Prenatal exposure to air pollutants can trigger autophagy and senescence in newborns; autophagy-related biomarkers vary with air pollution levels.
Exposure to nitrogen dioxide (NO2) and particulate matter smaller than 10 microns in diameter (PM10) during pregnancy, initiated processes of autophagy and senescence in the newborn. These processes might explain the deleterious effect of air pollutants on respiratory health in infancy.
Previous studies have already demonstrated an elevated risk for respiratory morbidity and impaired lung function in babies with prenatal exposure to air pollution. However, the cellular mechanisms are largely unknown. “Autophagy is a physiological process that helps cells to fight oxidative stress damage,” said Olga Gorlanova, MD, at the 2023 ERS International Congress. Air pollution exposure leads to an oxidative stress response in the fetus that may initiate autophagy. Degradation of damaged cell components can then lead to senescent cells that produce different senescence-associated secretory phenotypes (so-called SASP; eg, cytokines, chemokines, metalloproteinases, and growth factors). SASP can promote remodeling, inflammation, infectious susceptibility, angiogenesis, and proliferation, while hindering tissue repair and regeneration.
With her study, Dr. Gorlanova and colleagues wanted to shed light on the association between NO2 and PM10 exposure during pregnancy and a predefined set of autophagy-related biomarkers obtained from the cord blood of healthy-term newborns. Based on the autophagy/SASP biomarker profile, they tried to find out whether all infants respond to air pollution in the same way.
The study population consisted of healthy-term newborns (N=449) from the Basel-Bern Infant Lung Development (BILD) cohort. The BILD study started in 1999 in Bern and aims to recruit 1000 babies by 2025. It investigates the effects of genetics and the environment (particularly air pollution) on lung development in babies and children.
An analysis of 11 proteins in the cord blood, among other Beclin-1, SIRT1, different cytokines and metalloproteinases was performed and related to the air pollutant exposure.
Exposure to NO2 was associated with an increase in the protein Beclin-1 and a decrease in SIRT1 and IL-8. Beclin-1 is a protein that is central to initiating autophagy whereas SIRT1 play a protective role in stress resistance, inflammation, and ageing. Another important study result was that newborns from the cluster with low air pollution exposure had a low level of autophagy, senescence, inflammatory cytokines and remodeling SASP proteins.
“Therefore, we believe, that autophagy may play a role in the defense against oxidative stress damage related to prenatal air pollution exposure in newborns. In addition, there is a dose-dependent relationship between prenatal air pollution and autophagy-related biomarkers,” Dr. Gorlanova concluded.
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