A review and rationale for studying the cardiovascular effects of drinking water arsenic in women of reproductive age

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Toxicology and Applied Pharmacology (Impact Factor: 3.71). 09/2007; 222(3):344-50. DOI: 10.1016/j.taap.2007.02.016
Source: PubMed


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.

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    • "In recent years, exposure to high levels of inorganic arsenic (iAs) through consumption of contaminated drinking water, concentrations above 10 g/L and frequently greater than 50 g/L, has been associated with the development of a number of chronic human health effects (Kwok, 2007; Tseng, 2008; Zheng et al., 2014). Yet, few data are available to evaluate the impact of more widespread low-moderate levels of drinking water iAs contamination, those less than 10 g/L (van Halem et al., 2009), in particular among women of reproductive age. "
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    ABSTRACT: We conducted a pilot study of associations between drinking water contaminated by inorganic arsenic (iAs), mostly <10μg/L, and self-reported chronic diseases in 297 pregnant women. Adjusted for confounding variables, we identified a positive association between iAs and heart disease (OR=1.63, 95%CI 0.81-3.04, p=0.094), which was stronger for women living at their current residence ≥10 years (OR=2.47, 95%CI 0.87-10.43, p=0.058). Confounder-adjusted associations were also suggested for iAs with kidney disease (OR=1.32, 95%CI 0.77-2.21, p=0.265) and with high blood pressure (OR=1.36, 95%CI 0.68-2.39, p=0.300). A post hoc power analysis indicated the need for a larger study with more statistical power.
    Full-text · Article · Nov 2015
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    • "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 [6]. Epidemiological studies reported increased incidence of hypertension in arsenic-exposed populations [7] [8] [9]. Further, evidences showed that arsenic induced hypertension in rats [10] [11] and mice [12]. "
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    ABSTRACT: The groundwater pollutant arsenic can cause various cardiovascular disorders. Angiotensin II, a potent vasoconstrictor, plays an important role in vascular dysfunction by promoting changes in endothelial function, vascular reactivity, tissue remodeling and oxidative stress. We investigated whether modulation of angiotensin II signaling and redox homeostasis could be a mechanism contributing to arsenic-induced vascular disorder. Rats were exposed to arsenic at 25, 50 and 100ppm of sodium arsenite through drinking water consecutively for 90days. Blood pressure was recorded weekly. On the 91st day, the rats were sacrificed for blood collection and isolation of thoracic aorta. Angiotensin converting enzyme and angiotensin II levels were assessed in plasma. Aortic reactivity to angiotensin II was assessed in organ-bath system. Western blot of AT1 receptors and G protein (Gαq/11), ELISA of signal transducers of MAP kinase pathway and reactive oxygen species (ROS) generation were assessed in aorta. Arsenic caused concentration-dependent increase in systolic, diastolic and mean arterial blood pressure from the 10th, 8th and 7th week onwards, respectively. Arsenic caused concentration-dependent enhancement of the angiotensin II-induced aortic contractile response. Arsenic also caused concentration-dependent increase in the plasma levels of angiotensin II and angiotensin converting enzyme and the expression of aortic AT1 receptor and Gαq/11 proteins. Arsenic increased aortic protein kinase C activity and the concentrations of protein tyrosine kinase, extracellular signal-regulated kinase-1/2 and vascular endothelial growth factor. Further, arsenic increased aortic mRNA expression of Nox2, Nox4 and p22phox, NADPH oxidase activity and ROS generation. The results suggest that arsenic-mediated enhancement of angiotensin II signaling could be an important mechanism in the arsenic-induced vascular disorder, where ROS could augment the angiotensin II signaling through activation of MAP kinase pathway. Copyright © 2015. Published by Elsevier Ireland Ltd.
    Full-text · Article · Jun 2015 · Chemico-biological interactions
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    • "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). "
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    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.
    Full-text · Article · Mar 2012 · Archives of Toxicology
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