The atmospheric pollution can cause lung cancer by promoting the cell inflammation that have mutated for other reasons, according to research published in ‘Nature’ that also describes the mechanisms involved. The novelty of this study is that it focuses on this inflammation reaction, something that could be addressed with a anti-inflammatory appropriate. This supposes a paradigm shift, by emphasizing the role of inflammation over that of genetic mutations. Furthermore, this model would explain majority of lung cancer cases in non-smokers.
Those responsible for this study are researchers from the Francis Crick Institute of London, who have made a epidemiological study with data from 32,957 individuals to determine the correlation between fine particles of air pollution and lung cancer, and have used mouse models to find out the cellular processes they could be behind.
Air pollution is a cocktail of many toxic components and the term PM (abbreviations in English of ‘particulate matter’) is used to describe a mixture small solid and liquid particles found in the air.
these particles they are divided into categories according to their size and the especially fine (such as PM2.5 and PM0.1) are the most worrisome as for the detrimental health effects.
He increased exposure to pollution is associated with a increased incidence of lung cancer and one of the main causes are precisely those fine particles 2.5 micrometers or less (PM2.5), which They can penetrate deep into the lung.
The interaction between the environmental triggers and the genetic mutations associated with this cancer (such as those of the EGFR or KRAS genes, two of the genes with the most frequent mutations in non-small cell lung cancer -that is, non-small cell-) is not well known.
Investigation
Led by Charles Swanton, the team investigated the relationship between exposure to PM2.5 and the frequency of lung cancer in 32,957 individuals with a EGFR gene mutation from four countries (England, Taiwan, South Korea and Canada). This type also occurs in non-smoking patients.
The authors report that exposure to increasing levels of PM2.5 is associated with a increasing estimated incidence of EGFR-mutant lung cancer.
For example, observations of a cohort of 228 non-smokers with lung cancer from Canada found a higher frequency of cases after three years of high exposure to atmospheric pollutants PM2.5 (73%) compared to a low exposure (40%).
The study suggests that three years of exposure to high levels of pollution They may be enough for this cancer to arise, sums up the magazine.
cellular processes
The researchers used mouse models to investigate the cellular processes that they could underlie cancer progression in relation to air pollution.
Among others, they discovered that PM2.5 appears trigger an influx of immune cells and the interleukin 1 beta release (a proinflammatory signaling molecule) in lung cells. It was observed that this increased inflammation and favored tumor progression in EGFR and KRAS cancer models. Furthermore, it was shown that the blocking of that interleukin during exposure to PM2.5 prevented EGFR-driven cancer development.
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“Taken together, these results suggest that PM2.5 could act as tumor promoters and further aggravate the existing cancer mutations,” describes Nature.
Understanding this relationship can open pathways to prevention and provide an argument for initiatives for address air quality like a public health priority.
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