Background: Air pollution increases inflammation and reactive oxygen species that induce the autophagy pathway, thereby leading to airway inflammation and remodelling. However, it is not clear whether prenatal air pollution may impact proteins involved in the autophagy pathway.

Objectives: To investigate the associations of prenatal air pollution with biomarkers indicative of autophagy, senescence and remodelling in newborns.

Methods: We included 449 healthy term newborns from the BILD birth cohort study. We measured 11 different proteins in the serum and plasma of cord blood. We assessed the association of whole pregnancy residential exposure to nitrogen dioxide (NO2) and particulate matter (PM10) with protein levels using multiple Tobit regression model. We performed unsupervised hierarchical clustering (based on protein concentration) and network construction of identified clusters.

Results: Adjusted models showed that NO2 exposure was associated with decreased expression of SIRT1 and IL-8 and increased Beclin-1 level.  Clustering of 11 proteins resulted in four clusters with different air pollution exposure levels, of which one cluster had low concentration of nine proteins, and one cluster showed increased pro-inflammatory response with high levels of IL-8 and IL-1b. Both these clusters had a low air pollution level.  Network analysis revealed distinct protein–protein correlation patterns among clusters.
 
Conclusions: Our finding in healthy term newborns showed that prenatal air pollution exposure is associated with the autophagy-related proteins. We identified four distinct clusters of subjects, suggesting a different response pattern to air pollution in newborns.