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Administrative data

Link to relevant study record(s)

Description of key information

Butylaminoethanol or Butylethanolamine (BEA) is expected to be absorbed well after oral exposure, based on oral LD50 of 892-1310 mg/kg bw in rats, its low molecular weight (117.2 g/mol), high water solubility (1000 g/L) and LogPow of 0.64. Concerning the absorption after exposure via inhalation, as the chemical has vapour pressure of 13.94 Pa (a value not indicative for absorption by inhalation), it is clear, that the substance is moderately available for inhalation. Given its lipophilicity (LogPow 0.64) - if absorbed - it is expected to be absorbed directly across the respiratory tract epithelium or through aqueous pores and/or be metabolized by the alveolar and bronchial tissue. BEA may be absorbed to a limited extent following dermal exposure into the stratum corneum and into deeper layers of the epidermis, due to its high water solubility. Nevertheless, BEA does not quite meet the criterion of having a LogPow value < 0 that would support this assumption. Moreover, irritating properties of BEA due to its charged form (free base) can affect the absorption, slowing the passage through biological membranes. Concerning distribution in the body, BEA is expected to distribute into the inner of cells and into the intravascular compartment. The substance does not indicate a significant potential for accumulation. BEA is expected to be metabolised via Phase I reactions leading to hydroxylated derivatives and/or derivatives of oxidative deamination. Further, they can either be involved into intermediary metabolism for further oxidative reactions or be excreted. BEA and its metabolites are expected to be eliminated mainly via the urine.

Even if there are indications that the inhalation and dermal absorption rates of BEA are low on the basis of physical-chemical properties and available toxicological data, a worst-case approach i.e. 100 % absorption, are assumed for the purposes of derivation of dermal or inhalative systemic DNEL.

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential
Absorption rate - oral (%):
Absorption rate - dermal (%):
Absorption rate - inhalation (%):

Additional information


The toxicokinetic profile of butylethanolamine (BEA) was not determined by actual absorption, distribution, metabolism or excretion measurements. Rather, the physico-chemical properties of this substance were integrated with its available toxicological data as well as the data on the read-across substance dibutylethanolamine (CAS 102-81-8) to create a prediction of the toxicokinetic behavior. The read-across substance shows very similar physico-chemical properties (high water solubility (miscible in all proportions in water, similar LogPow, no hydrolysis in water)) and is thus believed to behave very similar in aqueous solutions.


Toxicological profile of Butylethanolamine

BEA is acutely toxic via oral route of exposure. An oral LD50of 892 mg/kg bw was established in an animal study in rats (BASF, 1977; Report No. XXVI/45). No mortalities were observed in an acute inhalation study in rats (LC0of 24.7 mg/L; BASF, 1977; Report No. XXVI/45); but mucous membrane irritation was observed. In an acute dermal study, BEA did not produce systemic effects in animals (LD50>2000 mg/kg bw; Latven, 1977). The substance was irritating to rabbits’ skin and produced severe damage to eyes (BASF, 2007; Report No. 18H0033/072033; BASF 1977; Report No. XXVI/45). Since BEA has pH of 11.9 (GESTIS, 2011) no testing of skin sensitisation was conducted. BEA was not mutagenic in any of the bacterial strains tested (BASF, 1997, Report No. 40M0579/964373) and did not induce gene mutations at the hprt locus in mouse lymphoma L5178Y cells (OECD 476, Covance Laboratories Ltd., 2012a; Report No. 8260615). Additionally, no relevant increases in the number of cells containing micronuclei in human lymphocytes were detected (OECD 487, Covance Laboratories Ltd., 2012b; Report No. 8260614). Corrosion/irritation is primary effect of BEA and, in analogy to other alkanolamines, the effects by prolonged exposures are confined to local effects of respiratory tract and no systemic toxicity could be reached. The only systemic effects observed in the Combined Repeated Dose and Reproduction/Developmental Toxicity Screening Test in Wistar Rats (OECD 422; BASF, 2013, Project No. 87R0286/05I017, conducted with dibutylethanolamine) were transiently reduced food consumption, body weight and body weight gain. Reproductive and developmental parameters were not affected.

Toxicokinetic analysis of Butylethanolamine

BEA is a colourless liquid without specific odour (MW of 117.2 g/mol) at 20 °C. The substance is soluble in water (1000 g/L at 20 °C) and has a LogPow of 0.64. It has a low vapour pressure of 13.94 Pa (at 20 °C) and melts at -2.5 °C under atmospheric conditions. BEA is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyse under environmental conditions.



Oral absorption is favoured for small water-soluble molecules with MW up to 200 which can pass through aqueous pores or can be carried with the bulk passage of water (TGD, Part I, Appendix IV, 2003). Based on the molecular weight of 117.2 g/mol, the high water solubility and the logPow of 0.64, BEA is expected to be readily absorbed via the gastrointestinal (GI) tract by passive diffusion. This thesis is supported by the fact that the substance induced systemic toxicity effects in rats via oral route (Cat 4, harmful if swallowed; BASF, 1977; Report No. XXVI/45). In this study, Sprague-Dawley rats were administered 414, 607, 892, 1310, 1917, 2818, 4138 mg/kg bw/day of the test substance. In the higher dose groups (1310-4138 mg/kg bw) irregular respiration, apathy, staggering, diarrhea containing blood and a bad general state was observed until all animals died. In the other groups, except in the 414 mg/kg bw dose group, gasping, spastic gait, ruffled fur, bad general state was observed. In animals that died prior to study ending, dilatation of the heart and congestion, hyperemia, anemic stomach with liquid content, atonic and reddened intestine was seen. The LD50 was set at 892-1310 mg/kg bw. From this study, systemic exposure to the test substance is indicated, possibly mediated by passive diffusion along the gastrointestinal tract (for what a logPow is indicative; ECHA R7.c, 2008). However, liquid content of the intestinal tract might be more indicative for local corrosive effects of the test substance rather than systemic availability.100 % oral absorption is considered appropriate based on this acute toxicity data and on the physico-chemical properties which are in the range suggestive of absorption from the gastro-intestinal tract.

Substances with logPow values above 0 have the potential for absorption directly across the respiratory tract epithelium. BEA has a moderate logPow value of 0.64 and is according to this criterion favourable for absorption directly across the respiratory tract epithelium by passive diffusion. Further parameter which should be considered is the volatility. Substances with low volatility have a vapour pressure of less than 0.5 kPa. A vapour pressure of 13.94 Pa is indicative for low volatility, assuming low availability for inhalation and consequently low systemic exposure (ECHA R7.c, Table R. 7.12 -2, 2008). Based on low volatility of BEA, exposure by inhalation is not really relevant for this substance. It is unlikely, that considerable amounts of the substance reach the lung and when this occurs, the substance is expected to be absorbed directly across the respiratory tract epithelium or through aqueous pores due to the logPow of 0.64. This was confirmed in the acute inhalation study in rats (BASF, 1977; Report No. XXVI/45). In this study, rats were exposed to a saturated vapour atmosphere of the test substance for 8 hours. The mean nominal concentration of the test substance was 24.69 mg/L. No animal died. Mucous membrane irritation was observed and no abnormalities at necropsy. Irritating to the mucous membranes can intensify the absorption. Based on these data, a low absorption can be expected for inhalation (in this case, absorption by inhalation cannot be higher than that by oral route). However, for the purpose of derivation of inhalative systemic DNEL a absorption rate of 100% is assumed, follwing a worst-case approach.


Similarly, based on the physico-chemical properties of BEA, the substance is likely to penetrate the skin to only a limited extent as it is very soluble in water (water solubility of 1000 g/L). According to TGD, Part I, Appendix IV (2003), absorption through the skin is anticipated to be limited if water solubility higher than 10,000 mg/L and logPow is below 0. In case of BEA, the criterion for very high water solubility meets but the criterion for logPow does not meet (it is slightly above 0). The molecular weight of 117.2 g/mol is also suggestive of absorption through the skin. However, the substance BEA may be too water solouble to cross lipid rich environment of the stratum corneum and achieve deeper layers of the epidermis. Low penetration rate is supported by the result of the acute dermal study in rats where no systemic effects of toxicity were observed in treated animals (Latven, 1977). Further, the charged molecules of BEA will be hindered to be absorbed through the skin. Additionally, BEA has highly irritating properties, which were confirmed in the acute inhalation study described above, skin irritation study in rabbits (BASF, 2007; Report No. 18H0033/072033) and in eye irritation study (BASF, 1977, XXVI/45). Based on these properties of BEA and taken into account the fact that the irritating property of the substance is primary effect, systemic effect cannot be reached, which is why a reduced dermal absorption rate is highly likely. Despite these assumptions, a dermal absorption of 100% is assumed for BEA for the purposes of derivation of dermal systemic DNEL, following a worst-case approach.


Distribution and accumulative potential

A significant amount of BEA via oral route is expected to be available for distribution. As the cell membranes require a substance to be soluble in both water and lipids to be taken up, BEA is expected to reach the inner cell compartment due to its optimal molecular weight of 117.2 g/mol, its LogPow of 0.64 and a sufficiently high solubility in water (1000 g/L). The substance is also expected to be distributed into the intravascular compartment. As it is known that “substances with LogPow values of 3 or less would be unlikely to accumulate with the repeated intermittent exposure patterns normally encountered in the workplace” (TGD, Part 1), no enhanced risk for accumulation will be associated with the substance.



BEA is not expected to undergo hydrolysis in gastrointestinal tract or in body fluids, due to the absence of hydrolysable functional groups. It is expected to be excreted unchanged due to its high water solubility and optimal molecular weight. If case of entering the cell inner, BEA can undergo Phase I reactions: hydroxylation at α-carbon leading to hydroxyl derivatives (i.e. 4-[(2-hydroxyethyl)amino]butan-1-ol, or 4-[(2-hydroxyethyl)amino]butan-2-ol) or oxidative deamination with splitting-off of butylamine and hydroxyacetaldehyde, hydroxyacetic acid or oxoacetic acid. Further possible reactions are oxidation of 4-[(2-hydroxyethyl)amino]butan-1-ol to aldehyde 4-[(2-hydroxyethyl)amino]butanal with subsequent oxidation to 4-[(2-hydroxyethyl)amino]butanoic acid. Primary and secondary metabolites can be involved into intermediary metabolism or excreted unchanged or in form of conjugates. Excretion Since BEA is a stable compound and sufficiently soluble in water, it can be filtered by the kidneys and undergo primarily urinary excretion. Molecular weight of BEA (117.2 g/mol) and vapour pressure of 13.94 Pa are also suggestive of excretion via the urine (ECHA Guidance R7c., 2008). Excretion via the urine is a major pathway for the oxidised and/or hydroxylated derivatives of BEA as well. Metabolites which re-enter the system are expected to occur in a lesser extent.