Chemical Information Profile 

for 

Indium Tin Oxide 

[CAS No. 50926-11-9] 

Supporting Nomination for Toxicological Evaluation by the 

National Toxicology Program 

June 2009 

National Toxicology Program

National Institute of Environmental Health Sciences 

National Institutes of Health 

U.S. Department of Health and Human Services 

Research Triangle Park, NC 

http://ntp.niehs.nih.gov/
Data Availability Checklist for Indium Tin Oxide [50926-11-9] 

Abbreviations: H = human; L = Lepus (rabbit); M = mouse; R = rat

Note: No judgement of whether the available data are adequate for evaluation of these endpoints in the context of 

human health hazard or risk assessment has been made. 

ENDPOINT H M R L ENDPOINT H M R L

ADME Developmental Toxicity 

Absorption X Developmental abnormalities 

Distribution X Embryonic/fetal effects 

Metabolism Newborn effects 

Excretion Carcinogenicity

Acute Toxicity (up to 1 week) Dermal 

Dermal Inhalation 

Inhalation* X Oral 

Injection Anticarcinogenicity

Ocular Anticarcinogenic effects 

Oral Genotoxicity

Subchronic Toxicity (1 to <26 weeks) Cytogenetic effects X

Dermal Microbial gene mutation 

Inhalation** Gene mutation in vitro 

Injection Gene mutation in vivo 

Oral Germ cell effects 

Chronic Toxicity (≥26 weeks) Neurotoxicity

Dermal Behavioral activity 

Inhalation* X Motor activity 

Injection Immunotoxicity 

Oral Immunotoxic effects X

Synergism/Antagonism Cardiovascular Toxicity

Synergistic effects Cardiovascular effects 

Antagonistic effects Mechanistic Data

Cytotoxicity Target Organs/Tissues** X 

Cytotoxic effects X X Endocrine modulation 

Reproductive Toxicity Effect on enzymes 

Fertility effects Modes of action 

Maternal effects Effect on metabolic pathways 

Paternal effects Structure-Activity Relationships** X X X X

*Rats: pharyngeal aspiration. **Data available for Syrian golden hamsters via intratracheal instillation. 

The above table provides an overview of the data summarized in this profile. From left to right, column 1 and 6 

list the endpoints and columns 2-5 and 7-10 identify the four species (human, rat, mouse, and rabbit) that were 

considered. An "X" is entered in each box that corresponds to an endpoint and species for which data are 

included in the profile. Blank cells indicate that no data were available in the literature.
Indium Tin Oxide Nomination Summary

Chemical Name: Indium Tin Oxide 

Formula: In.Sn.O 

CAS RN: 50926-11-9 

Molecular Wt.: Varies with composition 

[Structure not available] 

Basis for Nomination: Indium tin oxide (ITO) was nominated by the National Institute of 

Environmental Health Sciences for comprehensive toxicological characterization based on 

increasing potential for worker exposures due to its growing use in liquid crystal displays 

(LCDs), concern for pulmonary toxicity and carcinogenicity based on previous findings from 

NTP rodent toxicology studies of indium phosphide and effects observed in exposed workers, 

and lack of adequate toxicity data. Numerous wet chemical (aqueous or organic solvent) and 

thermal processes are available for producing ITO powders and thin film coatings. Commonly, 

indium oxide and tin oxide powders are blended together then compacted by hot or cold isostatic 

pressing or by sintering to make ITO sputtering targets (compressed blocks of ITO powder). 

ITO may be formed directly during a coating process, e.g., reactive sputtering from indium-tin 

alloy targets in the presence of oxygen. Its primary application is as a thin coating on glass or 

plastics used for touch panels (electrochromic, electroluminescent, and LCDs); plasma displays; 

flat panel displays (televisions, computer screens, cell phones, etc.); field emission displays; heat 

reflective coatings; solar panels; cathode-ray tubes; energy efficient windows; gas sensors; and 

photovoltaics. It is also coated on aircraft and automobile windshields for demisting and deicing. 

Workers engaged in finishing compacted ITO targets by wet grinding in a Japanese plant that 

manufactured ITO sputtering targets exhibited lung disease, the severity of which generally 

increased with duration of exposure and with serum indium concentrations. Two of five cases 

from the same Japanese plant experienced bilateral pneumothorax and at least one of these cases 

died. One of the five workers, diagnosed with lung fibrosis, improved upon removal to another 

work area. A cohort study of 108 workers from this plant reported that 23 (21%) had significant 

interstitial changes and 14 (13%) had emphysematous changes. Only modest lung function 

decrements were noted. These conditions were reported to most likely be due to inhalation of 

micrometer-sized ITO particles. High serum concentrations of indium in a large fraction of the 

workers and former workers indicated indium dissolution from ITO particles. Biomarkers of 

interstitial lung changes increased with increasing mean serum indium concentrations in 20 of 93 

workers who were exposed to indium metal (~10%), ITO (~50%), or other insoluble indium 

compounds (~40%) at two ITO target manufacturing plants and two recycling plants, and in nine 

of 40 (22.5%) workers who had extended exposure to other insoluble indium species. Indium 

was suggested as the main toxicant, as well as in studies with other indium compounds such as 

indium oxide and indium phosphide. Alveolitis and/or other lung inflammatory responses were 

observed in rats given two different ITO doses by pharyngeal aspiration. Particles and 

proteinaceous materials were observed in the alveolar lumen but no fibrotic response was seen 

up to 60-days post-treatment. In a hamster subchronic study, intratracheal instillation caused 

significant increases in relative lung weight and slight to moderate inflammatory lung lesions. In 

a similar study, two of ten animals had a slight increase in the number of seminiferous tubules 

with disorganization or vacuolization. Body, testis, epididymis, seminal vesicle weights, and 

caudal sperm count were comparable to controls. ITO was cytotoxic in mouse and rat peritoneal 

macrophages and rat alveolar macrophages but not to rat or mouse epithelial cells. It also 

induced micronuclei in rats in vivo but not in vitro. 
Chemical Information Profile for Indium Tin Oxide 

A. Chemical Information 

Molecular Identification 

Chemical Name: Indium Tin Oxide (ITO) (9CI) 

CAS RN: 50926-11-9* 

Synonyms: Tin indium oxide 

Trade Names: F-ITO; Hyviz; Indium tin oxide, Vacuum Deposition Grade, 99.999%; Microsolver 

LIT 41A; New Pro Coat EC-L; S 100 (electrode); SUPP-HX; UFP-HX; X 101 (oxide) [Note: These 

were given in the Registry record; however, only SUFP-HX and UFP-HX were confirmed in a 

Google search (mentioned in U.S. patents).] 

Hill Formula: In.Sn.O (usually given as In2O3:SnO2 as product, Hill formula = In2O5Sn) 

Line Formula: Not available 

Smiles Notation: Not available 

PubChem SID: 3764630** (PubChem, undated) 

InChI: Not available 

Molecular Weight: Varies with composition 

Purity of Commercial Products: nanopowder is available at purities from 99 to >99.99999% at 

wt. % ratios (oxide weight ratio or In-Sn atomic ratios) of 90:10 (most common), 95:5, and 80:20

(AZoM.com, 2006; Degussa AG Advanced Nanomaterials, 2006; Foyol Co., Ltd., 2008; Indium 

Corporation, undated; Nanophase Technologies, 2008; Reade Advanced Materials, 2006; Swarts 

[Indium Corp. of America], 2006; Tolcin, 2008) 

Additives in Commercial Products: Some nanopowders are coated with polymers to improve 

compatibility in coating formulations. 

Impurities in Commercial Products: Total aluminum, antimony, bismuth, chromium, copper, 

iron, lead, magnesium, nickel, potassium, sodium, titanium, and zinc at a total concentration of ~100 

ppm (Umicore, 2005) 

Mammalian Metabolites: Not available 

Biodegradation Products: Not available 

Environmental Transformation: Not available 

Physical-Chemical Properties 

Physical State: Yellow, yellow-green, gray-yellow, gray, or blue solid/powder 

Tin substitutes for indium in ITO crystals forming either stannous oxide (tin[II] monoxide) or 

stannic oxide (tin[IV] dioxide) at the doping levels commonly used (8-10%). Much of the Sn(IV) 

likely exists as interstitial atoms in the indium oxide cubic bixbyite lattice rather than as replacement 

atoms. Crystal grain size depends on processing parameters (e.g., deposition rate and substrate 

temperature). Typical ITO films are 1500-3500 Ǻngstroms thick (BizEsp, 2007; Zhou, 2005 thesis). 

ITO nanopowder primary particle size is ~7-75 nm. Standard- and fine-grade powder particle sizes 

are 0.1-15 μm with agglomerated particles ≥31 μm. ITO nanoparticles also are available as 

dispersions in water or organic solvents (AZoM.com, 2006; Chagnon, 2001; Degussa AG Advanced 

Nanomaterials, 2006; Foyol Co., Ltd., 2008; Indium Corporation, undated; Nanophase 

Technologies, 2008; Reade Advanced Materials, 2006; Swarts [Indium Corp. of America], 2006;

Tolcin, 2008). 

Specific Gravity or Density Value: 6.65-7.34 g/cm3

 (Registry, 2006); 7.14 g/cm3 (AZoM.com, 

2006) 

Boiling Point: Sublimes at 982 oC (Swarts [Indium Corp. of America], 2006) 

Melting Point: 1910 oC (Swarts [Indium Corp. of America], 2006) 

Vapor Pressure: Not available 

Solubility: Insoluble in water (Swarts [Indium Corp. of America], 2006) [Note: Solubility limit of 

Sn in In2O3 is <8 atomic % (Kim et al., 2006).] 

Log P = Log Kow: Not available 

1
Chemical Information Profile for Indium Tin Oxide 

Bioconcentration Factor(s) (species): Not available 

*This is the generic CAS RN; specific CAS RNs are given for specific formulations—e.g., 71243-84-0 for In1.69 Sn0.15O2.85, 

212075-26-8 for In0.01SnO2, and 180090-96-4 for In0.02Sn 0.98O1.99. 

**This is for the compound with CAS RN 71243-84-0. A PubChem compound and substance search produced no other 

records for other formulations (searched via chemical name and CAS RNs). 

B. Exposure Potential 

U.S. Annual Production 

Not available for ITO; no U.S. primary production of indium 

1997-2000: consumption of indium for coatings ranged from 34-39 metric tons (up from 15 metric 

tons in 1996); consumption for electronic components and semiconductors ranged from 9-13 

metric tons (up from the 5 metric tons in 1996) (Jorgenson and George, 2005). 

2001-2005: consumption of indium increased annually from 65-115 metric tons. The United States 

imported 79 to ~150 metric tons per year (Carlin, 2006). 

2006: U.S. indium "production" was largely from upgrading imported indium (99.97-99.99%) to 

purities up to 99.99999%; most indium products in the United States are currently produced by 

Indium Corporation of America and Umicore Indium Products. U.S. import of unwrought indium 

and indium powder was 100 metric tons (Tolcin, 2008). 

Worldwide Annual Production

- No production volumes for ITO were found. Most production of ITO targets and sputtering is done 

in Japan, China, and Korea. One Japanese company, Nikko Materials Co., Ltd. produces 45% of the 

global ITO target (Tolcin, 2008). 

- Refinery production of indium was 405 and 455 metric tons in 2004 and 2005, respectively; China 

was the lead indium producer with an output of 200 and 250 metric tons per year, respectively 

(Carlin, 2006). 

- More than 70% of indium produced in the world is used in flat panel displays (FPDs) but only ~30% 

of the ITO in the target deposits on the desired substrates during sputtering. Used targets, sputter 

chamber shields, and grinding sludge account for the remaining ITO. Reclaim reprocessing can 

recover ~ 60-65% of the indium from the non-deposited ITO (Carlin, 2006; Jorgenson and George, 

2005). 

- Secondary production of indium from reclaim processing of ITO scrap began to exceed primary 

production in 2006. The minimum world indium production used in ITO increased from 595 metric 

tons in 2005 to 774 metric tons in 2006 (Phipps et al., 2007). 

- World production of indium in 2009 is projected to be 1512 metric tons (551 metric tons primary 

and 961 metric tons secondary production); the projected demand is 1555 metric tons (1281 metric 

tons [82%] for FPDs and 274 tons for other uses) (Phipps et al., 2007). 

Production Processes 

- The most common method for producing ITO targets is sintering blended indium oxide and tin 

oxide powders (e.g., Okabe et al., 2000 pat.). 

- Indium oxide and tin oxide powders must be intimately mixed. ITO powders may be used directly. 

Powders are compacted by cold or hot isostatic pressing, sintering, or hot pressing. After 

compaction, the powders are heated for many hours at ~1500 oC for homogenization and 

recrystallization (BizEsp, 2007; Friz and Waibel, 2003). 

- After compaction of the powders, the targets are surface finished by polishing, machining, or 

grinding (Lo et al., 1997 pat.). 

- Umicore uses pressureless sintering to produce ceramic ITO sputtering targets (Umicore, 2005). 

- Co-precipitation from a solution containing both indium and tin ionic compounds also can be used. 

An aqueous solution of inorganic salts is basified, the precipitate washed to remove ionic 

compounds, and the intermediate indium tin hydroxide dried then subsequently heated to convert it 

to ITO (e.g., Kim et al., 2006). 

2
Chemical Information Profile for Indium Tin Oxide 

Nanoparticles

- Nanoscale monophasic ITO powders have been produced directly from organic salts in organic 

solvents (Ba et al., 2006; Lee and Choi, 2005). 

- ITO nanoparticles also are produced by sol-gel process in which controlled hydrolysis of metal 

alkoxides in aqueous solution leads to metal oxide nanoparticles, which must be washed, dried, and 

calcined (Ba et al., 2006; Zhang et al., 2004). 

- A nanopowder of ~37-nm particle size and said to be ITO, although it contained phases of indium 

oxide and tin oxide, was prepared by combustion of an emulsion containing indium nitrate and 

tetrabutyltin (Bickmore et al., 1999 pat.). 

- ITO nanostructure can also be synthesized by the following methods (Psuja et al., 2009): 

· hydrothermal method—mixed hydrochloric acid solution of metallic indium and tin and hydrous 

solution of sodium hydroxide in the form of sol are hydrothermally autoclaved and then sintered 

in air (Xu et al., 2005; cited by Psuja et al., 2009) 

· controlled growth technique—indium chloride and tin chloride dissolved in ethanol are dropped 

in 25% ammonia water with β-alanine and surfactant (Al-Dahoudi et al., 2001; cited by Psuja et 

al., 2009) 

· preparation of indium hydroxide, which is washed, centrifuged, dried, sintered, and then 

mechanically mixed with tin oxide 

· modified Pechini method—nitrides, α-hydroxyl acids, and multi-hydroxide alcohols are 

dissolved in water; metals are complexed by acid molecules at high temperature; crystallization 

of compounds via a violent combustion reaction to produce oxides 

Thin Films and Other Coatings

- Spray pyrolysis and sputtering from targets (preferred method) are thermal methods used to deposit 

thin ITO films (Gordon, 2000). Sputtering is done in a chamber at reduced pressure. In reactive 

sputtering from an In-Sn alloy target, oxygen is added to oxidize the metals [less popular process 

since pure ITO targets have become available for sputtering (BizEsp, 2007)]. For ITO thin film 

patterning, photoresists are typically used as masking layers. Sputtering processes include directcurrent magnetron and radiofrequency sputtering (Friz and Waibel, 2003; Zhou, 2005 thesis). 

- Other thermal methods include pulsed laser deposition in an ultra-high-vacuum chamber and 

reactive and ion-assisted sputtering (Friz and Waibel, 2003; Zhou, 2005 thesis). 

- Coatings may be produced on substrates by electrospinning sol-gel prepared ITO coatings on 

substrates followed by thermal processing (e.g., Zhang et al., 2004). 

- ITO inks are used for screen printing to give coatings with thicknesses of ~10-30 μm for LCDs, 

blackwall contacts, and solar-cell antireflection coatings. The post deposition crystallization 

temperature (≤600 oC) is held for more than an hour (Zhou, 2005 thesis). 

- Aqueous or organic solvent-based nanoscale ITO dispersions are applied to substrates by 

conventional coating processes such as spray, dipping, and spin coating. Formulations may include 

UV-cured acrylic coatings or other transparent plastics (Degussa AG Advanced Nanomaterials, 

2006). 

Recycling

- Spent sputtering materials, grinding sludge, and other indium-bearing wastes generated during FPD 

manufacture are recycled by wet chemical methods to reclaim the separate metals (acid dissolution, 

precipitation at different pH), which are sent back to the start of powder production (Ceramic 

Industry, 02-07-08; Schlott et al., 1997 pat.).

- A simpler process was patented in which ground-up target material (<250 μm powder) was returned 

to a compaction step using hot isostatic pressing at a temperature low enough to prevent 

recrystallization and retain the primary grain size (0.1-10 μm) of the original targets (Schlott et al., 

1997 pat.). 

- LCD panels from dismantled computers, etc., may be smashed into glass cullet and the indium 

recovered by acid dissolution, etc. Each 15-inch LCD display contains about 0.5 g ITO (King 

County Solid Waste Division, DNRP, 2008). 

3
Chemical Information Profile for Indium Tin Oxide 

Uses 

- Generally used as a thin coating on glass or plastics for: touch panels; electrochromic, 

electroluminescent, and LCDs; plasma displays; flat panel displays; field emission displays; touch or 

laptop computer screens; cell phones; heat reflective coatings; solar panels; cathode-ray tubes; 

energy efficient windows; gas sensors; and photovoltaics (AZoM.com, 2006; Gordon, 2000; 

Jorgenson and George, 2005). 

- Coated on aircraft and automobile windshields for demisting and deicing (AZoM.com, 2006; 

Gordon, 2000; Jorgenson and George, 2005). 

- Coated on glass for manufacture of transparent ITO electrodes, microscope slides, infrared mirrors, 

etc. (PGO, undated). 

- Can be used as a waveguide for photonic crystals (Giessen, 2005). 

- Nanopowder is used to create an ITO target, a key material used in coating an ITO thin film for use 

on LCDs, etc. (AZoNano, 2006). 

- Applications from the environmental and life sciences journal and patent literature not mentioned in 

the commercial literature include: 

· photocatalyst component for pollution control and water disinfection 

· chemical sensors and biosensors (may be implantable) 

· heaters in droplet-based microfluidic devices (e.g., "lab-on-a-chip;" some may be commercial) 

· protein and DNA microarrays (e.g., for hybridization and PCR) 

· transparent cell and tissue culture platforms that allow optical monitoring of functions (no 

cytotoxicity) 

· electroporation (e.g., for viral gene transfection) 

[See Appendix 1 for more details.] 

Occupational Exposure

- Greatest potential for exposure is due to industrial use, particularly as the use of ITO in the 

production of LCDs increases (Homma et al., 2003, 2005). 

- The primary routes of exposure are inhalation, ingestion, and eye and skin contact (Swarts [Indium 

Corp. of America], 2006). Workers handling powdered ITO or engaged in machining, polishing, or 

wet grinding of ITO targets after compaction may inhale ITO. [Workers in Japan engaged in wet 

grinding of targets have developed mild to severe interstitial lung disease despite respiratory 

protection (e.g., Homma et al., 2003, 2005).] 

General Population Exposure 

Foods and Beverages, Cosmetics, etc.: Not available 

Ambient Environment: Not available 

Environmental Occurrence 

Natural Occurrence: Not known to occur naturally 

U.S. Environmental Releases: Not available 

Concentrations in Environmental Media: Not available 

C. Regulatory Information 

U.S. Regulations 

ITO was on the Priority Testing List (TSCA section 8(a)) from 2001-2006. Effective June 3, 2004, it 

was added to the Health and Safety Data Reporting rule (TSCA section 8(d)), requiring submission of 

unpublished health effects studies on pharmacokinetics, genotoxicity, subchronic and chronic toxicity, 

and reproductive/developmental toxicity when purity of the indium compound is ≥90% by weight of 

test substance (U.S. EPA, 2004). In the 56th TSCA Interagency Testing Committee (ITC) Report, data 

were requested on concentrations to which workers may be exposed during manufacturing and 

downstream uses and numbers of workers associated with manufacturing and downstream uses (U.S. 

EPA, 2005). It was removed from Priority Testing List in Report 58 (U.S. EPA, 2006). A history of 

other U.S. EPA and ITC actions may be found in Appendix 2. 

4
Chemical Information Profile for Indium Tin Oxide 

Exposure Limits (Standards and Criteria): Not available for ITO 

ACGIH TLV: 0.1 mg/m3

 TWA (time-weighted average) for In2O3 (as In) 

NIOSH REL: 0. 1 mg/m3

 TWA for In2O3 (as In); 2 mg/m3 TWA for SnO2

OSHA PEL: None listed for either compound 

European Union Scientific Committee Regulations 

Not available 

Canadian Domestic Substances List (DSL) and Non Domestic Substances List (NDSL) 

ITO is not listed in the DSL or NDSL. Indium oxide [1312-43-2] and tin oxide [1332-29-2 and 18282-

10-5] are both on the public portion of the DSL (published May 4, 1994) (Environment Canada, 2008). 

D. Toxicological Information 

General Toxicity 

Data for indium oxide (In2O3) and tin oxide (SnO2) are also given below. ITO may cause severe 

irritation and burns to the skin or eyes. It may also burn the gastrointestinal tract if ingested. 

Respiratory irritation is possible from inhalation; chronic exposure may cause lung damage (Swarts 

[Indium Corp. of America], 2006). 

Human Studies: Most of the following case reports and cohort studies are from the same Japanese 

processing plant where ITO sputtering targets are produced for transparent conductive films used in 

flat panel displays. Workers were engaged in finishing compacted (press molded) and sintered ITO 

targets by wet surface grinding in a well ventilated area while wearing dust masks with >95% filter 

efficiency. Mean diameter of airborne ITO particles was 2.5 μm (0.1-11 μm). Dust may have been 

suspended after splashes from the wet grinding dried on surfaces (Chonan et al., 2007). 

- A 27-year-old male employed from 1994-1997 as an operator of a wet surface grinder was 

diagnosed in 1998 with interstitial pneumonia; diagnosis was consistent with inhalation of ITO 

particles. 

· Liver damage (possibly not indium-induced), emaciation, and splenomegaly were 

observed. 

· The indium serum concentration collected one year before death was 290 μg/L compared to 

a mean of 0.1 μg/L reported for healthy unexposed males (n=377). 

· The patient died three years later of bilateral pneumothorax. 

· Both tin and indium were spectroscopically identified in his lungs (Homma et al., 2003). 

- A 30-year-old male engineer exposed for 4 years to ITO aerosols from wet surface grinding was 

diagnosed with pulmonary fibrosis with cholesterol granulomas and emphysema; these were 

reported most likely due to inhalation of ITO. 

· Indium serum concentration was 51 μg/L compared to normal values (<0.1 μg/L). 

· Brown particles in lung tissues contained 61% indium and 4% tin compared to 74% indium 

and 8% tin in the target material. 

· The mean count diameter of the ITO particles sampled in the workplace (air was not 

specified; might have been surface wipes [deposits due to splashing]) was 10 μm. 

· The patient recovered when removed to another area in the company (Homma et al., 2005). 

- Among 115 ITO workers in the same Japanese plant, three workers who had been engaged in 

surface grinding for 8-12 years had severely injured lungs, which was reflected in significantly 

elevated KL-6 (MUC-1; Krebs von den Lungen-6), a marker of diffuse interstitial lung disease. 

They had high serum indium concentrations and high resolution computed tomography (HRCT) 

revealed interstitial and/or emphysematous changes in all three workers. One worker, a 

nonsmoker, had severe obstructive changes by spirometry parameters and later experience 

bilateral pneumothorax (Taguchi and Chonan, 2006 [PMID:16886812]). 

- Of 108 males at the same Japanese plant, 23 (21%) showed significant interstitial changes. 

Fourteen (two nonsmokers) (13%) had emphysematous changes. 

· Elevated serum KL-6 was found in 40 of the workers. 

5
Chemical Information Profile for Indium Tin Oxide 

· Although serum indium concentration and KL-6 concentration were not significantly 

different in surface grinders vs. those in other work rooms, the prevalence of interstitial 

changes and emphysematous changes in the two groups were 40% vs. 14% and 27% vs. 

8%, respectively. Most workers were rotated to different operations, which may have 

obscured exposure differences among them. 

· Of the 108 workers, the 78 who were currently exposed had serum indium concentrations 

of 7.8 ± 4.3 μg/L. Serum concentrations of 27 formerly employed employees were 8.3 ±

4.4 μg/L, and concentrations in nonexposed employees (38) were 0.3 ± 2.6 μg/L. 

· The range of serum indium concentrations increased with increasing years of exposure and 

increasing interstitial changes score while the mean age of the workers in each of the 

quartiles was 33-34 years. 

· The first quartile (mean 2.1 years of experience) had serum concentrations in the range 

0.2-2.9 μg/L and an interstitial changes score of zero. 

· In the second and third quartiles (2.9 and 4.1 mean years of experience), serum indium 

concentrations were 3.2-8.0 and 8.3-21.7 μg/L and the number of interstitial changes were 

0-10 (score 0.5-1.0). 

· In the fourth quartile (9.9 mean years of experience), the serum indium concentrations were 

22.2-126.8 μg/L and the number of interstitial changes were 0-14.5 (score 3.0). 

· Modest lung function decrements were noted in those workers with interstitial changes. 

· Recent efforts to reduce exposure included semi-closure of open systems such as wet 

surface grinding and stricter enforcement of dust respirator use (Chonan et al., 2007). 

- Workers were studied from two ITO manufacturing plants and two ITO recycling plants (total 93 

workers, 93 nonexposed workers) where the major indium species in the dusts to which the 

workers were exposed were ITO (>50%), In2O3 or In(OH)3 (~40%), and indium metal (~10%). 

All of these species are difficultly water soluble. Dusts were said to consist "largely of 

respirable-sized particles." 

· No differences were observed in lung effects between those who had inhaled mainly ITO 

and those who had inhaled tin-free indium compounds. 

· Although no differences were observed between exposed and nonexposed workers in 

parameters of spirometry or in prevalence of interstitial changes, dose-effect and doseresponse relations were very clear when the workers were grouped by serum indium 

concentration ranges. 

· The prevalence of interstitial and emphysematous changes as well as several biochemical 

indicators of lung damage, especially KL-6, generally increased with increasing blood 

serum indium concentrations. 

· The group with the greatest changes had a mean serum concentration of 80.4 μg/L. 

· Significant changes in KL-6 were observed in groups with mean serum concentrations 

between 24.2 and 80.4 μg/L (20 workers). 

· The overall serum geometric mean of exposed workers was 8.25 μg/L (maximum 116.9 

μg/L) compared to 0.25 μg/L in unexposed workers (Hamaguchi et al., 2008). 

Other studies of biological monitoring of workers exposed to water-insoluble indium compounds are 

included for comparison. 

- In a study of Japanese indium plant workers that does not clearly state in its abstract whether 

exposure was to ITO, no findings of interstitial lung changes were noted in the 40 workers upon 

HRCT examination; but serum KL-6 concentrations were elevated (>500 U/mL) in nine men 

(22.5%) who had significantly longer indium exposure, higher serum indium concentrations, and 

higher surfactant protein D (SP-D) concentrations, which were indicative of interstitial changes in 

the lungs (Nogami et al., 2008 [PMID:18260313]). 

- Arithmetic mean values for indium in whole blood, serum, and urine of 107 Japanese workers 

exposed to partially respirable particles of water-insoluble indium compounds for a mean 

duration 4.56 years were 16.8, 14.6, and 2.45 μg/L, respectively. Values at the 90th percentile 

6
Chemical Information Profile for Indium Tin Oxide 

were 42.7, 36.1, and 6.88 μg/L, respectively. The mean blood indium concentrations in 24 

unexposed workers were 0.57 μg/L (0.98 μg/L at the 90th percentile) (Miyaki et al., 2003). [The 

serum value 14.6 μg/L falls within the range of the workers with mean exposure duration of 4.1 

years reported by Chonan et al. (2007).] 

- Taiwanese optoelectronics workers (103) had mean whole blood concentrations of 0.22 μg/L 

[reported as ppb] compared to 0.14 μg/L in blood of 67 referents (unexposed office workers). 

There was little difference among the three groups of optoelectronic workers (15 in equipment 

maintenance, 52 dopants and thin film workers, and 36 fabrication supervisors and engineers). 

The mean concentrations of indium in urine were not significantly different from that of the 

controls (0.02-0.03 μg/L). The workers were also exposed to gallium, arsenic, and antimony. 

Although gallium and arsenic concentrations in the urine were significantly correlated with 

malondialdehyde plasma concentrations, a marker of lipid peroxidation, no such correlation for 

indium in urine was observed (Liao et al., 2004 [PMID:15354058], 2006 [PMID:16902371]). 

- Personal air samplers worn by production workers, engineers, and office administrators (72 

workers/group) at two semiconductor manufacturing plants in the Science-Based Industrial Park 

in Hsinchu City, Taiwan, collected inhalable air samples indicating mean (range) airborne indium 

concentrations of 8.4 (0.14-100.62), 7.38 (0.25-99.3), and 2.08 (0.12-17.66) μg In/m3

, 

respectively. Urine concentrations for the three groups were 6.98 (3.05-35.89), 5.88 (3.02-34.09), 

and 1.24 (0.05-7.27) μg In/L, respectively. All but one of the 216 indium inhalation exposure 

concentrations were less than the NIOSH REL for indium and indium compounds (100 μg/m3

) 

(NIOSH, 2005). (Exposures at this plant were probably to water-insoluble gallium arsenide and 

indium arsenide. Arsenic posed the greatest risk for the production workers and engineers since 

arsenic exposures frequently exceeded the exposure limit) (Chen et al., 2007a,b). 

Animal Studies: Not available 

Indium Oxide: Although extensive toxicity testing of hydrated indium (III) oxide [In(OH)3] has been 

done its comparability to indium oxide is questionable therefore results from studies using In(OH)3 are 

not included here. 

Human Studies: Not available 

Animal Studies: Necrotizing pneumonia was reported in rats and rabbits injected intravenously 

(i.v.) with indium oxide. Toxic effects in rats dosed intratracheally (i.t.) included pneumonia and 

early fibrosis in the lungs, hyperplasia in lung lymph nodes, dystrophic changes in liver and kidneys, 

and inflammatory changes in the heart. Lung inflammatory changes and growth depression were 

observed in rats that inhaled indium oxide for three months. It was nontoxic in rats when ingested 

(Smith et al., 1978). 

Tin Oxide

Human Studies: Workers exposed to tin oxide (stannic oxide) in dusts or fumes for at least three 

years while engaged in metal casting (tin foundries), scrap metal recycling, or tin plating 

accumulated tin in their lungs without any effect on lung function, reports of fibrosis, "clinically 

significant emphysema," or adverse effect on mortality. One case control study in Belgium reported 

an odds ratio of 3.72 for risk of chronic kidney failure for persons occupationally exposed to tin, but 

no distinction was made as to the tin speciation (IPCS, 2005; Monteiles, 2005). Tin oxide is 

generally regarded as an agent that produces nonfibrotic pneumoconiosis, a benign disease with 

insignificant pulmonary effects. Recently, interstitial lung disease has been reported in Turkish 

tinsmiths who recoat tin-covered copper kitchen utensils. Turkish tinners (24), who had worked at 

the occupation for a mean of 41.4 years, had a high incidence (46%) of diffuse parenchymal lung 

diseases that appeared to be attributable to combined exposure to sulfuric acid (in a preliminary step 

followed by rinsing) and powdered ammonium chloride (used to pretreat the copper surface) as well 

as to tin oxide vapors while applying the tin, either by rubbing a pure tin bar or by sprinkling small 

balls of granulated tin on the hot copper surface. Two-thirds of the workers had a history of 

potential exposure to environmental asbestos, but asbestosis was ruled out; and 75% smoked 

7
Chemical Information Profile for Indium Tin Oxide 

tobacco. High resolution computed tomography results were consistent with "respiratory 

bronchiolitis interstitial lung disease" in nine workers, a "usual interstitial pneumonia" in one 

worker, and a "non-specific interstitial pneumonia" in another (Dikensoy et al., 2008). Another 

study of 26 tinsmiths from the same Turkish province reported that 11 exhibited aortic valve 

sclerosis and left ventricle diastolic dysfunction. One of the workers had been seen before and 

determined to have a reversible toxic myocarditis due to tin [oxide] fumes exposure. The signs 

vanished after the worker refrained from exposure for six months (Gunay et al., 2006

[PMID:16326401]). 

Animal Studies: Rats given a 50-mg dose of tin smelter dust i.t. showed dust accumulation in the 

lungs without connective tissue changes one year post exposure. Toxic effects observed in shortterm experiments with rats exposed to tin salts were not observed in rats dosed with tin oxide

(Monteiles, 2005). 

Chemical Disposition, Metabolism, and Toxicokinetics 

Absorption and Clearance: Not available 

Human Studies: High concentrations of indium in sera of workers exposed by inhalation to ITO 

indicated indium dissolution from ITO particles; indium appeared to be distributed to several organs 

(e.g., liver and spleen) via blood, which authors noted may lead to chronic adverse health effects. 

Two former ITO workers in Japan had serum indium concentrations of 51 and 290 μg/L three to 

four years after leaving the factory compared to a mean concentration of 0.1 μg/L reported for 377 

unexposed workers (Chonan et al., 2007; Homma et al., 2003, 2005). 

Animal Studies: Two-phase elimination of ITO from female Wistar rat lungs was observed after a 

single pharyngeal aspiration of ITO particles (2 or 20 mg/rat). [See acute animal studies for particle 

characterization.] By 15 days post-exposure, ~60% of the 2 mg and ~40% of the 20 mg dose were 

eliminated. Little more was cleared at the subsequent observation points up to 60 days. No blood, 

tissue, or urine concentrations were reported (Laloy et al., 2007). 

Indium Oxide

Absorption and Clearance: Minor absorption of indium was observed when rats were exposed to 

indium oxide via inhalation, i.t. instillation, or ingestion. More indium was absorbed in the lungs 

and tracheobronchial lymph nodes than in the gastrointestinal tract, likely due to the longer retention 

time when indium oxide is deposited in the lungs. After inhalation, lung clearance was slow. 

Twelve weeks after a three-month inhalation exposure to indium oxide (mean concentration of 64 

μg/m3

), 58% of the indium oxide still in the lungs at the end of the exposure had been removed from 

the lungs and 69% from the tracheobronchial lymph nodes. The biological half life was calculated 

as 2.5 months in the lung and 1.75 months in the tracheobronchial lymph nodes. After nose-only 

exposure of rats to nanoparticulate (64 nm) indium oxide for one hour (~2.5 mg/m3

) 40% was 

deposited in the lower respiratory tract and 60% was in the nasopharyngeal region. Wide 

distribution to organs (greatest in the kidneys and liver) indicated "small but significant absorption," 

particularly during the first 24 hours of exposure. The half-life for clearance after this short 

exposure was 8 to 10 days. Fresh tissues from rats that were fed a diet with 8% indium oxide for 

three months contained ppm levels of indium (Morrow et al., 1957; Smith et al., 1978). 

Human Studies: Not available 

Animal Studies: When rats inhaled indium oxide (average concentration 64 mg/m3

) for two weeks, 

indium oxide mobilized significantly to tracheobronchial lymph nodes, but little absorption and 

distribution was observed. Indium concentrations in μg/g after two weeks (concentrations after 12 

weeks are in parentheses) were 490 (10,000) in lungs, 250 (1,300) in tracheobronchial lymph nodes, 

1.8 (9.2) in kidney, 0.33 (3.1) in liver, 0.25 (16) in spleen, and 0 (3.4) in bone. Tissue 

concentrations were higher at 24 weeks post exposure, but still represented only 10% of the lung 

burden with exclusion of the tracheobronchial lymph nodes. Kidneys, spleen, liver, and bone 

contained ≤2 μg In/g after consuming a diet with 8% indium oxide for three months. When rats 

8
Chemical Information Profile for Indium Tin Oxide 

were given indium oxide i.v. at 30 mg/kg bw, the principal deposits were in lung, liver, and spleen 

(Smith et al., 1978). 

Tin Oxide

Absorption and Clearance: The International Commission on Radiological Protection (ICRP) 

developed a human model for absorption of inhaled tin oxide and other compounds categorized as 

Type M (i.e., ~70% of the tin deposited in the alveolar interstitial regions is transferred to blood, and 

~10% of the tin deposited in the bronchi and bronchiole regions and 5% of the tin deposited in the 

gastrointestinal tract are rapidly absorbed) (IPCS, 2005). Ingested tin is poorly absorbed, even from 

soluble compounds. Tin compounds ingested by rats were excreted in the feces in amounts greater 

than 90 to 99% of the original low dose (within 48 hours in one experiment). When given 

parenterally, most was excreted in the urine with a limited amount excreted in the bile. The 

biological half-life for inorganic tin in rat femur was calculated at 34 to 40 days and in mouse whole 

body, approximately 30 days (JECFA, 1982). 

Human Studies: Long-term exposure (3 to 5 years) to tin oxide in dust and fumes from some 

extraction and treatment procedures of tin ores and concentrates, especially bagging of concentrates, 

and from certain smelting operations, caused stannosis (loading of tin in the lungs), a mild 

pneumoconiosis. Small dense shadows were apparent in lung X-rays. Autopsy of a worker who 

had no symptoms for 18 years after his last exposure revealed black pigmentation in pleura, lung 

parenchyma, and lymph nodes. The nodes near the bifurcation of the bronchi and bronchioles 

showed the heaviest pigmentation (HSDB, 2005a). 

Animal Studies: Rats given tin oxide (1-4 i.v. doses of 250 to 1000 mg/kg bw) and observed for up 

to 26 months for long-term retention, showed phagocytosis and storage of tin in mononuclear cells 

of the reticuloendothelial system, especially the spleen, liver, bone marrow, and some lymph nodes, 

but no fibrosis or neoplasia was seen. Retention was also noted at some injection sites. The same 

disposition pattern was observed in New Zealand white rabbits given tin oxide (1-5 i.v. doses of 250 

mg/kg bw) over a 6- to 26-month survival period (Fischer and Zimmerman, 1969; JECFA, 1982). 

Acute Exposures

In a recent rat study (TSCA test submission) the toxic effects of well characterized ITO particles 

(90:10 In-Sn ratio) produced by Umicore (the sponsor) were compared to those induced by indium 

trioxide, stannic oxide, or a mixture of the two. ITO impurities included 300 ppm zirconium, 100 ppm 

silicon, and <100 ppm each lead and antimony. The mass median diameter of 75% of the particles was 

<20 μm, with 58% <10 μm and 41% <20 μm. 

Route: pharyngeal aspiration [inhaled from its placement on base of fully extended 

tongue] 

Species: rats 

Dose/Duration: 2 or 20 mg (~1.5 or 15 mg In)/single dose 

Observation Time: ≤ 60 days 

Effects: lung inflammatory response indicated by increase in lactate dehydrogenase 

(LDH) activity 3 days after ITO treatment; increased total protein and total cells 

in bronchoalveolar lavage fluid in ITO-treated rats (> In2O3 > mixture of In2O3 + 

SnO2 > SnO2). ITO produced a stronger dose-response at 15 days; higher dose 

induced alveolitis (thickening of the alveolar wall by 3 days with nodules around 

particle aggregates). Fibrotic response, as measured by lung hydroxyproline and 

collagen, was not induced by ITO or the other indium and tin materials within 

observation period. ITO-reported effects included alveolitis; increase in 

macrophages, lymphocytes, and polymorphonucleated neutrophils; perivascular 

inflammatory infiltrates; and the presence of particles and proteinaceous material 

in the alveolar lumen (histological response to the other indium and tin materials 

9
Chemical Information Profile for Indium Tin Oxide 

at 60 days was not reported). A slight but significant increase in tumor necrosis 

factor-alpha was seen only in rats treated with the higher ITO dose. 

Source(s): Laloy et al. (2007) [TSCA test submission from Umicore]; Lison et al. (2009 

[PMID:19176593]) 

Indium Oxide

LC50/LD50 Values: i.p. LD50 = 396 mg In/kg bw [mice] (Smith et al., 1978) 

Route: oral (intragastric) 

Species: mice 

Dose/Duration: 10 g/kg bw (8270 mg In/kg bw) 

Observation Time: not provided 

Effects: 23% or 45% mortality [conflicting reports from same author] 

Source(s): Smith et al. (1978) 

Route: i.v. 

Species: rats 

Dose/Duration: up to 175 mg/kg bw 

Observation Time: not provided 

Effects: extensive necrotizing pneumonia and lung edema at doses as low as 30 mg/kg bw 

(25 mg In/kg bw); respiratory difficulties followed by convulsions, which are 

common when relative large amounts of insoluble dust are i.v. injected at doses 

≥90 mg/kg bw 

Source(s): Smith et al. (1978) 

Route: i.v. 

Species: rabbits 

Dose/Duration: 35-68 mg/kg bw 

Observation Time: not provided 

Effects: reduced food intake; weight loss; extensive pneumonia and abnormally heavy 

lungs on necropsy 

Source(s): Smith et al. (1978) 

Results from an animal study using a single i.t. instillation dose are included because of the long-term 

retention of indium oxide in the lower respiratory tract. 

Route: i.t. 

Species: rats 

Dose/Duration: 50 mg (41.4 mg In) 

Observation Time: 8 months 

Effects: 36% mortality and depressed growth in 70% of surviving animals; granular 

dystrophy of liver and kidney cells; cloudy swelling of myocardium fibers with 

focal lymphoid-histiocyte infiltration in the stroma; large dust accumulation, 

weak fibrosis of the stroma, and hyperplasia of the lung lymphoid follicles; dust 

deposits, focal desquamative pneumonia, meso- and peribronchitis, alveolar 

membrane proliferation, and beginning fibrosis of the interstitial tissue of lungs 

Source(s): Smith et al. (1978) 

Tin Oxide

LC50/LD50 Values: oral LD50 > 20,000 mg/kg bw [mice and rats] (RTECS, 2008) 

 i.p. LD50 > 6600 mg/kg bw [mice and rats] (RTECS, 2008) 

10
Chemical Information Profile for Indium Tin Oxide 

Route: i.t. 

Species: rats 

Dose/Duration: 50 mg deposited 

Observation Time: 1 year 

Effects: dust accumulation in lungs (unaccompanied by fibrosis) 

Source(s): Monteiles (2005)

Subchronic Exposures 

Route: i.t. 

Species: Syrian golden hamsters, male 

Dose/Duration: 6.0 mg/kg (4.5 mg In/kg) 1x/wk for 16 wk 

Observation Time: not provided 

Effects: no significant difference in body weight gain compared to controls; significant 

increase in relative lung weight (2.6 times) compared to controls; slight to 

moderate inflammatory lesions in lungs—slight cholesterol cleft and fibrotic 

proliferation; mild inflammatory cell infiltration, thickening of alveolar wall and 

pleura, and alveolar cell hyperplasia; and moderate exudation and accumulation 

of alveolar macrophages with expanded cytoplasm with or without ITO particles, 

necrotic cell debris, and few neutrophils within alveolar septae, alveolar spaces, 

or bronchiolar lumens 

Notes: ITO particles, purity >99.99%, contained 74.4% (wt%) indium and 7.8% tin. 

Mean count diameter of the particles was 0.95 μm. 

Source(s): Tanaka et al. (2002)

Indium Oxide

Route: oral 

Species: rats 

Dose/Duration: 8% indium oxide (6.6% In) in diet for 3 months 

Observation Time: not provided 

Effects: increased weight and food consumption; no histological changes or clinical signs 

of toxicity attributable to indium oxide 

Source(s): Smith et al. (1978) 

Route: inhalation (submicron-sized particles in a chamber) 

Species: rats 

Dose/Duration: 64 mg/m3

 for 4 hour/day for 3 months 

Observation Time: 24 weeks post-exposure 

Effects: significant growth depression in males (especially in month 1, averaged 90 g 

below weight of the controls); increased lung weight; pulmonary inflammatory 

reactions (alveolar phagocytes or alveolar epithelial cells on membrane walls); 

enlarged tracheobronchial lymph nodes; 2- to 3-fold increase in absolute 

neutrophil count in blood 

Source(s): Smith et al. (1978) 

Route: inhalation 

Species: rats 

Dose/Duration: 24-97 mg/m3

 for 224 hours 

Observation Time: up to 12 weeks post-exposure 

Effects: widespread alveolar edema; fluid was microscopically granular and contained 

few alveolar phagocytes, polymorphonuclear cells, and nuclear debris; alveolar 

walls altered with spindle-shaped and other type cells; little change in lesion 

11
Chemical Information Profile for Indium Tin Oxide 

during and after exposure; no fibrosis from healing process; concluded that effect 

on alveolar stasis resembling alveolar proteinosis in which alveolar clearance is 

reduced 

Source(s): HSDB (2002) 

Tin Oxide

Route: oral 

Species: rats 

Dose/Duration: ≤1% in diet, 7 days/week for 4 weeks 

Observation Time: not provided 

Effects: no adverse effects on body weight or to cardiovascular, hematopoietic, hepatic, 

or renal systems 

Source(s): ATSDR (1992); IPCS (2005)

Chronic Exposures 

Not available 

Synergistic/Antagonistic Effects

Not available for ITO 

Indium Oxide: Not available 

Tin Oxide: Suppressed the fibrogenic effect of silica dusts on rat lungs in vivo (Wang et al., 1994

[PMID:7946006]) 

Cytotoxicity

The responses of rat (RLE) and mouse (LA-4) epithelial cells to ITO, indium trioxide, and tin oxide 

showed insignificant toxicity, while silica at 200 μg/mL induced a significant increase in LDH activity 

after a 24-hour exposure. Both ITO and silica particles induced significant increases in mouse and rat 

peritoneal macrophages at 50 and 100 μg/mL. Significant increases in LDH were induced in rat 

alveolar macrophages by ITO and all of the other test articles except tin oxide. The response to ITO 

was dose-dependent and similar in intensity to that induced by silica (Laloy et al., 2007; Lison et al., 

2009 [PMID:19176593]). 

Indium Oxide: See above. 

Tin Oxide: Weak to no toxic effects in rabbit alveolar macrophages in vitro and in vivo (Labedzka et 

al., 1989 [PMID:2538328]; Wang, 1988); not cytotoxic in 3T3 fibroblasts (Rushe et al., 2005 

[PMID:15744616]). See also ITO discussion above. 

Reproductive and Developmental Toxicity 

Human Studies: Not available for ITO 

Animal Studies: In male Syrian golden hamsters i.t. instilled with ITO (6.0 mg/kg bw 1x/wk for 16 

wk), body weight, testis, epididymis, and seminal vesicle weights, and caudal sperm count were 

comparable to those of controls. Two of 10 animals had a slight increase in the number of 

seminiferous tubules displaying disorganization or vacuolization; a significant increase in incidence 

of tubules with vacuolization was observed in the epithelium (14.6% versus 7.2% for controls) 

(Omura et al, 2002). [Note: Water-soluble indium trichloride has been reported to induce 

developmental abnormalities in rats via oral or i.v. exposure (e.g., Nakajima et al., 2007 

[PMID:17646080]; Ungváry et al., 2001 [PMID:11261900]). However, indium concentrations 

measured in serum of ITO workers (e.g., Homma et al., 2003) were much lower than those expected 

in rats given one-time doses of indium trichloride. See Structure-Activity Relationships below.] 

Indium Oxide: Not available 

Tin Oxide: Not available 

Carcinogenicity 

Not available 

Anticarcinogenicity 

Not available 

12
Chemical Information Profile for Indium Tin Oxide 

Genetic Toxicity 

ITO increased micronuclei frequency in type II pneumocytes recovered from rats 3 days after a second 

administration of 2 mg (inflammatory dose) but not in RLE cells in vitro treated with 50-200 μg/mL. 

Suggests genotoxic response is related to reactive oxygen species products from inflammatory cells 

(Lison et al., 2009 [PMID:19176593]) 

Indium Oxide: Not available 

Tin Oxide: Negative in the Rec assay with Bacillus subtilis (ATSDR, 1992) 

Neurotoxicity 

Not available 

Immunotoxicity 

Not available for ITO 

Indium Oxide: Not available 

Tin Oxide: Weak to no toxic effects in rabbit alveolar macrophages in vitro and in vivo (Labedzka et 

al., 1989 [PMID:2538328]; Wang, 1988) 

E. Mechanistic Data 

Target Organs/Tissues 

Human: Lungs, liver, and spleen (Homma et al., 2003, 2005) 

Animal: Lungs [hamsters] (Tanaka et al., 2002) 

Endocrine Modulation 

Not available 

Effect on Enzymes 

Not available 

Modes of Action 

Not available 

Structure-Activity Relationships 

The results from ADME studies of indium trichloride administered by various routes (i.v., i.p., i.t., and 

oral) and toxicological data reported from studies in laboratory animals are given below. Most of the 

data were from studies of embryotoxic and teratogenic effects. 

Indium Trichloride [CAS No. 10025-82-8; PubChem CID:24812 (undated)] is used in electroplating 

and its radioisotopes are used in the treatment of tumors and in organ scanning. 

ADME: After i.v. administered, indium trichloride was mainly excreted in the urine; when given 

i.p., it accumulated in the liver, passed into the small intestine, then was excreted in the feces 

(HSDB, 2005b). Oral exposure of male Swiss mice to indium trichloride (≤ 250 mg/kg) did not 

affect the liver but urinary N-acetyl glucosaminidase in the kidney decreased (Chapin et al., 1995 

[PMID:7589924]). In patients treated i.v. with 111indium chloride 24 or 48 hours before 

orchidectomy, uptake into the testes was observed. The radionuclide also was found in the 

seminiferous tubules (Nettleton et al., 2004). The biological half-life of 114indium trichloride in 

mice treated by i.v. injection was 1.9 days during the fast phase of removal and 69 days for the slow 

phase (HSDB, 2005b). In rats administered 114indium trichloride by i.p. injection on four 

consecutive days then sacrificed one hour after the last injection, indium accumulated primarily in 

the liver, spleen, and kidney. The highest concentrations were reported in the cytosolic fraction 

followed by the mitochondria from tissue homogenates. Indium observed in the serum accounted 

for 90% of the total activity in whole blood and it was exclusively bound to transferrin (Van Hulle et 

al., 2001 [PMID:11253025]). 

Toxicity: Mouse i.p. LD50: 9500 μg/kg bw; rat i.p. and i.v. LD50 values: 2370 and 4460 μg/kg bw, 

respectively. A single i.v. injection caused severe necrosis of the renal proximal tubules in both 

mice and rats, while a single i.p. injection induced an increase in smooth endoplasmic reticulum in 

the tubule cells (HSDB, 2005b). Intratracheal administration of indium trichloride caused severe 

13
Chemical Information Profile for Indium Tin Oxide 

lung damage and fibrosis in rats, while inhalation caused inflammatory changes in rat lungs (Blazka 

et al., 1994a [PMID:8005375], 1994b [PMID:7925195]). 

Reproductive/Developmental Toxicity: Oral exposure of male Swiss mice to indium trichloride (≤

250 mg/kg) did not affect the reproductive system. In female mice, no changes were observed in the 

ability to become pregnant, but fetal development was affected (i.e., increase in intrauterine deaths) 

(Chapin et al., 1995 [PMID:7589924]). A significant increase in fetal mortality and malformations 

(mainly in the tail and rib) were reported in Wistar rats given indium chloride (300 mg/kg) by i.v. 

injection (0.4 mg In/kg) on day 9 of pregnancy (fetuses were examined on day 20). Results from 

orally treated rats also were higher compared to controls but they were not statistically significant 

(Nakajima et al., 1998 abstr., 1998 [PMID:9876012]). In a separate experiment in which indium 

trichloride was administered i.v. on gestation day 10, caudal hypoplasia (e.g., apoptosis in tailbud) 

was observed in embryos on day 11. Similar results also were reported for 10 day old rat embryos 

treated in vitro (Nakajima et al., 2008 [PMID:18547785]). Bone and cartilage malformations were 

observed in 21 day old fetuses from Sprague-Dawley rats given a single i.v. injection of indium 

trichloride on gestation day 10 (Nakajima et al., 2007 [PMID:17646080]). In a comparative species 

study, mice and rats were observed to be susceptible to the embryotoxicity of indium at similar 

developmental stages but mice were less susceptible to the teratogenicity of indium based on gross 

malformation (Nakajima et al., 2000 [PMID:10910472]). The embryotoxic and teratogenic effects 

of indium trichloride also have been observed in rabbits (Ungváry et al., 2000 [PMID:10681097]). 

Other Biological Effects: Daily oral administration of indium trichloride to Sprague-Dawley rats 

(200 mg/kg) on gestation days 6-15 produced hemodynamic effects. The cardiac index was 

increased, while cardiac output to kidneys, ovaries, uterus, and placenta was decreased (brain, lungs, 

and liver unaffected). Furthermore, the placenta had decreased blood flow and increased vascular 

resistance. The results, in combination with maternal survival over fetal mortality in the presence of 

noradrenaline, indicated the hemodynamic changes to be harmful to the fetus (Morvai et al., 2001 

[PMID:11261901]). Dose dependent apoptosis and necrosis also were induced in rat thymocytes 

(Bustamante et al., 1997 [PMID:9129167]). In hamsters, it inhibited erythrocyte δ-aminolevulinic 

acid dehydratase (ALAD) activity. No significant changes occurred in hepatic ALAD activity, but 

renal ALAD was statistically decreased (Conner et al., 1995 [PMID:7538452]). 

Brief summaries of the toxicological data for two other indium compounds, indium phosphide and 

indium arsenide, both of which are pulmonary and testicular toxicants, are given below. Physical and 

chemical characteristics contributing to different toxicity (potency) of various indium compounds are 

not well understood. 

Indium Phosphide (InP) [CAS No. 22398-80-7; PubChem CID:31170 (PubChem, undated)] is used 

in the semiconductor industry. Absorption from the gastrointestinal tract was minimal following 

oral treatment of mice and rats. At 5000 mg/kg i.p. or oral, indium was detected primarily in the 

liver and lungs of mice. In oral studies of InP in rats, most was excreted in the feces; urinary 

elimination half-time was ~321 hours. Following i.t. instillation of InP, indium was mostly found in 

the lungs (HSDB, 2005c). InP given to male and female B6C3F1 mice and F344/N rats via 

inhalation for three weeks produced gray to black discoloration and enlargement of the lungs; 

inflammatory and proliferative lesions in the lungs consisting of alveolar proteinosis, chronic 

inflammation, interstitial fibrosis, and alveolar epithelial hyperplasia; inflammation of the larynx; 

hyperplasia of the bronchial and mediastinal lymph nodes; and microcytic erythrocytosis in both 

species. InP particles were observed throughout the respiratory tract and in lymph nodes. The 

retained lung burdens of indium were proportional to exposure dose and duration, and elimination 

was slow. In a two-year inhalation study in mice and rats, InP was carcinogenic. An increase in the 

incidence of benign and malignant neoplasms of the lungs was seen in both sexes of both species. 

An increased incidence of liver neoplasms was also seen in male and female mice, while marginal 

increases in the incidences of small intestine neoplasms were seen in males only. In rats, an 

increased incidence of pheochromocytomas of the adrenal gland was also reported in males and 

14
Chemical Information Profile for Indium Tin Oxide 

females; marginal increases were seen in the incidences of mononuclear cell leukemia in males and 

females, fibroma of the skin in males, and carcinoma of the mammary gland in females. InP was 

negative in the micronucleus test using murine erythrocytes (NTP, 2001). It was a testicular 

toxicant in hamsters; it decreased reproductive organ weight and caudal sperm count and induced 

severe histopathologic changes in the testes (Omura et al., 2000). It also induced slight to severe 

inflammatory lesions in the lungs (e.g., diffuse alveolar cell hyperplasia) of hamsters; effects were 

more severe compared to animals given ITO [see above] (Tanaka et al., 2002). 

Indium Arsenide (InAs) [CAS No. 1303-11-3; PubChem CID:91500 (PubChem, undated)] is also 

used in the semiconductor industry. The oral LD50 is >15,000 mg/kg in mice (HSDB, 2002). The 

subcutaneous LD50 is 32,500 mg/kg in mice (ChemIDplus, undated). In hamsters, i.t. instillation of 

>99.9999% pure InAs, mean particle diameter 1.58 μm, produced proteinosis-like lesions or 

localized hyperplastic lesions (e.g., alveolar/bronchiolar cell hyperplasia with squamous cell 

metaplasia or squamous cell hyperplasia with keratinization), squamous cyst, inflammation, and 

interstitial fibrosis in the lungs (Tanaka et al., 2003). Like InP, InAs is a testicular toxicant but 

induces greater damage than InP (Omura et al., 2000). 

Isomers: Not available 

Congeners: Not available 

Reactive Moieties: Indium oxide [See toxicity data above.] 

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Umicore. 2005. Technical data: Indium tin oxide (ITO) sputtering target. Internet address: 

http://www.thinfilmproducts.umicore.com/pdf/indium_tin_oxide_ITO.pdf. Last accessed on August 19, 2008. 

Ungváry, G., Szakmáry, E., Tátrai, E., Hudák, A., Náray, M., and Morvai, V. 2000. Embryotoxic and teratogenic 

effects of indium chloride in rats and rabbits. J Toxicol Environ Health A, 59(1):27-42. Abstract from PubMed 

10681097. PubMed abstract Internet address: 

http://www.ncbi.nlm.nih.gov/sites/entrez?orig_db=PubMed&db=pubmed&cmd=Search&TransSchema=title&term=

10681097. Last accessed on May 26, 2009. 

Ungváry, G., Tátrai, E., Szakmáry, E., and Náray, M. 2001. The effect of prenatal indium chloride exposure on 

chondrogenic ossification. J Toxicol Environ Health A, 62(5):387-396. Abstract from PubMed 11261900. PubMed 

abstract Internet address: 

http://www.ncbi.nlm.nih.gov/sites/entrez?orig_db=PubMed&db=pubmed&cmd=Search&TransSchema=title&term=

11261900. Last accessed on May 8, 2009. 

Van Hulle, M., De Cremer, K., Cornelis, R., and Lameire, N. 2001. In vivo distribution and speciation of 

[114mIn]InCl3 in the Wistar rat. J Environ Monit, 3(1):86-90. Abstract from PubMed 11253025. PubMed abstract 

Internet address: 

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11253025. Last accessed on May 26, 2009.

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macrophages in vitro and in vivo (Chinese). Zhongua Laodong Weisheng Zhiyebing Zazhi, 6(5):277-280. Abstract 

from CAPLUS 1990:71928. 

Wang, F.S., Liu, L.F., Chen, N.M., and Li, Y.R. 1994. A study on cellular reactions and fibrogenic effects of 

mineral dusts. Biomed Environ Sci, 7(2):116-121. Abstract from PubMed 7946006. PubMed abstract Internet 

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Chemical Information Profile for Indium Tin Oxide 

address: 

http://www.ncbi.nlm.nih.gov/sites/entrez?orig_db=PubMed&db=pubmed&cmd=Search&TransSchema=title&term=

7946006. Last accessed on May 8, 2009. 

Xu, H., Zhu, G., and Zhou, H. 2005. Preparation of monodispersed Tin-Doped Indium Oxide Powders by 

Hydrotermal Method. J. Am. Ceram. Soc. 88(4):986-988. Cited by Psuja et al. (2009). 

Zhang, J., Au, K.H., and Chang, S.Y. 2004. Investigation of sol-gel derived indium tin oxide thin films with 

poly(ethylene glycol) as an additive. J Ceram Proc Res, 5(3):208-213. Internet address: http://jcpr.kbslab.co.kr/english/journal/JCPR/vol5num3/208-213.pdf. Last accessed on August 4, 2008. 

Zhou, J. 2005 thesis. Indium tin oxide (ITO) deposition, patterning, and Schottky contact fabrication. Department of 

Microelectronic Engineering, Rochester Institute of Technology, Rochester, NY, 89 pp. Internet address: 

http://www.rit.edu/kgcoe/ue/thesisguidelinespages/2006_Jianming_Zhou.pdf. Last accessed on August 4, 2008. 

Acknowledgements

Support to the National Toxicology Program for the preparation of Chemical Information Profile for 

Indium Tin Oxide was provided by Integrated Laboratory Systems, Inc., through NIEHS Contract Nos. 

N01-ES-35515 (2006-2008) and HHSN273200800008C (2009). Contributors included: Scott A. 

Masten, Ph.D. (Project Officer, NIEHS); Marcus A. Jackson, B.A. (Principal Investigator, ILS, Inc.); 

Bonnie L. Carson, M.S. (ILS, Inc.); Claudine A. Gregorio, M.A. (ILS, Inc.); Nathanael P. Kibler, B.A. 

(ILS, Inc.); and Sherry D. Blue, A.A. (ILS, Inc.). 

Search Strategy

On May 8, 2006, the Registry file on STN International was searched. In the file, 198 indium tin oxides 

with different ratios of the constituent elements were registered. Most of these, including the one 

registered as 71243-84-0, had only one record in Chemical Abstracts and no records in other STN 

databases except MEDLINE. That number was used erroneously instead of 50926-11-9 in the 51st Report 

of the Toxic Substances Control Act (TSCA) Interagency Testing Committee (ITC) and carried over into 

the ensuing U.S. EPA rule promulgated in 2001 (the only citation for 71243-84-0 in CAPLUS). The 

TSCA ITC had used the correct CAS number in the 47th Report and published a correction in the 52nd

Report in 2003. Various trade names in the Registry record for 50926-11-9 were not confirmed in 

Internet searches via the Google search engine and were omitted from the search strategy. 

Files MEDLINE, AGRICOLA, CABA, EMBASE, ESBIOBASE, BIOTECHNO, IPA, BIOSIS, and 

TOXCENTER were searched simultaneously on May 9, 2006, for indium tin oxide (ITO). [Note that 

CANCERLIT and NIOSHTIC, files once routinely included in searches, are no longer available on STN]. 

Reviews were sought for components indium sesquioxide and stannic oxide. [Reviews for the latter 

compounds were retrieved from HSDB and by searches at http://ww.inchem.org, which includes 

documents published by the World Health Organization, and searches at the Agency for Toxic Substances 

and Disease Registry (ATSDR) website (http://www.atsdr.cdc.gov/toxpro2.html) for toxicology profiles.] 

The 708 titles from the ITO answer set L20 were examined, but only 57 records were selected to be 

printed in full. These were retrieved in the following groups: health-related (6), substrate for biological 

studies (23), other uses (19), processing (7), and not immediately classifiable (2). Records on the 

common applications listed in the trade literature were usually not retrieved. The applications records 

that were retrieved were examined for the potential of human exposure (e.g., implants) and possible 

contact of ITO with cultured cells and tissues and with DNA, enzymes, and other proteins. 

In 2006, production information was sought at the U.S. EPA Inventory Update Rule (IUR) site and at the 

U.S. Geological Survey website (http://www.usgs.gov). Google and the Google Scholar search engines 

were used to clarify the use of indium tin oxide (or tin-doped indium oxide) for a number of applications 

22
Chemical Information Profile for Indium Tin Oxide 

including cell culture, water treatment, biochips/microfluidics, and glucose monitors/sensors and other 

biosensors after examination of the STN results. 

Searches for combinations of three atoms from the same elemental groups as indium (aluminum, gallium, 

thallium); tin (silicon and germanium but not lead); and oxygen (sulfur, selenium, and tellurium) did not 

find structural analogs of interest. Internet searches for other elements with "tin oxide" or "doped indium 

sesquioxide" (or oxide) (Google search, Google Scholar, and PubMed) were more fruitful. Compounds 

of possible interest as structural analogs found by the latter approach were antimony tin oxide (Sb is a 

Group V element, not Group III) and indium sesquioxide doped with silicon, germanium, gallium, and 

cadmium. (Other elements used for doping indium sesquioxide include Cr, Er, F, Au, Ir, Li, Mn, Mo 

[most Google hits], Ag, Ti, and Zn.). Other tin-doped oxides [("tin doped" AND oxide) NOT indium] of 

some interest would be titania, silica, cadmium oxide, and zinc oxide. No toxicity studies were found for 

any of these in PubMed. 

The history of the May 9, 2006, STN International session is reproduced below. 

L1 34 S 71243-84-0 

 SET DUPORDER FILE 

L2 31 DUP REM L1 (3 DUPLICATES REMOVED) 

L3 295 S 50926-11-9 

L4 286 DUP REM L3 (9 DUPLICATES REMOVED) 

L5 950 S INDIUM(W)(TIN OR STANNIC)(W)OXIDE 

L6 14 S F(W)ITO 

L7 7 DUP REM L6 (7 DUPLICATES REMOVED) 

L8 7 S L7 NOT FLUORINE 

L9 7 S L8 NOT L4 

L10 7 SORT L7 1-7 TI 

L11 1020 S L3 OR L5 

L12 33 S TIN(W)DOPED(W)INDIUM(W)(OXIDE OR TRIOXIDE OR SESQUIOXIDE) 

L13 5 S TIN(W)INDIUM(W)OXIDE 

L14 38 S L12 OR L13 

L15 78 S IN2O3(4A)SNO2 

L16 32 S L14 NOT L11 

L17 69 S L15 NOT L11 

L18 1121 S L11 OR L14 OR L15 

L19 708 DUP REM L18 (413 DUPLICATES REMOVED) 

L20 708 SORT L19 1-708 TI 

 SAVE L20 X0370BIOMED/A 

L21 4649 S (STANNIC OR TIN)(W)OXIDE OR 18282-10-5 

L22 3 S STANNIC(W)(ANHYDRIDE OR DIOXIDE) 

L23 84 S TIN(W)(IV)(W)OXIDE 

L24 814 S TIN(W)(PEROXIDE OR DIOXIDE) 

L25 4773 S L21 OR L22 OR L23 OR L24 

L26 3762 S L25 NOT L18 

L27 2 S L26 AND REVIEW/DT 

L28 0 S METAL(6A)OXIDE? AND REVIEW/DT AND (TIN OR STANNIC OR INDIUM) 

L29 19 S OXIDE? AND REVIEW/DT AND (TIN OR STANNIC OR INDIUM) 

L30 15 DUP REM L29 (4 DUPLICATES REMOVED) 

L31 15 SORT L30 1-15 TI 

L32 615 S INDIUM(W)(OXIDE OR TRIOXIDE OR SESQUIOXIDE) 

L33 477 S 1312-43-2 

L34 661 S L32 OR L33 

L35 414 S L34 NOT (L18 OR L25) 

L36 1 S L35 AND REVIEW/DT 

L37 57 S (L26 OR L35)AND REVIEW? 

L38 56 S L37 NOT REVIEW/DT 

L39 48 DUP REM L38 (8 DUPLICATES REMOVED) 

L40 16 S L39 AND (2000-2006)/PY 

L41 16 DUP REM L40 (0 DUPLICATES REMOVED) 

L42 16 SORT L41 1-16 TI 

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Chemical Information Profile for Indium Tin Oxide 

L43 32 S L39 NOT L40 

L44 32 SORT L43 1-32 TI 

2008 Update: The same search strategy for ITO was repeated on STN International in a simultaneous 

search of the above-named files plus FSTA, FROSTI, PASCAL, and NTIS on July 8, 2008, with 

publications limited to 2006-2008. The titles of 425 database records were examined. Publications for 

indium oxide, tin oxide, or both plus the word doping or doped in this time period were limited to those 

that were reviews or those that contained "?toxic?," "inhal?," "pneumo?," "pulmonary," or "lung OR 

lungs." These limitations resulted in 53 records after duplicate removal. Examination of the titles 

indicated that most of the retrievals discussed information already covered in the dossier. Only 45 

records were selected for printing (MEDLINE, 25; EMBASE, 4; TOXCENTER, 13; PASCAL, 1; and 

BIOSIS, 2). The printed records contained eight pairs of duplicates. Another 17 were removed from 

further consideration, often because they were about uses already covered in the dossier (a complete list 

of reasons for removal is available). The final selections of 20 new records (MEDLINE, 11; 

TOXCENTER, 7; EMBASE, 2) included four on lung disease in ITO workers, three on lung disease in 

tin workers, seven on processing and exposure potential, and six on uses with exposure potential. 

In July 2008, additional Internet searches were done using Google and Google Scholar to find references 

to help clarify the discussion on ITO technology and to find particle sizes available in commercial ITO 

products. While searching for "indium tin oxide" AND "inhalation OR lungs OR pulmonary," a 2007 

TSCA test submission that is not in the TSCATS database was found: Laloy et al. (2007). Subsequent 

check of TSCATS found no other TSCA test submissions. In August, searches regarding regulations 

pertinent to ITO in the United States, European Union, and Canada were conducted using various Internet 

sites, including Regulations.gov, GPO Access, Health Canada's The Substances List, and OECD's 

eChemPortal. 

2009 Update: STN International database files MEDLINE, AGRICOLA, CABA, IPA, 

BIOSIS, TOXCENTER, FSTA, FROSTI, EMBASE, ESBIOBASE, BIOTECHNO, and NTIS were 

searched simultaneously on April 14, 2009, updating earlier searches. 

L1 0 S 71243-84-8 

L2 717 S 71243-84-0 OR 50926-11-9 

L3 2000 S INDIUM(W)(TIN OR STANNIC)(W)OXIDE 

L4 78 S TIN(W)DOPED(W)INDIUM(W)(OXIDE OR TRIOXIDE OR SESQUIOXIDE) 

L5 0 S IN203(4A)SNO2 

L6 2202 S L2 OR L3 OR L4 

 SET DUPORDER FILE 

L7 454 S L6 AND (2008-2009)/PY 

L8 338 DUP REM L7 (116 DUPLICATES REMOVED) 

L9 338 SORT L8 1-338 TI 

 SAVE L9 X3702009UP/A 

L10 6437 S (STANNIC OR TIN)(W)(OXIDE OR DIOXIDE) 

L11 112 S TIN(W)IV(W)(OXIDE OR DIOXIDE) 

L12 1 S TIN(W)PEROXIDE 

L13 6494 S L10 OR L11 OR L12 

L14 12 S L13 AND REVIEW/DT 

L15 101 S OXIDE? AND REVIEW/DT AND (TIN OR STANNIC OR INDIUM) 

L16 969 S INDIUM(W)(OXIDE OR TRIOXIDE OR SESQUIOXIDE) OR 1312-43-2 

L17 101 S (L15 OR L16) AND REVIEW/DT 

L18 1 S 18282-10-5 AND REVIEW/DT 

L19 12 S L14 OR L18 

L20 1124 S INDIUM(W)(CHLORIDE OR TRICHLORIDE) OR 10025-82-8 

L21 16 S L20 AND REVIEW/DT 

L22 116 S L17 OR L19 OR L21 

L23 106 DUP REM L22 (10 DUPLICATES REMOVED) 

L24 105 S L23 NOT L8 

L25 105 SORT L24 1-105 TI 

 SAVE L25 X370OTHER09/A 

24
Chemical Information Profile for Indium Tin Oxide 

Appendix 1. Life Science Applications 

Indium tin oxide applications in environmental and life sciences found in the patent and experimental 

literature include the following: 

• Component of sensors to detect inorganic or organic chemicals in media such as atmospheric 

emissions, breath, and food (e.g., Lewis, 2000 pat.). 

• Photocatalyst component for degrading water pollutants and disinfecting water (e.g., Eggins et 

al., 1999) and a conductive paint electrode to electrochemically inactivate marine bacteria (Lim et 

al., 2003 [PMID:12474252]). 

• ITO microelectrode arrays in molecular biosensors with immobilized proteins (e.g., membrane 

proteins, antibodies, enzymes), nucleic acids/nucleotides, and even networks of excitable cells 

and microorganisms (e.g., Pancrazio et al., 1999 [PMID:10625143]; Tang et al., 2006 

[PMID:16448043]). In similar applications, ITO films were used as heaters for DNA PCR in a 

micro total analytical system that included pumps and valves (Fukuba et al., 2003) and ITO 

microelectrodes were used in biosensors for DNA hybridization (e.g., Armistead and Thorp, 2000 

[PMID:10959961]). ITO has been studied in the development of glucose biosensors, which may 

be miniaturized and implantable (e.g., Beach et al., 2005). 

• Numerous studies of cultured cells and tissues on ITO-coated glass or ITO electrodes as cellculture platforms (CCPs) take advantage of the transparency of ITO, its lack of adverse effects, 

and better cell adhesion and growth than achieved on conventional cell culture plastic (e.g., 

Tomai et al., 2000 [PMID:11065276]). Systems in which electrical field stimulation is 

accompanied by optically monitoring a physiological response are amenable to high-throughput 

screening (Burnett et al., 2004 pat.). ITO microelectrode arrays in which murine spinal cord 

tissue was grown were used to trigger tissue network responses for up to eight months in warm 

saline before electrode breakdown via oxidation and loss of light transmittance (Gross et al., 1993 

[PMID:8107494]). 

• ITO conductive growth surfaces were used to permit introduction of nonpermeant molecules 

(e.g., antibodies and genes) into adherent mammalian cells by electroporation (e.g., Raptis and 

Firth, 1990 [PMID:2271121]; Yamauchi et al., 2005 [PMID:16114943]). 

• Patterns of ITO microelectrodes are used in digital droplet-based microfluidics biochips to induce 

surface tension imbalances that move nanoliter volumes of liquid droplets along the line of 

electrodes. Such microsystems are called lab-on-a-chip and bio-MEMs (microfluidic 

electromechanical devices), which automate highly repetitive laboratory tasks involving microand nanoscale amounts of fluids. Such biochips (which may use other methods to move the 

fluids) are being manufactured for commercial use (Chakrabarty and Su, 2005). 

• Possible uses that would involve direct human exposure include implanted or worn biosensors, 

bio-MEMs (perhaps for drug delivery), and other biomedical devices with ITO microelectrodes. 

For example, ITO incorporation in contact lenses might allow for monitoring glucose or oxygen 

in tears (Mitsubayashi et al., 2001). In biocompatibility studies for materials to be chronically 

implanted as microelectrodes, ITO showed the least protein adsorption, a requirement for 

"electrode recording sites." Such electrodes might be useful for neural stimulation of movement 

for paralyzed individuals or for amputee prosthetics (Selvakumaran et al., 2002). 

References 

Armistead, P.M., and Thorp, H.H. 2000. Modification of indium tin oxide electrodes with nucleic acids: detection of 

attomole quantities of immobilized DNA by electrocatalysis. Anal Chem, 72(16):3764-3670. Abstract from PubMed 

10959961. PubMed abstract Internet address: 

http://www.ncbi.nlm.nih.gov/sites/entrez?orig_db=PubMed&db=pubmed&cmd=Search&TransSchema=title&term=

10959961. Last accessed on May 4, 2009. 

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Chemical Information Profile for Indium Tin Oxide 

Beach, R.D., Conlan, R.W. Godwin, M.C., and Moussy, F. 2005. Towards a miniature implantable in vivo telemetry 

monitoring system dynamically configurable as a potentiostat or galvanostat for two- and three-electrode biosensors. 

Instrumentation and Measurement, IEEE Transactions 54(1):61-72. Abstract at Internet address: 

http://ieeexplore.ieee.org/xpl/absprintf.jsp?arnumber=1381799&page=FREE. Last accessed on June 1, 2006. 

Burnett, P., Robertson, J.K., and Zivin, R.A. [assignee: Standard Mems, Inc.]. 2004 pat. Electrophysiology assay 

methods. World Patent number WO 2004012585. February 12, 2004. PCT Int Appl, 52 pp. Abstract from 

TOXCENTER 2004:41480 (also CAPLUS 2004:120658). 

Chakrabarty, K., and Su, F. 2005. Design automation challenges for microfluidics-based biochips. Paper presented 

at the Symposium on Design, Test, Integration and Packaging [DTIP] of MEMS/MOEMS at Montreux, 

Switzerland, June 1-3, 2005. TIMA Labs/DTIP. TIMA Laboratory [Techniques of Informatics and Microelectronics 

for Computer Architecture], Grenoble, France. Internet address: http://www.ee.duke.edu/~krish/cr1113.pdf. Last 

accessed on June 1, 2006. 

Eggins, B.R., Byrne, J.A., Dunlop, P.S.M., and Davidson, A. 1999. TiO2 particulate films on indium tin oxide 

coated glass and their use for water treatment. Topical Issues Glass, 3(Photons, Glasses and Coatings):57-62. 

Abstract from TOXCENTER 2000:154108 (also CAPLUS 2000:370741). 

Fukuba, T., Naganuma, T., and Fujii, T. 2003. Microfabricated flow-through PCR device for in situ gene analysis in 

extreme environments. In: Proceedings of the 7th International Conference on Miniaturized Chemical and 

Biochemical Analysis Systems, Squaw Valley, California, October 5-9, 2003, pp. 725-728. Internet address: 

http://www.chem.ualberta.ca/~microtas/Volume1/180-220.pdf. Last accessed on June 1, 2006. 

Gross, G.W., Rhoades, B.K., Reust, D.L., and Schwalm, F.U. 1993. Stimulation of monolayer networks in culture 

through thin-film indium-tin oxide recording electrodes. J Neurosci Methods, 50(2):131-143. Abstract from PubMed 

8107494. PubMed abstract Internet address: 

http://www.ncbi.nlm.nih.gov/sites/entrez?orig_db=PubMed&db=pubmed&cmd=Search&TransSchema=title&term=

8107494. Last accessed on May 4, 2009. 

Lewis, N.S. [assignee: California Institute of Technology]. 2000 pat. Method and device to analyze components of 

fluids in clinical, environmental, and food samples using sensors with conductive elements and chemically sensitive 

resistors. World Patent number WO 20000026638. May 11, 2000. PCT Int Appl, 70 pp. Abstract from 

TOXCENTER 2000:147256 (also from CAPLUS 2000:314908). 

Lim, T.-K., Murakami, T., Tsuboi, M., Yamashita, K., and Matsunaga, T. 2003. Preparation of a colored conductive 

paint electrode for electrochemical inactivation of marine bacteria. Biotechnol Bioeng, 81(3):299-304. Abstract from 

PubMed 12474252. PubMed abstract Internet address: 

http://www.ncbi.nlm.nih.gov/sites/entrez?orig_db=PubMed&db=pubmed&cmd=Search&TransSchema=title&term=

12474252. Last accessed on May 4, 2009. 

Mitsubayashi, , K., Tatsuro, E., Satoshi, S., and Karube, I. 2001. Optical-transparent oxygen sensor with a thinner 

membrane structure. Anal Sci, 17(Supplement):i773-i776. Internet address: 

http://wwwsoc.nii.ac.jp/jsac/analsci/ICAS2001/pdfs/0700/0773_4h08n.pdf. Last accessed on June 1, 2006. 

Pancrazio, J.J., Whelan, J.P., Borkholder, D.A., Ma, W., and Stenger, D.A. 1999. Development and application of 

cell-based biosensors. Ann Biomed Eng, 27(6):697-711. Abstract from Pubmed 10625143. PubMed abstract Internet 

address: 

http://www.ncbi.nlm.nih.gov/sites/entrez?orig_db=PubMed&db=pubmed&cmd=Search&TransSchema=title&term=

10625143. Last accessed on May 4, 2009. 

Raptis, L., and Firth, K.L. 1990. Electroporation of adherent cells in situ. DNA Cell Biol, 9(8):615-621. Abstract 

from PubMed 2271121. PubMed abstract Internet address: 

http://www.ncbi.nlm.nih.gov/sites/entrez?orig_db=PubMed&db=pubmed&cmd=Search&TransSchema=title&term=

2271121. Last accessed on May 4, 2009. 

Selvakumaran, J., Hughes, M.P., Keddie, J.L., and Ewins, D.J. 2002. Assessing biocompatibility of materials for 

implantable microelectrodes using cytotoxicity and protein adsorption studies. Microtechnologies in Medicine and 

Biology, 2nd Annual International IEEE-EMB Special Topics Conference, Madison, WI, May 2-4, 2002, pp. 261-

264. Abstract at Internet address: http://ieeexplore.ieee.org/xpl/absprintf.jsp?arnumber=1002326&page=FREE. Last 

accessed on June 1, 2006. 

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Chemical Information Profile for Indium Tin Oxide 

Tang, C.S., Dusseiller, M., Makohliso, S., Heuschkel, M., Sharma, S., Keller, B., and Voros, J. 2006. Dynamic, 

electronically switchablesurfaces for membrant protein microarrays. Anal Chem, 78(3):711-717. Abstract from 

PubMed 16448043. PubMed abstract Internet address: 

http://www.ncbi.nlm.nih.gov/sites/entrez?orig_db=PubMed&db=pubmed&cmd=Search&TransSchema=title&term=

16448043. Last accessed on May 4, 2009. 

Tomai, E., Klein, S., Firth, K., and Raptis, L. 2000. Growth on indium-tin-oxide-coated glass enhances 32Pphosphate uptake and protein labelling of adherent cells. Prep Biochem Biotechnol, 30(4):313-320. Abstract from 

PubMed 11065276. PubMed abstract Internet address: 

http://www.ncbi.nlm.nih.gov/sites/entrez?orig_db=PubMed&db=pubmed&cmd=Search&TransSchema=title&term=

11065276. Last accessed on May 4, 2009. 

Yamauchi, F., Kato, K., and Iwata, H. 2005. Layer-by-layer assembly of poly(ethyleneimine) and plasmid DNA 

onto transparent indium-tin oxide electrodes for temporally and spatially specific gene transfer. Langmuir, 

21(18):8360-8367. Abstract from PubMed 16114943. PubMed abstract Internet address: 

http://www.ncbi.nlm.nih.gov/sites/entrez?orig_db=PubMed&db=pubmed&cmd=Search&TransSchema=title&term=

16114943. Last accessed on May 4, 2009. 

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Chemical Information Profile for Indium Tin Oxide 

28

Appendix 2. History of U.S. EPA and ITC Actions on Indium Tin Oxide 

CAS No. 050926119 

Chemical Indium tin oxide 

Category Indium Chemicals 

Action Recommended Report 47 Date 11/30/2000 

 Notice 66FR17767 FR Date 04/03/2001 

Rationale In view of the fact that indium phosphide causes tumors in rats and mice and 

that indium chemicals are increasingly used in the semiconductor and other 

industries, existing exposure limits may be inadequate to protect workers. 

[Indium chemicals were added to the Priority Testing List.] (ITC Reports

[select Chemicals and enter CAS No.]) 

PAIR (Preliminary Assessment Information Reporting) rule: 7/26/01 66FR38955

HaSDR (Health and Safety Data Reporting) rule: 5/4/04 69FR24517

Action: Removed from Priority Testing List in Report 58 7/11/06 71FR39188