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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

L. Luyten,Y. Dockx,Eline B. Provost,N. Madhloum,H. Sleurs,K. Neven,B. Janssen,H. Bové,F. Debacq-Chainiaux,Nele Gerrits,W. Lefebvre,M. Plusquin,C. Vanpoucke,P. De Boever,T. Nawrot

Published 2020 in BMC Medicine

ABSTRACT

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 PM 2.5 (particulate matter with a diameter ≤ 2.5 μm) or NO 2 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 ENVIR ON AGE birth cohort. We modeled daily prenatal and postnatal PM 2.5 and NO 2 exposure levels for each participant’s home address using a high-resolution spatiotemporal model. Results An interquartile range (IQR) increase in PM 2.5 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 NO 2 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 NO 2 exposure. We observed a postnatal effect of short-term PM 2.5 exposure on the CRAE and a childhood NO 2 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.

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