Researchers have discovered a new mechanism through which pollutant air particles may trigger lung cancer development in people who may never have smoked.
“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 from the Francis Crick Institute and the Cancer Research UK’s 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.”
It’s not new that the particles in our air can lead to health side effects, but this breakthrough research reveals how air pollution translates to lung cancer.
It’s something that makes the threat of climate change and fossil fuels immediate and urgent, as air pollution can be found anywhere in the world where there’s a densely populated road or suburb. It also makes the case for electrification and decarbonisation much, much stronger.
“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,” added Swanton.
The new findings were uncovered when analysing the gene EGFR, which has been observed in half of the people with lung cancer “who have never smoked”. Nearly half a million people were studied in Taiwan, South Korea and the UK. Exposure to increased levels of airborne particles was linked to the mutation of EGFR genes.
Pollutant particles “prompted rapid changes in airway cells which had mutations in EGFR and in another gene linked to lung cancer called KRAS”, which drove both genes to cancer development, according to the news release. It adds:
“They also found that air pollution drives the influx of macrophages which release the inflammatory mediator, interleukin-1β, driving the expansion of cells with the EGFR mutations in response to exposure to PM2.5, and that blockade of interleukin-1β inhibited lung cancer initiation. These findings were consistent with data from a previous large clinical trial showing a dose dependent reduction in lung cancer incidence when people were treated with the anti-IL1β antibody, canakinumab.”
Additionally, using high-quality mutation profiling equipment, the team identifies EDGR driver mutations in 18 per cent of normal lung samples. KRAS was found in 33 per cent of the samples. Swanton added that they were “likely a consequence of aging”. He elaborated:
“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 harbouring driver gene mutations.”
“We have known about the link between pollution and lung cancer for a long time, and we now have a possible explanation for it,” said Tony Mok from the Chinese University of Hong Kong.
“As consumption of fossil fuels goes hand in hand with pollution and carbon emissions, we have a strong mandate for tackling these issues – for both environmental and health reasons.”
Swanton added that the next step in the research is finding out why some lung cells with the genes mutate in response to pollution while others don’t.
These findings were presented in full at the ESMO Congress 2022.