Arsenic Exposure and Hypertension: A Systematic Review
Arsenic Exposure and Hypertension: A Systematic Review
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 = 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 = 76.6%) and 2.57 (95% CI: 1.56, 4.24; p-value for heterogeneity = 0.13; I = 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 = 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.
Hypertension is a major risk factor for mortality and morbidity worldwide (Lopez et al. 2006; Murray and Lopez 1997; Oparil et al. 2003; Whitworth 2003). Risk factors for hypertension include high salt intake, increased body mass index (BMI), genetic predisposition, and exposure to psychosocial stress (Oparil et al. 2003; Whitworth 2003). Additional evidence, however, suggests that environmental factors play a role in hypertension development (Houston 2007;Klahr 2001; Laclaustra et al. 2009; Navas-Acien et al. 2007, 2008; Oparil et al. 2003; Tellez-Plaza et al. 2008; Vaziri 2008). The identification and mitigation of environmental exposures related to hypertension could contribute to reducing the worldwide burden of hypertension-related disease.
Among environmental exposures, epidemiologic and experimental evidence supports the possibility that arsenic plays a role in hypertension and other cardiometabolic diseases [Chen Y et al. 2011; Medrano et al. 2010; Navas-Acien et al. 2005; Smedley and Kinniburgh 2002; U.S. Department of Health and Human Services (DHHS) 2005; Wang CH et al. 2007; Wu et al. 1989]. Arsenic-contaminated drinking water represents a major public health problem internationally (Chappell et al. 2002; Chen CJ et al. 1995; Hinkle and Polette 1999; Mukherjee et al. 2006; Rahman et al. 1999). The World Health Organization and U.S. Environmental Protection Agency (EPA) standard for arsenic levels in drinking water is 10 μg/L (DHHS 2005; Whitworth 2003). In the United States alone, millions of persons are exposed to arsenic concentrations > 10 μg/L; whereas persons in Bangladesh, China, India, Cambodia, Ghana, Argentina, Mexico, and other countries around the world are exposed to arsenic levels in drinking water that are well beyond 10 μg/L (Navas-Acien et al. 2005; DHHS 2005). Epidemiologic studies conducted in arsenic-endemic areas in Taiwan and Bangladesh have found a positive relationship between inorganic arsenic exposure from drinking water and hypertension (Chen CJ et al. 1995; Rahman et al. 1999). Experimental studies have indicated that arsenic exposure may be involved in the development of hypertension through the promotion of inflammation, oxidative stress, and endothelial dysfunction (Aposhian et al. 2003; Balakumar et al. 2008; Lee et al. 2003; Smedley and Kinniburgh 2002; DHHS 2005).
To evaluate the potential relationship between arsenic and hypertension, we conducted a systematic review of epidemiologic studies that have investigated the association between inorganic arsenic exposure (using environmental measures or biomarkers) and hypertension outcomes [using hypertension status and systolic and diastolic blood pressure (SBP and DBP, respectively)].
Abstract and Introduction
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 = 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 = 76.6%) and 2.57 (95% CI: 1.56, 4.24; p-value for heterogeneity = 0.13; I = 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 = 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.
Introduction
Hypertension is a major risk factor for mortality and morbidity worldwide (Lopez et al. 2006; Murray and Lopez 1997; Oparil et al. 2003; Whitworth 2003). Risk factors for hypertension include high salt intake, increased body mass index (BMI), genetic predisposition, and exposure to psychosocial stress (Oparil et al. 2003; Whitworth 2003). Additional evidence, however, suggests that environmental factors play a role in hypertension development (Houston 2007;Klahr 2001; Laclaustra et al. 2009; Navas-Acien et al. 2007, 2008; Oparil et al. 2003; Tellez-Plaza et al. 2008; Vaziri 2008). The identification and mitigation of environmental exposures related to hypertension could contribute to reducing the worldwide burden of hypertension-related disease.
Among environmental exposures, epidemiologic and experimental evidence supports the possibility that arsenic plays a role in hypertension and other cardiometabolic diseases [Chen Y et al. 2011; Medrano et al. 2010; Navas-Acien et al. 2005; Smedley and Kinniburgh 2002; U.S. Department of Health and Human Services (DHHS) 2005; Wang CH et al. 2007; Wu et al. 1989]. Arsenic-contaminated drinking water represents a major public health problem internationally (Chappell et al. 2002; Chen CJ et al. 1995; Hinkle and Polette 1999; Mukherjee et al. 2006; Rahman et al. 1999). The World Health Organization and U.S. Environmental Protection Agency (EPA) standard for arsenic levels in drinking water is 10 μg/L (DHHS 2005; Whitworth 2003). In the United States alone, millions of persons are exposed to arsenic concentrations > 10 μg/L; whereas persons in Bangladesh, China, India, Cambodia, Ghana, Argentina, Mexico, and other countries around the world are exposed to arsenic levels in drinking water that are well beyond 10 μg/L (Navas-Acien et al. 2005; DHHS 2005). Epidemiologic studies conducted in arsenic-endemic areas in Taiwan and Bangladesh have found a positive relationship between inorganic arsenic exposure from drinking water and hypertension (Chen CJ et al. 1995; Rahman et al. 1999). Experimental studies have indicated that arsenic exposure may be involved in the development of hypertension through the promotion of inflammation, oxidative stress, and endothelial dysfunction (Aposhian et al. 2003; Balakumar et al. 2008; Lee et al. 2003; Smedley and Kinniburgh 2002; DHHS 2005).
To evaluate the potential relationship between arsenic and hypertension, we conducted a systematic review of epidemiologic studies that have investigated the association between inorganic arsenic exposure (using environmental measures or biomarkers) and hypertension outcomes [using hypertension status and systolic and diastolic blood pressure (SBP and DBP, respectively)].
