Lung cells become cancerous when exposed to airborne pollutants

September 15, 2022
Lung cells become cancerous when exposed to airborne pollutants

A new mechanism has been identified through which very small pollutant particles in the air may trigger lung cancer development in people who have never smoked, according to the ESMO Congress 2022 reports from the European Society for Medical Oncology (ESMO). Pollutant particles are typically found in vehicle exhaust and smoke from fossil fuels, and have been associated with non-small cell lung cancer (NSCLC) risk – accounting for as much as 250,000 lung cancer deaths globally per 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 Charles Swanton, the Francis Crick Institute in London, UK.

“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 findings are based on human and laboratory research on mutations in a gene called EGFR which are seen in about half of people with lung cancer who have never smoked.

In a study of nearly half a million people living in England, South Korea, and Taiwan, exposure to increasing concentrations of airborne particulate matter (PM) of 2.5 micrometres (μm) in diameter was linked to increased risk of NSCLC with EGFR mutations.

In the laboratory studies, the Crick Institute scientists showed that the 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.

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.

Commenting on the results, Tony Mok, from the Chinese University of Hong Kong, said: “This research is intriguing and exciting as it means that we can ask whether, in the future, it will be possible to use lung scans to look for pre-cancerous lesions in the lungs and try to reverse them with medicines such as interleukin-1βinhibitors.”

Like Swanton, he stresses the importance of reducing air pollution to lower the risk of lung diseases, including cancer.

“We have known about the link between pollution and lung cancer for a long time, and we now have a possible explanation for it. 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,” Mok concluded.

The late-breaking data is likely to introduce new approaches to lung cancer prevention and treatment.

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Category: Features, Health alert, Uncategorized

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