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1 Dept of Respiratory Medicine and Allergy, University Hospital, Umeå, Sweden and 2 Institute for Working Life, Dept of Occupational Chemistry, Umeå, Sweden
CORRESPONDENCE: E. Ädelroth, Dept of Respiratory Medicine and Allergy, University Hospital, S-90185, Umeå, Sweden. Fax: 46 90141369
Keywords: asthma, airway responsiveness, diesel exhaust, induced sputum
Received: September 7, 2000
Accepted January 18, 2001
This work was supported by the Swedish Heart and Lung Foundation.
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 µm (PM10) 300 µg·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.
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