This isn’t exactly a breath of fresh air.
Air pollution can cause lung cancer without mutating cells, a new study found.
Published Wednesday in the journal Nature, the study analyzed the presence of lung cancer in non-smokers, using mice as their test subjects.
The researchers found that, instead of causing mutations, the exposure to pollution resulted in inflammation which fostered tumor growth in tissue with existing mutations.
Typically inactive, the cancer-causing mutations naturally accumulate as time goes on, according to Professor Charles Swanton, of London’s Francis Crick Institute, one of the study authors.
“We’ve demonstrated that air pollution wakes these cells up in the lungs, encouraging them to grow and potentially form tumours,” Swanton said in a statement.
Globally, air pollution causes an estimated 9 million “preventable” deaths every year, as the World Health Organization says that 99% of the world breathes toxic air.
While lung cancer is often associated with those who smoke, air pollution can trigger the lethal disease, too.
“The idea is that exposures to carcinogens could promote cancer without actually doing anything to the DNA,” medical geneticist Serena Nik-Zainal, from the University of Cambridge, said in a statement. “Not every carcinogen is a mutagen.”
To investigate the phenomenon, Swanton put his team to work. They gathered both environmental and epidemiological data from Taiwan, South Korea, Canada and the UK, focusing on individuals who carried mutations in EGFR gene, which they claimed is present more often in non-smokers.
Mimicking the gene mutation in mice, the research team then exposed the rodents to air pollution, or particulate matter 2.5 (PM2.5), observing the lack of cell mutations and increase of inflammation.
“The major mechanism by which air pollution causes cancer is not due to the induction of new mutations,” University of California, San Francisco, cancer researcher Allan Balmain said in a statement. “It’s that sustained inflammation that becomes chronic that is essential to get these mutated cells to grow into tumors.”
The study authors wrote that they “found a significant association between PM2.5 levels and the incidence of lung cancer for 32,957 EGFR-driven lung cancer cases” included in the data sets analyzed.
PM2.5 – which derives its name from the the size of the particulate matter, measuring 2.5 micrometers or less in diameter – has been linked to other negative health conditions such as heart attacks and strokes. The pollutant particles, which are a result of smoke, vehicle exhaust and power plant emissions, are tiny enough to get into the lungs and, therefore, the bloodstream.
But researchers also noticed that some immune cells rushing to the inflammation site contained an inflammation-promoting protein, IL-1β. By blocking the protein, the incidence of lung cancer in the mice decreased.
The study’s results informed the authors’ plea to lawmakers for improved initiatives to combat pollution that could “reduce disease burden.”
“The mechanism we’ve identified could ultimately help us to find better ways to prevent and treat lung cancer in never-smokers,” said Swanton. “If we can stop cells from growing in response to air pollution, we can reduce the risk of lung cancer.”