Alumina

101.96

101.947823

254-434-2

LMI26O6933

0351

DTXSID1052791

White crystalline powder|White powder, balls or lumps or various mesh

D - Dermatologicals

28181010

3

0.31860

DERBY BROWN

4.0 g/cm³ @ Temp: 20 °C

2000 °C (approx)

2980 °C

2980°C

1.765

Miscible with ethanol.INsoluble

Keep container tightly closed in a dry and well-ventilated place. strongly hygroscopic.

17 mm Hg ( 20 °C)

Non-toxic

Noncombustible solid, but dusts may form explosive mixtures in air.

Odorless

Very hygroscopic; an electrical insulator, electrical resistivity at 300 °C about 1.2x10+13 ohms-cm; very hard, about 8.8 on Mohs' scale; when heated above 800 °C, becomes insoluble in acid; specific gravity increases from 2.8 to 4.0 when heated above 800 °C|White powder, hexagonal; MP: 2054 °C; BP: 2977 °C; density: 3.99 g/cu cm; insoluble in water, organic solvents; slightly soluble in alkaline solutions /Alpha-alumina/|Heat of formation: -130.0 kJ/mol; Gibbs energy of formation: -159.0 kJ/mol; molar entropy: 259.4 J/mol-K; molar heat capacity at constant pressure: 45.7 J/mol-K at 298.15 K|Enthalpy of fusion: 111.1 kJ/mol /Alpha-alumina/|Density: 3.97 g/cu cm; Mohs' hardness: 9; index of refraction: 1.761 (alpha), 1.769 (beta) /Corundum/|Ridgeway's hardness scale: 12; Knoop hardness: 21 kN/sq m|Mean specific heat: 795.5 J/kg-K from 25-1,800 °C; thermal conductivity: 10.9 W/m-K at 500 °C, 6.2 W/m-K at 1000 °C; linear thermal expansion coefficient: 8.6/deg C X 10+6, from 20-1000 °C

Insoluble in water.

Non-Redox-Active Inorganic Compounds

Known Catalytic Activity

ALUMINUM OXIDE is chemically amphoteric (behaves as a weak acid in the presence of base and as a weak base in the presence of acid). May act catalytically. May cause the exothermic polymerization of ethylene oxide. May cause the vigorous polymerization of vinyl chloride [MCA SD-75, 1970]. The degree of subdivision of the aluminum oxide may affect the vigor of such reactions.

Noncombustible solid, but dusts may form explosive mixtures in air.

8

UN1219 - class 3 - PG 2 - Isopropanol, solution

R36/37/38

26-24/25-16-7-36

BD1200000

Xi,F

Aluminum oxide should be stored in a well-closed container in a cool, dry, place. It is very hygroscopic.

Stable under normal shipping and handling conditions.

P210-P261-P305 + P351 + P338

H225-H319-H336

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

Materials to avoid: strong acids, strong bases, chlorine trifluoride, ethylene oxide, halogenated hydrocarbon, oxygen difluoride, sodium nitrate, vinyl compounds|Chlorine trifluoride, hot chlorinated rubber, acids, oxidizers [Note: Hydrogen gas may be formed when finely divided iron contacts moisture during crushing & milling operations].

Certification of this color additive when used to color drugs is not necessary for the protection of the public health, and therefore batches thereof are exempt from the certification pursuant to section 721(c) of the act.

Krewski D et al; Human Health Risk Assessment for Aluminum, Aluminum Oxide, and Aluminum Hydroxide, J Toxicol Environ Health B Crit Rev. 2007 ; 10(Suppl 1): 1-269. doi:10.1080/10937400701597766, is an NIH Public Access Author Manuscript that is a compendium of information on aluminium compounds used in industrial settings, and as pharmaceuticals, food additives, cosmetics and as other household products.|ATSDR; Toxicological Profile for Aluminum, 357 pp., September 2008. The ATSDR toxicological profile identifies and reviews the key literature that describes a hazardous substance's toxicologic properties. Other pertinent literature is presented in less detail.[Available from, as of June 15, 2010: http://www.atsdr.cdc.gov/ToxProfiles/tp22.pdf]

Not combustible.

Not Classified| |Warning|H335 (100%): May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]|P261, P271, P304+P340, P312, P403+P233, P405, and P501|The GHS information provided by 1 company from 1 notification to the ECHA C&L Inventory.|Danger|H335: May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]|P260, P261, P264, P270, P271, P304+P340, P312, P314, P403+P233, P405, and P501

Skin: No recommendation is made specifying the need for personal protective equipment for the body. Eyes: No recommendation is made specifying the need for eye protection. Wash skin: No recommendation is made specifying the need for washing the substance from the skin (either immediately or at the end of the work shift). Remove: No recommendation is made specifying the need for removing clothing that becomes wet or contaminated. Change: No recommendation is made specifying the need for the worker to change clothing after the work shift. (NIOSH, 2016)|Local exhaust or breathing protection. Protective gloves. Safety goggles, or eye protection in combination with breathing protection.|Extra personal protection: P1 filter respirator for inert particles.|(See protection codes)

Not combustible.

Do not use halocarbon extinguishers. The product itself does not burn. Wear self contained breathing apparatus for fire fighting if necessary.|In case of fire in the surroundings: all extinguishing agents allowed.

Sweep spilled substance into containers; if appropriate, moisten first to prevent dusting. Wash away remainder with plenty of water.

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.|SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.|Provide appropriate exhaust ventilation at places where dust is formed.

May cause minor irritation to lungs and eyes. /Aluminum powder/

Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 15 mg/cu m. /Total dust/|Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 5 mg/cu m. /Respirable fraction/|Vacated 1989 OSHA PEL TWA 10 mg/cu m is still enforced in some states. /Total/|Vacated 1989 OSHA PEL TWA 5 mg/cu m is still enforced in some states. /Resp/

NIOSH has concluded that the documentation cited by OSHA was inadequate to support the proposed PEL (as an 8-hour Time-Weighted Average) of 10 mg/cu m for alpha-alumina.

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Wash away remainder with plenty of water.

Evaporation at 20 °C is negligible; a harmful concentration of airborne particles can, however, be reached quickly.

Inhalation of high concentrations of dust may cause irritation of the eyes and respiratory tract.

The substance may have effects on the central nervous system.

PREVENT DISPERSION OF DUST!

Use local exhaust or breathing protection.

Protective gloves.

Wear safety goggles or eye protection in combination with breathing protection.

| 0 - Materials that, under emergency conditions, would offer no hazard beyond that of ordinary combustible materials.| 0 - Materials that will not burn under typical fire conditions, including intrinsically noncombustible materials such as concrete, stone, and sand.| 1 - Materials that in themselves are normally stable but that can become unstable at elevated temperatures and pressures.

SEDIMENT: In 1984, aluminum oxide was detected in sediments in the west branch of the Grand Calumet River, in Indiana and Illinois, at mean, median and maximum concentrations (% composition) of 8.60, 7.73 and 12.46, respectively(1).

Observations that aluminium inhalation reduced the ability of quartz to produce lung fibrosis in some experimental animals lead to its application in humans. ... Symptomatic improvement was reported in 49 nonferrous metal workers treated with metallic aluminium. Forty-three percent of those treated with hydrated aluminium oxide reported improvement compared to 30% of those treated with metallic aluminium oxide. There was no objective measure of improvement in these cases. In 1946, E. J. King & C. L. Sutherland reviewed the evidence for the use of aluminium to prevent or treat silicosis and concluded that there was no definitive evidence that aluminium prevented further development or caused reversal of established disease. ... Carefully planned and properly controlled studies were recommended. This led to an investigation that was conducted in pottery workers and coal miners of the efficacy of inhalation of 50 mg pure metallic aluminium dust, of which > 90% was respirable, for 15 minutes, 3 times weekly, for up to 3.5 years; comparison was made with inhalation of 5 mg of carbon black containing 1 mg/kg aluminium powder. No regression of the x-ray picture or improvement of functional capacity was seen.|To elucidate the interaction between aluminum and certain essential trace metals, an experiment was performed on rats fed diets with suboptimal or optimal levels of zinc or copper. Half of each group of animals were fed the same diet but with 1000 ppm aluminum added. Changes were noted after 120 days. Severe testicular damage was seen in rats fed either the low zinc or the low copper diet. The lesions included a wide range of spermatogenic cell degeneration and tubular atropy. When aluminum was added to the diet, the testicular destruction of zinc deficient rats was significantly reduced. This indicated that the presence of aluminum in the diet protected the testes against the damage cauesed by zinc deficiency. Pituitary glands were examined. Hypertrophy of basophiles was more pronounced in rats fed the suboptimal zinc or copper diet. When aluminum was added to their diet, the changes were reversed. The mechanisms by which aluminum protects male gonadal functions against zinc deficiency are discussed. This study is the first to demonstrate the preventive effect of aluminum against testicular damage caused by zinc deficiency. /Aluminum/|Desferrioxamine, traditionally used as an iron chelator, has been shown to increase urinary aluminum output in humans and aluminum loaded mice, rats and rabbits. However, major side effects of desferrioxamine treatment have been observed and the drug may accumulate in dialysis patients receiving repeated doses. In recent years, it has been reported that some dicarboxylic or tricarboxylic acids such as succinic, malic or citric may be considered as possible alternatives to desferrioxamine in the management of aluminum accumulation. Ethylene-di-(o- hydroxyphenylacetic acid) like compounds may also have potential as alternatives to desferrioxamine in the treatment of aluminum accumulation and aluminum induced toxicity. /Aluminum/|/Investigators/ have shown that intratracheal instillation of 40 mg aluminum oxide without adsorbed fluorides only resulted in an increase in fibronectin concentration, whereas aluminum oxide with adhered fluorides led to a significant increase in macrophages and neutrophils in bronchoalveolar lavage (BAL) fluid. This is indicative of the greater irritancy potential of the latter fluoride associated particles.

LD50 Rat oral > 5,000 mg/kg bw

Occurs in nature as the minerals: bauxite, bayerite, boehmite, corundum, diaspore, gibbsite

Exposure to aluminum oxide-containing dust in prodn of abrasives from bauxite has been described as a hazard.|Recycled aluminum oxide is reduced electrolytically in pots. Pot fumes contain fluoride dust, sulfur dioxide, cox, and pitch volatiles. Itching of the legs results from exposure to the fumes.|Aluminum oxide particles from corroded air conditioners ... .|Main health hazard in primary aluminum production is fluoride exposure, not exposure to aluminum or aluminum oxide.|For more Probable Routes of Human Exposure (Complete) data for Aluminum oxide (7 total), please visit the HSDB record page.

Inhalation exposure to 100 mg/hr aluminium, in the form of powder, or 92 mg Al/ per 2 hr, as a fume, each day for 9-13 months showed a significant retention of aluminium in the lungs of both groups of animals. The aluminium retention in the lungs in rats and hamsters exposed to fume was much greater than when exposed to powder. Following exposure to fresh air, aluminium oxide was cleared rapidly from the lungs of the both powder and fume groups. Weight of wet lung, ash and aluminium oxide content of lungs in exposed animals increased. The initial pulmonary tissue response was proliferation of macrophages within alveolar spaces as well as lipoid pneumonia. The focal aggregates of macrophages were located around the small bronchioles and small pulmonary arterioles; lymphoid hyperplasia was observed. After chronic exposure to aluminium powder, rats showed focal deposits of hyaline in alveolar walls, and focal areas of lipoid pneumonia developed in hamsters.|... The concentrations of aluminum in tissues of female New Zealand rabbits exposed to /aluminum oxide/ dust at a concentration of 0.56 mg Al/cu m for 5 months (8 hr/day, 5 days/week) were determined. The amount of aluminum in the brains of the animals was nearly two and a half times as high as that of the control animals. The concentrations in other tissues were only slightly increased.|Radiolabeled 26Al inhalation studies were performed using tagged gamma aluminum oxide. The results showed that the material acted as an insoluble dust. about 45% was cleared from the lung after one day, with slow mechanical clearance from the lungs of the balance. After 72 days, only 0.2% of the alumina remained in the lung. The lung may provide long-term sequestration for small percentage of inhaled, insoluble alumina.|/Investigators/ evaluated the accumulation and clearance of aluminum oxide in Sprague-Dawley rats following intratracheal instillation. Rats were instilled with 1 mg/kg of smelter grade alumina obtained via electrostatic precipitator (MMAD = 1.2 um) once per week for 20 weeks. Groups of rats were sacrificed periodically during the exposure period and up to 19-weeks post exposure. Aluminum was measured by flame and flameless atomic absorption spectroscopy. Exposed rats steadily accumulated aluminum during the exposure period up to a lung burden of about 500 ug Al/g tissue.Only 9% was cleared during the 19-week post-exposure period. Extrapulmonary tissues such as brain, bone, kidney, liver, and spleen had aluminum levels that were essentially the same as, but slightly above, those of non-exposed control animals (0.17-2.63 ug Al/g tissue.|For more Absorption, Distribution and Excretion (Complete) data for Aluminum oxide (6 total), please visit the HSDB record page.

The mean plasma half-life of aluminum after iv admin in dogs is approx 4.5 hr. /Aluminum/|The shorter half-life for the urinary elimination of aluminum was about 8 hr. /Aluminum/

... Six 8 wk old female Swiss Webster mice were fed for 10 weeks purified diets containing 100 (control), 500 or 1000 ug aluminum/g diet. Brain and liver lipid peroxidation was determined by evaluating the production of 2-thiobarbituric acid reactive substances in brain and liver homogenates in the presence or absence of 50 uM ferrous iron. 2-Thiobarbituric acid reactive substances production in the absence of iron in brain homogenates from mice fed the 1000 ... ug/g diet was higher (30%) than that in the ... control group (3.1 vs 2.4 nmol 2-thiobarbituric acid reactive substances/mg protein). The addition of ferrous iron increased 2-thiobarbituric acid reactive substances production in brain homogenates from all 3 dietary groups. The iron induced 2-thiobarbituric acid reactive substances production was 26% higher in the 1000 ... ug/g /group/ brain homogenates than in the ... /control/ group (4.9 vs 3.9 nmol 2-thiobarbituric acid reactive subtances/mg protein). Brain 2-thiobarbituric acid reactive substances production in the presence and absence of iron was similar between the 100 and 500 ... ug/g /diet/ groups. 2-Thiobarbituric acid reactive substances production in liver homogenates measured either with or without iron was similar for the 3 groups. These results show that, in mice, dietary aluminum intoxication leads to increased brain 2-thiobarbituric acid reactive substance production, suggesting that enhanced lipid peroxidation may be one possible mechanism underlying the neurological damage associated with increased tissue aluminum. /Aluminum/|Evidence is presented indicating that dementias are associated with a relative insufficiency of magnesium in the brain. Such insufficiency may be attributable to low intake or retention of magnesium; high intake of a neurotoxic metal, such a aluminum, which inhibits activity of magnesium requiring enzymes; or impaired transport of magnesium and/or enhanced transport of the neurotoxic metal into brain tissue. It is proposed that Alzheimer's disease involves a defective transport process, characterized by both an abnormally high incorporation of aluminum and an abnormally low incorporation of magnesium into brain neurons. The hypothesis has advanced that an altered serum protein contributes to the progression of Alzheimer's disease by having a greater affinity for aluminum than for magnesium, in contrast to the normal protein, which binds magnesium better than aluminum. The altered protein crosses the blood-brain barrier more efficiently than the normal protein and competes with the normal protein in binding to brain neurons. Binding of the altered protein to the target neurons would both facilitate aluminum uptake and impede magnesium uptake. Evidence suggests that albumin is the serum protein that is altered. /Aluminum/|Aluminum is established as a neurotoxin, although the basis for its toxicity is unknown. It recently has been shown to alter the function of the blood brain barrier, which regulates exchanges between the central nervous system and peripheral circulation. The blood brain barrier owes its unique properties to the integrity of cell membranes that comprise it. Aluminum affects some of the membrane-like functions of the blood brain barrier. It increases the rate of transmembrane diffusion and selectively changes saturable transport systems without disrupting the integrity of the membranes or altering CNS hemodynamics. Such alterations in the access to the brain of nutrients, hormones, toxins, and drugs could be the basis of CNS dysfunction. Aluminum is capable of altering membrane function at the blood-brain barrier; many of its effects on the CNS as well as peripheral tissues can be explained by its actions as a membrane toxin. /Aluminum/|Chronic, oral administration of aluminum to rats increases the in vivo concentration of cyclic AMP and the phosphorylation of microtubule-associated protein-2 and the 200 kd neurofilament subunit. In the present study, the effect of this treatment on endogenous protein phosphorylation in soluble and particulate fractions prepared from cerebral cortices was examined. Chronic aluminum treatment significantly elevated the basal and cyclic AMP-dependent phosphorylation of 11-12 endogenous proteins in the soluble fraction prepared from cerebral cortices. Endogenous protein phosphorylation in the soluble fraction occurring in the presence of calcium(+2) alone or calcium(+2) phorbol 12-myristate 13-acetate and phosphatidylserine was not significantly altered by aluminum treatment. In the particulate fraction the phosphorylation of several proteins was significantly decreased by aluminum administration; however the phosphorylation of the majority of protein substrates remained unaltered. Aluminum treatment did not alter the activities of cyclic AMP-dependent protein kinase or protein tyrosine kinase in the soluble and particulate fractions. The activity of calcium(+2)/phospholipid-dependent protein kinase (protein kinase C) was increased in the particulate fraction of aluminum fed rats. These results clearly demonstrate that specific effects on protein kinase activities result from in vivo aluminum administration. /Aluminum/

Sodium is the main component of the process solution and is also the largest contaminant of the product. ... Gallium is a ubiquitous component of aluminous ores. Its chemistry is similar to that of aluminum, so it accumulates in Bayer process solutions until an equilibrium is reached at about 0.2 g/L. The gallium content of Al2O3 is a linear function of the gallium concentration in the solution. ... Silicon is a component of many aluminum alloys, yet the specification for Al2O3 is less than 0.02% SiO2. ... Potassium is undesirable in the Al2O3 because it may destroy the graphite in Hall-Heroult cells by intercalation, i.e., it diffuses between the layers of the graphite structure, thus expanding its volume. Although it is soluble in Bayer solutions, there has not been a recorded instance of K2O concentrations becoming high enough to affect the Al2O3 quality.... Iron(III)oxide (Fe2O3) as an impurity in Al2O3. ... Calcium also is a common impurity.

Exposure Routes: inhalation, ingestion, skin and/or eye contact Symptoms: irritation eyes, skin, respiratory system Target Organs: Eyes, skin, respiratory system (NIOSH, 2016)

Eye: If this chemical contacts the eyes, immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Contact lenses should not be worn when working with this chemical. Skin: If irritation occurs, gently blot or brush away excess. Breathing: If a person breathes large amounts of this chemical, move the exposed person to fresh air at once. Other measures are usually unnecessary. Swallow: If this chemical has been swallowed, get medical attention immediately. (NIOSH, 2016)|(See procedures)

Fresh air, rest.

Rinse and then wash skin with water and soap.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/SIGNS AND SYMPTOMS/ The aluminium lung concentrations in 4 workers exposed to aluminium oxide for 10 to 37 years were 400 to 1080 mg/kg, respectively and correlated well with the extent of fibrosis.|/SIGNS AND SYMPTOMS/ Aluminium oxide refinery workers exposed to some low temperature transitional aluminas demonstrated little evidence of pulmonary fibrosis and pneumoconiosis. The noted adverse effects were consistent with non-specific chronic industrial bronchitis associated with excessive, prolonged exposures to nuisance dust.|/SIGNS AND SYMPTOMS/ /In 1947/ a lung disease seen in 23 furnace feeders and ore bin operators, who had worked for 23 months to 15 years in a facility manufacturing the aluminium oxide abrasive, corundum /was described/. These workers were exposed to fumes containing considerable amounts of very fine aluminium oxide as well as silica and smaller quantities of many other substances. The disease was characterized by dyspnea, sudden attacks of extreme breathlessness, pneumothorax, and diffuse, irregular, lace-like, granular shadows rapidly progressing to a non-nodular fibrosis. This became known as Shaver's disease, a pulmonary fibrosis seen in workers in bauxite refining or exposed to finely divided aluminium powders, especially flake (pyro) powders. The fumes were shown to contain 30% silicon dioxide and 55% aluminium oxide; the silicon particle size (0.02 to 05 um) was smaller than that associated with classical silicosis.|/SIGNS AND SYMPTOMS/ Effects of short-term exposure: Inhalation of high concentrations of dusts of this substance may cause eyes and upper respiratory tract irritation. Effects of long-term exposure: The substance may have effects on the central nervous system.|For more Human Toxicity Excerpts (Complete) data for Aluminum oxide (29 total), please visit the HSDB record page.

Alumina

The substance can be absorbed into the body by inhalation of its aerosol.|inhalation, ingestion, skin and/or eye contact

irritation eyes, skin, respiratory system

Cough.

Redness.

Eyes, skin, respiratory system

93% as a chem intermediate for aluminum metal; 7% for misc uses (1973)

Grades: Technical; CP /chemically pure: a grade designation signifying a minimum of impurities, but not 100% purity/; fibers; high purity; fused; calcined|MAIN COMPONENT OF TECHNICAL ALUMINUM OXIDE IS ALPHA-ALUMINUM OXIDE ; AMT OF GAMMA-ALUMINUM OXIDE DEPENDS ON CALCINATING TEMP USED.|Whiskers, polycrystalline filaments as Fiber FP and Saffil fiber.|Continuous monofilaments|For more Formulations/Preparations (Complete) data for Aluminum oxide (6 total), please visit the HSDB record page.

Alpha-alumina is the main component of technical grade alumina; corundum is natural aluminum oxide; emery is an impure crystalline variety of aluminum oxide|Although "alumina" denotes pure Al2O3, the term is commonly applied to any ceramic whose major constituent is alumina, even if the ceramic contains other components.|The five principal producing countries, in descending order of quantity of alumina produced, China, Australia, Brazil, the United States, and Jamaica, accounted for 70% of world production; China and Australia together accounted for more than 50%.|Typical Properties of Metallurgical Alumina

Method: OSHA ID-109-SG; Procedure: flame atomic absorption; Analyte: aluminum oxide; Matrix: air; Detection Limit: 0.5 ug/mL.|Method: AOAC 917.01; Procedure: gravimetric method; Analyte: aluminum oxide; Matrix: liming materials (limestone, marl, slag, burnt lime, hydrated lime); Detection Limit: not provided.

Cosmetics -> Abrasive; Opacifying; Viscosity controlling