The link between air pollution and lung cancer has long been clear. The only question was: how?
In the classic 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 wrong.
New research presented last weekend in Paris may have found the right explanation. And this, according to researcher Charles Swanton, turns our understanding of tumor growth upside down. Mutations alone aren’t the only culprit.
“Everyone develops such mutations in their body, which is 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, so to speak.
And that’s exactly what happens when we inhale the particulates. Jargon: PM2.5, which means that the particles are no larger than 2.5 microns, about one-thirtieth the thickness of a hair. These particles can be found everywhere, mainly as a result of all types of combustion engines: in industry, but also in traffic. When people inhale them, they create small inflammations that awaken the mutated cells in our body. Just like a flame is needed to ignite the gas.
The fact that particulate matter primarily causes inflammation and not mutation isn’t necessarily good news. It means that chronic exposure to particulates causes otherwise harmless mutations to develop in cancer cells.
The finding could also explain lung cancer in non-smokers.
“The mechanism we have identified could ultimately help us find better ways to prevent and treat lung cancer in nonsmokers. If we can prevent cell growth in response to air pollution, we can reduce the risk of lung cancer.” .
