Indium phosphide

145.79

147.89300

244-959-5

SD36LG60G1

DTXSID3031444

Brittle mass with metallic appearance|Black, cubic crystals

0

0.32580

pieces

4.81 g/cm³

1070 °C

Insoluble in water.Slightly soluble in mineral acids

High heat produces toxic phosphorus oxide fumes

Explosive reaction with dinitrogen tetraoxide + acetonitrile. Violent reaction with mercury(II) bromide at 350 deg C.

Dielectric constant: 10.8; Energy gap: 1.3 eV at 25 °C; electron mobility: approx 4600 sq cm/volt-sec. Hole mobility: approx 150 sq cm/volt-sec. Solid solutions of InP can cover the energy gap continuously from 0.3 to 1.3 ev.|Standard molar enthalpy (heat) of formation at 298.15 K = -88.7 kJ/mol; Standard molar Gibbs energy of formation at 298.15 K = -77.0 kJ/mol; Standard molar entropy at 298.15 K = 59.8 J/mol-K; Molar heat capacity at constant pressure at 298.15 K = 45.4 J/mol-K|Can react with moisture or acids to liberate phosphine (PH3); when heated to decomposition, it may emit toxic fumes of POx

3288

3

24/25-45-53

NL1800000

T

Warehouse ventilated, low temperature and dry

P201-P281-P308 + P313

H350-H361f-H372

Can react with moisture or acids to liberate phosphine (PH3);

IARC Vol 86: Cobalt in Hard Metals and Cobalt Sulfate, Gallium Arsenide, Indium Phosphide and Vanadium Pentoxide p. 197 (2006); IARC Monographs provide critical reviews of data on carcinogenicity for agents to which humans are known to be exposed and on specific exposure situations.[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: http://monographs.iarc.fr/ENG/Classification/index.php, p. V86 197 (2006)]

|Danger|H350: May cause cancer [Danger Carcinogenicity]|P201, P202, P260, P264, P270, P281, P308+P313, P314, P405, and P501|H350 (97.84%): May cause cancer [Danger Carcinogenicity]|Aggregated GHS information provided by 185 companies from 6 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Flammable in the form of dust when exposed to heat or flame.|Mixtures with sulfur ignite when heated.

Explosive reaction with dinitrogen tetraoxide + acetonitrile. Violent reaction with mercury(II) bromide at 350 °C.

Recommended Exposure Limit: 10 hr Time Weighted Avg: 0.1 mg/cu m. [Note: The REL also applies to other indium compounds (as In).] /Indium/

D003; A solid waste containing indium phosphide may become characterized as a hazardous waste when subjected to testing for reactivity as stipulated in 40 CFR 261.23, and if so characterized, must be managed as a hazardous waste.[40 CFR 261.23 (USEPA); U.S. National Archives and Records Administration's Electronic Code of Federal Regulations. Available from, as of July 19, 2014: http://www.ecfr.gov]

This research work investigated the physical and chemical properties of a new type of wastewater produced from the semiconductor industry. The wastewater generated from indium phosphide (InP) wafer backgrinding and sawing processes was characterized in term of its particle size distribution (PSD), zeta potential, suspended and dissolved solids, total organic carbon, and turbidity. The wastewater contained high concentration of fine InP dusts with a size ranging from 0.07 - 1.44 millimicrons. ...

Indium phosphide (InP) quantum dots (QDs) have emerged as a presumably less hazardous alternative to cadmium-based particles, but their cytotoxicity has not been well examined. Although their constituent elements are of very low toxicity to cells in culture, they nonetheless exhibit phototoxicity related to generation of reactive oxygen species by excited electrons and/or holes interacting with water and molecular oxygen. Using spin-trap electron paramagnetic resonance (EPR) spectroscopy and reporter assays, we find a considerable amount of superoxide and a small amount of hydroxyl radical formed under visible illumination of biocompatible InP QDs with a single ZnS shell, comparable to what is seen with CdTe. A double thickness shell reduces the reactive oxygen species concentration approximately two-fold. Survival assays in five cell lines correspondingly indicate a distinct reduction in toxicity with the double-shell InP QDs. Toxicity varies significantly across cell lines according to the efficiency of uptake, being overall significantly less than what is seen with CdTe or CdSe/ZnS. This indicates that InP QDs are a useful alternative to cadmium-containing QDs, while remaining capable of electron-transfer processes that may be undesirable or which may be exploited for photosensitization applications./Indium phosphide quantum dots/

... 2 Yr Study in Rats: Groups of 60 male and 60 female /F344/N/ rats were exposed to particulate aerosols of indium phosphide at concn of 0, 0.03, 0.1 or 0.3 mg/cu m /for/ 6 hr/ day 5 days/wk for 22 wk (0.1 and 0.3 mg/cu m groups) or 105 wk (0 and 0.03 mg/cum groups). Animals in the 0.1 and 0.3 mg/cu m group were maintained on filtered air from exposure termination at wk 21 until the end of the studies. 2 Yr Study in Mice: Groups of 60 male and female /B6C3F1/ mice were exposed to particulate aerosols of indium phosphide at concn of 0, 0.03, 0.1 or 0.3 mg/cu m /for/ 6 hr/day 5 days/wk for 21 wk (0.1 and 0.3 mg/cu m groups) or 105 wk (0 and 0.3 mg/cu m groups). Animals in the 0.1 and 0.3 mg/cu m groups were maintained on filtered air from exposure termination at wk 21 until the end of the studies. Conclusions: Under the conditions of these 2 yr inhalation studies, there was clear evidence of carcinogenic activity of indium phosphide in male and female F344/N rats based on incr incidences of benign and malignant neoplasms of the lung. Incr incidences of pheochromocytoma of the adrenal medulla in males and females were also considered exposure related. Marginal incr in incidences of mononuclear cell leukemia in males and females, fibroma of the skin in males, and carcinoma of the mammary gland in females may have been related to exposure to indium phosphide. There was clear evidence of carcinogenic activity of indium phosphide in male B6C3F1 mice based on incr incidences of malignant neoplasms of the lung and benign and malignant neoplasms of the liver. Marginal incr in incidences of adenoma and carcinoma of the small intestine may have been related to exposure to indium phosphide. There was clear evidence of carcinogenic activity of indium phosphide in female B6C3F1 mice based on incr incidences of benign and malignant neoplasms of the lung. Incr incidences of liver neoplasms were also considered exposure related. ... Conclusions: Under the conditions of these 2 yr inhalation studies, there was clear evidence of carcinogenic activity of indium phosphide in male and female F344/N rats based on incr incidences of benign and malignant neoplasms of the lung. Incr incidences of pheochromocytoma of the adrenal medulla in males and females were also considered exposure related. Marginal incr in incidences of mononuclear cell leukemia in males and females, fibroma of the skin in males, and carcinoma of the mammary gland in females may have been related to exposure to indium phosphide. There was clear evidence of carcinogenic activity of indium phosphide in male B6C3F1 mice based on incr incidences of malignant neoplasms of the lung and benign and malignant neoplasms of the liver. Marginal incr in incidences of adenoma and carcinoma of the small intestine may have been related to exposure to indium phosphide. There was clear evidence of carcinogenic activity of indium phosphide in female B6C3F1 mice based on incr incidences of benign and malignant neoplasms of the lung. Incr incidences of liver neoplasms were also considered exposure related.|Groups of 10 male and 10 female /F344/N/ rats were exposed to aerosols of indium phosphide with a mass median aerodynamic diameter of approx 1.2 um at concn of 0, 1, 3, 10, 30 or 100 mg/cu m by inhalation /6 hr day/5 days/wk (weeks 1-4 and weeks 10-14) or 7 days/wk (weeks 5-9). One male in the 100 mg/cu m group died before the end of the study. Body weight gains of all males were less than those of chamber controls. As a result of the indium phosphide exposure, the lungs of all exposed rats had a gray to black discoloration and were significantly enlarged, weighing 2.7-4.4 fold more than those of chamber controls. Indium phosphide particles were observed throughout the respiratory tract and in the lung associated lymphnodes. ... Inflammatory and proliferative lesions occurred in the lungs of all exposed groups of rats and consisted of alveolar proteinosis, chronic inflammation, interstitial fibrosis and alveolar epithelial hyperplasia. Pulmonary inflammation was attended by incr leukocyte and neutrophil counts in the blood. ... Indium phosphide caused inflammation at the base of the epiglottis of the larynx and hyperplasia of the bronchial and mediastinal lymph nodes. ... Indium phosphide ... induced a microcytic erythrocytosis consistent with bone marrow hyperplasia and hematopoietic cell proliferation in the spleen. Hepatocellular necrosis was suggested by incr serum activities of alanine aminotransferase and sorbitol dehydrogenase in all groups of males and in 10 mg/cu m or greater females and was confirmed microscopically in 100 mg/cu m males and females.|Groups of 10 male and 10 female /B6C3f1) mice were exposed to aerosols of indium phosphide with a mass median aerodynamic diameter of approx 1.2 um at concn of 0, 1, 3, 10, 30 or 100 mg/cu m by inhalation /6 hr day/5 days/wk (weeks 1-4 and weeks 10-14) or 7 days/wk (weeks 5-9). Although the effects of indium phosphide exposure were similar in rats and mice, mice were more severely affected in that all males and females in the 100 mg/cu m groups either died or were removed moribund during the study. One male and three females in the 30 mg/cu m group were also removed before the end of the study. In general body weight gains were significantly less in males and females exposed to 3 mg/cu m or greater compared to chamber controls. Mice exposed to 30 or 100 mg/cu m were lethargic and experienced rapid, shallow breathing. /In mice/ the lungs were discolored and enlarged 2.6 -4.1 fold greater than chamber controls due to exposure induced alveolar proteinosis. Indium phosphide particles were observed in the nose, trachea, and lymph nodes of some exposed males and females. Alveolar proteinosis, chronic active inflammation, interstitial fibrosis, and alveolar epithelial hyperplasia were observed. ... Hyperplasia in the bronchial lymph nodes and squamous metaplasia, necrosis and suppurative inflammation of the larynx were observed in some exposed males and females. Exposure to indium phosphide induced a microcytic erythrocytosis which was consistent with the observed hematopoietic cell proliferation in the spleen.|Genetic Toxicology: No significant incr in the frequencies of micronucleated normochromatic erythrocytes were noted in peripheral blood samples of male or female mice exposed to indium phosphide for 14 wk. ... There was a significant incr in micronucleated polychromatic erythrocytes in 30 mg/cu m male mice, there was no incr in female mice, and the percentage of polychromatic erythrocytes was not altered in males or females.

TERRESTRIAL FATE: 95% of natural indium exists as the isotope (115)In which has a half-life of 4.4X10+14 years and decays by beta-ray emission (Emax = 0.48 MeV)(1). Monovalent and bivalent indium compounds tend to disproportionate into the trivalent compounds and indium metal; the trivalent compounds are most stable(2). Due to the ionic nature of indium salts, volatilization from soil surfaces will not be important(SRC).

... Fischer 344 rats /were exposed/ to 0, 1, 10 and 100 mg/kg bw particulate indium phosphide (80% of the particles were < 0.8 um in diameter) by intratracheal instillation. Indium, determined by use of AAS /atomic absorption spectroscopy/ was detected at concentrations of 25 ng/g and 58 ng/g in liver and spleen, respectively, 1 day after instillation of 1 mg/kg bw indium phosphide. On day 7, the concentrations were 14 and 19 ng/g in these organs. Indium concentrations in serum increased significantly from day 1 to day 7 in animals that had received the highest dose. Toxic effects were obvious in the lungs but all rats survived. In this experiment, toxicity of indium phosphide was found to be much lower than that of more soluble compounds, such as indium chloride and indium nitrate.|The absorption of indium phosphide particles (2.4 um in diameter) following admin by oral gavage or ip injection of single doses of 0, 1,000, 3,000 or 5,000 mg/kg indium phosphide to male ICR mice, which were observed for up to 14 days /was evaluated/. Absorption from the gastrointestinal tract was minimal in less than 0.125 ug indium/mL of serum was detected at all doses. Following ip injection, there was a dose related incr in indium concn in serum (0.13, 0.6 and 1.75 ug/mL). After a dose of 5,000 mg/kg, indium was detected primarily in the liver and lungs (approx 150 ug/g tissue), with some being detected in the kidneys and testes (less than 20 ug/g tissue).|The distribution of indium phosphide particles (1.73 um diameter) in male F344 rats following a single oral dose, 14 days of oral dosing, or a single intratracheal instillation of 10 mg/kg indium phosphide. Indium phosphide was poorly absorbed from the intestinal tract in both oral studies, with most being excreted in the feces. Less than 0.23% of the admin dose was excreted in the urine over a 10 day recovery period. Absorbed indium was evenly distributed among the major organs, although less than 0.67% of the dose was retained in tissues or urine following 24 hr in both oral studies, indicating that the indium was not accumulating in the bodies of rats following multiple dosing. The urinary elimination half time was determined to be about 321 hr. Intratracheal admin of indium phosphide, the majority of the tissue indium was in the lungs and less than 0.36% of the dose being evenly distributed to the other major organs.

Analysis of genetic alterations in indium phosphide-induced hepatocellular adenomas and carcinomas revealed mutations in H-ras and alpha-catenin that were identical to those found in human hepatocellular neoplasms. This suggests a similar pathway of carcinogenesis in both species.

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

indium phosphide

Indium phosphide (InP): ACTIVE|Gallium arsenide can substitute for indium phosphide in solar cells and in many semiconductor applications.|One of the key advantages of indium phosphide is its potential for the fabrication of very small devices. Because indium phosphide and its ternary (InGaAs) and quaternary (InGaAsP) derivatives have relatively higher refractive indices than those of other optical materials, these compounds allow for devices with much sharper and smaller bends. As their energy band gap is also closer to light energy, electro-optical effects are stronger than those in other materials (which again translates into shorter distances and lower drive voltages). As a result, extremely small devices can be produced: dice are typically < 5 mm and for many functions (e.g. lasers, modulators) they are 1 mm or less.|This research work investigated the physical and chemical properties of a new type of wastewater produced from the semiconductor industry. The wastewater generated from indium phosphide (InP) wafer backgrinding and sawing processes was characterized in term of its particle size distribution (PSD), zeta potential, suspended and dissolved solids, total organic carbon, and turbidity. The wastewater contained high concentration of fine InP dusts with a size ranging from 0.07 - 1.44 mm. In spite of its high concentration of suspended solids resulting in high turbidity up to 371 NTU /nephelometric turbidity unit/, the wastewater contained very low organic matters (TOC < 2.2 mg L(-1)) and other inorganic impurities (SO4(2-) < 0.21 mg L(-1) and Na+ < 0.16 mg L(-1)). Based on the experimental data collected, the treatment technologies using chemical precipitation and ultrafiltration were applied to the wastewater. Both processes could effectively remove InP particles from the wastewater, however the coagulants in chemical precipitation introduced other ionic contents into the process resulting in difficulties of water recycling in the later stage. In comparison, ultrafiltration was more promising for InP wastewater treatment and recycling. Based on the results of this study, a full-scale UF system was built in a local semiconductor plant and it has successfully reclaimed water from the InP wastes for the past six months without any quality issue being raised.|An electrothermal atomic absorption (ETAAS) method for the determination of traces of iron (0.1-1.0 microgram g-1) in Fe-doped indium phosphide (InP) has been developed. In order to overcome the indium matrix-effect and to achieve a useful detection limit, a preliminary solvent-extraction of Fe(III) with acetylacetone (HAA) is necessary. After sample dissolution with hydrochloric acid (1 + 1) the digest is evaporated to dryness, Fe(II) is oxidized to Fe(III) with nitric acid, the residue is dissolved in 0.01 mol L-1 HCl and the iron is extracted at pH 2.0 with 0.5 mol L-1 HAA in toluene. The organic phase is injected into the graphite furnace and the iron is directly evaluated by external organic standard calibration. The limit of detection (3SB) resulting from further in-situ preconcentration is 0.03 microgram g-1. When the method was applied to the analysis of real samples containing 0.2-0.7 microgram g-1 Fe, the RSD was in the range 8-21%. Results were compared with those independently obtained on the decomposed sample solution with inductively coupled /plasma/ atomic emission spectrometry (ICP-AES). The detection limit of the ICP-AES method, that needs matrix-matched standards, is 0.20 microgram g-1.|The most common valence of indium is three. Monovalent and bivalent compounds of indium with oxygen, sulfur, and halogens are also known. The trivalent indium compounds are the most stable. The lower valence compounds tend to disproportionate to give the corresponding trivalent compounds and indium metal. /Indium and Indium compounds/