Lung cancer is the leading cause of cancer death worldwide. In fact, it is estimated that this disease, characterized by its difficult detection in early stages and whose symptoms become palpable in advanced stages, is responsible for approximately 1.8 million deaths each year globally.
Among the main causes of lung cancer is smoking, exposure to smoke from smokers or occupational exposure to carcinogenic substances such as asbestos. Also, as it seems logical to think, air pollution has always been associated with a higher incidence of lung cancer, however, until now the mechanisms by which this pollution could interact with lung cells were unknown by scientists.
Now, however, a team of researchers from the Francis Creek Institute in London and the University of California in San Francisco seem to have found one of the keys, relating this type of cancer to the so-called particulate matter (PM), that is, particle pollution.
Some of these particles, such as dust or soot, are large enough to be detected with the naked eye. But others, such as PM 10 or PM 2.5 (with sizes of 10 and 2.5 micrometers respectively) are only detectable under the microscope.
These particles, especially the finer ones (PM 2.5), can travel deep into the lungs of people, and that is why the specialized doctor in oncology, Charles Swanton, and his colleagues, decided to investigate the relationship between exposure to these particles and the mutation of two of the genes most frequently associated with lung cancer: the so-called genes EGFR y KRAS.
Thus, after analyzing the cases of In 32,957 patients with lung cancer caused by the EGFR gene mutation in four different countries, the researchers found a direct relationship between this type of cancer and PM 2.5.
The researchers used mouse models to investigate cellular processes that might underlie cancer progression in relation to air pollution, and found than PM 2.5 triggered an influx of immune cells and the release of interleukin-1β (a proinflammatory signaling molecule) in lung cells responsible for aggravation of lung inflammation and the progression of tumors.
They also showed that Interleukin-1β blockade during PM 2.5 exposure prevents the development of cancer driven by EGFR. Furthermore, heThe authors also identified the type II alveolar cells (AT2) as the cells in which lung tumors are likely to occur induced by the presence of PM 2.5.
Taken together, the results suggest that theas PM 2,5 could act as tumor promoters and further aggravate existing cancer mutations, so the researchers argue that uA better understanding of this relationship may open the way for the prevention of this type of cancer, as well as provide an argument in favor of initiatives to address air quality as a public health priority.