Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205, USA.
Environ Health Perspect. 2012 Apr;120(4):494-500. doi: 10.1289/ehp.1103988. Epub 2011 Dec 2.
Environmental exposure to arsenic has been linked to hypertension in persons living in arsenic-endemic areas.
We summarized published epidemiologic studies concerning arsenic exposure and hypertension or blood pressure (BP) measurements to evaluate the potential relationship.
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.
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; I(2) = 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; I(2) = 76.6%) and 2.57 (95% CI: 1.56, 4.24; p-value for heterogeneity = 0.13; I(2) = 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; I(2) = 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.
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.
环境砷暴露已与生活在砷流行地区的人患高血压有关。
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,以评估潜在的关系。
我们检索了 PubMed、Embase 和 TOXLINE,并应用了预先确定的排除标准。我们从 11 项横断面研究中提取或推导了关联测量值,并使用逆方差加权随机效应模型计算了汇总比值比(OR)。
比较最高和最低砷暴露类别的高血压汇总 OR 为 1.27(95%置信区间[CI]:1.09,1.47;异质性检验 p 值<0.001;I²=70.2%)。在饮用水中砷浓度中等至高的人群中,汇总 OR 分别为 1.15(95%CI:0.96,1.37;异质性检验 p 值=0.002;I²=76.6%)和 2.57(95%CI:1.56,4.24;异质性检验 p 值=0.13;I²=46.6%),在排除有影响力的研究后。在饮用水中砷浓度低的人群中,相应的汇总 OR 为 1.56(95%CI:1.21,2.01;异质性检验 p 值=0.27;I²=24.6%)。纳入 6 项具有可用数据的研究进行剂量-反应评估显示,随着砷暴露量的增加,高血压的几率呈上升趋势。很少有研究评估了砷暴露水平对收缩压和舒张压(SBP 和 DBP)测量值的影响,而且这些研究的结果尚无定论。需要进一步的证据来评估环境砷暴露与高血压之间的剂量-反应关系。
在这项系统评价中,我们发现了砷与高血压患病率之间的关联。由于研究数量少、存在有影响力的研究以及缺乏前瞻性证据,因此对环境砷暴露对高血压的因果效应的解释受到限制。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。