Aluminium sodium tetrahydroxide

Endpoint summary

Description of key information

Sodium aluminate is corrosive to the skin and mucous membranes. Acute toxicity data is based on information from aluminium and aluminium compounds as structural analogues for read-across.
Oral: LD50 > 2000 mg/kg bw (aluminium oxide, nanosized and bulk material)
Inhalation: LC50 > 1000 mg Al/m³ air (aluminium flakes)
Inhalation: LC50 > 5090 mg Al/m³ air (75% aluminium oxide, 25% aluminium hydroxide)

Additional information

There are no data available on the acute toxicity of sodium aluminate.

Sodium aluminate is a strong base (pH > 11.5) and thus fulfils the criteria for classification as corrosive. In accordance with Column 2, Section 8.5., of Annex VIII to the REACh Regulation (EC No. 1907/2006), acute toxicity studies do not generally need to be conducted if the substance is classified as corrosive to the skin.

Available information on the acute toxicity of other aluminium compounds was, however, taken into account as supporting information, since the pathways leading to toxic outcomes are likely to be dominated by the chemistry and biochemistry of the aluminium ion (Al³⁺) (Krewski et al., 2007; ATSDR, 2008).

Oral

An acute oral toxicity study was performed with aluminium oxide (bulk material with a particle size of 50 -200 µm as well as nanosized particles of 30 and 40 nm, respectively) in female Wistar rats in a study similar to OECD Guideline 420. Aluminium oxide nanoparticles and the bulk sample were administered by a single oral gavage at doses 5, 50, 300 and 2000 mg Al₂O₃/kg bw. Parameters monitored during the study included mortality and clinical signs. There was no mortality related to the acute oral exposure to aluminium oxide (nanoparticles and bulk sample) at any dose. Under the conditions of this study, the oral LD50 of all three types of Al₂O₃ is above 2000 mg/kg bw (Balasubramanyam et al., 2009a, b).

Inhalation

The acute inhalation irritation properties of Catapal Alumina Fines (fine powder) were investigated in rats in a GLP-compliant study similar to OECD Guideline 403. The test material was reported to consist of 75 % aluminium oxide and 25% aluminium hydroxide. Ten male and ten female rats were exposed for 4 h to an aerosol generated from the undiluted test material (fine powder) at an exposure concentration of 5.09 mg/L (5090 mg/m³). The mass median aerodynamic diameter (MMAD) for the test material was 4.64 µm (geometric standard deviation - 3.16 µm). 20 sham-exposed animals served as negative control group. Animals were observed for up to 3 days for clinical signs and mortality. Gross necropsy examinations were performed on 5 animals per sex per group sacrificed at 24 and 72 h after exposure, respectively. Nasal turbinate, lungs and trachea from all Al-exposed and control group animals were examined microscopically.

No mortality was observed. Clinical signs of piloerection were noted in male and female rats during exposure period and in all males and females during 1.5 h and 2 h post-exposure, respectively. Decreased activity was observed in the treated male and female rats during exposure period and 1.0 h and 1.5 h post administration, respectively. Ptosis was observed in the treated male and female rats during exposure period only. All animals appeared to be normal and no toxic signs were observed at 24, 48 and 72 h post-exposure. No body weight changes were noted during the post-exposure observation period. Macroscopic examination at the end of the 24 and 72 h observation periods did not reveal any aluminium-related changes of the internal organs of the treated animals compared to the control group. The results showed no histopathological changes in the nasal turbinate, trachea and lungs of the animals exposed to the test material. In summary, no irritation effects were observed in male and female rats following an acute inhalation exposure to Catapal Alumina Fines at exposure concentration of 5.09 mg/L under conducted experimental conditions (Holbert, 1990). The LC50 was suggested to be > 5.09 mg/mL (5090 mg/m³). However, some caution is required in interpreting results and a conclusion due to a short period of post exposure observation (3 days instead of 14 days).

In another study, no mortalities and no signs of general toxicity were reported in rats (6 per group) exposed to airborne aluminium flakes (coated with < 2% palmitic and stearic acids) for 4 h at 10, 50, 100, 200 and 1000 mg Al/m³. Animals were examined at 24 h, 14 days, 3 months and 6 months post-exposure. No changes in lung function were found. BALF analyses showed an influx of polymorphonuclear neutrophils that was still evident six months after exposure at 50 mg/m³. At this concentration and above, increased lactate dehydrogenase, glucose-6-phosphate dehydrogenase, and alkaline phosphatase activity in lavage fluid were reported. At 200 mg/m³ and higher, multifocal microgranulomas in lungs were observed. This study provided evidence for a mild, acute inflammatory response in rats on inhalation of aluminium flakes and also for the retention of the insoluble flakes in the lungs resulting in a persistent irritation response at doses greater than 10 mg/m³ (Thomson et al., 1986). The LC50 was considered to be > 1000 mg/m³.

There is no information available on the occurrence of death following acute inhalation exposure to various forms of aluminium in humans (ATSDR, 2008).

Dermal

There is no information available indicating mortality or systemic effects after acute dermal exposure to various forms of aluminium in humans or animals (ATSDR, 2008).

This is supported by the notion that, in general, aluminium absorption via the skin is very low (ca. 0.01%) (Flarend et al., 2001).

Justification for classification or non-classification

Sodium aluminate is corrosive to the skin and mucous membranes. Based on read-across from aluminium and other aluminium compounds as structural analogues, the available data on the acute toxicity of sodium aluminate is conclusive but not sufficient for classification according to DSD (67/548/EEC) and CLP (1272/2008/EC).