Scientists said on Saturday they had identified the mechanism by which air pollution triggers lung cancer in non-smokers, a discovery one expert hailed as “an important step for science – and for society”. The research illustrated the health risk posed by small particles. are created by the burning of fossil fuels, raising new calls for more urgent action to combat climate change. It could also pave the way for a new field of cancer prevention, according to Charles Swanton of the UK’s Francis Crick Institute.
Swanton presented the research, which has not yet been published in a peer-reviewed journal, at the annual conference of the European Society of Medical Oncology in Paris. Air pollution has long been thought to be linked to a higher risk of lung cancer in people who have never smoked. But we didn’t really know if pollution directly causes lung cancer – or how,” Swanton told AFP.
Traditionally, exposure to carcinogens, such as those in cigarette smoke or pollution, was thought to cause DNA mutations that then become cancer. But there was an “inconvenient truth” with that model, Swanton said: previous research had shown that DNA mutations can be present without causing cancer — and that most carcinogens in the environment don’t cause those mutations. A research team from the Francis Crick Institute and University College London analyzed the health data of more than 460,000 people in England, South Korea and Taiwan.
They found that exposure to small PM2.5 pollution particles – which are less than 2.5 microns in diameter – led to an increased risk of mutations in the EGFR gene. In laboratory studies on mice, the team showed that the particles caused changes in the EGFR gene as well as the KRAS gene, both of which have been linked to lung cancer. They ended up analyzing nearly 250 samples of human lung tissue that had never been exposed to carcinogens from smoking or heavy pollution.
Even though the lungs were healthy, they found DNA mutations in 18 percent of the EGFR genes and 33 percent of the KRAS genes. It’s just sitting there,” Swanton said, adding that mutations appear to increase with age. “They probably aren’t enough to drive cancer by themselves,” he said. But when a cell is exposed to pollution, it can trigger a “wound-healing response” that causes inflammation, Swanton said.
And if that cell “has a mutation, it creates cancer,” he added. We’ve provided a biological mechanism behind what was previously a mystery,” he said. In another experiment in mice, the researchers showed that the antibody could block a mediator — called interleukin 1 beta — that ignites inflammation and stops cancer. Swanton said he hopes the finding “it will provide a fertile ground for the future of what could be molecular cancer prevention, where we can offer people a pill, perhaps every day, to reduce the risk of cancer”.
Suzette Delaloge, who heads the cancer prevention program at France’s Gustave Roussy Institute, said the research was “quite revolutionary because we had practically no previous demonstration of this alternative way of cancer.” “This means we can ask whether, in the future, it will be possible to use lung scans to look for precancerous lesions in the lungs and try to reverse them with drugs such as interleukin 1 beta inhibitors,” he said. Other research links PM2.5 to 250,000 deaths on the lungs annually.the cancer itself.
You and I have a choice whether we smoke or not, but we don’t have a choice about the air we breathe,” said Swanton, who is also chief clinical officer at Cancer Research UK, which was the lead sponsor of the research. With probably five times more people exposed to unhealthy levels of pollution than tobacco, you can see that this is a pretty big global problem,” he added. We can only tackle this if we recognize the really close links between climate health and human health.”
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