Rafael Ogaz-González1, Ángel Mérida-Ortega2, Luisa Torres-Sánchez3, Lourdes Schnaas4, César Hernández-Alcaraz5, Mariano E Cebrián6, Stephen J Rothenberg7, Rosa María García-Hernández8, Lizbeth López-Carrillo9. 1. Centro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública, Av. Universidad 655, Col. Santa María Ahuacatitlán, Cuernavaca, Morelos, Mexico. Electronic address: rafaogaz@hotmail.com. 2. Centro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública, Av. Universidad 655, Col. Santa María Ahuacatitlán, Cuernavaca, Morelos, Mexico. Electronic address: angel.merida@espm.insp.mx. 3. Centro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública, Av. Universidad 655, Col. Santa María Ahuacatitlán, Cuernavaca, Morelos, Mexico. Electronic address: ltorress@insp.mx. 4. Subdirección de Investigación en Intervenciones Comunitarias, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Calle Montes Urales 800, Miguel Hidalgo, Lomas Virreyes, Ciudad de México, Mexico. Electronic address: lschnaas@hotmail.com. 5. Centro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública, Av. Universidad 655, Col. Santa María Ahuacatitlán, Cuernavaca, Morelos, Mexico. Electronic address: cesar.hernandez@insp.mx. 6. Departamento de Toxicología, Centro de Investigación y de Estudios Avanzados del IPN, Av. Instituto Politécnico Nacional, 2508, Delegación Gustavo A. Madero, San Pedro Zacatenco, Ciudad de México, Mexico. Electronic address: mcebrian@cinvestav.mx. 7. Centro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública, Av. Universidad 655, Col. Santa María Ahuacatitlán, Cuernavaca, Morelos, Mexico. Electronic address: rothenberg@insp.mx. 8. Departamento de Toxicología, Centro de Investigación y de Estudios Avanzados del IPN, Av. Instituto Politécnico Nacional, 2508, Delegación Gustavo A. Madero, San Pedro Zacatenco, Ciudad de México, Mexico. Electronic address: rmgarcia@cinvestav.mx. 9. Centro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública, Av. Universidad 655, Col. Santa María Ahuacatitlán, Cuernavaca, Morelos, Mexico. Electronic address: lizbeth@insp.mx.
Abstract
BACKGROUND: Maternal 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) serum levels during pregnancy have been negatively linked to child neurodevelopment in contrast to intake of omega-3 and -6 (ω-3 and ω-6) fatty acids. OBJECTIVES: To assess whether maternal dietary intake of ω-3 and ω-6 during pregnancy modifies the association between exposure to DDE and child neurodevelopment from age 42-60 months. METHODS: Prospective cohort study with 142 mother-child pairs performed in Mexico. DDE serum levels were determined by electron capture gas chromatography. Dietary ω-3 and ω-6 intake was estimated by questionnaire. Child neurodevelopment was assessed by McCarthy Scales. RESULTS: Docosahexaenoic (DHA) fatty acid intake significantly modified the association between DDE and motor component: increased maternal DDE was associated with lower motor development in children whose mothers had lower DHA intake (βlog2DDE = -1.25; 95% CI: -2.62, 0.12), in contrast to the non-significant increase among children whose mothers had higher DHA intake (βlog2DDE-motor = 0.50; 95% CI: 0.55, 1.56). Likewise, arachidonic fatty acid (ARA) intake modified the association between DDE and memory component: increased maternal DDE was associated with a significantly larger reduction in the memory component in children whose mothers had lower ARA intake (βlog2DDE = -1.31; 95% CI: -2.29, -0.32) than children whose mothers had higher ARA intake (βlog2DDE-memory = 0.17; 95% CI: -0.78, 1.11). CONCLUSIONS: Dietary intake of DHA and ARA during pregnancy may protect against child neurodevelopment damage associated with prenatal maternal DDE levels.
BACKGROUND: Maternal 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) serum levels during pregnancy have been negatively linked to child neurodevelopment in contrast to intake of omega-3 and -6 (ω-3 and ω-6) fatty acids. OBJECTIVES: To assess whether maternal dietary intake of ω-3 and ω-6 during pregnancy modifies the association between exposure to DDE and child neurodevelopment from age 42-60 months. METHODS: Prospective cohort study with 142 mother-child pairs performed in Mexico. DDE serum levels were determined by electron capture gas chromatography. Dietary ω-3 and ω-6 intake was estimated by questionnaire. Child neurodevelopment was assessed by McCarthy Scales. RESULTS:Docosahexaenoic (DHA) fatty acid intake significantly modified the association between DDE and motor component: increased maternal DDE was associated with lower motor development in children whose mothers had lower DHA intake (βlog2DDE = -1.25; 95% CI: -2.62, 0.12), in contrast to the non-significant increase among children whose mothers had higher DHA intake (βlog2DDE-motor = 0.50; 95% CI: 0.55, 1.56). Likewise, arachidonic fatty acid (ARA) intake modified the association between DDE and memory component: increased maternal DDE was associated with a significantly larger reduction in the memory component in children whose mothers had lower ARA intake (βlog2DDE = -1.31; 95% CI: -2.29, -0.32) than children whose mothers had higher ARA intake (βlog2DDE-memory = 0.17; 95% CI: -0.78, 1.11). CONCLUSIONS: Dietary intake of DHA and ARA during pregnancy may protect against child neurodevelopment damage associated with prenatal maternal DDE levels.
Authors: Liliana A Zúñiga-Venegas; Carly Hyland; María Teresa Muñoz-Quezada; Lesliam Quirós-Alcalá; Mariana Butinof; Rafael Buralli; Andres Cardenas; Ricardo A Fernandez; Claudia Foerster; Nelson Gouveia; Juan P Gutiérrez Jara; Boris A Lucero; María Pía Muñoz; Muriel Ramírez-Santana; Anna R Smith; Noemi Tirado; Berna van Wendel de Joode; Gloria M Calaf; Alexis J Handal; Agnes Soares da Silva; Sandra Cortés; Ana M Mora Journal: Environ Health Perspect Date: 2022-09-29 Impact factor: 11.035