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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

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Administrative data

Link to relevant study record(s)

Description of key information

Key value for chemical safety assessment

Additional information

2 -(methylamino)ethanol, compound with sulfur dioxide is a liquid with a small molecular weight and high water solubility at room temperature (MW = 139, water solubility = unlimited miscibility). These physicochemical properties indicate a good bioavailability via the dermal and oral route of the substance.

Systemic effects after acute exposure show that 2 -(methylamino)ethanol, compound with sulfur dioxide becomes bioavailable. In the acute oral toxicity study (BASF, 1979), 2/10 rats at 3160 mg/kg, 5/10 rats at 3830 mg/kg, 7/10 at 4640 mg/kg and 9/10 rats at 5000 mg/kg died. Clinical signs were: dyspnoea, apathy, poor general condition, exsiccosis, ruffled fur, markedly yellow urine, atony, diarrhoea, spastic gait, stagger, excitation, abnormal posture, lack of pain reaction and narcosis, indicating systemic availability.

For further assessment, a weight of evidence approach with methylethanolamin and sulfites will be done.

In a teratology study, monomethylethanolamine-supplementation resulted in elevated levels of both choline (43%) and acetylcholine (27%) when compared to levels detected in the choline-deficient derived pups (Zahniser et al., 1978). Measurable (11.7±1.8 nmol/g) amounts of dimethylethanolamine (DMAE) were detected in the brains of monomethylethanolamine-exposed pups (one-day-old). In addition, phosphatidylcholine and phosphatidyl aminoethanol levels in the brain were significantly (p<0.05) lower relative to the choline-deficient-fed pups. In another report, addition of DMAE or monomethylethanolamine to cultured hepatocytes isolated from choline-deficient rats resulted in the biosynthesis of phosphatidyldimethylethanolamine or phosphatidylmonomethylethanolamine in the place of phosphatidylcholine. Phosphatidyldimethylethanolamine corrected, to a limited extent, the choline-deficient reduction in Very low density lipoprotein (VLDL) secretion. Without VLDL secretion, fat and cholesterol accumulate in the liver, producing liver damage (Oregon State University, 2000).

SO2 transforms into sulfite after inhalation and exposure leads to a dose-dependent and significant increase of the contents of sulfite in brain, heart, and lung tissues (Meng, 2005). Endogenously generated sulfite resulted in significant systemic exposure in the highly sulfite oxidase-deficient groups. The histological data and results of gross pathological examinations indicate that all organs except the testicles were refractory to theses high concentrations of sulfite (Gunnison, 1987). Following oral administration of 10 or 50 mg SO2/kg (as NaHSO3 mixed with Na235SO3), 70-95% of the 35S was absorbed from the intestine and voided in the urine of mice, rats and monkeys within 24 hours. The majority of the remaining 35S was eliminated via faeces, the rate being species-dependent. Only 2% or less of 35S remained in the carcass after one week (Gunnison & Palmes, 1976; Gibson & Strong, 1973). In conclusion, soluble sulfite substances may be considered to be readily absorbed from the digestive tract of mice and rats; these studies also showed that only small amounts of ingested SO2 are eliminated via exhalation. Given the somewhat variable but high extent of oral absorption (70-95%), it appears most appropriate to conservatively assume 100 % absorption of sulfite substances after ingestion.Sulfites are cleared from the body almost exclusively by oxidation to sulfate. Exposure to sodium dithionite leads to composition products such as hydrogen sulfite which can be absorbed from the rat gastrointestinal tract and is oxidised in vivo to sulfate, principally by hepatic sulfite oxidase (cytochrom-c oxidoreductase). With lesser amounts, it is metabolised by the kidneys, intestines, heart, and lungs. About 70 to 95 % of the radioactivity orally applied hydrogen sulfite dose appeared in rodent and monkey urine within 3 days as sulfate. Only a small fraction (8 - 10%) of the absorbed hydrogen sulfite was eliminated intact (ACGIH, 1991; Gunnison, 1977). Physiologically, sulfite oxidase is involved in the methionine and cysteine metabolism.The endogenous sulfite amount in the body resulting from amino acid degradation is in the range of 0.3 - 0.4 mmol/kg. This is reported to be about 15 - to 130 - fold higher than the estimated value for exogenous sulfite exposure (Institute of Food Technologists and Committee on Public Information, 1976). In conclusion, sodium dithionite is not stable under physiological conditions. The rate of decomposition increases with increasing acidity. Upon contact with moisture, it is oxidised to hydrogen sulfite (HSO3-), sulfite (SO32-) and hydrogen sulfate (HSO4-), and under strongly acidic conditions it may liberate sulfur dioxide. Under anaerobic conditions (such as in the lower gastrointestinal tract), hydrogen sulfite (HSO3-) and thiosulfate (S2O32-) may be formed. Thiosulfate is eliminated mainly unchanged via renal excretion, but some amounts can also be enzymatically oxidized in the liver to sulfate. Under physiologically relevant conditions, the substance readily dissociates in aqueous solution to sulfite and hydrogensulfite anions. Bioaccumulation is not expected because of the strong anionic and hydrophilic nature of the substance, as well as its experimentally verified rapid oxidation in vivo to sulfate with subsequent renal elimination.