Air pollution could lead to an explosion in lung cancer cases

The deleterious effects of air pollution range from insignificant (but still bad) to very relevant (and very, very bad). been linked to lung inflammation, strokes and death. The link between air pollution and cancer is particularly worrying: the European Environment Agency estimated last year that more than 10% of cancers on the continent are caused by exposure to pollution.

But for years, the specific way in which air pollution causes cancer has been the subject of debate. Traditionally, researchers believed that environmental factors associated with cancer directly cause a person’s DNA to break and repair in an error-prone way, which could plant the seeds for a malignant tumor cell. This theory has been proven for UV and other forms of radiation, for example, but for the fine particle air pollution known as PM 2.5, the science is not so clear cut. PM 2.5 are tiny droplets in the air – smaller than a grain of sand, a human hair, dust and pollen particles – which can be a mixture of metals, organic compounds and hundreds different chemicals. They form as a result of pollution emitted by vehicles, power plants, fires and smokestacks, and people inhale unhealthy levels of them every year.

In a new study by researchers in the UK, the relationship between PM 2.5 and a type of lung cancer found in non-smokers and light smokers has taken center stage. The team looked at nearly 33,000 cases of this lung cancer in the UK, Canada, South Korea and Taiwan; and genetically modified mice that developed lung cancer when exposed to PM 2.5. Based on these experiments, they were able to confirm the existence of a second pathway that causes cancer: widespread lung inflammation, resulting from air pollution. Their results were published on April 5 in Nature.

This new theory is based on the notion that mutations that can lead to lung cancer may already exist in a small number of a person’s cells, having arisen on their own due to a random change. Pollutants like PM 2.5 then alter the environment of the lungs to facilitate the proliferation and growth of these cells into a tumor in their own right.

“The idea is that exposures to carcinogens could promote cancer without doing anything for DNA,” said Serena Nik-Zainal, a medical geneticist at the University of Cambridge who was not involved in the study. . Nature News. “Not all carcinogens are mutagens.”

In a multi-institutional study to identify the causes of cancer called the TRACERx study, researchers focused on lung cancer with a mutation in the EGFR gene, which is involved in cell growth and survival. They first mapped EGFR lung cancer cases to a country’s PM 2.5 pollution levels, finding that high levels of the particles were linked to an increase in cases associated with the mutation.

But then they took it a step further by genetically modifying mice to have a mutated human EGFR gene that would lead to lung cancer. The researchers exposed 31 of these mice to two different levels of fine particles and measured cancer development seven weeks later.

Mice exposed to low and high concentrations of particles developed more lung damage than mice that were not exposed to air pollution. Mice exposed to the highest pollution levels also had larger clusters of mutated EGFR cells in their lungs.

Importantly, the mice exposed to the particles had no more mutations in their tumors than the control mice, suggesting that the pollution was not causing their DNA to change. Instead, the researchers found an increased number of immune cells called macrophages in the lungs of mice exposed to air pollution. These immune cells release an inflammation-causing protein, and researchers strongly suspect that the resulting inflammation is what fuels the growth of pre-existing mutated EGFR cells.

Allan Balmain, a cancer geneticist at the University of California, San Francisco, wrote in an accompanying commentary that the research was a “multidisciplinary analytical and technical tour de force that helps show how pollution interacts with lung cells to promote changes that ultimately result in malignancy.”

“These results have major implications for how we think about cancer prevention,” he added, since the researchers showed that mice treated with an antibody targeting the inflammatory protein prevented the formation of lung tumors, even when ‘they were exposed to air pollution.

In the short term, cancer researchers can focus on identifying foods or drugs that can protect against dangerous inflammation caused by harmful air pollution. However, to truly address this crisis for humanity, and not just the individuals who can access these therapies, we need widespread change as soon as possible. The best, and only, long-term solution is to stop emitting air pollution.

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