Altered cord blood mitochondrial DNA content and pregnancy lead exposure in the PROGRESS cohort
Introduction: Lead (Pb) crosses the placenta and can cause oxidative stress, reduced fetal growth and neurological problems. The principal source of oxidative stress in human cells is mitochondria. Therefore, disruption of normal mitochondrial function during pregnancy may represent a primary mechan...
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Elsevier
2019-04-01
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Series: | Environment International |
Online Access: | http://www.sciencedirect.com/science/article/pii/S0160412018313801 |
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record_format |
Article |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Marco Sanchez-Guerra Cheng Peng Letizia Trevisi Andres Cardenas Ander Wilson Citlalli Osorio-Yáñez Megan M. Niedzwiecki Jia Zhong Katherine Svensson Maria Teresa Acevedo Maritsa Solano-Gonzalez Chitra J. Amarasiriwardena Guadalupe Estrada-Gutierrez Kasey J.M. Brennan Lourdes Schnaas Allan C. Just Hannah E. Laue Rosalind J. Wright Martha Maria Téllez-Rojo Robert O. Wright Andrea A. Baccarelli |
spellingShingle |
Marco Sanchez-Guerra Cheng Peng Letizia Trevisi Andres Cardenas Ander Wilson Citlalli Osorio-Yáñez Megan M. Niedzwiecki Jia Zhong Katherine Svensson Maria Teresa Acevedo Maritsa Solano-Gonzalez Chitra J. Amarasiriwardena Guadalupe Estrada-Gutierrez Kasey J.M. Brennan Lourdes Schnaas Allan C. Just Hannah E. Laue Rosalind J. Wright Martha Maria Téllez-Rojo Robert O. Wright Andrea A. Baccarelli Altered cord blood mitochondrial DNA content and pregnancy lead exposure in the PROGRESS cohort Environment International |
author_facet |
Marco Sanchez-Guerra Cheng Peng Letizia Trevisi Andres Cardenas Ander Wilson Citlalli Osorio-Yáñez Megan M. Niedzwiecki Jia Zhong Katherine Svensson Maria Teresa Acevedo Maritsa Solano-Gonzalez Chitra J. Amarasiriwardena Guadalupe Estrada-Gutierrez Kasey J.M. Brennan Lourdes Schnaas Allan C. Just Hannah E. Laue Rosalind J. Wright Martha Maria Téllez-Rojo Robert O. Wright Andrea A. Baccarelli |
author_sort |
Marco Sanchez-Guerra |
title |
Altered cord blood mitochondrial DNA content and pregnancy lead exposure in the PROGRESS cohort |
title_short |
Altered cord blood mitochondrial DNA content and pregnancy lead exposure in the PROGRESS cohort |
title_full |
Altered cord blood mitochondrial DNA content and pregnancy lead exposure in the PROGRESS cohort |
title_fullStr |
Altered cord blood mitochondrial DNA content and pregnancy lead exposure in the PROGRESS cohort |
title_full_unstemmed |
Altered cord blood mitochondrial DNA content and pregnancy lead exposure in the PROGRESS cohort |
title_sort |
altered cord blood mitochondrial dna content and pregnancy lead exposure in the progress cohort |
publisher |
Elsevier |
series |
Environment International |
issn |
0160-4120 |
publishDate |
2019-04-01 |
description |
Introduction: Lead (Pb) crosses the placenta and can cause oxidative stress, reduced fetal growth and neurological problems. The principal source of oxidative stress in human cells is mitochondria. Therefore, disruption of normal mitochondrial function during pregnancy may represent a primary mechanism behind the adverse effects of lead. We sought to assess the association of Pb exposure during pregnancy with mitochondrial DNA (mtDNA) content, a sensitive marker of mitochondrial function, in cord blood. Materials and methods: This study comprised mother-infant pairs from the Programming Research in Obesity, Growth, Environment and Social Stressors (PROGRESS) study, a prospective birth-cohort that enrolled 1050 pregnant women from Mexico City who were receiving prenatal care between December 2007 and July 2011. Quantitative PCR was used to calculate relative MtDNA content (mitochondrial-to-nuclear DNA ratio (mtDNA/nDNA)) in cord blood. Lead concentrations in both maternal blood (2nd and 3rd trimester and at delivery day) and in cord blood were measured by ICP-MS. Multivariable regression models adjusting for multiple confounders were fitted with 410 mother-infant pairs for whom complete data for mtDNA content, lead levels, and covariates were available. Results: Maternal blood Pb measured in the second (mean 3.79 μg/dL, SD 2.63; β = 0.059, 95% CI 0.008, 0.111) and third trimester (mean 3.90 μg/dL; SD 2.84; β = 0.054, 95% CI 0.002, 0.107) during pregnancy and PB in cord blood (mean 3.50 μg/dL, SD 2.59; β = 0.050, 95% CI 0.004; 0.096) were associated with increased cord blood mtDNA content (mean 1.46, SD 0.44). In two-way interaction analyses, cord blood Pb marginally interacted with gestational age leading to an increase in mtDNA content for pre-term births (Benjamini-Hochberg False Discovery Rate correction; BH-FDR = 0.08). Conclusion: This study shows that lead exposure in pregnancy alters mtDNA content in cord blood; therefore, alteration of mtDNA content might be a mechanism underlying the toxicity of lead. Keywords: mtDNA content, Lead exposure, Pregnancy, Mitochondrial dysfunction, Cord blood |
url |
http://www.sciencedirect.com/science/article/pii/S0160412018313801 |
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doaj-537d37962e744c95a9d06ac0e4b0c4642020-11-24T21:37:11ZengElsevierEnvironment International0160-41202019-04-01125437444Altered cord blood mitochondrial DNA content and pregnancy lead exposure in the PROGRESS cohortMarco Sanchez-Guerra0Cheng Peng1Letizia Trevisi2Andres Cardenas3Ander Wilson4Citlalli Osorio-Yáñez5Megan M. Niedzwiecki6Jia Zhong7Katherine Svensson8Maria Teresa Acevedo9Maritsa Solano-Gonzalez10Chitra J. Amarasiriwardena11Guadalupe Estrada-Gutierrez12Kasey J.M. Brennan13Lourdes Schnaas14Allan C. Just15Hannah E. Laue16Rosalind J. Wright17Martha Maria Téllez-Rojo18Robert O. Wright19Andrea A. Baccarelli20Department of Developmental Neurobiology, National Institute of Perinatology, Montes Urales 800, Lomas Virreyes, Mexico City 11000, Mexico; Correspondence to: M. Sanchez-Guerra, Department of Developmental Neurobiology, National Institute of Perinatology, Mexico City 11000, Mexico.Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USADepartment of Global Health and Social Medicine, Harvard Medical School, Boston, MA, USADivision of Chronic Disease Research Across the Lifecourse, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim HealthCare Institute, Boston, MA, USADepartment of Statistics, Colorado State University, Fort Collins, CO 80523, USADepartment of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Center for Nutrition and Health Research, National Institute of Public Health, Ministry of Health, Cuernavaca, Morelos, MexicoDepartment of Preventive Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USADepartment of Environmental Health Sciences, Columbia University, Mailman School of Public Health, New York, NY, USADepartment of Preventive Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USADepartment of Developmental Neurobiology, National Institute of Perinatology, Montes Urales 800, Lomas Virreyes, Mexico City 11000, MexicoCenter for Nutrition and Health Research, National Institute of Public Health, Ministry of Health, Cuernavaca, Morelos, MexicoDepartment of Preventive Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USADepartment of Developmental Neurobiology, National Institute of Perinatology, Montes Urales 800, Lomas Virreyes, Mexico City 11000, MexicoDepartment of Environmental Health Sciences, Columbia University, Mailman School of Public Health, New York, NY, USADepartment of Developmental Neurobiology, National Institute of Perinatology, Montes Urales 800, Lomas Virreyes, Mexico City 11000, MexicoDepartment of Preventive Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USADepartment of Environmental Health Sciences, Columbia University, Mailman School of Public Health, New York, NY, USAKravis Children's Hospital, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Mindich Child Health and Development Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USACenter for Nutrition and Health Research, National Institute of Public Health, Ministry of Health, Cuernavaca, Morelos, MexicoDepartment of Preventive Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USADepartment of Environmental Health Sciences, Columbia University, Mailman School of Public Health, New York, NY, USA; Correspondence to: A. Baccarelli, Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, 722 West 168th Street, New York, NY 10032, USA.Introduction: Lead (Pb) crosses the placenta and can cause oxidative stress, reduced fetal growth and neurological problems. The principal source of oxidative stress in human cells is mitochondria. Therefore, disruption of normal mitochondrial function during pregnancy may represent a primary mechanism behind the adverse effects of lead. We sought to assess the association of Pb exposure during pregnancy with mitochondrial DNA (mtDNA) content, a sensitive marker of mitochondrial function, in cord blood. Materials and methods: This study comprised mother-infant pairs from the Programming Research in Obesity, Growth, Environment and Social Stressors (PROGRESS) study, a prospective birth-cohort that enrolled 1050 pregnant women from Mexico City who were receiving prenatal care between December 2007 and July 2011. Quantitative PCR was used to calculate relative MtDNA content (mitochondrial-to-nuclear DNA ratio (mtDNA/nDNA)) in cord blood. Lead concentrations in both maternal blood (2nd and 3rd trimester and at delivery day) and in cord blood were measured by ICP-MS. Multivariable regression models adjusting for multiple confounders were fitted with 410 mother-infant pairs for whom complete data for mtDNA content, lead levels, and covariates were available. Results: Maternal blood Pb measured in the second (mean 3.79 μg/dL, SD 2.63; β = 0.059, 95% CI 0.008, 0.111) and third trimester (mean 3.90 μg/dL; SD 2.84; β = 0.054, 95% CI 0.002, 0.107) during pregnancy and PB in cord blood (mean 3.50 μg/dL, SD 2.59; β = 0.050, 95% CI 0.004; 0.096) were associated with increased cord blood mtDNA content (mean 1.46, SD 0.44). In two-way interaction analyses, cord blood Pb marginally interacted with gestational age leading to an increase in mtDNA content for pre-term births (Benjamini-Hochberg False Discovery Rate correction; BH-FDR = 0.08). Conclusion: This study shows that lead exposure in pregnancy alters mtDNA content in cord blood; therefore, alteration of mtDNA content might be a mechanism underlying the toxicity of lead. Keywords: mtDNA content, Lead exposure, Pregnancy, Mitochondrial dysfunction, Cord bloodhttp://www.sciencedirect.com/science/article/pii/S0160412018313801 |