Fine particulate air pollution can increase the proliferation of pre-existing lung cancer-specific gene mutations, leading to further tumor development as suggested a study published in the journal Natural.

This has been verified in animal models by an international group of scientists after being carried out an epidemiological study where they have investigated the correlation between fine particulate matter (PM2.5) air pollution and certain types of lung cancer.

Increased exposure to pollution is associated with a higher incidence of lung cancer, and one of the main causes is particulate matter (PM), especially fine particulate matter 2.5 micrometers or less (PM2.5), which They can penetrate deep into the lungs. The interaction between environmental triggers and genetic mutations associated with lung cancer (such as mutations in the EGFR or KRAS genes, the two most frequently mutated genes in non-small cell lung cancer) is not well understood.

Charles Swanton, of the Francis Crick Institute in London and the paper’s corresponding author, and his colleagues investigated the relationship between exposure to these tiny PM2.5 particles and the frequency of lung cancer in 32,957 EGFR mutant lung cancer patients from four different countries (UK, Taiwan, South Korea, and Canada). The authors of the paper demonstrated that exposure to elevated PM2.5 levels was associated with an expected increased incidence of EGFR mutant lung cancer. Furthermore, data from 407,509 UK Biobank participants supports this association.

A cohort observation of 228 people with lung cancer from Canada found a higher frequency of lung cancer cases after three years of high exposure to the air pollutant PM2.5 (73%) than low exposure (40%), according to the study. An association among this Canadian cohort was not observed over a 20-year period, suggesting that three years of exposure to high levels of pollution may be sufficient for the emergence of this cancer.

To investigate the possible underlying cellular processes cancer development in relation to air pollution the scientists used a mouse model. They found that PM2.5 appeared to trigger immune cell influx and the release of interleukin-1 (a pro-inflammatory signaling molecule) in lung cells. It was also found to exacerbate inflammation and promote tumor development in the EGFR and KRAS cancer models. Interleukin-1 blockade during PM2.5 exposure was shown to prevent EGFR-driven cancer development. The authors also identified alveolar cell type II (AT2) as a possible cell that initiates lung tumors in the presence of PM2.5.

Overall, these results suggest that fine particulate air pollution, PM2.5, may act as a tumor promoter and further exacerbate existing cancer mutations.. Work on finding these links could pave the way for disease prevention, as well as provide a case for initiatives to address air quality as a public health priority.

Victor Briz, Ramón y Cajal researcher at the National Center for Environmental Health of the Carlos III Health Institute, has stated in a statement to SMC Spain that the significance and importance of this study “lies not only in the confirmation by reliable statistical data of the relationship between pollution and lung tumor development, but in that going a step further, by investigating and elucidating the mechanisms involved using animal models“. Using a genetically modified mouse model, he continued, “the authors conclusively demonstrated that air pollution particles trigger an inflammatory response in the lungsmediated by macrophages (immune system cells) and interleukin-1 (proinflammatory molecules), which are responsible for stimulating the proliferation of certain cells of the lung epithelium (cells with EGFR mutations to be precise)”.

In addition, Briz points out that in the work “they also show that This type of mutation accumulates naturally with age. and not the result of other environmental factors (such as tobacco or pollution itself) and, therefore, everyone is susceptible to it; Hence the importance of reducing the level of environmental pollution“.

Although the authors acknowledged minor methodological limitations in their study, such as the estimation of particle exposure by region (rather than individual exposure) or the use of previously unpurified alveolar tissue from different cell types in genetic analyses, these were minimal in comparison with provide a wealth of scientific evidence to support their conclusions.