Donaldson K, Stone V, Seaton A, MacNee W
Biomedicine Research Group, School of Life Sciences, Napier University, Edinburgh, Scotland.
Environ Health Perspect. 2001 Aug;109 Suppl 4(Suppl 4):523-7. doi: 10.1289/ehp.01109s4523.
Well-documented air pollution episodes throughout recent history have led to deaths among individuals with cardiovascular and respiratory disease. Although the components of air pollution that cause the adverse health effects in these individuals are unknown, a small proportion by mass but a large proportion by number of the ambient air particles are ultrafine, i.e., less than 100 nm in diameter. This ultrafine component of particulate matter with a mass median aerodynamic diameter less than 10 microm (PM(10) may mediate some of the adverse health effects reported in epidemiologic studies and for which there is toxicologic evidence to support this contention. The exact mechanism by which ultrafine particles have adverse effects is unknown, but these particles have recently been shown to enhance calcium influx on contact with macrophages. Oxidative stress is also to be anticipated at the huge particle surface; this can be augmented by oxidants generated by recruited inflammatory leukocytes. Atheromatous plaques form in the coronary arteries and are major causes of morbidity and death associated epidemiologically with particulate air pollution. In populations exposed to air pollution episodes, blood viscosity, fibrinogen, and C-reactive protein (CRP) were higher. More recently, increases in heart rate in response to rising air pollution have been described and are most marked in individuals who have high blood viscosity. In our study of elderly individuals, there were significant rises in CRP, an index of inflammation. In this present review, we consider the likely interactions between the ultrafine particles the acute phase response and cardiovascular disease.
近代史上有充分记录的空气污染事件已导致心血管和呼吸系统疾病患者死亡。尽管导致这些个体出现不良健康影响的空气污染成分尚不清楚，但按质量计占比小但按数量计占比大的环境空气颗粒物是超细颗粒物，即直径小于100纳米。这种质量中位空气动力学直径小于10微米的颗粒物（PM10）中的超细成分可能介导了一些流行病学研究中报告的不良健康影响，并且有毒理学证据支持这一观点。超细颗粒物产生不良影响的确切机制尚不清楚，但最近已表明这些颗粒在与巨噬细胞接触时会增强钙内流。在巨大的颗粒表面也可预期会产生氧化应激；募集的炎性白细胞产生的氧化剂可增强这种氧化应激。冠状动脉中形成动脉粥样硬化斑块，这是与颗粒空气污染在流行病学上相关的发病和死亡的主要原因。在暴露于空气污染事件的人群中，血液粘度、纤维蛋白原和C反应蛋白（CRP）较高。最近，已描述了随着空气污染加剧心率增加的情况，并且在血液粘度高的个体中最为明显。在我们对老年人的研究中，炎症指标CRP显著升高。在本综述中，我们考虑了超细颗粒物、急性期反应和心血管疾病之间可能的相互作用。
