背景:暴露于环境化学物质与心力衰竭的风险增加有关,但对左心室功能障碍(LVD)标志物的影响仍不确定.
目的:建立关于早期HF标记物及其与环境污染物关联的证据基础,我们进行了系统评价和荟萃分析.
方法:搜索,10月13日,2023年,包括PubMed,Embase,和没有过滤器的WebofScience,专注于报告心肌几何结构的观察性研究,结构,或没有心脏病史的个体的功能改变。这包括一般的成年人,工人,年轻人,和老人。使用ROBINS-I工具在研究和项目层面评估偏倚风险。
结果:系统评价包括17项研究,涉及接触空气污染的43.358人和接触重金属的2038人。大约41%的关联效应指标报告了心肌结构或功能的显着异常。污染物类别的元分析表明,LV收缩和舒张异常与PM2.5[-0.069(-0.104,-0.033);-0.044(-0.062,-0.025)]和PM10[-0.055(-0.087,-0.022);-0.030(-0.050,-0.013)]和NO2[-0.042(-0.071,-0.013);-0.021(-0.037],-以及导线暴露与左心室收缩异常之间的正相关[-0.033(-0.051,-0.016)]。
结论:为了增强对调查结果的信心并改善基线暴露的归因,作者建议进行更多的纵向和病例对照研究.这些研究应该考虑共同暴露,对于弱势群体,并确定可能需要调节的心脏毒性化合物。当检查心肌异常和环境暴露之间的联系时,还建议探索使用不良结果路径(AOP)方法的支持性使用以确认因果关系。
BACKGROUND: Exposure to environmental chemicals has been associated with an elevated risk of heart failure (HF). However, the impact on early markers of HF, such as left ventricular dysfunction (LVD), remains limited.
OBJECTIVE: To establish a foundation of evidence regarding early HF markers and their association with environmental pollutants, a systematic
review and meta-analysis was conducted.
METHODS: The search, conducted on October 13th, 2023, encompassed PubMed, Embase, and Web of Science without filters, focusing on observational studies reporting myocardial geometrical, structural, or functional alterations in individuals without a history of heart disease. This included the general adult population, workers, young people, and the elderly. The risk of bias was assessed using the ROBINS-I tool at both study and item levels.
RESULTS: The systematic
review included 17 studies involving 43.358 individuals exposed to air pollution and 2038 exposed to heavy metals. Approximately 41% of the effect measures of associations reported significant abnormalities in myocardial structure or function. The metanalyses by pollutants categories indicated positive associations between LV systolic and diastolic abnormalities and exposure to PM2.5 [-0.069 (-0.104, -0.033); -0.044 (-0.062, -0.025)] and PM10 [-0.055 (-0.087, -0.022); -0.030 (-0.050, -0.010)] and NO2 [-0.042 (-0.071, -0.013); -0.021 (-0.037, -0.004)], as well as positive associations between lead exposure and LV systolic abnormalities [-0.033 (-0.051, -0.016)].
CONCLUSIONS: Existing evidence shows that specific early markers of HF may be associated with exposure to chemical pollutants. It is recommended to include such endpoints in new longitudinal and case-control studies to confirm further risk associations. These studies should consider co-exposures, account for vulnerable groups, and identify cardiotoxic compounds that may require regulation. When examining the link between myocardial abnormalities and environmental exposure, it is also advisable to explore the supportive use of Adverse Outcome Pathway (AOP) approaches to confirm a causal relationship.