Hallberg Lance M, Ward Jonathan B, Wickliffe Jeffrey K, Ameredes Bill T
Sealy Center for Environmental Health and Medicine, University of Texas Medical Branch, Galveston, TX, USA.
Department of Preventive Medicine and Community Health, University of Texas Medical Branch, Galveston, TX, USA.
Environ Health Insights. 2017 Jun 19;11:1178630217714215. doi: 10.1177/1178630217714215. eCollection 2017.
Since its beginning, more than 117 years ago, the compression-ignition engine, or diesel engine, has grown to become a critically important part of industry and transportation. Public concerns over the health effects from diesel emissions have driven the growth of regulatory development, implementation, and technological advances in emission controls. In 2001, the United States Environmental Protection Agency and California Air Resources Board issued new diesel fuel and emission standards for heavy-duty engines. To meet these stringent standards, manufacturers used new emission after-treatment technology, and modified fuel formulations, to bring about reductions in particulate matter and nitrogen oxides within the exhaust. To illustrate the impact of that technological transition, a brief overview of pre-2007 diesel engine exhaust biomarkers of genotoxicity and health-related concerns is provided, to set the context for the results of our research findings, as part of the Advanced Collaborative Emissions Study (ACES), in which the effects of a 2007-compliant diesel engine were examined. In agreement with ACES findings reported in other tissues, we observed a lack of measurable 2007-compliant diesel treatment-associated DNA damage, in lung tissue (comet assay), blood serum (8-hydroxy-2'-deoxyguanosine [8-OHdG] assay), and hippocampus (lipid peroxidation assay), across diesel exhaust exposure levels. A time-dependent assessment of 8-OHdG and lipid peroxidation also suggested no differences in responses across diesel exhaust exposure levels more than 24 months of exposure. These results indicated that the 2007-compliant diesel engine reduced measurable reactive oxygen species-associated tissue derangements and suggested that the 2007 standards-based mitigation approaches were effective.
自117多年前诞生以来,压燃式发动机,即柴油发动机,已发展成为工业和交通运输中至关重要的一部分。公众对柴油排放对健康影响的担忧推动了排放控制法规制定、实施及技术进步的发展。2001年,美国环境保护局和加利福尼亚空气资源委员会发布了重型发动机新的柴油燃料和排放标准。为满足这些严格标准,制造商采用了新的排放后处理技术并改进了燃料配方,以减少尾气中的颗粒物和氮氧化物。为说明这一技术转变的影响,本文简要概述了2007年前柴油发动机排气中遗传毒性生物标志物及与健康相关的问题,以此为我们作为先进合作排放研究(ACES)一部分的研究结果设定背景,在该研究中对符合2007年标准的柴油发动机的影响进行了研究。与其他组织报告的ACES研究结果一致,我们观察到在不同柴油尾气暴露水平下,在肺组织(彗星试验)、血清(8-羟基-2'-脱氧鸟苷[8-OHdG]试验)和海马体(脂质过氧化试验)中,均未检测到与符合2007年标准的柴油处理相关的DNA损伤。对8-OHdG和脂质过氧化的时间依赖性评估还表明,在超过24个月的暴露中,不同柴油尾气暴露水平下的反应没有差异。这些结果表明,符合2007年标准的柴油发动机减少了可测量的与活性氧相关的组织紊乱,并表明基于2007年标准的缓解方法是有效的。