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Goal The goal of this study was to evaluate the association between groundwater arsenic and fasting blood glucose in the context of other groundwater chemicals, in Bangladesh. Methods Fasting blood glucose, gender, body mass index, sociodemographic variables, and diabetes medication use were measured among adults ≥ 35 years of age (n = 6587) participating in the Bangladesh Demographic and Health Survey (BDHS) 2011. Groundwater chemicals in 3534 well water samples were measured in the British Geological Survey (BGS) and Department of Public Health Engineering (DPHE) 1998–99 survey. We assigned the nearest BGS-DPHE well's chemical exposure to each BDHS participant. We used survey-estimation linear regression methods to model natural log-transformed fasting blood glucose, among those using groundwater as their primary drinking-water source, as a function of groundwater arsenic. We considered possible interactions between categorical arsenic exposure and each of 14 other groundwater chemicals dichotomized at their medians. The chemicals considered as possible effect modifiers included: aluminum, barium, calcium, iron, potassium, lithium, magnesium, manganese, sodium, phosphorous, silicon, sulfate, strontium, and zinc. Results Compared to persons exposed to groundwater arsenic ≤ 10 μg/L, the adjusted geometric mean ratio (GMR) of fasting blood glucose was 1.01 (95% confidence interval: 0.98, 1.04) for individuals exposed to groundwater arsenic concentrations > 10 μg/L and ≤ 50 μg/L, and was 1.01 (0.97, 1.03) for those with > 50 μg/L arsenic. There were no Bonferroni-significant interactions with other chemicals, after accounting for the large number of chemicals tested as modifiers. Conclusions In our analysis of groundwater chemistry data from 1998/99 and fasting blood glucose outcomes measured in nearby populations approximately a decade later, there was no overall association of fasting blood glucose with nearby historical groundwater arsenic. This null association was not significantly modified by the historical levels of other groundwater chemicals. These null results are inconclusive regarding shorter-term potential toxicity of arsenic for glucose regulation, if there are differences between the historical concentrations measured in nearby groundwater and the actual drinking water chemical exposures in the population during the etiologically relevant period for more acute phenotypes like fasting blood glucose. Drinking water supply-relevant, longitudinal exposure assessment with less measurement error is needed to more precisely evaluate the joint impacts of drinking water chemicals and establish if there is a sensitive time window for glycemic outcomes.

Background Drinking water salinity has contributed to scarcity of potable water in southwest coastal Bangladesh. Drinking saline water has been associated with high blood pressure among communities in southwest coastal Bangladesh, but the effect of water salinity on kidney health is unknown. We aimed to understand the association between drinking water salinity and urinary protein excretion from the baseline findings of a community-based stepped-wedge randomised trial. Methods We collected 24-h urine from 1185 participants from 532 households and 16 communities in three districts (Khulna, Satkhira, and Bagerhat) of southwest coastal Bangladesh between Nov 17, and Dec 21, 2016, and measured urinary sodium and total protein. We measured electrical conductivity in sampled households' stored drinking water. We estimated water chloride concentration by using a published conversion factor and then estimated daily sodium intake by drinking water assuming sodium ions will be coupled with chloride in water. Among normotensive participants who reported exclusively drinking household stored water, and did not report kidney or heart diseases or diabetes, we determined the effects of daily sodium intake by water and urinary sodium on total protein using hierarchical models accounting for household and community level clustering, and adjusted for age, sex and, weight. Findings Mean urinary sodium was 164 mmoL/24 h and total protein was 402 mg/24 h. Mean sodium intake through drinking water was 17 mmoL per day. For each 1000 μS/cm higher in drinking water electrical conductivity, there was a 8·2 mmoL/24 h (95% CI 5·3–11·1) higher excretion of 24-h urinary sodium. For each 10 mmoL increase in estimated daily sodium intake through drinking water, there was a 15·9 mg/24 h (95% CI 0·3–31·6) increase in total protein. We estimated a 62·9 mg/24 h (95% CI 29·7–96·1) increase in total protein for each 100 mmoL/24 h increase urinary sodium. We identified 37% participants that had mild proteinuria (total protein: 300–500 mg/24 h) and 20% had moderate or substantial proteinuria (total protein: >500 mg/24 h). Interpretation Drinking water sodium and urinary sodium were associated with increased protein excretion—a powerful marker for progressive kidney disease—in southwest coastal Bangladesh. Interventions aimed at lowering drinking water salinity could provide benefit to kidney health. Funding Wellcome Trust, UK.