New research suggests that exposure to per- and polyfluoroalkyl substances (PFAS) may impair kidney function through disruptions in gut microbiota, the community of bacteria and microorganisms that reside in the digestive system.
PFAS, often dubbed “forever chemicals,” are used in everyday products such as furniture and food packaging. These chemicals persist in the environment and human bodies, breaking down extremely slowly. PFAS exposure has been linked to several health issues, including cardiovascular disease, cancer, and chronic kidney disease, though the biological pathways remain unclear.
“Nearly everyone has PFAS in their blood, and these chemicals are associated with numerous health risks. But without known interventions to reduce PFAS levels, it’s difficult to provide actionable recommendations,” said Hailey Hampson, PhD, a postdoctoral fellow at the Keck School of Medicine of USC and lead author of the study.
Funded partly by the National Institutes of Health, the study investigates the relationship between PFAS exposure, gut microbiota changes, and kidney function. Researchers found that increased PFAS exposure correlated with poorer kidney function four years later, with changes in the gut microbiome and related metabolites accounting for up to 50% of the decline in kidney health. The findings were recently published in the journal Science of the Total Environment.
“This research offers early insights for policymakers to develop strategies to mitigate PFAS-related health risks,” said Jesse A. Goodrich, PhD, senior author of the study and assistant professor at the Keck School of Medicine.
The research team analyzed data from 78 participants, aged 17 to 22, enrolled in the Southern California Children’s Health Study—a long-term effort examining pollution’s impact on health. More than half the participants were Hispanic, a demographic at higher risk for chronic kidney disease.
At the study’s outset, researchers collected blood and stool samples to measure PFAS exposure and evaluate gut microbiota composition. A follow-up conducted four years later assessed kidney function.
The results revealed that for every standard deviation increase in PFAS exposure, kidney function worsened by 2.4%. Further statistical analysis identified two distinct groups of bacteria and metabolites that played a role in this decline—one group accounted for 38% of the change, while the other explained 50%. Both sets of beneficial bacteria, which typically reduce inflammation, were suppressed with higher PFAS exposure.
“We observed that PFAS exposure altered the gut microbiome by reducing anti-inflammatory bacteria and metabolites, while increasing harmful inflammatory ones,” Hampson said.
The research highlights inflammation and oxidative stress as possible mechanisms linking PFAS exposure to kidney damage, offering a direction for future studies.
Goodrich acknowledged that the study’s small sample size is a limitation, stressing the need for larger studies to confirm the findings and develop preventive measures. The team plans to extend their research by examining metabolites in specific tissues, including the kidneys, to deepen understanding of PFAS’s impact.
(Inputs from ANI)