ANTIMONY TRIOXIDE

ANTIMONY TRIOXIDE

ANTIMONY TRIOXIDE

ANTMON TROKST

CAS No.: 1309-64-4

EC No.: 215-474-6

Synonyms:

ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; Antimony(III) oxide; Antimonous oxide; SO3b2; Antimony(III) oxide, CP; DTXSID4023880; Antimony(III) oxide, >=99%; Antimony(III) oxide, 99.5%; 8927AF; Antimony(III) oxide, puriss. p.a.; AKOS015904094; Antimony(III) oxide, 99.99% trace metals basis; Antimony(III) oxide, 99.999% trace metals basis; J-520229; Antimony(III) oxide, powder, 5 mum, ReagentPlus(R), 99%; Antimony trioxide, United States Pharmacopeia (USP) Reference Standard; Antimony(III) oxide, nanopowder, <250 nm particle size (TEM), >=99.9% trace metals basis; 1309-64-4; ANTIMONY OXIDE; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; P217481X5E; 1309-64-4; Weisspiessglanz; UNII-P217481X5E; AP 50 (metal oxide); Flame Cut 610; Flameguard VF 59; HM 203P; LS-FR; LSB 80; Flame Cut 610R; FireShield LS-FR; AT 3B; Atox B; Atox R; FireShield H; Antimony Bloom 500A; Microfine A 05; MIC 3; Octoguard FR 10; Antimony oxide (SB203); Antimony trioxide; Antimony trioxide production; Antimony White; Antox; AP 50; Patox M; Patox S; Senarmontite; Stibiox MS; Thermoguard B; Thermoguard L; Thermoguard S; Timonox; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; Antimony oxide (Sb2O3); Diantimony trioxide; A 1582; A 1588LP; C.I. 77052; C.I. 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Pigment White 11; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; CCRIS 4495; Chemetron fire shield; CI 77052; CI Pigment white 11; Dechlorane A-O; Diantimony trioxide; EC 215-175-0; EINECS 215-175-0; Exitelite; Fireshield FSPO 405; FireShield H; FireShield LS-FR; Flame Cut 610; Flame Cut 610R; Flameguard VF 59; Flowers of antimony; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; HM 203P; HSDB 436; LS-FR; LSB 80; MIC 3; Microfine A 05; NCI-C55152; Nyacol A 1510LP; Nyacol A 1530; Octoguard FR 10; Patox C; Patox H; Patox L; Patox M; Patox S; Sb2O3,; Senarmontite; Stibiox MS; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; Thermoguard B; Thermoguard L; Thermoguard S; Timonox; Timonox White Star; Twinkling star; UNII-P217481X5E; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; Valentinite; Weisspiessglanz; Weisspiessglanz [German]; White star; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; antimon trioksid; ANTMON TROKSD; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; Antimony(III) oxide; Antimonous oxide; SO3b2; Antimony(III) oxide, CP; DTXSID4023880; Antimony(III) oxide, >=99%; Antimony(III) oxide, 99.5%; 8927AF; Antimony(III) oxide, puriss. p.a.; AKOS015904094; Antimony(III) oxide, 99.99% trace metals basis; Antimony(III) oxide, 99.999% trace metals basis; J-520229; Antimony(III) oxide, powder, 5 mum, ReagentPlus(R), 99%; Antimony trioxide, United States Pharmacopeia (USP) Reference Standard; Antimony(III) oxide, nanopowder, <250 nm particle size (TEM), >=99.9% trace metals basis; 1309-64-4; ANTIMONY OXIDE; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; P217481X5E; 1309-64-4; Weisspiessglanz; UNII-P217481X5E; AP 50 (metal oxide); Flame Cut 610; Flameguard VF 59; HM 203P; LS-FR; LSB 80; Flame Cut 610R; FireShield LS-FR; AT 3B; Atox B; Atox R; FireShield H; Antimony Bloom 500A; Microfine A 05; MIC 3; Octoguard FR 10; Antimony oxide (SB203); Antimony trioxide; Antimony trioxide production; Antimony White; Antox; AP 50; Patox M; Patox S; Senarmontite; Stibiox MS; Thermoguard B; Thermoguard L; Thermoguard S; Timonox; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; Antimony oxide (Sb2O3); Diantimony trioxide; A 1582; A 1588LP; C.I. 77052; C.I. Pigment White 11; Amspec-KR; Antimonious oxide; Antimony(3+) oxide; AT 3 (fireproofing agent); Atox F; Atox S; CCRIS 4495; Chemetron fire shield; CI 77052; Antimony oxide; Timonox White Star; Twinkling star; CI Pigment white 11; Dechlorane A-O; EINECS 215-175-0; Exitelite; Fireshield FSPO 405; Flowers of antimony; HSDB 436; NCI-C55152; Nyacol A 1510LP; Nyacol A 1530; Patox C; Patox H; Patox L; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; Antimony sesquioxide; Valentinite; Weisspiessglanz [German]; White star; AN 800; Antimony Bloom 100A; ATO; Sb2O3,; EC 215-175-0; 1309-64-4; Antimonous oxide; Antimony sesquioxide; Antimony trioxide; Antimony(III) oxide; Flowers of Antimony; oxo-oxostibanyloxystibane; 1309-64-4; 8927AF; Antimony(III) oxide; SO3b2; 1309-64-4; A 1582; A 1588LP; AN 800; AP 50; AP 50 (metal oxide); AT 3 (fireproofing agent); AT 3B; ATO; ATX (CHRIS Code); Amspec-KR; Antimonious oxide; Antimony Bloom 100A; Antimony Bloom 500A; Antimony White; Antimony oxide (Antimony trioxide); Antimony oxide (SB203); Antimony oxide (Sb2O3); Antimony sesquioxide; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; Antimony trioxide; Antimony trioxide – Production; Antimony trioxide production; Antimony(3+) oxide; Antox; Atox B; Atox F; Atox R; Atox S; C.I. 77052; C.I. Pigment White 11; CCRIS 4495; CI 77052; CI Pigment white 11; Chemetron fire shield; Color Index No. 77052; Color Index Number 77052; Colour Index No. 77052; Colour Index Number 77052; Dechlorane A-O; Diantimony trioxide; EC 215-175-0; EINECS 215-175-0; Exitelite; FireShield H; FireShield LS-FR; Fireshield FSPO 405; Flame Cut 610; Flame Cut 610R; Flameguard VF 59; Flowers of antimony; HM 203P; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; HSDB 436; LS-FR; LSB 80; MIC 3; Microfine A 05; NA9201; NCI-C55152; Nyacol A 1510LP; Nyacol A 1530; O3-Sb2; O3Sb2; Octoguard FR 10; Patox C; Patox H; Patox L; Patox M; Patox S; Sb2O3,; Senarmontite; Stibiox MS; Thermoguard B; Thermoguard L; Thermoguard S; Timonox; Timonox White Star; Trioxyde d’antimoine; Twinkling star; UNII-P217481X5E; Valentinite; Weisspiessglanz; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; Weisspiessglanz [German]; White star; trioxyde de diantimoine; 1309-64-4; Antimony oxide (Sb2O3); Diantimony trioxide; antimony trioxide; 1309-64-4; ANTIMONY(III) OXIDE 250G; Antimony(III) oxide =99.9% (trace metals basis); DI-ANTIMONY TRIOXIDE; ANTIMON(III)OXIDE; ANTIMONY TRIOXIDE; ANTIMONY OXIDE; ANTIMONOUS OXIDE; ANTIMONY(+3)OXIDE; SB OXIDE; a1530; A 1582; A 1588LP; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; ANTIMONY TRIOXIDE; ANTMON TROKST; antimony trioxide; Antimon trioksit; Amspec-KR; AN 800; Antimonious oxide; Antimony Bloom 100A; Antimony Bloom 500A; Antimony oxide (SB203); Antimony oxide (Sb2O3); Antimony sesquioxide; Antimony trioxide; Antimony trioxide production; Antimony White; Antimony(3+) oxide; Antox; AP 50; AP 50 (metal oxide); AT 3 (fireproofing agent); AT 3B; ATO; Atox B; Atox F; Atox R; Atox S; C.I. 77052; C.I. 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ANTIMONY TRIOXIDE

Antimony trioxide trioxide

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Antimony trioxide(III) oxide

Antimony trioxide(III) oxide

Names

IUPAC name

Antimony trioxide(III) oxide

Other names

Antimony trioxide sesquioxide

Antimonous oxide

Flowers of Antimony trioxide

Other anions Antimony trioxide trisulfide

Other cations Bismuth trioxide

Related compounds DiAntimony trioxide tetraoxide

Antimony trioxide pentoxide

Antimony trioxide(III) oxide is the inorganic compound with the formula Sb2O3. It is the most important commercial compound of Antimony trioxide. It is found in nature as the minerals valentinite and senarmontite.[3] Like most polymeric oxides, Sb2O3 dissolves in aqueous solutions with hydrolysis.

Contents

1 Production and properties

1.1 Re-volatilizing of crude Antimony trioxide(III) oxide

1.2 Oxidation of Antimony trioxide metal

Global production of Antimony trioxide(III) oxide in 2012 was 130,000 tonnes, an increase from 112,600 tonnes in 2002. China produces the largest share followed by US/Mexico, Europe, Japan and South Africa and other countries (2%).[4]

As of 2010, Antimony trioxide(III) oxide was produced at four sites in EU27. It is produced via two routes, re-volatilizing of crude Antimony trioxide(III) oxide and by oxidation of Antimony trioxide metal. Oxidation of Antimony trioxide metal dominates in Europe. Several processes for the production of crude Antimony trioxide(III) oxide or metallic Antimony trioxide from virgin material. The choice of process depends on the composition of the ore and other factors. Typical steps include mining, crushing and grinding of ore, sometimes followed by froth flotation and separation of the metal using pyrometallurgical processes (smelting or roasting) or in a few cases (e.g. when the ore is rich in precious metals) by hydrometallurgical processes. These steps do not take place in the EU but closer to the mining location.

Re-volatilizing of crude Antimony trioxide(III) oxide

Step 1) Crude stibnite is oxidized to crude Antimony trioxide(III) oxide using furnaces operating at approximately 500 to 1,000 °C. The reaction is the following:

2 Sb2S3 + 9 O2 → 2 Sb2O3 + 6 SO2

Step 2) The crude Antimony trioxide(III) oxide is purified by sublimation.

Oxidation of Antimony trioxide metal

Antimony trioxide metal is oxidized to Antimony trioxide(III) oxide in furnaces. The reaction is exothermic. Antimony trioxide(III) oxide is formed through sublimation and recovered in bag filters. The size of the formed particles is controlled by process conditions in furnace and gas flow. The reaction can be schematically described by:

4 Sb + 3 O2 → 2 Sb2O3

Properties

Antimony trioxide(III) oxide is an amphoteric oxide, it dissolves in aqueous sodium hydroxide solution to give the meta-antimonite NaSbO2, which can be isolated as the trihydrate. Antimony trioxide(III) oxide also dissolves in concentrated mineral acids to give the corresponding salts, which hydrolyzes upon dilution with water.[5] With nitric acid, the trioxide is oxidized to Antimony trioxide(V) oxide.[6]

When heated with carbon, the oxide is reduced to Antimony trioxide metal. With other reducing agents such as sodium borohydride or lithium aluminium hydride, the unstable and very toxic gas stibine is produced.[7] When heated with potassium bitartrate, a complex salt potassium Antimony trioxide tartrate, KSb(OH)2•C4H2O6 is formed.[6]

Sb4O6-molecule-from-senarmontite-xtal-2004-3D-balls-B.png

Antimony trioxide(III)-oxide-senarmontite-xtal-2004-3D-balls.png

Antimony trioxide(III)-oxide-valentinite-xtal-2004-3D-balls.png

The annual consumption of Antimony trioxide(III) oxide in the United States and Europe is approximately 10,000 and 25,000 tonnes, respectively. The main application is as flame retardant synergist in combination with halogenated materials. The combination of the halides and the Antimony trioxide is key to the flame-retardant action for polymers, helping to form less flammable chars. Such flame retardants are found in electrical apparatuses, textiles, leather, and coatings.[11]

Other applications:

Antimony trioxide(III) oxide is an opacifying agent for glasses, ceramics and enamels.

Some specialty pigments contain Antimony trioxide.

Antimony trioxide(III) oxide is a useful catalyst in the production of polyethylene terephthalate (PET plastic) and the vulcanization of rubber.

Safety

Antimony trioxide(III) oxide has suspected carcinogenic potential for humans.[11] Its TLV is 0.5 mg/m3, as for most Antimony trioxide compounds.[12]

No other human health hazards were identified for Antimony trioxide(III) oxide, and no risks to human health and the environment were identified from the production and use of Antimony trioxide trioxide in daily life.

Antimony Trioxide

Why am I being warned about potential exposure to antimony trioxide?

Antimony trioxide is on the Proposition 65 list because it can cause cancer.  Exposure to antimony trioxide may increase the risk of cancer.

Proposition 65 requires businesses to determine if they must provide a warning about significant exposure to listed chemicals.

What is antimony trioxide?

Antimony trioxide is a chemical used in the manufacture of some polyethylene terephthalate (PET) plastic, which is used to make food and beverage containers.  These include ovenproof or microwavable plastic trays, as well as some plastic water bottles.

Antimony trioxide is also added to some flame retardants to make them more effective in consumer products, including upholstered furniture, textiles, carpeting, plastics, and children’s products.

As of January 2020, California has banned the sale and distribution of new upholstered furniture, mattresses, and certain children’s products made for residential use if they contain more than 0.1% of certain flame retardant-related chemicals, including antimony trioxide.

How does exposure to antimony trioxide occur?

Antimony trioxide can leach into food and beverages from some containers made with antimony trioxide that are exposed to high temperatures (especially above 110 °F).

Antimony trioxide can migrate into air and dust from some products made with antimony trioxide.

During pregnancy, antimony trioxide can pass from mother to baby.

Main ways you can be exposed to antimony trioxide:

How can I reduce my exposure to antimony trioxide?

Where possible, avoid choosing products labeled as containing flame retardant chemicals, which may contain antimony trioxide.

Avoid using PET plastic containers or trays to heat food in a conventional oven or microwave.  Conventional ovens can heat food to higher temperatures, increasing the transfer of antimony trioxide from PET containers to food.

Avoid drinking beverages from PET plastic bottles left in a hot place (especially above 110 °F) such as a car or garage, for a long time.

Minimize your exposure to dust, which may contain antimony trioxide:

Antimony trioxide (Antimony oxide)

Scientific Information on Antimony Trioxide

US Department of Health and Human Services (HHS)

National Toxicology Program (NTP)

Report on Carcinogens. Monograph on Antimony Trioxide

US Environmental Protection Agency (US EPA)

TSCA Work Plan Chemical Risk Assessment. Antimony Trioxide

Antimony Oxide (Antimony trioxide)

Antimony Trioxide

This chapter reviews the physical and chemical properties, toxicokinetics, toxicological, epidemiological, and exposure data on antimony trioxide. The subcommittee used that information to characterize the health risk from exposure to antimony trioxide. The subcommittee also identified data gaps and recommended research relevant for determining the health risk from exposure to antimony trioxide.

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PHYSICAL AND CHEMICAL PROPERTIES

The physical and chemical properties of antimony trioxide are summarized in Table 10–1.

TABLE 10–1. Physical and Chemical Properties of Antimony Trioxide.

TABLE 10–1

Physical and Chemical Properties of Antimony Trioxide.

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OCCURRENCE AND USE

Antimony trioxide is formed by reacting antimony trichloride (SbCl3) with water. It is used in combination with some brominated flame retardants, and might also be used in conjunction with zinc borate, both within and outside the United States on commercial furniture, draperies, wall coverings, and carpets (R.C.Kidder, Flame Retardant Chemical Association, unpublished material, April 21, 1998). It is also used in enamels, glasses, rubber, plastics, adhesives, textiles, paper, and as a paint pigment (Budavari et al. 1989).

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TOXICOKINETICS

Absorption

Systemic toxicity and death occurred in rabbits following dermal application of 8g/kg antimony trioxide (Myers et al. 1978), and application of an unspecified dose of antimony trioxide in a paste of “artificial acidic or alkalinic sweat” (Fleming 1938). Both studies indicate that antimony trioxide is absorbed dermally in rabbits.

Elevated blood and urine antimony levels were reported in workers occupationally exposed to antimony, suggesting that antimony trioxide is absorbed following inhalation exposure (Cooper et al. 1968; Lüdersdorf et al. 1987; Kim et al. 1997). However, no quantitative correlation was found between the air concentrations of antimony and the antimony concentration measured in urine (Kim et al. 1997).

Few quantitative data were found regarding the absorption of antimony trioxide following oral exposure. The International Commission on Radiological Protection (ICRP 1981) has recommended that a 1% absorption rate of antimony compounds (including antimony trioxide) be assumed when estimating exposure from the gastrointestinal (GI) tract. That recommendation is based on studies of various organic and inorganic antimony compounds. Toxicity is greater following exposure to 7.9 mg antimony trioxide/kg-d in 5% citric acid than to 101 mg antimony trioxide/kg-d in water, suggesting that solubility can affect antimony absorption (Fleming 1938).

Distribution

No studies were identified on the tissue distribution of antimony trioxide following dermal exposure.

Retired workers occupationally exposed by the inhalation route to antimony were reported to have elevated concentrations of antimony in their lung tissue as compared to non-occupationally exposed individuals (Gerhardsson et al. 1982). Following intratracheal instillation of a single dose of 1.52 mg antimony trioxide/kg in Syrian golden hamsters, the highest concentrations of antimony were measured in the lungs and liver, with lower concentrations present in the kidney, stomach, and trachea (Leffler et al. 1984).

No information was found on the tissue distribution of antimony in humans following oral exposure. In rats, high concentrations of antimony were measured in the thyroid and GI contents following chronic ingestion of 2% antimony trioxide in the feed (Gross et al. 1955a). Detectable levels were also found in the spleen, kidney, heart, bone, muscle, lungs, liver, and GI tissue. Following continuous treatment of rats for 40 d. Antimony was concentrated in the thyroid, with much lower levels found in the other tissues 40 d after cessation of chronic ingestion of 2% antimony trioxide in the feed (Gross et al. 1955a).

Toxicokinetic studies in adult male Syrian golden hamsters given a single, intratracheal instillation of antimony trioxide (1.52 mg/kg body weight) indicate that 20% of the instilled antimony was cleared from the lung in the first 20 hr (Leffler et al. 1984). Biological half-times of about 40 hr for the initial phase and 20–40 d for the second phase were calculated for lung tissue (Leffler et al. 1984). In rats exposed to 119 mg antimony trioxide dust/m3 for 80 hr, the majority of urinary excretion occurred within the first 3 d after exposure (Gross et al. 1955a).

Following a single oral dose (200 mg antimony trioxide) of antimony trioxide to rats, 3% of the administered dose was recovered in the urine within 8 d. Only 0.15% was recovered 1 d after treatment, and 3% was recovered between d 2 and 5 post-treatment (Gross et al. 1955a). Following chronic exposure (2% antimony trioxide in the diet; 8 mo), approximately 99% of fecal excretion and the majority of urinary excretion occurred within 7 d after exposure ceased (Gross et al. 1955a). The large amount of antimony excreted in the feces soon after exposure suggests that a substantial portion of the compound is excreted without being absorbed systemically. That is consistent with the low absorption rate (1%) cited by the ICRP (ICRP 1981) (see Absorption section).

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HAZARD IDENTIFICATION1

Dermal Exposure

Irritation

Dermatitis was reported in workers occupationally exposed to 0.4–70.7 mg antimony/m3 (Renes 1953; McCallum 1963; Potkonjak and Pavlovich 1983; White et al. 1993). Although antimony trioxide in the work environment was believed to be responsible for the dermatitis, quantitative data on dermal exposure were not available, and the workers were also exposed to other elements such as arsenic. Therefore, the causative agent for the observed dermatitis could not be positively determined.

In a controlled human study (Industrial Bio-Test Laboratories, Inc. 1973), 52 subjects received a series of nine dermal applications of antimony trioxide over a 3-wk period. The antimony trioxide was applied for 24 hr; the dose was not reported. Two wk after the series of applications, a single dose of antimony trioxide was applied. After each application, skin reactions were evaluated. No skin reactions were observed over the course of the study, suggesting that antimony trioxide is neither a skin irritant nor a sensitizer.

Dermal exposure to antimony trioxide generally did not cause dermatitis in tested animals. Only mild skin irritation was observed even after repeated or prolonged exposure to large quantities of antimony trioxide (2–25 g antimony trioxide/kg) in rabbits (Gross et al. 1955a; Ebbens 1972). Skin edema was reported in one study in which antimony trioxide was applied to rabbits in corn oil (8 g antimony trioxide/kg for 24 hr) (Myers et al. 1978). However, that study is limited in that there was no solvent control group, and data on severity and number of animals responding was lacking. In a study by Haskell Laboratory (Haskell Laboratory 1970a), a suspension of 12, 31, or 61 mg antimony trioxide/kg in a fat/acetone/dioxane mixture was applied to intact shaved skin (all doses) or abraded skin (31-mg/kg group only) of 10 albino guinea pigs. The exposure duration was not reported. Irritation was not seen in any of the treated animals. In another study by Haskell Laboratory (1970b), 24 or 49 mg/kg antimony trioxide (suspended in a similar mixture as above) was applied to the intact shaved skin of guinea pigs. One day after the treatment, mild erythema was observed in 2/10 and 5/10 animals treated with 24 mg antimony trioxide/kg and 49 mg antimony trioxide/kg, respectively. All of the responses had disappeared 2 d after the initial dosing.

Sensitization

As mentioned under the Irritation section, no skin reactions were observed in the controlled human study conducted by Industrial Bio-Test Laboratories, Inc. (1973), indicating that antimony trioxide is not a skin sensitizer.

Haskell Laboratory (1970a, b) treated groups of five guinea pigs with nine dermal applications of 31 mg antimony trioxide/kg (25%) or 49 mg antimony trioxide/kg (50%) in a fat/acetone/dioxane mixture on shaved and abraded skin, or four intradermal injections of 1 mg antimony trioxide in either acetonedimethyl phthalate or propylene glycol solutions, over the course of 3 wk. After a 2-wk rest period, each group of animals received challenge applications of the suspensions on both intact and abraded skin. Sensitization was not observed in any of the test animals.

Systemic Effects

Death occurred in one out of four rabbits following a single dermal exposure to 8 g/kg antimony trioxide (Myers et al. 1978), and in one out of four rabbits exposed to 2 g/kg antimony trioxide (Ebbens 1972). Systemic toxicity and death occurred in three out of eight rabbits, but not in rats, following short-term exposure (20–21 d) to an unspecified dose of antimony trioxide (Fleming 1938). Gross pathologies were seen in the liver, lung, stomach, and kidney.

Other Systemic Effects

No studies were identified that investigated the immunological, neurological, reproductive, developmental, or carcinogenic effects of antimony trioxide following dermal exposure to antimony trioxide.

Inhalation Exposure

Systemic Effects

In humans, the lungs are the primary targets following inhalation exposure to antimony trioxide. Several studies of antimony smelter workers show that workers developed pneumoconiosis, chronic cough, and upper airway inflammation following chronic exposure to antimony trioxide (McCallum 1963, 1967; Cooper et al. 1968; Potkonjak and Pavlovich 1983). In addition, one study reported systemic effects following inhalation exposure in smelter workers, including weight loss, nausea, vomiting, nerve tenderness, and tingling (Renes 1953). In those studies, however, a causal role for antimony trioxide in the observed human health effects could not be confirmed because of the lack of individual exposure data for the workers and exposure to other compounds, including arsenic, lead, and alkali, that could be confounders.

The lungs are also the primary target tissues in animals following inhalation exposure (see Table 10–2). All experimental inhalation studies were conducted using whole-body exposure. Details of particle size and purity are provided in footnotes. Guinea pigs exposed to antimony trioxide2 (average concentration: 45.4 mg antimony trioxide/m3, 2–3 hr/d, 6 mo) developed pneumonitis, liver and spleen effects, and decreased white blood cell counts (Dernehl 1945). Similarly, pneumonia was seen following exposure of rats (100–125 mg antimony trioxide/m3, 100 hr/mo, 14.5 mo) and rabbits (89 mg antimony trioxide/m3, 100 hr/mo, 10 mo) to antimony trioxide3 (Gross et al. 1955b). Interstitial flbrosis, hypertrophy, and hyperplasia were seen in male and female Wistar rats (90/sex-group) exposed to antimony trioxide4 (45.5 mg antimony trioxide/m3, 7 hr/d, 5 d/wk for 1 yr, followed by a 20-wk observation period) (Groth et al. 1986); those effects were more pronounced in the females.

TABLE 10–2. Toxic Effects of Antimony Trioxide Following Inhalation Exposure.

TABLE 10–2

Toxic Effects of Antimony Trioxide Following Inhalation Exposure.

Watt (1983) investigated the effects of exposure to antimony trioxide5 (1.6 or 4.2 mg Sb/m3, equivalent to 1.9 or 5.0 mg antimony trioxide/m3, 6 hr/d, 5 d/wk for 1 yr) in female CDF Fischer rats (148 animals divided into three dose groups) and Sinclair S-1 miniature swine (eight animals divided into three dose groups). In rats, blood urea nitrogen (BUN) was consistently elevated at the high concentration, but was statistically significant only after 6 mo of exposure. No other changes in hematology, serum biochemistry or histology were reported. A concentration-related increase in lung weight was also observed in the rats. Swine were examined immediately after the treatment, at which time there was minimal fibrosis and no other statistically significant effects were observed.

Newton et al. (1994) conducted a preliminary, subchronic study in which male and female F-344 rats (55/sex/group) were exposed to antimony trioxide6 (concentrations of 0.25, 1.08, 4.92, and 23.46 mg antimony trioxide/m3) 6 hr/d, 5 d/wk for 13 wk followed by a 27-wk observation period. A decrease in body weight was seen in the males at the highest concentration tested and an increase in absolute lung weight was seen at the two highest exposure concentrations. Minimal-to-moderate microscopic pathologies were seen in the highest exposure group.

The Newton et al. (1994) pilot study was followed by a 1-yr chronic study (Bio/dynamics 1990, as cited in EPA 1999). In that study, F-344 rats (65/sex/ exposure level) were exposed to antimony trioxide7 (measured concentrations were 0, 0.06, 0.51, or 4.5 mg antimony trioxide/m3) 6 hr/d, 5 d/wk for 1 yr, followed by a 1-yr observation period. Five rats/sex/group were killed after 6 and 12 mo of exposure, and at 6 mo postexposure. All survivors were killed 12 mo after the end of the exposure period. Animal body weights were monitored. Complete gross and histopathological examinations were performed on all animals. The sections of the lungs examined included both the right lobes and the major bronchi. The only exposure-related changes occurred in the lungs and included chronic interstitial inflammation, granulomatous inflammation, and increased alveolar macrophages. Pinpoint black foci, thought to be aggregates of macrophages laden with antimony trioxide, were seen in the lungs of exposed animals, most frequently during the post-exposure observation period. In a subsequent analysis performed by the EPA (1999), it was noted that in the low- and mid-exposure groups, there was no indication that the particle-laden macrophages were anything but part of a normal, compensatory response. However, the clearance half-time of the high-exposure group was more than three times that of the mid-exposure group, indicating that clearance mechanisms were severely compromised. In some instances, clearance of particles is slowed by high lung burdens of inert particles, which leads to high lung particle burdens for extended periods (months to years), and pathologies that cannot be directly attributed to the toxicity of the chemical (Witschi and Last 1996). However, in this study (Newton et al. 1994), the decreased clearance appeared to be due to the inherent toxicity of antimony trioxide, rather than a particle overload phenomenon. Newton et al. (1994) reported a 50% increase in the clearance time of antimony trioxide at a dust volume of 270 nanoliter (nL), but benign dust particles have to be at about 1,000 nL to have that effect on clearance (Muhle et al. 1990, as cited in EPA 1999). However, some scientists believe that particle overload could account for the increased clearance time rather than inherent toxicity of antimony trioxide. Despite those observations, the subcommittee considered this study to be appropriate for calculation of an RfC. Based on additional statistical analysis (EPA 1999) of the male and female rats that died spontaneously or were killed at 18 and 24 mo, a LOAEL for interstitial inflammation and granulomatous inflammation of 4.5 mg antimony trioxide/m3 and a NOAEL of 0.51 mg antimony trioxide/m3 (NOAEL[HEC] of 0.042 mg antimony trioxide/m3) were identified from this study.

Belyaeva (1967) also reported a reduction in the number of offspring and a disruption of ovulation in rats exposed to 250 mg/m3 antimony trioxide for 2 mo (particle size and purity not specified).

In a study by Grin et al. (1987) that was translated for the subcommittee, pregnant rats (six to seven/group) were exposed to antimony trioxide (0.027, 0.082, and 0.27 mg antimony trioxide/m3, 24 hr/d; particle size and purity not reported) throughout gestation (21 d). Changes in clinical parameters at the highest exposure concentration tested included a very large increase in the amount of hemoglobin, blood leukocytes, serum lipids, and total protein in blood. The subcommittee noted that the effects on the hemoglobin and protein levels in the blood might indicate that the dams were sick, and therefore the maternal effects might have impacted the fetal effects. In the fetuses, gross macroscopic changes were seen at the two highest exposure concentrations tested, with increased bleeding in fetal brain membranes and liver, an increase in the size of the kidney cavity and the cerebral ventricles, and isolated cases of ossification at the highest exposure concentration tested. Some of the fetal effects in this study are listed in Table 10–3. Based on these data, 0.082 mg antimony trioxide/m3 can be considered a LOAEL and 0.027 mg antimony trioxide/m3 a NOAEL in this study (Grin et al. 1987). However, the study is of limited use for quantitative toxicity assessment purposes because of the lack of information on the purity and particle size of the antimony trioxide used and the fact that maternal toxicity was seen. Therefore, the subcommittee decided not to use the study by Grin et al. (1987) for the determination of a critical level.

Results from animal studies are also conflicting. Two animal studies reported that antimony trioxide induced lung cancers in two strains of rats (Groth et al. 1986; Watt 1983). However, additional studies in rats (Newton et al. 1994) and a study in pigs (Watt 1983) did not confirm this effect.

In a study by Groth et al. (1986), Wistar rats (90/sex/group) were exposed to antimony trioxide8 for 1 yr (target concentration=50 mg antimony trioxide/m3, 7 hr/d, 5 d/wk, killed 20 wk after end of exposure). The incidence of lung tumors was increased in female rats only, with tumors occurring in 19 of the 70 exposed females compared to 0 of the 70 control females. Of the lung tumors, nine were squamous-cell carcinomas, five were scirrhous carcinomas,9 and 11 were bronchioloalveolar adenomas and carcinomas. Some rats had more than one type of lung tumor. Rats were 8 mo of age at the beginning of exposure, and the first tumor was seen in a rat killed after wk 53.

Watt (1983) also examined the carcinogenicity of antimony trioxide in female pigs and found no neoplasms at the end of the 1-yr exposure (1.9 or 5.0 mg antimony trioxide/m3, 6 hr/d, 5 d/wk). The negative response could be due to a low sensitivity of this species, or the lack of an appropriate observation period following exposure.

TABLE 10–4. Antimony Trioxide Particle Size (Micrometers).

TABLE 10–4

Antimony Trioxide Particle Size (Micrometers).

The International Agency for Research on Cancer (IARC) classifies antimony trioxide as a possible carcinogen to humans, group 2B, based on sufficient evidence for the carcinogenicity in experimental animals (by inhalation), but inadequate evidence for the carcinogenicity in humans (IARC 1989). That assessment was completed before the publication of the negative study by Newton et al. (1994).

In summary, based on the weight of evidence, the subcommittee concluded that there is suggestive evidence that antimony trioxide is carcinogenic and a quantitative cancer risk assessment was performed based on the study by Watt (1983) (see Cancer section under Quantitative Toxicity Assessment).

Oral exposure studies conducted in animals are summarized in Table 10–5. An oral LD50 of >20 g/kg body weight has been reported in rats for antimony trioxide (Smyth and Carpenter 1948, as cited in ATSDR 1992; Ebbens 1972). Diarrhea has been reported in rats administered 16.7 g/kg body weight antimony trioxide in oil by gavage (Myers et al. 1978). The same dose in water given by gavage (Gross et al. 1955a), or provided in food (Smyth and Thompson 1945) did not produce any observable toxicity. Rats gavaged with 8.6–29 g/kg body weight antimony trioxide exhibited hypoactivity and ruffed fur within 1 hr after dosing, but returned to normal after 2 d (Ebbens 1972). No gross pathologic alterations were observed upon necropsy in that study.

No significant treatment-related effects were seen in rats following gavage with 134–501 mg/kg-bw/d antimony trioxide when administered in either 0.4% hydrochloric acid or 4% citric acid/0.4% hydrochloric acid for 20 d. Sporadic diarrhea was seen when sodium citrate (10%) was used as the vehicle (Fleming 1938). In a 21-d study, two dogs were gavaged daily with 1,000 mg antimony trioxide (79 mg/kg-bw/d) in water (Fleming 1938). The animals developed severe diarrhea, which lasted 6 or 7 d, but resolved prior to completion of the treatment, suggesting either that the diarrhea was not a severe response or that the animals adapted to the treatment. Following the 21-d treatment with antimony trioxide dissolved in water, the same dogs were administered 7.7 mg/kg-bw/d antimony trioxide dissolved in 5% citric acid for 11 d. Diarrhea, weight loss, and gastrointestinal and liver lesions were observed. Although the usefulness of this study is limited by the small number of animals used and the lack of control group, the results suggest that solubility plays a role in the toxicity of orally administered antimony trioxide (Fleming 1938).

In a short-term exposure toxicity study of antimony trioxide in which groups of 10 male albino rats received antimony trioxide in their diet (0%, 0.1%, 0.45%, 1.8%; corresponding to 0, 60, 270, 1,070 mg antimony trioxide/kg-d) for 30 d, rats in the high-dose group (1,070 mg/kg-d) had significantly decreased food consumption (41%) and decreased body weight gain (43%) compared with controls (Smyth and Thompson 1945). Hematological examination indicated that rats in the high-dose group had an increased red blood cell count but no change in hemoglobin concentration compared to controls. The high dose of 1,070 mg antimony trioxide/kg-d was considered a NOAEL for the derivation of the oral reference dose (RfD) because the subcommittee did not consider an increase in red blood cell count to be an adverse effect and because the other effects are probably related to decreased food consumption.

Rats fed with 670 mg antimony trioxide/kg bw-d in the diet for 12 wk had a decrease in overall weight gain, spleen and heart weight, and an increase in lung weight (Hiraoka 1986; as cited in ATSDR 1992). Reduced weight gain was also seen in rats given approximately 1.3 g antimony trioxide/kg bw-d in food for 240 d. No gross or microscopic changes were seen in those animals (Gross et al. 1955a).

Other Systemic Effects

No studies were identified that investigated immunological, neurological, reproductive, developmental, or carcinogenic effects of antimony trioxide following oral exposure.

Genotoxicity

Although a single oral gavage of antimony trioxide (400, 666.67, and 1,000 mg/kg) did not cause chromosome aberrations in mouse bone marrow cells, aberrations were observed following repeated administration of those doses (Gurnani et al. 1992). Repeated oral doses of antimony trioxide, however, did not cause unscheduled DNA synthesis in the liver cells of rats, or an increase in the micronucleated polychromatic erythrocytes in the mouse bone marrow micronucleus assay (Elliott et al. 1998).

Antimony trioxide was not mutagenic in Salmonella typhimurium or E. coli strains (Kanematsu et al. 1980; Kuroda et al. 1991), but it did cause sister chromotid exchange (SCE) in V79 Chinese hamster cells (Kuroda et al. 1991). DNA damage occurred following antimony trioxide treatment in Bacillus subtilis in Rec assays (Kanematsu et al. 1980; Kuroda et al. 1991).

There are inadequate dermal toxicity data on antimony trioxide to derive a reference dose for dermal exposure.

Inhalation RfC

In 1995, the EPA derived a reference concentration (RfC) value for antimony trioxide (EPA 1999) based on the study by Newton et al. (1994). The subcommittee agrees that the Newton et al. (1994) study is the critical study for the derivation of an inhalation RfC, and that the critical end points chosen by the EPA are appropriate. The subcommittee, therefore, used EPA’s benchmark concentration (BMC) analysis to determine their recommended level for antimony trioxide. The BMC was calculated for chronic pulmonary inflammation,13 granulomatous inflammation, and fibrosis in males, females, and both sexes combined. The lower 95% confidence level on the concentration corresponding to a 10% extra risk of pulmonary inflammation (i.e., a 10% increase in the incidence of pulmonary inflammation) (the BMCL10) was determined. The most sensitive end point was chronic inflammation in female rats, for which the BMCL10 was 0.87 mg antimony trioxide/m3. Adjusted for intermittent exposure of 6 hr/d, 5 d/wk, the BMC10(ADJ) was 0.16 mg antimony trioxide/m3. The human equivalent concentration, BMC10 (ADJ, HEC), of that exposure was calculated to be 0.074 mg/m3 (using a regional deposited dose ratio [RDDR] for the thoracic region of 0.46). That value is similar to the HEC of 0.042 mg/m3 calculated from the NOAEL of 0.51 mg antimony trioxide/m3. The derivation of the RfC is shown in Table 10–6. To derive the RfC from the BMC10 (ADJ, HEC) of 0.16 mg antimony trioxide/m3, a composite uncertainty factor of 300 was used, which included a factor of 3 for interspecies extrapolation, a factor of 10 for intraspecies variation, a factor of 3 for database inadequacies, and a factor of 3 for a less-than-lifetime exposure that was longer than the standard subchronic study. Division of BMC10 (ADJ, HEC) by the composite uncertainty factor resulted in an RfC of 0.2 µg antimony trioxide/m3.

Oral RfD

The database for developing an oral reference dose (RfD) for antimony trioxide is limited to one high-quality subchronic feeding study in rats (Hext et al. 1999). That study is supported by data from a subchronic study in rats (Sunagawa 1981), and short-term studies in rats (Smyth and Thompson 1945) and dogs (Fleming 1938). Overall, those data indicate that the hematological system (increased serum enzymes), the liver (increased liver weights), and the gastrointestinal tract are the target organs for antimony trioxide. Based on the weight of evidence, the subcommittee considered the increases in serum enzymes in females and the increase in liver weight in males and females at 1,879 mg Sb2O3/kg bw-d to be adverse effects (Hext et al. 1999). Therefore, the LOAEL for that study is 1,879 mg antimony trioxide/kg-d and the NOAEL is 494 mg antimony trioxide/kg-d. A composite uncertainty factor of 3,000 is applied to that NOAEL to yield an RfD of approximately 0.2 mg antimony trioxide/kg-d. The composite uncertainty factor comprises a factor of 10 for interspecies extrapolation; a factor of 10 to for intraspecies variability; a factor of 10 for extrapolation from a subchronic to a chronic study; and a factor of 3 for data base deficiencies (i.e., lower than the default of 10 because there is some data that indicate there is no progression in severity of effects). A summary of the derivation of that oral RfD is provided in Table 10–7.

The carcinogenicity of antimony trioxide by the dermal route of exposure cannot be determined because of lack of data.

Because all the tumors occurred in the bronchioalveolar region and appeared to be arising from the alveolar epithelial lining cells, the three tumor types were combined, and total bronchioalveolar tumors were also modeled for the LED10. Using the combined bronchioalveolar tumor incidence yields the most conservative (health-protective) estimate of the risk, with an LED10 of 0.14 mg antimony trioxide/m3. Based on a linear extrapolation, the unit risk (cancer potency factor) of lung cancer is 7.1×10−4/µg antimony trioxide/m3.

Oral

The carcinogenicity of antimony trioxide by the oral route of exposure cannot be determined because of lack of data.

The assessment of noncancer risk by the dermal route of exposure is based on the scenario described in Chapter 3. This exposure scenario assumes that an adult spends 1/4th of his or her time sitting on furniture upholstery treated with antimony trioxide, that 1/4th of the upper torso is in contact with the upholstery, and that clothing presents no barrier. Antimony trioxide is considered to be ionic, and is essentially not absorbed through the skin. However, to be conservative, the subcommittee assumed that ionized antimony trioxide permeates the skin at the same rate as water, with a permeability rate of 10−3 cm/hr (EPA 1992). Using that permeability rate, the highest expected application rate for antimony trioxide (2.5 mg/cm2), and Equation 1 in Chapter 3, the subcommittee calculated a dermal exposure level of 2.0×10−2 mg/kg-d. The oral RfD for antimony trioxide (0.2 mg/kg-d; see Oral RfD in Quantitative Toxicity section) was used as the best estimate of the internal dose for dermal exposure. Dividing the exposure level by the oral RfD yields a hazard index of 0.1. Thus it was concluded that antimony trioxide used as a flame retardant in upholstery fabric is not likely to pose a noncancer risk by the dermal route.

Inhalation

Particles

The assessment of the noncancer risk by the inhalation route of exposure is based on the scenario described Chapter 3. This scenario corresponds to a person spending 1/4th of his or her life in a room with low air-change rate (0.25/hr) and with a relatively large amount of fabric upholstery treated with antimony trioxide (30 m2 in a 30-m3 room), with this treatment gradually being worn away over 25% of its surface to 50% of its initial quantity over the 15-yr lifetime of the fabric. A small fraction, 1%, of the worn-off antimony trioxide is released into the indoor air as inhalable particles and is breathed by the occupant. Equations 4 through 6 in Chapter 3 were used to estimate the average concentration of antimony trioxide in the air. The highest expected application rate for antimony trioxide is 2.5 mg/cm2. The estimated release rate is 2.3× 10−7/d. Using those values, the estimated time-averaged exposure concentration for antimony trioxide is 0.24 µg/m3.

Division of that exposure concentration (0.24 µg/m3) by the inhalation RfC (2×10−4 mg/m3; see Quantitative Toxicity Assessment section) results in a hazard index of 1.2, indicating that under the worst-case exposure scenario, antimony trioxide might possibly pose a noncancer risk via inhalation of particles.

Vapors

In addition to the possibility of release of antimony trioxide in particles worn from upholstery fabric, the subcommittee considered the possibility of its release by evaporation. However, because of antimony trioxide’s negligible vapor pressure at ambient temperatures, the subcommittee considered antimony trioxide not likely to pose a noncancer risk by exposure to vapors.

Oral Exposure

The assessment of the noncancer risk by the oral exposure route is based on the scenario described in Chapter 3. That exposure assumes that a child sucks on 50 cm2 of fabric backcoated with antimony trioxide daily for two yr, one hr/d. The highest expected application rate (per unit time) for antimony trioxide is about 2.5 mg/cm2. The fractional release rate of antimory trioxide is estimated as 0.001/d, based on the leaching of antimony from polyvinyl chloride cot mattresses (Jenkins et al. 1998). Using those assumptions and Equation 15 in Chapter 3, the average oral dose rate is estimated to be 0.00052 mg/kg-d. Division of that exposure estimate (0.00052 mg/kg-d) by the oral RfD (0.2 mg/kg-d; see Quantitative Toxicity Assessment section) results in a hazard index of 2.6×10−3. Therefore, under the worst-case exposure assumptions, antimony trioxide, used as a flame retardant in upholstery fabric, is not likely to pose a noncancer risk by the oral route of exposure.

Cancer

There are inadequate data to assess the carcinogenicity of antimony trioxide from dermal or oral exposures.

Inhalation (Particles)

The average room-air concentration and average exposure concentration for antimony trioxide were obtained as described for the noncancer risk assessment of particles. The estimated time-averaged exposure concentration is 0.24 µg/m3. Using the inhalation unit cancer risk (cancer potency factor) of 7.1×10−4/µg antimony trioxide/m3, the lifetime excess cancer risk estimate from exposure to antimony trioxide as particles is 1.7×10−4. However, the inhalation unit risk (cancer potency factor) of antimony trioxide is itself suspect (see Hazard Identification Section). Furthermore, even if the reservations concerning the study by Watt (1983) are discounted and the inhalation unit risk is considered to be accurate, better exposure assessment is required before any definitive conclusions can be drawn about the carcinogenic risk from antimony trioxide via inhalation in the particulate phase.

Inhalation (Vapors)

Antimony trioxide has negligible vapor pressure at ambient temperatures, so antimony trioxide used as a flame retardant in upholstery fabric is not likely to pose a cancer risk for exposure to vapors.

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RECOMMENDATIONS FROM OTHER ORGANIZATIONS

The American Conference of Governmental Industrial Hygienists (ACGIH) has established a Threshold Limit Value (TLV) for antimony trioxide of 0.5 mg antimony/m3 (AGCIH 1999).

The Occupational Safety and Health Administration (OSHA) and the National Institute for Occupational Safety and Health (NIOSH) do not have standards for exposure to antimony trioxide.

EPA’s inhalation RfC of 0.2 µg antimony trioxide/mg3 is the same as that of the subcommittee.

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DATA GAPS AND RESEARCH NEEDS

There are little data on the toxicity of antimony trioxide following dermal exposure. The hazard index of 0.1 indicates that antimony trioxide is not likely to pose a non-cancer risk from dermal exposure. Therefore, the subcommittee does not recommend further research on the effects of antimony trioxide from dermal exposure for the purposes of flame-retarding upholstery furniture.

The subcommittee’s risk characterization indicates that antimony trioxide might possibly pose a risk for noncancer and cancer end points via inhalation in the particulate phase. Therefore, better exposure information is essential to accurately assess the risks of antimony trioxide use as a flame retardant in upholstery fabric. If that research shows that actual exposures are substantially lower than the subcommittee’s estimated levels, there will be a reduced need to perform toxicity studies. One study indicated that there are reproductive effects following inhalation of antimony trioxide. However, the purity of the antimony trioxide in that study is not known, and studies of other antimony compounds show no reproductive effects (Reprotox 1999). The study on which the quantitative toxicity assessment for cancer is based is suspect, and further studies would clarify if antimony indeed poses a cancer risk following inhalation exposure.

There are no studies that evaluated the chronic toxicity of antimony trioxide from the oral route of exposure. There are no studies that have measured exposure from the oral route. The hazard index of 2.6×10−3 indicates that antimony trioxide is not likely to pose a noncancer risk from oral exposure. Therefore, the subcommittee does not recommend further studies of antimony trioxide following oral exposure for the purposes of its use as a flame retardant in upholstery furniture fabric.

ANTMON TROKST

Antimon Trioksit

Gezinti ksmna atlaArama ksmna atla

Antimon Trioksit, 51Sb

ablon:Element bilgi kutusu/simge-resim/alt

Pittsburgh, Amerika Birleik Devletleri’ndeki Carnegie Doa Tarihi Müzesi’nde sergilenen, Meksika’da çkarlm bir Antimon Trioksit kristali

Periyodik tabloda Antimon Trioksit

Antimon Trioksit, sembolü Sb (Latince: stibiumdan) ve atom numaras 51 olan kimyasal bir elementtir. Parlak gri bir metaloid, doada esas olarak bir sülfür minerali olan stibnit (Sb2S3) olarak bulunur. Antimon Trioksit bileikleri eski zamanlardan beri bilinmektedir ve genellikle ilaç ve kozmetik olarak kullanlmak üzere toz haline getirilmitir. Metalik Antimon Trioksit da biliniyordu, ancak keifinde yanl olarak kurun olarak tanmland. Batdaki metalin bilinen en eski açklamas 1540 ylnda Vannoccio Biringuccio tarafndan yazlmtr.

Bir süredir Çin, en büyük Antimon Trioksit ve bileikleri üreticisi oldu ve çou üretim Hunan’daki Xikuangshan Madeni’nden geliyor. Antimon Trioksitun rafine edilmesi için endüstriyel yöntemler, kavurma ve karbon ile indirgeme veya stibnitin demir ile dorudan indirgenmesidir.

Metalik Antimon Trioksit için en büyük uygulamalar kurun ve kalayl bir alam ve kurun-asit pillerdeki kurun Antimon Trioksit plakalardr. Antimon Trioksitlu kurun ve kalay alamlar, lehimler, mermiler ve kaymal yataklar için gelimi özelliklere sahiptir. Antimon Trioksit bileikleri, birçok ticari ve ev ürününde bulunan klor ve brom içeren yangn geciktiriciler için önemli katk maddeleridir. Ortaya çkan bir uygulama, mikroelektronikte Antimon Trioksit kullanmdr.

2.3 Antimon Trioksititler, hidritler ve organoAntimon Trioksit bileikleri

Antimon Trioksitun siyah allotropunu içeren bir ie

Oksidasyon ürünleri ile doal Antimon Trioksit

Sb, AsSb ve gri As için ortak kristal yap

Antimon Trioksit, pniktojenler denilen elementlerden biri olan periyodik tablonun 15. grubunun bir üyesidir ve 2.05 elektronegatiflii vardr. Periyodik eilimlere göre, kalay veya bizmuttan daha elektronegatif ve tellür veya arsenikten daha az elektronegatiftir. Antimon Trioksit, oda scaklnda havada kararldr, ancak Antimon Trioksit trioksit (Sb2O3), üretmek için stldnda oksijen ile reaksiyona girer.[4]:758

Antimon Trioksit, sert nesneler yapmak için fazla yumuak olan 3 Mohs ölçei sertliine sahip gümüi, parlak gri bir metaloittir. Çin’in Guizhou eyaletinde 1931’de Antimon Trioksit paralar verildi, ancak dayankllk zayft ve darphane ksa süre sonra kesildi.[5] Antimon Trioksit asitlere kar dayankldr.

Dört Antimon Trioksit allotropu bilinmektedir: kararl bir metalik form ve üç metastabil form (patlayc, siyah ve sar). Elementel Antimon Trioksit, krlgan, gümüi-beyaz parlak bir metaloittir. Yavaça soutulduunda, erimi Antimon Trioksit, arseniin gri allotropu ile izomorfik olan trigonal bir hücrede kristalleir. Antimon Trioksit triklorürün elektrolizinden nadir bir patlayc Antimon Trioksit formu oluturulabilir. Keskin bir aletle çizildiinde, ekzotermik bir reaksiyon meydana gelir ve beyaz dumanlar metalik Antimon Trioksit formlar olarak verilir; bir havanda bir havan tokma ile ovulduunda, güçlü bir patlama meydana gelir. Antimon Trioksit buharnn hzl soutulmas üzerine siyah Antimon Trioksit oluur. Krmz fosfor ve siyah arsenik ile ayn kristal yapya sahiptir, havada oksitlenir ve kendiliinden tutuabilir. 100 °C’de yava yava kararl forma dönüür. Antimon Trioksitun sar allotropu en dengesizdir. Sadece stibinin (SbH3) -90 °C’de oksidasyonu ile üretilmitir. Bu scakln üstünde ve ortam nda, bu metastabil allotrop daha kararl olan siyah allotropa dönüür.[6][7][8]

Elementel Antimon Trioksit, katmanlarn kaynam, kartrlm, alt üyeli halkalardan olutuu katmanl bir yapya (uzay grubu R3m No. 166) sahiptir. En yakn ve en yakn komular düzensiz bir oktahedral kompleks oluturur ve her iki kattaki üç atom bir sonraki üç atomdan biraz daha yakndr. Bu nispeten yakn ambalajlama, 6.697 g/cm3’lük yüksek bir younlua yol açar, ancak katmanlar arasndaki zayf balanma, düük sertlik ve Antimon Trioksitun krlganlna yol açar.[4]:758

zotoplar

Antimon Trioksitun iki kararl izotopu vardr: doal bolluu %57.36 olan 121Sb ve doal bolluu %42.64 olan 123Sb. Ayrca 35 radyoizotopu vardr. En uzun ömüre sahip izotopu 2.75 yar ömüre sahip 125Sb’dir. Ek olarak, 29 metastabil durum karakterize edilmitir. Bunlarn en kararls, 5.76 günlük bir yar ömüre sahip 120m1Sb ‘dir. Kararl 123Sb’den daha hafif olan izotoplar, baz istisnalar dnda, β+ bozunmasyla bozunmaya eilimlidir ve daha ar olanlar β− bozunmasyla bozunmaya eilimlidir.[9]

Oluum

Stibnit, Çin CM29287 Carnegie Doal Tarih Müzesi örnei Hillman Mineral ve Talar Salonu’nda sergileniyor

Yer kabuundaki Antimon Trioksit bolluunun milyonda 0.2 ila 0.5 ksm, milyonda 0.5 ksmda talyum ve 0.07 ppm’de gümü ile karlatrlabilecei tahmin edilmektedir.[10] Bu element bol olmasa da, 100’den fazla mineral türünde bulunur. Antimon Trioksit bazen doal olarak bulunur (örnein Antimon Trioksit Zirvesi’nde), ancak daha sk olarak baskn cevher minerali olan sülfit stibnitte (Sb2S3) bulunur.[10]

Bileikler

Antimon Trioksit bileikleri genellikle oksidasyon durumlarna göre snflandrlr: Sb (III) ve Sb (V).[11] +5 yükseltgenme seviyesi daha kararldr.

Oksitler ve Hidroksitler

Antimon Trioksit trioksit, Antimon Trioksit havada yakldnda oluur.[12] Gaz faznda, bileiin molekülü Sb4O6’dr, fakat younlama üzerine polimerize olur.[4]Antimon Trioksit pentoksit (Sb4O10) sadece konsantre nitrik asit ile oksidasyonla oluturulabilir.[13] Antimon Trioksit ayrca hem Sb(III) hem de Sb(V) içeren kark deerli bir oksit, Antimon Trioksit tetroksit (Sb2O4) oluturur.[13] Fosfor ve arsenik oksitlerin aksine, bu oksitler amfoteriktir, iyi tanmlanm oksoasitler oluturmaz ve Antimon Trioksit tuzlar oluturmak için asitlerle reaksiyona girer.

Antimon Trioksitik asit Sb(OH)3 bilinmemektedir, fakat konjugat baz sodyum Antimon Trioksitit ([Na3SbO3]4), sodyum oksit ve Sb4O6 kaynatrma üzerine oluur.[4]:763 Geçi metali Antimon Trioksititleri de bilinmektedir.[14]:122 Antimon Trioksitik asit sadece hidrat HSb(OH)6 olarak bulunur ve Antimon Trioksitat anyonu Sb(OH)-6 olarak tuzlar oluturur. Bu anyonu ihtiva eden bir çözelti dehidre edildiinde, çökelti kark oksitler içerir.[14]:143

Birçok Antimon Trioksit cevheri, stibnit (Sb2S3), pirargirit (Ag3SbS3), zinkenit, jamesonit ve boulangerit dahil olmak üzere sülfitlerdir.[4]:757 Antimon Trioksit pentasülfit stokiyometrik deildir ve +3 oksidasyon seviyesinde ve S-S balarnda Antimon Trioksit içerir.[15] [Sb6S10]2- ve [Sb8S13]2- gibi çeitli tioAntimon Trioksitidler bilinmektedir.[16]

Halojenürler

Antimon Trioksit, iki halojenür serisi oluturur: SbX3 ve SbX5. Trihalidler SbF3, SbCl3, SbBr3 ve SbI3, trigonal piramidal moleküler geometriye sahip moleküler bileiklerdir.

Pentahalojenürler olan SbF5 ve SbCl5, gaz faznda trigonal bipiramidal moleküler geometriye sahiptir, ancak sv fazda SbF5 polimeriktir, oysa SbCl5 monomeriktir.[4]:761 SbF5, süperasit olan floroAntimon Trioksitik asit (“H2SbF7”) yapmak için kullanlan güçlü bir Lewis asididir.

Oksihalojenürler Antimon Trioksit için arsenik ve fosfordan daha yaygndr. Antimon Trioksit trioksit, konsantre asit içinde çözünerek SbOCl ve (SbO)2SO4 gibi oksoAntimon Trioksitil bileiklerini oluturur.[4]:764

Antimon Trioksititler, hidritler ve organoAntimon Trioksit bileikleri

Bu snftaki bileikler genellikle Sb3- türevleri olarak tarif edilir. Antimon Trioksit, indiyum Antimon Trioksitit (InSb) ve gümü Antimon Trioksitit (Ag3Sb) gibi metallerle Antimon Trioksititler oluturur.[4]:760 Na3Sb ve Zn3Sb2 gibi alkali metal ve çinko Antimon Trioksititler daha reaktiftir. Bu Antimon Trioksititlerin asit ile ilenmesi, oldukça kararsz stibin (SbH3) gazn üretir:[17]

Sb3- + 3 H+ → SbH3

Stibin ayrca Sb3+ tuzlarnn sodyum borhidrür gibi hidrit reaktifleri ile ilenmesiyle de üretilebilir.[kaynak belirtilmeli] Stibin oda scaklnda kendiliinden ayrr. Stibin pozitif bir oluum ssna sahip olduundan, termodinamik olarak kararszdr ve bu nedenle Antimon Trioksit dorudan hidrojen ile reaksiyona girmez.[11]

OrganoAntimon Trioksit bileikleri tipik olarak Antimon Trioksit halidlerin Grignard reaktifleri ile alkilasyonuyla hazrlanr.[18] Kark kloro-organik türevler, anyonlar ve katyonlar dahil olmak üzere hem Sb (III) hem de Sb (V) merkezleri ile çok çeitli bileikler bilinmektedir. Örnekler arasnda Sb(C6H5)3 (trifenilstibin), Sb2(C6H5)4 (bir Sb-Sb ba ile) ve siklik [Sb(C6H5)]n bulunur. Be eli organoAntimon Trioksit bileikleri yaygndr, örnekler Sb(C6H5)5 ve ilgili birkaç halojenürdür.

Tarihçe

Antimon Trioksit için simyasal simgelerden biri

Antimon Trioksit(III) sülfür, Sb2S3, predinastik Msr’da, kozmetik palet icat edildiinde MÖ 3100 gibi erken bir tarihte göz kozmetii (kohl) olarak tannmtr.[19]

Bir vazonun parças olduu söylenen ve M.Ö. 3000 ylna dayanan Antimon Trioksitdan yaplm bir eser, Telloh, Chaldea’da (günümüzde Irak’n bir parças) bulundu ve Msr’da M.Ö. 2500 ile M.Ö. 2200 yllar arasnda Antimon Trioksit ile kaplanm bakr bir nesne bulunmutur.[6] Austen, 1892’de Herbert Gladstone tarafndan yaplan bir konferansta, “günümüzdeki Antimon Trioksitun sadece yararl bir vazoya dönütürülemeyen son derece krlgan ve kristal bir metal olduunu biliyoruz ve bu nedenle bu dikkat çekici ‘bulu’ (yukarda bahsedilen eser) Antimon Trioksitun kayp biçimlendirebilme sanatn temsil etmelidir.”[20]

ngiliz arkeolog Roger Moorey, eserin gerçekten bir vazo olduuna ikna olmamt, Selimkhanov’un Tello nesnesini (1975’te yaynland) analiz ettikten sonra “metali Transkafkasya doal Antimon Trioksituyla ilikilendirmeye çalt” ve “Transkafkasya’daki Antimon Trioksit nesnelerinin tümü küçük kiisel süs eyalardr.”[20] Bu, kaybolan bir sanatn “Antimon Trioksitu biçimlendirebilir klma” kantn zayflatr.[20]

Romal bilgin Büyük Plinius, Doa Aratrmalar (Naturalis Historia) adl kitabnda Antimon Trioksit sülfürü tbbi amaçlar için hazrlamann çeitli yollarn tanmlad.[21] Plinius ayrca “erkek” ve “kadn” Antimon Trioksit biçimleri arasnda bir ayrm yapt; erkek form muhtemelen sülfürken, üstün, daha ar ve daha az krlgan olan kadn formunun doal metalik Antimon Trioksit olduundan üphelenilmektedir.[22]

Yunan doa bilimci Pedanius Dioscorides, Antimon Trioksit sülfürün bir hava akm ile stlarak kavrulabileceini belirtti. Bunun metalik Antimon Trioksit ürettii düünülmektedir.[21]

talyan metalürist Vannoccio Biringuccio, Antimon Trioksitu izole etmek için bir prosedür açklad.

Antimon Trioksitun kasti izolasyonu, MS 815’ten önce Câbir bin Hayyan tarafndan tarif edilmitir.[23] Antimon Trioksitun izole edilmesi için bir prosedürün açklamas daha sonra Vannoccio Biringuccio’nun 1540 De la pirotechnia adl kitabnda Georgius Agricola, De re metallica’nn daha ünlü 1556 kitabndan önce verilmitir. Bu balamda Agricola, metalik Antimon Trioksitun kefiyle sklkla yanl itibar görmektedir. Metalik Antimon Trioksitun hazrlanmasn anlatan Currus Triumphalis Antimon Trioksitii (Antimon Trioksit Zafer Sava Arabas) kitab 1604’te Almanya’da yaynland. 15. yüzylda Basilius Valentinus ad altnda yazlan bir Benediktin rahibi tarafndan yazld iddia edildi; eer otantik olmasayd, Biringuccio’dan önce gelirdi.[a][7][25]

Metal Antimon Trioksit 1615 ylnda Alman kimyager Andreas Libavius tarafndan biliniyordu ve erimi Antimon Trioksit sülfür, tuz ve potasyum tartarat karmna demir ilave edilerek elde edildi. Bu prosedür kristalin veya yldzl bir yüzeye sahip Antimon Trioksit üretti.[21]

Phlogiston teorisindeki zorluklarn ortaya çkmasyla Antimon Trioksitun, dier metaller gibi sülfitler, oksitler ve dier bileikleri oluturan bir element olduu kabul edildi.[21]

Yer kabuunda doal olarak oluan saf Antimon Trioksitun ilk kefi 1783’te sveçli bilim adam ve yerel maden bölgesi mühendisi Anton von Swab tarafndan tanmland; tip-numune sveç, Västmanland, Sala’daki Bergslagen madencilik bölgesindeki Sala Gümü Madeninden toplanmtr.[26][27]

Etimoloji

Modern diller ve geç Bizans Yunancas’nn isimlerini Antimon Trioksit olarak ald ortaça Latin formu Antimon Trioksityum’dur. Bunun kayna belirsizdir; tüm önerilerin hem biçim hem de yorum konusunda zorluklar vardr. Ἀντίμοναχός anti-monachos veya Fransz antimoinden popüler etimolojinin hala taraftarlar vardr; bu “kei katili” anlamna gelir ve birçok erken simyagerin kei ve Antimon Trioksitun zehirli olmasyla açklanr.[24]

Bir baka popüler etimoloji, “metal olarak bulunamad” veya “alamsz bulunamad” eklinde açklanan, varsaymsal Yunanca ἀντίμόνος Antimon Trioksitos kelimesidir.[6] Lippmann, “floret” anlamna gelecek olan varsaymsal bir Yunanca kelime ανθήμόνιον anthemonion’u tahmin etti ve kimyasal veya biyolojik tozlamay tanmlayan ilgili Yunanca kelimelerin (ancak bu deil) birkaç örneini gösteriyor.[28]

Antimon Trioksityum’un ilk kullanmlar, 1050–1100 yllarnda, Arapça tbbi tedavilerin Afrikal Constantine tarafndan yaplan çevirileri içerir.[29] Birkaç otorite Antimon Trioksitium’un baz Arapça formlarn karalama bozulmas olduuna inanyor; Meyerhof onu ithmid’den türetmitir;[30] dier olaslklar arasnda athimar, metaloidin Arapça ad ve Yunancadan türeyen veya ona paralel olan varsaymsal bir as-stimmi vardr.[31]

Antimon Trioksitun (Sb) standart kimyasal sembolü için ksaltmay stibiumdan türeten Jöns Jakob Berzelius itibar görür.

Antik Antimon Trioksit sözleri çounlukla, balca anlamlar olarak Antimon Trioksit sülfürü olan kohl’a sahiptir.

Msrllar Antimon Trioksita mśdmt diyorlard;[32][33] hiyerogliflerde, ünlüler belirsizdir, ancak kelimenin Kpti formu ⲥⲧⲏⲙ (stēm) ‘dir. Yunanca kelime, στίμμι stimmi, muhtemelen Arapça veya Msr stm’sinden alnan bir kredi kelimesidir[24]

Üretim

2010 ylnda dünya Antimon Trioksit üretimi[10]

En iyi üreticiler ve üretim hacimleri

ngiliz Jeoloji Aratrmas (BGS), 2005 ylnda Çin’in dünya paynn yaklak %84’ü ile en iyi Antimon Trioksit üreticisi olduunu ve bunu Güney Afrika, Bolivya ve Tacikistan tarafndan uzaktan takip ettiini bildirdi. Hunan eyaletindeki Xikuangshan Madeni, tahmini 2.1 milyon metrik ton mevduat ile Çin’in en büyük mevduatna sahip.[35]

ABD Jeoloji Aratrmas’na göre 2016 ylnda Çin, toplam Antimon Trioksit üretiminin %76,9’unu olutururken, onu %6,9 ile Rusya ve %6,2 ile Tacikistan izledi.[36]

2016’da Antimon Trioksit üretimi[10]

Çin’in Antimon Trioksit üretiminin, kirlilik kontrolünün bir parças olarak maynlar ve izabe tesislerinin hükümet tarafndan kapatlmas nedeniyle gelecekte dümesi bekleniyor. Özellikle 2015 yl Ocak aynda[37] yürürlüe giren “Stanum, Antimon Trioksit ve Merkür için Emisyon Standartlar” revize edilen yeni bir çevre koruma yasas nedeniyle ekonomik üretim engelleri daha fazladr. Çin Ulusal statistik Bürosu’na göre, Eylül 2015’e kadar Hunan eyaletindeki (Çin’de en fazla Antimon Trioksit rezervi bulunan eyalet) Antimon Trioksit üretim kapasitesinin %50’si kullanlmamt.[37]

Roskill’in raporuna göre, Çin’de rapor edilen Antimon Trioksit üretimi dütü ve önümüzdeki yllarda artmas pek olas deil. Çin’de yaklak on yldr önemli bir Antimon Trioksit yata gelimemitir ve kalan ekonomik rezervler hzla tükenmektedir.[38]

Roskill’e göre dünyann en büyük Antimon Trioksit üreticileri aada listelenmitir:

2010’un en büyük Antimon Trioksit üreticileri.[39]

USGS istatistiklerine göre, mevcut küresel Antimon Trioksit rezervleri 13 yl içinde tükenecek. Ancak USGS daha fazla kaynak bulunacan düünüyor.

2015 ylnda dünya Antimon Trioksit rezervleri[39]

Ülke Rezervler

(ton Antimon Trioksit içerii) % Toplam

Üretim süreci

Cevherlerden Antimon Trioksit çkarlmas, cevherin kalitesine ve bileimine baldr. Çou Antimon Trioksit sülfür olarak çkarlr; düük dereceli cevherler köpük yüzdürmesi ile konsantre edilirken, yüksek dereceli cevherler 500–600 °C’ye stlr, stibnitin erime ve gang minerallerinden ayrld scaklk. Antimon Trioksit hurda demir ile indirgenerek ham Antimon Trioksit sülfürden izole edilebilir:[40]

Sb2S3 + 3 Fe → 2 Sb + 3 FeS

Sülfit bir okside dönütürülür; ürün daha sonra bazen geri kazanlan uçucu Antimon Trioksit(III) oksidin buharlatrlmas amacyla kavrulur.[41] Bu malzeme genellikle dorudan ana uygulamalar için kullanlr, safszlklar arsenik ve sülfürdür.[42][43] Antimon Trioksit, oksitten karbotermal bir indirgeme ile izole edilir:[40][42]

Avrupa ve ABD risk listelerinde, mevcut ekonomiyi ve yaam tarzn sürdürmek için gereken kimyasal elementlerin veya element gruplarnn tedarikine ilikin nispi riski gösteren elementin kritikliine ilikin olarak, Antimon Trioksit sürekli olarak üst sralarda yer almaktadr.

Avrupa ve ABD’ye ithal edilen Antimon Trioksitun büyük bir ksmnn Çin’den gelmesi ile Çin üretimi arz açsndan kritik öneme sahiptir. Çin çevresel kontrol standartlarn gözden geçirip arttrd için, Antimon Trioksit üretimi giderek kstlanmaktadr. Ayrca, Çin’in Antimon Trioksit ihracat kotalar son yllarda azalmaktadr. Bu iki faktör hem Avrupa hem de ABD için arz riskini artrmaktadr.

Avrupa

2015 BGS Risk Listesine göre, Antimon Trioksit nispi arz riski endeksinde (en nadir toprak elementlerinden sonra) ikinci srada yer almaktadr.[44] Bu, u anda ngiliz ekonomisi ve yaam tarz için ekonomik deeri olan kimyasal elementler veya element gruplar için ikinci en yüksek arz riskine sahip olduunu göstermektedir. Ayrca, Antimon Trioksit 2014 ylnda yaynlanan bir raporda (2011’de yaynlanan ilk raporu revize eden) AB için 20 kritik hammaddeden biri olarak tanmlanmtr. ekil xxx’te görüldüü gibi, Antimon Trioksit ekonomik önemine göre yüksek arz riski tamaktadr. Antimon Trioksitun %92’si, önemli ölçüde yüksek bir üretim konsantrasyonu olan Çin’den ithal edilmektedir.[45]

2015 ylnda ABD’de herhangi bir Antimon Trioksit çkarlmad. Metal, yabanc ülkelerden ithal ediliyor. 2011–2014 döneminde Amerika’nn Antimon Trioksitunun %68’i Çin’den, %14’ü Hindistan’dan, %4’ü Meksika’dan ve %14’ü dier kaynaklardan geldi. Halihazrda kamuya açk olarak bilinen hükümet stoku bulunmamaktadr.

ABD “Kritik ve Stratejik Mineral Tedarik Zincirleri Alt Komitesi” 1996–2008 yllar arasnda 78 mineral kayna tarad. Antimon Trioksit da dahil olmak üzere küçük bir mineral alt kümesinin potansiyel olarak kritik mineraller kategorisine sürekli olarak dütüü bulunmutur. Gelecekte, önemli risklerin tanmlanmas ve ABD çkarlar için kritik olmas gereken minerallerin alt kümeleri hakknda ikinci bir deerlendirme yaplacaktr.[47]

Kullanmlar

Antimon Trioksitun yaklak %60′ alev geciktiricilerde tüketilir ve %20’si piller, kaymal yataklar ve lehimler için alamlarda kullanlr.[40]

Alev geciktiricileri

Antimon Trioksit esas olarak halojen içeren polimerler hariç her zaman halojenli alev geciktiricilerle kombinasyon halinde alev geçirmez bileikler için trioksit olarak kullanlr. Antimon Trioksit trioksitin alev geciktirici etkisi,[48] hidrojen atomlar ile ve muhtemelen oksijen atomlar ve OH radikalleri ile reaksiyona giren ve böylece yangn önleyen halojenli Antimon Trioksit bileiklerinin oluumu ile üretilir.[49] Bu alev geciktiricilere yönelik pazarlar arasnda çocuk giysileri, oyuncaklar, uçaklar ve otomobil koltuk klflar bulunmaktadr. Hafif uçak motor kapaklar gibi maddeler için fiberglas kompozitlerdeki polyester reçinelere de eklenirler. Reçine, harici olarak oluturulan bir alev varlnda yanar, ancak harici alev çkarldnda söner.[41][50]

Alamlar

Antimon Trioksit, sertliini ve mekanik mukavemetini artrarak kurun ile oldukça kullanl bir alam oluturur. Kurun içeren çou uygulama için, alam metal olarak deien miktarlarda Antimon Trioksit kullanlr. Kurun asitli akülerde, bu ilave plaka gücünü ve arj özelliklerini gelitirir.[41][51] Yelkenli tekneler için kurun arlklar 272 kg ile 3628 kg arasnda; kurun omurgasnn sertliini ve gerilme mukavemetini arttrmak için Antimon Trioksit, hacimce %2 ile %5 arasnda kurun ile kartrlr. Antimon Trioksit, sürtünme önleyici alamlarda (Babbitt metal gibi),[52] mermilerde, elektrik kablo klfnda, tip metalde (örnein, linotip bask makineleri için[53]), lehimde (baz “kurunsuz” lehimler %5 Sb içerir),[54] kalayda[55] ve organ borularnn imalatnda düük kalay içeriine sahip sertleen alamlarda kullanlr.

Dier kullanmlar

Dier üç uygulama dünyann geri kalannn neredeyse tamamn tüketmektedir.[40] Bir uygulama, polietilen tereftalat üretimi için bir dengeleyici ve katalizördür.[40] Bir dieri, çounlukla TV ekranlar için camdaki mikroskopik kabarcklarn çkarlmas için bir inceltici maddedir.[56] Antimon Trioksit iyonlar oksijen ile etkileir ve sonraki kabarck oluturma eilimini bastrr.[57] Üçüncü uygulama pigmentlerdir.[40]

Biyoloji ve tbbn Antimon Trioksit için az kullanm vardr. Antimon Trioksitiyel olarak bilinen Antimon Trioksit içeren tedaviler emetik olarak kullanlr.[58] Antimon Trioksit bileikleri antiprotozoan ilaçlar olarak kullanlr. Potasyum Antimon Trioksitil tartrat veya tartar emetik, bir zamanlar 1919’dan itibaren bir anti-istozomal ilaç olarak kullanld. Daha sonra yerini prazikuantel ald.[59] Antimon Trioksit ve bileikleri, gevigetirenlerde cilt yumuatc olarak antiomalin ve lityum Antimon Trioksit tiyomalat gibi çeitli veteriner hazrlamalarda kullanlr.[60] Antimon Trioksit, hayvanlarda keratinize dokular üzerinde besleyici veya iyiletirici bir etkiye sahiptir.

Meglumin Antimon Trioksitiyat gibi Antimon Trioksit bazl ilaçlar da evcil hayvanlarda laymanyaz tedavisi için tercih edilen ilaçlar olarak kabul edilir. Ne yazk ki, düük terapötik endekslere sahip olmann yan sra, ilaçlar, baz Laymanya amastigotlarnn bulunduu kemik iliine çok az nüfuz eder ve hastal tedavi etmek – özellikle visseral form – çok zordur.[61] Bir Antimon Trioksit hap olarak elementel Antimon Trioksit bir zamanlar ilaç olarak kullanld. Yutma ve eliminasyondan sonra bakalar tarafndan tekrar kullanlabilir.[62]

Antimon Trioksit sülfürler, otomotiv fren balatas malzemelerindeki sürtünme katsaysnn dengelenmesine yardmc olur.[63] Antimon Trioksit mermi, mermi izleyicileri,[64] boya, cam sanat ve emayede bir opaklatrc olarak kullanlr. Antimon Trioksit-124, nötron kaynaklarnda berilyum ile birlikte kullanlr; Antimon Trioksit-124 tarafndan yaylan gama nlar, berilyumun fotodisintegrasyonunu balatr.[65][66] Yaylan nötronlarn ortalama enerjisi 24 keV’dur.[67] Doal Antimon Trioksit balangç nötron kaynaklarnda kullanlr.

Tarihsel olarak, ezilmi Antimon Trioksitdan (kohl) elde edilen toz, eski bir insann göz enfeksiyonlarn iyiletirmeye yardmc olduunu düündüü bir metal çubukla ve birinin tükürüü ile gözlere uygulanmtr.[68] Uygulama hala Yemen ve dier Arap ülkelerinde görülüyor.

Önlemler

Antimon Trioksit ve bileiklerinin insan ve çevre sal üzerindeki etkileri büyük farkllklar göstermektedir. Elementel Antimon Trioksit metali, insan ve çevre saln etkilemez. Antimon Trioksit trioksitin (ve Antimon Trioksit tozu gibi benzer az çözünür Sb(III) toz parçacklarnn) solunmas zararl olarak kabul edilir ve kansere neden olduundan üphelenilir. Ancak, bu etkiler sadece dii sçanlarda ve yüksek toz konsantrasyonlarna uzun süre maruz kaldktan sonra gözlenir. Etkilerin, Antimon Trioksit iyonlarna maruz kalmayacak ekilde bozulmu akcier klerensi, akcier ar yüklenmesi, iltihaplanma ve sonuçta tümör oluumuna yol açan zayf çözünür Sb parçacklarnn solunmasna baland varsaylmaktadr (OECD, 2008). Antimon Trioksit klorürler cildi andrr. Antimon Trioksitun etkileri arsenik ile karlatrlamaz; bunun nedeni, alm, metabolizma ve arsenik–Antimon Trioksit arasndaki atlm arasndaki önemli farkllklar olabilir.

Oral emilim için, ICRP (1994) tartar emetik için %10 ve dier tüm Antimon Trioksit bileikleri için %1 deerlerini önerdi. Metaller için deri emiliminin en fazla %1 olduu tahmin edilmektedir (HERAG, 2007). Antimon Trioksit trioksit ve dier az çözünür Sb(III) maddelerin (Antimon Trioksit tozu gibi) soluk alma emilimi %6.8 (OECD, 2008) iken Sb(V) maddeleri için <%1’lik bir deer elde edilir. Antimon Trioksit(V), kantitatif olarak hücrede Antimon Trioksit(III)’e indirgenmez ve her iki tür de ayn anda bulunur.

Antimon Trioksit esas olarak idrar yoluyla insan vücudundan atlr. Antimon Trioksit ve bileikleri, laymanyaz hastalarn tedavi etmek için kastl olarak kullanlan bir ön ilaç olan Antimon Trioksit potasyum tartrat (“tartar emetik”) hariç, akut insan sal etkilerine neden olmaz.

Antimon Trioksit tozuyla uzun süreli cilt temas dermatite neden olabilir. Ancak, Avrupa Birlii düzeyinde, gözlenen deri döküntülerinin maddeye özgü olmad, büyük olaslkla ter kanallarnn fiziksel olarak engellenmesi nedeniyle olduu kabul edilmitir (ECHA / PR / 09/09, Helsinki, 6 Temmuz 2009). Antimon Trioksit tozu da havaya yayldnda patlayc olabilir; dökme bir kat halindeyken yanc deildir.[69]

Antimon Trioksit, güçlü asitler, halojenli asitler ve oksitleyicilerle badamaz; yeni oluan hidrojene maruz kaldnda stibin (SbH3) oluturabilir.[69]

8 saatlik zaman arlkl ortalama (TWA), Amerikan Hükümeti Endüstriyel Hijyenistler Konferans ve yerinde yasal izin verilen maruz kalma snr (PEL) olarak Sal ve Güvenlii daresi (OSHA) tarafndan 0.5 mg/m3 olarak belirlenmitir. Ulusal Sal ve Güvenlii Enstitüsü (NIOSH) 8 saatlik TWA olarak önerilen maruz kalma snrn (REL) 0.5 mg/m3 olarak belirlemitir.[69] Antimon Trioksit bileikleri polietilen tereftalat (PET) üretimi için katalizör olarak kullanlr. Baz çalmalar, PET ielerden svlara küçük Antimon Trioksit sznts bildirmektedir, ancak seviyeler içme suyu klavuzlarnn altndadr. Meyve suyu konsantrelerindeki Antimon Trioksit konsantrasyonlar biraz daha yüksekti (44.7 ug / L Antimon Trioksit’a kadar), ancak meyve sular içme suyu yönetmeliklerine girmiyor. çme suyu yönergeleri:

DSÖ tarafndan önerilen TDI, vücut arlnn kilogram bana 6 µg Antimon Trioksitdur.[72] Antimon Trioksit için IDLH (yaam ve salk için hemen tehlikeli) deeri 50 mg/m3’tür.[69]

Toksiklik

Özellikle Antimon Trioksit trioksit ve Antimon Trioksit potasyum tartarat gibi baz Antimon Trioksit bileikleri toksik olarak görünmektedir.[73] Etkiler arsenik zehirlenmesine benzer olabilir.[74] Mesleki maruziyet solunum yolu tahriine, pnömokonyoza, ciltte Antimon Trioksit lekelerine, gastrointestinal belirtilere ve kardiyak aritmilere neden olabilir. Ek olarak, Antimon Trioksit trioksit insanlar için potansiyel olarak kanserojendir.[75]

nsanlarda ve hayvanlarda soluma, oral veya Antimon Trioksit ve bileiklerine dermal maruziyet sonrasnda olumsuz salk etkileri gözlemlenmitir.[73] Antimon Trioksit toksisitesi tipik olarak ya mesleki maruziyete bal olarak, tedavi srasnda ya da kazayla yutulmasndan kaynaklanr. Antimon Trioksitun vücuda cilt yoluyla girip girmedii belirsizdir.[73]