Scientists have recently brought to light a new understanding of how pollution particles cause lung cancer even to non-smokers. The groundbreaking study provides a new perspective on how pollution poses cancer risks and gives us a glimpse of a possible breakthrough in cancer treatment and prevention.
Most of us are familiar with the fact that other risk factors aside from tobacco smoke can result in cancer. We are reminded time and time again that exposure to secondhand smoke, asbestos, radon, and air pollution can result in an increased risk of getting cancer. All available science currently points to pollution as one of the deadliest causes of lung cancer.
CDC tells us that smoke contains harmful chemicals that can damage or change the DNA of cells. DNA is the cell's "instruction manual," controlling normal cell growth and function. When a cell's DNA is damaged, it can cause it to grow out of control and form a cancer tumor.
Harmful Fumes Can Activate Dormant Mutations to Trigger Cancer Cells
This particular research by a group of scientists from Francis Crick Institute and University College London warns the public that particles coming from car fumes and smoke from burning fossil fuels can activate dormant mutations in the lung cell to develop into full-blown dangerous cancer cells.
The same study claimed that exposure to the said pollution particles accounts for over 250,000 lung cancer deaths globally per year. As reported by the South China Morning Post, the research team from the Francis Crick Institute and University College London examined the health records of over 460,000 people in England, South Korea, and Taiwan before arriving at these groundbreaking findings.
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Swanton's team emulated the effects of pollution particles in the mutation of dormant EGFR genes in lab rats. This revealed an increased possibility of developing cancer when exposed to pollutant particles.
Findings Suggest New Ways Prevent Cancer
The researchers discovered that exposure to tiny PM2.5 pollution particles (less than 2.5 microns in diameter) increased the risk of EGFR gene mutations. This proves that air pollution might be deadlier than scientists previously thought.
This finding led to another discovery that might accelerate lung cancer treatment and prevention development. PM2.5 particles can trigger the body to release interleukin-1 beta (IL1B), which is an antibody that can prevent antigens from starting developing cancer cells. This immunoglobulin can make humans less vulnerable to risks caused by PM2.5 exposure. This finding could pave the way for better and more enhanced ways to prevent exposure to carcinogens.
Prof Charles Swanton of the Francis Crick Institute said at the European Society for Medical Oncology's annual conference in Paris, "The risk of lung cancer from air pollution is lower than from smoking, but we have no control over what we all breathe."
According to the WHO, exposure to air pollution levels have increased significantly in some parts of the world, primarily in low and middle-income countries with large populations. These new findings might spark more Clean Air movements and a basis to forward zero-emission industries.
