Abstract

Background: A growing body of evidence shows that cardiovascular disease in adulthood, in particular that of the microcirculation, could find its roots during prenatal development. In this study we investigated the association between pre- and postnatal black carbon and particulate air pollution exposure on heat-induced skin hyperemia as a dynamic marker of the microvasculature. Methods: In 139 children between the age of 4 to 6 who are followed longitudinally within the ENVIRONAGE birth cohort, we measured skin perfusion by Laser Doppler probes using the Periflux6000. Residential black carbon (BC) and particulate (PM10 and PM2.5) air pollution levels were modelled for each participant’s home address using a high-resolution spatiotemporal model. We assessed the association between skin hyperemia and pre- and postnatal air pollution using linear regression models while adjusting for relevant covariates. Results: Prenatal residential BC exposure averaged (IQR) 1.38 (1.05 - 1.62) µg/m³, PM10 18.72 (14.44 - 22.78) µg/m³ and PM2.5 13.43 (9.19 - 17.26) µg/m³. An IQR increment in BC exposure during the third trimester of pregnancy was associated with a 13.8 % (95% CI: -22.7 to -3.9; p = 0.008) lower skin hyperemia. Similar effect estimates were retrieved for PM10 and PM2.5 (respectively 11.7 % (95% CI: -20.6 to -1.8; p = 0.022) and 14.2 % (95% CI: -25.1 to -1.8; p = 0.027) lower skin hyperemia). Postnatal exposure to BC, PM10 or PM2.5 was not associated with skin hyperemia at the age 4 to 6 and did not alter the previous reported prenatal associations. Conclusion: These findings support that BC and particulate air pollution exposure even at low concentrations during prenatal life can have long-lasting consequences on the microvasculature. This proposes a role of prenatal air pollution exposures in the microvascular origin of cardiovascular disease development later in life.

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