二噁英暴露所致心血管损害及其机制的研究进展
Research progress on PCDD/Fs-induced cardiovascular damage and related mechanisms
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摘要:
多氯二苯并二噁英/呋喃（简称二噁英）是来源于人类活动和工业排放的持久性环境污染物，可经由食物链层层富集，在人体内蓄积，造成多种健康损害，包括心血管损害。近年来，心血管疾病一直是造成我国及全球死亡的首要原因。因此，本文着眼于二噁英的心血管系统毒性，对相关流行病学及毒理学文献进行了综述。首先，本文回顾了已有的流行病学报道，归纳了二噁英暴露分别与高血压、缺血性心脏病、其他心血管不良结局的发（患）病率和死亡率的关联性研究。其次，本文总结了二噁英致心血管毒性的毒理学研究，提示二噁英可引起实验动物发生动脉粥样硬化性改变、血压水平改变、心肌结构及舒缩功能改变。最后，本文简述了既往文献发现的二噁英所致心血管系统毒性的可能机制，包括芳香烃受体介导、引起氧化损伤、激活炎性反应及造成脂质代谢紊乱等相关通路。以上归纳与综述提示，二噁英暴露会对实验动物及人类的心血管系统造成不良影响，增加心血管疾病的患病风险，但其具体机制尚未明确。
Abstract: Polychlorinated dibenzo-dioxins and polychlorinated dibenzo-furans (PCDD/Fs) are persistent organic pollutants derived from anthropogenic activities and industrial processes, and can be bio-magnified through food chain and bio-accumulate in human bodies, causing various adverse health effects, including cardiovascular impairments. Cardiovascular diseases have been the leading cause of death in China and across the world. Focusing on cardiovascular toxicity of PCDD/Fs, related epidemiological and toxicological studies were reviewed in the present paper. First, epidemiological studies showed associations between PCDD/Fs exposure and the incidence/prevalence and mortality rates of hypertension, ischemic heart disease, and other adverse cardiovascular outcomes. Second, toxicological studies showed that PCDD/Fs caused atherosclerosis formation and changes of blood pressure levels, myocardial structure, and cardiac contractility. Last, previously proposed mechanisms on the cardiovascular toxicity of PCDD/Fs included activating aryl hydrocarbon receptor, oxidative stress, or inflammation, and disturbing lipid metabolism. Above summaries indicated that PCDD/Fs exposure would induce adverse effects on the cardiovascular systems of animals and humans, and elevate the risk of cardiovascular diseases. However, the specific mechanisms remain to be elucidated.
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