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

- Prenatal NO2 exposure was inversely associated with infant growth.
- Birth outcomes mediate the prenatal NO2 exposure and infant growth association.
- Placental mtDNA content was positively associated with infant length.
- Placental mtDNA mediates the prenatal NO2 exposure and infant length association.

BackgroundThe 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.ObjectiveIn 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.MethodsIn 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.ResultsPrenatal NO2 exposure was inversely associated with all infant growth parameters. A 10 µg/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.ConclusionsOur 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.