The link between air pollution and lung cancer has long been clear. The only question was: how?
In the classical view it is simple. Polluted air is full of tiny dust particles that affect the DNA of certain cells in our body and cause mutations in the genetic code. If a cell accumulates too many mutations, it develops into a cancer cell. But writes De Morgen, that theory is probably incorrect.
New research presented last weekend in Paris may have found the right explanation. And that, according to researcher Charles Swanton, turns our knowledge about the growth of cancers upside down. Mutations alone are not the only culprit.
“Everyone develops such mutations in their body, that’s part of the aging process. But our research shows that you still need a second step in the process: a inflammatory response which ensures that the mutated cells are activated, as it were.”
And that is exactly what happens when we inhale particulate matter. In the jargon: PM2.5, which means the particles are no bigger than 2.5 microns, about one-thirtieth the thickness of a hair. These particles can be found everywhere, mainly as a result of all kinds of combustion engines: in industry, but also in traffic. When people inhale them, small inflammations arise that wake up the mutated cells in our body. Just like a flame is needed to ignite gas.
The fact that particulate matter mainly causes the inflammation and not the mutation is not necessarily good news. It means that chronic exposure to particulate matter causes otherwise harmless mutations to develop into cancer cells.
The finding may also explain lung cancer in non-smokers.
“The mechanism we identified could ultimately help us find better ways to prevent and treat lung cancer in never-smokers. If we can prevent cells from growing in response to air pollution, we can reduce the risk of lung cancer.”