| GHS classification | This chemical does not meet GHS hazard criteria for 57.8% (1112 of 1924) of all reports.DangerH302 (24%): Harmful if swallowed [Warning Acute toxicity, oral]P203, P261, P264, P264+P265, P270, P272, P280, P301+P317, P302+P352, P305+P351+P338, P318, P321, P330, P333+P317, P337+P317, P362+P364, P405, and P501 (click each P-code to see the statement)Aggregated GHS information provided per 1924 reports by companies from 27 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies. |
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| Regulatory information | Chemical: Chromium(III) oxide (Cr2O3)Chromium oxide (Cr2O3) is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Chromium oxide (Cr2O3) are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)Status: Active Update: 30-03-2023 https://echa.europa.eu/registration-dossier/-/registered-dossier/15477Chromium oxide (Cr2O3): Does not have an individual approval but may be used under an appropriate group standardThe New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.) |
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| Other safety information | IMAP assessments - Chromium(III) oxide (Cr2O3): Human health tier I assessment |
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| Fire hazards | Not combustible. |
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| Hazards summary | CrIII compounds do not cause chrome ulcerations but may cause allergic dermatitis in workers with prior sensitization to CrVI compounds. [ILO Encyclo] CrIII is an essential trace mineral in the human diet. [ATSDR Case Studies] An eye and respiratory tract irritant[ICSC] May cause GI irritation if ingested[MSDSonline] See Chromium. |
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| FDA requirements | Certification of this color additive when used in coloring externally applied drugs, including those intended for use in the area of the eye, in amounts consistent with good manufacturing practice, is not necessary for the protection of the public health, and therefore batches thereof are exempt from the certification pursuant to section 721(c) of the act.Certification of this color additive when used in coloring externally applied cosmetics, including cosmetics intended for use in the area of the eye, in amounts consistent with good manufacturing practice, is not necessary for the protection of the public health, and therefore batches thereof are exempt from the certification pursuant to section 721(c) of the act.Certification of this color additive, when used as a color additive in contact lenses in amounts not to exceed the minimum reasonably required to accomplish the intended coloring effect, is not necessary for the protection of the public health, and therefore batches thereof are exempt from the certification pursuant to section 721(c) of the act. |
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| RCRA requirements | D007A solid waste containing chromium may or may not become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste. /Chromium/ |
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| OSHA Standards | Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 0.5 mg/cu m. /Chromium(III) compounds, as Cr/ |
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| EPA Hazardous Waste Number | D007A waste containing chromium may or may not be characterized as a hazardous waste following testing by the Toxicity Characteristic Leaching Procedure as prescribed by the Resource Conservation and Recovery Act (RCRA) regulations. /Chromium/ |
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| NIOSH Recommendations | Recommended Exposure Limit: 10-hour Time-Weighted Average: 0.5 mg/cu m. /Chromium(III) compounds (as Cr)/ |
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| Clean Water Act requirements | Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /Chromium and compounds/ |
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| Hazard Classes and Categories | Acute Tox. 4 (24%)Respiratory sensitization - Category 1 |
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| State drinking water guidelines | (MN) MINNESOTA 20000 ug/L /Chromium III ion/ |
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| Fire fighting | In case of fire in the surroundings, use appropriate extinguishing media. |
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| First aid measures | Fresh air, rest.Rinse skin with plenty of water or shower.First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.Rinse mouth. |
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| Firefighting Hazards | Chromium oxides |
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| Fire fighting procedures | Wear self-contained breathing apparatus for firefighting if necessaryUse water spray, alcohol-resistant foam, dry chemical or carbon dioxideRespiratory protection from chromium metal and insoluble chromium salts while fighting fires: self-contained breathing apparatus with a full facepiece operated in pressure-demand or other positive pressure mode. /Chromium metal and insoluble chromium salts/ |
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| Storage conditions | Keep container tightly closed in a dry and well-ventilated place. Hygroscopic Handle and store under inert gas. Keep in a dry place. Storage class (TRGS 510): Non Combustible Solids |
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| Cleanup methods | ACCIDENTAL RELEASE MEASURESPersonal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Avoid breathing dust. Environmental precautions: Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.If chromium metal or insoluble chromium salts are spilled, the following steps should be taken: 1. Remove all ignition sources where metallic chromium has been spilled. 2. Ventilate area of spill. 3) Collect spilled material in the most convenient and safe manner and deposit in sealed containers for reclamation or for disposal in a secured sanitary landfill. Liquid containing chromium metal or insoluble chromium salts should be absorbed in vermiculite, dry sand, earth, or a similar material. /Chromium metal and insoluble chromium salts/ |
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| Disposal methods | Wastewater treatment sludge from the production of chrome green pigments is a poor candidate for incineration. /Chrome green pigments/Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contaminated packaging: Dispose of as unused product.Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D007, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste. /Chromium/SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.For more Disposal Methods (Complete) data for Chromium (III) oxide (9 total), please visit the HSDB record page. |
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| Spillage disposal | Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. |
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| Preventive Measures | SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.For more Preventive Measures (Complete) data for Chromium (III) oxide (12 total), please visit the HSDB record page. |
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| Eye Prevention | Wear safety goggles. |
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| Inhalation Risk | A harmful concentration of airborne particles can be reached quickly when dispersed. |
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| Skin Prevention | Protective gloves. |
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| Treatment | There is no know antidote for chromium poisoning. Exposure is usually handled with symptomatic treatment. (L16) |
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| Interactions | In inhalation chambers, male Wistar rats of the strain TNO-W74 were continuously exposed to submicron aerosols of sodium dichromate and to a pyrolyzed Cr(VI)/Cr(III) (3:2) oxide mixture. The sodium dichromate (Na2Cr2O7) aerosol had the chromium concentrations of 25, 50 and 100 micrograms/cu m, the chromium oxide mixture (Cr5O12) had the chromium concentration of 100 micrograms/cu m. After 18 months of inhalation the rats were held under conventional conditions for a further year. The experimental groups consisted of 20 rats and the control group of 40 rats. More than 90% of the rats in each group reached 2 years. At the end of the study the mortality rates amounted to 35%, 45% and 25% in the 3 sodium dichromate aerosol groups, respectively, and 50% in the chromium oxide mixture aerosol group, which was not significantly different from that of the controls (42.5%), living under the same conditions in filtered fresh air. In all sodium dichromate exposed groups significant effects were neither found clinically nor from hematology and clinical chemistry compared to the controls. In the chromium oxide mixture group, however, there was a number of significant findings. Elevated white and red blood cell counts and serum cholesterol as well as decreased serum total immunoglobulin levels at different stages of the study were observed together with few local lung effects determined histopathologically in this group. We assume that these effects are mainly due to the increased chromium lung burden of the rats. At the end of the study the lung chromium retention was about 10 times higher for the rats exposed to chromium oxide versus sodium dichromate at an aerosol Cr-concentration of 100 micrograms/cu m, while the kidney chromium retention was measured to be nearly equal in both groups. Three primary lung tumors (2 adenomas and 1 adenocarcinoma) and 1 malign tumor of the pharynx were found at the highest Cr-concentration (100 micrograms/cu m) of the sodium dichromate aerosol, 1 primary adenoma of the lung was in the chromium oxide mixture group exposed also to a Cr-concentration of 100 micrograms/cu m. No primary lung tumors were observed in the other experimental and control groups. These results indicate a weak carcinogenicity at 100 micrograms/cu m for the rats continuously exposed to submicron Na2Cr2O7 and Cr5O12 aerosols. Thus, there may be a small carcinogenic risk from occupational relevant chromium air levels. /Pyrolzed Cr(VI)/Cr(III) oxide mixture/ |
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| Health effects | Chromium in its trivalent state is not very toxic. It may be oxidized to hexavalent chromium, a known carcinogen. Hexavalent chromium has also been shown to affect reproduction and development. (A12) |
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| Adverse effects | ACGIH Carcinogen - Not Classifiable. |
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| Exposure routes | Oral (L16)inhalation (L16)dermal (L16) |
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| Toxicity summary | IDENTIFICATION AND USE: Chromic oxide (Cr(2)O(3)) is a green powder. It is not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses. It is used in abrasives and electric semiconductorsin alloysin printing fabrics and banknotes. It is also used in dyeing polymerscolorant for latex paints, in manufacturing of chromium metal and aluminum-chromium master alloys. It's other uses include catalyst in organic synthesis, green granules in asphalt roofing, component of refractory brick. Chromic oxide is a color additive in drug use. HUMAN EXPOSURE AND TOXICITY: Fine chromic oxide particles were insoluble in the culture mediumon the contrary, Cr(2)O(3) nanoparticles released soluble hexavalent chromium into the culture medium. Human lung carcinoma A549 cells and human keratinocyte HaCaT cells showed an increase in intracellular reactive oxygen species (ROS) level and activation of antioxidant defense systems on exposure to Cr(2)O(3) nanoparticles. The cellular influences of Cr(2)O(3) nanoparticles matched those of hexavalent chromium. Human lung epithelial cells exposure to chromic oxide nanoparticles led to DNA damage, which was detected by comet assay and cytokinesis block micronucleus assay. The cell exposure lead to mitochondria-mediated apoptosis. ANIMAL STUDIES: In rats in a 13-week nose-only inhalation study that included a 13-week recovery period, chromic oxide caused pathological changes in the bronchial and mediastinal lymphatic tissue and lungs, consisting of the presence of pigment-laden macrophages, lymphoid and septal hyperplasia, and interstitial inflammation similar to that observed with other inert dusts. In experiments with rats 4/20 animals developed lung sarcomas 16-19 months after a single intraperitoneal injection of 20 mg chromic oxide. No effects on reproduction were reported in nine pairs of rats fed up to 5% chromium(III) oxide in a supplemented bread, 5 days/week for 60 days before grossly observable malformations or adverse effects occurred in the pups. Exposure to chromic oxide increased sister chromatid exchanges in Chinese hamster V79 cells. Exposure for 18 hr to Cr(2)O(3) induced in Chinese hamster cells a statistically significant increase in the mutation frequency of up to 10-fold over the control. ECOTOXICITY STUDIES: In seeds of Triticum aestivum exposure to 25-100 ug/mL Cr(2)O(3) nanoparticles inhibited the seed germination and seedling growth in concentration dependent manner.Trivalent chromium may also form complexes with peptides, proteins, and DNA, resulting in DNA-protein crosslinks, DNA strand breaks, DNA-DNA interstrand crosslinks, chromium-DNA adducts, chromosomal aberrations and alterations in cellular signaling pathways. It has been shown to induce carcinogenesis by overstimulating cellular regulatory pathways and increasing peroxide levels by activating certain mitogen-activated protein kinases. It can also cause transcriptional repression by cross-linking histone deacetylase 1-DNA methyltransferase 1 complexes to CYP1A1 promoter chromatin, inhibiting histone modification. Chromium may increase its own toxicity by modifying metal regulatory transcription factor 1, causing the inhibition of zinc-induced metallothionein transcription. (A12, L16, A34, A35, A36) |
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| Average Daily Intake | According to the 2012 TSCA Inventory Update Reporting data, 17 reporting facilities estimate the number of persons reasonably likely to be exposed during the manufacturing, processing, or use of chromium (III) oxide may be as low as <10 workers up to the range of 100-499 workers per plantthe data may be greatly underestimated due to confidential business information (CBI) or unknown values(1).NIOSH (NOES Survey 1981-1983) has statistically estimated that 88,897 workers (11,984 of these are female) were potentially exposed to chromium (III) oxide in the US(1). Occupational exposure to chromium (III) oxide may occur through inhalation and dermal contact with this compound at workplaces where chromium (III) oxide is produced or used(SRC).Dental technicians working in areas of cast prothetics containing chromium and no effective ventilation were exposed to chromium (III) oxide levels 0.15-9.6 mg/cu m(1). |
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| Ecotoxicity excerpts | /PLANTS/ In this study, seeds of Triticum aestivum L. (Poaceae) were exposed to 0-100 ug/mL chromium oxide nanoparticles (Cr2O3, Nps) to study the phytotoxic effects on seed germination and seedling growth. It has been observed that 25-100 ug/mL Cr2O3, Nps inhibited the seed germination and seedling growth in concentration dependent manner. The present study suggests that release of Cr2O3, Nps in environment may adversely affect the wheat production. |
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| Signs and Symptoms | Cough.Redness.Chromium in its trivalent state is not very toxic, but it may be oxidized to hexavalent chromium. Breathing hexavalent chromium can cause irritation to the lining of the nose, nose ulcers, runny nose, and breathing problems, such as asthma, cough, shortness of breath, or wheezing. Ingestion of hexavalent chromium causes irritation and ulcers in the stomach and small intestine, as well as anemia. Skin contact can cause skin ulcers. (L16) |
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| TSCA Test Submissions | Chromic Oxide (CAS #1308-38-9) was one of two materials evaluated for subchronic toxicity. The test material was administered via nose-only inhalation to Fischer 344 rats (15/sex/group) at exposure concentrations of 4.4, 15, and 44 mg/cu m, with one control group. Exposures were conducted for 6 hr/day, for 13 weeks, except weekends and holidays. After 13 weeks of exposure, 10 animals/sex/group were sacrificed and given a complete necropsy and histologic examination along with hematologic, serum biochemistry, urologic, ophthalmologic and sperm characterizations. The remaining animals underwent a 13-week post exposure recovery, followed by a complete necropsy and limited histologic examination. During weeks 7 and 8, additional Fischer rats (5/sex/group) were exposed for 5 consecutive days at each exposure level, then evaluated for bronchoalveolar fluid (BALF) parameters. There were no exposure-related effects in clinical signs, ophthalmologic, body weight-gain, or sperm characteristic evaluations. None of the hematologic, serum biochemical, or urinalysis parameters were significantly different from controls. The BALF parameters were not significantly different, however, yellow crystalline material was observed in the mononuclear cells of all treated groups. Gross examination at terminal sacrifice revealed treatment- and concentration-related green discoloration in the lungs and mediastinal lymph nodes which, in the recovery group, occurred with slightly decreased incidence and severity. The mean, absolute and relative lung weights of male rats in the highest exposure group were significantly different from controls (p</= 0.01), although no other organs showed treatment-related differences. Black pigment was observed in the peribronchial lymphoid tissue, macrophages, and mediastinal lymph nodes in all treatment groups and corresponded with trace to moderate microscopic changes in the lung and mediastinal lymph nodes. These changes included interstitial inflammation, septal cell hyperplasia, and lymphoid hyperplasia at the two highest exposureslymphoid hyperplasia only at the lowest exposure concentration. |
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| Natural Pollution Sources | Chromium (III) oxide occurs in chromium-rich tremolite skarns, metaquartzites, and chlorite veins (Outokumpu, Finland)on greywacke pebbles in a glacial boulder clay deposit (Callowhill Upper, Ireland)as pebbles in streams (Merume River, Guyana)a very rare component in chondrite meteorites(1). |
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| Human Toxicity Excerpts | /HUMAN EXPOSURE STUDIES/ The International Agency for Research on Cancer considers the carcinogenicity of welding fume of priority for re-evaluation. Genotoxic effects in experimental animals are still inconclusive. Here, we investigated the association of personal exposure to metals in respirable welding fumes during a working shift with oxidatively damaged guanosine in DNA of white blood cells (WBC) and in postshift urine samples from 238 welders. Medians of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) were 2.35/10(6) dGuo in DNA of WBC and 4.33 ug/g creatinine in urine. The median of 8-oxo-7,8-dihydroguanosine (8-oxoGuo) was 7.03 ug/g creatinine in urine. The extent of both urinary parameters was higher in welders applying techniques with high particle emission rates to stainless steel than in tungsten inert gas welders (8-oxodGuo: 9.96 vs. 4.49 ug/L, 8-oxoGuo: 15.7 vs. 7.7 ug/L), but this apparent difference diminished after creatinine adjustment. We applied random intercept models to estimate the influence of airborne and systemic exposure to metals on oxidatively damaged guanosine in WBC and urine together with covariates. We observed a highly significant nonlinear association of urinary 8-oxoGuo with serum ferritin (P < 0.0001) and higher 8-oxoGuo concentrations for respirable iron >1,000 ug/cu m compared to < or = 57 ug/cu m. Similar effects were found for manganese. Airborne chromium but not nickel was associated with all oxidatively modified guanosine measures, whereas urinary chromium as well as nickel showed associations with urinary modified guanosines. In summary, oxidatively damaged urinary guanosine was associated with airborne and systemic exposure to metals in welders and showed a strong relation to body iron stores. /Chromium oxide//ALTERNATIVE and IN VITRO TESTS/ Chromium oxide (Cr2O3 ) nanoparticles (NPs) are being increasingly used as a catalyst for aromatic compound manufacture, abrading agents and as pigments (e.g.,Viridian). Owing to increased applications, it is important to study the biological effects of Cr2O3 NPs on human health. The lung is one of the main exposure routes to nanomaterialstherefore, the present study was designed to determine the genotoxic and apoptotic effect of Cr2O3 NPs in human lung epithelial cells (A549). The study also elucidated the molecular mechanism of its toxicity. Cr2O3 NPs led to DNA damage, which was deduced by comet assay and cytokinesis block micronucleus assay. The damage could be mediated by the increased levels of reactive oxygen species. Further, the oxygen species led to a decrease in mitochondrial membrane potential and an increase in the ratio of BAX/Bcl-2 leading to mitochondria-mediated apoptosis induced by Cr2O3 NPs, which ultimately leads to cell death. Hence, there is a need of regulations to be imposed in NP usage. The study provided insight into the caspase-dependent mechanistic pathway of apoptosis./ALTERNATIVE and IN VITRO TESTS/ Chromium(III) oxide (Cr(2)O(3)) is used for industrial applications such as catalysts and pigments. In the classical form, namely the fine particle, Cr(2)O(3) is insoluble and chemically stable. It is classified as a low-toxicity chromium compound. Recently, industrial application of nanoparticles (a new form composed of small particles with a diameter of < or =100 nm, in at least one dimension) has been increasing. Cellular effects induced by Cr(2)O(3) nanoparticles are not known. To shed light upon this, the release of soluble chromium from Cr(2)O(3) nano- and fine-particles in culture medium was compared. Fine Cr(2)O(3) particles were insoluble in the culture mediumon the contrary, Cr(2)O(3) nanoparticles released soluble hexavalent chromium into the culture medium. Cr(2)O(3) nanoparticles showed severe cytotoxicity. The effect of Cr(2)O(3) nanoparticles on cell viability was higher than that of fine particles. Cr(2)O(3) nanoparticles showed cytotoxicity equal to that of hexavalent chromium (K(2)Cr(2)O(7)). Human lung carcinoma A549 cells and human keratinocyte HaCaT cells showed an increase in intracellular reactive oxygen species (ROS) level and activation of antioxidant defense systems on exposure to Cr(2)O(3) nanoparticles. Exposure of Cr(2)O(3) nanoparticles led to caspase-3 activation, showing that the decrease in cell viability by exposure to Cr(2)O(3) nanoparticles was caused by apoptosis. Cellular responses were stronger in the Cr(2)O(3) nanoparticles-exposed cells than in fine Cr(2)O(3) - and CrCl(3) -exposed cells. Cellular uptake of Cr(2)O(3) particles were observed in nano- and fine-particles. The cellular influence of the extracellular soluble trivalent chromium was lower than that of Cr(2)O(3) nanoparticles. Cr(2)O(3) nanoparticles showed cytotoxicity by hexavalent chromium released at outside and inside of cells. The cellular influences of Cr(2)O(3) nanoparticles matched those of hexavalent chromium. In conclusion, Cr(2)O(3) nanoparticles have a high cytotoxic potential. |
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| Federal Drinking Water Standards | Maximum contaminant level for inorganic contaminants: Contaminant: ChromiumMCL 0.1 mg/L. /Chromium/ |
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| Federal drinking water guidelines | Maximum contaminant level goal for inorganic contaminants: Contaminant: ChromiumMCLG 0.1 mg/L. /Chromium/ |
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