Contact electrification between water and a solid surface is crucial for physicochemical processes at water–solid interfaces. However, the nature of the involved processes remains poorly understood, especially in the initial stage of the interface formation. Here we report that H₂O₂is spontaneously produced from the hydroxyl groups on the solid surface when contact occurred. The density of hydroxyl groups affects the H₂O₂yield. The participation of hydroxyl groups in H₂O₂generation is confirmed by mass spectrometric detection of¹⁸O in the product of the reaction between 4-carboxyphenylboronic acid and¹⁸O–labeled H₂O₂resulting from¹⁸O₂plasma treatment of the surface. We propose a model for H₂O₂generation based on recombination of the hydroxyl radicals produced from the surface hydroxyl groups in the water–solid contact process. Our observations show that the spontaneous generation of H₂O₂is universal on the surfaces of soil and atmospheric fine particles in a humid environment.

Male BALB/c mice fed with either a regular or high fat diet were exposed to 0, 5 or 20 mg/kg perfluorooctane sulfonate (PFOS) for 14 days. Increased body weight, serum glucose, cholesterol and lipoprotein levels were observed in mice given a high fat diet. However, all PFOS-treated mice got reduced levels of serum lipid and lipoprotein. Decreasing liver glycogen content was also observed, accompanied by reduced serum glucose levels. Histological and ultrastructural examination detected more lipid droplets accumulated in hepatocytes after PFOS exposure. Moreover, transcripitonal activity of lipid metabolism related genes suggests that PFOS toxicity is probably unrelevant to PPARα's transcription. The present study demonstrates a lipid disturbance caused by PFOS and thus point to its role in inhibiting the secretion and normal function of low density lipoproteins.