Teresa Verenice Muñoz-Rocha1, Marcela Tamayo Y Ortiz2, Martín Romero3, Ivan Pantic4, Lourdes Schnaas5, David Bellinger6, Birgit Claus-Henn7, Rosalind Wright8, Robert O Wright9, Martha María Téllez-Rojo10. 1. National Institute of Public Health, Universidad No. 655 Colonia Santa María, Ahuacatitlán, Cerrada Los Pinos y Caminera, C.P. 62100, Cuernavaca, Morelos, Mexico. Electronic address: verenice.munoz@insp.mx. 2. National Institute of Public Health, Universidad No. 655 Colonia Santa María, Ahuacatitlán, Cerrada Los Pinos y Caminera, C.P. 62100, Cuernavaca, Morelos, Mexico; CONACYT- National Council of Science and Technology, Avenida Insurgentes Sur 1582, D.F., Benito Juárez, Crédito Constructor, 03940, Ciudad de, Mexico. Electronic address: marcela.tamayo@insp.mx. 3. National Institute of Public Health, Universidad No. 655 Colonia Santa María, Ahuacatitlán, Cerrada Los Pinos y Caminera, C.P. 62100, Cuernavaca, Morelos, Mexico. Electronic address: martin.romero@insp.mx. 4. National Institute of Perinatology, Calle Montes Urales #800, D.F., Miguel Hidalgo, Lomas Virreyes, 11000 Ciudad de, Mexico. Electronic address: ivandpantic@gmail.com. 5. National Institute of Perinatology, Calle Montes Urales #800, D.F., Miguel Hidalgo, Lomas Virreyes, 11000 Ciudad de, Mexico. Electronic address: lschnaas@hotmail.com. 6. Department Environmental Health, Harvard T.H. Chan School of Public Health, 677 Huntington Ave, Boston, MA 02115, United States,. Electronic address: david.bellinger@childrens.harvard.edu. 7. Department of Environmental Health, Boston University School of Public Health, 715 Albany Street, Boston, MA 02118, United States,. Electronic address: bclaus@bu.edu. 8. Department of Pediatrics, Icahn School of Medicine at Mount Sinai, 1428 Madison Ave, New York, NY 10029, United States. Electronic address: rosalind.wright@mssm.edu. 9. Department of Preventive Medicine, Icahn School of Medicine at Mount Sinai, 1428 Madison Ave, New York, NY 10029, United States. Electronic address: robert.wright@mssm.edu. 10. National Institute of Public Health, Universidad No. 655 Colonia Santa María, Ahuacatitlán, Cerrada Los Pinos y Caminera, C.P. 62100, Cuernavaca, Morelos, Mexico. Electronic address: mmtellez@insp.mx.
Abstract
BACKGROUND: Normal prenatal neurodevelopment follows stages that are potentially influenced by both chemical and psychosocial environments. Exposure to elevated manganese during this critically vulnerable period has been found to be neurotoxic. Independently, maternal prenatal depression has been associated with subsequent neurodevelopmental decrements in children. The association between child neurodevelopment and prenatal co-exposure to manganese and maternal depression has not been sufficiently studied. METHODS: During pregnancy and at birth, we measured maternal blood and cord blood manganese levels respectively. Maternal depression was assessed in the 3rd trimester of pregnancy using the Edinburgh Depression Scale. Neurodevelopment was evaluated at 24 months of age with the Bayley Scales of Infant Development. A multivariate multiple regression model was used to analyze cognitive, language and motor scores simultaneously for 473 children from the PROGRESS birth cohort in Mexico City. RESULTS: Over 25% of our study participants reported having depressive symptoms. 3rd trimester blood manganese as well as depressive symptoms were independently negatively associated with all neurodevelopment scores in adjusted models. In stratified analyses, the negative association between manganese (maternal as well as cord blood) and 24-month language scores was stronger among women with depressive symptoms. Receptive language was mostly affected. Inverted U-shaped curves were seen for the association between with cord blood manganese and neurodevelopment scores. CONCLUSIONS: Our findings are in line with previous studies of manganese and depression neurotoxicity. The prenatal period may be particularly sensitive to manganese and depression co-exposures and should be of interest for public health interventions to promote healthy emotional and nutritional pregnancies.
BACKGROUND: Normal prenatal neurodevelopment follows stages that are potentially influenced by both chemical and psychosocial environments. Exposure to elevated manganese during this critically vulnerable period has been found to be neurotoxic. Independently, maternal prenatal depression has been associated with subsequent neurodevelopmental decrements in children. The association between child neurodevelopment and prenatal co-exposure to manganese and maternal depression has not been sufficiently studied. METHODS: During pregnancy and at birth, we measured maternal blood and cord blood manganese levels respectively. Maternal depression was assessed in the 3rd trimester of pregnancy using the Edinburgh Depression Scale. Neurodevelopment was evaluated at 24 months of age with the Bayley Scales of Infant Development. A multivariate multiple regression model was used to analyze cognitive, language and motor scores simultaneously for 473 children from the PROGRESS birth cohort in Mexico City. RESULTS: Over 25% of our study participants reported having depressive symptoms. 3rd trimester blood manganese as well as depressive symptoms were independently negatively associated with all neurodevelopment scores in adjusted models. In stratified analyses, the negative association between manganese (maternal as well as cord blood) and 24-month language scores was stronger among women with depressive symptoms. Receptive language was mostly affected. Inverted U-shaped curves were seen for the association between with cord blood manganese and neurodevelopment scores. CONCLUSIONS: Our findings are in line with previous studies of manganese and depression neurotoxicity. The prenatal period may be particularly sensitive to manganese and depression co-exposures and should be of interest for public health interventions to promote healthy emotional and nutritional pregnancies.
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