That exposure to air pollution is not good for health is not a big news. Neither is the fact that, in particular, pollutants in the air are correlated with a greater risk of the onset of various types of cancer, first of all lung cancer. Less clear, however, are the how and why of the phenomenon: and it is precisely this that a team of scientists from the Frances Crick Institute in London, in the United Kingdom, and other research institutes have dealt with, who in an article just published in the magazine Nature it has, in fact, investigated the mechanisms that link environmental factors and genetic mutations to better understand the nature of this correlation and try to propose countermeasures.
The fine powders
According to estimates by the World Health Organization, the increase in cases of lung cancer linked to the continuous release of pollutants into the atmosphere, and the consequent greater exposure to these poisons, causes a total of approximately 250,000 deaths a year. The best solution, clearly, would be to stop polluting; but it is also the most difficult solution to achieve, at least in the short term. To be more involved in the phenomenon are the notorious PM2.5, the smallest fine particles (with a diameter of less than two and a half microns) which, precisely by virtue of their size, easily penetrate the airways and reach the innermost layers of the alveoli lungs, from where they then pass into the blood and then reach all body tissues.
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I study
To understand the effects of exposure to PM2.5, the authors of the work just published analyzed the frequency of the onset of lung cancer in approximately 33,000 people (residents in England, Taiwan, South Korea and Canada) who carry the EGFR mutation , a genetic anomaly known to be associated with the onset of the disease, and cross-referenced this information with that relating to exposure to fine dust. In this way it emerged that, effectively, exposure to PM2.5 increases the risk of the onset of lung cancer for subjects carrying the mutation; moreover, a further even more in-depth analysis, conducted by sequencing the mutations of 228 Canadian people, revealed a significant increase in the frequency of the disease in the subgroup most exposed to PM2.5. And, even more worryingly, this increase in frequency has emerged in just three years of observations, which suggests that the effect of pollutants is quite fast.
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The signal that triggers the development of the tumor
To understand the cellular processes underlying the phenomenon, the researchers studied mouse models and discovered that PM2.5 triggers a huge influx of immune system cells into the lungs and the consequent release of interleukin 1-β, a molecule linked to the inflammatory: this seems to be the phenomenon that “wakes up” the EGFR mutation and triggers the development of cancer. So much so that in a subset of mice treated with an antibody that blocks the production of interleukin 1-β, the onset of lung cancer linked to exposure to PM2.5 decreased again. “Clearly,” concluded Allan Balmein of the Family Comprehensive Cancer Center at the University of California, San Francisco, who was not directly involved in the study and author of a commentary piece to the article, “it is not possible to think of preventing, or reducing, the air pollution by giving millions of people a very expensive anti-interleukin treatment.However, thanks to this discovery we could try to implement more realistic prevention measures, for example by introducing or increasing in the diet foods that contain anti-inflammatory substances. -oxidants and/or anti-inflammatory effects”.
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