Ozone enhances the airway inflammation initiated by diesel exhaust

Exposure to air pollution is associated with adverse health effects, with particulate matter (PM) and ozone (03) both indicated to be of considerable importance. Diesel engine exhaust (DE) and 03 generate substantial inflammatory effects in the airways. However, as yet it has not been determined whether a subsequent 03 exposure would add to the diesel-induced airway inflammatory effects. Healthy subjects underwent two separate exposure series: A 1-h DE exposure at a PM-concentration of 300 mu g/m(3), followed after 5 h by a 2-h exposure to filtered air and 0.2 ppm 03, respectively. Induced sputum was collected 18 h after the second exposure. A significant increase in the percentage of neutrophils (PMN) and concentration of myeloperoxidase (MPO) was seen in sputum post DE+O-3 vs. DE+air (p < 0.05 and < 0.05, respectively). Significant associations were observed between the responses in MPO concentration and total PMN cells (p = 0.001), and also between MPO and matrix metalloproteinase-9 (MMP-9) (p < 0.001). The significant increase of PMN and MPO after the DE+O-3 exposures, compared to DE+air, denotes an O-3-induced magnification of the DE-induced inflammation. Furthermore, the correlation between responses in MPO and number of PMNs and MMP-9 illustrate that the PMNs are activated, resulting in a more potent inflammatory response. The present study indicates that O-3 exposure adds significantly to the inflammatory response that is established by diesel exhaust. This interaction between exposure to particulate pollution and O-3 in sequence should be taken into consideration when health effects of air pollution are considered. (c) 2006 Elsevier Ltd. All rights reserved.