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Key value for chemical safety assessment

Additional information

Genetic toxicity

There are studies available in which the mutagenic properties of Fatty acids, C16-18 (even numbered), aluminum salt were investigated, including a bacterial mutation and mammalian cell gene mutation assay. Clastogenic properties of the test substance have not been investigated. However, there are reliable data on analogue substances which are considered suitable for read-across, including docosanoic (CAS 112-85-6), stearic (CAS 57-11-4) as well as aluminium hydroxide (CAS 21645-51-2). For details on the read-across approach please refer to the analogue justification in section 13 of the technical dossier.

Gene mutations in bacteria

The potential to induce gene mutations in bacteria of Fatty acids, C16-18 (even numbered), aluminum salts was investigated according to OECD 471 with Salmonella typhimurium tester strains TA 98, TA 100, TA 102, TA 1535 and TA 1537 (Schreib, 2012). Concentrations ranging from 3.16 to 5000 µg per plate were tested with and without metabolic activation in a plate incorporation assay (incubation for 48 hours). The test substance did not increase the number of revertant colonies in any tester strain either in the absence or presence of metabolic activation. Cytotoxicity was observed without metabolic activation starting at 1580 µg/plate or 500 µg/plate in TA 1535 and TA 100/TA1537, respectively. Precipitation started at 100 µg/plate (without S9) and at 316 µg/plate (with S9). Under the conditions of the study, Fatty acids, C16-18 (even numbered), aluminum salts were non-mutagenic in bacteria.

Gene mutations in mammalian cells 

An in vitro mammalian cell gene mutation test according to OECD guideline 476 was performed with Fatty acids, C16-18 (even numbered), aluminum salts in mouse lymphoma L5178Y cells (Trenz, 2012). Cells were treated with metabolic activation at several test substance concentrations ranging from 10 – 1500 µg/mL and at concentrations of 2 - 500 µg/mL in the absence of metabolic activation for 4 hours. In a second experiment, cells were exposed for 4 or 24 hours without metabolic activation to concentrations ranging from 15 – 500 µg/mL or 10 – 100 µg/mL, respectively. No increase in the mutation frequency above the Global Evaluation Factor (GEF) was seen in the presence of S9 mix. Treatment with 500 µg/mL test item without metabolic activation for 4 hours induced a mutation frequency of up to 126.9 mutants/10E+06 cells thereby exceeding slightly the GEF in a dose-dependent manner. The second experiment did not confirm mutagenicity of the test substance: exposure to up to 500 µg/mL for 4 hours did not result in a dose-dependent increase in mutation frequencies exceeding the GEF. Similar results were found after long-term exposure for 24 h. In conclusion, Fatty acids, C16-18 (even numbered), aluminum salt is considered to be non-mutagenic in the conducted study.

Chromosome aberrations

No studies are available on clastogenic properties toxicity of Fatty acids, C16-18 (even numbered), aluminum salt. However, there are reliable data on analogue substances which are considered suitable for read-across. According to the general rules defined in Regulation (EC) No. 1907/2006, Annex XI, Item 1.5 for the grouping of substances and read-across approach, similarities between substances may be based on “common functional groups” and “common precursors and/or the likelihood of common breakdown products via physical and biological processes, which result in structurally similar chemicals”. Bonds between metal salts and carboxylic acids are known to readily dissociate into the corresponding metal and carboxylic acid in the ambient environment (at neutral pH) and in the digestive tract (at low pH) where complete dissociation occurs, as determined for aluminium di- and tristearate in the US HPV Chemical Challenge Program (2007). Thus, nearly complete dissociation of aluminum fatty acid salts into aluminium, stearic (C18) and/or palmitic (C16) acid is expected to occur in the digestive tract after oral ingestion thereby indicating that toxicity of Fatty acids, C16-18 (even numbered), aluminum salt can be evaluated based on reliable data for the dissociation products and structural analogues of those. The first dissociation product, C16 and 18 fatty acids are stepwise degraded within the mitochondrium matrix by β (–) Oxidation in which C2 units are released (CIR, 1987). Therefore, read-across to saturated fatty acids of different chain length is feasible because of the likelihood of common breakdown products. The second dissociation product,aluminium exists in 4 different forms in the living organisms, including free ions, low-molecular-weight complexes, physically bound macromolecular complexes, and covalently bound macromolecular complexes (Ganrot 1986). As the pathways leading to toxic outcomes are mainly dominated by the chemistry and biochemistry of the aluminium ion (Al3+) (Krewski et al., 2007; ATSDR, 2008), different aluminium compounds may serve as surrogates for read-across to the free metal component of Fatty acids, C16-18 (even numbered), aluminum salt.

As noted in Regulation (EC) No. 1907/2006, Article 13 (1) "information on intrinsic properties of substances may be generated by means other than tests, provided that the conditions set out in Annex XI are met.” Information shall therefore be generated whenever possible by means other than vertebrate animal tests, which includes the use of information from structurally related or surrogate substances (grouping or read-across) “to avoid the need to test every substance for every endpoint”. For details on the read-across approach please refer to the analogue justification in section 13 of the technical dossier.

As no data are available on clastogenic properties ofFatty acids, C16-18 (even numbered), aluminum salts, read-across to reliable data on the analogue and surrogate substances aluminium hydroxide (CAS 21645-51-2) and docosanoic acid (CAS 112-85-6) was performed.

A GLP-compliant mammalian erythrocyte micronucleus test according to OECD guideline 474 was performed with aluminium hydroxide (Covance Laboratories Ltd., 2010). 6 male Sprague Dawley rats received 500, 1000 and 2000 mg test substance /kg bw/day viaoral gavage in two doses 24 hours apart.Control animals received either the concurrent vehicle (carboxymethylcellulose in deionised water (1% CMC)) or 20 mg/kg bw cyclophosphamide as positive control substance. A bone marrow sample was collected 24 hours after the final test substance administration. No signs of systemic toxicity were observed. Mean values of micronuclei frequency were comparable among the different treatment groups. Animals of the positive control group showed a statistically significant increase in the micronuclei frequency. Thus, aluminium hydroxide administered to male rats at doses up to the maximum recommended dose of 2000 mg/kg bw/day did not induce micronuclei in bone marrow polychromatic erythrocytes.


Docosanoic acid was tested in a guideline study according to OECD 473 (Nakajima, 2002). Properly maintained chinese hamster lung cells were exposed to docosanoic acidat concentrations of 875, 1750 and 3500 µg/mL for 6 hours with and without metabolic activation. In addition, cells were treated with 350, 700, 1400, 2800 µg/mL without metabolic activation for 24 hours and with 288, 575, 1150 and 2300 µg/mL without metabolic activation for 48 hours, respectively.The test item induced cytotoxicity at the highest concentration used after 24 and 48 hours of exposure. No difference in the aberration rate or polyploidy was determined up to the maximum concentrations compared to control plates after short- and long-term exposures.



Taken the available mentioned data on Fatty acids, C16-18 (even numbered), aluminum salt and read-across substances into account, genotoxic effects after exposure to Fatty acids, C16-18 (even numbered), aluminum salt are considered to be non-genotoxic. 

References not included in IUCLID:

ATSDR (Agency for Toxic Substances and Disease Registry) (2008).Toxicological Profile for Aluminum.Atlanta: Department of Health and Human Services, Public Health Service.

CIR (1987). Final report on the safety assessment of oleic acid, lauric acid, palmitic acid, myristic acid, stearic acid. J. of the Am. Coll. of Toxicol.6 (3): 321-401

Ganrot, P.O. (1986). Metabolism and possible health effects of aluminum. Environ Health Perspect 65:363-441.  


Krewski et al. (2007). Human Heaklth Risk Assessment for Aluminium, Aluminium Oxide, and Aluminium Hydroxide. J Toxicol Environ Heakth B Crit Rev 10(1):1-269

U.S. High Production Volume (HPV) Chemical Challenge Program (2007)

Justification for selection of genetic toxicity endpoint
No study was selected as hazard assessment was based on a weight of evidence from all available studies, which showed non-mutagenic potential of either the target substance or structural surrogates of dissociation products.

Short description of key information:
Gene mutation in bacteria: negative Ames test with S. typhimurium TA 98, TA 100, TA 102, TA 1535 and TA 1537 , with and without metabolic activation (OECD Guideline 471, GLP).

Cytogenicity: negative result in in vivo erythrocyte micronucleus test with the read-across substance aluminium hydroxide (OECD Guideline 474, GLP) and in in vitro mammalian chromosome aberration test in chinese hamster lung cells with the read-across substance docosanoic acid, with and without metabolic activation (OECD Guideline 473, GLP).

Gene mutation in mammalian cells: negative result in mouse lymphoma L5178Y cells, with and without metabolic activation (OECD Guideline 476, GLP).

Endpoint Conclusion: No adverse effect observed (negative)

Justification for classification or non-classification

The available data on genetic toxicity do not meet the classification criteria according to Regulation (EC) 1272/2008 or Directive 67/548/EEC, and are therefore conclusive but not sufficient for classification.