, is associated with adverse effects in asthmatic airways, even in the presence of inhaled corticosteroid therapy. The increase in airway responsiveness may provide an important link to epidemiological findings of exacerbations of asthma following exposure to particulate matter.
Nordenhäll
C
C
Dept of Respiratory Medicine and Allergy, University Hospital, Umeå, Sweden.
Pourazar
J
J
Ledin
M C
MC
Levin
J O
JO
Sandström
T
T
Adelroth
E
E
D000328:Adult; D000403:Airway Resistance / Q000187:drug effects / Q000276:immunology; D001249:Asthma / Q000175:diagnosis / Q000209:etiology* / Q000276:immunology; D016535:Bronchial Hyperreactivity / Q000175:diagnosis / Q000209:etiology* / Q000276:immunology; D001985:Bronchial Provocation Tests; D005260:Female; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D001335:Vehicle Emissions / Q000009:adverse effects*
D015850:Interleukin-6; D001335:Vehicle Emissions