Exposure to tobacco smoke in early life is associated with accelerated biological aging, study finds

Exposure to environmental factors during pregnancy and early childhood can significantly -- and sometimes irreversibly -- alter our metabolism and physiology, thereby determining our health status later in life. It can also accelerate the process of biological ageing, which has been associated with a higher risk of metabolic, cardiovascular or neurodegenerative diseases. At the cellular level, ageing is a continuous process that starts early in life, and which can be measured thanks to of epigenetic clocks. Epigenetic clocks use the levels of DNA methylation in certain regions of the genome to infer biological aging of a person.

"The epigenetic clock allows us to assess whether someone's biological age is older or younger than his or her chronological age," explains Mariona Bustamante, ISGlobal researcher and last author of the study. Several studies have shown an association between an acceleration in epigenetic ageing and certain environmental exposures, but most were performed in adults and focusing on single exposures. In this study, the team led by Bustamante investigated for the first time the association between the early-life exposome (83 prenatal exposures and 103 in early childhood) and the epigenetic age of 1,173 children between 6 and 11 years of age from the Human Early Life Exposome (HELIX) project, based on six birth cohorts in six European countries, including Spain, and coordinated by ISGlobal researcher Martine Vrijheid.

After selecting the best suited epigenetic clock for the study and adjusting for multiple factors, the research team found that exposure to maternal tobacco smoke during pregnancy was associated with an acceleration in epigenetic ageing. Regarding the postnatal exposome, the analysis showed association with two exposures: parental smoking and indoors levels of black carbon, an air pollutant which results from the incomplete combustion of fuels (and is indirectly measured by particulate matter absorbance or PM_abs).

Intriguingly, two other variables were associated with a slowing in biological ageing: the organic pesticide DMDTP and a persistent organic pollutant (polychlorinated biphenyl-138). "Further research is needed to explain these results, but the former could be due to a higher intake of fruits and vegetables while the latter could be explained by its correlation with body mass index," says Paula de Prado-Bert, first author of the study.

"The positive association between epigenetic age acceleration and exposure to tobacco smoke during pregnancy and early childhood go in line with previous results obtained in the adult population," says Bustamante. The epigenetic modifications could affect pathways involved in inflammation, toxin elimination, and cell cycle, with a subsequent impact on health.

Admittedly, these associations do not prove a causality, but this and future early life exposome studies will help guide health policies to reduce certain environmental exposures and promote a "healthy ageing" from early life stages.