Even as childhood obesity and poor diets dominate discussions about adolescent liver disease, the study adds a less visible but potentially decisive factor to the picture: everyday exposure to chemicals that linger in bodies and environments for decades. By showing how PFAS, genetics and lifestyle can converge during adolescence to shape lifelong liver health, the findings raise a pressing question for regulators and families alike: how much disease risk is being set in motion long before symptoms ever appear?
A new study led by researchers at the Southern California Superfund Research and Training Program for PFAS Assessment, Remediation and Prevention (ShARP) Center and the University of Hawai’i has found that exposure to certain widely used “forever chemicals” is associated with a higher risk of liver disease in adolescents.
The synthetic compounds, known as per- and polyfluoroalkyl substances (PFAS), were linked to a significantly increased likelihood of developing metabolic dysfunction-associated steatotic liver disease (MASLD), previously called fatty liver disease.
The researchers found that PFAS exposure may nearly triple the risk of the condition in adolescents.
The findings were published in the journal Environmental Research.
MASLD affects an estimated 10% of children overall and up to 40% of children with obesity.
The chronic disease often develops without obvious symptoms, though some patients report fatigue, discomfort or abdominal pain. Over time, MASLD raises the risk of type 2 diabetes, cardiovascular disease, advanced liver injury, cirrhosis and liver cancer.
“MASLD can progress silently for years before causing serious health problems,” said Lida Chatzi, MD, PhD, a professor of population and public health sciences and pediatrics and director of the ShARP Center, which is funded by the National Institute of Environmental Health Sciences to study PFAS health impacts, advance cleanup technologies and support affected communities.
“When liver fat starts accumulating in adolescence, it may set the stage for a lifetime of metabolic and liver health challenges. If we reduce PFAS exposure early, we may help prevent liver disease later. That’s a powerful public-health opportunity.”
PFAS are manufactured chemicals commonly used in nonstick cookware, stain- and water-repellent fabrics, food packaging and some cleaning products. They persist in the environment and accumulate in the human body over time.
More than 99% of people in the United States have measurable levels of PFAS in their blood, and at least one PFAS has been detected in about half of U.S. drinking water supplies.
“Adolescents are particularly more vulnerable to the health effects of PFAS as it is a critical period of development and growth,” said the study’s first and corresponding author Shiwen “Sherlock” Li, PhD, an assistant professor of public health sciences at the University of Hawai’i.
“In addition to liver disease, PFAS exposure has been associated with a range of adverse health outcomes, including several types of cancer.”
Linking PFAS, genetics and lifestyle
The researchers analyzed data from 284 adolescents and young adults in Southern California who were enrolled in two long-running USC studies.
Participants were already considered at higher metabolic risk because their parents had type 2 diabetes or were overweight. Blood tests were used to measure PFAS levels, while liver fat was assessed using MRI scans.
Higher blood concentrations of two common PFAS, perfluorooctanoic acid (PFOA) and perfluoroheptanoic acid (PFHpA), were associated with a greater likelihood of MASLD. Adolescents with double the amount of PFOA in their blood were nearly three times more likely to have the disease.
The risk was even higher among those with a specific genetic variant, PNPLA3 GG, which is known to influence liver fat accumulation. Among young adults, smoking further intensified the liver-related effects linked to PFAS exposure.
“These findings suggest that PFAS exposures, genetics and lifestyle factors work together to influence who has greater risk of developing MASLD as a function of your life stage,” said Max Aung, PhD, MPH, an assistant professor of population and public health sciences at the Keck School of Medicine of USC.
“Understanding gene and environment interactions can help advance precision environmental health for MASLD.”
Li noted that the study is the first to investigate the relationship between PFAS and MASLD in children using gold-standard diagnostic criteria, and the first to examine how genetic and lifestyle factors may interact with PFAS exposure.
The prevalence of MASLD also increased as participants aged, reinforcing evidence that puberty and early adulthood may represent periods of heightened vulnerability to environmental exposures.
The findings build on earlier USC research showing that, among adolescents undergoing bariatric surgery for obesity, exposure to PFHpA was linked to more severe liver disease, including inflammation and fibrosis.
“Taken together, the two studies show that PFAS exposures not only disrupt liver biology but also translate into real liver disease risk in youth,” Chatzi said. “Adolescence seems to be a critical window of susceptibility, suggesting PFAS exposure may matter most when the liver is still developing.”
The study’s co-authors include researchers from USC, Brown University, Emory University, the University of California at Irvine, Johns Hopkins University, Children’s Hospital Los Angeles and West Virginia University.
Funding was provided by the National Institutes of Health, the U.S. Environmental Protection Agency and the Hastings Foundation.
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