A one-year-old child receives a blood stem cell transplant from a 30-year-old donor. Seventeen years later, the child is a young adult. A blood test, however, tells a different story. The DNA of his blood cells reads 47 years old.

The cells never adjusted to their new body. They kept counting from the donor’s age.

This case comes from research on leukemia survivors, and it shows something most of us never consider. Your cells carry a clock of their own. That clock can run faster or slower than your birthday suggests. Scientists call this epigenetic aging, and they can now measure it with a blood sample.

The bigger news is what speeds the clock up. In 2025, a Stanford team reviewed 102 studies covering more than 180,000 people. Air pollution and cigarette smoke pushed biological age upward in about four out of five studies.

As a doctor who has worked with stem cells for years, I find this research practical. It turns “aging” into something we can measure, and partly influence. Here is what the evidence shows.

What epigenetic aging is and how scientists measure it

Your DNA sequence stays almost the same from birth to old age. What changes is the way cells read it. Small chemical tags called methyl groups attach to specific spots on the DNA. This process is DNA methylation. The tags do not change your genetic code. They work like sticky notes that tell the cell which genes to use and which to ignore.

Identical twins show how much these notes matter. In 2005, Mario Fraga and colleagues reported in PNAS that twins start life with nearly identical methylation patterns. In older twin pairs, the patterns had drifted apart, more so in twins who had lived different lives.

With age, the pattern of these tags shifts in a predictable way. Some spots gain methyl groups. Others lose them. Read enough of these spots together, and you can estimate a person’s age from DNA alone.

In 2013, Steve Horvath at UCLA published the first clock that works across many tissues (Horvath, Genome Biology 2013). It uses 353 spots on the DNA called CpG sites. The clock works in blood, liver, brain, and other tissues. Its estimates matched real age with a correlation above 0.90, which is very high for a biological test.

Since then, researchers have built three generations of clocks:

1. First-generation clocks, such as Horvath and Hannum, estimate chronological age. When a person’s DNA age is higher than their real age, we call it epigenetic age acceleration.
2. Second-generation clocks, such as PhenoAge and GrimAge, add health markers from blood tests. They predict disease and death better than age alone. GrimAge even includes a DNA-based estimate of smoking history.
3. Third-generation clocks, such as DunedinPACE, measure the speed of aging. A value of 1.0 means one biological year per calendar year. A value of 1.2 means your body ages about 20% faster.

This matters because the gap between DNA age and real age carries information. People whose DNA age runs ahead of their calendar age face higher risks of age-related disease and death. That link has appeared across many cohorts, and it explains why these clocks now appear in clinical research.

The clocks are also for sale. Several companies offer epigenetic age tests directly to consumers. I will return to what those results can and cannot tell you. For now, the key idea is simple. Biological age is a number that can move, and the next sections show what moves it.

For the everyday habits linked to this number, see our article on how lifestyle choices affect your biological age.

Air pollution, smoke and chemicals: what the 2025 review found

The largest summary of this evidence came in 2025. Raj Fadadu, Anne Bozack and Andres Cardenas at Stanford published it in Environmental Research (Fadadu et al., 2025). They analyzed 102 studies with epigenetic data from more than 180,000 people. Most studies had a low risk of bias.

The results were not uniform, and that is useful information in itself:

• Cigarette smoke: 53 of 66 studies (80%) linked it to faster epigenetic aging.
• Air pollution: 15 of 19 studies (79%) found the same link.
• Synthetic and workplace chemicals: 5 of 8 studies (63%) showed acceleration.
• Metals: only 7 of 13 studies (54%) found acceleration, so the picture here is mixed.

Smoking surprised nobody. The air pollution result deserves more attention, because you cannot quit the air you breathe.

Fine particles called PM2.5 are the main concern. They are about 30 times thinner than a human hair and reach deep into the lungs. A study of adults aged 60 to 69 in China compared seven markers of biological age. PM2.5 exposure pushed several of them upward and also raised blood pressure.

The Lothian Birth Cohort 1936 in Scotland added a time dimension. Researchers followed 525 people and collected 1,782 blood samples between ages 70 and 80. They matched each person’s address history with yearly air pollution data. Exposure in young and middle adulthood was linked to older Horvath age decades later. Men with higher exposure in midlife also had shorter telomeres, the protective caps at the ends of chromosomes.

That finding changes how I think about prevention. The air you breathed at 35 may still show up in your blood at 75.

Consider a bus driver in a large city and a farmer in the hills. Their genes may be similar. Their daily dose of PM2.5 is not, and the Lothian data suggest the difference adds up over decades.

Workplace data point the same way. Factory workers exposed to benzene showed faster aging on two clocks, Hannum and Skin-Blood. Workers exposed to trichloroethylene, a solvent used in degreasing, also looked biologically older. This held even at levels below 10 parts per million.

For more on urban air and health, read our article on air quality in cities.

Heavy metals: a mixed picture with clear signals

Metals are complicated, because the body needs some of them and is harmed by others. Sudipta Dutta, Douglas Ruden and colleagues reviewed this evidence in Genes (Dutta et al., Genes 2024). Three studies show the pattern well.

The first looked at iron. A large genetic study examined four blood markers of iron status, including ferritin, the protein that stores iron. Higher ferritin and higher transferrin saturation raised all four measures of biological age tested. More iron was not better. This matters for people who take iron supplements without a proven deficiency. Iron is essential, but extra iron brings no bonus. Check ferritin with your doctor before you start.

The second came from American Indian communities in the United States. Researchers measured six metals in the body and five epigenetic clocks. Non-essential metals, meaning tungsten, arsenic, and cadmium, were linked to faster aging on GrimAge and DunedinPACE. Essential metals, meaning selenium, zinc, and molybdenum, were linked to slower aging.

The cadmium signal. In that study, cadmium showed the strongest link. Each step up in cadmium level (one standard deviation) matched about 1.23 extra years on the GrimAge clock. For most people, cigarette smoke is a main source of cadmium. Some foods grown in contaminated soil add more.

The third study followed 290 adults in Detroit, a post-industrial city with a long pollution history. Their average age was 51. Lead was linked to faster GrimAge aging. Mercury was linked to faster PhenoAge aging. Manganese, on the other hand, went with slower PhenoAge aging. Copper followed a U-shaped curve, so both too little and too much went with older biological age.

What should you take from this? A practical example helps. A 55-year-old smoker who lives near an old industrial site carries several of these exposures at once. The metals add up, and the Detroit data showed that the total mixture pushed two clocks upward.

The mixed 54% result from the Stanford review also teaches caution. Metal studies vary in design, sample size, and the clocks they use. For now, the clearest message concerns cadmium and lead, where the signal repeats across studies.

Stress, trauma and pregnancy: when the mind ages the cells

Epigenetic clocks respond to more than chemicals. Psychological stress leaves a mark too, and the studies here are some of the most striking in the field.

Young military veterans with a median age of 32 showed a clear pattern. The more severe their lifetime PTSD, the older their DNA looked on the Hannum clock. A second study followed 179 veterans of Iraq and Afghanistan over time. PTSD and alcohol-use disorders were both linked to faster biological aging across the follow-up.

The largest analysis came from the Psychiatric Genomics Consortium for PTSD. It included more than 2,000 participants from diverse backgrounds. Both childhood trauma and lifetime PTSD severity were linked to faster epigenetic aging.

The study I find most encouraging involved 40 paramedicine students in Australia. Over 12 months, all of them faced work-related trauma. They saw patient deaths, suicide scenes, and aggressive patients. Distress and PTSD symptoms went together with older biological age. Students who had joined a psychological support group at the start showed a different result. Their GrimAge acceleration was significantly lower, both at baseline and after the traumatic exposures.

This is a small study, and it needs repeating. Still, it suggests something concrete. Support given before trauma may protect the body at a molecular level.

Why would stress change DNA tags at all? Chronic stress keeps cortisol, the main stress hormone, high for long periods. In 2015, Anthony Zannas and colleagues reported in Genome Biology that cumulative life stress was linked to faster epigenetic aging. Many of the affected DNA sites respond directly to cortisol signals. Stress hormones, in other words, can write on the same sticky notes that the clocks read.

I see a practical version of this in orthopedics. Patients who come to me after a serious car accident often carry two injuries. We treat the fracture with great care. The psychological injury too often goes untreated. These data give one more reason to treat both.

Pregnancy adds a second generation to the story. One study followed 89 mothers and their newborns. Researchers measured the mothers’ biological age in the third trimester with three clocks. Some mothers had more stressful life events, PTSD symptoms, and difficulty regulating emotions. They showed faster GrimAge and PhenoAge shortly after birth. Their babies showed the opposite shift. Infants of mothers with more PTSD symptoms had a lower epigenetic gestational age, which suggests slower development.

The Drakenstein Child Health Study in South Africa looked at 271 mother-child pairs. It assessed trauma, PTSD, depression, alcohol, and tobacco use during pregnancy. Maternal PTSD was linked to a lower epigenetic gestational age at birth. The link held even after the researchers accounted for other factors.

Think about what this means in daily life. A pregnant woman living through violence or loss is not only suffering emotionally. Her stress may shape how her baby’s cells develop. That makes mental health care in pregnancy a medical priority, and not a luxury.

For the physical side of this connection, see our article on depression and chronic disease.

What transplants, oxygen and cancer reveal about the clock

Some of the most surprising findings come from the laboratory and from transplant medicine. Masaki Matsuyama, Arne Søraas and colleagues summarized them in Experimental Biology and Medicine in 2020.

Each tissue keeps its own time

Go back to the transplant story from the start of this article. Researchers studied leukemia survivors whose donors were more than 10 years older or younger than them. Up to 17 years after transplant, the new blood cells kept the donor’s biological age. The body around them did not reset the clock.

This tells us that blood cells carry their own aging program. Other tissues may do the same, each running at its own pace.

A second finding caught my attention as a regenerative medicine physician. Some donors received G-CSF, a drug that pushes stem cells from the bone marrow into the blood before collection. Blood produced from those cells looked about five years younger than the donor. Cells taken directly from the bone marrow, without G-CSF, showed no such effect. We do not yet know why, and it deserves more study.

Too much oxygen speeds aging

Oxygen keeps us alive, but it has a cost. Skin cells called fibroblasts aged faster in standard lab incubators, which hold 21% oxygen. Cells grown at 1% oxygen aged about 40% more slowly, even though they divided more times.

Inside the body, most tissues live with far less oxygen than the air. The brain, liver, and kidneys sit at about 2% to 3%. The bone marrow niche, where blood stem cells live, sits at 1% to 2%. A protein called HIF1α senses oxygen levels and influences the enzymes that add or remove methyl groups. Low oxygen may be one way the body protects its stem cells from rapid aging. This concerns the environment inside tissues, not the air you breathe. Devices sold as “hypoxia therapy” for anti-aging have no human evidence behind them.

Cancer breaks the clock

Cancer cells show DNA ages that make no sense. Breast cancer cells from one 51-year-old woman read 138 years in one cell line and 11 years in another. In leukemia patients, unusual shifts in the DNA age of normal blood cells predicted relapse months before standard tests. Epigenetic disruption may begin before cancer becomes visible.

What can slow the clock

Research on reversing epigenetic age is still early. Three approaches stand out:

• Rapamycin, a drug that acts on cell metabolism, slowed DNA methylation aging in cultured cells.
• Calorie restriction kept DNA methylation patterns younger in mice.
• Partial reprogramming, a brief exposure to the factors used to make stem cells, rejuvenated old muscle stem cells without turning them into stem cells. Our article on cellular reprogramming explains how this works.

None of these is a ready treatment for people. The practical steps today come from the exposure data. Stopping smoking removes the single exposure with the most consistent evidence. Two more steps target factors from the studies. Reduce your time in heavy traffic, and use a HEPA filter at home on high-pollution days. After a trauma, ask for psychological help early.

A word on consumer tests. An epigenetic age result can motivate change, and that has value. Individual results still vary between clocks and between labs, though. I would not base medical decisions on a single commercial test.

What your biological age can and cannot tell you

Biological age is not destiny. It is a measurement, and measurements can change.

The Stanford review of 102 studies gives the clearest map so far. Cigarette smoke and air pollution accelerate epigenetic aging in about 80% of studies. Workplace chemicals follow close behind. Metals show a mixed picture, with cadmium and lead as the clearest warning signs. Trauma and chronic stress leave measurable marks, even in the next generation.

The transplant data remind us that cells keep their own time. The oxygen data show that the environment inside the body matters as much as the one outside. The Australian paramedic study adds a hopeful detail. Support given early may slow the clock.

If you want to act on this research now, start with the exposures that have the strongest evidence. Quit smoking, and limit your time in polluted air. Take psychological stress as seriously as blood pressure. For a broader view of why we age, our article on aging theories is a good next read.

The child from the transplant story carries blood that is decades older than he is. Most of us will never face that situation. Still, the air we breathe and the stress we carry keep adjusting our own clocks every year.

References

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3. Horvath S. DNA methylation age of human tissues and cell types. Genome Biol. 2013;14(10):R115.
4. Breaking new ground on human health and well-being with epigenetic clocks: a systematic review and meta-analysis of epigenetic age acceleration associations. Ageing Res Rev. 2024;102:102552.
5. Ryan J, Wrigglesworth J, Loong J, Fransquet PD, Woods RL. A systematic review and meta-analysis of environmental, lifestyle, and health factors associated with DNA methylation age. J Gerontol A Biol Sci Med Sci. 2020;75(3):481-94.
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