According to new research, the link between per- and polyfluoroalkyl substances, or PFAS, and kidney damage may be due to regulation of the gut microbiota, which is made up of bacteria and other microorganisms that live in the digestive tract. PFAS are chemicals that are made and used in a variety of items, including furniture and food packaging. They are often referred to as “forever chemicals” because once they accumulate in the environment or human body, they take a long time to decompose.
How PFAS chemicals harm kidney function through gut health
The group of chemicals is known to increase the risk for many health problems, including heart disease, cancer, and chronic kidney disease, but the biological mechanisms behind that risk are poorly understood. “Almost everyone has PFAS in their blood, and these chemicals are linked to many negative health effects. But we don’t have any known interventions to reduce PFAS in the body, so we can’t really give recommendations to help.” “Can,” said Haley Hampson, PhD, a postdoctoral fellow in population and public health sciences at the Keck School of Medicine of USC, lead author of the new study.
The findings of the research, partially funded by the National Institutes of Health, are beginning to connect the dots between that problem and possible solutions. Building on previous studies that linked kidney damage to both PFAS and gut problems, the research team analyzed the three factors together for the first time. They found that increased PFAS exposure was associated with worse kidney function after four years, and changes in the gut microbiome and related metabolites explained up to 50 percent of the reduction in function. The results were recently published in the journal Science of the Total Environment.
The findings, which add to other Keck School of Medicine studies of PFAS, including longitudinal research, provide early clues about how to protect the kidneys from PFAS-related damage. Jessie A. Goodrich, PhD, said, “Our findings are an important piece of the puzzle about the many different health risks of PFAS, which can provide information to policymakers who want to protect the public from exposure to these chemicals. Help develop policies.” , assistant professor of population and public health sciences at the Keck School of Medicine and senior author of the study.
Research findings and implications
Researchers analyzed data from 78 participants ages 17 to 22 enrolled in the Southern California Children’s Health Study, a large-scale longitudinal effort to understand the effects of pollution on health. Fifty-six percent of the sample was Hispanic, a group that faces a greater risk of chronic kidney disease. At baseline, the researchers collected blood and stool samples, which allowed them to measure PFAS exposure, gut microbiome bacteria, and circulating metabolites (these metabolites, many of which are produced by the gut microbiome, are present in the blood). At a follow-up appointment four years later, researchers collected a second round of data on kidney function.
They found that when PFAS exposure increased by one standard deviation, kidney function was 2.4% worse at follow-up visits. The researchers then conducted a statistical analysis to determine whether a third factor – gut bacteria and associated metabolites – contributed to that association.
The analysis revealed two distinct groups of bacteria and metabolites, helping to explain the effects of PFAS exposure on kidney function. One group reported a 38 percent change in kidney function, and the other group reported a 50 percent change. Both groups of bacteria and metabolites had beneficial activities, such as reducing inflammation in the body, which were disrupted as PFAS exposure increased.
“We observed that exposure to PFAS was potentially altering the composition of the microbiome, which was associated with lower levels of beneficial bacteria and fewer anti-inflammatory metabolites,” Hampson said. The findings provide a roadmap for researchers wanting to better understand the connection between PFAS and kidney health. Hampson and colleagues observed a decrease in anti-inflammatory metabolites, as well as the bacteria that produce them, and an increase in inflammatory metabolites.
“This points to inflammation and oxidative stress as a possible mechanism, so this is an area where future research could focus,” she said. One limitation of the study is its small sample size. Goodrich said larger studies are needed to determine if and how the findings can be used to protect against PFAS-induced kidney damage. Next, the research team will move beyond measuring metabolites in the blood to detecting their presence in specific tissues of the body, including the kidneys.
