A new study uncovers a crucial clue about the link between exposure to crystalline silica – which, if prolonged, causes the progressive lung disease silicosis – and a form of lung cancer.
The team, from the University of Louisville, KY, reports the findings in the journal Nature Communications.
They hope their discovery will speed up the development of new treatments for lung cancer associated with silicosis.
Silicosis is a progressive, debilitating and incurable lung disease that results after many years of inhaling large quantities of crystalline silica (silicon dioxide) – a compound found in rocks, stone, clay and sand.
Exposure to crystalline silica occurs in occupations where the compound forms a fine powder that can be inhaled.
These jobs include quarrying, mining, stone masonry, sandblasting, road construction, pottery, tunneling and rock drilling.
In the US, about 2 million people are potentially exposed to breathable silica dust because of their jobs. In the developing world, due to rapid industrialization and where working conditions are less well regulated, this figure could be over 10 million.
Silicosis continues to progress even if exposure stops because once the tiny particles are in the lungs, it is impossible to cough them up.
The body tries to get rid of the silica particles by getting macrophages – cells that ingest bits of debris for disposal – to mop them up.
But unfortunately, the crystalline silica kills off the macrophages, causing persistent sterile inflammation in the lung tissue, which can eventually lead to cancer.
Crystalline silica in breathable form is recognized as a human carcinogen by various bodies, including the International Agency for Research on Cancer and the US National Toxicology Program.
While crystalline silica is recognized as being potentially cancer-causing, it has not been easy to discern silicosis-associated lung cancer because other factors could be involved. For example, workers likely to be exposed to silica are often smokers.
In their study, the team found in mice that develop spontaneous lung tumors, exposure to crystalline silica accelerated tumor progression. They also saw this happen in mice implanted with human lung tumors.
When they looked in more detail at the underlying biology, they found that silica exposure triggered a molecule called leukotriene B4 (LTB4), which helps regulate inflammation, especially in the lungs.
The molecule works by binding to a receptor called BLT1. When the researchers removed this receptor in the mice, they were significantly protected from tumor growth spurred by silica exposure.
The researchers suggest the findings point to possible new treatment targets for both silicosis and associated lung cancer.
Senior author Haribabu Bodduluri, a professor of microbiology and immunology, says:
“We believe this is a significant step in our understanding of how environmental exposure alters the way lung cancer progresses. It is our hope that this new information will allow for the more rapid development of treatments for this currently incurable disease.”
In May 2014, Medical News Today learned about another study where scientists found a protein that may slow pulmonary fibrosis – a progressive, fatal lung disease with a survival that rarely exceeds 5 years after diagnosis.