As the weather warms, daydreams of summer set in; the sounds of birds chirping, the smell of freshly mown grass, the feel of a cool swim on a warm day. But as the flowers begin to bloom so do algae unleashing a green scum across bodies of water and toxins that can affect the health of anyone exposed to too much.
Microcystin-LR is the most common and the most potent toxin produced by freshwater blue-green algae. It was first identified as a potent liver toxin in the 1980s and has since been linked to liver damage and cancer. Today, levels of the toxin are monitored in drinking and recreation waters for a designated maximum amount that people can safely ingest known as a tolerable daily intake value.
“It’s ubiquitous, every continent in the world has algae,” said Pharmaceutical Sciences Assistant Professor John Clarke. “We’re trying to assess whether individuals living with liver disease may be at greater risk.”
Clarke recently received an Outstanding New Environmental Scientist (ONES) grant from the National Institute of Environmental Health Sciences (NIEHS) of $2.1 million over the next five years to further his research into how exposure to microcystin may contribute to the progression of nonalcoholic fatty liver disease (NAFLD)—a condition characterized by the accumulation of extra fat in liver cells.
“We often talk about the hits that the liver takes that drive the progression of [NALFD],” said Clarke, explaining that his research team is looking into how microcystin may act as one of these “hits” driving the disease forward and possibly predisposing the liver to cancer later on. His research will help determine whether the designated tolerable daily intake value of microcystin should be different for those living with NAFLD.
NAFLD is the most common chronic liver disease in the United States and estimated to effect approximately 25% of people worldwide. While the condition begins as an accumulation of fat in the liver, it can progress through several stages where the liver becomes inflamed (known as nonalcoholic steatohepatitis or NASH) and eventually causes fibrosis—a buildup of scar tissue in the liver.
Clarke explained that fibrosis is a natural part of the liver’s repair processes after toxin exposure. In a healthy liver, once the toxins are removed, the liver repairs itself, reversing the fibrosis.
Previous research out of Clarke’s lab found that when a healthy liver was exposed to microcystin it caused fibrosis, which then repaired itself. However, when a NAFLD liver was exposed to the same toxin the fibrosis stayed.
When fibrosis becomes very severe and permanent, the liver disease has progressed to a stage known as cirrhosis. Both fibrosis and cirrhosis increase the risk of developing hepatocellular carcinoma, the most common type of primary liver cancer.
“You don’t just get cancer overnight, it’s small changes that happen over time,” said Clarke.
The concern is that microcystin causes some of these small changes that given time may lead to cancer.
Clarke explained, “When we looked at the comparison of healthy livers to those with NASH we saw a lot of cancer-related genes that had changed after exposure to microcystin.”
The most common exposure to microcystin is through drinking water, especially when taken from surface water. In 2014, microcystin levels in some parts of Ohio exceeded tolerable daily intake values after an algal bloom in Lake Erie leading to the shutdown of the water supply to more than 400,000 people.
Even when drinking water is treated, it is often done so by killing off all algae which can in turn release more microcystin into the water. Other avenues of exposure can come through accidental ingestion while swimming, or through eating fish and shellfish that have been exposed to the toxin.
“I hope that my research will help people better understand how our environment impacts our overall health,” Clarke said.