Why air pollution can trigger lung cancer in people who have never smoked

British scientists have discovered a new biological mechanism that, due to air pollution, can cause lung cancer even in people who have never smoked in their lives. Pollutant microparticles can induce mutations in specific genes (EGFR and KRAS), which in turn trigger cancer.

Researchers from the Francis Crick Institute and University College London (UCL), led by Dr Charles Swanton, who made the announcement at the European Society of Medical Oncology (ESMO Congress 2022), hope their discovery will open up the pave the way for new approaches to the prevention and treatment of lung cancer especially among non-smokers.

The “culprit” microscopic PM 2.5 particles (25 millionths of a meter in diameter), commonly found in vehicle exhausts and smoke from burning fossil fuels, are mainly associated with non-small cell lung cancer (NSCLC), the which is responsible for more than 250,000 deaths worldwide each year.

“The same particles in the air that come from burning fossil fuels and contribute to climate change have a direct impact on human health through an important but previously overlooked mechanism of causing cancer in lung cells. The risk of lung cancer from air pollution air pollution is less than smoking, but we have no control over what we all breathe in. Globally, more people are exposed to unsafe levels of air pollution than to toxic chemicals in cigarette smoke,” said Swanton.

The new findings are based on laboratory and human research, particularly on the EGFR gene, which is present in about half of people with lung cancer who have never smoked. Analysis of data from almost half a million people in England, South Korea and Taiwan shows that exposure to elevated concentrations of PM2.5 particles in the air is associated with an increased risk of mutations in the gene in question and – for that reason – of NSCLC cancer.

Laboratory research has shown that the same particulate pollutants also cause mutations in a gene (KRAS) associated with lung cancer. It was also found that air pollution prompts an increase in macrophage cells that release the substance interleukin-1β, which in turn facilitates the expansion of cells with mutations in the EGFR gene.

The researchers found that mutations in the EGFR and KRAS genes are actually present in normal lung tissue, possibly due to aging. When lung cells with these pre-existing mutations are exposed to air pollution, the likelihood of cancer increases at a faster rate than if the cells in question had not been exposed to the pollutants.

“The next step,” according to Swanton, “is to find out why some lung cells with mutations become cancerous when exposed to the pollutants, while others do not.”

Dr Tony Mok of the Chinese University of Hong Kong said: “The new research is interesting because it means we can ask whether in the future it will be possible to use lung scans to find pre-cancerous changes in the lungs and then try reverse them with drugs such as interleukin-1β inhibitors.At present, we do not know whether it will be possible to use the EGFR gene ‘profile’ in blood or other samples to identify those non-smokers who are predisposed to lung cancer”.

In any case, the scientists pointed out the importance of reducing air pollution in order to reduce the risk of lung diseases, including cancer. As Swanton said, “We’ve known for a long time about the link between pollution and lung cancer, but now we have a possible explanation for it. As fossil fuel consumption goes hand in hand with pollution and emissions coal, we have every reason to address these issues, both for environmental and health reasons.”

RES-EMP

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