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二氧化氮和超细颗粒主导了经催化式柴油颗粒过滤器处理的吸入柴油机废气的生物学效应。

Nitrogen dioxide and ultrafine particles dominate the biological effects of inhaled diesel exhaust treated by a catalyzed diesel particulate filter.

机构信息

* 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;

出版信息

Toxicol Sci. 2013 Oct;135(2):437-50. doi: 10.1093/toxsci/kft162. Epub 2013 Jul 28.

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.

摘要

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。

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