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Maternal and infant inflammatory markers in relation to prenatal arsenic exposure in a U.S. pregnancy cohort.

ABSTRACT: INTRODUCTION:Accumulating evidence indicates that arsenic (As), a potent environmental toxicant, may increase cardiovascular disease risk and adversely affect endothelial function at high levels of exposure. Pregnancy is a vulnerable time for both mother and child; however, studies examining the association between prenatal As exposure and plasma biomarkers of inflammation and endothelial function in mothers and newborns are lacking. METHODS:We examined maternal urinary As levels at gestational weeks 24-28 and levels of inflammatory biomarkers in plasma from 563 pregnant women and 500 infants' cord blood. We assessed a multiplexed panel of circulating inflammatory and endothelial function markers, including tumor necrosis factor alpha (TNF?), monocyte chemoattractant protein 1 (MCP1), intercellular adhesion molecule (ICAM1) and vascular cell adhesion molecule (VCAM1). RESULTS:Compared with the bottom tertile, the highest tertile of maternal urinary As during pregnancy was associated with a 145.2ng/ml (95% CI 4.1, 286.3; p=0.04) increase in cord blood ICAM1 and 557.3ng/ml (95% CI -56.4, 1171.1; p=0.09) increase in cord blood VCAM1. Among mothers, the highest tertile of maternal urinary As during pregnancy was related to a 141.8ng/ml (95% CI 26.1, 257.5; p=0.02) increase maternal plasma VCAM1 levels. Urinary As was unrelated to MCP1 or TNF? in maternal plasma and cord blood. In structural equation models, the association between maternal urinary As and infant VCAM was mediated by maternal levels of VCAM (?mediation: 0.024, 95% CI: 0.002, 0.050). CONCLUSION:Our observations indicate that As exposure during pregnancy may affect markers of vascular health and endothelial function in both pregnant women and children, and suggest further investigation of the potential impacts on cardiovascular health in these susceptible populations.

SUBMITTER: Farzan SF

PROVIDER: S-EPMC5477637 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature

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Maternal and infant inflammatory markers in relation to prenatal arsenic exposure in a U.S. pregnancy cohort.

Farzan Shohreh F SF Brickley Elizabeth B EB Li Zhigang Z Gilbert-Diamond Diane D Gossai Anala A Chen Yu Y Howe Caitlin G CG Palys Thomas T Karagas Margaret R MR

Environmental research 20170412

<h4>Introduction</h4>Accumulating evidence indicates that arsenic (As), a potent environmental toxicant, may increase cardiovascular disease risk and adversely affect endothelial function at high levels of exposure. Pregnancy is a vulnerable time for both mother and child; however, studies examining the association between prenatal As exposure and plasma biomarkers of inflammation and endothelial function in mothers and newborns are lacking.<h4>Methods</h4>We examined maternal urinary As levels ...[more]

PMID: 28410520

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Project description:BackgroundShortening 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.ObjectivesWe 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.MethodsIn 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 ≤16weeks' gestation. Demographic information was collected using a structured questionnaire.ResultsOf 1184 singleton livebirths, 16.4% (n=194) were low birthweight (<2500g), 21.9% (n=259) preterm (<37weeks' gestation), and 9.2% (n=109) both low birthweight and preterm. The median concentrations of arsenic in drinking water and maternal toenails were 2.2μg/L (range: below the level of detection [LOD]-1400) and 1.2μg/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=-19.7g [95% CI: -26.7, -13.3] to 90th percentile=-10.9g [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=-28.0g [95% CI: -43.8, -9.9] to 20th percentile=-14.9g [95% CI: -30.3, -1.7] per natural log water arsenic increase). Similar pattern was observed for maternal toenail arsenic.ConclusionsThe 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.

Dataset Information

Maternal and infant inflammatory markers in relation to prenatal arsenic exposure in a U.S. pregnancy cohort.

Publications

Maternal and infant inflammatory markers in relation to prenatal arsenic exposure in a U.S. pregnancy cohort.

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