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Biological age & clocks
Research brief

Smoking, DNA methylation-based telomere shortening and epigenetic age in six immune cell types

In blood immune cells from 74 nonsmokers and 69 smokers, smoking was associated with greater methylation-based telomere shortening, epigenetic age acceleration and faster aging pace, with effects differing by cell type. [1]

Automatic summary · not editorially reviewed

The key findings

  1. The study compared 74 nonsmokers and 69 smokers using six major immune cell types isolated from whole blood of the same individuals. [1]

  2. Telomere shortening in all cell types was significantly associated with smoking status, with smokers showing greater shortening. [1]

  3. The smoking effect on epigenetic age acceleration correlated with AHRR cg05575921 demethylation, with myeloid cells showing the greatest and T cells the least effect. [1]

The source at a glance

Study type / format
Abstract of a comparative study of human blood immune cell types
Population / context
74 nonsmokers and 69 smokers providing whole blood samples.
Summary based on
Study abstract
Original publication
June 30, 2026

Smoking compared across six isolated immune cell types

The abstract describes a comparison of 74 nonsmokers and 69 smokers. Six major immune cell types were isolated from whole blood samples of the same individuals. The researchers compared smoking effects on methylation-based telomere length (DNAmTL) shortening, age acceleration from six DNA methylation age models, aging pace (DunedinPACE) and a stochastic epigenetic mitotic timer of cancer (stemTOC).

Supporting source [1]

Greater telomere shortening and age acceleration in smokers

Telomere shortening in all cell types was significantly associated with smoking status, with smokers showing greater shortening. CD8+ T cells had the greatest DNAmTL shortening and CD15+ granulocytes the least. Among the six age models, the strongest association with smoking was for GrimAge2, followed by FitAge and PhenoAge, with smokers showing greater age acceleration. The Hannum, Horvath and Skin_Blood models were generally not significantly associated with smoking in isolated cell types. DunedinPACE was significantly associated with smoking in all cell types and whole blood, with higher aging pace in smokers. stemTOC was not significantly associated with smoking in isolated cell types.

Supporting source [1]

Cell-type differences and abstract-only scope

The effect size of smoking on epigenetic age acceleration across cell types correlated with the smoking effect measured by mean AHRR cg05575921 demethylation, with myeloid cells showing the greatest effect and T cells the least. The authors conclude that smoking is associated with these methylation-based measures and that effects differ among cell types, suggesting shifts in cell composition may matter. These are associations, not proof of causation, and the abstract does not report follow-up duration or detailed adjustment. The full text was not reviewed.

Supporting source [1]

How to interpret this

Abstract only; the full text was not reviewed. The abstract reports associations, not causation, and does not give follow-up duration or detailed adjustment.

Based on the study abstract; the full paper, tables and supplementary data were not reviewed.

Source & supporting passages

Read the quoted passagesIn the language of the original source
  1. Finding 1 ↑

    74 nonsmokers and 69 smokers
  2. Finding 2 ↑

    Telomere shortening in all cell types was
  3. Finding 3 ↑

    myeloid cell types showing the greatest effect

AI-assisted summary with linked source passages. No independent editorial or clinical review.

Our editorial method

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