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Review
, 120 (4), 494-500

Arsenic Exposure and Hypertension: A Systematic Review

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Review

Arsenic Exposure and Hypertension: A Systematic Review

Lalita N Abhyankar et al. Environ Health Perspect.

Abstract

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; 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.

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.

Conflict of interest statement

The authors declare they have no actual or potential competing financial interests.

Figures

Figure 1
Figure 1
Summary of search and screening process. aA total of 138 studies were not in English. bChen Y et al. (2007) and Jones et al. (2011) were the only studies including both hypertension and BP level end points.
Figure 2
Figure 2
ORs of hypertension by arsenic exposure levels. The area of each square is proportional to the inverse of the variance of the estimated log OR. Horizontal lines represent 95% CIs. In the Chen Y et al. (2007) study, arsenic concentrations in drinking water were estimated based on time-weighted arsenic concentrations (ΣCiTi Ti, where “Ci and Ti denote the well arsenic concentration and drinking duration for the ith well”).
Figure 3
Figure 3
Evaluation of dose response for arsenic exposure and hypertension. Blue symbols indicate studies conducted in populations with low arsenic levels in drinking water (average < 50 μg/L); black symbols indicate studies conducted in populations with moderate-to-high arsenic levels in drinking water (average > 50 μg/L). The size of each data point is inversely weighted based on the inverse of the variance of the estimated log OR. For the Wang SL et al. (2007) study, actual arsenic levels for each hair tertile were not provided, and values defining the arsenic exposure tertiles were approximated based on the geometric mean of hair arsenic.
Figure 4
Figure 4
Difference (95% CI) in mean SBP and DBP by arsenic exposure level. The area of each square is proportional to the inverse of the variance of the estimated. NA: not available [the study by Chen Y et al. (2007) did not include standard errors or data that would allow estimation of the standard errors for mean systolic and diastolic blood pressure SBP and DBP levels, and a 95% CI could not be calculated for this study]. aProfessions include taxidermists, garden fence makers, weekend cottage constructors, wood impregnators, electric pylon impregnators, and new house constructors (Jensen and Hansen 1998).

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References

    1. Aposhian HV, Zakharyan RA, Avram MD, Kopplin MJ, Wollenberg ML. Oxidation and detoxification of trivalent arsenic species. Toxicol Appl Pharmacol. 2003;193:1–8. - PubMed
    1. Appel LJ, Robinson KA, Guallar E, Erlinger T, Masood SO, Jehn M, et al. Utility of blood pressure monitoring outside of the clinic setting. Evid Rep Technol Assess (Summ) 2002;63:1–5. - PMC - PubMed
    1. Balakumar P, Kaur T, Singh M. Potential target sites to modulate vascular endothelial dysfunction: current perspectives and future directions. Toxicology. 2008;245:49–64. - PubMed
    1. Barchowsky A, Dudek EJ, Treadwell MD, Wetterhahn KE. Arsenic induces oxidant stress and NF-κB activation in cultured aortic endothelial cells. Free Radic Biol Med. 1996;21:783–790. - PubMed
    1. Barchowsky A, Roussel RR, Klei LR, James PE, Ganju N, Smith KR, et al. Low levels of arsenic trioxide stimulate proliferative signals in primary vascular cells without activating stress effector pathways. Toxicol Appl Pharmacol. 1999;159:65–75. - PubMed
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