Arsenic exposure and hypertension: a systematic review.
Arsenic exposure and hypertension: a systematic review.
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DOI：
10.1289/ehp.1103988
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发表时间：
2012-04
影响因子：
10.4
通讯作者：
Navas-Acien A
中科院分区：
文献类型：
--
作者：
Abhyankar LN;Jones MR;Guallar E;Navas-Acien A
背景：砷的环境暴露与生活在砷流行地区的人的高血压有关。目的：我们总结了已发表的有关砷暴露与高血压或血压 (BP) 测量的流行病学研究，以评估潜在关系。数据来源和提取：我们检索了 PubMed、Embase 和 TOXLINE，并应用了预定的排除标准。我们确定了 11 项横断面研究，从中提取或导出关联性度量，并使用逆方差加权随机效应模型计算汇总优势比 (OR)。数据综合：比较最高和最低砷暴露类别的高血压的汇总 OR 为 1.27 [95% 置信区间 (CI)：1.09、1.47；异质性的 p 值 = 0.001； I2 = 70.2%]。在饮用水中砷浓度为中等到高的人群中，合并 OR 为 1.15（95% CI：0.96, 1.37；异质性 p 值 = 0.002；I2 = 76.6%）和 2.57（95% CI：1.56, 4.24；异质性 p 值 = 0.13；I2 = 46.6%）分别排除一项有影响力的研究之前和之后。饮用水中砷浓度较低的人群中相应的汇总 OR 为 1.56（95% CI：1.21，2.01；异质性 p 值 = 0.27；I2 = 24.6%）。包括六项可用数据研究在内的剂量反应评估显示，随着砷暴露的增加，高血压的发病率呈增加趋势。很少有研究评估砷暴露水平对收缩压和舒张压（分别是收缩压和舒张压）测量值的变化，并且这些研究报告了不确定的结果。结论：在这项系统评价中，我们确定了砷与高血压患病率之间的关联。由于研究数量少、存在影响力的研究以及缺乏前瞻性证据，解释环境砷对高血压的因果影响受到限制。需要更多的证据来评估环境砷暴露与高血压之间的剂量反应关系。
Background: Environmental exposure to arsenic has been linked to hypertension in persons living in arsenic-endemic areas. Objective: We summarized published epidemiologic studies concerning arsenic exposure and hypertension or blood pressure (BP) measurements to evaluate the potential relationship. Data sources and extraction: We searched PubMed, Embase, and TOXLINE and applied predetermined exclusion criteria. We identified 11 cross-sectional studies from which we abstracted or derived measures of association and calculated pooled odds ratios (ORs) using inverse-variance weighted random-effects models. Data synthesis: The pooled OR for hypertension comparing the highest and lowest arsenic exposure categories was 1.27 [95% confidence interval (CI): 1.09, 1.47; p-value for heterogeneity = 0.001; I2 = 70.2%]. In populations with moderate to high arsenic concentrations in drinking water, the pooled OR was 1.15 (95% CI: 0.96, 1.37; p-value for heterogeneity = 0.002; I2 = 76.6%) and 2.57 (95% CI: 1.56, 4.24; p-value for heterogeneity = 0.13; I2 = 46.6%) before and after excluding an influential study, respectively. The corresponding pooled OR in populations with low arsenic concentrations in drinking water was 1.56 (95% CI: 1.21, 2.01; p-value for heterogeneity = 0.27; I2 = 24.6%). A dose–response assessment including six studies with available data showed an increasing trend in the odds of hypertension with increasing arsenic exposure. Few studies have evaluated changes in systolic and diastolic BP (SBP and DBP, respectively) measurements by arsenic exposure levels, and those studies reported inconclusive findings. Conclusion: In this systematic review we identified an association between arsenic and the prevalence of hypertension. Interpreting a causal effect of environmental arsenic on hypertension is limited by the small number of studies, the presence of influential studies, and the absence of prospective evidence. Additional evidence is needed to evaluate the dose–response relationship between environmental arsenic exposure and hypertension.
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影响因子：
6.1
作者：
Klahr, S
通讯作者：
Klahr, S
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作者：
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作者：
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