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EC number: 215-185-5 | CAS number: 1310-73-2
Endpoint summary
Administrative data
Link to relevant study record(s)
Description of key information
Short description of key information on bioaccumulation potential result:
When humans are dermally exposed to low (non-irritating) concentrations, the uptake of NaOH should be relatively low due to the low absorption of ions. For this reason the uptake of NaOH is expected to be limited under normal handling and use conditions. Under these conditions the uptake of OH-, via exposure to NaOH, is not expected to change the pH in the blood. Furthermore the uptake of sodium, via exposure to NaOH, is much less than the uptake of sodium via food under these conditions. For this reason NaOH is not expected to be systemically available in the body under normal handling and use conditions. (EU RAR, 2007; section 4.1.2.1, page 63).
Key value for chemical safety assessment
Additional information
Sodium is a normal constituent of the blood and an excess is excreted in the urine. A significant amount of sodium is taken up via the food because the normal uptake of sodium via food is 3.1-6.0 g per day according to Fodor et al. (1999). Exposure to NaOH could potentially increase the pH of the blood. However, the pH of the blood is regulated between narrow ranges to maintain homeostasis. Via urinary excretion of bicarbonate and via exhalation of carbon dioxide, the pH is maintained at the normal pH of 7.4-7.5 (EU RAR, 2007, section 4.1.2.1, page 63).
Mean daily sodium intakes of populations in Europe range from about 3-5 g (about 8 -11 g sodium hydroxide) and are well in excess of dietary needs (about 1.5 g sodium/day in adults) (EFSA, 2006). The main source of sodium in the diet is from processed foods (about 70 -75% of the total intake), with about 10 -15% from naturally occuring sodium in unprocessed foods and about 10 -15% from discretionary sodium added during cooking and at the table. The major effect of increased sodium intake is elevated blood pressure. The effect of sodium on blood pressure is linked to that of chloride. This is a continuous relationship which embraces the levels of sodium habitually consumed and it is not possible to determine a threshold level of habitual sodium consumption below which there is unlikely to be any adverse effect on blood pressure. Evidence that high sodium intake may have a direct adverse effect on heart function, independent of any secondary effect due to changes in blood pressure, is not conclusive. The Panel (EFSA, 2006) concludes that the available data are not sufficient to establish an upper level (UL) for sodium from dietary sources.
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