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首页> 外文期刊>Toxicological sciences: An official journal of the Society of Toxicology >Nitrogen dioxide and ultrafine particles dominate the biological effects of inhaled diesel exhaust treated by a catalyzed diesel particulate filter
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Nitrogen dioxide and ultrafine particles dominate the biological effects of inhaled diesel exhaust treated by a catalyzed diesel particulate filter

机译：二氧化氮和超细颗粒支配着催化柴油机微粒过滤器处理的吸入柴油机废气的生物效应

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摘要

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), 43ppm; nitrogen dioxide (NO2), 4ppm; carbon monoxide (CO), 6ppm; hydrocarbons, 11ppm; particles, 3.2 × 105/cm3, 60-70nm mode, 269μg/m3; (2) treated exhaust (+DPF), NO, 20ppm; NO2, 16ppm; CO, 1ppm; hydrocarbons, 3ppm; and particles, 4.4 × 105/cm3, 7-8nm mode, 2μg/m3. 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.
机译：我们研究了催化柴油机微粒过滤器（DPF）对柴油机废气毒性的影响。在第1天（单次暴露）和3天（重复暴露）下，大鼠从有或没有DPF后处理的康明斯ISM重型柴油发动机或经过HEPA过滤的空气中吸入4小时。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）后评估生物效应。污染物的浓度为（1）未处理的废气（-DPF），一氧化氮（NO），43ppm;二氧化氮（NO2），4ppm;一氧化碳（CO）为6ppm;碳氢化合物，11ppm;颗粒，3.2×105 / cm3，60-70nm模式，269μg/ m3; （2）处理过的废气（+ DPF），NO，20ppm; NO2，16ppm;一氧化碳，1ppm;碳氢化合物，3ppm;和颗粒，4.4×105 / cm3，7-8nm模式，2μg/ m3。一次暴露于-DPF排气会导致肺灌洗液中的中性粒细胞，总蛋白和细胞因子增加，与生长相关的癌基因/角质形成细胞趋化因子，巨噬细胞炎性蛋白1α和单核细胞趋化蛋白1增加，以及白介素的基因表达增加-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-在肺中转化酶1，在心脏中转化ET-1。暴露于柴油机废气后，肺中bigET-1与ET-1肽的比率增加，同时肺中的内皮一氧化氮合酶基因表达降低，这提示内皮功能障碍。 + DPF排气不仅没有降低毒性，还导致伤害和炎症加剧，与NO2浓度增加4倍相一致。在暴露于-DPF和+ DPF后，bigET-1与ET-1的比率也同样升高。因此，内皮功能障碍似乎与沉积的颗粒数量有关，而不是与颗粒质量或NO 2浓度有关。使用催化的DPF减少颗粒物质的潜在好处可能会因NO2排放增加和反应性超细颗粒的释放而混淆。

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