Airway inflammation after controlled exposure to diesel exhaust particulates

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 volu nteers. DEP were collected from the exhaust of a stationary diesel engine a nd were resuspended in an exposure chamber. Ten nonsmoking healthy voluntee rs were exposed for 2 h at rest to a controlled concentration of DEP (monit ored at 200 mu g/m(3) particulate matter of less than 10 mu m aerodynamic d iameter [PM10]) or air in a double-blind, randomized, crossover study. Expo sures were followed by serial spirometry and measurement of pulse, blood pr essure, exhaled carbon monoxide (CO), and methacholine reactivity, as well as sputum induction and venesection for up to 4 h after exposure, and a rep eat of all these procedures at 24 h after exposure. There were no changes i n cardiovascular parameters or lung function following exposure to DEP. Lev els of exhaled CO were increased ater exposure to DEP, and were maximal at 1 h (aic 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. E xposure to DEPs at high ambient concentrations leads to an airway inflammat ory response in normal volunteers.