Scientists have long known that air pollution may be linked to an increased risk of lung cancer in people who have never smoked, but new research describes a mechanism that may help explain how.
The findings, presented Saturday at the Presidential Symposium of the European Society for Medical Oncology in Paris, suggest that air pollution may trigger lung cancer in people with no history of smoking, as certain air pollutant particles may promote changes in airway cells.
In particular, greater exposure to airborne particles or particulate pollution – 2.5 micrometers in diameter or less – can lead to rapid changes in airway cells that show mutations in a gene called EGFR, which are seen in about half of people with lung cancer who have ever smoked, and another lung cancer-related gene called KRAS, according to the research, led by scientists from the Francis Crick Institute of London and other institutions around the world.
“We have found that driver mutations in the EGFR and KRAS genes, which are commonly found in lung cancers, are in fact present in normal lung tissue and are likely a consequence of aging,” said scientist Charles Swanton. at the Francis Crick Institute and Chief Clinician at Cancer Research. UK, which presented the results, said in a press release on Saturday.
“In our research, these mutations alone only weakly potentiated cancer in laboratory models. However, when lung cells with these mutations were exposed to air pollutants, we saw more cancers and these grew faster than when lung cells with these mutations were not exposed to pollutants, suggesting that air pollution favors the initiation of lung cancer in the cells harboring the driver. genetic mutations,” Swanton said. “The next step is to find out why some lung cells with mutations become cancerous when exposed to pollutants while others do not.”
According to the US Environmental Protection Agency, particulate matter or particulate pollution in the air is a mixture of solid particles and liquid droplets. Some are emitted as dirt, dust, soot, or smoke, and they can come from coal and natural gas power plants, cars, agriculture, unpaved roads, and construction sites, among other places. sources.
The researchers analyzed data from 463,679 people to find associations between their exposure to air pollution and cancer risk.
Fine particles, with a diameter of 2.5 micrometers (PM 2.5) or less, are the smallest air pollutant and yet among the most dangerous. When inhaled, these pollutants can penetrate deep into lung tissue, where they can enter the bloodstream and contribute to asthma, cardiovascular disease and other respiratory illnesses.
As part of their analysis, the researchers found that increasing levels of air pollutants at PM 2.5 were associated with overall increases in the risk of EGFR-related non-small cell lung cancer in England, South Korea and Taiwan. Up to 33% of normal lung tissue samples in the study had EGFR and KRAS driver mutations, even in the absence of cancer.
“The first thing is that we look at epidemiological data on air pollution levels and lung cancer risk in non-smokers, finding a good correlation in England, South Korea and Taiwan,” Swanton said in a video posted by the European Society of Medicine. Oncology on Saturday.
“Second, we use animal models to show that by exposing mice to pollution – these mice are prone to EGFR or KRAS mutations – we see a dramatic increase in the number, size and grade of cancers in these mice after exposure to pollution,” he added. said.
The researchers looked at 247 samples of normal lung tissue, looking closely at tissue from humans and mice after exposures to air pollutants, and then studied the consequences of that exposure in mouse models.
“What we found is that exposure to air pollution in mice and humans drives an inflammatory axis,” which transforms cells, Swanton said in the video.
“And only if that stem cell has an EGFR mutation is a tumor initiated,” he said. “What we found through biopsy of normal lung tissue is that EGFR and KRAS mutations occur in normal lung tissue in over 50% of normal lung biopsies, and these occur with aging. .”
These mutations in the EGFR and KRAS genes “could very well be the reason why the non-smoking population ends up developing lung cancer. It’s a question we’ve been asking for a number of years: why is- Do otherwise healthy people unrelated to second-hand smoke or primary smoking still develop lung cancer?” Dr. Albert Rizzo, chief medical officer of the American Lung Association, told CNN on Monday.
“So we know that air pollution was listed as a carcinogen many years ago by the World Health Organization, and I think this study just adds further evidence that it is ‘a particular mechanism for these PM 2.5 particles leading to the development of lung cancer in this population,’ said Rizzo, who was not involved in the research.
“We really should make sure to limit exposure to PM as much as possible,” he added. “We don’t have much control over our genetics right now, but we can control air pollution.”
Research has shown that exposure to PM 2.5 air pollution may be associated with decreased lung function and an increased risk of cardiac arrest, among other health problems. A study, published in the Proceedings of the National Academy of Sciences in 2019, estimated that particles in the air were responsible for 107,000 premature deaths in the United States in 2011, costing society $886 billion.
“The same particles in the air that derive from the burning of fossil fuels, exacerbating climate change, directly impact human health via an important and previously overlooked carcinogenic mechanism in lung cells,” Swanton said in the press release.
“The risk of lung cancer from air pollution is lower than from smoking, but we have no control over what we all breathe,” he said. “Globally, more people are exposed to dangerous levels of air pollution than the toxic chemicals found in cigarette smoke, and this new data links the importance of addressing the climate health and improving human health.”
The new research suggests that, rather than causing mutations in cells that lead to cancer, airborne PM 2.5 pollutants may activate existing mutations, wrote Richard Smith, chairman of the UK Health Alliance on Climate Change, in an opinion piece in the medical journal BMJ. In Monday.
“This mechanism may be important in other cancers with carcinogens other than air pollution,” Smith wrote.
“The habitual invisibility of today’s air pollution must prevent us from giving it the attention it deserves, but the roots of medical neglect of air pollution must lie in the intertwined factors of the feeling that doctors can do nothing about air pollution and failures in the training of doctors,” he wrote.
“There are tips doctors can offer individuals – recognizing the importance of polluted air, reducing internal pollution at home, accessing local air pollution information, changing travel routes , avoid particularly toxic days and perhaps even help alleviate the problem drive less or not all of them – but the response needed is political action at local, national and global levels.
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