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EC number: 237-301-3 | CAS number: 13732-62-2
- 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
Carcinogenicity
Administrative data
Description of key information
Key value for chemical safety assessment
Justification for classification or non-classification
Based on the current data, Morpholinium toluene-4-sulphonate is not subject to classification for canceraogenicity according to Directive 67/548/EEC (DSD) and Regulation (EC) No 1272/2008 (GHS/CLP).
Additional information
No studies are available for morpholinium tuluene-4 -sulphonate. Two studies were performed with morpholine.
In the first combined chronic/carcinogenicity study (Harbison et al., 1989), Morpholine (99.2 %) was administered by whole body inhalation exposure to Sprague-Dawley rats at mean concentrations of 0, 36, 181 or 543 mg/m³ (6 h/day, 5 days/week) for 52 weeks (10 animals/sex/group) or for 104 weeks (60 animals/sex/group). No treatment-related changes in mortality, body weights, organ weights, or clinical pathology parameters were observed. Ophthalmoscopic examinations at week 103 revealed signs of eye irritation. Histological findings were limited to ocular and anterior nasal cavity effects, consistent with the known irritating properties of Morpholine. At the doses tested, there was no evidence of increased incidence of carcinogenesis due to chronic Morpholine inhalation. Since only local effects were noted, under the conditions of this study, the NOAEC was >543 mg/m³ for both carcinogenicity and toxicity.
In a second carcinogenicity study (Kitano et al., 1997), the effects of dietary Morpholine administration at a dose level of 0.5 % (approx. 220 mg/kg bw) to male Fischer 344 rats (10 or 20 animals/group) were investigated for a period of 23 weeks (i) in combination with sodium nitrite given in the drinking water following an initiation phase, (ii) without sodium nitrite following an initiation phase and (iii) in combination with sodium nitrite without initiation phase. In an additional experiment, male Fischer 344 rats (14 or 5 animals/group) received a dietary treatment with Morpholine (2.0 %) for 1 hour with subsequent administration of sodium nitrite for determination of N-nitroso compounds in the stomach and to detect DNA adduct generation. Both experiments were run with concurrent control groups. Morpholine alone was not tested. The initiation treatment decreased the body weight of rats compared to non-initiated groups. The group that was initiated and received sodium nitrite in the drinking water and Morpholine in the diet was significantly lower in body weight than the group that was only initiated. However, the liver and kidneys weights were increased. The combination of initiation followed by sodium nitrite and Morpholine caused an increase in the number and area of GST-P positive liver foci as compared to the group that was only initiated, indicating that Morpholine plus sodium nitrite, but not Morpholine alone, has a tumour promoting effect. Treatment with Morpholine or Morpholine plus sodium nitrite did not clearly lead to an increased tumour incidence. No tumours were induced by Morpholine plus sodium nitrite in the absence of initiation. The mean N-nitrosomorpholine yield in the group given Morpholine plus sodium nitrite was 6720 µg. No DNA adducts related to Morpholine treatment were detected immunohistochemically.
Overall, there was no evidence of carcinogenic activity of Morpholine.
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