Exposure to chemicals from burning fuels or organic matter accelerate markers of DNA aging

Aging is something that happens to everyone and is associated with a great number of disabilities and diseases including: cardiovascular disease, dementia, cancer, arthritis, and osteoporosis. You might consider aging to just be a part of life but there is very real evidence that changes within your cell are responsible for your aging. These can include a build up of mutations in your DNA, loss of the protective end caps on DNA (called telomeres), and changes to DNA marks called methylations which can alter the expression of genes. There has been a few studies in recent years that have shown that the pattern of methylation marks on parts a person’s DNA can be used to calculate a methylation age or epigenetic clock and this epigenetic clock can be compared to a person chronological age (their ‘real’ age) to determine how fast or slow someone is aging. The idea being that if someone’s epigenetic clock says they are older than their actual age then they are relatively older compared to someone who’s epigenetic clock is younger than their actual age. Studies have shown that the epigenetic clock can be used to predict mortality later in life. With this in mind, a team of researchers from China and Boston wanted to know how exposure to compounds created during burning of fossil fuels and organic matter might accelerate the aging of the epigenetic clock.

The team was interested in a class of compounds called polycyclic aromatic hydrocarbons (PAH’s) which are ring like structures that are formed by incomplete combustion of fuels (diesel) and organic matter (forest fires, incinerators). Using exposure data from 3 different cohorts, the team built and validated a model using information from Chinese and Caucasian populations. After validation of the model, the researchers looked for associations between 10 urinary PAH metabolites and accelerated aging of the epigenetic clock in a subset of the Chinese population (539 people in total). They found that total exposure to PAH and exposure to two specific metabolites (9-OH-Phenanthrene and 1-OH-Pyrene) was associated with a larger difference between chronological age and epigenetic age and a faster epigenetic aging rate. In other words, exposure to PAH’s was associated with faster aging in the cell and DNA. For every 1-unit increase in the two PAH species, there was approximately a 0.5 year increase in epigenetic age compared to chronological age and a 1.2% increase in epigenetic aging rate.

So what does this all mean? Epigenetic aging is still relatively poorly understood. We know that it is associated with mortality risk and we know that certain diseases (cancer, Alzheimer’s) and exposures (cigarette smoke) can change it. We don’t yet know how much of an increase in the epigenetic age could be problematic or how epigenetic aging might cause disease or overall aging. PAH’s have been investigated in the context of cancer, heart disease, and lung disease but there is still more work that is needed before we know the full impact of PAH’s on human health. This study intriguingly suggests that PAH may accelerate aging in people which may accelerate the onset of disease. More work is needed to understand how this process may be triggered. There are several limitations to this study that need to be addressed: 1) methylation age was measured in the blood of participants and we don’t have any data on how methylation may different between different organs. Exposure to PAH may accelerate the epigenetic clock in tissues that come in contact with PAH (blood, lungs, skin) but perhaps not in other tissues, 2) The results were primarily carried out in Chinese populations and we don’t know how they may differ in people of different ethnic backgrounds, 3) This was a cross-sectional study and so we do not know whether these epigenetic changes happen rapidly after PAH exposure or if exposure over time is needed, 4) Finally, we don’t know how genetics might alter the relationship between PAH exposure and epigenetic age. That is to say, there may be some people who are not able to clear the PAH from their body as readily leading to longer exposure and perhaps more epigenetic aging. In these people, epigenetic age would be higher for the same PAH exposure level. In conclusion, epigenetic changes as we age could play a large role in the onset of age related disease and exposure to environmental pollutants could alter the rate of aging making these diseases manifest earlier in life.


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