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EC number: 246-140-8 | CAS number: 24304-00-5
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- Ecotoxicological Summary
- Aquatic toxicity
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Endpoint summary
Administrative data
Key value for chemical safety assessment
Genetic toxicity in vitro
Description of key information
Aluminium nitride dissolves into aluminium and ammonia/ammonium ion. The Al compound is considered the relevant moiety for risk assessment. The genotoxic potential of aluminium is assessed by a weight of evidence approach regarding several in vitro and in vivo studies with various highly soluble aluminium compounds. In summary these studies are considered negative with respect to genotoxicity, therefore aluminium nitride is considered to be not genotoxic.
Link to relevant study records
- Endpoint:
- in vitro DNA damage and/or repair study
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- weight of evidence
- Justification for type of information:
- For details and justification of read-across please refer to the read-across report attached to IUCLID section 13.
- Reason / purpose for cross-reference:
- read-across source
- Species / strain:
- other: Human Jurkat T-lymphocytes
- Metabolic activation:
- without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- cytotoxicity
- Vehicle controls validity:
- not applicable
- Untreated negative controls validity:
- valid
- True negative controls validity:
- not examined
- Positive controls validity:
- valid
- Conclusions:
- Aluminum chloride solution is considered to be non-mutagenic in a Comet assay.
- Executive summary:
In an in vitro Comet assay, human Jurkat T-lymphocyte cells cultured in vitro were exposed to aluminum chloride solution at concentrations of 0.05, 0.1, 0.5, 1.0 and 5 mM in the absence of mammalian metabolic acivation.
For assessment of cytotoxicity, apoptosis, cell proliferation and cell viability were measured. Aluminum chloride induced >50% caspase-9 positive cells at 5 mM concentration. Aluminum chloride solution showed no effects on cell proliferation and cell viability at the concentrations tested. No significant increase of DNA damage, measured by using an index of DNA damage (IDD, average tail lenghth of 50 cells) were observed.
Therefore, Aluminum chloride solution is not genotoxic in the Comet assay.
This information is used in a read-across approach in the assessment of the target substance. For details and justification of read-across please refer to the read-across report attached to IUCLID section 13.
- Endpoint:
- in vitro DNA damage and/or repair study
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- weight of evidence
- Justification for type of information:
- For details and justification of read-across please refer to the read-across report attached to IUCLID section 13.
- Reason / purpose for cross-reference:
- read-across source
- Species / strain:
- bacteria, other: Bacillus subtilis
- Metabolic activation:
- without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- not specified
- Vehicle controls validity:
- not specified
- Untreated negative controls validity:
- not specified
- True negative controls validity:
- not specified
- Positive controls validity:
- valid
- Conclusions:
- Under the described test conditions, the test compound AlCl3 is considered to be negative in the Bacillus subtilis Rec Assay.
- Executive summary:
In a Bacillus subtilis Rec Assay, the strain H17 Rec+ (rec+ arg try) and M45Rec- (rec45 arg try) were exposed to aluminum chloride. Only minor information were presented about the test compound concentration, the solubility and the used solvent/vehicle. Moreover, it is not clear, if postive controls were used during the test . Due to the simplicicity of the assay and the well described protocol of Rec Assay it can nevertheless be stated, that under the decribed test conditions, the test compound aluminum chloride is considered to be negative in the Bacillus subtilis Rec Assay.
This information is used in a read-across approach in the assessment of the target substance. For details and justification of read-across please refer to the read-across report attached to IUCLID section 13.
- Endpoint:
- in vitro cytogenicity / micronucleus study
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- weight of evidence
- Justification for type of information:
- For details and justification of read-across please refer to the read-across report attached to IUCLID section 13.
- Reason / purpose for cross-reference:
- read-across source
- Species / strain:
- lymphocytes: human
- Metabolic activation:
- without
- Genotoxicity:
- other: The results obtained are considered not biologically relevant.
- Cytotoxicity / choice of top concentrations:
- no cytotoxicity
- Vehicle controls validity:
- not applicable
- Untreated negative controls validity:
- valid
- True negative controls validity:
- not examined
- Positive controls validity:
- valid
- Additional information on results:
- N.A.
- Conclusions:
- The results obtained in the in vitro mammalian cell micronucleus test after treatment with aluminum sulfate are considered not biologically relevant. In certain dose groups a slight increase in micronuclei frequency was observed in comparison to the untreated control, but no dose relationship was observed.
- Executive summary:
In a mammalian cell micronucleus test conducted similar to OECD guideline 487, human lymphocytes were exposed in vitro to aluminum sulfate at concentrations of 0, 500, 1000, 2000 and 4000 µM without metabolic activation for 48 hours.
Micronuclei frequency was counted in 2000 cells for each concentration of each donor, showing a slight increase in micronucleus frequency. This increase is considered not biologically relevant, as in both donor blood experiments no dose-relationship was observed (the micronucleus frequency of the highest dose tested in donor 1 was even below the negative control values). The positive controls did induce distinct and biologically relevant increases of the micronucleus frequency. Under the test conditions, aluminum sulfate induced micronuclei without a dose relationship in human lymphocytes.The results show a certain degree of variability between the two donors and question the relevance of the slight increase of micronuclei frequency. Moreover, the dose levels used induced no apparent toxicity (change in frequency of binucleate cells) and no relationship between toxicity, dose and the level of micronucleated cells was observed.
This information is used in a read-across approach in the assessment of the target substance. For details and justification of read-across please refer to the read-across report attached to IUCLID section 13.
- Endpoint:
- in vitro gene mutation study in mammalian cells
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- weight of evidence
- Justification for type of information:
- For details and justification of read-across please refer to the read-across report attached to IUCLID section 13.
- Reason / purpose for cross-reference:
- read-across source
- Species / strain:
- mouse lymphoma L5178Y cells
- Metabolic activation:
- without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- cytotoxicity
- Vehicle controls validity:
- valid
- Untreated negative controls validity:
- not examined
- Positive controls validity:
- valid
- Additional information on results:
- TEST-SPECIFIC CONFOUNDING FACTORS
- Effects of pH: after adding the chemical to the medium, a dramatic change in pH occured over the 4h expression period - Remarks on result:
- other: all strains/cell types tested
- Conclusions:
- The test substance AlCl3 did not induce gene mutation in the TK locus in L5178Y mouse lymphoma cells under the tested experimental conditions.
- Executive summary:
In a mammalian cell gene mutation assay conducted similar to OECD guideline 490, L5178Y mouse lymphoma cells cultured in vitro were exposed to AlCl3, solved in water, at concentrations of 570, 580, 590, 600, and 625 µg/mL in the absence of mammalian metabolic activation. The induced mutation frequencies without metabolic activation were not increased by more than 2 fold in comparison to the untreated control, except the 625 µg/mL dose group dose with a 2.2 fold increase. The results of the mutant frequencies did not fulfill the criteria for a positive study result outcome. The positive control did induce the appropriate response.
In summary, the test item AlCl3 did not induce gene mutation in L51178Y mouse lymphoma cells.
This study is classified as acceptable and satisfies the requirement for test guideline OECD 490 for in vitro mutagenicity (mammalian forward gene mutation) data.
This information is used in a read-across approach in the assessment of the target substance. For details and justification of read-across please refer to the read-across report attached to IUCLID section 13.
- Endpoint:
- genetic toxicity in vitro, other
- Remarks:
- review article - results of various in vitro and in vivo studies are reported
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- weight of evidence
- Justification for type of information:
- For details and justification of read-across please refer to the read-across report attached to IUCLID section 13.
- Reason / purpose for cross-reference:
- read-across source
- Remarks on result:
- other: Report is a review article
- Conclusions:
- Based on the results it can be stated that aluminum compounds are not genotoxic in the absence of cytotoxicity.
- Executive summary:
In a review article by Krewski et al., 2007 several in vitro studies regarding the genotoxic potential of aluminum compounds are summarized. Some early studies reported chromosome aberrations upon aluminum chloride exposure, i.e. in spermatocytes of grasshoppers (10 mg/0.21 g bw, Manna and Parida, 1965), in mammalian peritoneal cells (Nashed et al., 1975) and bone marrow cells (0.1 M aluminum chloride 1 mL/30 g bw, acute ip. dose, Manna and Das, 1972). More recently, Roy et al., 1990 reported micronuclei formation and sister chromatic exchange upon 11.6 µmol/mL aluminum chloride in human blood lymphocytes. Stimulation of chromosomal protein crosslinking by aluminum chloride has been reported by Wedrychowski et al., 1986a, and 1986b in ascites hepatoma cells from Sprague-Dawley rats. No crosslinking, in either cytotoxic or non-cytotoxic concentrations of aluminum chloride could be seen in Burkitt human lymphoma cells transformed with an Epstein-Barr virus (Costa et al., 1996).
In bacteria, aluminium compounds have been considered to be non-mutagenic. At concentrations of 1 to 10 mM, Al2O3, AlCl3 and Al2(SO4)3 were negative in the REC-assay with Bacillus subtilis (Kada et al, 1980). The absence of mutagenic effects of aluminium compounds on various bacterial strains including Salmonella typhimurium and Escherichia coli demonstrated in earlier studies has been supported by the findings of more recent studies (Marzin & Phi 1985, Shimizu et al. 1985).
In the study by Oberly et al., 1982 aluminum chloride did not induce forward mutations at the thymidine kinase locus in the mouse lymphoma assay (see IUCLID entry in section 7.6.1 for details).
Importantly, two in vitro studies (Migliore et al, 1999 and Banasik et al., 2004) found genotoxic effects of aluminum compounds only concomitant to cytotoxicity (see IUCLID entries in section 7.6.1 for details).
The cell toxicity of aluminum prior genotoxic effects is supported by the Caicedo et al., 2007 (see IUCLID entry in section 7.6.1 for details) who analyzed the DNA damage provoked by the aluminum metal ion in human Jurkat T-cells. The study used aluminum concentrations of 0.05, 0.1, 0.54, 1 and 5 mM for 48 hours; DNA damage was assessed by single cell electrophoresis (comet assay). Only the highest concentration of 5 mM induced significant DNA damage, concomitant with apoptosis rates exceeding 50 percent. Another comet assay study by Lankoff et al., 2006 used aluminum chloride in doses of 1, 2, 5, 10 and 25 µg/ml exposing human peripheral blood lymphocytes for 72 hours. Olive tail moments increased in association with apoptosis up to a concentration of 10 µg/mL aluminum chloride, while the highest concentration had lower values of the olive tail moment together with an apoptosis rate greater 20 percent.
Based on the results it can be stated that aluminum compounds are not genotoxic in the absence of cytotoxicity and the author stated, that in agreement with their non-carcinogenic activity, aluminum compounds failed to show positive results in most short-term and animal experiments to determine genotoxic potential of aluminum compounds lead to contradictory results with a suggestion of an anti-genotoxic potential.
This information is used in a read-across approach in the assessment of the target substance. For details and justification of read-across please refer to the read-across report attached to IUCLID section 13.
- Endpoint:
- in vitro gene mutation study in bacteria
- Type of information:
- read-across from supporting substance (structural analogue or surrogate)
- Adequacy of study:
- weight of evidence
- Justification for type of information:
- For details and justification of read-across please refer to the read-across report attached to IUCLID section 13.
- Reason / purpose for cross-reference:
- read-across source
- Species / strain:
- S. typhimurium TA 1535, TA 1537, TA 98 and TA 100
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- no cytotoxicity
- Vehicle controls validity:
- not examined
- Untreated negative controls validity:
- valid
- True negative controls validity:
- not examined
- Positive controls validity:
- valid
- Species / strain:
- S. typhimurium TA 1538
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- no cytotoxicity
- Vehicle controls validity:
- not examined
- Untreated negative controls validity:
- valid
- True negative controls validity:
- not examined
- Positive controls validity:
- valid
- Species / strain:
- E. coli WP2 uvr A
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- no cytotoxicity
- Vehicle controls validity:
- not examined
- Untreated negative controls validity:
- valid
- True negative controls validity:
- not examined
- Positive controls validity:
- valid
- Conclusions:
- No biologically relevant increase in the mutant count, in comparison with the negative control was observed under the descriped test conditions. Therefore, Ammonia is considered to be non-mutagenic with and without metabolic activation.
- Executive summary:
In a reverse gene mutation assay in bacteria, strains TA 98, TA 100, TA 1535, TA 1537 and TA 1538 of S. typhimurium and a strain of E. coli (WP2uvrA) were exposed to Ammonia (99.9%) at concentrations of 0, 500, 1000, 2500, 5000, 10000 and 25000 ppm per plate in the presence and absence of mammalian metabolic activation. The positive controls induced the appropriate responses in the corresponding strains. There was no evidence of induced mutant colonies over background.
This study is classified as acceptable. This study satisfies the requirement for Test Guideline OECD 471 for in vitro mutagenicity (bacterial reverse gene mutation) data.
This information is used in a read-across approach in the assessment of the target substance. For details and justification of read-across please refer to the read-across report attached to IUCLID section 13.
Referenceopen allclose all
TABLE 1: Concentrations of Metals Required to Induce a a Significant Harmful Effect (DNA Damage, Apoptosis, Viability, and Proliferation Inhibition) on T-Helper Jurkat Cells | |||||
Metal Concentrations (mM) |
DNA Damage |
Apoptosis | Viability | Proliferation Inhibition | Average Concentration of Four Parameters |
V | 0.05 | 0.05 | 1.0 | 0.05 | 0.29 |
Ni | 0.05 | 0.1 | 5.0 | 0.5 | 1.41 |
Co | 5.0 | 5.00 | 0.5 | 0.1 | 2.65 |
Cu | >5 | 0.5 | 5.0 | 0.1 | >2.65 |
Nb | >5 | 0.5 | 0.5 | >5 | >2.75 |
Mo | >5 | 1.0 | >5 | 0.5 | >2.87 |
Zr | 5.0 | 0.5 | 5.0 | >5 | >3.875 |
Be | >5 | 5.0 | 1.0 | 5.0 | >4 |
Cr | >5 | >5 | >5 | >5 | >5 |
Al | >5 | 5.0 | >5 | >5 | >5 |
Fe | >5 | 5.0 | >5 | >5 | >5 |
Significant effect: | |||||
DNA damage: IDD>75. | |||||
Apoptosis:>50% caspase 9-positive cells. | |||||
Viability: >50% PI-positive cells. | |||||
Proliferation inhibition: p<0.05 significance in metal-treated cells CPMs reduction compared to untreated controls. |
Table 1: Donor A_ Results
Chemical | Dose [µM] | BN scored | MN BN1 | MN BN/1000 +/-SD | BN (%)1 |
negative control | 0 | 2000 | 12 | 6.0 +/- 1.4 | 33.0 |
Griseofulvin | 43 | 2000 | 131 | 65.5 +/- 34.6*** | 22.7 |
Mitomycin C | 0.51 | 2000 | 121 | 60.5 +/- 12.0*** | 22.5 |
Al2(SO4)3 | 500 | 2000 | 14 | 7.0 +/- 2.8 | 21.2 |
1000 | 2000 | 23 | 11.5 +/- 2.1* | 25.0 | |
2000 | 2000 | 30 | 15.0 +/-1.4** | 27.5 | |
4000 | 2000 | 11 | 5.5 +/- 0.7 | 29.5 |
Table 2: Donor B_Results
Chemical | Dose [µM] | BN scored | MN BN1 | MN BN/1000 +/-SD | BN (%)1 |
negative control | 0 | 2000 | 8 | 4.0 +/- 1.4 | 45.6 |
Griseofulvin | 43 | 1555 | 46 | 29.4 +/- 0.8*** | 18.9 |
Mitomycin C | 0.51 | 2000 | 209 | 104.5+/- 7.8*** | 17.9 |
Al2(SO4)3 | 500 | 2000 | 19 | 9.5 +/- 3.5* | 47.2 |
1000 | 2000 | 28 | 14.0 +/-0.0*** | 46.7 | |
2000 | 2027 | 20 | 9.9 +/-3.0* | 53.2 | |
4000 | 2000 | 18 | 9.0 +/- 0.0* | 33.9 |
1: MN BN: number micronucleated binucleated cells, BN (%): binucleated cells/total cells
* Fishers exact test: *P<0.05, **P< 0.01, ***P<0.001
Table1: Mutagenic response after treatment with AlCl3
Chemical | Dose [µg/mL] | Percent total survival | Mutation frequency | Increase over solvent (-fold) |
Solvent | 0 | 100 | 2.5 | - |
EMS | 620 | 31 | 85.0 | 34.0 |
AlCl3 | 625 | 63 | 5.6 | 2.2 |
600 | 38 | 5.0 | 2.0 | |
590 | 42 | 4.9 | 2.0 | |
580 | 88 | 4.3 | 1.7 | |
570 | 69 | 5.0 | 2.0 |
Various studies cited in a review article.
Table 5: Mutagenic activity of Ammonia | |||||||||||||
No. Compound | Dose µg/plate | TA 100 | TA 1535 | WP2 uvrA | TA98 | TA 1537 | TA1538 | ||||||
-S9 | +S9 | -S9 | +S9 | -S9 | +S9 | -S9 | +S9 | -S9 | +S9 | -S9 | +S9 | ||
Control | 0 | 191.8 +/- 39.5a | 190.6 +/- 49.3 | 31.3 +/- 7.0 | 27.8 +/- 8.4 | 32 +/- 5.0 | 28.8 +/- 6.1 | 48.3 +/- 7.7 | 60.7 +/- 14.1 | 11.4 +/- 3.0 | 10.3 +/- 3.8 | 31.8 +/- 8.6 | 58.3 +/-14.2 |
2NF | 2 | 700 +/- 52.8 | -b | - | - | - | - | 503.3 +/-121.9 | - | - | - | 295.6 +/-46.5 | - |
ENNG | 5 | - | - | 1001.4 +/- 168.5 | - | 136.8 +/- 39.8 | - | - | - | - | - | - | - |
9AC | 80 | - | - | - | - | - | - | - | - | 745 +/-59.1 | - | - | - |
B(a)P | 5 | - | - | - | - | - | - | - | 546 +/- 29.8 | - | 96.8 +/-24.6 | - | 510.5 +/- 183.8 |
2.5 | - | 956.4 +/-212.4 | - | - | - | - | - | 389.5 +/- 43.3 | - | - | - | - | |
2AA | 4 | - | - | - | - | - | 132 +/-50.7 | - | - | - | - | - | - |
2 | - | - | - | 138.5 +/- 24.8 | - | - | - | - | - | - | - | - | |
Ammonia | 500 ppm | 243 | 229 | 25 | 31 | 36 | 31 | 64 | 63 | 11 | 9 | 13 | 37 |
1000 ppm | 251 | 220 | 23 | 40 | 32 | 33 | 56 | 76 | 13 | 7 | 27 | 59 | |
2500 ppm | 198 | 181 | 29 | 35 | 28 | 31 | 43 | 66 | 8 | 9 | 23 | 53 | |
5000 ppm | 207 | 195 | 20 | 21 | 33 | 28 | 43 | 53 | 10 | 6 | 34 | 55 | |
10000 ppm | 197 | 185 | 23 | 34 | 33 | 30 | 69 | 60 | 7 | 13 | 32 | 52 | |
25000 ppm | 227 | 220 | 19 | 31 | 19 | 20 | 57 | 68 | 13 | 10 | 25 | 40 |
a= mean +/- S.D.
b= not tested
2NF= 2 -nitrofluorene
ENNG= N-ethyl-N-nitro-N-nitrosoguandine
9AC= 9 -aminoacridine
B(a)P= benzo(a)pyrene
2AA= 2-aminoanthracene
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Additional information
No substance specific genotoxicity studies are available for aluminium nitride (target substance). The genotoxic potential of aluminium nitride is assessed by its dissolution products aluminium and ammonium ions. Ammonium is an endogenous compound, formed at concentrations of 79 mmol/kg bw/day. Therefore, the nitride component of aluminium nitride is considered to be of minor impact and negligible for the assessment of the genotoxicity. The genotoxic potential of aluminium nitride is thus based on the aluminium component and assessed by read across with aluminium salts, mainly aluminium chloride and aluminium sulfate. Due to a lower water solubility of aluminium nitride compared to the source substances the resulting bioavailability (toxicity potential) would also be expected to be lower. Therefore, the read-across to the source substances aluminium chloride and aluminium sulfate is adequately protective. Details on the read-across rational are provided in section 13.
Aluminium chloride was tested negative in the Bacillus subtilis Rec mutagenicity screening assay. This assay is detecting DNA damage, which is subjected to cellular recombination repair (Kada et al., 1980). Caicedo et al., 2007 reported, that aluminium chloride was tested negative in an in vitro Comet assay. Oberly et al., 1982 reported negative results in a L5178Y mouse lymphoma mutagenicity assay (OECD 476) using aluminium chloride. Two in vitro studies (Banasik et al., 2005 (in vitro MNT), Lima et al., 2007 (in vitro CA)) found genotoxic effects of aluminium chloride only concomitant to severe cytotoxicity. The positive effect is not considered relevant due to the increased cytotoxicity, disqualifying a distinction of genotoxic from cell toxic events.
In a mammalian cell micronucleus test conducted similar to OECD guideline 487, human lymphocytes were exposed in vitro to aluminium sulfate at concentrations of 0, 500, 1000, 2000 and 4000 µM without metabolic activation for 48 hours. The results revealed a slight increase in micronucleus frequency. As in both blood donor experiments no dose-relationship was observed (the micronucleus frequency of the highest dose tested in donor 1 was even below the negative control values). Overall, the results are considered ambiguous due to the before mentioned reasons.
Supporting data was received by the review article by Krewski et al., 2007. In a weight of evidence evaluation of the data presented by Krewski, it can be stated, that aluminium compounds are not genotoxic in the absence of cytotoxicity.
As above explained, the nitride component of aluminium nitride is considered to be of minor impact and negligible for the assessment of the genotoxicity of aluminium nitride. Nevertheless, one study by Shimizu et al., 2005 is available, in which ammonia was tested negative in a reverse gene mutation assay in bacteria (OECD 471).
In summary of the available data from various read-across partners with higher solubility compared to AlN, no genotoxic effects at non-cytotoxic concentrations were observed. Therefore, it can be concluded that aluminium nitride can be considered as not genotoxic.
Justification for classification or non-classification
Based on data from soluble aluminium compounds, aluminium nitride is considered negative regarding mutagenicity.
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