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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

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Description of key information

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Additional information

The toxicokinetics of sodium bicarbonate have been described already on page 13 of the OECD SIDS dossier (2002). Please find hereafter the text:

The major extracellular buffer in the blood and the interstitial fluid of vertebrates is the bicarbonate buffer system, described by the following equation:

                      H2O + CO2 <=> H2CO3 <=> H++ HCO3-

Carbon dioxide from the tissues diffuses rapidly into red blood cells, where it is hydrated with water to form carbonic acid. This reaction is accelerated by carbonic anhydrase, an enzyme present in high concentrations in red blood cells. The carbonic acid formed dissociates into bicarbonate and hydrogen ions. Most of the bicarbonate ions diffuse into the plasma. Since the ratio of H2CO3 to dissolved CO2 is constant at equilibrium, pH may be expressed in terms of bicarbonate ion concentration and partial pressure of CO2 by means of the Henderson-Hasselbach equation: pH = pk + log[HCO3-]/aPCO2


The blood plasma of man normally has a pH of 7.40. Should the pH fall below 7.0 or rise above 7.8, irreversible damage may occur. Compensatory mechanisms for acid-base disturbances function to alter the ratio of HCO3- to PCO2, returning the pH of the blood to normal. Thus, metabolic acidosis may be compensated for by hyperventilation and increased renal absorption of HCO3-. Metabolic alkalosis may be compensated for by hypoventilation and the excess of HCO3- in the urine (Johnson and Swanson, 1987). Renal mechanisms are usually sufficient to restore the acidbase balance (McEvoy, 1994). The uptake of sodium, via exposure to sodium bicarbonate, is much less than the uptake of sodium via food. Therefore, sodium bicarbonate is not expected to be systemically available in the body. Furthermore it should be realised that an oral uptake of sodium bicarbonate will result in a neutralisation in the stomach due to the gastric acid.


Since the publication of the OECD SIDS dossier no additional relevant studies on toxicokinetics were found.