New publications
Study links early tobacco exposure to accelerated aging
Last reviewed: 02.07.2025
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
In a recent study published in the journal Science Advances, scientists examined the impact of early-life tobacco exposure on diseases associated with aging. They found that exposure to tobacco in the womb was associated with accelerated biological aging.
The study shows that reducing early life tobacco exposure is critical to improving healthy aging as it significantly influences biological aging 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 health systems. Recent reviews have emphasized the importance of quantifying biological age (BA) using various biomarkers to accurately predict health outcomes. Particular attention has been 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 aging using multiple biomarkers, including telomere length (TL) and composite algorithms of clinical parameters. Additionally, the combined effects of genetic predisposition and tobacco exposure on accelerating biological aging were investigated, which could provide insights for preventive and therapeutic interventions aimed at healthy aging. The study used data from the UK Biobank, a population-based cohort study that included 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 leukocytes 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 higher indices of body mass index (BMI) and Townsend Deprivation Index (TDI), as well as a higher prevalence of underlying medical conditions.
Further statistical analysis revealed consistent associations between early life tobacco exposure and accelerated biological aging.
Of particular note, subjects with in utero exposure showed significant increases in both KDM-BA and PhenoAge acceleration, along with a marked reduction 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, a clear dose-response relationship was observed with respect to age of smoking onset, with earlier onset being associated with greater acceleration of biological aging indices.
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 with never smokers.
Research into the combined effects of genetic predisposition and early life tobacco exposure highlights significant impacts on accelerated aging.
Those with elevated polygenic risk scores (PRS) and either prenatal exposure or early smoking initiation showed the most pronounced acceleration of biological aging indicators.
Stratified analyses further revealed subtle interactions between early life tobacco exposure and demographic or lifestyle factors.
For example, younger participants exposed in the womb showed increased acceleration of biological aging measures, while the effects were enhanced in those living in areas with high levels of deprivation.
This study examines how early tobacco exposure, including during fetal development, childhood and adolescence, is associated with higher rates of biological aging in adulthood.
In a large-scale analysis, prenatal tobacco exposure and age at smoking initiation were significantly associated with accelerated aging rates and shorter 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.