Scientists link ‘forever chemicals’ exposure to liver damage
Scientists have identified a link between exposure to “forever chemicals” and liver damage, as well as a potential connection to non-alcoholic fatty liver disease, in a study published on Wednesday.
Exposure to such compounds — also known as per- and polyfluoroalkyl substances or PFAS — was associated with elevated levels of a liver enzyme called ALT, which serves as a biomarker for liver damage, the scientists concluded in an Environmental Health Perspectives article.
The authors synthesized the results of more than 100 peer-reviewed studies in both humans and rodents, ultimately finding that three of the most common types of PFAS detected in humans — PFOA, PFOS and PFNA — are all connected to elevated levels of ALT in human blood.
“PFAS are ubiquitous, and we know that all adults in the United States have detectable levels of PFAS in their bodies,” Leda Chatzi, a professor of population and public health sciences at the University of Southern California’s Keck School of Medicine, said in a statement.
“There is growing interest in the long-term health effects of PFAS exposure, and this study supports that there is evidence that PFAS are associated with liver injury,” Chatzi added.
Known for their presence in jet-fuel firefighting foam and industrial discharge, PFAS are also key components in a variety of household products, such as nonstick pans, waterproof apparel and cosmetics.
Thus far, scientists have determined a “probable link” between PFAS and diagnosed high cholesterol, ulcerative colitis, thyroid disease, testicular cancer, kidney cancer and pregnancy-induced hypertension.
The Environmental Health Perspectives study, however, is the first to establish such a link between PFAS and liver damage.
These so-called forever chemicals earned this epithet due to their propensity to break down slowly and accumulate in the environment and in human tissue, including in the liver, according to the authors.
In addition to making the connection between PFAS exposure and liver damage, the authors also identified a possible link to non-alcoholic fatty liver disease.
The liver enzyme ALT is likewise elevated in humans who have this disease — a condition in which excess fat accumulates in the liver — suggesting a potential connection between PFAS and what the authors described as a “dramatic and unexplained rise” in the disease in recent years.
Non-alcoholic fatty liver disease has become a serious public health threat that impacts 25 percent of adults worldwide, while U.S. cases are expected to grow by about one-third by 2030, according to the study.
Evidence from animal studies have shown that PFAS, which are endocrine-disrupting compounds, could cause metabolic shifts that lead to fatty liver disease, the authors noted.
Epidemiological studies, they continued, have demonstrated connections between PFAS exposure and cholesterol, triglycerides and uric acid — all of which are biomarkers of fatty liver disease.
Acknowledging that the human research connecting PFAS to liver disease is still limited, study lead author Sarah Rock stressed that ample evidence from animal research demonstrates the toxic nature of PFAS to the liver.
“A challenge for PFAS researchers is that humans are exposed to mixtures of hundreds if not thousands of these chemicals,” Rock, a PhD student at the Keck School of Medicine, said in a statement. “Mixture analyses is one potential tool for addressing this complexity in the future.”
Although some U.S. manufacturers have stopped using PFOA and PFOS, the researchers warned that the risk of exposure remains, due to the long-lasting nature of these compounds.
“This research clearly shows that PFAS need to be taken seriously as a human health concern because even after they are phased out, they persist in the environment,” PhD student Elizabeth Costello, also a lead author on the study, said in a statement.
“There is enough evidence, we believe, to demonstrate a need to clean up sources of exposure to PFAS and to prevent future exposures,” Costello added.
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