Prenatal exposure to environmental air pollution and psychosocial stress jointly contribute to the epigenetic regulation of the serotonin transporter gene in newborns

Antenatal exposures to maternal stress and to particulate matter with an aerodynamic diameter of less than 2.5 μm (PM2.5) have been independently associated with developmental outcomes in early infancy and beyond. Knowledge about their joint impact, biological mechanisms of their effects and timing-effects, is still limited. Both PM2.5 and maternal stress exposure during pregnancy might result in altered patterns of DNA methylation in specific stress-related genes, such as the serotonin transporter gene (SLC6A4 DNAm), that might, in turn, influence infant development across several domains, including bio-behavioral, cognitive and socioemotional domains. Here, we investigated the independent and interactive influence of variations in antenatal exposures to maternal pandemic-related stress (PRS) and PM2.5 on SLC6A4 DNAm levels in newborns. Mother–infant dyads (N = 307) were enrolled at delivery during the COVID-19 pandemic. Infants’ methylation status was assessed in 13 CpG sites within the SLC6A4 gene’s region (chr17:28562750–28562958) in buccal cells at birth and women retrospectively report on PRS. PM2.5 exposure throughout the entire gestation and at each gestational trimester was estimated using a spatiotemporal model based on residential address. Understanding the interplay between environmental and individual-level stressors has important implications for the improvement of mother-infant health during and after the pandemic.

NAZZARI Sarah;  CAGLIERO Lucia;  GRUMI Serena;  PISONI Enrico;  MALLUCCI Giulia;  BERGAMASCHI Roberto;  MACCARINI Julia;  GIORDA Roberto;  PROVENZI Livio; 

2024-02-08

SPRINGERNATURE

JRC132769

1359-4184 (online),   

https://www.nature.com/articles/s41380-023-02206-9,    https://publications.jrc.ec.europa.eu/repository/handle/JRC132769,   

10.1038/s41380-023-02206-9 (online),