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

Shohreh F. Farzan, Elizabeth B. Brickley, Zhigang Li, Diane Gilbert-Diamond, Anala Gossai, Yu Chen, Caitlin G. Howe, Thomas Palys, Margaret R. Karagas

Research output: Contribution to journalArticle

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 (TNFα), 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 145.2 ng/ml (95% CI 4.1, 286.3; p=0.04) increase in cord blood ICAM1 and 557.3 ng/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 141.8 ng/ml (95% CI 26.1, 257.5; p=0.02) increase maternal plasma VCAM1 levels. Urinary As was unrelated to MCP1 or TNFα 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 (βmediation: 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.

Original languageEnglish (US)
Pages (from-to)426-433
Number of pages8
JournalEnvironmental Research
Volume156
DOIs
StatePublished - Jul 1 2017

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Arsenic
pregnancy
arsenic
Mothers
Pregnancy
Blood
Fetal Blood
blood
Plasmas
plasma
Chemokine CCL2
Biomarkers
adhesion
tumor
biomarker
Tumor Necrosis Factor-alpha
Health
Association reactions
Pregnant Women
protein

Keywords

  • Arsenic
  • Endothelial
  • Inflammatory markers
  • New Hampshire
  • Pregnancy cohort

ASJC Scopus subject areas

  • Biochemistry
  • Environmental Science(all)

Cite this

Maternal and infant inflammatory markers in relation to prenatal arsenic exposure in a U.S. pregnancy cohort. / Farzan, Shohreh F.; Brickley, Elizabeth B.; Li, Zhigang; Gilbert-Diamond, Diane; Gossai, Anala; Chen, Yu; Howe, Caitlin G.; Palys, Thomas; Karagas, Margaret R.

In: Environmental Research, Vol. 156, 01.07.2017, p. 426-433.

Research output: Contribution to journalArticle

Farzan, SF, Brickley, EB, Li, Z, Gilbert-Diamond, D, Gossai, A, Chen, Y, Howe, CG, Palys, T & Karagas, MR 2017, 'Maternal and infant inflammatory markers in relation to prenatal arsenic exposure in a U.S. pregnancy cohort', Environmental Research, vol. 156, pp. 426-433. https://doi.org/10.1016/j.envres.2017.03.056
Farzan, Shohreh F. ; Brickley, Elizabeth B. ; Li, Zhigang ; Gilbert-Diamond, Diane ; Gossai, Anala ; Chen, Yu ; Howe, Caitlin G. ; Palys, Thomas ; Karagas, Margaret R. / Maternal and infant inflammatory markers in relation to prenatal arsenic exposure in a U.S. pregnancy cohort. In: Environmental Research. 2017 ; Vol. 156. pp. 426-433.
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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 (TNFα), 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 145.2 ng/ml (95{\%} CI 4.1, 286.3; p=0.04) increase in cord blood ICAM1 and 557.3 ng/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 141.8 ng/ml (95{\%} CI 26.1, 257.5; p=0.02) increase maternal plasma VCAM1 levels. Urinary As was unrelated to MCP1 or TNFα 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 (βmediation: 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.",
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AU - Farzan, Shohreh F.

AU - Brickley, Elizabeth B.

AU - Li, Zhigang

AU - Gilbert-Diamond, Diane

AU - Gossai, Anala

AU - Chen, Yu

AU - Howe, Caitlin G.

AU - Palys, Thomas

AU - Karagas, Margaret R.

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N2 - 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 (TNFα), 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 145.2 ng/ml (95% CI 4.1, 286.3; p=0.04) increase in cord blood ICAM1 and 557.3 ng/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 141.8 ng/ml (95% CI 26.1, 257.5; p=0.02) increase maternal plasma VCAM1 levels. Urinary As was unrelated to MCP1 or TNFα 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 (βmediation: 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.

AB - 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 (TNFα), 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 145.2 ng/ml (95% CI 4.1, 286.3; p=0.04) increase in cord blood ICAM1 and 557.3 ng/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 141.8 ng/ml (95% CI 26.1, 257.5; p=0.02) increase maternal plasma VCAM1 levels. Urinary As was unrelated to MCP1 or TNFα 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 (βmediation: 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.

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