Anne Debost-Legrand1, Charline Warembourg2, Catherine Massart3, Cécile Chevrier2, Nathalie Bonvallot4, Christine Monfort2, Florence Rouget5, Fabrice Bonnet6, Sylvaine Cordier7. 1. National Institute of Health and Medical Research (Inserm), U1085, Institut de Recherche en Santé, Environnement et Travail (Irset), F-35043 Rennes, France; Centre Hospitalier Universitaire de Clermont-Ferrand, Service de Santé Publique, F-63000 Clermont-Ferrand, France; Centre Hospitalier Universitaire de Clermont-Ferrand, EA 4681, PEPRADE, Université d'Auvergne, F- 63000 Clermont-Ferrand, France. 2. National Institute of Health and Medical Research (Inserm), U1085, Institut de Recherche en Santé, Environnement et Travail (Irset), F-35043 Rennes, France; Université de Rennes I, F-35043 Rennes, France. 3. Laboratory of Hormonology, CIC-P INSERM 1414, CHU Rennes, F-35000 Rennes, France. 4. National Institute of Health and Medical Research (Inserm), U1085, Institut de Recherche en Santé, Environnement et Travail (Irset), F-35043 Rennes, France; Ecole des Hautes études en Santé Publique (EHESP), F-35043 Rennes, France. 5. National Institute of Health and Medical Research (Inserm), U1085, Institut de Recherche en Santé, Environnement et Travail (Irset), F-35043 Rennes, France; Université de Rennes I, F-35043 Rennes, France; Département de Pédiatrie, CHU Rennes, F-35000 Rennes, France. 6. Université de Rennes I, F-35043 Rennes, France; Service Endocrinologie, CHU de Rennes, F-35000 Rennes, France; Inserm U1018, Centre de Recherche en Epidémiologie et Santé des Populations, F-94807 Villejuif, France. 7. National Institute of Health and Medical Research (Inserm), U1085, Institut de Recherche en Santé, Environnement et Travail (Irset), F-35043 Rennes, France; Université de Rennes I, F-35043 Rennes, France. Electronic address: sylvaine.cordier@inserm.fr.
Abstract
BACKGROUND: Experimental evidence suggests that developmental exposure to persistent organic pollutants (POP) and to some non persistent pesticides may disrupt metabolic regulation of glucose metabolism and insulin secretion, and thereby contribute to the current epidemic of obesity and metabolic disorders. Quasi-experimental situations of undernutrition in utero have provided some information. However, the evidence in humans concerning the role of the prenatal environment in these disorders is contradictory, and little is known about long-term outcomes, such as type 2 diabetes, of prenatal exposure. OBJECTIVES: Our aim was to evaluate the effects of prenatal exposure to POP and organophosphate pesticides on fetal markers of glucose metabolism in a sample of newborns from the Pelagie mother-child cohort in Brittany (France). METHODS: Dialkylphosphate (DAP) metabolites of organophosphate pesticides were measured in maternal urine collected at the beginning of pregnancy. Cord blood was assayed for polychlorinated biphenyl congener 153 (PCB153), p,p'-dichlorodiphenyl dichloroethene (DDE) and other POP. Insulin and adiponectin were determined in cord blood serum (n=268). RESULTS: A decrease in adiponectin and insulin levels was observed with increasing levels of DDE, but only in girls and not boys. Adiponectin levels were not related to the concentrations of other POP or DAP metabolites. Decreasing insulin levels were observed with increasing PCB153 concentrations. Insulin levels increased with DAP urinary levels. Additional adjustment for BMI z-score at birth modified some of these relations. CONCLUSIONS: Our observations bring support for a potential role of organophosphate pesticides and POP in alterations to glucose metabolism observable at birth.
BACKGROUND: Experimental evidence suggests that developmental exposure to persistent organic pollutants (POP) and to some non persistent pesticides may disrupt metabolic regulation of glucose metabolism and insulin secretion, and thereby contribute to the current epidemic of obesity and metabolic disorders. Quasi-experimental situations of undernutrition in utero have provided some information. However, the evidence in humans concerning the role of the prenatal environment in these disorders is contradictory, and little is known about long-term outcomes, such as type 2 diabetes, of prenatal exposure. OBJECTIVES: Our aim was to evaluate the effects of prenatal exposure to POP and organophosphate pesticides on fetal markers of glucose metabolism in a sample of newborns from the Pelagie mother-child cohort in Brittany (France). METHODS:Dialkylphosphate (DAP) metabolites of organophosphate pesticides were measured in maternal urine collected at the beginning of pregnancy. Cord blood was assayed for polychlorinated biphenyl congener 153 (PCB153), p,p'-dichlorodiphenyl dichloroethene (DDE) and other POP. Insulin and adiponectin were determined in cord blood serum (n=268). RESULTS: A decrease in adiponectin and insulin levels was observed with increasing levels of DDE, but only in girls and not boys. Adiponectin levels were not related to the concentrations of other POP or DAP metabolites. Decreasing insulin levels were observed with increasing PCB153 concentrations. Insulin levels increased with DAP urinary levels. Additional adjustment for BMI z-score at birth modified some of these relations. CONCLUSIONS: Our observations bring support for a potential role of organophosphate pesticides and POP in alterations to glucose metabolism observable at birth.
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