Dhaka Community Hospital Trust

Dhaka, Bangladesh

Dhaka Community Hospital Trust

Dhaka, Bangladesh
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Rahman M.L.,Harvard University | Valeri L.,Harvard University | Kile M.L.,Oregon State University | Mazumdar M.,Harvard University | And 7 more authors.
Environment International | Year: 2017

Background Shortening of gestation and intrauterine growth restriction (IUGR) are the two main determinants of birthweight. Low birthweight has been linked with prenatal arsenic exposure, but the causal relation between arsenic and birthweight is not well understood. Objectives We applied a quantile causal mediation analysis approach to determine the association between prenatal arsenic exposure and birthweight in relation to shortening of gestation and IUGR, and whether the susceptibility of arsenic exposure varies by infant birth sizes. Methods In a longitudinal birth cohort in Bangladesh, we measured arsenic in drinking water (n = 1182) collected at enrollment and maternal toenails (n = 1104) collected ≤ 1-month postpartum using inductively coupled plasma mass spectrometry. Gestational age was determined using ultrasound at ≤ 16 weeks' gestation. Demographic information was collected using a structured questionnaire. Results Of 1184 singleton livebirths, 16.4% (n = 194) were low birthweight (< 2500 g), 21.9% (n = 259) preterm (< 37 weeks' gestation), and 9.2% (n = 109) both low birthweight and preterm. The median concentrations of arsenic in drinking water and maternal toenails were 2.2 μg/L (range: below the level of detection [LOD] − 1400) and 1.2 μg/g (range: < LOD − 46.6), respectively. Prenatal arsenic exposure was negatively associated with birthweight, where the magnitude of the association varied across birthweight percentiles. The effect of arsenic on birthweight mediated via shortening of gestation affected all infants irrespective of birth sizes (β range: 10th percentile = − 19.7 g [95% CI: − 26.7, − 13.3] to 90th percentile = − 10.9 g [95% CI: − 18.5, − 5.9] per natural log water arsenic increase), whereas the effect via pathways independent of gestational age affected only the smaller infants (β range: 10th percentile = − 28.0 g [95% CI: − 43.8, − 9.9] to 20th percentile = − 14.9 g [95% CI: − 30.3, − 1.7] per natural log water arsenic increase). Similar pattern was observed for maternal toenail arsenic. Conclusions The susceptibility of prenatal arsenic exposure varied by infant birth sizes, placing smaller infants at greater risk of lower birthweight by shortening of gestation and possibly growth restriction. It is important to mitigate prenatal arsenic exposure to improve perinatal outcomes in Bangladesh. © 2017 Elsevier Ltd


Kile M.L.,Oregon State University | Faraj J.M.,University of Massachusetts Amherst | Ronnenberg A.G.,University of Massachusetts Amherst | Quamruzzaman Q.,Dhaka Community Hospital Trust | And 4 more authors.
BMC Public Health | Year: 2016

Background: In the Ganges Delta, chronic arsenic poisoning is a health concern affecting millions of people who rely on groundwater as their potable water source. The prevalence of anemia is also high in this region, particularly among women. Moreover, arsenic is known to affect heme synthesis and erythrocytes and the risk of arsenic-induced skin lesions appears to differ by sex. Methods: We conducted a case-control study in 147 arsenic-exposed Bangladeshi women to assess the association between anemia and arsenic-induced skin lesions. Results: We observed that the odds of arsenic-related skin lesions were approximately three times higher among women who were anemic (hemoglobin < 120 g/L) compared to women with normal hemoglobin levels [Odds Ratio (OR) = 3.32, 95 % Confidence Intervals (CI): 1.29, 8.52] after adjusting for arsenic levels in drinking water and other covariates. Furthermore, 75 % of the women with anemia had adequate iron stores (serum ferritin ≥12 μg/L), suggesting that the majority of anemia detected in this population was unrelated to iron depletion. Conclusions: Considering the magnitude of arsenic exposure and prevalence of anemia in Bangladeshi women, additional research is warranted that identifies the causes of anemia so that effective interventions can be implemented while arsenic remediation efforts continue. © 2016 Kile et al.


Mazumdar M.,Boston Childrens Hospital | Valeri L.,Harvard University | Rodrigues E.G.,Boston Childrens Hospital | Ibne Hasan M.O.S.,Dhaka Community Hospital Trust | And 7 more authors.
Birth Defects Research Part A - Clinical and Molecular Teratology | Year: 2015

BACKGROUND: Arsenic induces neural tube defects in many animal models. Additionally, studies have shown that mice with specific genetic defects in folate metabolism and transport are more susceptible to arsenic-induced neural tube defects. We sought to determine whether 14 single-nucleotide polymorphisms in genes involved in folate metabolism modified the effect of exposure to drinking water contaminated with inorganic arsenic and posterior neural tube defect (myelomeningocele) risk. METHODS: Fifty-four mothers of children with myelomeningocele and 55 controls were enrolled through clinical sites in rural Bangladesh in a case-control study of the association between environmental arsenic exposure and risk of myelomeningocele. We assessed participants for level of myelomeningocele, administered questionnaires, conducted biological and environmental sample collection, and performed genotyping. Inductively coupled plasma mass spectrometry was used to measure inorganic arsenic concentration in drinking water. Candidate single-nucleotide polymorphisms were identified through review of the literature. RESULTS: Drinking water inorganic arsenic concentration was associated with increased risk of myelomeningocele for participants with 4 of the 14 studied single-nucleotide polymorphisms in genes involved in folate metabolism: the AA/AG genotype of rs2236225 (MTHFD1), the GG genotype of rs1051266 (SLC19A1), the TT genotype of rs7560488 (DNMT3A), and the GG genotype of rs3740393 (AS3MT) with adjusted odds ratio of 1.13, 1.31, 1.20, and 1.25 for rs2236225, rs1051266, rs7560488, and rs3740393, respectively. CONCLUSION: Our results support the hypothesis that environmental arsenic exposure increases the risk of myelomeningocele by means of interaction with folate metabolic pathways. © 2015 Wiley Periodicals, Inc.


PubMed | Dhaka Community Hospital Trust, Harvard University, University of Massachusetts Amherst and Oregon State University
Type: | Journal: BMC public health | Year: 2016

In the Ganges Delta, chronic arsenic poisoning is a health concern affecting millions of people who rely on groundwater as their potable water source. The prevalence of anemia is also high in this region, particularly among women. Moreover, arsenic is known to affect heme synthesis and erythrocytes and the risk of arsenic-induced skin lesions appears to differ by sex.We conducted a case-control study in 147 arsenic-exposed Bangladeshi women to assess the association between anemia and arsenic-induced skin lesions.We observed that the odds of arsenic-related skin lesions were approximately three times higher among women who were anemic (hemoglobin< 120 g/L) compared to women with normal hemoglobin levels [Odds Ratio (OR)= 3.32, 95% Confidence Intervals (CI): 1.29, 8.52] after adjusting for arsenic levels in drinking water and other covariates. Furthermore, 75% of the women with anemia had adequate iron stores (serum ferritin 12 g/L), suggesting that the majority of anemia detected in this population was unrelated to iron depletion.Considering the magnitude of arsenic exposure and prevalence of anemia in Bangladeshi women, additional research is warranted that identifies the causes of anemia so that effective interventions can be implemented while arsenic remediation efforts continue.


PubMed | Dhaka Community Hospital Trust, University of Massachusetts Boston, Boston Childrens Hospital, Bangladesh Medical College and Harvard University
Type: Journal Article | Journal: Birth defects research. Part A, Clinical and molecular teratology | Year: 2015

Arsenic induces neural tube defects in many animal models. Additionally, studies have shown that mice with specific genetic defects in folate metabolism and transport are more susceptible to arsenic-induced neural tube defects. We sought to determine whether 14 single-nucleotide polymorphisms in genes involved in folate metabolism modified the effect of exposure to drinking water contaminated with inorganic arsenic and posterior neural tube defect (myelomeningocele) risk.Fifty-four mothers of children with myelomeningocele and 55 controls were enrolled through clinical sites in rural Bangladesh in a case-control study of the association between environmental arsenic exposure and risk of myelomeningocele. We assessed participants for level of myelomeningocele, administered questionnaires, conducted biological and environmental sample collection, and performed genotyping. Inductively coupled plasma mass spectrometry was used to measure inorganic arsenic concentration in drinking water. Candidate single-nucleotide polymorphisms were identified through review of the literature.Drinking water inorganic arsenic concentration was associated with increased risk of myelomeningocele for participants with 4 of the 14 studied single-nucleotide polymorphisms in genes involved in folate metabolism: the AA/AG genotype of rs2236225 (MTHFD1), the GG genotype of rs1051266 (SLC19A1), the TT genotype of rs7560488 (DNMT3A), and the GG genotype of rs3740393 (AS3MT) with adjusted odds ratio of 1.13, 1.31, 1.20, and 1.25 for rs2236225, rs1051266, rs7560488, and rs3740393, respectively.Our results support the hypothesis that environmental arsenic exposure increases the risk of myelomeningocele by means of interaction with folate metabolic pathways.

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