Low-level arsenic exposure, AS3MT gene polymorphism and cardiovascular diseases in rural Texas counties
F. Marie Hall Institute for Rural and Community Health, Texas Tech University Health Science Center, 3601 4th Street, STOP 6232, Lubbock, TX 79430-6232, USA. Environmental Research
(Impact Factor: 4.37).
02/2012; 113:52-7. DOI: 10.1016/j.envres.2012.01.003
Most Americans living in rural areas use groundwater for drinking. Exposure to low-level (around the current U.S. standard 10 μg/L) arsenic in drinking water is associated with increased mortality of cardiovascular diseases. The current study was to determine if coronary heart disease, hypertension, and hyperlipidemia were associated with low-level arsenic exposure and AS3MT gene single nucleotide polymorphism (SNP) A35991G (rs10748835) in rural Texas. Subjects (156 men, 343 women, 40-96 years of age with a mean of 61) were residents from rural counties Cochran, Palmer, and Bailey, Texas. Groundwater arsenic concentration at each subject's home was estimated with ArcGIS inverse distance weighted interpolation based on the residential location's distances to surrounding wells with known water arsenic concentrations. The estimated groundwater arsenic concentration ranged from 2.2 to 15.3 (mean 6.2) μg/L in this cohort. Logistic regression analysis showed that coronary heart disease was associated with higher arsenic exposure (p<0.05) and with AS3MT genotype GG vs. AA (p<0.05) after adjustments for age, ethnicity, gender, education, smoking status, alcoholism, and anti-hyperlipidemia medication. Hypertension was associated with higher arsenic exposure, while hyperlipidemia was associated with genotype AG vs. AA of the AS3MT gene (p<0.05). Thus, coronary heart disease and its main risk factors were associated with low-level arsenic exposure, AS3MT polymorphism or both.
Available from: Tanvir Abir
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ABSTRACT: Background. There is inconclusive evidence from cross-sectional and cohort studies that arsenic exposure is a risk factor involved in the development of hypertension. Methods. A database search, using several keywords, was conducted to identify relevant studies. Separate odds ratio estimates for arsenic exposure with concentration only and arsenic exposure with duration, including biomarker, were extracted from studies that met all inclusion criteria. The extracted odds ratios (OR) comparing the highest exposure categories with the lowest in each study were pooled using the random effects methods of meta-analysis. Heterogeneity of odds ratios in the included studies were analyzed using I(2) statistics. Results. Eight studies were analyzed. Using the exposure as arsenic concentration in the drinking water, the OR estimate was 1.9 (95% CI: 1.2-3.0), with the I(2) = 92%, while using the exposure as concentration and duration, the OR estimate was 1.4 (95% CI: 0.95-2.0) with the I(2) = 80%. Meta-regression was done and the quality of exposure measurement was found to be significantly associated with the effect measure. For a one unit increase in the score from exposure assessment, the odds ratio decreased by 6%. No publication bias was evident. The only major weaknesses of this study were heterogeneity across studies and small sample size. Conclusions. The study findings provide limited evidence for a relationship between arsenic and hypertension. In summary, the relationship between arsenic exposure and hypertension is still inconclusive and needs further validation through prospective cohort studies.
Available from: Katarina Paunovic
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ABSTRACT: Arsenic is constantly present in drinking water supply systems of Zrenjanin municipality across decades. It presents a great public health problem in Serbia, but its relationship with acute coronary syndrome (ACS) has not been studied previously.
The aims of this study were to assess the incidence of ACS in two areas from Zrenjanin municipality consuming different levels of arsenic in drinking water, and to explore the association between arsenic exposure and the probability of fatal outcome of ACS.
The research was a registry-based ecological study of two populations consuming water with different arsenic levels, based on current guidelines (10 μg/L). Median arsenic in the area above national standard was 80 μg/L; median arsenic in the other area was 1 μg/L. Newly diagnosed cases of ACS were obtained from the National Registry for Acute Coronary Syndrome from 2006 to 2010.
The two populations were comparable by age, gender, and prevalence of risk factors for ACS. Standardized incidence rates (SIR) of ACS were higher for people consuming arsenic above standard (average five-year SIR was 237.00 per 100.000; 95% CI=214.93-260.74), in comparison to people consuming arsenic within limits (average SIR=124.40 per 100.000; 95% CI=96.00-158.56). Exposure to arsenic above limits was insignificantly associated with fatal outcome of ACS for the whole population, men and women.
Consumption of arsenic above national standards was associated with higher risk for the occurrence of acute coronary syndrome and with insignificantly higher probability of fatal outcome of ACS in Zrenjanin municipality.
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ABSTRACT: Inorganic arsenic (iAs) is a complete transplacental carcinogen in mice. Previous studies have demonstrated that in utero exposure to iAs promotes cancer in adult mouse offspring, possibly acting through epigenetic mechanisms. Humans and rodents enzymatically convert iAs to its methylated metabolites. This reaction requires S-adenosylmethionine (SAM) as methyl group donor. SAM is also required for DNA methylation. Supplementation with folate, a major dietary source of methyl groups for SAM synthesis, has been shown to modify iAs metabolism and the adverse effects of iAs exposure. However, effects of gestational folate supplementation on iAs metabolism and fetal DNA methylation have never been thoroughly examined. In the present study, pregnant CD1 mice were fed control (i.e. normal folate, or 2.2mg/kg) or high folate diet (11mg/kg) from gestational day (GD) 5 to 18 and drank water with 0 or 85ppm of As (as arsenite) from GD8 to 18. The exposure to iAs significantly decreased body weight of GD18 fetuses and increased both SAM and S-adenosylhomocysteine (SAH) concentrations in fetal livers. High folate intake lowered the burden of total arsenic in maternal livers but did not prevent the effects of iAs exposure on fetal weight or hepatic SAM and SAH concentrations. In fact, combined folate-iAs exposure caused further significant body weight reduction. Notably, iAs exposure alone had little effect on DNA methylation in fetal livers. In contrast, the combined folate-iAs exposure changed the CpG island methylation in 2,931 genes, including genes known to be imprinted. Most of these genes were associated with neurodevelopment, cancer, cell cycle, and signaling networks. The canonical Wnt-signaling pathway, which regulates fetal development, was among the most affected biological pathways. Taken together, our results suggest that a combined in utero exposure to iAs and a high folate intake may adversely influence DNA methylation profiles and weight of fetuses, compromising fetal development and possibly increasing the risk for early-onset of disease in offspring.
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