Air pollution alters lung tissue and cancer susceptibility

Scientists studying the impact of fine particulate matter on the respiratory system believe tumours are caused indirectly through structural changes, raising hopes for new treatments. 

A mechanism explaining how fine air pollution particles could increase the chances of developing lung cancer has been identified in a study published by eLife

The team involved carried out research at Nanjing University and the University of Macau, using samples of fine particulate matter (FPM) taken from seven different locations across China, focusing on the effects on cytotoxic T-cells (CTLs), which are the body’s main defence against tumour growth.

One group of mice was administered with lung cancer cells exposed to the particulates, another treated with cells that had not been exposed. FPM is recognised as a Group 1 carcinogen, and considered a substantial threat to global health, but until now the mechanism allowing these tiny, inhalable particles to cause tumours has remained a mystery.

selective focus photography of anatomy lungs

In all cases, the test subjects that had not been exposed to FPM had CTLs recruited by the body and sent to the lungs to destroy the cancer cells, while those that had been exposed struggled with this function. Those involved in the research now believe FPM dramatically compresses lung tissue structure, effectively making it far more difficult for CTLs to travel through the lungs to areas where tumours are developing, blocking them from performing their role. 

‘Despite its potential to cause mutations, recent research suggests that FPM does not directly promote – and may even inhibit – the growth of lung cancer cells,’ said the study’s first author, Zhenzhen Wang. ‘This suggests that FPM might lead to cancer through indirect means that support tumour growth. For example, some studies suggest FPM can prevent immune cells from moving to where they are needed.’

Further investigation and analysis of the structure changes to lung tissue revealed that this was down to a collagen subtype, collagen IV. The team then discovered that FPM triggers high levels of this due to the enzyme peroxidasin. 

‘The most surprising find was the mechanism by which this process occurred,’ added Wang. ‘The peroxidasin enzyme stuck to the FPM in the lung, which increased its activity. Taken together, this means that wherever FPM lands in the lung, increased peroxidasin activity leads to structural changes in the lung tissue that can keep immune cells out and away from growing tumour cells.’

In related news, research by the World Health Organisation last year revealed that over half of the world’s population lives without protection from PM2.5, a deadly form of particulate matter pollution linked to around 4.2 million fatalities each year.

Photo by Robina Weermeijer


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