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Cardiovascular health and particulate vehicular emissions: a critical evaluation of the evidence

机译:心血管健康和车辆微粒排放:证据的严格评估

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A major public health goal is to determine linkages between specific pollution sources and adverse health outcomes. This paper provides an integrative evaluation of the database examining effects of vehicular emissions, such as black carbon (BC), carbonaceous gasses, and ultrafine PM, on cardiovascular (CV) morbidity and mortality. Less than a decade ago, few epidemiological studies had examined effects of traffic emissions specifically on these health endpoints. In 2002, the first of many studies emerged finding significantly higher risks of CV morbidity and mortality for people living in close proximity to major roadways, vs. those living further away. Abundant epidemiological studies now link exposure to vehicular emissions, characterized in many different ways, with CV health endpoints such as cardiopulmonary and ischemic heart disease and circulatory-disease-associated mortality; incidence of coronary artery disease; acute myocardial infarction; survival after heart failure; emergency CV hospital admissions; and markers of atherosclerosis. We identify numerous in vitro, in vivo, and human panel studies elucidating mechanisms which could explain many of these cardiovascular morbidity and mortality associations. These include: oxidative stress, inflammation, lip-operoxidation and atherosclerosis, change in heart rate variability (HRV), arrhythmias, ST-segment depression, and changes in vascular function (such as brachial arterialrncaliber and blood pressure). Panel studies with accurate exposure information, examining effects of ambient components of vehicular emissions on susceptible human subjects, appear to confirm these mechanisms. Together, this body of evidence supports biological mechanisms which can explain the various CV epidemiological findings. Based upon these studies, the research base suggests that vehicular emissions are a major environmental cause of cardiovascular mortality and morbidity in the United States. As a means to reduce the public health consequences of such emissions, it may be desirable to promulgate a black carbon (BC) PM_(2.5) standard under the National Ambient Air Quality Standards, which would apply to both on and off-road diesels. Two specific critical research needs are identified. One is to continue research on health effects of vehicular emissions, gaseous as well as paniculate. The second is to utilize identical or nearly identical research designs in studies using accurate exposure metrics to determine whether other major PM pollutant sources and types may also underlie the specific health effects found in this evaluation for vehicular emissions.
机译:公共卫生的主要目标是确定特定污染源与不良健康结果之间的联系。本文对检查诸如黑碳(BC),碳质气体和超细PM的车辆排放对心血管(CV)发病率和死亡率的影响的数据库进行了综合评估。不到十年前,很少有流行病学研究专门研究交通排放对这些健康终点的影响。 2002年,出现了许多研究中的第一项,发现居住在主要道路附近的人与远离道路的人相比,患心血管疾病和死亡的风险明显更高。现在,大量的流行病学研究将暴露与车辆排放联系起来,车辆排放以多种不同方式表征,并与心血管健康终点(例如心肺和缺血性心脏病以及与循环疾病相关的死亡率)相关。冠状动脉疾病的发生率;急性心肌梗塞;心力衰竭后的存活率;紧急简历医院入院;和动脉粥样硬化的标志物。我们确定了许多体外,体内和人类实验研究,阐明了可以解释许多这些心血管疾病发病率和死亡率关联的机制。其中包括:氧化应激,炎症,嘴唇过氧化和动脉粥样硬化,心率变异性(HRV)变化,心律不齐,ST段压低以及血管功能变化(例如肱动脉口径和血压)。小组研究利用准确的暴露信息,检查了车辆排放的环境成分对易感人群的影响,似乎证实了这些机制。总之,这一证据支持可以解释各种心血管流行病学发现的生物学机制。基于这些研究,研究基础表明在美国,机动车排放是导致心血管疾病死亡率和发病率的主要原因。作为减少此类排放给公众健康造成影响的一种手段,可能希望颁布《国家环境空气质量标准》下的黑碳(BC)PM_(2.5)标准,该标准将同时适用于公路和非公路用柴油。确定了两个特定的关键研究需求。一种是继续研究车辆排放物,气体以及颗粒物对健康的影响。第二个是在使用准确的暴露指标的研究中利用相同或几乎相同的研究设计,以确定其他主要的PM污染物来源和类型是否也可能是本次评估中发现的针对车辆排放的特定健康影响的基础。

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