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EC number: 233-135-0 | CAS number: 10043-01-3
- 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
Biological effects monitoring
Administrative data
- Endpoint:
- biological effects monitoring
- Type of information:
- migrated information: read-across based on grouping of substances (category approach)
- Adequacy of study:
- key study
- Reliability:
- 1 (reliable without restriction)
- Rationale for reliability incl. deficiencies:
- other: Reliable without restrictions. Guideline study
Data source
Reference
- Reference Type:
- study report
- Title:
- Unnamed
- Year:
- 1 997
Materials and methods
Test guideline
- Qualifier:
- according to guideline
- Guideline:
- other: existing WHO Guidelines for aluminium exposure in healthy, non-occupationally exposed humans.
- GLP compliance:
- not specified
- Type of study / information:
- Various methods for sampling, sample preparation and determination of aluminium in biological and environmental samples have been developed and described.
Because of the ubiquitous distribution of aluminium in nature, care must be taken during sampling and sample preparation to avoid contamination. Most analytical errors are due to contamination of the sample with aluminium from air, vessels and reagents during sampling and preparation for analysis. To prevent aluminium contamination, the use of aluminium-free polyethylene, polypropylene, teflon or quartz materials is recommended. Containers and laboratory materials have to be washed with warm, dilute nitric acid and subsequently rinsed with de-ionized water prior to use (Andersen, 1987).
Air is sampled with high volume samplers using low-ash cellulose or cellulose ester filters for particulate aluminium (NIOSH, 1984). Biological samples need to be preserved by cooling, freezing or lyophilization. Preservation with 10% formalin is not recommended because of a high risk of aluminium contamination (Bouman et al., 1986).
Homogeneity of the samples is an absolute prerequisite for accurate analysis. To prepare samples for analysis, inorganic samples are usually dissolved in nitric acid or extracted with water. Solutions are filtered with a membrane filter and the particulate residue is analysed separately (Dunemann & Schwedt, 1984).
Water (DIN, 1993) and urine should be acidified with HNO3 or HCl to pH < 2 to prevent adsorption effects and the precipitation of salts. This ensures that aluminium remains in solution. Water samples for speciation analysis should be stored, without acidification, in high-density polyethylene bottles (Berden et al., 1994; Fairman et al., 1994). Prior to analysis biological tissues must be homogenized and separated or extracted. Blood and urine samples may be separated by centrifugation and diluted, or, if appropriate, analysed directly without pretreatment.
Test material
- Reference substance name:
- Aluminium sulphate
- EC Number:
- 233-135-0
- EC Name:
- Aluminium sulphate
- Cas Number:
- 10043-01-3
- Molecular formula:
- Al.3/2H2O4S; General formula Al2(OH)x(SO4)(3-x/2), with x=0 and x=3 and x ranging from 0 to 3.
- IUPAC Name:
- Aluminium sulphate
Constituent 1
Results and discussion
Any other information on results incl. tables
Hazards to neurological development and brain function from exposure to aluminium have been identified through animal studies.However, aluminium has not been demonstrated to pose a health risk to healthy, non-occupationally exposed humans.
There is no evidence to support a primary causative role of aluminium in Alzheimer's disease (AD), and aluminium does not induce AD pathology in vivo in any species, including humans.
The hypothesis that exposure of the elderly population in some regions to elevated levels of aluminium in drinking-water mayexacerbate or accelerate Alzheimer's disease (AD) lacks adequate supporting data.
The data in support of the hypothesis that particular exposures, either occupational or via drinking-water, may be associated with non-specific impaired cognitive function are also inadequate.
There is insufficient health-related evidence to justify revisions to existing WHO Guidelines for aluminium exposure inhealthy, non-occupationally exposed humans. As an example, there is an inadequate scientific basis for setting a health-based standard foraluminium in drinking-water.
Subpopulations at special risk
In people of all ages with impaired renal function, aluminium accumulation has been shown to cause the clinical syndrome ofencephalopathy, vitamin-D-resistant osteomalacia and microcytic anaemia. The sources of aluminium are haemodialysis fluid and aluminium-containing pharmaceutical agents (e.g., phosphate binders).Intestinal absorption can be exacerbated by the use of citrate-containing products. Patients with renal failure are thus at risk of neurotoxicity from aluminium.
Iatrogenic aluminium exposure poses a hazard to patients with chronic renal failure. Premature infants have higher body burdens of aluminium than other infants. Every effort should be made to limitsuch exposure in these groups.
Occupationally exposed population
Workers having long-term, high-level exposure to fine aluminium particulates may be at increased risk of adverse health effects.However, there are insufficient data from which to develop with any degree of certainty occupational exposure limits with regards to the adverse effects of aluminium. Exposure to stamped pyrotechnic aluminium powder most often coated with mineral oil lubricants has caused pulmonary fibrosis(aluminosis), whereas exposure to other forms of aluminium has not been proven to cause pulmonary fibrosis. Most reported cases hadexposure to other potentially fibrogenic agents.
Irritant-induced asthma has been associated with inhalation of aluminium sulfate, aluminium fluoride or potassium aluminium tetrafluoride, and with the complex environment within the potrooms during aluminium production.
Environmental effects
Aluminium-bearing solid phases in the environment are relatively insoluble, particularly at circumneutral pH values, resulting in low concentrations of dissolved aluminium in most natural water.
In acidic or poorly buffered environments subjected to strong acidifying inputs,concentrations of aluminium can increase to levels resulting in adverse effects on both aquatic organisms and terrestrial plants. However, there exist large species, strain and life historystage differences in sensitivity to this metal.
The detrimental biological effects from elevated concentrations of inorganic monomeric aluminium can be mitigated in the presence oforganic acids, fluorides, silicate and high levels of calcium and magnesium.
There is a substantial reduction in species richness associated with the mobilization of the more toxic forms of aluminium in acid-stressed waters. This loss of species diversity is observed at alltrophic levels.
Applicant's summary and conclusion
- Conclusions:
- Jones & Bennett(1985) (Summary Exposure Assessment for Aluminium", a Technical Report prepared by the Monitoring and Assessment Centre,,Kings College London, University of London with the support of the United Nations Environment Programme) summarized the data on aluminium concentrations in the environment and produced a list of representative values as follows:
1.Atmospheric aluminium
• urban air 1000 ng/m3 (160-7000 ng/m3),
• rural air 200 ng/m3(150-325 ng/m3),
2.Lithospheric aluminium
•agricultural soil 70 000 mg/kg (10 000-300 000 mg/kg),
3.Hydrospheric aluminium
•fresh water (dissolved) 50 µg/litre (1-2250 µg/litre),
•ocean (dissolved) 2 µg/litre (1-5 µg/litre),
4.Biospheric aluminium
•terrestrial plants 100 mg/kg (50-600 mg/kg).
•Food 8 m/kg
5. Aluminium in man
•Body burden 60 mg (30-60)
•Serum/plasma 7 µg/litre (1.5-15 µg/litre),
•Tissues 3 µg/litre (1-70 µg/litre), - Executive summary:
EVALUATIONS BY INTERNATIONAL BODIES
Total human intake of aluminium from all environmental pathways
In calculating total human exposures one must be aware of the quality of the sampling and analytical procedures, particularly when using data from earlier studies. Total intake of aluminium must consider all routes of exposure, i.e. inhalation, oral and dermal.
For humans, non-occupationally exposed to aluminium, oral intakeof aluminium represents the major route of exposure.The total daily intake of aluminium in adults ranges from 2.5 to13 mg/day, depending upon the country of origin as well as the age and sex of the subject. The variation reflects different dietary habits as well as the level of additives used in food processing. For infants(under 6 months) daily intakes range from 0.27 to 0.53 mg/day for those consuming soya-based formulae and 0.03 to 0.05 mg/day forinfants consuming cow's milk formulae (UK MAFF, 1993). Similar values were reported fromCanada (respectively, 0.08 and 0.69) (Dabeka &McKenzie, 1990). Aluminium intake from breast milk has been calculated to be < 0.04 mg/day (UK MAFF, 1993).
In conclusion, the total intake of aluminium by the general population varies between 2.5 and 13 mg/day. In most countries over 95% of this comes from food and less than 1% from airborne aluminium.These intakes can be increased greatly (10 to 100 times) through the use of aluminium-containing antacids andbuffered analgesics. Total daily exposure to aluminium from all sources, other than medicines, and for all age groups has been shown to be less than the PTWI of 1 mg/kg per day (WHO, 1993).
On the basis of non-health-related criteria, a WHO Drinking-WaterGuideline of 0.2 mg/litre has been proposed (WHO, 1993). No health- based guideline was recommended.
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