An international team of scientists has made a breakthrough in identifying how air pollution causes lung cancer in people who have never smoked, a finding that could help medical experts prevent and treat tumors.
The researchers found that the fine particles in polluted air cause inflammation in the lungs, which activates dormant preexisting cancer genes. Previously, air pollution was believed to trigger genetic mutations that led to cancer.
The findings, based on research led by the Francis Crick Institute in London and funded by Cancer Research UK, were announced at the European Society of Medical Oncology Congress in Paris on Saturday.
As fewer people smoke, air pollution is showing itself more clearly as a cause of lung tumors.
It is estimated that 300,000 lung cancer deaths per year worldwide are caused by very fine pollutant particles with a diameter of less than 2.5 microns, known as PM2.5 (particulate matter), which are emitted by vehicle exhaust. and the burning of fossil fuels.
“Our study has fundamentally changed the way we view lung cancer in people who have never smoked,” said project leader Charles Swanton, professor of personalized cancer medicine at University College London.
“Cells with cancer-causing mutations naturally accumulate as we age, but are normally dormant. We’ve shown that air pollution wakes up these cells in the lungs, encouraging them to grow and potentially form tumors.”
The project is part of the UK’s £14m cancer research program to understand how lung cancer starts and progresses.
Scientists analyzed data on MP2.5 exposure and lung cancer in 400,000 people in the UK, Taiwan and South Korea, and performed laboratory experiments on mice, human cells and tissues.
Two important environmental carcinogens, tobacco smoke and ultraviolet light, damage DNA and create mutations that generate tumors. But the researchers found no evidence that the MP2,5 particles created mutations directly in DNA, which led them to look for a different explanation.
They found that the particles cause inflammation, which activates preexisting mutations in genes that promote the development of many lung cancers.
“The mechanism we’ve identified may help us find better ways to prevent and treat lung cancer in people who have never smoked,” 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.”
The findings could be applicable to other cancers associated with air pollution, including mesothelioma and throat and mouth tumors, said Emilia Lim, also a researcher at Crick.
“Ninety-nine percent of the world’s population live in areas that exceed the World Health Organization’s annual limits for PM2.5, highlighting the public health challenges posed by air pollution worldwide,” he added.
One way to counteract the harmful effect of air pollution may be to block a molecule called interleukin-1beta, which plays a key role in the inflammatory response to PM2,5. The team found that this approach worked in mice.
Tony Mok, a professor of medical oncology at the Chinese University of Hong Kong, who was not involved in the study, said the research results were “intriguing and encouraging.”
“That means we can ask whether, in the future, it will be possible to use CT scans to look for precancerous lesions in the lungs and try to reverse them with drugs,” he said.
He joined Swanton in emphasizing the importance of reducing air pollution to lower the risk of disease.
“We’ve known for a long time about the link between pollution and lung cancer, and now we have a possible explanation for it,” Mok said.
“As the consumption of fossil fuels goes hand in hand with pollution and carbon emissions, we have a strong incentive to address these issues for environmental and health reasons.”
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