Arsenic Exposure and Subclinical Endpoints of Cardiovascular Diseases.
Arsenic Exposure and Subclinical Endpoints of Cardiovascular Diseases.
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DOI：
10.1007/s40572-014-0011-2
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发表时间：
2014-06-01
影响因子：
7.9
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中科院分区：
文献类型：
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机制证据表明，饮用水中砷暴露会增加活性氧的产生，并影响炎症反应和内皮一氧化氮的动态平衡。这些砷诱导的事件可能导致内皮功能障碍，从而增加动脉粥样硬化和心血管疾病的风险。我们回顾了越来越多的流行病学证据，这些证据评估了砷暴露与中间标志物和预测未来心血管风险的亚临床措施之间的关联。横断面研究表明，高水平或低至中等水平的砷暴露与亚临床动脉粥样硬化、QT间期延长和血管内皮细胞功能障碍的循环标志物呈正相关。其他中间终点的证据是有限的，如氧化应激和炎症的标志物、QT离散度和血脂谱。需要进行前瞻性研究，以加强砷对心血管疾病亚临床终点影响的因果推断，特别是在较低的砷暴露水平下。
Mechanistic evidence suggests that arsenic exposure from drinking water increases the production of reactive oxygen species and influences inflammatory responses and endothelial nitric oxide homeostasis. These arsenic-induced events may lead to endothelial dysfunction that increases the risk of atherosclerosis and cardiovascular disease. We reviewed accumulating epidemiologic evidence that evaluated the association between arsenic exposure and intermediate markers and subclinical measures that predict future cardiovascular risk. Cross-sectional studies have indicated positive associations between high or low-to-moderate levels of arsenic exposure with indices of subclinical atherosclerosis, QT interval prolongation, and circulating markers of endothelial dysfunction. The evidence is limited for other intermediate endpoints such as markers of oxidative stress and inflammation, QT dispersion, and lipid profiles. Prospective studies are needed to enhance the causal inferences of arsenic's effects on subclinical endpoints of cardiovascular disease, especially at lower arsenic exposure levels.