Drinking water arsenic has been shown to be associated with a host of adverse health outcomes at exposure levels >300 microg of As/L. However, the results are not consistent at exposures below this level. We have reviewed selected articles that examine the effects of drinking water arsenic on cardiovascular outcomes and present a rationale for studying these effects on women of reproductive age, and also over the course of pregnancy when they would potentially be more susceptible to adverse cardiovascular and reproductive outcomes. It is only recently that reproductive effects have been linked to drinking water arsenic. However, there is a paucity of information about the cardiovascular effects of drinking water arsenic on women of reproductive age. Under the cardiovascular challenge of pregnancy, we hypothesize that women with a slightly elevated exposure to drinking water arsenic may exhibit adverse cardiovascular outcomes at higher rates than in the general population. Studying sensitive clinical and sub-clinical indicators of disease in susceptible sub-populations may yield important information about the potentially enormous burden of disease related to low-level drinking water arsenic exposure.
"Several studies have associated high-level of arsenic exposure from drinking water with elevated risk of vascular diseases, including peripheral vascular disease, hypertension, ischemic heart disease and carotid atherosclerosis . Epidemiological studies reported increased incidence of hypertension in arsenic-exposed populations   . Further, evidences showed that arsenic induced hypertension in rats   and mice . "
"Arsenic levels greater than 10 lg/L (the standard set by WHO) in the groundwater are found in Taiwan, Chile, Argentina, Hungary, Bangladesh, India, Thailand, Vietnam , China, and the USA (Ahmed et al. 2006; Kwok 2007; Sun 2004). Chronic fluorosis is commonly found in many regions of the world, among which India and China are the worst affected (Hussain et al. 2010). "
[Show abstract][Hide abstract] ABSTRACT: Epidemiological and experimental studies have demonstrated the atherogenic effects of environmental toxicant arsenic and fluoride. Inflammatory mechanism plays an important role in the pathogenesis of atherosclerosis. The aim of the present study is to determine the effect of chronic exposure to arsenic and fluoride alone or combined on inflammatory response in rabbit aorta. We analyzed the expression of genes involved in leukocyte adhesion [P-selectin (P-sel) and vascular cell adhesion molecule-1(VCAM-1)], recruitment and transendothelial migration of leukocyte [interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1)] and those involved in pro-inflammatory cytokines [interleukin-6 (IL-6)]. We found that fluoride and arsenic alone or combined increased the expression of VCAM-1, P-sel, MCP-1, IL-8, and IL-6 at the RNA and protein levels. The gene expressions of inflammatory-related molecules were attenuated when co-exposure to the two toxicants compared with just one of them. We also examined the lipid profile of rabbits exposed to fluoride and (or) arsenic. The results showed that fluoride slightly increased the serum lipids but arsenic decreased serum triglyceride. We showed that inflammatory responses but not lipid metabolic disorder may play a crucial role in the mechanism of the cardiovascular toxicity of arsenic and fluoride.
Archives of Toxicology 03/2012; 86(6):849-56. DOI:10.1007/s00204-012-0803-9 · 5.98 Impact Factor
"); three of these studies measured individual arsenic exposure based on measured well water concentrations (Chen Y et al. 2007; Kwok et al. 2007; Yildiz et al. 2008), and two studies used a biomarker of exposure (Table 2) (Jones et al. 2011; Wang SL et al. 2007). Five studies defined hypertension based on established cutoffs for SBP and DBP levels measured with a standardized protocol and self-reported physician diagnosis or antihypertensive treatment (Chen CJ et al. 1995; Chen Y 2007; Jones et al. 2011; Rahman et al. 1999; Wang SL et al. 2007). "
[Show abstract][Hide abstract] ABSTRACT: 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.
Environmental Health Perspectives 12/2011; 120(4):494-500. DOI:10.1289/ehp.1103988 · 7.98 Impact Factor
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