Air pollution may trigger lung cancer in non-smokers, discover scientists

Researchers have found a new way that exposure to air pollution’s microscopic particles can cause lung cancer in people who have never smoked.

They discovered that particles associated with climate change promote cancerous changes in airway cells, opening up new avenues for preventing and treating lung cancer.

The research was presented at the “ESMO Congress 2022” by scientists from the Francis Crick Institute and University College London, with support from Cancer Research UK.

It is estimated that over 250,000 people die annually from lung cancer due to exposure to the particles typically found in vehicle exhaust and smoke from fossil fuels.

When they informed the public that “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,” they were correct.

“But we have no control over what we all breathe,” despite the fact that exposure to air pollution poses a lower risk of lung cancer than smoking does.

These new data link the importance of addressing climate health to improving human health, according to Charles Swanton of the Francis Crick Institute. “Globally, more people are exposed to unsafe levels of air pollution than to toxic chemicals in cigarette smoke,” he said.

Approximately half of the people with lung cancer who have never smoked have mutations in a gene called EGFR, which is the basis for the new findings based on human and laboratory research.

An increased risk of NSCLC with EGFR mutations was found in a study of nearly half a million people from England, South Korea, and Taiwan who were exposed to increasing concentrations of airborne particulate matter (PM) 2.5 micrometres (I’m) in diameter.

Researchers demonstrated in the lab that exposure to the same pollutant particles (PM2.5) accelerated the transition to a cancer stem cell-like state in airway cells with mutations in EGFR and another gene linked to lung cancer called KRAS.

“We found that driver mutations in EGFR and KRAS genes, commonly found in lung cancers, are actually present in normal lung tissue and are likely the result of ageing,” said Swanton.

However, “we saw more cancers and these occurred more quickly than when lung cells with these mutations were not exposed to pollutants,” indicating that air pollution promotes the initiation of lung cancer in cells harbouring driver gene mutations.

The next step, according to Swanton, is to figure out why some mutated lung cells become cancerous when exposed to pollutants while others do not.

The research is intriguing and exciting, according to Tony Mok of the Chinese University of Hong Kong, who was not involved in the study.

The discovery “means that we can ask whether 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-1I inhibitors,” Mok said.

Discussions are still very hypothetical, he added, because “we don’t yet know whether it will be possible to use highly sensitive EGFR profiling on blood or other samples to find non-smokers who are predisposed to lung cancer and may benefit from lung scanning.”