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Living in Polluted Air for Three Years Raises Your Risk of Lung Cancer, Warns Study!


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New data from a comprehensive study show that exposure to high concentrations of fine particles in the air can increase the risk of developing lung cancer in as little as three years.

The study also provides new insight into the progression of the disease.

Contaminated haze seems to be especially harmful to healthy lung tissue, which has genetic changes that put it at risk of becoming cancerous.

A study of nearly 33,000 people with lung cancer found that elevated levels of micropollutants were associated with an increased risk of EGFR-induced lung cancer, which primarily affects non-smokers or people who smoke lightly.

Charles Swanton, a cancer researcher at the Francis Crick Institute in the UK, says: “Cells with cancer-causing mutations naturally accumulate with age, but are usually inactive. We have shown that air pollution awakens these cells in the lungs, stimulating them to proliferate and may have been tumors.”

The researchers say these results confirm that air pollution is a major cause of lung cancer and highlight the need for action to reduce pollution and protect public health.

Particulate matter (PM) contributes to air pollution, affecting almost every place on earth and causing 8 million deaths each year. Fine particles less than 2.5 micrometers (PM2.5) can penetrate deep into the lungs and are associated with many health problems such as heart disease and lung cancer.

“Traditionally, carcinogens are thought to cause tumors by causing direct DNA damage,” the study authors wrote in their published paper.

The new data supports the 76-year-old idea, as Swanton tweeted, “that cancer starts with two steps: acquisition of a driver gene (initiation) and then a second step where a cancer risk factor acts on these latent cells to cause disease.” .”

Mouse models have also shown that exposure to air pollution induces changes in lung cells that can lead to cancer, with PM2.5 particles appearing to enhance the second step of this process.

To better understand how air pollution causes cancer, Swanton and an international team of researchers conducted a three-part analysis.

Using environmental and epidemiological datasets of 32,957 people from England, Taiwan, and South Korea, they examined PM2.5 levels associated with EGFR-mutated lung cancer, which is caused by a mutation in the EGFR gene.

According to the results, the incidence of EGFR-mutated lung cancer increases with exposure to PM2.5. Additional data from 407,509 UK biobank members supports this association.

A smaller dataset of 228 non-smokers in Canada showed that after three years of exposure to high levels of PM2.5 air pollution, the risk of EGFR-induced lung cancer increased from 40% to 73%. This association was not found among the same Canadian group 20 years later.

Taken together, these data, together with published data, suggest that there is an association between the incidence of EGFR-induced lung cancer and PM2.5 exposure levels, and that 3 years of air pollution exposure may be sufficient for this association to occur.

The team also used an induced mutation in EGFR in mouse models to study cellular processes that may be responsible for cancer growth due to air pollution. They found that PM2.5 induces an influx of immune cells and the release of interleukin-1 (an inflammation-causing signaling molecule) into lung cells.

In addition, blocking interleukin-1 during PM2.5 exposure has been shown to stop the development of EGFR-induced cancer.

These data confirm that PM2.5 can induce tumor growth and exacerbate existing cancer mutations. The researchers also found that lung cells, called alveolar type II (AT2) cells, were more likely to develop lung cancer when PM2.5 was present.

Finally, tests done on healthy lung tissue from 295 people showed that a large percentage of them had genetic mutations that can lead to cancer, meaning that exposure to high levels of PM2.5 could put their health at greater risk.

“Overall, 54 of 295 (18%) non-cancerous lung tissue samples contained an EGFR driver mutation,” write Swanton et al.

The researchers acknowledge that their work has some limitations. For example, mouse models of tumor-prone cancer, even without PM2.5, may not show the full range of mutations found in healthy adult tissues. But they give scientists the opportunity to study early tumor growth in a controlled environment.

Co-author and cancer cell biologist William Hill of the Francis Crick Institute concluded: “Finding ways to prevent or reduce inflammation caused by air pollution will go a long way in reducing the risk of lung cancer in people who have never smoked, as well as reducing exposure to people In general, air pollution is an urgent problem.

The peer-reviewed study was published in the journal Nature.

Source: Science Alert

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