A team of scientists led by the Francis Crick Institute and the University College London has recently identified a mechanism through which very small pollutant particles in the air may trigger lung cancer in people who have never smoked. Such particles – typically found in vehicle exhaust and smoke from burning fossil fuels – appear to be associated with the risk of non-small cell lung cancer (NSCLC), accounting for over 250,000 deaths globally each year.
“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 study lead author Charles Swanton, the Francis Crick Institute and Cancer Research UK Chief Clinician.
“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.”
The scientists studied mutations in a gene called EGFR, which are found in approximately half of people with lung cancer who are non-smokers. In a study of over half a million participants from the UK, South Korea, and Taiwan, researchers found that exposure to increasing concentrations of airborne particulate matter (PM2.5) was associated to an increased risk of NSCLC with EGFR mutations.
Moreover, laboratory studies indicated that these pollutants also cause mutations in another gene linked to lung cancer called KRAS, and drive the influx of macrophages that release the inflammatory mediator interleukin-1β, which causes the expansion of cells with the EGFR mutations in response to exposure to PM2.5.
“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 ageing. In our research, these mutations alone only weakly potentiated cancer in laboratory models,” Dr. Swanton explained.
“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,” he concluded.