Lung Cancer Linked to Air Pollution: Scientists Demonstrate How Vehicle Exhaust, Smoke May Trigger the Chronic Illness in ‘Never Smokers’

A late-breaking data recently showed that a new mechanism had been identified through which very tiny pollutant particles in the air may stimulate lung cancer in individuals who have never smoked, paving the way to new prevention strategies and developments of treatments.

According to a EurekAlert! report, the data were shared at the ESMO Congress 2022 by scientists from the Francis Crick Institute and University College London, funded by Cancer Research UK.

The particles, which are usually present in the vehicle exhaust and smoke from fossil fuels, are linked to non-small cell lung cancer or NSCLC risk, accounting for more than 250,000 lung cancer deaths worldwide every year.

The same particles in the air were deriving from the combustion of fossil fuels, exacerbating climate change, and are directly affecting human health through an essential and previously overlooked cancer-causing mechanism in lung cells.

The danger of Lung Cancer from Air Pollution

The danger of lung cancer from air pollution is lower than from smoking. Unfortunately, one doesn't have control over what he's breathing.

Globally, more people are exposed to unsafe air pollution levels compared to toxic chemicals in cigarette smoke. These new data link essentiality of addressing climate health to enhancing human health, according to Charles Swanton, the Francis Crick Institute and Cancer Research UK Chief Clinician, London, UK, who presented the study findings at the ESMO 2022 Presidential Symposium.

The new findings are based on human and laboratory research on mutations in genes known as EGFR, which are seen in roughly half of the people with lung cancer who have never smoked.

In laboratory studies, the Francis Crick Institute scientists revealed that the same pollutant particles known as PM2.5 promoted quick changes in airway cells, which had mutations in EGFR and in another gene associated with lung cancer known as KRAS, which drives them towards a cancer cell-like state.

EGFR Mutations

The study authors also discovered that air pollution is driving the influx of macrophages that release the interleukin-1β, the inflammatory mediator that drives the expansion of cells with the EGFR mutations in response to PM2.5 exposure interleukin-1β blockade inhibited lung cancer initiation.

A similar Medical Xpress report said that such findings were consistent with data from large clinical trials demonstrating a dose-dependent reduction in lung cancer occurrence when people were treated with the anti-IL1β antibody, canakinumab.

In the final series of experiments, the researchers used state-of-the-art, ultradeep mutational profiling of tiny samples of normal lung tissue and discovered EGFR and KRAS driver mutations in 18 percent and 33 percent of normal lung specimens, respectively.

The study investigators discovered that driver mutations in KRAS and EGFR genes, commonly found in lung cancers, actually exist in normal lung tissue and are likely consequences of aging.

EGFR Profiling

Tony Mok, from the Chinese University of Hong Kong, who was not part of the study, said the work is intriguing and exciting since it means that "we can ask if, in the future," it will be plausible to use lung scans in search for pre-cancerous lesions in the lungs and attempt to reverse them with medicines like interleukin-1β inhibitors.

It's unknown yet if it will be possible to use highly sensitive EGFR profiling on blood or other specimens to find non-smokers who are predisposed to lung cancer and may benefit from lung scanning. Thus, discussions remain quite speculative, a similar Euronews report specified.

The report about the new mechanism is shown on OncoInfoTV's YouTube video below:

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