Accelerated biological ageing is associated with exposure to tobacco smoke during pregnancy and early childhood, as well as with indoor exposure to black carbon. These are conclusions of analysis led by the Barcelona Institute for Global Health (ISGlobal), an institution supported by the “la Caixa” Foundation, the first to evaluate associations between a large number of early-life environmental exposure and epigenetic age in children.
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 epigenetic clocks. Epigenetic clocks use the level of DNA methylation in a certain region of the genome to infer the biological ageing 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 Marion’s Bustamante, ISGlobal researcher and last author of the study. Several studies have shown an association between acceleration in epigenetic ageing and certain environmental exposures, but most were performed in adults and focusing on signal exposure. In the study, the team led by Bustamante investigated for the first time the association between the early-life exposome ( 83 prenatal exposure and 103 in early childhood) and the epigenetic age of 1,173 children between 6 and 11 years of age from the Human Early Exposome (HELIX) project, based on six birth cohorts in six European countries, including Spain, and coordinated by ISGlobal researcher Martine Virjheid.
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After selecting the best suited epigenetic clock for 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 associated with two exposure: parental smoking and indoor levels of black carbon, an air pollutant that results from the incomplete combustion of fuel (and is indirectly measured by particulate matter absorbance or PMabs).
Intriguing, two other variables were associated with a slowing in biological ageing: the organic pesticide DMDTP and a president 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”, said Bustamante. The epigenetic modification could affect pathways involved in inflammation, toxin elimination, and cells cycle with a subsequent impact on health.
Admittedly, these associations do not prove 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.
By: Peace Chigozie
