Air pollution containing high levels of airborne particles smaller than 2.5 micron isn’t just bad for the heart and lungs, it is bad for the liver too.
While most studies have linked exposure to particle pollution to heart, lung and other respiratory diseases, a new study suggests that ultra-small airborne particles may also damage the liver and possibly set the stage for metabolic disease and liver failure.
Known as PM2.5, these particles with diameters smaller than 2.5 micrometers, or about 3% the width of a strand of hair, induce liver fibrosis in animal models after a 10-week exposure to PM2.5 levels observed in a highly polluted city.
Liver fibrosis, commonly known as scarring of the liver, is the liver’s response to injury or inflammation in which fibrous scar tissues are formed to repair damaged tissues. But when excessive scar tissues are formed, the liver gradually loses its function, leading to metabolic disease, liver dysfunction and sometimes liver cancer. The major causes of liver fibrosis are hepatitis B and C, excess alcohol consumption and non-alcoholic fatty liver disease.
To investigate how PM2.5 promotes liver scarring, the researchers performed further molecular and cellular analyses in the laboratory.
They discovered that PM2.5 triggered inflammatory stress response in liver cells that in turn activated the transforming growth factor beta (TGF-β) signaling, and suppressed peroxisome proliferator-activated receptor gamma (PPAR-γ) to promote collagen deposition — a hallmark of fibrosis.
TGF-β signaling is part of the body’s tissue repair program to promote the growth of new collagen-rich tissues to heal wound and inflammation. In a healthy system, this process is balanced by PPAR-γ which, among other things, suppresses TGF-β activity at the end of the healing process to resolve inflammation and prevent excessive scarring.
Short-term (10 weeks) exposure to ambient PM2.5, however, could disrupt this healing process, as suggested by the study, and lead to excess scar tissues accumulating in the liver.
“Our work has a major impact on medical care and health policy-making for the populations under air pollution environment,” said Kezhong Zhang, Ph.D., principal investigator of the study.
“Liver fibrosis is an advanced stage of chronic liver injuries caused by chronic hepatitis viral infection, obesity, alcoholism or autoimmune diseases. Our work defined that air pollution, specifically PM2.5 pollutant, is an independent risk factor of liver fibrosis. This is very significant in terms of identifying new health risk factors and understanding liver diseases. The molecular and cellular mechanisms we revealed in this work have very important implications in clinical disease diagnosis and treatment associated with air pollution.”
The study is scheduled to be published in the Journal of Hepatology.
A previous study carried out by the same team suggested that PM2.5 exposure induced symptoms similar to non-alcoholic steatohepatitis in mice after a 10-week exposure to “real-world” PM2.5 levels. Mice exposed to ambient PM2.5 displayed impaired glucose metabolism in the liver, glucose intolerance and insulin resistance. The study was published in the Journal of Hepatology January 2013 Volume 58.