A subset of individuals from the case-control study had saliva DNA of sufficient quality and were included in the genetic analyses (Figure 1). Control children were excluded from the main study if the child was diagnosed with cancer or a condition considered to be related to arsenic exposure (i.e. arsenic-related keratosis). Various candidate gene studies of neural tube defects in humans have examined one or a few genes (Finnell et al., 2021), particularly those that are orthologs of risk genes in mice or genes involved in folate pathways (Greene & Copp, 2014). Determinants of neural tube defects include a combination of environmental, nutritional, and genetic risk factors (Greene & Copp, 2014; Harris & Juriloff, 2007). At minimum, more surveillance for spina bifida is needed in high arsenic areas such as Bangladesh.
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Previous work in Bangladesh in a large pregnancy cohort has shown high correlations between pregnant women’s toenail arsenic measurements during the first trimester and 1 month post-partum and also with measurements from their infant’s toenails at age 1 month . We were not able to assess all pregnancies that included neural tube defects because Bangladesh does not have a birth defect surveillance program that collects this information from ultrasonography centers or from all deliveries. We used biomarkers (e.g. toenail arsenic) to minimize this bias. If arsenic exposure was related to these more severe outcomes, our results could represent a downward bias towards or beyond the null . It is possible that even higher arsenic exposures are needed to demonstrate a primary effect. In Folbp2 knockout mice, for example, mice with this specific defect in folate transport had higher rates of NTDs after arsenic exposure, and mice nullizygous for genes encoding proteins in cellular uptake of folate were more susceptible to arsenic-induced NTDs https://wakelet.com/@spinracasinoen.
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Our study is the largest study to date to investigate spina bifida only (larger studies included all NTDs), and we were able to further restrict our analyses to only myelomeningocele in sensitivity analyses. In humans, the strongest evidence for arsenic-folic acid interactions comes from trials in which folic acid has been shown to reduce blood arsenic concentrations 34,35,36. The interaction between arsenic and folate may be explained by arsenic’s interference with folate-related functions, such as the depletion of S-adenosylmethionine (SAM), a key methyl donor for pathways implicated in neural tube closure . Animal studies have consistently shown arsenic to be a potent teratogen, inducing neural tube defects in several animal models 7,8,9,10,11.
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We found similar evidence of effect modification when we restricted the analysis to cases with myelomeningocele, a more severe type of spina bifida. The cutoff for mother’s toenail arsenic concentrations was defined by the median of study population (0.46 µg/g toenail). Serum folate concentrations were higher among mothers who reported folic acid use during pregnancy compared to those who did not report folic acid use (10.20 ng/ml and 7.96 ng/ml, respectively).
We collected various biomarkers to investigate how arsenic contributes to the risk of spina bifida. Environmental exposure to arsenic is of particular concern and may be a potential contributor to spina bifida risk, especially in areas of the world with high arsenic exposures and micronutrient deficiencies. Folic acid supplement use reduces the risk of spina bifida , and fortification of staple foods with folic acid has been successful in decreasing spina bifida rates in multiple countries 4, 5.
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