Lung cancer has long been associated with smoking, or exposure to concentrations of dangerous toxic substances such as asbestos. But new research adds to a growing body of work that suggests trace pollutants can cause lung cancer in individuals who have never smoked and have lived apart from industrial sources of airborne carcinogens, such as factory smokestacks.
Scientists at the Francis Crick Institute and University College London estimate that a quarter million people die annually as a result of small toxic particles that are commonly found in and around population centers, and often far beyond.
They also linked this risk to the issue of climate change. “The same particles in the air that derive from the combustion of fossil fuels, exacerbating climate change, are directly impacting human health via an important and previously overlooked cancer-causing mechanism in lung cells,” said Charles Swanton of the Francis Crick Institute.
“The risk of lung cancer from air pollution is lower than from smoking, but we have no control over what we all breathe. Globally, more people are exposed to unsafe levels of air pollution than to toxic chemicals in cigarette smoke, and these new data link the importance of addressing climate health to improving human health.”
These trace particles trigger mutations in the EGFR gene, which is a typical cause of lung cancer in non-smokers. The researchers reviewed data from large populations in Taiwan, South Korea and England and discovered that “the same pollutant particles (PM2.5) promoted rapid changes in airway cells which had mutations in EGFR and in another gene linked to lung cancer called KRAS, driving them towards a cancer stem cell like state.”
The presence of these mutations did not always indicate cancer, however. When a person breathes in small particulate matter, small inflammations occur that can awaken the mutated cells in the body.
Swanton reported: “We found that driver mutations in EGFR and KRAS genes, commonly found in lung cancers, are actually present in normal lung tissue and are a likely consequence of aging. 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 occurred more quickly than when lung cells with these mutations were not exposed to pollutants, suggesting that air pollution promotes the initiation of lung cancer in cells harboring driver gene mutations. The next step is to discover why some lung cells with mutations become cancerous when exposed to pollutants while others don’t.
“Everyone develops mutations, it’s just part of the aging process,” he added. “But our research shows that you need a second step in the process: an inflammatory reaction which activates the mutated cells. … We’ve provided a biological mechanism behind what was previously an enigma.”
Research on Trace Pollutants Unlocks Lung Cancer Enigma
