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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Administrative data

Link to relevant study record(s)

Description of key information

Short description of key information on bioaccumulation potential result:

Hydrogen peroxide will rapidly dissociate in contact with organic matter.

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential

Additional information

The toxicokinetics of hydrogen peroxide have been reviewed in the course of preparing the EU risk assessment report for the substance (European Commission 2003) and the following text is copied from the EU RAR, page 104-105:

"Hydrogen peroxide is a normal metabolite in the aerobic cell, but there is uncertainty about the true levels of the substance in biological media due to analytical difficulties. The steady state level appears to depend on the balance between its generation and degradation. Hydrogen peroxide passes readily across biological membranes (permeability constant corresponds to that of water) and, because it slowly reacts with organic substrates, it can diffuse at considerable distances in the cell. There are two main hydrogen peroxide metabolising enzymes, catalase and glutathione peroxidase, which control H2O2 concentration at different levels and in different parts of the cell as well as in the blood. At low physiological levels hydrogen peroxide is mainly decomposed by GSH peroxidase whereas the contribution of catalase increases with the increase of hydrogen peroxide concentration. Red blood cells remove hydrogen peroxide efficiently from the blood due to a very high catalase activity whereas in the serum catalase activity is low. Both animal studies and human case reports indicate that at high uptake rates hydrogen peroxide passes the absorption surface entering the adjacent tissues and blood vessels where it is degraded liberating oxygen bubbles. One ml of 30% H2O2 yields approximately 100 ml of oxygen; thus mechanical pressure injury may be produced. The hazard of oxygen embolisation is particularly high if the substance is administered into closed body cavities where the liberated oxygen (under pressure) cannot freely escape. In most cases the consequences of venous embolisation are not catastrophic because the lung functions as an effective filter for microbubbles under normal conditions (Butler and Hills, 1979). However, in experiments with dogs, when the lungs were overloaded with a bolus injection of 30 ml of air, or when the animals were pretreated with a vasodilator (aminophylline) prior to venous infusion of microbubbles of air, embolisation was detected in the femoral artery with Doppler monitoring. Regarding hydrogen peroxide inhalation or skin contact at rates that would correspond to occupational exposures, there are no data on the systemic fate of the substance. In view of the high degradation capacity for hydrogen peroxide in blood it is however unlikely that the endogenous steady state level of the substance is affected. In biological systems, hydrogen peroxide may also undergo iron-catalyzed reactions (Fenton reaction, Haber-Weiss reaction) resulting in the formation of hydroxyl radicals. The cellular toxicity of hydrogen peroxide appears to depend largely on the generation of hydroxyl radicals. Genetically determined traits (acatalasaemia, glucose-6-phosphate dehydrogenase deficiency of the erythrocytes) render humans more susceptible to peroxide toxicity."

The available information on the toxicokinetics of hydrogen peroxide is considered as reliable and sufficient. Additional tests on the toxicokinetics of the substance are deemed not necessary.

Discussion on bioaccumulation potential result:

See the Endpoint summary for a discussion.