Prenatal ambient air pollution exposure, infant growth and placental mitochondrial DNA content in the INMA birth cohort


Por: Clemente DBP, Casas M, Janssen BG, Lertxundi A, Santa-Marina L, Iñiguez C, Llop S, Sunyer J, Guxens M, Nawrot TS and Vrijheid M

Publicada: 1 ago 2017 Ahead of Print: 20 may 2017
Resumen:
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 10 mu g/m(3) 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.

Filiaciones:
Clemente DBP:
 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.

Casas M:
 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

Lertxundi A:
 Universidad del País Vasco UPV-EUH, Spain

 Health Research Institute, Biodonostia, San Sebastian, Spain

Santa-Marina L:
 Public Health Division of Gipuzkoa, Basque Government, Spain

:
 Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain

 University of Valencia, Valencia, Spain

:
 University of Valencia, Valencia, Spain

Sunyer J:
 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

Guxens M:
 ISGlobal, Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain

 Universitat Pompeu Fabra, Barcelona, Spain

 Department of Child and Adolescent Psychiatry/Psychology, Erasmus University Medical Centre - Sophia Children's Hospital, Rotterdam, The Netherlands

Nawrot TS:
 Center for Environmental Sciences, Hasselt University, Diepenbeek, Belgium

 Department of Public Health & Primary Care, Unit Environment & Health, Leuven University, Leuven, Belgium

Vrijheid M:
 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
ISSN: 00139351





ENVIRONMENTAL RESEARCH
Editorial
ACADEMIC PRESS INC ELSEVIER SCIENCE, 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 157 Número:
Páginas: 96-102
WOS Id: 000403524000013
ID de PubMed: 28535425
imagen Green Accepted, Green Submitted

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