Being exposed to high levels of air pollution increases the risk of lung cancer. This is not new, however, a new study carried out by members of the Francis Crick Institute and University College London (United Kingdom) has gone further, and has discovered the mechanism by which pollution causes lung cancer in non-smokers.
As explained at the 2022 European Society for Medical Oncology (ESMO) congress, very small polluting particles called PM2.5 generated by the burning of fossil fuels, for example, in car exhaust pipes, increased the risk of mutations in the EGFR gene and in the KRAS gene, which promoted the development of non-small cell lung cancer.
According to the researchers, these polluting particles are responsible for more than 250,000 deaths a year as a result of lung cancer in the world. Although not yet published, the research has analyzed the health of more than 460,000 people from South Korea, England and Taiwan.
In addition, the work studied the effects of exposure to PM2.5 in mice and analyzed almost 250 samples of human lung tissue that had never been exposed to carcinogenic substances, such as tobacco or strong pollution.
Pollution causes mutations in the EGFR and KRAS genes
The results showed that people exposed to pollution particles had more mutations in the EGFR gene. In addition, tests in mice corroborated this change in genes, and changes in the KRAS gene were also observed, both of which are associated with the development of lung cancer. In the tissue sample, DNA mutations were found in 18% of the EGFR genes and 33% of the KRAS genes.
People exposed to pollution particles had more mutations in the EGFR gene and changes in the KRAS gene, both associated with the development of lung cancer
“We found that driver mutations in the EGFR and KRAS genes, which are commonly found in lung cancers, are actually present in normal lung tissue and are likely a consequence of aging. In our research, these mutations alone only weakly potentiated cancer in laboratory models”, explains Charles Swanton, lead author of the study.
In addition, he adds that “however, when lung cells with these mutations were exposed to air pollutants, we saw more cancers and they appeared more quickly than when lung cells with these mutations were not exposed to pollutants, which suggests that the Air pollution promotes the initiation of lung cancer in cells that carry driver mutations. The next step is to discover why some lung cells with mutations become cancerous when exposed to contaminants and others do not,” Swanton said.
They also found that air pollution promoted the influx of macrophages that release the inflammatory mediator interleukin-1β, driving the expansion of cells with EGFR mutations in response to PM2.5 exposure, and that blockade of interleukin-1β 1β inhibits the initiation of lung cancer.
All these results indicate the importance of taking measures to reduce air pollution, which is found at very high levels, especially in large cities. In addition, the researchers believe that interleukin-1β inhibitor drugs could help reverse precancerous lesions in the lungs. More studies need to be done in this regard to draw more precise conclusions.
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