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Our final study population included 294 cases and 163 controls. Toenail arsenic concentrations were not available for 27 cases and 2 controls. Reasons for study refusal were similar among cases and controls and primarily included concerns about giving blood.
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- A challenge faced in conducting genomic research in the study population was a lack of a replication sample, preventing us from validating the current findings in another study population.
- To our knowledge, our study is the first to report an association between a variant in SULT1C2 and spina bifida risk.
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- Mother’s arsenic exposure modified the protective association of folic acid with spina bifida.
Neurosurgeons at NINS further classified cases based on examination, observations during surgery, and review of neuroimaging studies. Cases were eligible to enroll in the study if they were diagnosed with myelomeningocele or meningocele following examination by a physician, were less than a year old, received medical care from NINS, and if parents were able to identify the primary water source used during early pregnancy. Trio designs, which are suited to studying health outcomes that develop early in life (Lupo et al., 2017), can be used to detect de novo mutations and permit assessment using the transmission disequilibrium test to determine if alleles are over-transmitted from parents to case children (Wolujewicz et al., 2021). Biological pathways examined in candidate gene studies of neural tube defects involve the non-canonical Wnt/PCP and SHH signaling pathways (Wolujewicz & Ross, 2019), similar to the animal genetic models of neural tube defects.
We included families with children with lipomeningocele as controls because our study was primarily designed to investigate associations between arsenic and spina bifida (myelomeningocele and meningocele), and lipomeningocele would be present in the population that would give rise to cases. In our analysis including genetic variants spanning the genome, we did not observe significant differences in measured serum folate among mothers of cases and controls and did not identify any significant associations between genetic variants in genes relevant in folate pathways and case status in the child, maternal, or trio models. The genetic association analysis includes data from child-parent trios, allowing us to explore family-based, genome-wide association analyses in a unique study population with myelomeningocele and meningocele, subtypes of spina bifida, from Bangladesh, a country with relatively high prevalence of neural tube defects with a population that is underrepresented in genome-wide association studies (Gurdasani et al., 2019). In the current study, we build upon this previous analysis, performing a genome-wide scan of variants to assess genetic contributors to neural tube defect risk in a larger case-control population. In this study, we investigated the association of genetic variants spanning the genome with risk of spina bifida (i.e., myelomeningocele and meningocele) in a subset of families enrolled from December 2016 through December 2022 in a case-control study in Bangladesh, a population often underrepresented in genetic studies. A recent study from an area of Turkey with high arsenic exposures reported higher levels of arsenic in plasma samples of 100 mothers of NTD cases as compared to mothers from 70 controls .