‘Forever chemicals’ linked to another devastating, lifelong condition: study – New York Post

Lead

A Swedish team led by Kim Kultima analyzed blood samples in 2025 from 900 people recently diagnosed with multiple sclerosis (MS) and matched controls and found that higher blood concentrations of PFOS and PCBs were associated with roughly double the odds of an MS diagnosis. The work, reported in a press release and covered by media, evaluated individual and combined exposures and adjusted for known lifestyle and genetic risk factors. Researchers also identified an interaction between a previously protective gene variant and PFOS exposure, complicating prior genetic assumptions. The finding adds to mounting evidence that persistent industrial chemicals may influence autoimmune disease risk.

Key takeaways

• Study population: Blood samples from 900 newly diagnosed MS patients in Sweden were compared with control samples from people without MS.
• Primary finding: Individuals with the highest PFOS and PCB concentrations had about twice the odds of having MS compared with those with the lowest concentrations.
• Mixed exposures: Increased combined exposure to multiple chemicals correlated with higher MS odds even after adjusting for lifestyle and genetic factors.
• Gene–environment interaction: A gene variant previously associated with lower MS risk showed higher MS odds when PFOS exposure was elevated.
• Persistent contaminants: PCBs remain in the environment decades after the 1979 U.S. ban; PFAS, including PFOS, continue to be detected widely, including in newborns.
• Health context: PFAS and related compounds have prior links to immune disruption, liver effects, high cholesterol, fertility issues and several cancers.
• Risk reduction: Experts recommend actions such as filtering drinking water and avoiding nonstick cookware and grease-resistant packaging to lower personal exposure.

Background

PFAS (per- and polyfluoroalkyl substances) and polychlorinated biphenyls (PCBs) are classes of synthetic chemicals valued for their water-, oil- and stain-repellent properties but notorious for environmental persistence. PFOS is a long-studied PFAS molecule; PCBs were widely used until their phase-out and ban in many countries, including the United States in 1979. Both groups resist degradation, accumulate in soil and sediment, and bioaccumulate in animal and human tissues, producing long-term exposure risks.

Over the past two decades, observational and experimental studies have linked PFAS and PCBs to a range of adverse outcomes: immune modulation, altered lipid metabolism, impaired reproductive outcomes, developmental effects and increased risks for several cancers. Separately, multiple sclerosis is an autoimmune disease of the central nervous system that disrupts nerve signaling and frequently causes lasting disability; its causes are believed to arise from a combination of genetic susceptibility and environmental triggers. Identifying environmental contributors remains central to prevention strategies and to understanding disease mechanisms.

Main event

The Swedish research team measured PFOS, several PCB congeners and other contaminants in blood samples drawn from 900 people recently diagnosed with MS and compared those concentrations to samples from people without MS. Statistical models adjusted for known lifestyle risks (for example, smoking and vitamin D proxies) and recognized genetic risk alleles. The investigators examined both single-chemical associations and combined exposures to reflect real-world simultaneous contact with multiple contaminants.

Key quantitative results showed that participants in the highest exposure groups for PFOS and for PCBs had approximately double the odds of an MS diagnosis relative to participants in the lowest exposure groups. The association persisted when the researchers controlled for potential confounders, suggesting a robust correlation in this case-control dataset. The team also analyzed dose–response patterns and found that increasing total exposure correlated with progressively higher odds of MS.

Importantly, the authors assessed gene–environment interplay by looking at variants previously thought to modify MS risk. Contrary to expectations, a variant earlier associated with reduced MS risk appeared to confer higher odds when combined with elevated PFOS levels. The authors interpreted this as evidence that inherited and environmental factors may interact in complex, sometimes counterintuitive ways to affect disease probability.

Analysis & implications

The study strengthens observational evidence linking persistent environmental contaminants to immune-mediated disease, but it does not by itself establish causation. Case-control designs are susceptible to reverse causation and unmeasured confounding; however, the biological plausibility is supported by prior mechanistic data showing PFAS and PCBs can alter immune function, including both suppression and inappropriate activation. This mechanistic plausibility increases the weight of the association but does not replace the need for longitudinal and experimental confirmation.

From a public-health perspective, the findings raise concern because PFAS exposures are widespread—surveillance studies show detectable levels in the blood of most populations, including newborns—and PCBs persist long after their manufacture ceased. If a causal link were confirmed, the population attributable burden could be substantial given the ubiquity of exposure. That would argue for more aggressive regulatory limits, remediation of contaminated sites, and expanded monitoring of drinking water and food supplies.

Clinically, the result suggests that exposure history could be a relevant element in research on MS etiology and possibly in risk assessment, though routine individual testing for PFAS or PCBs as part of MS workups is premature. For researchers, the observed gene–environment interaction points to the value of combining genomics with detailed exposure assessment to reveal pathways of disease initiation and progression. Policymakers may need to weigh this accumulating evidence when setting exposure standards and prioritizing cleanup efforts.

Comparison & data

The table summarizes the principal effect sizes reported in the analysis: roughly twofold odds for individuals in the highest measured concentration categories compared with those in the lowest. These figures come from adjusted comparisons within the Swedish sample and should be interpreted as association estimates rather than guarantees of causal magnitude. Differences across populations, exposure timing and measurement methods could change the numerical estimates in other settings.

Reactions & quotes

Study authors emphasized both the size of associations and the need to explore biological mechanisms and interactions with inherited risk.

“People with the highest concentrations of PFOS and PCBs had approximately twice as high odds of being diagnosed with MS, compared with those with the lowest concentrations.”

Kim Kultima (study lead)

The first author highlighted that combined exposures and gene–environment interplay were central to the findings.

“An increase in total exposure was linked to higher odds of MS, even after adjusting for previously known lifestyle and genetic risk factors.”

Aina Vaivade (first author)

Unconfirmed

• Whether the observed associations reflect a causal effect of PFOS or PCBs on MS onset remains unproven and requires prospective, mechanistic and experimental confirmation.
• The timing of relevant exposures (prenatal, early life or adult exposures) that might most influence MS risk has not been identified in this case-control analysis.
• The specific gene variant interaction observed needs replication in independent cohorts before it can be considered a reliable modifier of risk.

Bottom line

This Swedish case-control analysis adds to a growing body of evidence linking persistent industrial chemicals to disruptions of the immune system and to autoimmune diseases, here showing an association between higher PFOS and PCB blood levels and roughly double the odds of an MS diagnosis. The data are biologically plausible given prior studies of immune effects, but they stop short of proving causation; prospective cohorts and mechanistic studies are necessary next steps.

In the meantime, public-health measures that reduce population-level exposure—improved drinking-water treatment, tighter limits on PFAS in consumer products, continued remediation of PCB-contaminated sites and consumer-level steps such as filtering water and avoiding certain packaging—are prudent risk-mitigation strategies. For researchers and policymakers, the paper underscores the importance of integrating exposure science with genetics to clarify how environmental contaminants contribute to chronic disease.

Sources

• New York Post — news report
• U.S. Environmental Protection Agency (EPA) — official PFAS information and guidance
• U.S. Centers for Disease Control and Prevention (CDC) — overview of multiple sclerosis