Researchers have found a link between the buildup of per- and polyfluoroalkyl substances in the body and poorer sleep, with the effect most evident among younger adults. The study looked at blood measurements and sleep data from 144 participants aged 19 to 24 to explore how PFAS exposure might influence rest. This summary comes from a recent peer‑reviewed study that aims to understand the sleep implications of PFAS in early adulthood.
PFAS are widely used in everyday products to repel water and oil, including nonstick cookware, waterproof clothing, and food packaging. Because these chemicals resist breakdown, they are often described as forever chemicals and can persist in the environment and the body for long periods.
Exposure to PFAS has been linked to several health concerns, including cancer and metabolic diseases, as well as disruptions to reproductive and immune function, and effects on fetal development during pregnancy.
To assess sleep connections, researchers collected blood samples and sleep information from 144 participants aged 19 to 24, drawing on toxicology databases and clinical data to map links between PFAS levels and sleep metrics.
Among the seven PFAS types tested, four showed a significant association with shorter sleep duration or poorer sleep quality, notably PFDA, PFHxS, PFOA, and PFOS.
The study found that the presence of PFDA, PFHxS, and PFOA in the body was linked to about 80 minutes less sleep, and higher levels of many PFAS correlated with even greater reductions in sleep time.
People with elevated PFAS in their blood were also more likely to report difficulty falling asleep, waking during the night, and feeling tired during the day.
To explore potential mechanisms, the team examined four PFAS types using toxicology databases that connect chemicals to diseases and to changes in gene expression, building an integrated view of possible pathways affecting sleep.
Researchers analyzed more than 600 genes and identified seven genes that PFAS exposure appears to activate and that may influence sleep patterns.
A key factor highlighted is the immune-related gene HSD11B1, which helps produce the cortisol hormone that helps regulate the body’s sleep-wake rhythm.
Another gene linked to sleep and PFAS exposure is cathepsin B, a protein connected to cognitive function and memory. The enzyme it produces is a precursor to amyloid beta proteins found in the brains of individuals with Alzheimer’s disease, offering a potential link between PFAS exposure and neurological health considerations.
Earlier work has produced devices designed to remove PFAS from wastewater, reflecting ongoing efforts to reduce environmental PFAS exposure and its reach into human health.
Notes from a peer‑reviewed study indicate that the observed sleep disruptions may arise from a combination of hormonal regulation changes, immune signaling shifts, and subsequent impacts on brain function, all of which warrant further investigation to better understand long-term outcomes.