Scientists have discovered a new mechanism
through which very small pollutant particles in the air may trigger lung cancer
in people who have never smoked,
Particles linked to climate change also promote
cancerous changes in airway cells, they found, paving the way to new approaches
for lung cancer prevention and treatment.
Scientists of the Francis Crick Institute and
University College London, funded by Cancer Research UK, presented the data at
the ‘ESMO Congress 2022’.
According to them, the particles which are
typically found in vehicle exhaust and smoke from fossil fuels, are associated
with non-small cell lung cancer (NSCLC) risk, accounting for over 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,” they informed.
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,” said Charles Swanton from the Francis Crick Institute.
The new 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) 2.5 micrometres
(Im) in diameter was linked to increased risk of NSCLC with EGFR mutations.
In the laboratory
studies, scientists showed 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.
“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,” said
Swanton.
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.
“The next step is to
discover why some lung cells with mutations become cancerous when exposed to
pollutants while others don’t,” said Swanton.
Tony Mok from the
Chinese University of Hong Kong, who was not involved in the study, said that
the research is intriguing and exciting.
“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-1I inhibitors,” said Mok.
“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, so discussions are still very speculative,” he
added.