Exposure to air pollution is associated with adverse health effects, with particulate matter (PM) and ozone (O 3 ) both indicated to be of considerable importance. Diesel engine exhaust (DE) and O 3 generate substantial inflammatory effects in the airways. However, as yet it has not been determined whether a subsequent O 3 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 300μg/m 3 , followed after 5h by a 2-h exposure to filtered air and 0.2ppm O 3 , respectively. Induced sputum was collected 18h 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.