Gestational organophosphate pesticide exposure and childhood cardiovascular outcomes

Introduction: The general population is chronically exposed to organophosphate pesticides through various routes including ingestion, hand-to-mouth contact, inhalation, and dermal contact. Exposure to organophosphate pesticides during pregnancy impairs fetal development, but the potential long-term...

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Main Authors: Danielle R. Stevens, Sophia M. Blaauwendraad, Paige A. Bommarito, Michiel van den Dries, Leonardo Trasande, Suzanne Spaan, Anjoeka Pronk, Henning Tiemeier, Romy Gaillard, Vincent W.V. Jaddoe, Kelly K. Ferguson
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Language:English
Published: Elsevier 2024-11-01
Series:Environment International
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Online Access:http://www.sciencedirect.com/science/article/pii/S0160412024006688
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author Danielle R. Stevens
Sophia M. Blaauwendraad
Paige A. Bommarito
Michiel van den Dries
Leonardo Trasande
Suzanne Spaan
Anjoeka Pronk
Henning Tiemeier
Romy Gaillard
Vincent W.V. Jaddoe
Kelly K. Ferguson
author_facet Danielle R. Stevens
Sophia M. Blaauwendraad
Paige A. Bommarito
Michiel van den Dries
Leonardo Trasande
Suzanne Spaan
Anjoeka Pronk
Henning Tiemeier
Romy Gaillard
Vincent W.V. Jaddoe
Kelly K. Ferguson
author_sort Danielle R. Stevens
collection DOAJ
description Introduction: The general population is chronically exposed to organophosphate pesticides through various routes including ingestion, hand-to-mouth contact, inhalation, and dermal contact. Exposure to organophosphate pesticides during pregnancy impairs fetal development, but the potential long-term effects of gestational organophosphate pesticide exposure are less well understood. Methods: We investigated associations between gestational organophosphate pesticide exposure and cardiovascular outcomes in 643 children in the Generation R Study, a prospective pregnancy cohort based in Rotterdam, The Netherlands. Urinary organophosphate pesticide metabolites (dimethyl [∑DMAP], diethyl [∑DEAP], and total dialkyl phosphate [∑DAP] metabolites) were quantified in three urine samples collected from pregnant participants, and their children were followed until age 10 years at which time cardiac magnetic resonance imaging, ultrasonography, blood pressure, and serum biomarkers assessed cardiovascular health. Linear regression models estimated associations (β and 95 % confidence interval [CI]) between a one-interquartile range (IQR) increase in averaged gestational exposure biomarker concentrations and z-scored pediatric cardiovascular outcomes. We investigated effect modification of associations by PON1 genotype. Results: Carotid intima-media thickness z-score was lower (β: -0.14 [95 % CI: −0.25, −0.02]) and HDL cholesterol z-score was higher (β: 0.14 [95 % CI: 0.02, 0.25]) for increases in ∑DEAP concentrations. Carotid intima-media distensibility z-score was lower (β: -0.08 [95 % CI: −0.19, 0.03]) for increases in ∑DMAP concentrations, and systolic blood pressure z-score was higher (β: 0.10 [95 % CI: −0.01, 0.21]) for increases in ∑DMAP and ∑DAP. Among those with PON1-161CC and PON1-L55MTT genotypes, higher organophosphate pesticide concentrations conferred an excess risk of adverse vascular and glycemic outcomes, respectively. Conclusions: We observed heterogenous associations between gestational organophosphate pesticide exposure and pediatric cardiovascular health: an anti-atherogenic profile was observed for increases in ∑DEAP concentrations, and impairments in multiple aspects of cardiovascular health was observed for increases in ∑DMAP concentrations. PON1-161 and PON1-L55M single nucleotide polymorphisms modified associations for vascular and glycemic outcomes, respectively.
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spelling doaj-art-37ee204fa69d46e7a61a0f09449e4f972024-11-22T07:35:39ZengElsevierEnvironment International0160-41202024-11-01193109082Gestational organophosphate pesticide exposure and childhood cardiovascular outcomesDanielle R. Stevens0Sophia M. Blaauwendraad1Paige A. Bommarito2Michiel van den Dries3Leonardo Trasande4Suzanne Spaan5Anjoeka Pronk6Henning Tiemeier7Romy Gaillard8Vincent W.V. Jaddoe9Kelly K. Ferguson10Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Durham, NC, United StatesThe Generation R Study Group, Erasmus Medical Center, University Medical Center, Rotterdam, the Netherlands; Department of Pediatrics, Erasmus Medical Center, University Medical Center, Rotterdam, the NetherlandsEpidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Durham, NC, United StatesISGlobal, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, Spain; CIBER Epidemiología y Salud Pública (CIBERESP), Spain; Department of Child and Adolescent Psychiatry/Psychology, Erasmus Medical Center, Erasmus University Medical Centre, Rotterdam, the NetherlandsDepartment of Pediatrics, Division of Environmental Pediatrics, NYU Grossman School of Medicine, New York, NY, United States; Department of Population Health, NYU Grossman School of Medicine, New York, NY, United States; NYU Wagner School of Public Service, New York, NY, United StatesDepartment of Risk Analysis for Products in Development, TNO, Utrecht, 3584 CB, the NetherlandsDepartment of Risk Analysis for Products in Development, TNO, Utrecht, 3584 CB, the NetherlandsDepartment of Child and Adolescent Psychiatry/Psychology, Erasmus Medical Center, Erasmus University Medical Centre, Rotterdam, the Netherlands; Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Boston, MA 02115, United StatesThe Generation R Study Group, Erasmus Medical Center, University Medical Center, Rotterdam, the Netherlands; Department of Pediatrics, Erasmus Medical Center, University Medical Center, Rotterdam, the NetherlandsThe Generation R Study Group, Erasmus Medical Center, University Medical Center, Rotterdam, the Netherlands; Department of Pediatrics, Erasmus Medical Center, University Medical Center, Rotterdam, the NetherlandsEpidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Durham, NC, United States; Corresponding author at: National Institute of Environmental Health Sciences, Epidemiology Branch, 111 TW Alexander Drive, Research Triangle Park, NC 27709, United States.Introduction: The general population is chronically exposed to organophosphate pesticides through various routes including ingestion, hand-to-mouth contact, inhalation, and dermal contact. Exposure to organophosphate pesticides during pregnancy impairs fetal development, but the potential long-term effects of gestational organophosphate pesticide exposure are less well understood. Methods: We investigated associations between gestational organophosphate pesticide exposure and cardiovascular outcomes in 643 children in the Generation R Study, a prospective pregnancy cohort based in Rotterdam, The Netherlands. Urinary organophosphate pesticide metabolites (dimethyl [∑DMAP], diethyl [∑DEAP], and total dialkyl phosphate [∑DAP] metabolites) were quantified in three urine samples collected from pregnant participants, and their children were followed until age 10 years at which time cardiac magnetic resonance imaging, ultrasonography, blood pressure, and serum biomarkers assessed cardiovascular health. Linear regression models estimated associations (β and 95 % confidence interval [CI]) between a one-interquartile range (IQR) increase in averaged gestational exposure biomarker concentrations and z-scored pediatric cardiovascular outcomes. We investigated effect modification of associations by PON1 genotype. Results: Carotid intima-media thickness z-score was lower (β: -0.14 [95 % CI: −0.25, −0.02]) and HDL cholesterol z-score was higher (β: 0.14 [95 % CI: 0.02, 0.25]) for increases in ∑DEAP concentrations. Carotid intima-media distensibility z-score was lower (β: -0.08 [95 % CI: −0.19, 0.03]) for increases in ∑DMAP concentrations, and systolic blood pressure z-score was higher (β: 0.10 [95 % CI: −0.01, 0.21]) for increases in ∑DMAP and ∑DAP. Among those with PON1-161CC and PON1-L55MTT genotypes, higher organophosphate pesticide concentrations conferred an excess risk of adverse vascular and glycemic outcomes, respectively. Conclusions: We observed heterogenous associations between gestational organophosphate pesticide exposure and pediatric cardiovascular health: an anti-atherogenic profile was observed for increases in ∑DEAP concentrations, and impairments in multiple aspects of cardiovascular health was observed for increases in ∑DMAP concentrations. PON1-161 and PON1-L55M single nucleotide polymorphisms modified associations for vascular and glycemic outcomes, respectively.http://www.sciencedirect.com/science/article/pii/S0160412024006688OrganophosphatesPesticidesPregnancyCardiovascular diseasesGene polymorphismEndocrine disrupters
spellingShingle Danielle R. Stevens
Sophia M. Blaauwendraad
Paige A. Bommarito
Michiel van den Dries
Leonardo Trasande
Suzanne Spaan
Anjoeka Pronk
Henning Tiemeier
Romy Gaillard
Vincent W.V. Jaddoe
Kelly K. Ferguson
Gestational organophosphate pesticide exposure and childhood cardiovascular outcomes
Environment International
Organophosphates
Pesticides
Pregnancy
Cardiovascular diseases
Gene polymorphism
Endocrine disrupters
title Gestational organophosphate pesticide exposure and childhood cardiovascular outcomes
title_full Gestational organophosphate pesticide exposure and childhood cardiovascular outcomes
title_fullStr Gestational organophosphate pesticide exposure and childhood cardiovascular outcomes
title_full_unstemmed Gestational organophosphate pesticide exposure and childhood cardiovascular outcomes
title_short Gestational organophosphate pesticide exposure and childhood cardiovascular outcomes
title_sort gestational organophosphate pesticide exposure and childhood cardiovascular outcomes
topic Organophosphates
Pesticides
Pregnancy
Cardiovascular diseases
Gene polymorphism
Endocrine disrupters
url http://www.sciencedirect.com/science/article/pii/S0160412024006688
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