title: Nitrogen dioxide and ultrafine particles dominate the biological effects of inhaled diesel exhaust treated by a catalyzed diesel particulate filter.
abstract: We studied the impact of a catalyzed diesel particulate filter (DPF) on the toxicity of diesel exhaust. Rats inhaled exhaust from a Cummins ISM heavy-duty diesel engine, with and without DPF after-treatment, or HEPA-filtered air for 4h, on 1 day (single exposure) and 3 days (repeated exposures). Biological effects were assessed after 2h (single exposure) and 20h (single and repeated exposures) recovery in clean air. Concentrations of pollutants were (1) untreated exhaust (-DPF), nitric oxide (NO), 43 ppm; nitrogen dioxide (NO2), 4 ppm; carbon monoxide (CO), 6 ppm; hydrocarbons, 11 ppm; particles, 3.2×10(5)/cm(3), 60-70nm mode, 269 μg/m(3); (2) treated exhaust (+DPF), NO, 20 ppm; NO2, 16 ppm; CO, 1 ppm; hydrocarbons, 3 ppm; and particles, 4.4×10(5)/cm(3), 7-8nm mode, 2 μg/m(3). Single exposures to -DPF exhaust resulted in increased neutrophils, total protein and the cytokines, growth-related oncogene/keratinocyte chemoattractant, macrophage inflammatory protein-1α, and monocyte chemoattractant protein-1 in lung lavage fluid, as well as increased gene expression of interleukin-6, prostaglandin-endoperoxide synthase 2, metallothionein 2A, tumor necrosis factor-α, inducible nitric oxide synthase, glutathione S-transferase A1, heme oxygenase-1, superoxide dismutase 2, endothelin-1 (ET-1), and endothelin-converting enzyme-1 in the lung, and ET- 1 in the heart. Ratio of bigET-1 to ET-1 peptide increased in plasma in conjunction with a decrease in endothelial nitric oxide synthase gene expression in the lungs after exposure to diesel exhaust, suggesting endothelial dysfunction. Rather than reducing toxicity, +DPF exhaust resulted in heightened injury and inflammation, consistent with the 4-fold increase in NO2 concentration. The ratio of bigET-1 to ET-1 was similarly elevated after -DPF and +DPF exhaust exposures. Endothelial dysfunction, thus, appeared related to particle number deposited, rather than particle mass or NO2 concentration. The potential benefits of particulate matter reduction using a catalyzed DPF may be confounded by increase in NO2 emission and release of reactive ultrafine particles.
authors.affiliation: * Inhalation Toxicology Laboratory, Environmental Health Science and Research Bureau, Research and Radiation Directorate, Health Canada, Environmental Health Centre, Tunney's Pasture, Ottawa, Ontario K1A 0K9, Canada;
authors.forename: Subramanian
authors.initials: S
authors.lastname: Karthikeyan
authors.forename: Errol M
authors.initials: EM
authors.lastname: Thomson
authors.forename: Prem
authors.initials: P
authors.lastname: Kumarathasan
authors.forename: Josée
authors.initials: J
authors.lastname: Guénette
authors.forename: Debbie
authors.initials: D
authors.lastname: Rosenblatt
authors.forename: Tak
authors.initials: T
authors.lastname: Chan
authors.forename: Greg
authors.initials: G
authors.lastname: Rideout
authors.forename: Renaud
authors.initials: R
authors.lastname: Vincent
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid; D002384:Catalysis; D016207:Cytokines / Q000097:blood / Q000378:metabolism; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D016232:Endothelins / Q000378:metabolism; D009585:Nitrogen Dioxide / Q000633:toxicity*; D010316:Particle Size; D051381:Rats; D011916:Rats, Inbred F344; D001335:Vehicle Emissions
chemical_list: D016207:Cytokines; D016232:Endothelins; D001335:Vehicle Emissions; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost; D009585:Nitrogen Dioxide
keywords: diesel emission particles; diesel exhaust; diesel particulate filter; inflammation.; inhalation; nitrogen dioxide