Children's microvascular traits and ambient air pollution exposure during pregnancy and early childhood: Prospective evidence to elucidate the developmental origin of particle-induced disease

Leen J. Luyten, Yinthe Dockx, Eline B. Provost, Narjes Madhloum, Hanne Sleurs, Kristof Y. Neven, Bram G. Janssen, Hannelore Bové, Florence Debacq-Chainiaux, Nele Gerrits, Wouter Lefebvre, Michelle Plusquin, Charlotte Vanpoucke, Patrick De Boever, Tim S. Nawrot

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Résumé

Background: Particulate matter exposure during in utero life may entail adverse health outcomes later in life. The microvasculature undergoes extensive, organ-specific prenatal maturation. A growing body of evidence shows that cardiovascular disease in adulthood is rooted in a dysfunctional fetal and perinatal development, in particular that of the microcirculation. We investigate whether prenatal or postnatal exposure to PM2.5 (particulate matter with a diameter ≤ 2.5 μm) or NO2 is related to microvascular traits in children between the age of four and six. Methods: We measured the retinal microvascular diameters, the central retinal arteriolar equivalent (CRAE) and central retinal venular equivalent (CRVE), and the vessel curvature by means of the tortuosity index (TI) in young children (mean [SD] age 4.6 [0.4] years), followed longitudinally within the ENVIRONAGE birth cohort. We modeled daily prenatal and postnatal PM2.5 and NO2 exposure levels for each participant's home address using a high-resolution spatiotemporal model. Results: An interquartile range (IQR) increase in PM2.5 exposure during the entire pregnancy was associated with a 3.85-μm (95% CI, 0.10 to 7.60; p = 0.04) widening of the CRVE and a 2.87-μm (95% CI, 0.12 to 5.62; p = 0.04) widening of the CRAE. For prenatal NO2 exposure, an IQR increase was found to widen the CRVE with 4.03 μm (95% CI, 0.44 to 7.63; p = 0.03) and the CRAE with 2.92 μm (95% CI, 0.29 to 5.56; p = 0.03). Furthermore, a higher TI score was associated with higher prenatal NO2 exposure. We observed a postnatal effect of short-term PM2.5 exposure on the CRAE and a childhood NO2 exposure effect on both the CRVE and CRAE. Conclusions: Our results link prenatal and postnatal air pollution exposure with changes in a child's microvascular traits as a fundamental novel mechanism to explain the developmental origin of cardiovascular disease.

langue originaleAnglais
Numéro d'article128
journalBMC Medicine
Volume18
Numéro de publication1
Les DOIs
Etat de la publicationPublié - 26 mai 2020

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