Yang et al. (2026)
- Authors: Hyo-Seon Yang, Jin-Seok Lee, Mi-Hyun Kang, Mi-Kyung Song, Ji-Yun Kang, Hyung Doo Kim, Hwan-Cheol Kim, Jong-Han Leem, Chang-Gue Son, Kyuhong Lee
- Institutes: Respiratory Safety Research Center, Korea Institute of Toxicology, Jeongeup, Republic of Korea, Institute of Bioscience & Integrative Medicine, Daejeon University, Daejeon, Republic of Korea, Department of Occupational and Environmental Medicine, Inha University, Incheon, Republic of Korea
- Publisher: Environmental Research
- Link: DOI
Summary
This study establishes a critical link between humidifier disinfectant exposure and the development of ME/CFS through a dual human and animal research model. By identifying specific mitochondrial damage and neuroinflammation as primary mechanisms, it validates toxic environmental exposure as a potential trigger for the disease. These findings provide a biological basis for symptoms in affected populations and offer new avenues for diagnosing ME/CFS via mitochondrial biomarkers.
What was researched?
The study investigated the mechanistic link between exposure to humidifier disinfectants containing polyhexamethyleneguanidine phosphate 💊 (PHMG-p) and the onset of ME/CFS. It specifically focused on how this chemical affects mitochondrial morphology, energy production, and neural health in the brain.
Why was it researched?
Large-scale human casualties in South Korea were linked to humidifier disinfectants, with many survivors developing chronic fatigue symptoms. Researchers aimed to determine if PHMG-p directly causes ME/CFS pathology through systemic toxic effects.
How was it researched?
The researchers analyzed mitochondrial abnormalities in the blood cells of human patients with disinfectant-linked ME/CFS. They further validated these findings by exposing mice to PHMG-p via intratracheal administration and assessing their behavior, mitochondrial function, and brain tissue integrity.
What has been found?
Patients and exposed mice exhibited significant mitochondrial swelling, disrupted cristae, and reduced oxidative phosphorylation (OXPHOS) complex expression. Additionally, the researchers observed blood-brain barrier disruption, neuroglial activation, and glymphatic system dysfunction in the hypothalamus of the exposed mice.
Discussion
The study successfully bridges the gap between environmental toxicology and clinical ME/CFS symptoms. While the animal model uses a specific administration route, the consistent mitochondrial findings across species strengthen the evidence for a shared pathological pathway.
Conclusion & Future Work
PHMG-p acts as a potent environmental trigger for ME/CFS by inducing mitochondrial and neurological dysfunction. Future research should explore whether stabilizing mitochondrial function can reverse these toxic effects in affected patients.