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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Key value for chemical safety assessment

Additional information

No data are available for (2 -Hydroxyethyl)ammonium nitrate. But data are available for sodium nitrate and monoethanolamin.

Sodium nitrate: In aqueous environments, such as the body, sodium nitrate is completely dissociated into the sodium (Na+) and the nitrate (NO3-) ions. Nitrate is reduced to nitrite by the enzyme nitrate reductase. After ingestion, nitrates are reduced to nitrites by bacteria in the lower intestine of the adult. However, in babies, which have a physiological gastric achlorhydria (lack of HCl in the stomach), the reduction occurs in the stomach and duodenum from which the nitrites are readily absorbed into the blood stream. Furthermore, methemoglobin-reductase (NADH-cytochrome b5 reductase) in infants has not yet reached full activity. After absorption, nitrites convert oxyhemoglobin into methemoglobin and thus interfere with oxygen transport in the blood, resulting in methemoglobineamia (“blue baby syndrome”). Nitrites can also cause vasodilation, which, like methemoglobineamia, is dose-related. The sodium cation is an essential ion, and is present in the blood and various body fluids, playing an important role in sustaining health. Most of the sodium is generally 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 could potentially increase the pH of the blood. However, the pH of the blood is regulated between narrow ranges to maintain homeostasis. Based on low MW, high water solubility, assumed low logPow high absorption is expected. However, the ion formation of the substance inmediately when in contact with a fluid decreases the absorption. Therefore, 50% absorption is taken for oral, dermal and inhalation exposure.

The major effect of increased sodium intake is elevated blood pressure which is linked to that of chloride. This is a continuous relationship which embraces the levels of sodium habitually consumed. For that reason, 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 might 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.

Monoethanolamin (MEA):

No information is available on toxicokinetics of MEA regarding the oral and inhalation route.

The absorption, distribution and metabolism of topically administered [14C]-MEA was studied in vivo, using athymic nude mice and human skin grafted onto athymic nude mice (Klain et al, 1985). The substance was applied at a chemical dose of 4.0 µg and a radioactive dose of 3.6 µCi to a 1.45 cm² graft area, using ethanol as vehicle. The same dose was applied to a similar area of non-grafted mice or administered intraperitoneally to another group of non-grafted mice. Expired air and urine were collected over a period for 24 hours. Radioactivity was determined periodically. At the end of the sampling period skin and selected organs were analysed. The results indicated that topical applied MEA penetrates the skin and is widely distributed in the body, radioactivity being detected in all the tissues and organs examined. Percutaneous penetration of the skin appears however to be relatively slowly, demonstrated by a marked time lag in the initial appearance of labelled carbon dioxide between topical and intraperitoneal treatment. Radioactivity in expired CO2was detected 5 min after an intraperitoneal administration of MEA, while no radioactivity in expired air was detected during the first 20 min post-topical application. The substance is readily metabolised in the skin as well as in other organs and tissues in the mouse. Liver is a major site for metabolism, containing over 24% of the applied radioactive dose. Further recovery of the administered radioactive dose was at skin administration site (24.3%), as exhaled CO2(over 18%), in urine (4.6%), in kidneys (2.5%) and in feces (1.8%). Lungs, brain, and the heart contained 0.55, 0.27, and 0.15% of the dose, respectively. Extensive metabolisation was indicated by appearance of labelled carbon dioxide in skin and hepatic amino acids, proteins and incorporation into phospholipids, and by recovery of over 18% of radioactive dose as14CO2. Urea, glycine, serine, choline, and uric acid were the urinary metabolites of MEA.

Skin penetration of MEA was also studied in vitro (Klain et al, 1985) by applying 5 µl of solution to 0.8 cm² area of pig skin, resulting in a dose of 4 µg/cm² and a radioactive dose of approximately 0.05 µCi. The results show that percutaneous penetration of MEA was quite slow, with ca. 5% penetrating the skin 50 hours post-application. Ca. 11% was lost from the skin due to evaporation and the bulk of the dose 62% remained in the skin. In separate experiments 7 to 9 times as much radioactivity was recovered from the upper 100 µm layer (mostly epidermis) as compared to the recovery from the remaining dermis. It should be noted that the in vitro penetration rate of MEA in pig skin was considerably slower than the rate observed in the in vivo experiment. This discrepancy may be due to several experimental variables, including the differences in species, the thickness of the skin, or the presence of the microcirculation system in human or mouse skin which would facilitate the removal of the chemical from the skin.


In another study (Sun, 1996) the skin penetration of MEA was tested in an in vitro model with full thickness skin preparations from mice, rats, humans and rabbits. [14C]-MEA was applied to skin discs as either an undiluted liquid or as an aqueous solution at target doses of 4 mg/cm2. An "infinite dose" or an amount of the test compound that would not be entirely absorbed by the skin during the 6 h exposure period was used to allow the calculation of steady-state penetration rates and permeability constants. The steady-state penetration rates were determined to be 42.5, 123.1, 73.8, and 7.9 μg/cm²/h for the undiluted dose of [14C]-MEA, while the permeability constants were calculated to be 0.42 x 10-4, 1.21 x 10-4, 0.72 x 10-4, and 0.08 x 10-4cm/hr for rat, mouse, rabbit, and human skin preparations, respectively. Comparing undiluted and water diluted doses of MEA, the results showed that there was generally less skin penetration of the undiluted material than that for the diluted test substance.The results suggest that the potential percutaneous absorption of MEA would be less for humans than it would be for rats, rabbits, and mice.

Pilgeram described a study wherefollowing an intraperitoneal application of 1,2 -14C-ethanolamine 12 % of the total dose could be recovered within 24 hours. Of these the majority was exhaled in form of CO2(9.2 %), another 2.84 % were excreted via the urine (Pilgeram, 1953)



The results indicate that topically applied MEA penetrates the skin, is widely distributed and is extensively metabolised in the body. A major site for metabolism is the liver. Extensive metabolism was indicated by the incorporation of radiolabelled carbon into hepatic amino acids, proteins and phospholipids. Urea and glycine were the major urinary metabolites of MEA.

Regarding a quantitative figure for dermal absorption, the results of the in vivo study are preferred above the results of the in vitro studies. In the in vivo study (Klain, 1985) the potential absorbed dose amounted to about 75% after 24 hours exposure. As workers are not exposed externally for more than 8 hours and assuming that a lower amount of substance was present in the skin (potentially absorbed amount) at t=8 hours compared to t=24 hours and that not the whole amount of substance present in the skin will eventually become systemically available, a correction factor of 2 will be used to derived the dermal absorption figure workers, i.e., 75/2 = 37.5%. For consumers the percentage of 75% is proposed as the default exposure duration for consumers is 24 hours (note that this is a very conservative figure for consumers as consumers will probably not be exposed for 24 hours/day).