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.
Silicosis is a progressive, debilitating and incurable lung disease that results after
many years of inhaling large quantities of crystalline silica.
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.
Difficult to discern silicosis-associated lung cancer
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.