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EC number: 247-852-1 | CAS number: 26628-22-8
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Endpoint summary
Administrative data
Key value for chemical safety assessment
Genetic toxicity in vitro
Description of key information
Sodium azide was found to be genotoxic without and with metabolic activation only in Salmonella typhimurium strains TA100 and TA1535, but not in TA98, TA1537, and TA1538 (NTP, 1991; De Flora, 1981). The mutagenic effect of sodium azide in Salmonella typhimurium is specific to strains, which possess a certain histidine mutation (his G 46) (Owais 1988, Olsen 1993, Shelton 1994). Lesions are caused by the conversion of azide to the proximal mutagen β-L-azidoalanine (Owais 1988). L-azidoalanine appears to be formed by the action of O-acetylserine (thiol)-lyase using O-acetylserine and azide as substrates. In both plants and bacteria tested, azide substitutes for the natural substrate sulfide in this reaction (Owais and Kleinhofs, 1988, see IUCLID section 7.6.1).
Mammalian cells lack the O-acetylserine (thiol)-lyase activity and cannot synthesize L-azidoalanine. A search for the metabolite in animal cells has been negative (Owais and Kleinhofs, 1988). Therefore, this metabolic pathway is not relevant for human risk assessment.
The lack of genotoxicity is further supported by experimental data. No chromosomal aberrations or unscheduled DNA synthesis were observed in human lymphocytes and in Chinese hamster ovary cell line CHO cells (NTP 1991, Sander 1978, Slamenova 1980). Moreover, in a 6-thioguanine mutation assay with the mammalian CHO cell line no increased mutation rates were observed after treatment with sodium azide (Slamenova, 1980). Results of three studies on sister chromatide exchange (SCE) rates are available. In one study for SCE in CHO cells treatment with sodium azide yielded a positive result (NTP, 1991). In contrast, Arenaz & Nilan, 1981 reported negative results for SCE in CHO cells and in human lymphocytes. The absence of a genotoxic effect in nearly all mammalian test systems is consistent with the lack of evidence of carcinogenic activity in the 2-year NTP bioassay conducted with F344/N rats receiving oral gavage dose of sodium azide (NTP, 1991).
Link to relevant study records
- Endpoint:
- in vitro gene mutation study in mammalian cells
- Type of information:
- experimental study
- Adequacy of study:
- weight of evidence
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- test procedure in accordance with national standard methods with acceptable restrictions
- Qualifier:
- equivalent or similar to guideline
- Guideline:
- OECD Guideline 476 (In Vitro Mammalian Cell Gene Mutation Test)
- Deviations:
- yes
- Remarks:
- no metabolic activation, no statistic examination performed
- GLP compliance:
- no
- Type of assay:
- other: in vitro gene mutation study in mammalian cells
- Target gene:
- no data
- Species / strain / cell type:
- Chinese hamster lung fibroblasts (V79)
- Details on mammalian cell type (if applicable):
- - Type and identity of media: MEM Eagle with 10% calf serum, 2.5% FCS, penicillin (200 U/mL) and streptomycin (100 µg/mL)
- Properly maintained: yes
- Periodically checked for Mycoplasma contamination: yes
- Periodically checked for karyotype stability: no data
- Periodically "cleansed" against high spontaneous background: no data - Metabolic activation:
- without
- Test concentrations with justification for top dose:
- 20-h treatment: 0, 30, 100, 300 µg/mL
60-min treatment: 0, 10 ,25, 50 µg/mL - Vehicle / solvent:
- 20-h treatment: MEM medium
60-min treatment: PBS pH 5.3 - Untreated negative controls:
- no
- Negative solvent / vehicle controls:
- no
- True negative controls:
- no
- Positive controls:
- yes
- Positive control substance:
- other: UV irradiation
- Details on test system and experimental conditions:
- no data
- Evaluation criteria:
- no data
- Statistics:
- no data
- Species / strain:
- Chinese hamster lung fibroblasts (V79)
- Metabolic activation:
- without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- not determined
- Vehicle controls validity:
- not examined
- Untreated negative controls validity:
- not examined
- Positive controls validity:
- valid
- Additional information on results:
- TEST-SPECIFIC CONFOUNDING FACTORS
- Effects of pH: the observed cytotoxicity of sodium azide was substantially increased with lower pH as found in human fibroblasts
- Conclusions:
- In Chinese hamster cells, neither 20-h treatment in medium nor 60-min treatment in an acidic environment lead to significantly increased occurrence of 6-thioguanine resistant mutations. The results of the DNA-synthesis inhibition test, as well as the mutagenicity testing, do not suggest the possibility that treatment with sodium azide might induce DNA-damage in the observed human and Chinese hamster cells. The cytostatic effect of sodium azide on the fibroblasts studied is probably not accompanied by a genotoxic effect.
- Executive summary:
In a mammalian cell gene mutation assay, Chinese hamster cells (V79) were exposed to sodium azide at concentrations of 0,10 ,25, 50 µg/mL during a 60 -min treatment in an acidic environment and 0, 30, 100, 300 µg/mL for a 20 -h treatment in medium. This assay was conducted in absence of mammalian metabolic activation. In Chinese hamster cells, neither 20 -h treatment in medium nor 60 -min treatment in an acidic environment lead to significantly increased occurrence of 6 -thioguanine resistant mutations. The results of the DNA-synthesis inhibition test, as well as the mutagenicity testing, do not suggest the possibility that treatment with sodium azide might induce DNA-damage in the observed human and Chinese hamster cells. The cytostatic effect of sodium azide on the fibroblasts studied is probably not accompanied by a genotoxic effect. Moreover, it has to be highlighted, that the study was not conducted to sufficiently high-test concentrations. Therefore, the negative results should be interpretated under reservation.
- Endpoint:
- in vitro gene mutation study in bacteria
- Type of information:
- experimental study
- Adequacy of study:
- weight of evidence
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- test procedure in accordance with national standard methods with acceptable restrictions
- Qualifier:
- equivalent or similar to guideline
- Guideline:
- OECD Guideline 471 (Bacterial Reverse Mutation Assay)
- Deviations:
- yes
- Remarks:
- only 4 strains tested, information on bacterial cultures, substance preparation/storage insufficient
- GLP compliance:
- not specified
- Type of assay:
- bacterial reverse mutation assay
- Specific details on test material used for the study:
- - Name of test material (as cited in study report): sodium azide
- Substance type: powder
- Source of test material: Radian Corporation, Austin, TX.
- Physical state: solid
- Analytical purity: >99%
- Lot/batch No.: 32880
- Stability under test conditions: Sodium azide was stable as a bulk chemical for at least 2 weeks at up to 60°C when protected from light.
- Storage condition of test material: Stored at room temperature in the dark. - Target gene:
- hisitidine
- Species / strain / cell type:
- S. typhimurium TA 1535, TA 1537, TA 98 and TA 100
- Additional strain / cell type characteristics:
- not specified
- Metabolic activation:
- with and without
- Metabolic activation system:
- S9 mix (from Arochlor 1254-induced male Sprague Dawley rat or Syrian hamster liver)
- Test concentrations with justification for top dose:
- 0.03 / 0.1 / 0.3 / 1.0 / 3.3 / 10.0 / 33.3 µg/plate
- Vehicle / solvent:
- - Vehicle(s)/solvent(s) used: buffer
- Justification for choice of solvent/vehicle: not given - Untreated negative controls:
- yes
- Negative solvent / vehicle controls:
- yes
- Positive controls:
- yes
- Positive control substance:
- other: 4-nitro-o-phenylendiamine (TA98), sodium azide (TA100 and TA1535), 9-aminoacridine (TA1537)
- Remarks:
- without metabolic activation
- Untreated negative controls:
- yes
- Negative solvent / vehicle controls:
- yes
- Positive controls:
- yes
- Positive control substance:
- other: 2-aminoanthracene
- Remarks:
- with metabolic activation
- Details on test system and experimental conditions:
- METHOD OF APPLICATION: in buffer or S9-mix
DURATION
- Exposure duration: 20 minutes
- Expression time (cells in growth medium): 48h
- Evaluation criteria:
- no data
- Statistics:
- no data
- Species / strain:
- S. typhimurium TA 102
- Metabolic activation:
- with and without
- Genotoxicity:
- not determined
- Cytotoxicity / choice of top concentrations:
- not determined
- Vehicle controls validity:
- not examined
- Untreated negative controls validity:
- not examined
- True negative controls validity:
- not examined
- Positive controls validity:
- not examined
- Species / strain:
- S. typhimurium TA 100
- Metabolic activation:
- with and without
- Genotoxicity:
- positive
- Cytotoxicity / choice of top concentrations:
- not specified
- Vehicle controls validity:
- valid
- Positive controls validity:
- valid
- Species / strain:
- S. typhimurium TA 1535
- Metabolic activation:
- with and without
- Genotoxicity:
- positive
- Cytotoxicity / choice of top concentrations:
- not specified
- Vehicle controls validity:
- valid
- Positive controls validity:
- valid
- Species / strain:
- S. typhimurium TA 1537
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- not specified
- Vehicle controls validity:
- valid
- Positive controls validity:
- valid
- Species / strain:
- S. typhimurium TA 98
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- not specified
- Vehicle controls validity:
- valid
- Positive controls validity:
- valid
- Additional information on results:
- no data
- Conclusions:
- Sodium azide (dose range of 0.03 to 33.3 µg/plate) produced a strong, dose-related increase in mutant colonies in Salmonella thyphimurium strains TA100 and TA1535 when tested in a preincubation protocol with/without Aroclor 1254-induced male Sprague-Dawley rat or Syrian hamster liver S9; no mutagenic activity was observed in strains TA1537 or TA98 with/without S9.
- Executive summary:
Sodium azide was nominated by the National Cancer Institute for evaluation of its carcinogenic activity because of the high potential for human exposure and the lack of adequate carcinogenicity testing. Besides subacute, subchronic acid chronic in vivo studies in rats, the genetic toxicity was evaluated by testing the ability of the chemical to induce mutations in various strains of Salmonella thyphimurium.
Sodium azide (dose range of 0.03 to 33.3 µg/plate) produced a strong, dose-related increase in mutant colonies in S. thyphimurium strains TA100 and TA1535 when tested in a preincubation protocol with/without Aroclor1254-induced male Sprague-Dawley rat or Syrian hamster liver S9; no mutagenic activity was observed in strains TA1537 or TA98 with/without S9.
- Endpoint:
- in vitro DNA damage and/or repair study
- Type of information:
- experimental study
- Adequacy of study:
- supporting study
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- test procedure in accordance with national standard methods with acceptable restrictions
- Qualifier:
- equivalent or similar to guideline
- Guideline:
- OECD Guideline 479 (Genetic Toxicology: In Vitro Sister Chromatid Exchange Assay in Mammalian Cells)
- Deviations:
- yes
- Remarks:
- : no metabolic activation, highest concentration shows no clear sign of toxicity
- GLP compliance:
- not specified
- Type of assay:
- sister chromatid exchange assay in mammalian cells
- Target gene:
- no data
- Species / strain / cell type:
- Chinese hamster Ovary (CHO)
- Details on mammalian cell type (if applicable):
- - Type and identity of media: Mc Coys 5A medium + 15% FCS + 0.1% gentamycin
- Additional strain / cell type characteristics:
- not specified
- Species / strain / cell type:
- lymphocytes: human
- Details on mammalian cell type (if applicable):
- - Type and identity of media: Gibco chromosome medium 1A, supplemented with phytohemagglutin
- Metabolic activation:
- without
- Test concentrations with justification for top dose:
- lymphocytes: 1h exposure: 0.5 mM - 50 mM mol/L
lymphocytes: 4h exposure: 0.1 µM - 100 µM mol/L
CHO Cells: 2h exposure: 0.5 µM - 1 mM mol/L - Vehicle / solvent:
- - Vehicle(s)/solvent(s) used: physiol. saline, pH 6.8
- Untreated negative controls:
- yes
- Negative solvent / vehicle controls:
- not specified
- True negative controls:
- no
- Positive controls:
- yes
- Positive control substance:
- mitomycin C
- Remarks:
- 0.05 µg/mL
- Details on test system and experimental conditions:
- CHO:
METHOD OF APPLICATION: in medium
- Cell density at seeding (if applicable): ~5 X10^5
DURATION
- Preincubation period: 24 hours
- Exposure duration: 2 hours
- Fixation time (start of exposure up to fixation or harvest of cells): Deduced 24 hours
SPINDLE INHIBITOR (cytogenetic assays): Colcemid
STAIN (for cytogenetic assays): Giemsa (Perry and Wolff 1974)
NUMBER OF REPLICATIONS: One
METHODS OF SLIDE PREPARATION AND STAINING TECHNIQUE USED: Not specified except by reference (Perry and Wolff 1974)
NUMBER OF METAPHASE SPREADS ANALYSED PER DOSE (if in vitro cytogenicity study in mammalian cells): 49 - 51
DETERMINATION OF CYTOTOXICITY
- Method: Only indicated cultures with lethality
Human lymphocytes:
METHOD OF APPLICATION: in medium
DURATION
- Preincubation period: 48 hours
- Exposure duration: 1 or 4 hours
- Fixation time (start of exposure up to fixation or harvest of cells): Deduced 48 hours
SPINDLE INHIBITOR (cytogenetic assays): Colcemid
STAIN (for cytogenetic assays): Giemsa (Perry and Wolff 1974)
NUMBER OF REPLICATIONS: 2 - 3
METHODS OF SLIDE PREPARATION AND STAINING TECHNIQUE USED: Not specified except by reference (Perry and Wolff 1974)
NUMBER OF METAPHASE SPREADS ANALYSED PER DOSE (if in vitro cytogenicity study in mammalian cells): 40 - 120 (number of cells evaluated for all the replication tests) - Evaluation criteria:
- no data
- Statistics:
- not specified
- Species / strain:
- Chinese hamster Ovary (CHO)
- Metabolic activation:
- without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- cytotoxicity
- Remarks:
- Lethal at 5 X 10^-5 M and above
- Vehicle controls validity:
- valid
- Untreated negative controls validity:
- not examined
- Positive controls validity:
- valid
- Species / strain:
- lymphocytes: human
- Metabolic activation:
- without
- Genotoxicity:
- positive
- Remarks:
- slightly but significantly increased. However, the increase was probably due to the inhibition by azide of catalase and peroxidase which would lead to an increase in H2O2, a known inducer of SCEs.
- Cytotoxicity / choice of top concentrations:
- not specified
- Vehicle controls validity:
- valid
- Untreated negative controls validity:
- not examined
- Positive controls validity:
- valid
- Species / strain:
- lymphocytes: human
- Metabolic activation:
- without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- not specified
- Vehicle controls validity:
- valid
- Untreated negative controls validity:
- not examined
- Positive controls validity:
- valid
- Additional information on results:
- CHO cells:
- No increase in SCE after 2h exposure of CHO cells with concentrations from 0.5 µM - 10 µM.
- Cytotoxicity observed in CHO cells at concentrations exceeding 50 µM.
Lymphocytes:
- Slight but significant increase of SCE at 1h exposure to 50 mM.
- No increase in SCE of human lymphocytes after 4h exposure up to 100 µM. - Remarks on result:
- other: 2h treatment
- Conclusions:
- The data suggest, that sodium azide does not interact with DNA in a manner that either produces SCEs in CHO cells. A slight but significant increase of SCEs in human lymphocytes has been observed after 1h incubation with 50 mM sodium azide. However, this increase was probably due to the inhibition by azide of catalase and peroxidase, which would lead to an increase in H2O2, a known inducer of SCEs.
- Executive summary:
Previous reports from this laboratory and others indicate that sodium azide is a unique mutagen. It is highly mutagenic in S. typhimurium TA1530 as well as in barley, rice, peas, and yeast. However, azide apparently does not produce chromosome breaks in barley, vicia or human lymphocytes.
In a mammalian cell cytogenetics assay (Sister-chromatid exchanges, SCE), human whole blood or Chinese hamster K1 (CHO) cells were exposed for 1, 2, or 4 h respectively to various concentrations of sodium azide ranging from 10^-7 to 5 x 10^-2 M in the absence of metablic activation. Cells were harvested and chromosomes stained by the FPG technique. In human lymphocytes, concentrations above 10^-4 induced lethality (after 4h treatment) whereas CHO cells were sensitive to concentrations up to 10^-5M. The lower concentrations of azide produced no significant increase in SCE frequency above controls; only in the highest concentration of the 1h treatment group (50 mM) a slight increase of SCE could be seen. Concurrent mitomycin C treatments produced significant increases in SCE levels. The presented data suggest, that this highly mutagenic compound does not interact with DNA in a manner that either produces chromosome aberrations or SCEs. Thus, azide appears to be unique among mutagenic compounds. In fact, it has been suggested that azide acts strictly as a base substitution mutagen. It has been reported that azide requires metabolic activation in both barley and S. typhimurium. To date, however no mutagenic metabolite has been detected in mammalian cells.
- Endpoint:
- genetic toxicity in vitro, other
- Remarks:
- Type of genotoxicity: other: metabolic activation to proximate carcinogen
- Type of information:
- experimental study
- Adequacy of study:
- supporting study
- Reliability:
- 4 (not assignable)
- Rationale for reliability incl. deficiencies:
- secondary literature
- Qualifier:
- no guideline available
- GLP compliance:
- no
- Type of assay:
- other: mechanistic study
- Species / strain / cell type:
- not specified
- Vehicle / solvent:
- no data
- Details on test system and experimental conditions:
- no data
- Evaluation criteria:
- no data
- Statistics:
- no data
- Additional information on results:
- Inorganic azide mutagenicity is mediated through a metabolically synthesized organic azide, L-azidoalanine. L-Azidoalanine appears to be formed by the action of O-acetylserine (thiol)-lyase (EC 4.2.99.8) using O-acetylserine and azide as substrates. In both plants and bacteria tested, azide substitutes for the natural substrate sulfide in this reaction. In whole animal tests, azide was ineffective in inducing dominant lethals in rats at concentrations up to 10 mg/kg/day or in inducing sperm head abnormalities. Azide has also been reported as non-carcinogenic.
Animal cells are known to synthesize L-cysteine from L-methionine rather than from inorganic sulfide and O-acetylserine. Thus, they lack the O-acetylserine (thiol)-lyase activity and could not synthesize L-azidoalanine. A search for the metabolite in animal cells has been negative.
Azide (L-azidoalanine) mutagenesis is highly attenuated by a deficiency in the excision of UV-like DNA damage (uvr-). Thus a premutation lesion recognizable by the bacterial excision-repair enzymes must be formed. Mutagenesis appears to proceed from this by 'direct mispairing' pathway. Azide (L-azidoalanine) mutagenicity is highly specific and involves a stereoselective process as D-azidoalanine exhibits a lower mutagenicity as the L-form, but the molecular nature of the specificity has not been determined. - Remarks on result:
- other: For detailed information on the mode of action please refer to box " Additional information on results"
- Conclusions:
- Azide (L-azidoalanine) mutagenicity is highly specific and involves a stereoselective process as D-azidoalanine exhibits a lower mutagenicity as the L-form, but the molecular nature of the specificity has not been determined.
- Executive summary:
Inorganic azide mutagenicity is mediated through a metabolically synthesized organic azide, L-azidoalanine. L-Azidoalanine appears to be formed by the action of O-acetylserine (thiol)-lyase (EC 4.2.99.8) using O-acetylserine and azide as substrates. In both plants and bacteria tested, azide substitutes for the natural substrate sulfide in this reaction. In whole animal tests, azide was ineffective in inducing dominant lethals in rats at concentrations up to 10 mg/kg/day or in inducing sperm head abnormalities. Azide has also been reported as non-carcinogenic.
Animal cells are known to synthesize L-cysteine from L-methionine rather than from inorganic sulfide and O-acetylserine. Thus, they lack the O-acetylserine (thiol)-lyase activity and could not synthesize L-azidoalanine. A search for the metabolite in animal cells has been negative.
Azide (L-azidoalanine) mutagenesis is highly attenuated by a deficiency in the excision of UV-like DNA damage (uvr-). Thus a premutation lesion recognizable by the bacterial excision-repair enzymes must be formed. Mutagenesis appears to proceed from this by 'direct mispairing' pathway. Azide (L-azidoalanine) mutagenicity is highly specific and involves a stereoselective process, but the molecular nature of the specificity has not been determined.
Referenceopen allclose all
The results show that sodium azide will not induce increased occurrence of 6-thioguanine resistant colonies.
Table 1: Mutagenicity of sodium azide in Salmonella thyphimurium
Stain | Dose (µg/plate) | Revertants / plate a | |||||||
- S9mix | + 10% hamster S9 | + 10% rat S9 | |||||||
Trial 1 | Trial 2 | Trial 1 | Trial 2 | Trial 1 | Trial 2 | ||||
TA100 | 0 | 102±5.3 | 112±1.7 | 108±9.7 | 115±8.2 | 111±8.1 | |||
0.03 | 167±20 | ||||||||
0.1 | 255±9.2 | ||||||||
0.3 | 446±11.7 | 137±11.3 | 88±3.3 | 114±4.2 | 122±5.2 | ||||
1 | 175±2.1 | 127±1.5 | 123±0.3 | 140±5.8 | |||||
3.3 | 755±10.3 | 3.6±14.2 | 276±17.2 | 290±10.7 | 293±11.5 | ||||
10 | 1083±19.7 | 1011±35.6 | 817±37 | 929±58.8 | 951±44.7 | ||||
33.3 | 1313±10.7 | 1124±38.6 | 1363±8.8 | 1390±49.1 | |||||
Trial summary | Positive | Positive | Positive | Positive | Positive | ||||
Positive control | 526±12 | 1006±58 | 1278±34.7 | 593±4.4 | 627±18.2 | ||||
TA1535 | 0 | 20±2.6 | 25±3.1 | 13±2 | 10±0.7 | 9±2.9 | 9±0.9 | ||
0.03 | 119±8.4 | ||||||||
0.1 | 247±7.7 | ||||||||
0.3 | 296±12 | 474±16.3 | 33±2.5 | 16±3.8 | 24±2.9 | 28±8.8 | |||
1 | 5.8±25.5 | 78±3.7 | 45±4.4 | 77±14.1 | 50±4.5 | ||||
3.3 | 818±40.4 | 688±28.8 | 262±5.1 | 161±13 | 290±34.3 | 251±5.8 | |||
10 | 1147±53.6 | 957±62.1 | 927±21.8 | 795±3.2 | 928±8.4 | 899±29.6 | |||
33.3 | 1403±34.2 | 1335±24.1 | 1317±40.4 | 1325±36.1 | 1320±64.1 | ||||
Trial summary | Positive | Positive | Positive | Positive | Positive | Positive | |||
Positive control | 512±18.9 | 444±17 | 400±19.3 | 300±6.3 | 311±6.4 | 374±12.8 | |||
TA1537 | 0 | 8±1 | 15±1.2 | 13±3.2 | |||||
0.3 | 11±1 | 24±2.6 | 15±12 | ||||||
1 | 8±0.7 | 22±2.8 | 8±2.3 | ||||||
3.3 | 8±0.9 | 17±4.9 | 9±2.2 | ||||||
10 | 9±1.7 | 13±0.6 | 9±2.5 | ||||||
33.3 | 10±1.8 | 16±1.2 | 10±2.4 | ||||||
Trial summary | Negative | Negative | Negative | ||||||
Positive control | 119±225 | 376±12 | 493±132.1 | ||||||
TA98 | 0 | 46±2.4 | 53±3.4 | 60±5 | |||||
0.3 | 41±6.9 | 27±1.8 | 65±8 | ||||||
1 | 45±72 | 31±5.8 | 54±3.9 | ||||||
3.3 | 52±6.7 | 31±3.5 | 62±6.5 | ||||||
10 | 51±6.9 | 26±2.9 | 51±7.2 | ||||||
33.3 | 54±2.8 | 30±0.3 | 59±4.2 | ||||||
Trial summary | Negative | Negative | Negative | ||||||
Positive control | 850±18 | 1170±9.5 | 509±20.5 |
a Revertants are presented as mean ± the standard error from three plates.
Table 1: Effects of various concentrations of sodium azide on SCE induction in human lymphocytes
Treatment dose |
|
Treatment time [h] |
Number of cells analyzed |
SCEs/cell ± SE |
100 µM |
a |
4 |
80 |
8.00 ±0.307 |
50 µM |
b |
4 |
117 |
7.25 ±0.241 |
10 µM |
b |
4 |
110 |
7.65 ±0.297 |
5 µM |
b |
4 |
91 |
7.41 ±0.260 |
1 µM |
b |
4 |
120 |
7.79 ±0.239 |
0.5 µM |
a |
4 |
80 |
7.48 ±0.334 |
0.1 µM |
a |
4 |
80 |
6.88 ±0.261 |
0.05 µg/mL Mitomycin C |
b |
4 |
92 |
45.84 ±1.23 * |
Control |
|
|
120 |
7.48 ±0.244 |
|
|
|
|
|
50 mM |
a |
1 |
40 |
10.35 ±0.647 * |
10 mM |
a |
1 |
64 |
9.03 ±0.549 |
5 mM |
a |
1 |
67 |
9.40 ±0.471 * |
1 mM |
|
1 |
20 |
8.63 ±0.467 |
0.5 mM |
|
1 |
40 |
8.03 ±0.492 |
0.05 µg/mL Mitomycin C |
a |
4 |
40 |
38.03 ±1.80 * |
Control |
|
|
60 |
8.113 ±0.326 |
a Average of 2 experiments
b Average of 3 experiments
* Significant (p<0.05)
Table 2: Effects of various concentrations of sodium azide on SCE induction inChinese hamster K1 cell line
Treatment dose |
|
Treatment time [h] |
Number of cells analyzed |
SCEs/cell ± SE |
1 mM |
|
2 |
--- |
Lethal |
500 µM |
|
2 |
--- |
Lethal |
100 µM |
|
2 |
--- |
Lethal |
50 µM |
|
2 |
--- |
Lethal |
10 µM |
|
2 |
50 |
11.20 ±0.512 |
5 µM |
|
2 |
49 |
11.90 ±0.456 |
1 µM |
|
2 |
51 |
12.05 ±0.490 |
0.5 µM |
|
2 |
50 |
10.46 ±0.554 |
Control |
|
2 |
50 |
10.70 ±0.572 |
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Genetic toxicity in vivo
Endpoint conclusion
- Endpoint conclusion:
- no study available
Additional information
Justification for classification or non-classification
Sodium azide is used as a positive control in the Ames test (OECD 471). Mutagenicity in bacteria is mediated through a bacteria specific metabolic process that is not available in mammalian cells. Since the mutagenic metabolite, azidoalanine is not synthesized by animals, bacterial mutagenicity is considered irrelevant for risk human assessment. Results from in vitro tests in mammalian cells are negative in almost all available reports. This fact is strengthened by the absence of carcinogenic effects of sodium azide in a 2-year carcinogenicity study on rats. Consequently, a classification for mutagenicity is not warranted.
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