title: Ozone enhances the airway inflammation initiated by diesel exhaust.
abstract: 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 300 microg/m(3), followed after 5h by a 2-h exposure to filtered air and 0.2 ppm O(3), 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.
authors.affiliation: Department of Respiratory Medicine and Allergy, University Hospital, SE-901 85 Umeå, Sweden. jenny.bosson@lung.umu.se
authors.forename: Jenny
authors.initials: J
authors.lastname: Bosson
authors.forename: Jamshid
authors.initials: J
authors.lastname: Pourazar
authors.forename: Bertil
authors.initials: B
authors.lastname: Forsberg
authors.forename: Ellinor
authors.initials: E
authors.lastname: Adelroth
authors.forename: Thomas
authors.initials: T
authors.lastname: Sandström
authors.forename: Anders
authors.initials: A
authors.lastname: Blomberg
mesh_terms: D000328:Adult; D000393:Air Pollutants / Q000633:toxicity*; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D007958:Leukocyte Count; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D018375:Neutrophil Activation; D009504:Neutrophils / Q000187:drug effects / Q000473:pathology; D010126:Ozone / Q000633:toxicity*; D052638:Particulate Matter / Q000633:toxicity; D009195:Peroxidase / Q000378:metabolism; D011014:Pneumonia / Q000201:enzymology / Q000209:etiology* / Q000473:pathology; D013183:Sputum / Q000166:cytology / Q000201:enzymology; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D000393:Air Pollutants; D052638:Particulate Matter; D001335:Vehicle Emissions; D010126:Ozone; D009195:Peroxidase; D020780:Matrix Metalloproteinase 9