Marc Hoylaerts, Center for Molecular and Vascular Biology, Leuven, Belgium.
Hamostaseologie. 2012;32(1):5-13. doi: 10.5482/ha-1179. Epub 2011 Oct 18.
Ambient environmental air pollutants include gaseous and particulate components. In polluted air, especially particulate matter seems responsible for cardiovascular complications: It consists of a heterogeneous mixture of solid and liquid particles with different diameters ranging from large thoracic to ultrafine particles, with a diameter <100 nm. Ultrafines can penetrate deeply into the lung to deposit in the alveoli. Cardiovascular manifestations result both from short-term and long-term exposure and have been linked to interference with the autonomic nervous system, direct translocation into the systemic circulation, pulmonary inflammation and oxidative stress. Thrombotic complications associated with air pollution comprise arterial and probably venous thrombogenicity. This review describes the existing epidemiological and experimental evidence to explain the rapid induction of myocardial infarction within 1-2 hours after exposure to polluted air and advances several explanations as to why more chronic exposure will lead to enhanced venous thrombogenicity. Mechanisms such as platelet activation, endothelial dysfunction, coagulation factor changes and microvesicle production are discussed.
环境空气污染物包括气态和颗粒成分。在污染的空气中，特别是颗粒物似乎是导致心血管并发症的原因：它由不同直径的固体和液体颗粒的不均匀混合物组成，直径范围从大到超细颗粒，直径<100nm。超细颗粒可以深入肺部沉积在肺泡中。心血管表现既来自短期暴露也来自长期暴露，与干扰自主神经系统、直接转移到全身循环、肺部炎症和氧化应激有关。与空气污染相关的血栓并发症包括动脉和可能的静脉血栓形成。本综述描述了现有的流行病学和实验证据，以解释暴露于污染空气后 1-2 小时内心肌梗死的快速发生，并提出了为什么更多的慢性暴露会导致增强的静脉血栓形成的几个解释。讨论了诸如血小板激活、内皮功能障碍、凝血因子变化和微泡产生等机制。
