The burning of coal, oil and petrol not only harms the climate – it also produces exhaust gases that increase the risk of lung cancer, even for non-smokers. Researchers are now finding out why this is so. And they discover a possible way to prevent this.
Scientists from Great Britain have presented an explanation as to why non-smokers also develop lung cancer. Researchers from the Francis Crick Institute and University College London used patient charts, animal studies and sample collection to explore how lung cancer is linked to air pollution from exhaust fumes from burning fossil fuels. They presented the results of their study, which has not yet been published in a specialist journal, at the annual meeting of the European Society for Medical Oncology in Paris.
Cancer researcher Charles Swanton from the Francis Crick Institute, who was involved in the study, told the AFP news agency that a connection between air pollution and an increased risk of lung cancer has long been suspected. “But we didn’t really know if pollution directly causes lung cancer – and if so, how.”
It has long been thought that exposure to carcinogens, such as those found in cigarette smoke or exhaust fumes, causes DNA mutations that lead to cancer. According to Swanton, this does not fit with the fact that research has shown that on the one hand DNA mutations can occur without causing cancer, and on the other hand that most carcinogenic substances in the environment do not cause mutations.
Swanton and his colleagues analyzed the files of more than 460,000 patients in England, South Korea and Taiwan. The analysis showed that people who are more exposed to air pollution with particulate matter of particle size PM2.5 have an increased risk of mutations in the EGFR gene, Swanton said.
In the laboratory, his research team showed in mice that the PM2.5 particles caused changes in the EGFR gene as well as in the KRAS gene, which in turn are both associated with lung cancer. Finally, the research team examined nearly 250 lung samples from people who had never been exposed to air pollution or tobacco smoke. Although their lungs were healthy, 18 percent of the samples had mutations in the EGFR gene and 33 percent had mutations in the KRAS gene.
“They just sit there,” Swanton said of genetic changes, which he says increase with age. “On their own, they probably aren’t enough to cause cancer.” However, if a cell is exposed to air pollution, for example, this can trigger “a wound healing reaction” with inflammatory processes, Swanton explained. If the affected cell is affected by a corresponding gene mutation, cancer develops.
Apart from the explanation for the development of lung cancer, Swanton and his colleagues also developed an approach to prevent lung cancer. In experiments with mice, they showed that the messenger substance interleukin 1 beta, which triggers the inflammatory process, can be stopped by an antibody.
This can prevent lung cancer from developing in advance, Swanton said. He hopes that on this basis “molecular cancer prevention” can be developed, for example in the form of a tablet that people can take daily as a precaution.
Cancer researcher Suzette Delaloge, who was not involved in the study, said the study was “a pretty important step for science – and for society, I hope.” It opens “a huge door both for knowledge and for new ways of preventing” cancer, Delalog said.
(This article was first published on Sunday, September 11, 2022.)