アルシニジンガリウム

Metals -> Arsenic Compounds, Inorganic

Carcinogens

5.31 at 77 °F (NTP, 1992) - Denser than water; will sink

5.3176 @ 25 °C

Lattice constant 5.6-54 Angstroms; dielectric constant 11.1; intrinsic resistivity @ 300 deg K= 3.7X10+8 ohm-cm; electron lattice mobility @ 300 deg K= 10,000 square cm/volt-sec; intrinsic charge density @ 300 deg K= 1.4X10+6/cc; electron diffusion constant @ 300 deg K= 310 square cm/sec; hole diffusion constant= 11.5 square cm/sec

5.31

Cubic crystals, dark gray with metallic sheen

Gray cubic crystals

less than 1 mg/mL at 68 °F (NTP, 1992)

<1 mg/mg in DMSO, 95% ethanol, methanol, and acetone; soluble in hydrochloric acid

In water, <1 mg/ml @ 20 °C

When heated to decomposition it emits very toxic fumes of /arsenic/.

DANGEROUS WHEN HEATED TO DECOMP ... IT EMITS TOXIC FUMES OF ARSENIC /SRP: INCLUDING ARSINE/. /ARSENIC CMPD/

2260 °F (NTP, 1992)

1238 °C

1238 °C

2260 °F

Gallium arsenide is an insoluble, high-boiling solid which may react very slowly with water or water vapor to evolve toxic gases such as arsine. It is used as a high-performance material in the semiconductor industry.

Gray crystals or powder; [CAMEO]

Dark gray crystals with a metallic greenish-blue sheen or gray powder.

Hardness 4.5; thermal expansion coefficient: 5.9x10-6; thermal conductivity 0.52 watt units; specific heat 0.086 cal/g/deg c; intrinsic electron concn 10+7; energy gap @ room temp 1.38 electron volts; electron mobility 8800 square cm/volt sec; effective mass for electrons 0.06 m(-0)

Electroluminescent in infrared light

Forms a hydrate which is orthorhombic and it can form acidic salts

Danger

H350: May cause cancer [Danger Carcinogenicity]

P203, P260, P264, P270, P280, P318, P319, P405, and P501 (click each P-code to see the statement)

This chemical does not meet GHS hazard criteria for 6.2% (7 of 112) of reports.

Danger

H350 (88.4%): May cause cancer [Danger Carcinogenicity]

Chemical: Gallium arsenide (GaAs)

Hazard Traits - Carcinogenicity; Reproductive Toxicity

REACH registered substance: Gallium arsenide (EC: 215-114-8)

Restricted substance: Gallium arsenide

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

SYMPTOMS: Symptoms of exposure to this compound may include diarrhea, hypotension, weakness, cardiac failure, convulsions, coma, nervousness, headache, dizziness hypothermia, abdominal cramps, irritability, paralysis, cardiac arrhythmia, respiratory edema, dyspnea, cyanosis, coughing, peripheral neuropathy, optic neuritis, anesthesia, paresthesia, alopecia, dermatitis, cirrhosis of the liver, salivation, aplastic anemia, kidney damage, anuria, liver damage, jaundice, hematuria, proteinuria and leukopenia.

Its toxicity is due to arsenic, and exposed workers can be monitored by urine arsenic levels. [Harrison RJ, State of the Art Reviews: Occupational Medicine, Vol. 1, No. 1, pages 49-58.] Inhalation studies in experimental rats show that both gallium and arsenic are cleared within 14 days after treatment. [Webb DR et al. Pulmonary Clearance and Toxicity of Respirable Gallium Arsenide Particulates. Am Ind Hyg Assoc J. 1987 Jul;48(7):660-7.] Gallium arsenide is poorly absorbed; it is excreted primarily in the feces. [Rosenstock, p. 947] Toxic arsenic released when heated to decomposition; [CAMEO] Metalloid arsenic is generally regarded as nonpoisonous due to its insolubility in water and body fluids. [ATSDR Case Studies: Arsenic Toxicity] Gallium arsenide is classified as a human carcinogen. [IARC] Because of its ability to cause extensive pulmonary damage in the rat at a level of 10 µg/m3 and in the mouse at a level of 100 mg/m3 for particles of 1 µm or smaller and because of its ability to cause cancer in female rats (but not male rats), a TLV–TWA of 0.3 µg/m3 (0.0003 mg/m3) is recommended, with an A3, Confirmed Animal Carcinogen with Unknown Relevance to Humans, designation. [ACGIH] See Arsenic and the linked occupational diseases.

If material involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) Use water in flooding quantities as fog. Use foam, dry chemical, or carbon dioxide. /Arsenical cmpd, liquid, NOS/

If material involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) Use water in flooding quantities as fog. Use foam, dry chemical, or carbon dioxide. /Arsenical cmpd, solid, NOS/

8 hr Time-Weighted avg: 10 ug/cu m./Arsenic, inorganic cmpd (as As)/

Permissible Exposure Limit: Table Z-1 8-Hr Time Weighted Avg: 0.5 mg/cu m. /Arsenic, organic cmpd (as As)/

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Gallium arsenide is included on this list.

(a) The owner or operator of an existing glass melting furnace subject to the provisions of this subpart shall comply with either paragraph (a)(1) or (a)(2) of this section ... (1) Uncontrolled total arsenic emissions from the glass melting furnace shall be less than 2.5 Mg (2.7 ton) per year, or ... (2) Total arsenic emissions from glass melting furnace shall be conveyed to a control device and reduced by at least 85%. /Total arsenic/

(b) The owner or operator of a new or modified glass melting furnace subject to the provisions of this subpart shall comply with either paragraph (b)(1) or (b)(2) of this section ... (1) Uncontrolled total arsenic emissions from the glass melting furnace shall be less than 0.4 Mg (0.44 ton) per year, or ... (2) Total arsenic emissions from glass melting furnace shall be conveyed to a control device and reduced by at least 85%. /Total arsenic/

The owner or operator of each copper converter subject to the provisions of this subpart shall reduce inorganic arsenic emissions to the atmosphere by meeting the following design, equipment, work practice, and operational requirements: (1) Install, operate, and maintain a secondary hood system on each copper converter. Each secondary hood system shall consist of a hood enclosure, air curtain fan(s), exhaust system fan(s), and ductwork that conveys the captured emission to a control device ... (2) Optimize the capture of secondary inorganic arsenic emission by operating the copper converter and secondary hood systems at all times ... . /Inorganic arsenic/

For more Atmospheric Standards (Complete) data for GALLIUM ARSENIDE (6 total), please visit the HSDB record page.

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

ARSENIC IS RECOVERED AS A HYDRATE OF AN AS-GROUP III METAL COMPOUND FROM SOLN OR WASTEWATER.

Prompt cleanup and removal are necessary. Control runoff and isolate discharged material for proper disposal.

Floors and other accessible surfaces contaminated with inorganic arsenic may not be cleaned by the use of compressed air, and shoveling and brushing may be used only where vacuuming or other relevant methods have been tried and found not to be effective. /Inorganic arsenic compounds/

SMALL SPILLS AND LEAKAGE: If you spill this chemical, you should dampen the solid spill material with water, then transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

Chemical Treatability of Arsenic; Concentration Process: Chemical Precipitation; Chemical Classification: Metal; Scale of Study: Pilot Scale; Type of Wastewater Used: Domestic Wastewater + Pure Compound; Results of Study: 5ppm @ 4gpm @ pH= 7.0. Iron system-90% reduction; low lime system-80% reduction; high lime system-76% reduction; (3 coagulant systems were used; Iron system used 45 ppm as Fe of Fe2(SO4)3 @ pH= 6.0. Low lime system used 20 ppm Fe of Fe2(SO4)3 and 260 ppm of CaO @ pH= 10.0. High lime system used 600 ppm of CaO @ pH= 11.5. Chemical coagulation was followed by multimedia filtration). /Arsenic cmpd/

Chemical Treatability of Arsenic; Concentration Process: Chemical Precipitation; Chemical Classification: Metal; Scale of Study: Full Scale Continuous Flow; Type of Wastewater Used: Domestic Wastewater; Results of Study: Effluent character (ppb): 2.5, 56% reduction with lime; 3.3, 24% reduction with lime; (lime dose of 350-400 ppm as calcium oxide @ pH= 11.3). /Arsenic cmpd/

WELL VENTILATED & ALL POISONOUS FUME ... CONDENSED & DUST CONTENT REMOVED. ... EXHAUST HOODS ... WORKTABLES ... EQUIPPED WITH DOWN-DRAUGHT ... VENTILATION. /ARSENIC CMPD/

IN ... /FACTORIES/ WITH ARSENIC HAZARD, FLOORS ... SHOULD BE ... IMPERMEABLE ... TO PREVENT ABSORPTION & ... FLUSHED DOWN FREQUENTLY WITH WATER. /ARSENIC CMPD/

Lockers should be provided with separate compartments for work & personal clothes, & adjacent sanitary facilities of a high standard should be made available. Smoking, eating, & drinking at the workplace should not be allowed. /Arsenic & cmpd/

Employees exposed to arsenic shall wash their hands and exposed skin before eating or smoking during the work shift. No food shall be permitted in areas where arsenic is handled, processed, or stored. Employees shall not smoke in areas where arsenic is handled, processed, or stored. /Inorganic arsenic/

For more Preventive Measures (Complete) data for GALLIUM ARSENIDE (6 total), please visit the HSDB record page.

Tolerances for total residues of combined arsenic (calculated as As) in food are established as follows: (a) In edible tissues & in eggs of chickens & turkeys: 0.5 ppm in uncooked muscle tissue; 2 ppm in uncooked edible by-products; & 0.5 ppm in eggs. (b) In edible tissues of swine: 2 ppm in uncooked liver & kidney; 0.5 ppm in uncooked muscle tissue & by-products other than liver & kidney. /Arsenic/

0.0003 [mg/m3], respirable fraction

8 hr Time weighted Avg (TWA) 0.01 mg/cu m. /Arsenic and inorganic compounds, as As/

Excursion Limit Recommendation: Excursions in worker exposure levels may exceed 3 times the TLV-TWA for no more than a total of 30 minutes during a work day, and under no circumstances should they exceed 5 times the TLV-TWA, provided that the TLV-TWA is not exceeded. /Arsenic and inorganic compounds, as As/

A1: Confirmed human carcinogen. /Arsenic and inorganic compounds, as As/

Biological Exposure Index (BEI): Determinant: Inorganic arsenic plus methylated metabolites in urine; Sampling Time: end of workweek; BEI:35 ug As/L. The determinant may be present in biological specimens collected from subjects who have not been occupationally exposed, at a concentration which could affect interpretation of the result. Such background concentrations are incorporated in the BEI value. /Arsenic, elemental and soulble inorganic compounds/

0.0003 mg/m³ (respirable particulate matter) [2004]

Arsenic poisoning can be treated by chelation therapy, using chelating agents such as dimercaprol, EDTA or DMSA. Charcoal tablets may also be used for less severe cases. In addition, maintaining a diet high in sulfur helps eliminate arsenic from the body. (L20)

Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (T1, A17)

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical. [http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=1303-00-0]

Gallium arsenide (CAS # 1303-00-0) was evaluated for chronic inhalation toxicity and carcinogenicity in Fischer 344 rats (50/sex/exposure level) exposed to concentrations of 0, 0.01, 0.1, and 1.0 mg/cu m for 6 hours, 5 days/week for 104 weeks. There was no increased mortality relative to controls and 11-20 rats of each treatment group were available for 2-year terminal sacrifice and evaluation of consequential histopathology. Both decedent and surviving animals were examined microscopically. Treatment was associated with increased neoplastic lesions in female rats of 1.0 mg/cu m exposures, including significantly increased incidence of bronchiolar adenomas and carcinomas. Pheochromocytoma of the adrenal medulla, and mononuclear cell leukemia were likewise significantly increased in 1.0 mg/cu m females. No carinogenic toxicity was evident in male rats. Relative to controls, both male and female rats exhibited significantly increased incidences of non-neoplastic lesions of the lungs, including atypical hyperplasia, alveolar epithelial hyperplasia, chronic active inflammation, proteinosis, and alveolar epithelial metaplasia. Significantly increased incidences of non-neoplastic laryngeal lesions in 1.0 mg/cu m male rats included hyperplasia, chronic active inflammation, squamous metaplasia, and hyperplasia of the epiglottis.

Gallium arsenide (CAS # 1303-00-0) was evaluated for chronic inhalation toxicity and carcinogenicity in B6C3F1 mice (50/sex/exposure level) exposed to concentrations of 0, 0.1, 0.5, and 1.0 mg/cu m for 6 hours, 5 days/week for 104 weeks. At 2-year terminal sacrifice, 29-38 mice of each treatment group were available for evaluation of consequential histopathology. Both decedent and surviving animals were examined microscopically. Neither male nor female mice exhibited clearly evident carcinogenic toxicity. Increasing exposures were associated with significantly increased incidence of non-neoplastic lesions of the lung in both males and females, as characterized by alveolar epithelial hyperplasia, chronic and acute inflammation, alveolar proteinosis, histiocytic cellular infiltrate, and foreign body alveolus. Treated mice also exhibited concomitant slight enlargement of bronchial lymph nodes in association with inflammation of the lungs. The significance of increased preputial gland inflammation in high-exposure males was deemed equivocal relative to historical controls, as were slight increases in adenomas and carcinomas of Harderian glands in treated male mice due to histologic evaluation of only those tissues appearing abnormal on necropsy.

Gallium arsenide (CAS # 1303-00-0) was evaluated for carcinogenicity in Fischer 344 rats (50/sex/group) exposed by inhalation to particulate concentrations of 0, 0.01, 0.1, or 1.0 mg/m3, 6 hours plus T90/day, 5 days/week, for 105 weeks. All animals were examined microscopically, the presumed target organs - lungs, adrenal medulla, larynx, nose, and preputial gland in addition to stomach, liver, and spleen. Treatment was associated with nonneoplastic pulmonary lesions in males and females: proteinosis, focal chronic/active inflammation, typical and atypical alveolar epithelial hyperplasia, alveolar epithelial metaplasia, and squamous epithelial metaplasia. The severity of lesions correlated positively with dose level. A high incidence of pulmonary tumors including alveolar bronchiolar adenomas and carcinomas and adrenal pheochromocytomas was observed in high dose females, but not in males. Treated males had increased incidence of preputial gland tumors and hyperplasia; necrosis of the forestomach and glandular stomach relative to controls was considered not related directly to treatment. Mononuclear cell leukemia was elevated in liver and spleen of both treated males and females relative to controls, that in males was not outside the range of historical controls. No further protocol, interpretation of results, or statistical determinations were provided.

Gallium arsenide (CAS # 1303-00-0) was evaluated for carcinogenicity in B6C3F1 mice (50/sex/group) exposed by inhalation to particulate concentrations of 0, 0.1, 0.5, or 1.0 mg/cu m, 6 hours plus T90/day, 5 days/week, for 105 weeks. All animals were examined microscopically, including presumed target organs - lungs and nose, in addition to bronchial lymph nodes, female liver and spleen, and male preputial gland. No exposure-related neoplastic lesions were identified in the respiratory tracts of either sex in any exposure group. Treatment-related nonneoplastic pulmonary lesions included alveolar proteinosis, histiocytic cellular infiltrate, foreign body alveolus (presumed gallium arsenide), acute and chronic inflammation, and alveolar epithelial hyperplasia. Enlarged bronchiole lymph nodes were associated with pulmonary inflammation. Nasal lesions were comparable in severity and number to those found in control animals. Since only grossly abnormal harderian glands received microscopic examination, the biological significance of an unanticipated slightly increased incidence of harderian gland adenomas and carcinomas in treated males could not be determined. The increased incidence and severity of preputial gland inflammation in 1.0 mg/cu m males relative to controls was deemed of equivocal significance, since such lesions were unrelated to treatment in previous inhalation studies. No further protocol, interpretation of results, or statistical determinations were provided.

A single intracheal instillation of GaAs at 100 mg/kg produced mitochondrial swelling in renal proximal tubule cells similar to that observed with arsenical exposure.

Potential health & safety hazards posed by feedstock materials & residuals generated in the large-scale manufacture of gallium arsenide alloy based multi-junction photovoltaic cells are identified.

Gallium Arsenide

TR-492: Toxicology and Carcinogenesis Studies of Gallium Arsenide (CASRN 1303-00-0) in F344/N Rats and B6C3F1 Mice (Inhalation Studies) (2000 )

05/21/99

No Evidence

Clear Evidence

No Evidence

DUST OF...ARSENIDE OF GALLIUM WAS GENERALLY TOXIC WHEN INTRODUCED INTO RESPIRATORY SYSTEM (INTRATRACHEAL INJECTIONS IN WHITE RATS), CAUSING DYSTROPHY OF LIVER & KIDNEYS. IN LUNGS IT CAUSED INFLAMMATORY & SCLEROTIC CHANGES.

... Rats intratracheally instilled with a fraction of gallium arsenide (GaAs) particulates, characterized with a mean count diameter of 8.30 um and a mean volume diameter of 12.67 um, developed signs of systemic arsenic intoxication, pulmonary inflammation, and pneumocyte hyperplasia. The results of the present study confirm these findings and also show that a significantly smaller fraction of GaAs is a relatively more severe pneumotoxicant. Decreasing the particle mean count and mean volume diameter to 1.63 um and 5.82 um, respectively, increased the in vivo dissolution rate of galium arsenide, increased the severity of pulmonary lesions previously associated with galium arsenide exposure, and resulted in unique pathological sequalae in affected lung tissue. Pulmonary fibrosis, as indicated by analysis of lung 4-hydroxyproline content, was not considered statistically significant although histological examination of lung tissue revealed a mild fibrotic response.

Male rats received GaAs suspensions at doses of 50, 100, or 200 mg/kg via a single intratracheal instillation. Six days after treatment a dose dependent inhibition of blood 8 aminolevulinic acid dehydratase (ALAD) was observed, with activity decreasing to 5 percent of controls at the highest dose. There was a concomitant marked increase in the urinary excretion of aminolevulinic acid. Inhibition of blood aminolevulinic acid dehydratase following administration of GaAs was maximal (30 percent of control) 3 to 6 days post exposure. Inhibition of kidney and liver aminolevulinic acid dehydratase following GaAs exposure was also evident. Rats treated with 100 mg/kg GaAs exhibited swelling of kidney proximal tubule mitochondria 6 days following exposure. The inhibition of aminolevulinic acid dehydratase was partially prevented by excess zinc, suggesting that gallium is the primary inhibitor of aminolevulinic acid dehydratase following dissolution of GaAs in vivo and that competition for or displacement of zinc from the enzyme's active site may be involved in the mechanism of inhibition

A dose of 100 mg/kg GaAs given by intratracheal instillation to rats resulted in type 11 pneumocyte hyperplasia, alveolar proteinosis, and interstitial pneumonia as determined from histopathologic examination. An inflammatory response was also indicated by enzyme activity changes in bronchopulmonary lavage studies. Significant increases were found in total lung weight and lung lipid, protein, and DNA content. Similar, but less severe, effects were seen at 30 mg/kg, and at 2.5 mg/kg the biochemical effects were essentially absent.

For more Non-Human Toxicity Excerpts (Complete) data for GALLIUM ARSENIDE (18 total), please visit the HSDB record page.

If material involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) Use water in flooding quantities as fog. Use foam, dry chemical, or carbon dioxide. /Arsenical cmpd, liquid, NOS/

If material involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) Use water in flooding quantities as fog. Use foam, dry chemical, or carbon dioxide. /Arsenical cmpd, solid, NOS/

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Gallium arsenide is included on this list.

(a) The owner or operator of an existing glass melting furnace subject to the provisions of this subpart shall comply with either paragraph (a)(1) or (a)(2) of this section ... (1) Uncontrolled total arsenic emissions from the glass melting furnace shall be less than 2.5 Mg (2.7 ton) per year, or ... (2) Total arsenic emissions from glass melting furnace shall be conveyed to a control device and reduced by at least 85%. /Total arsenic/

(b) The owner or operator of a new or modified glass melting furnace subject to the provisions of this subpart shall comply with either paragraph (b)(1) or (b)(2) of this section ... (1) Uncontrolled total arsenic emissions from the glass melting furnace shall be less than 0.4 Mg (0.44 ton) per year, or ... (2) Total arsenic emissions from glass melting furnace shall be conveyed to a control device and reduced by at least 85%. /Total arsenic/

The owner or operator of each copper converter subject to the provisions of this subpart shall reduce inorganic arsenic emissions to the atmosphere by meeting the following design, equipment, work practice, and operational requirements: (1) Install, operate, and maintain a secondary hood system on each copper converter. Each secondary hood system shall consist of a hood enclosure, air curtain fan(s), exhaust system fan(s), and ductwork that conveys the captured emission to a control device ... (2) Optimize the capture of secondary inorganic arsenic emission by operating the copper converter and secondary hood systems at all times ... . /Inorganic arsenic/

For more Atmospheric Standards (Complete) data for GALLIUM ARSENIDE (6 total), please visit the HSDB record page.

Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /Arsenic & cmpd/

The national primary drinking water maximum contaminant level (MCL) for inorganic arsenic is 0.05 mg/l. /Inorganic arsenic/

For the maximum protection of human health from the potential carcinogenic effects due to exposure of arsenic through ingestion of contaminated water & contaminated aquatic organisms, the ambient water concn should be zero based on the nonthreshold assumption for this chemical. However, zero level may not be attainable at the present time. Therefore, the levels which may result in incremental increase of cancer risk over the lifetime are estimated at 1X10-5, 1X10-6, & 1X10-7. The corresponding criteria are 22 ng/l, 2.2 ng/l, & .22 ng/l, respectively .... For consumption of aquatic organisms only, excluding consumption of water, the levels are 175 ng/ml, 17.5 ng/l, & 1.75 ng/l, respectively. /Arsenic/

D004; A solid waste containing arsenic may or may not become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste.

(AZ) ARIZONA 10 ug/L /Arsenic/

(CT) CONNECTICUT 10 ug/l /Arsenic/

A number of experiments have demonstrated that GaAs dissociates in the lung or gut of mammals to gallium & arsenic with the latter behaving metabolically as any other inorganic arsenic species.

Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (L20)

After exposure to 75 mg/ml of GaAs, the analysis of tissues from pregnant rats showed that gallium levels in the maternal blood were 300 fold less than the arsenic concentrations. Thus the fetal changes were due to the arsenic, not the gallium. The gallium concentrations in the fetus were greater than in the mother. The increase in the material and fetal gallium tissue concentrations at 75 mg/cu m were not proportional to the increases at 37 mg/cu m.

After intratracheal instillation into hamsters of GaAs ..., the compound was absorbed from the lungs in 24 hr. The blood levels were lower in the GaAs treated group. The arsenic blood levels in the hamsters treated with GaAs peaked at 48 hr and remained constant for 48 hr. ... After 4 days 50 percent of the arsenate ... was excreted in the urine ... . The slower absorption of GaAs from the lungs may account for the lesser fecal excretion

Excretion of arsenic absorbed from GaAs is probably as rapid as that found after inorganic arsenic administration; about 35% of soluble sodium arsenite was excreted within 48 hours in humans. GaAs is absorbed slowly from the lung, so arsenic excretion is expected to continue for several weeks after GaAs exposure. GaAs remaining in the lung is eliminated slowly; a single intratracheal dose of 100 mg/kg was excreted in about 3 months and had a half life in the range of 2 weeks.

A dose of 30 mg/kg of GaAs introduced into the lung by intratracheal administration produced enzymatic changes in the body characteristic of soluble arsenic compounds; equivalent changes were observed only when 1000 mg/kg GaAs was given by oral administration. The cumulative absorption of GaAs from the lung as measured by the amount of arsenic found in blood and urine was approximately 10-20% of the administered dose, and this appeared over a period of several days ... . This absorption was fairly constant over the dose range of 10-100 mg/kg ... . After oral administration, the amount absorbed appeared to depend on dose in the range 10-1,000 mg/kg; at 1000 mg/kg, less than 1% was absorbed, but the percentage of the dose absorbed rose to almost 10% at the 10 mg/kg dose. These results are all based on arsenic data because no gallium was detected in either blood or urine. Lung and fecal analyses found more gallium than arsenic, suggesting that gallium was more poorly absorbed from the lung than was arsenic and greater amounts of gallium were cleared from the lung by mucociliary mechanisms and subsequently swallowed.

Gallium arsenide administered by oral gavage at single doses of 10, 100, or 1,000 mg/kg to male Fischer rats ... or male Syrian hamsters Yamauchi was only slightly soluble in the gastrointestinal tract and therefore absorption was minimal. Fourteen days after dosing with gallium arsenide, 90.7% + or - 35.4% of the arsenic and 99.4% + or - 38.7% of the gallium was eliminated in the feces in the 1,000 mg/kg group. Less than 0.02% of the arsenic was excreted in the urine, and 0.3% was detected in the blood. Gallium was not detected in the blood or urine. Five days after dosing in hamsters, more than 80% to 90% of the total arsenic dose from gallium arsenide was eliminated in the feces, and less than 0.15% was excreted in the urine.

Used in semiconductor applications; [Merck Index #4347]

Semiconductor Manufacturing [Category: Industry]

In semiconductor applications (transistors, solar cells, lasers)

Semiconductor in light-emitting diodes for telephone dials; magnetoresistance devices; thermistors; microwave generation

Infrared emitters; photoelectronic transmission of data by optical fibers

Gallium arsenide is used as a semiconductor, as well as in solar cells, x-ray detection diodes, and laser diodes. (L354)

...by passing mixture of hydrogen and arsenic vapor over Ga(III) oxide @ 600 °C: Goldschmidt, Skr Akad Oslo 1926, 8, 34, 100. Simplified procedure: Juza, Schulz, Z Anorg Allgem Chem 275, 65 (1954); Minden, Sylvania Technologist 11, 1, 19(Jan 1958). Vapor phase crystal growth: McAleer et al, J Electrochem Soc 108, 1168 (1961)

Obtained by the reaction of GaCl3 on As2O3 @ 800 °C

Gallium arsenide (GaAs): ACTIVE

Gallium arsenide single crystals have been grown by the Czochralski technique and by the floating zone method. Extensive twinning occurs.