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|Title: ||Prenatal ambient air pollution exposure, infant growth and placental mitochondrial DNA content in the INMA birth cohort|
|Authors: ||Clemente, Diana B. P.|
Janssen, Bram G.
Nawrot, Tim S.
|Issue Date: ||2017|
|Publisher: ||ACADEMIC PRESS INC ELSEVIER SCIENCE|
|Citation: ||ENVIRONMENTAL RESEARCH, 157, p. 96-102|
|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 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.|
|Notes: ||[Clemente, Diana B. P.; Casas, Maribel; Sunyer, Jordi; Guxens, Monica; Vrijheid, Martine] ISGiobal, Ctr Res Environm Epidemiol CREAL, Barcelona, Spain. [Clemente, Diana B. P.; Janssen, Bram G.; Nawrot, Tim S.] Hasselt Univ, Ctr Environm Sci, Diepenbeek, Belgium. [Clemente, Diana B. P.; Casas, Maribel; Sunyer, Jordi; Guxens, Monica; Vrijheid, Martine] Univ Pompeu Fabra, Barcelona, Spain. [Clemente, Diana B. P.; Casas, Maribel; Santa-Marina, Loreto; Iniguez, Carmen; Llop, Sabrina; Sunyer, Jordi; Guxens, Monica; Vrijheid, Martine] Inst Hlth Carlos III, CIBER Epidemiol & Salud Pabl CIBERESP, Madrid, Spain. [Lertxundi, Aitana] Univ Pais Vasco UPV EUH, Bilbao, Spain. [Lertxundi, Aitana] Biodonostia, Hlth Res Inst, San Sebastian, Spain. [Santa-Marina, Loreto] Basque Govt, Publ Hlth Div Gipuzkoa, San Sebastian, Spain. [Iniguez, Carmen] Fdn Promot Hlth & Biomed Res Valencian Reg FISABI, Valencia, Spain. [Iniguez, Carmen] Univ Valencia, Valencia, Spain. [Guxens, Monica] Erasmus Univ, Med Ctr, Sophia Childrens Hosp, Dept Child & Adolescent Psychiat Psychol, Rotterdam, Netherlands. [Nawrot, Tim S.] Leuven Univ, Unit Environm & Hlth, Dept Publ Health& Primary Care, Leuven, Belgium.|
|ISI #: ||000403524000013|
|Type: ||Journal Contribution|
|Appears in Collections: ||Research publications|
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