BackgroundMillions of people in Bangladesh are at risk of chronic arsenic toxicity from drinking contaminated groundwater, but little is known about diet as an additional source of As exposure.MethodsWe employed a duplicate diet survey to quantify daily As intake in 47 women residing in Pabna, Bangladesh. All samples were analyzed for total As, and a subset of 35 samples were measured for inorganic arsenic (iAs) using inductively coupled plasma mass spectrometry equipped with a dynamic reaction cell.ResultsMedian daily total As intake was 48 μg As/day [interquartile range (IQR), 33–67) from food and 4 μg As/day (IQR, 2–152) from drinking water. On average, iAs comprised 82% of the total As detected in dietary samples. After adjusting for the estimated inorganic fraction, 34% [95% confidence interval (CI), 21–49%] of all participants exceeded the World Health Organization’s provisional tolerable daily intake (PTDI) of 2.1 μg As/kg-day. Two of the 33 women who used a well with < 50 μg As/L exceeded this recommendation.ConclusionsWhen drinking water concentrations exceeded the Bangladesh drinking water standard of 50 μg As/L, ingested water was the dominant source of exposure. However, as drinking water As concentrations decrease, the relative contribution of dietary As sources becomes more important to ingested dose. The combined intake from both diet and drinking water can cause some individuals to exceed the PTDI in spite of using a tube well that contains < 50 μg As/L.
Drinking shallow groundwater with naturally elevated concentrations of arsenic is causing widespread disease in many parts of South and Southeast Asia. In the Bengal Basin, growing reliance on deep (>150 m) groundwater has lowered exposure. In the most affected districts of Bangladesh, shallow groundwater concentrations average 100 to 370 μg L−1, while deep groundwater is typically < 10 μg L−1. Groundwater flow simulations have suggested that, even when deep pumping is restricted to domestic use, deep groundwater in some areas of the Bengal Basin is at risk of contamination. However, these simulations have neglected the impedance of As migration by adsorption to aquifer sediments. Here we quantify for the first time As sorption on deeper sediments in situ by replicating the intrusion of shallow groundwater through injection of 1,000 L of deep groundwater modified with 200 μg L−1 of As into a deeper aquifer. Arsenic concentrations in the injected water were reduced by 70% due to adsorption within a single day. Basin-scale modelling indicates that while As adsorption extends the sustainable use of deep groundwater, some areas remain vulnerable; these areas can be prioritized for management and monitoring.
13 14More and more people in Bangladesh have recently become aware of the risk of drinking 15 arsenic-contaminated groundwater, and have been trying to obtain drinking water from less 16 arsenic-contaminated sources. In this study, arsenic intakes of 18 families living in one block of a rural 17 village in an arsenic-affected district of Bangladesh were evaluated to investigate their actual arsenic 18 intake via food, including from cooking water, and to estimate the contribution of each food category 19 and of drinking water to the total arsenic intake. Water consumption rates were estimated by the 20 self-reporting method. The mean drinking water intake was estimated as about 3 L/d without gender 21 difference. Arsenic intakes from food were evaluated by the duplicate portion sampling method. The 22 duplicated foods from each family were divided into four categories (cooked rice, solid food, cereals 23 for breakfast, and liquid food), and the arsenic concentrations of each food category and of the 24 drinking water were measured. The mean arsenic intake from water and food by male subjects was 25 0.18 ± 0.13 (n = 12) and that by female subjects was 0.096 ± 0.007 mg/d (n = 6), and the range for all 26 18 respondents was 0.043-0.49 mg/d. The average contributions to the total arsenic intake were, from 27 drinking water, 13%; liquid food, 4.4%; cooked rice, 56%; solid food, 11%; and cereals, 16%. Arsenic 28 intake via drinking water was not high despite the highly contaminated groundwater in the survey area 29 because many families had changed their drinking water sources to less contaminated ones. Instead, 30 cooked rice contributed most to the daily arsenic intake. Use of contaminated water for cooking by 31 several families was suspected based on comparisons of arsenic concentrations between drinking 32 water and liquid food, and between rice before and after cooking. Detailed investigation suggested that 33 six households used contaminated water for cooking but not drinking, leading to an increase of arsenic 34 intake via arsenic-contaminated cooking water. 35 36 2
Background: Arsenic is an epigenetic toxicant and could influence fetal developmental programming. Objectives: We evaluated the association between arsenic exposure and DNA methylation in maternal and umbilical cord leukocytes. Methods: Drinking-water and urine samples were collected when women were at ≤ 28 weeks gestation; the samples were analyzed for arsenic using inductively coupled plasma mass spectrometry. DNA methylation at CpG sites in p16 ( n = 7) and p53 ( n = 4), and in LINE-1 and Alu repetitive elements (3 CpG sites in each), was quantified using pyrosequencing in 113 pairs of maternal and umbilical blood samples. We used general linear models to evaluate the relationship between DNA methylation and tertiles of arsenic exposure. Results: Mean (± SD) drinking-water arsenic concentration was 14.8 ± 36.2 μg/L (range: < 1–230 μg/L). Methylation in LINE-1 increased by 1.36% [95% confidence interval (CI): 0.52, 2.21%] and 1.08% (95% CI: 0.07, 2.10%) in umbilical cord and maternal leukocytes, respectively, in association with the highest versus lowest tertile of total urinary arsenic per gram creatinine. Arsenic exposure was also associated with higher methylation of some of the tested CpG sites in the promoter region of p16 in umbilical cord and maternal leukocytes. No associations were observed for Alu or p53 methylation. Conclusions: Exposure to higher levels of arsenic was positively associated with DNA methylation in LINE-1 repeated elements, and to a lesser degree at CpG sites within the promoter region of the tumor suppressor gene p16 . Associations were observed in both maternal and fetal leukocytes. Future research is needed to confirm these results and determine if these small increases in methylation are associated with any health effects.
Results suggest that maternal arsenic exposure early in pregnancy negatively affects newborn birth weight and that maternal hair provides the best integrated measure of arsenic exposure.
BackgroundUrinary arsenic metabolites (UAs) are used as biomarkers of exposure and metabolism.ObjectivesTo characterize inter- and intraindividual variability in UAs in healthy individuals.MethodsIn a longitudinal study conducted in Bangladesh, we collected water and spot urine samples from 196 participants every 3 months for 2 years. Water arsenic (As) was measured by inductively coupled plasma–mass spectrometry and urinary As [arsenite, arsenate, monomethylarsonic acid (MMA), and dimethylarsinic acid (DMA)] were detected using high-performance liquid chromatography–hydride-generated atomic absorption spectrometry. We used linear mixed-effects models to compute variance components and evaluate the association between UAs and selected factors.ResultsThe concentrations of UAs were fairly reproducible within individuals, with intraclass correlation coefficients (ICCs) of 0.41, 0.35, 0.47, and 0.49 for inorganic As (InAs), MMA, DMA, and total urinary As (TUA). However, when expressed as a ratio, the percent InAs (%InAs), %MMA, and %DMA were poorly reproducible within individuals, with ICCs of 0.16, 0.16, and 0.17, respectively. Arsenic metabolism was significantly associated with sex, exposure, age, smoking, chewing betel nut, urinary creatinine, and season. Specificity and sensitivity analyses showed that a single urine sample adequately classified a participant’s urinary As profile as high or low, but TUA had only moderate specificity for correctly classifying drinking water exposures.ConclusionsEpidemiologic studies should use both urinary As concentrations and the relative proportion of UAs to minimize measurement error and to facilitate interpretation of factors that influence As metabolism.
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