Am. J. Respir. Crit. Care Med., Volume 162, Number 1, July 2000, 161-166

Airway Inflammation after Controlled Exposure to Diesel Exhaust Particulates

JULIA A. NIGHTINGALE, RICHARD MAGGS, PAUL CULLINAN, LOUISE E. DONNELLY, DUNCAN F. ROGERS, ROBERT KINNERSLEY, K. FAN CHUNG, PETER J. BARNES, MICHAEL ASHMORE, and ANTHONY NEWMAN-TAYLOR

Departments of Thoracic Medicine and Occupational and Environmental Medicine, Royal Brompton Hospital and National Heart and Lung Institute, Imperial College School of Medicine, and Imperial College Centre for Environmental Technology, Imperial College, London, United Kingdom

Epidemiologic evidence suggests a link between morbidity and mortality and levels of particulate matter in the atmosphere. We studied the inflammatory response to inhalation of diesel exhaust particulates (DEP) in normal volunteers. DEP were collected from the exhaust of a stationary diesel engine and were resuspended in an exposure chamber. Ten nonsmoking healthy volunteers were exposed for 2 h at rest to a controlled concentration of DEP (monitored at 200 µg/m³ particulate matter of less than 10 µm aerodynamic diameter [PM₁₀]) or air in a double-blind, randomized, crossover study. Exposures were followed by serial spirometry and measurement of pulse, blood pressure, exhaled carbon monoxide (CO), and methacholine reactivity, as well as sputum induction and venesection for up to 4 h after exposure, and a repeat of all these procedures at 24 h after exposure. There were no changes in cardiovascular parameters or lung function following exposure to DEP. Levels of exhaled CO were increased ater exposure to DEP, and were maximal at 1 h (air: 2.9 ± 0.2 ppm [mean ± SEM]; DEP: 4.4 ± 0.3 ppm; p < 0.001). There was an increase in sputum neutrophils and myeloperoxidase (MPO) at 4 h after DEP exposure as compared with 4 h after air exposure (neutrophils: 41 ± 4% versus 32 ± 4%; MPO: 151 ng/ml versus 115 ng/ml, p < 0.01), but no change in concentrations of inflammatory markers in peripheral blood. Exposure to DEPs at high ambient concentrations leads to an airway inflammatory response in normal volunteers.

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