'Forever Chemicals' Linked to Accelerated Aging in Older Men, Study Finds

The study of how environmental and behavioral factors impact the way genes work formed the backbone of the study methodology.

John Rigolizzo

Published: 2/27/2026, 1:58:59 PM EST

'Forever Chemicals' Linked to Accelerated Aging in Older Men, Study Finds — PFAS food packaging results chart. (Courtesy of Mind the Store campaign/Toxic-Free Future)

"Forever chemicals" are causing older Americans to age faster.

Polyfluoroalkyl substances, also knows as PFAS, are polymers used for everything from non-stick cookware to certain cosmetics. But they do not naturally degrade and contaminate drinking water, and are linked to various health issues. A study published Wednesday in the journal Frontiers in Aging found that PFAS are linked to chemicals that accelerate aging in men and Americans 50-64.

The study noted that over 200 million Americans are affected by PFAS contaminating drinking water, and has a half-life inside the body of about 8.5 years. PFAS exposure is linked to higher cholesterol levels, decreased antibody response to some vaccines, changes in liver enzymes, hypertension, and preeclampsia during pregnancy, small decreases in the weight of babies at birth, and risks of kidney and testicular cancers.

Epigenetics—the study of how environmental and behavioral factors impact the way genes work—formed the backbone of the study methodology. Examining the discrepancy between biological age and epigenetic age—called age acceleration—was also a core piece of the methodology. The study examined DNA serum of 326 U.S. adults aged 50 and up from the National Health and Nutrition Examination Survey of 1999-2000. The researchers examined the concentration of PFAS in the samples and cross-referenced them with 12 different DNA methylation algorithms to determine how PFAS exposure affected their bodies.

The study found that perfluorononanoic acid (PFNA) in particular was linked to a DNA biomarker called GrimAgeacc which predicts mortality, especially in male and middle-aged subjects. Midlife—from ages 50-64—was the critical window for PFNA-related aging, due to the natural onset of heart disease, metabolic disorders, and tissue degeneration. The researchers postulated that the genes regulating inflammation, DNA repair, protein metabolism, and cellular senescence are especially responsive to PFNA exposure. PFNA was also shown to affect lipid transport, peroxisomal signaling, and oxidative stress pathways.

Exposure to PFNA and another chemical called perfluorosulfonic acid (PFSA) was also linked to disruptions in the mTOR pathway, which regulates cellular growth and metabolism. Disruptions in the pathway are linked to age-related muscle dysfunction, impaired protein synthesis, and systemic metabolic decline; relatedly, PFAS have been shown to disrupt nutrient sensing and metabolic functions. The researchers concluded that PFNA and PFSA increase oxidative and inflammatory stress on the body, thereby accelerating the epigenetic aging process.

The results were limited by sex: the study reported that "no significant associations were observed in females."

Limiting factors included a small sample size, unsuited to detecting smaller effect sizes; and a limited age sampling and time frame which does not include younger age groups and more current populations that may have been affected by PFAS differently. And while the study found "robust associations" between PFAS and the epigenetic clock, the researchers could not rule out the possibility that biological aging has influence over PFAS metabolism rather than the other way around. They also refused to rule out false positives. The researchers recommended larger and more representative population samples and additional procedures.

However, based on their conclusions, the researchers recommended including certain algorithms into studies to gain further insight into how these chemicals impact aging; along with "targeted interventions and regulatory actions to mitigate the health impacts of PFAS exposure, particularly in high-risk populations."