Diana B P Clemente1, Maribel Casas2, Bram G Janssen3, Aitana Lertxundi4, Loreto Santa-Marina5, Carmen Iñiguez6, Sabrina Llop7, Jordi Sunyer2, Mònica Guxens8, Tim S Nawrot9, Martine Vrijheid2. 1. ISGlobal, Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain; Center for Environmental Sciences, Hasselt University, Diepenbeek, Belgium; Universitat Pompeu Fabra, Barcelona, Spain; CIBER de Epidemiologia y Salud Pública (CIBERESP), Institute of Health Carlos III, Madrid, Spain. Electronic address: diana.clementebatalhapardal@uhasselt.be. 2. ISGlobal, Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain; Universitat Pompeu Fabra, Barcelona, Spain; CIBER de Epidemiologia y Salud Pública (CIBERESP), Institute of Health Carlos III, Madrid, Spain. 3. Center for Environmental Sciences, Hasselt University, Diepenbeek, Belgium. 4. Universidad del País Vasco UPV-EUH, Spain; Health Research Institute, Biodonostia, San Sebastián, Spain. 5. CIBER de Epidemiologia y Salud Pública (CIBERESP), Institute of Health Carlos III, Madrid, Spain; Health Research Institute, Biodonostia, San Sebastián, Spain; Public Health Division of Gipuzkoa, Basque Government, Spain. 6. CIBER de Epidemiologia y Salud Pública (CIBERESP), Institute of Health Carlos III, Madrid, Spain; Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain; University of Valencia, Valencia, Spain. 7. CIBER de Epidemiologia y Salud Pública (CIBERESP), Institute of Health Carlos III, Madrid, Spain; University of Valencia, Valencia, Spain. 8. ISGlobal, Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain; Universitat Pompeu Fabra, Barcelona, Spain; CIBER de Epidemiologia y Salud Pública (CIBERESP), Institute of Health Carlos III, Madrid, Spain; Department of Child and Adolescent Psychiatry/Psychology, Erasmus University Medical Centre - Sophia Children's Hospital, Rotterdam, The Netherlands. 9. Center for Environmental Sciences, Hasselt University, Diepenbeek, Belgium; Department of Public Health & Primary Care, Unit Environment & Health, Leuven University, Leuven, Belgium.
Abstract
BACKGROUND: The association between prenatal air pollution exposure and postnatal growth has hardly been explored. Mitochondrial DNA (mtDNA), as a marker of oxidative stress, and growth at birth can play an intermediate role in this association. OBJECTIVE: In a subset of the Spanish birth cohort INMA we assessed first whether prenatal nitrogen dioxide (NO2) exposure is associated with infant growth. Secondly, we evaluated whether growth at birth (length and weight) could play a mediating role in this association. Finally, the mediation role of placental mitochondrial DNA content in this association was assessed. METHODS: In 336 INMA children, relative placental mtDNA content was measured. Land-use regression models were used to estimate prenatal NO2 exposure. Infant growth (height and weight) was assessed at birth, at 6 months of age, and at 1 year of age. We used multiple linear regression models and performed mediation analyses. The proportion of mediation was calculated as the ratio of indirect effect to total effect. RESULTS: Prenatal NO2 exposure was inversely associated with all infant growth parameters. A 10µg/m³ increment in prenatal NO2 exposure during trimester 1 of pregnancy was significantly inversely associated with height at 6 months of age (-6.6%; 95%CI: -11.4, -1.9) and weight at 1 year of age (-4.2%; 95%CI: -8.3, -0.1). These associations were mediated by birth length (31.7%; 95%CI: 34.5, 14.3) and weight (53.7%; 95%CI: 65.3, -0.3), respectively. Furthermore, 5.5% (95%CI: 10.0, -0.2) of the association between trimester 1 NO2 exposure and length at 6 months of age could be mediated by placental mtDNA content. CONCLUSIONS: Our results suggest that impaired fetal growth caused by prenatal air pollution exposure can lead to impaired infant growth during the first year of life. Furthermore, molecular adaptations in placental mtDNA are associated with postnatal consequences of air pollution induced alterations in growth.
BACKGROUND: The association between prenatal air pollution exposure and postnatal growth has hardly been explored. Mitochondrial DNA (mtDNA), as a marker of oxidative stress, and growth at birth can play an intermediate role in this association. OBJECTIVE: In a subset of the Spanish birth cohort INMA we assessed first whether prenatal nitrogen dioxide (NO2) exposure is associated with infant growth. Secondly, we evaluated whether growth at birth (length and weight) could play a mediating role in this association. Finally, the mediation role of placental mitochondrial DNA content in this association was assessed. METHODS: In 336 INMA children, relative placental mtDNA content was measured. Land-use regression models were used to estimate prenatal NO2 exposure. Infant growth (height and weight) was assessed at birth, at 6 months of age, and at 1 year of age. We used multiple linear regression models and performed mediation analyses. The proportion of mediation was calculated as the ratio of indirect effect to total effect. RESULTS: Prenatal NO2 exposure was inversely associated with all infant growth parameters. A 10µg/m³ increment in prenatal NO2 exposure during trimester 1 of pregnancy was significantly inversely associated with height at 6 months of age (-6.6%; 95%CI: -11.4, -1.9) and weight at 1 year of age (-4.2%; 95%CI: -8.3, -0.1). These associations were mediated by birth length (31.7%; 95%CI: 34.5, 14.3) and weight (53.7%; 95%CI: 65.3, -0.3), respectively. Furthermore, 5.5% (95%CI: 10.0, -0.2) of the association between trimester 1 NO2 exposure and length at 6 months of age could be mediated by placental mtDNA content. CONCLUSIONS: Our results suggest that impaired fetal growth caused by prenatal air pollution exposure can lead to impaired infant growth during the first year of life. Furthermore, molecular adaptations in placental mtDNA are associated with postnatal consequences of air pollution induced alterations in growth.
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