* 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;
Toxicol Sci. 2013 Oct;135(2):437-50. doi: 10.1093/toxsci/kft162. Epub 2013 Jul 28.
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.
我们研究了催化式柴油颗粒过滤器（DPF）对柴油废气毒性的影响。大鼠吸入康明斯 ISM 重型柴油发动机的废气，分别在有和没有 DPF 后处理或高效空气过滤器的情况下，每天吸入 4 小时，连续吸入 3 天。在清洁空气中恢复 2 小时（单次暴露）和 20 小时（单次和重复暴露）后，评估了生物效应。污染物浓度为：（1）未经处理的废气（-DPF），一氧化氮（NO），43ppm；二氧化氮（NO2），4ppm；一氧化碳（CO），6ppm；碳氢化合物，11ppm；颗粒，3.2×10（5）/cm（3），60-70nm 模式，269μg/m（3）；（2）经处理的废气（+DPF），NO，20ppm；NO2，16ppm；CO，1ppm；碳氢化合物，3ppm；颗粒，4.4×10（5）/cm（3），7-8nm 模式，2μg/m（3）。单次暴露于-DPF 废气会导致肺灌洗液中的中性粒细胞、总蛋白和细胞因子（生长相关癌基因/角质细胞趋化因子、巨噬细胞炎性蛋白-1α和单核细胞趋化蛋白-1）增加，白细胞介素-6、前列腺素内过氧化物合酶 2、金属硫蛋白 2A、肿瘤坏死因子-α、诱导型一氧化氮合酶、谷胱甘肽 S-转移酶 A1、血红素加氧酶-1、超氧化物歧化酶 2、内皮素-1（ET-1）和内皮素转换酶-1在肺中的基因表达增加，以及暴露于柴油废气后心脏中的 ET-1 增加。暴露于柴油废气后，血浆中大 ET-1 与内皮型一氧化氮合酶基因表达减少的比值增加，提示内皮功能障碍。+DPF 废气不仅没有降低毒性，反而导致更高的损伤和炎症，这与 NO2 浓度增加了 4 倍一致。-DPF 和+DPF 废气暴露后，大 ET-1 与 ET-1 的比值也升高。因此，内皮功能障碍似乎与沉积的颗粒数量有关，而不是颗粒质量或 NO2 浓度。使用催化式 DPF 减少颗粒物可能会因 NO2 排放增加和释放反应性超细颗粒而受到影响。
