According to the WHO, 92% of the world’s population breathes air that fails to meet the clean-air standards.
Usually, when we examine the effects of air pollution, we measure clinically obvious things – air flow, blood pressure, and heart rhythm. But the damage done by air pollution runs deeper than just experiencing difficulty in breathing–it can damage your DNA as well.
Let’s understand the impact of air pollution on our DNA.
Related article: How Caffeine Consumption is Hurting Your DNA
Key Topics:
What exactly is air pollution?
The presence of harmful substances in the air we breathe is Air pollution. Polluted air is a toxic cocktail of pollutants, with particulate matter (PM) being the most harmful, according to research.
Particulate matter refers to extremely small solid particles and liquid droplets that are found in the air around us. They can be made up of a variety of components, like nitrates, sulphates, dust particles, and allergens such as pollen. They are ejected into the air from motor vehicles, wood and crop burning, and factories.
Other pollutants include black carbon (BC), ozone (O3), nitrogen oxides (NOx), heavy metals, and polyaromatic hydrocarbons (PAHs). These compounds interact with substances and make the air polluted.
These pollutants altogether can be very harmful because they not only just irritate our lungs; they can also travel into our bloodstream, triggering oxidative stress, DNA strand breaks, and harmful epigenetic changes.
We now understand how these pollutants reach deeper in our cells, interact with our DNA, alter our genes and lead to mutations and conditions like cancer, and long-term health problems.
Let’s look at what science has to say about how daily exposure to polluted air is altering our DNA.
Air pollution and our DNA:
According to the review published in Clinical Epigenetics, exposure to polluted air can change DNA methylation (DNAm).
Normally, methylation helps in maintaining the cellular balance, but when harmful particles from traffic fumes, fine particulate matter (PM2.5), and industrial emissions enter our body, they disrupt this system.
Studies show that these air pollutants often cause a drop in the process of DNA methylation across the genome, resulting in hypomethylation, which can make DNA more unstable and prone to improper gene activation.
In some cases, it can also lead to hypermethylation, silencing genes that protect against inflammation or cancer.
These changes at the genetic level can result in long-term health risks like chronic lung disease, cardiovascular problems and even developmental issues if they happen during pregnancy or childhood.
As we already know, polluted air is not just one thing; it is a mixture of some of the most harmful components like gases, metals, and tiny particles, each having its own way of damaging our DNA.
Let me break down five of the major pollutants found in air pollution.
Particulate matter:
As we already discussed what particulate matter is, let us now look at how it affects our DNA and ultimately our health.
Particulate matter smaller than 2.5 µM (PM2.5) is so small that it doesn’t just stay in our lungs; it slips into the bloodstream.
Research published in the Journal of Toxicology shows that exposure to PM2.5 directly leads to DNA strand breaks. This damage can trigger mutagenesis (gene mutations) and even cancer development.
PM2.5, once they are inside these particles, can lead to the generation of reactive oxygen species (unstable molecules that attack DNA, proteins, and lipids). This results in oxidative DNA damage.
PM2.5 doesn’t just cause DNA damage–it also interferes with the body’s DNA repair machinery. The exposure to PM2.5 disrupts the function of genes that are normally responsible for fixing the broken DNA strands, such genes are OGG1, MTH1, and XRCC1.
This means that the cell will accumulate more and more mutations over time due to this disrupted repair mechanism. In some cases, PM2.5 can also trigger inflammatory responses, which adds another layer of stress, making the damage even harder for cells to cope with.
Nitrogen dioxide:
Nitrogen dioxide is formed by emissions from motor vehicles, industries, and gas stoves. High concentrations of the gas can be found near busy roads and indoors when using gas for cooking.
Nitrogen dioxide is a proven genotoxic agent. In an in vivo study published in the journal Chemosphere, where rats inhaled Nitrogen dioxide at concentrations commonly found in cities, researchers observed DNA damage in multiple organs–including lungs, brain, kidney, spleen, and heart.
In a dose-dependent manner, the damage was observed as DNA strand breaks and DNA-protein crosslinks, along with increased micronuclei formation in bone marrow cells.
Another study published in the Journal of Toxicology Letters demonstrated that when nasal epithelial cells from human patients were exposed to low concentrations of nitrogen dioxide, about 0.1ppm, which matches the levels we breathe in polluted urban air;
Scientists found DNA fragmentation in cells after just 30 minutes of exposure, and after 3 hours, cells showed micronucleus formation, which is a marker of genetic instability and damage. And importantly, it was observed that there was no cell death, meaning that the cells were still alive, carrying the altered DNA.
Ozone:
Ozone is an important constituent of ambient air pollution and represents a major public health concern. Oxidative injury due to ozone inhalation causes the generation of reactive oxygen species and can be genotoxic.
A 2017 study published in the journal PLOS on human airway cells and fibroblasts revealed that even 120 ppb of tropospheric ozone causes a significant rise in DNA strand breaks and micronuclei, both of which are markers of mutagenic DNA damage.
The researchers observed that the damage was notably stronger in the lung epithelial cells than in fibroblasts. This highlights how the ozone can be a potential harm to the respiratory cell DNA, directly.
Benzene & PAHs (polycyclic aromatic hydrocarbons):
PAHs are formed when fuels burn during traffic, in factories or while grilling and are well-known carcinogens. These chemicals bind to DNA and form PAH-DNA adducts.
DNA adducts are kind of like molecular sticky notes that twist the DNA structure and block correct reading or replication. Over time, this can result in harmful mutations.
Studies have continuously found PAH-DNA adducts in the blood and tissue samples of people who smoke or people who are regularly exposed to polluted urban air. These adducts result in increased risk of cancer, including breast and lung cancer.
Similarly, benzene is another common pollutant from traffic fumes and industrial emissions. Benzene does not bind to DNA directly, but benzene dioxide, which is a metabolite of benzene, does.
Studies show this metabolite can form harmful DNA adducts like 7-phenylguanine, and can also contribute to chromosome breaks in bone marrow and blood cells.
Workers like fuel attendants who are chronically exposed to benzene had measurable DNA strand breaks and their ability to repair damaged DNA was also reduced.
Heavy metals:
Heavy metals such as lead, arsenic, cadmium, nickel, and mercury, via industrial emissions, waste burning, and contaminated soil dust, find their way into the air, thereby polluting it.
Exposure to these heavy metals, which are commonly found in the environment, is a significant public health concern due to their link to adverse birth outcomes.
According to a review published in the journal Environmental International, exposure to heavy metals results in DNA methylation, causing hypermethylation and hypomethylation. Over time, this imbalance destabilises the genome, weakens the DNA repair mechanism, thus increasing the likelihood of genetic mutations and chronic diseases.
Heavy metals can also disrupt the proteins that wrap around the DNA-histone proteins. This can result in silencing the critical defence genes or switching on harmful genes.
In addition, they alter the activity of microRNAs; together, these epigenetic imbalances can create a dangerous environment in cells and eventually harm the DNA.
Read more: 7 Daily Tech Habits That Might Be Hurting Your DNA and How to Avoid Them.
Wrapping up:
Air pollution is no longer just an environmental threat; now, it has become a genetic one. We saw how polluted air can enter our cells and create havoc inside.
What makes this is its invisibility. We used to think that air pollution was just about facing difficulty in breathing due to smog or coughing due to the fumes, but we now know how these pollutants can damage our DNA and alter our genes.
Every breath of polluted air carries the potential to leave scars on our genome. The danger is silent, but it can be everlasting.
Resources:
- Ewa, Błaszczyk, and Mielżyńska-Švach Danuta. “Polycyclic Aromatic Hydrocarbons and PAH-Related DNA Adducts.” Journal of Applied Genetics, vol. 58, no. 3, 12 Dec. 2016, pp. 321–330, https://doi.org/10.1007/s13353-016-0380-3.
- Han, Ming, et al. “Nitrogen Dioxide Inhalation Induces Genotoxicity in Rats.” Chemosphere, vol. 90, no. 11, 1 Mar. 2013, pp. 2737–2742, https://doi.org/10.1016/j.chemosphere.2012.11.057.
- Kim, Nicholas, et al. “Epigenetic Toxicity of Heavy Metals − Implications for Embryonic Stem Cells.” Environment International, vol. 193, 18 Oct. 2024, p. 109084, www.sciencedirect.com/science/article/pii/S0160412024006706.
- Koehler, C., et al. “Ex Vivo Toxicity of Nitrogen Dioxide in Human Nasal Epithelium at the WHO Defined 1-h Limit Value.” Toxicology Letters, vol. 207, no. 1, 12 Aug. 2011, pp. 89–95, https://doi.org/10.1016/j.toxlet.2011.08.004.
- Liu, Jiayu, et al. “Fine Particulate Matter Exposure Induces DNA Damage by Downregulating Rad51 Expression in Human Bronchial Epithelial Beas-2B Cells in Vitro.” Toxicology, vol. 444, 1 Nov. 2020, pp. 152581–152581, https://doi.org/10.1016/j.tox.2020.152581.
- Poma, Anna, et al. “Effects of Ozone Exposure on Human Epithelial Adenocarcinoma and Normal Fibroblasts Cells.” PLOS ONE, vol. 12, no. 9, 8 Sept. 2017, p. e0184519, https://doi.org/10.1371/journal.pone.0184519.
- Rider, Christopher F., and Chris Carlsten. “Air Pollution and DNA Methylation: Effects of Exposure in Humans.” Clinical Epigenetics, vol. 11, no. 1, 3 Sept. 2019, https://doi.org/10.1186/s13148-019-0713-2.