Giorgini Paolo, Di Giosia Paolo, Grassi Davide, Rubenfire Melvyn, Brook Robert D, Ferri Claudio
University of L'Aquila, Department of Life, Health and Environmental Sciences - San Salvatore Hospital, Delta 6 Building - V.le San Salvatore, Coppito (L'Aquila), 67100. Italy.
Curr Pharm Des. 2016;22(1):28-51. doi: 10.2174/1381612822666151109111712.
Both high arterial blood pressure (BP) and elevated levels of fine particulate matter (PM2.5) air pollution have been associated with an increased risk for several cardiovascular (CV) diseases, including stroke, heart failure, and myocardial infarction. Given that PM2.5 and high BP are each independently leading risk factors for premature mortality worldwide, a potential relationship between these factors would have tremendous public health repercussions. Therefore, the aim of this review is to summarize recent evidence linking air pollution and BP. Epidemiological findings demonstrate that particulate pollutants cause significant increases in BP parameters in relation to both short and long-term exposures, with robust evidence for exposures to PM2.5. Moreover, recent epidemiological studies suggest a positive association between residence within regions with higher levels of ambient PM and an increased incidence and prevalence of overt hypertension. Studies provide consistent results that elevated concentrations of pollutants increase hospital admissions and/or emergency visits for hypertensive disorders and also support that PM levels increases BP in vulnerable subsets of individuals (pregnant women, high CV risk individuals). In this context, PM-mediated BP elevations may be an important pathway which acts as a potential triggering factor for acute CV events. Mechanistic evidence illustrates plausible pathways by which acute and chronic exposures to air pollutants might disrupt hemodynamic balance favoring vasoconstriction, including autonomic imbalance and augmented release of various pro-oxidative, inflammatory and/or hemodynamically-active mediators. Together these responses may underlie PM-induced BP elevations; however, full details regarding the responsible mechanisms require further studies. As a consequence of the ubiquity of air pollution, even a small effect on raising BP and/or the prevalence of hypertension, i.e. the major risk factor for mortality and morbidity worldwide, would have enormous global public health implications.
高动脉血压（BP）和空气中细颗粒物（PM2.5）污染水平升高均与包括中风、心力衰竭和心肌梗死在内的多种心血管（CV）疾病风险增加有关。鉴于PM2.5和高BP均为全球过早死亡的独立主要风险因素，这些因素之间的潜在关系将产生巨大的公共卫生影响。因此，本综述的目的是总结近期将空气污染与BP联系起来的证据。流行病学研究结果表明，无论是短期还是长期接触，颗粒物污染物都会导致BP参数显著升高，有充分证据表明接触PM2.5会出现这种情况。此外，最近的流行病学研究表明，居住在环境PM水平较高地区与显性高血压的发病率和患病率增加之间存在正相关。研究提供了一致的结果，即污染物浓度升高会增加高血压疾病的住院人数和/或急诊就诊次数，也支持PM水平会使易感个体亚组（孕妇、心血管高风险个体）的BP升高。在这种情况下，PM介导的BP升高可能是一个重要途径，作为急性心血管事件的潜在触发因素。机制证据说明了急性和慢性接触空气污染物可能破坏有利于血管收缩的血流动力学平衡的合理途径，包括自主神经失调以及各种促氧化、炎症和/或血流动力学活性介质的释放增加。这些反应共同构成了PM诱导BP升高的基础；然而，有关具体机制的详细信息还需要进一步研究。由于空气污染无处不在，即使对BP升高和/或高血压患病率（即全球死亡和发病的主要风险因素）产生微小影响，也将对全球公共卫生产生巨大影响。
