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Key value for chemical safety assessment

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Acute toxicity: via oral route (read-across):

No acute oral toxicity study with (2 -Hydroxyethyl)ammonium nitrate is available. The acute oral toxicity hazard of (2 -Hydroxyethyl)ammonium nitrate is considered reflected by the salt 2 -Aminoethanol hydrochloride (source chemical) based on structural similarity. In the key acute oral toxicity study (BASF AG, 1980; 78/908), groups of 5 Sprague Dawley rats/sex were given a single oral gavage dose of Härter 421 flüssig, i.e. the read across reference substance 2 -Aminoethanol hydrochloride, in aqueous carboxymethyl cellulose (0.5 %) at doses of 2150 or 5000 mg/kg bw (dose volume: 10 mL/kg bw) and observed for 14 days. Mortality incidence, clinical signs and body weights were assessed during the observation period. All survivors were necropsied at the end of the observation period. Oral administration of the test item resulted in no mortality, no relevant clinical findings and no effect on the body weight. At necropsy, there were no test item-related macroscopic findings. Under the conditions of this study, the combined oral LD50 for male and female rats was determined to be > 5000 mg/kg bw (significance level: 1 %). In a reliable key study conducted with the source chemical 2 -Aminoethanol a relevant acute oral toxicity hazard was identified. In this study (Union Carbide Corporation, 1988; 51 -86), groups of 5 rats/sex received 0.25, 0.5, 1.0 or 2 mL/kg bw of neat test substance and one group of 2 males received 4.0 mL/kg bw by single oral gavage administration, resulting in dose levels of 254, 509, 1018, 2036 and 4072 mg/kg bw. Rats were fasted overnight before dosing. All animals were observed daily for death or signs of toxicity during the 14 -day observation period. Body weights were recorded on days 0 (before treatment), 7 and 14 (prior to necropsy). At death or termination, each animal was subjected to a gross pathological examination. Based on the mortalitiy incidence noted in this study, the oral LD50 of 2 -Aminoethanol for both sexes combined was established at 1089 mg/kg bw.

In supporting acute oral toxicity studies in rats, oral LD50 values of 1515 mg/kg bw (BASF AG, 1966; XV/305) were determined for 2 -Aminoethanol, while an oral LD50 value of 3430 mg/kg bw (BASF AG, 1980; 80/360) was established for Sodium nitrate.

On this basis, the acute oral toxicity hazard of the target chemical (2 -Hydroxyethyl)ammonium nitrate was considered attributable to 2 -Aminoethanol and not to Sodium nitrate, for which a low hazard was identified. In view of the weight proportion of 2 -Aminoethanol in the target chemical (2 -Hydroxyethyl)ammonium nitrate (49.2 % w/w), the oral LD50 of 1089 mg/kg bw determined for 2 -Aminoethanol corresponds to an oral LD50 of 2213 mg/kg bw for (2 -Hydroxyethyl)ammonium nitrate (1089 mg/kg bw / 0.492). Of note, this assessment would be conservative, since a direct read-across from the salt 2 -Aminoethanol hydrochloride (with a weight proportion of 2 -Aminoethanol of 62.6 % w/w) to the target chemical (2 -Hydroxyethyl)ammonium nitrate (with a weight proportion of 2 -Aminoethanol of 49.2 % w/w) would lead to a considerably higher oral LD50 value which is supported by the LD50 value of higher than 5000 mg/kg for (2 -Hydroxyethyl)ammonium nitrate.

Acute toxicity: via inhalation route (read-across):

A key acute inhalation toxicity study is availabe for the source chemical 2 -Aminoethanol, which is known to display the highest acute toxicity hazard among the source chemicals identified. In this study (Union Carbide Corporation, 1988; 51 -86), 5 rats/sex were exposed to substantially saturated vapour of 2 -Aminoethanol for a period of 6 hours and then observed for 14 days. Mortality, clinical signs and body weights were assessed repeatedly during the observation period. At the end of the observation period, all animals were necropsied and examined macroscopically. There was no mortality. No clinical signs, effects on body weight or macroscopic findings attributable to the treatment with the test substance were noted during the study. The LC50 for 6 hours exposure to 2 -Aminoethanol vapour was ca. 520 ppm, corresponding to ca. 1300 mg/m³ based on the theoretical saturated vapour concentration of the test substance at room temperature. Using modified Haber's law (cn x t = constant; c: concentration, t: exposure duration) and a default value of n = 3 in accordance with Chapter R.7a (ECHA, 2012) for extrapolation from longer to shorter exposure duration (6 hours to 4 hours), the LC50(4 hours) of 2 -Aminoethanol is calculated to be >1487 mg/m³. As the weight proportion of 2 -Aminoethanol in (2 -Hydroxyethyl)ammonium nitrate is 49.2 % (w/w), the LC50(4hours) for (2 -Hydroxyethyl)ammonium nitrate is estimated to be >3022 mg/m³ (>1487 / 0.492).

Acute toxicity: dermal (read across):

In the key acute dermal toxicity study (BASF AG, 1980; 78/908), groups of 3 Sprague Dawley rats/sex were given a single dermal application of neat Härter 421 flüssig, i.e. the read across reference substance 2 -Aminoethanol hydrochloride (source chemical), at doses of 1000 or 4000 mg/kg bw (dose volume adjusted) and observed for 14 days. Mortality incidence, clinical signs and body weights were assessed during the observation period. All survivors were necropsied at the end of the observation period. Dermal administration of the test substance resulted in no mortality, no relevant clinical findings and no effect on the body weight. At necropsy, there were no test item-related macroscopic findings. Under the conditions of this study, the combined dermal LD50 for male and female rats was determined to be > 4000 mg/kg bw. This study was classified as appropriate for read across assessment, i.e. prediction of the endpoint for the target chemical (2 -Hydroxyethyl)ammonium nitrate.

Based on reliable supporting data, the corrosive source chemical 2 -Aminoethanol displayed the highest acute toxicity hazard for the dermal route with a LD50 of 2504 mg/kg bw determined in rabbits (Union Carbide Corporation, 1988; 51 -86), while Potassium nitrate revealed no acute toxicity hazard via the dermal route when tested in rats (Product Safety Labs, 2000; 9742).

Considering the weight proportion of the toxicologically relevant source chemical 2 -Aminoethanol in the target chemical (2 -Hydroxyethyl)ammonium nitrate (49.2 % w/w) and using a conservative approach, the LD50 of >4000 mg/kg bw determined for the source chemical 2 -Aminoethanol hydrochloride in the key study is considered to represent the appropriate dose descriptor for the acute dermal toxicity hazard related to (2 -Hydroxyethyl)ammonium nitrate. This assessment is considered conservative, since read-across from the LD50 value of 2504 mg/kg bw determined for the the source chemical 2 -Aminoethanol would result in a higher LD50 value for the target chemical (2 -Hydroxyethyl)ammonium nitrate, i.e. LD50 of 5089 mg/kg bw (2504 mg/kg bw / 0.492).

Justification for classification or non-classification

Considering acute toxicity data of the source chemicals idenitifed for read-across assessment (section 13), 2 -Aminoethanol is currently classified as Xn; R20/21/22 according to Directive 67/548/EEC (DSD) and as Acute Tox 4; H332, H312, H302 according to Regulation (EC) No 1272/2008 (CLP/GHS).

Referring to the acute toxicity effect levels identified for (2 -Hydroxyethyl)ammonium nitrate, the substance is not subject to classification for acute toxicity according to Directive 67/548/EEC and Regulation (EC) No 1272/2008. The criteria for specific target organ toxicity after single exposure (STOT SE) are not met.