Could ageing lung cells increase lung cancer risk?
A new study in Nature Medicine suggests that the lungs can carry their own “biological age”, separate from a person’s actual age, and that lungs which age faster at the cell level are linked to a higher risk of lung cancer. The signal holds on top of smoking history, not just because of it.
The work comes from a team at Stanford Medicine, led by Daisy Yi Ding with senior author Tony Wyss-Coray, and is open access. It draws on blood samples from more than 60,000 people across three large studies, with health records followed for around 15 years.
Key points
Researchers measured over 7,000 proteins in blood samples from 60,542 people across three cohorts (the UK Biobank, the Global Neurodegeneration Proteomics Consortium and the British 1946 birth cohort) and built molecular “clocks” to estimate the biological age of more than 40 cell types.
Ageing does not move at one speed through the whole body. Cell types age at different rates, even within the same person, and around one in four people showed faster ageing in at least one cell type.
For the lungs, faster ageing of two cell types, respiratory epithelial cells and alveolar type 2 cells, was linked to higher lung cancer risk.
The link was additive to smoking. Current smokers whose lung cells had also aged faster carried the highest risk of all, around 58 per cent higher than current smoking alone, while people who had never smoked carried the lowest.
This is observational research and a research tool only. It is not a test you can ask for yet.
What the researchers did
Most of us think of age as a single number. This study works from a different idea: that different cell types in the body age at different rates, and that some of this can be read from a blood sample.
The team measured the levels of thousands of proteins circulating in the blood, then used machine learning to estimate a biological age for each of more than 40 cell types, spanning nerve, immune, glial, hormone-producing, epithelial and musculoskeletal origins. They tested the approach across three separate groups of people and two different laboratory platforms, then looked at whether faster or slower ageing of particular cell types lined up with disease and survival over the following years.
The headline across the whole study is broad. Faster ageing of specific cell types was associated with higher disease risk and earlier death, while slower ageing of others was linked to better protection and longer survival. The strongest threads run through the brain and through overall mortality, with lung cancer as one clear example among several.
What it showed for the lungs
When the researchers looked specifically at lung cancer, two cell types stood out: the respiratory epithelial lineage and alveolar type 2 cells. People whose lung cells had aged faster than expected were at higher risk, and this added information beyond smoking status.
The numbers give a sense of the scale. Current smokers whose lung cells had aged faster in both types carried the highest risk, around 58 per cent higher than current smoking on its own. People who had never smoked sat at the bottom. Importantly, the lung-cell ageing signal held up even after the researchers accounted for age, sex, smoking status and how much someone had smoked over their lifetime.
There is a plausible biological thread here too. Alveolar type 2 cells act as the lung’s repair cells, and they are thought to be the cells from which the most common form of lung cancer can arise. A worn-down capacity to repair lung tissue may help create the conditions in which cancer can take hold.
In plain terms, two people with the same smoking history may carry different levels of risk depending on how their lung cells are ageing.
Cells age at different speeds, even inside one person
One of the wider findings is that ageing is uneven. Between a fifth and a quarter of people showed faster ageing in a single cell type, and a smaller group showed it across ten or more cell types at once. The more cell types that had aged faster, the worse a person’s survival over the 15 years, in a clear step-by-step pattern.
The same study found striking links elsewhere in the body. Faster ageing of brain support cells called astrocytes was strongly associated with Alzheimer’s disease risk, and faster ageing of muscle cells with motor neurone disease. On the other side, people with youthful immune and brain cell signatures tended to live longer. The lung cancer finding sits within this larger picture rather than standing alone.
What this does and does not mean
It is worth being precise about what the study shows.
It is observational. It points to associations between cell ageing and disease risk across large populations. It does not prove that fast-ageing lung cells cause lung cancer, and it does not tell an individual whether they will develop it.
The people studied were mostly older and mostly of white European background, which the authors flag as a limitation. The findings will need testing in younger and more diverse groups before they can be relied on more widely.
It is not available as a test. The researchers describe the tool as research-only for now. The senior author has also co-founded companies working to commercialise related technology, which is worth keeping in view when reading the coverage.
Why this is one to watch
For people affected by lung cancer, the value here is not a new test or treatment. It is the direction of travel.
For years, lung cancer risk has been framed almost entirely around smoking. Work like this adds to a growing body of evidence that biology varies between people in ways smoking history does not capture, which speaks to a question many people living with lung cancer already ask: why me, when others with the same history stayed well. It also strengthens the longer-term case for better, earlier ways to identify who is most at risk, including the large group of people who develop lung cancer having never smoked.
We will follow how this research develops, and what it could mean for earlier detection and fairer access to it across Europe.
Frequently asked questions
Does cell ageing cause lung cancer?
No. The study is observational, so it can show a strong link but not cause and effect. It found that faster-ageing lung cells were associated with higher lung cancer risk, independent of smoking, but it cannot prove the cells cause the cancer.
What is the “biological age” of a cell?
It is an estimate, based on proteins measured in the blood, of how old a cell type appears to be compared with a person’s actual age. The study found that some cell types can look biologically older or younger than the person they belong to.
Does this only apply to people who smoke?
No. Faster-ageing lung cells were linked to higher risk across smoking groups. The risk was highest in current smokers whose lung cells had also aged faster, and lowest in people who had never smoked, but the lung-cell signal added information beyond smoking history.
Is this a test I can have?
Not yet. The researchers describe the tool as research-only for now, with any consumer version likely some years away.
Sources
Research article (open access): Ding, D. Y. et al. “Plasma proteomic signatures of cellular aging predict human disease.” Nature Medicine (2026). https://www.nature.com/articles/s41591-026-04446-y
Research briefing: “Blood signatures of cell type-specific aging forecast disease risk and resilience.” Nature Medicine (2026). https://www.nature.com/articles/s41591-026-04447-x