Accelerated Biological Aging Associated With Exposure To Tobacco Smoke In Early Life: Study

BARCELONA, Spain — A new study has found that exposure to tobacco smoke in early life is associated with accelerated biological aging.

The findings of the study titled, “The early-life exposome and epigenetic age acceleration in children,” were published in the journal “Environment International.”

Accelerated biological aging is associated with exposure to tobacco smoke during pregnancy and early childhood and indoor exposure to black carbon.

These are the conclusions of an 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 exposures 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 aging, which has been associated with a higher risk of metabolic, cardiovascular, or neurodegenerative diseases.

At the cellular level, aging is a continuous process that starts early in life and can be measured thanks to epigenetic clocks. Epigenetic clocks use the levels of Deoxyribonucleic acid (DNA) methylation in certain regions of the genome to infer the 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,” explained Mariona Bustamante, ISGlobal researcher and last author of the study.

Several studies have shown an association between acceleration in epigenetic aging 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 aging.

Regarding the postnatal exposome, the analysis showed association with two exposures: parental smoking and indoors levels of black carbon, an air pollutant that results from the incomplete combustion of fuels (and is indirectly measured by particulate matter absorbance or PMabs).

Intriguingly, two other variables were associated with a slowing in biological aging: the organic pesticide Dimethyldithiophosphate (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,” said 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 modifications could affect pathways involved in inflammation, toxin elimination, and cell cycle, with a subsequent impact on health.

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

(With inputs from ANI)

Edited by Ojaswin Kathuria and Nikita Nikhil



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