A review and rationale for studying the cardiovascular effects of drinking water arsenic in women of reproductive age.
ABSTRACT 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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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. · 5.08 Impact Factor
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ABSTRACT: Arsenic speciation was performed based on liquid chromatographic separation followed by gradient hydride generation (GHG) and quartz atomizer atomic absorption spectrometric detection. The arsenic species, i.e., arsenate (As(V)), arsenite (As(III)), monomethylarsonic acid (MMA), dimethylarsinic acid (DMA) and trimethylarsine oxide (TMAO), were separated on C30-5 columns, and the concept of gradient hydride generation facilitates high conversion efficiency of the arsenic species into corresponding hydrides. The use of 2% L-cysteine in the GHG process gives rise to further improvements on the hydride generation efficiency of 13% to 32% for the arsenic species. The hydrides were separated in a unique design of gas–liquid separator, which not only ensures a complete separation but minimizes the dispersion of hydrides when delivering into the atomizer, resulting in a maximum of 13-fold improvement on the sensitivity of As(V) compared to previous studies. A separation process was finished within 800 s by injecting 100 µL sample solution, achieving detection limits of 0.9, 1.4, 1.4, 1.6, 1.5 µg/L, respectively, for As(V), As(III), MMA, DMA and TMAO. Precisions of less than 3% and 6% RSD were obtained for the five arsenic species at 100 µg/L and 20 µg/L, respectively. Three arsenic species, i.e., As(V), DMA and TMAO, were identified in Hijiki samples by this procedure.Journal of Analytical Atomic Spectrometry 01/2010; 25(1). · 3.40 Impact Factor
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ABSTRACT: Because dramatic cases of arsenic contamination of water resources, soils, vegetables, humans and animals increase, this review has focussed on the fate and behaviour of this element and what kind of health impacts are related with its release in surface or ground waters. In a first part, we point out how the primary minerals can lead to As mobilization and exportation by surface waters and suspended matter. We also emphasize the particular key role for As retention through both adsorption onto natural Fe(III) (hydr)oxides, Mn oxides and/or precipitation as Fe(III) arsenates. Nowadays, numerous and efficient systems for arsenic removal from any natural resources are available to produce good quality drinking water (with <10μg/l As); however it is not within the scope of the present review. In a second part we focus on recent knowledge about the human toxicity of the various arsenic species. Chronic exposure to As in drinking water lead to many health diseases and, although the mechanisms of toxification/detoxification are not well identified, the role of methylated species is discussed. Some epidemiologic studies are cited, but the exact relationship between past chronic As exposure and present health diseases has been questioned.Reviews in Environmental Science and Bio/Technology 11/2008; 7(4):307-323. · 2.26 Impact Factor