Microplastics in Water Generate Harmful Reactive Chemicals, Challenging Their 'Inert' Reputation

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A 2026 study reveals that microplastics in water surfaces produce reactive oxygen species, which can damage biological molecules, suggesting microplastics are chemically active and possibly harmful.
Microplastics—tiny particles resulting from the breakdown of larger plastic items—have been largely considered chemically inert, contributing to their widespread use in packaging and containers. However, new research from Columbia University challenges this assumption, showing that microplastics in water are not inert but actively generate harmful reactive chemicals. Published in Nature in October 2026, the study led by chemist Wei Min demonstrates that the interface between water and various microplastics facilitates the production of reactive oxygen species (ROS), known for causing oxidative damage to proteins, DNA, and lipids.
Min's team focused on the chemistry occurring at the boundary layer between water and plastic particles. Using polystyrene as a model, they observed that a yellow dye (methyl orange) dissolved in water containing microplastics degraded significantly over 10 days, indicating chemical activity attributable to ROS. Further experiments detected hydroxyl radicals—highly reactive ROS—directly at the plastic surfaces. This effect was consistent across six common plastics, including polyethylene, polypropylene, PVC, PET, and acrylic, with the most water-repellent plastics generating the highest radical levels.
The researchers attribute this to a disruption in the molecular hydrogen-bond network of water at hydrophobic plastic surfaces, which raises the energy levels of local water molecules and lowers the energy needed to form radicals from hydroxide ions. Additionally, plastic surfaces acquire a negative charge in water, further facilitating radical production. To exclude contamination or artifacts, the team employed multiple independent detection techniques and demonstrated that adding surfactants to disrupt the water-plastic interface reduced radical generation, supporting the conclusion that the phenomenon is intrinsic to the microplastic-water interface.
Biological relevance was also investigated. Proteins such as lysozyme aggregated on plastic surfaces due to radical-induced damage, and mouse red blood cells exposed to microplastics fragmented in proportion to the plastics’ radical production. These findings suggest microplastics' ROS generation could contribute to oxidative stress and related health issues, although the effect’s magnitude relative to internally produced ROS remains unclear.
The study acknowledges uncertainties regarding the extent of human exposure to microplastics, the impact of environmental aging on particles, and the influence of particle size, with smaller nanoplastics potentially posing greater risks due to larger surface areas. The researchers propose that engineering plastics to be less water-repellent might mitigate radical formation.
Concluding, Min emphasized the need for further study to determine the direct contribution of microplastic-generated ROS to disease in humans and animals. This research marks an important advance in understanding microplastics’ chemical activity and potential health impacts beyond their physical presence.


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