Study Links Early Life Tobacco Exposure to Accelerated Aging

In a recent study published in the journal Science Advances, researchers investigated the impact of early-life tobacco exposure on age-related diseases. They found that exposure to tobacco in the womb was associated with accelerated biological ageing.

The study shows that reducing early-life tobacco exposure is critical to improving healthy ageing as it significantly affects biological ageing and interacts with various factors such as age, gender, and diet.

Biological ageing is a complex process characterized by the accumulation of cellular changes that gradually deteriorate the integrity of tissues and organs. This leads to increased vulnerability to disease and mortality, and places a significant financial burden on healthcare systems. Recent reviews have highlighted the importance of quantifying biological age (BA) using various biomarkers to accurately predict health outcomes. Particular attention was paid to early life environmental exposures, especially tobacco exposure, as a significant risk factor for adverse health outcomes in adulthood.

The study examined the association between early life tobacco exposure and adult biological ageing using multiple biomarkers, including telomere length (TL) and composite algorithms of clinical parameters. In addition, the joint effects of genetic predisposition and tobacco exposure on accelerating biological ageing were investigated, which could provide insights for preventive and therapeutic interventions targeting healthy ageing. The study used data from the UK Biobank, a population-based cohort study of nearly half a million participants aged 37 to 73 years, enrolled between 2006 and 2010. After exclusions, 276,259 participants were included in the study. Early life tobacco exposure, including prenatal exposure and age at smoking initiation, was assessed using self-administered questionnaires. BA was determined using the Klemera-Doubal Biological Age (KDM-BA) and phenotypic age (PhenoAge) algorithms validated with NHANES data.

TL length in white blood cells was measured using quantitative polymerase chain reaction. Polygenic risk scores (PRS) were constructed using genetic variants associated with aging phenotypes and TL.

Baseline comparisons of participants showed that those with prenatal exposure tended to be somewhat younger, mostly male, and more likely to drink alcohol. They also had elevated markers such as body mass index (BMI) and Townsend deprivation index (TDI), as well as a higher prevalence of major medical conditions.

Further statistical analysis revealed consistent associations between early life tobacco exposure and accelerated biological aging.

Notably, in subjects with prenatal exposure, significant increases in both KDM-BA and PhenoAge acceleration were observed, along with marked reductions in telomere length (TL). Specifically, in utero exposure was associated with a 0.26 year increase in KDM-BA acceleration, a 0.49 year increase in PhenoAge acceleration, and a 5.34% decrease in TL.

In addition, there was a clear dose-response relationship with respect to age at smoking initiation, with earlier initiation correlating with greater acceleration in indices of biological aging.

For example, childhood tobacco exposure was associated with a 0.88-year increase in KDM-BA acceleration, a 2.51-year increase in PhenoAge acceleration, and a 10.53% decrease in TL compared to never smokers. p>

Research on the combined effects of genetic predisposition and early-life tobacco exposure highlights significant effects on accelerated aging.

Those with elevated polygenic risk scores (PRS) and either prenatal exposure or early smoking initiation showed the most pronounced acceleration in measures of biological aging.

Stratified analyzes further revealed subtle interactions between early life tobacco exposure and demographic or lifestyle factors.

For example, younger participants exposed in utero showed increased acceleration in measures of biological aging, while the effects were magnified in those living in areas of high deprivation.

This study examines how early life exposure to tobacco, including during fetal development, childhood, and adolescence, is associated with higher rates of biological aging in adulthood.

In a large analysis, prenatal tobacco exposure and age at smoking initiation were significantly correlated with accelerated rates of aging and shortened telomere length.

The results of this study highlight the multifaceted interactions between early life tobacco exposure, genetic predisposition, and environmental factors that shape the trajectory of biological aging.