A new study demonstrates that microplastics can produce reactive oxygen species when in contact with water, challenging assumptions about their chemical inertness.

Researchers at Columbia University investigated how common plastics behave at the interface with water, finding that water-repellent surfaces trigger chemical reactions that generate harmful molecules.

The team used polystyrene powder in water containing methyl orange dye, observing near-complete fading of the dye over 10 days. This degradation occurred only in water, not in solvents like ethanol, indicating a water-specific reaction.

Electron spin resonance confirmed the presence of hydroxyl radicals at the plastic-water interface. Fluorescent sensors visualized these reactive species concentrating on plastic surfaces over time.

Testing six plastic types revealed polyethylene and polypropylene generated the strongest reactions, while water-attracting plastics like PET produced fewer radicals. The researchers attributed this to how water molecules organize near hydrophobic surfaces, creating conditions where hydroxide ions more easily form radicals.

To address contamination concerns, the study employed multiple detection methods and controlled experiments. Adding surfactants that disrupt the plastic surface reduced radical production, supporting the conclusion that the interface itself drives the chemistry.

When exposed to polystyrene particles, proteins aggregated and mouse red blood cells suffered damage, effects partially reversed by adding caffeine to neutralize radicals. However, researchers noted this does not prove microplastics cause disease, only that they can generate reactive molecules under specific conditions.

The study used fresh laboratory powders rather than weathered environmental particles, which showed weaker reactions. Particle age and size variations, common in real-world exposure, were not fully tested but may influence the magnitude of effects.

If confirmed as biologically relevant, these findings suggest plastic design could incorporate changes to reduce water-repellency, potentially mitigating interface-driven chemistry. The researchers emphasize the need for further study on how this interface chemistry translates to disease mechanisms in animals and humans.

The work appears in Nature (2026), DOI: 10.1038/s41586-026-11141-y.