Arsenic exposure in children is a public health concern but is understudied in relation to the predictors, and effects of low-level exposure. We examined the extent and dietary predictors of exposure to inorganic arsenic in 5–8 year old children from Montevideo, Uruguay. Children were recruited at school; 357 were enrolled, 328 collected morning urine samples, and 317 had two 24-hour dietary recalls. Urinary arsenic metabolites, i.e. inorganic arsenic (iAs), methylarsonic acid (MMA), and dimethylarsinic acid (DMA), were measured using high-performance liquid chromatography with hydride generation and inductively coupled plasma mass spectrometry (HPLC-HG-ICP-MS), and the sum concentration (U-As) used for exposure assessment. Proportions of arsenic metabolites (%iAs, %MMA and %DMA) in urine were modelled in OLS regressions as functions of food groups, dietary patterns, nutrient intake, and nutritional status. Exposure to arsenic was low (median U-As: 9.9 µg/L) and household water (water As: median 0.45 µg/L) was not a major contributor to exposure. Children with higher consumption of rice had higher U-As but lower %iAs, %MMA, and higher %DMA. Children with higher meat consumption had lower %iAs and higher %DMA. Higher scores on ”nutrient dense” dietary pattern were related to lower %iAs and %MMA, and higher %DMA. Higher intake of dietary folate was associated with lower %MMA and higher %DMA. Overweight children had lower %MMA and higher %DMA than normal-weight children. In summary, rice was an important predictor of exposure to inorganic arsenic and DMA. Higher meat and folate consumption, diet rich in green leafy and red-orange vegetables and eggs, and higher BMI contributed to higher arsenic methylation capacity.
There was no association between low-level As exposure and general cognitive abilities.
Lead exposure remains an important public health problem. Contaminated foods may act as a source of lead exposure, while certain nutrients may reduce lead absorption. We examined the cross-sectional associations of dietary patterns and the intake of several nutrients and foods with blood (Pb-B) and urinary (Pb-U) lead concentrations in children (5-8y) from Montevideo, Uruguay. From two 24-hour recalls completed by caregivers, we derived the mean daily intake of select nutrients and food groups (dairy, milk, fruit, root vegetables, foods rich in heme and non-heme iron), as well as "nutrient dense" and "processed" food patterns. Pb-B (n=315) was measured using atomic absorption spectrometry; Pb-U (n=321) using ICP-MS. Pb-U was adjusted for specific gravity and log-transformed to approximate a normal distribution. Iron deficiency (ID) and dietary variables were tested as predictors of Pb-B and log-Pb-U in covariate-adjusted regressions. Median [5%, 95%] Pb-B and Pb-U were 3.8 [0.8-7.8] μg/dL and 1.9 [0.6-5.1] μg/L, respectively; ~25% of Pb-B above current U.S. CDC reference concentration of 5μg/dL. ID was associated with 0.75μg/dL higher Pb-B, compared to non-ID (p<0.05). Consumption of root vegetables was not associated with Pb-B or log-Pb-U. Higher scores on the nutrient-dense pattern were related with higher Pb-Bs, possibly due to consumption of green leafy vegetables. Dietary intake of iron or iron-rich foods was not associated with biomarkers of lead. Conversely, children consuming more calcium, dairy, milk and yogurt had lower Pb-B and log-Pb-U. Our findings appear consistent with existing recommendations on including calcium-rich, but not iron- or vitamin-C-rich foods in the diets of lead-exposed children, especially where the consumption of these foods is low.
Oxidative stress (OS) is a potential molecular mechanism for lead-induced toxicities, yet, we have limited understanding of the relation between low-level lead (Pb) exposure and OS, especially in children. This cross-sectional study examines the association between blood lead level (BLL) and two OS markers—urinary F2-8α isoprostane or isoprostane (a marker of lipid peroxidation) and 8-hydroxy-2-deoxy-Guanosine or 8-OH-dG (a marker of DNA damage) in 211 children, aged 5–8 years, from Montevideo, Uruguay. The role of dietary intakes of vitamin C and zinc in modifying the relation between BLL and OS was also examined. The mean (SD) BLL of the study children was 4.7 (2.2) μg/dL, with 30.2% children having BLL ≥5 μg/dL, the current reference level set by the US Centre for Disease Control for identifying, monitoring and management of children with elevated BLL. In covariate-adjusted analysis, there was a weak positive association between BLL and urinary isoprostane (adjusted for specific gravity) [β = 0.09, p< 0.1]. No association was found between children’s BLL and urinary 8-OH-dG. Interactions between dietary intakes of vitamin C or zinc and BLL on OS biomarkers were not consistent. However, when BLL and vitamin C or BLL and zinc were modeled together, BLL was independently associated with isoprostane concentration [β = 0.10, p< 0.05] but vitamin C or zinc intake was not. These findings suggest that there may be a potential adverse effect of BLL on OS in children with low-level Pb exposure. There is a need to study the effects of Pb on other OS measures, as well as the role of OS in mediating low-level Pb toxicity on functional outcomes.
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