Potassium Chromate

H315: Causes skin irritation [Warning Skin corrosion/irritation]

H317: May cause an allergic skin reaction [Warning Sensitization, Skin]

H319: Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H335: May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]

H340: May cause genetic defects [Danger Germ cell mutagenicity]

H350i: May cause cancer by inhalation [Danger Carcinogenicity]

H400: Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

H410: Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

P203, P261, P264, P264+P265, P271, P272, P273, P280, P302+P352, P304+P340, P305+P351+P338, P318, P319, P321, P332+P317, P333+P317, P337+P317, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

H301 (15.4%): Toxic if swallowed [Danger Acute toxicity, oral]

H315 (99.9%): Causes skin irritation [Warning Skin corrosion/irritation]

H317 (100%): May cause an allergic skin reaction [Warning Sensitization, Skin]

H319 (99.7%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H330 (15.3%): Fatal if inhaled [Danger Acute toxicity, inhalation]

H335 (99.9%): May cause respiratory irritation [Warning Specific target organ toxicity, single exposure; Respiratory tract irritation]

H340 (100%): May cause genetic defects [Danger Germ cell mutagenicity]

H350 (84.8%): May cause cancer [Danger Carcinogenicity]

H350i (15.2%): May cause cancer by inhalation [Danger Carcinogenicity]

H360FD (15%): May damage fertility; May damage the unborn child [Danger Reproductive toxicity]

H372 (15.2%): Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]

H400 (100%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

H410 (100%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

P203, P260, P261, P264, P264+P265, P270, P271, P272, P273, P280, P284, P301+P316, P302+P352, P304+P340, P305+P351+P338, P316, P318, P319, P320, P321, P330, P332+P317, P333+P317, P337+P317, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 693 reports by companies from 19 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

H301: Toxic if swallowed [Danger Acute toxicity, oral]

H314: Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]

H318: Causes serious eye damage [Danger Serious eye damage/eye irritation]

H334: May cause allergy or asthma symptoms or breathing difficulties if inhaled [Danger Sensitization, respiratory]

H350: May cause cancer [Danger Carcinogenicity]

H360: May damage fertility or the unborn child [Danger Reproductive toxicity]

H370: Causes damage to organs [Danger Specific target organ toxicity, single exposure]

H372: Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]

P203, P233, P260, P261, P264, P264+P265, P270, P271, P272, P273, P280, P284, P301+P316, P301+P330+P331, P302+P352, P302+P361+P354, P304+P340, P305+P354+P338, P308+P316, P316, P317, P318, P319, P321, P330, P333+P317, P342+P316, P362+P364, P363, P391, P403, P405, and P501 (click each P-code to see the statement)

H341: Suspected of causing genetic defects [Warning Germ cell mutagenicity]

P203, P233, P260, P261, P264, P264+P265, P271, P272, P280, P284, P301+P330+P331, P302+P352, P302+P361+P354, P304+P340, P305+P354+P338, P316, P317, P318, P321, P333+P317, P342+P316, P362+P364, P363, P403, P405, and P501 (click each P-code to see the statement)

H312: Harmful in contact with skin [Warning Acute toxicity, dermal]

H330: Fatal if inhaled [Danger Acute toxicity, inhalation]

H360FD: May damage fertility; May damage the unborn child [Danger Reproductive toxicity]

P203, P233, P260, P261, P264, P270, P271, P272, P273, P280, P284, P301+P316, P301+P330+P331, P302+P352, P302+P361+P354, P304+P340, P305+P354+P338, P316, P317, P318, P319, P320, P321, P330, P333+P317, P342+P316, P362+P364, P363, P391, P403, P403+P233, P405, and P501 (click each P-code to see the statement)

Fresh air, rest. Half-upright position. Artificial respiration may be needed. Refer for medical attention.

First rinse with plenty of water for at least 15 minutes, then remove contaminated clothes and rinse again. Refer for medical attention .

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Do NOT induce vomiting. Give one or two glasses of water to drink. Refer for medical attention .

INHALATION: move to fresh air.

INGESTION: give large amount of water; induce vomiting; treat peripheral vascular shock vigorously; get medical attention.

EYES: flush with water for at least 15 min.; get medical attention.

SKIN: flush with water; if irritation persists, get medical attention. (USCG, 1999)

Excerpt from ERG Guide 140 [Oxidizers]:

SMALL FIRE: Use water. Do not use dry chemicals or foams. CO2 or Halon® may provide limited control.

LARGE FIRE: Flood fire area with water from a distance. Do not move cargo or vehicle if cargo has been exposed to heat. If it can be done safely, move undamaged containers away from the area around the fire.

FIRE INVOLVING TANKS, RAIL TANK CARS OR HIGHWAY TANKS: For ammonium nitrate products: Do not fight cargo fire. Withdraw, evacuate and isolate area for at least 1600 meters (1 mile). Treat as an explosive (ERG Guide 112). Do not enter area for 24 hours or until expert advice has been provided. Fight fire from maximum distance or use unmanned master stream devices or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. ALWAYS stay away from tanks in direct contact with flames. For massive fire, use unmanned master stream devices or monitor nozzles; if this is impossible, withdraw from area and let fire burn. (ERG, 2024)

In case of fire in the surroundings, use appropriate extinguishing media.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

If material involved in fire: Extinguish fire using agent suitable for type of surrounding fire (Material itself does not burn or burns with difficulty.)

Respiratory protection from chromic acid and chromates while fighting fires: Self-contained breathing apparatus with a full facepiece operated in pressure-demand or other positive pressure mode.

From a secure, explosion-proof location, use water spray to cool exposed containers. If cooling streams are ineffective (venting sound increases in volume and pitch, tank discolors, or shows any signs of deforming), withdraw immediately to a secure position.

/When fire fighting wear/ self-contained breathing apparatus, with a full facepiece, operated in pressure-demand or other positive pressure mode. /Chromic acid & chromates/

Excerpt from ERG Guide 140 [Oxidizers]:

IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.

LARGE SPILL: Consider initial downwind evacuation for at least 100 meters (330 feet).

FIRE: If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. If ammonium nitrate products are in a tank, rail car or truck and involved in a fire, ISOLATE for 1600 meters (1 mile) in all directions; also, initiate evacuation including emergency responders for 1600 meters (1 mile) in all directions. (ERG, 2024)

Personal protection: chemical protection suit including self-contained breathing apparatus. Sweep spilled substance into containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations. Do NOT let this chemical enter the environment.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust; Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided; 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.

Environmental considerations: Land Spill: Dig a pit, pond, lagoon, holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Cover solids with a plastic sheet to prevent dissolving in rain or fire fighting water.

Environmental considerations: Water Spill: Add sodium bisulfite (NaHSO3). Neutralize with agricultural lime (CaO), crushed limestone (CaCO3), or sodium bicarbonate (NaHCO3). Adjust pH to neutral (pH=7).

Evacuate persons not wearing protective equiment from area of spill or leak until cleanup is complete. Remove all ignition sources. Collect powdered materials in the most convenient and safe manner and deposit sealed containers. Ventilate area after cleanup is complete. ... It may be necessary to contain and dispose of this chemical as a hazardous waste. If material or contaminated runoff enters waterwats, notify downstram users of potentially contaminated waters.

For more Cleanup Methods (Complete) data for POTASSIUM CHROMATE (6 total), please visit the HSDB record page.

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/

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D002, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

Product: Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Offer surplus and non-recyclable solutions to a licensed disposal company; Contaminated packaging: Dispose of as unused product.

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 POTASSIUM CHROMATE (11 total), please visit the HSDB record page.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust; Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. 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.

Appropriate engineering controls: Avoid contact with skin, eyes and clothing. Wash hands before breaks and immediately after handling the product.

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.

For more Preventive Measures (Complete) data for POTASSIUM CHROMATE (11 total), please visit the HSDB record page.

Excerpt from ERG Guide 140 [Oxidizers]:

Keep combustibles (wood, paper, oil, etc.) away from spilled material. Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Do not get water inside containers.

SMALL DRY SPILL: With clean shovel, place material into clean, dry container and cover loosely; move containers from spill area.

SMALL LIQUID SPILL: Use a non-combustible material like vermiculite or sand to soak up the product and place into a container for later disposal.

LARGE SPILL: Dike far ahead of liquid spill for later disposal. (ERG, 2024)

Provision to contain effluent from fire extinguishing. Dry. Well closed. Separated from combustible substances, reducing agents and food and feedstuffs. Store in an area without drain or sewer access.

Keep container tightly closed in a dry and well-ventilated place. Storage class (TRGS 510): Non-combustible, acute toxic Cat.3 / toxic hazardous materials or hazardous materials causing chronic effects

... Store in a location separate from other materials, especially flammables and combustibles. ... Store in a secure poison location. ... Potassium chromates must be stored to avoid contact with combustible, organic, or other easily oxidized materials (such as paper, wood, sulfur, aluminum, hydrazine, and plastics) since violent reactions occur. A regulated, marked area should be established where potassium chromate is handled, used, or stored. Where possible, automatically transfer material from drums or other storage containers to process containers. Sources of ignition, such as smoking and open flames, are prohibited where this chemical is handled, used, or stored. Metal containers involving the transfer of this chemical should be grounded and bonded. Wherever this chemical is used, handled, manufactured, or stored, use explosion-proof electrical equipment and fittings.

0.56 [mg/m3]

9.7 [mg/m3]

58 [mg/m3]

0.005 [mg/m3], as Cr(VI)

15 mg Cr(VI)/m3 ; A potential occupational carcinogen. (NIOSH, 2024)

250 mg/cu m (as Cr(II)). /Chromium(II) compounds (as Cr)/

25 mg/cu m (as Cr(III)). /Chromium(III) compounds (as Cr)/

15 mg/cu m (as Cr(VI)). /Chromic acid and chromates/

NIOSH considers chromic acid and chromates to be potential occupational carcinogens. /Chromic acid and chromates/

0.0001 [mg/m3], as Cr(VI), inhalable particulate matter

0.0005 [mg/m3], as Cr(VI), inhalable particulate matter

8 hr Time Weighted Avg (TWA): 0.5 mg/cu m. /Chromium and Cr(III) inorganic compounds, as Cr/

A4; Not classifiable as a human carcinogen. /Chromium and Cr(III) inorganic compounds, as Cr/

Peak Exposure Recommendation: Transient increases in workers' exposure levels may exceed 3 times the value of the TLV-TWA level for no more than 15 minutes at a time, on no more than 4 occasions spaced 1 hour apart during a workday, and under no circumstances should they exceed 5 times the value of the TLV-TWA level. In addition, the 8-hour TWA is not to be exceeded for an 8-hour work period. /Chromium and Cr(III) inorganic compounds, as Cr/

8 Hr Time Weighted Avg (TWA): 0.05 mg/cu m. /Water-soluble Cr(VI) inorganic compounds, as Cr/

For more Threshold Limit Values (TLV) (Complete) data for POTASSIUM CHROMATE (11 total), please visit the HSDB record page.

(as Cr(VI), inhalable fraction): 0.0002 mg/m

(as Cr): 0.005 mg/m

Intermediate Oral: 0.005 mg/kg/day (L134)

Chronic Oral: 0.001 mg/kg/day (L134)

A harmful concentration of airborne particles can be reached quickly when dispersed, especially if powdered.

The substance is corrosive to the eyes, skin and respiratory tract. Corrosive on ingestion. The substance may cause effects on the kidneys and liver. This may result in tissue lesions.

Repeated or prolonged contact may cause skin sensitization. Repeated or prolonged inhalation may cause asthma. Repeated or prolonged inhalation may cause nasal ulceration. This may result in perforation of the nasal septum. The substance may have effects on the kidneys. This may result in kidney impairment. This substance is carcinogenic to humans. Animal tests show that this substance possibly causes toxicity to human reproduction or development.

Bu. of Mines approved filter-type respirator; close-fitting safety goggles; rubber boots and apron; safety hat; face shield (USCG, 1999)

Eye/face protection: Face shield and safety glasses. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).

Skin protection: Handle with gloves.

Body Protection: Complete suit protecting against chemicals, The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

For more Personal Protective Equipment (PPE) (Complete) data for POTASSIUM CHROMATE (13 total), please visit the HSDB record page.

NO contact with combustible substances.

PREVENT DISPERSION OF DUST! AVOID ALL CONTACT! IN ALL CASES CONSULT A DOCTOR!

Use closed system or ventilation.

Protective gloves. Protective clothing.

Wear face shield or eye protection in combination with breathing protection.

Do not eat, drink, or smoke during work. Wash hands before eating.

Potassium chromate is a yellow crystalline solid. It is soluble in water. The primary hazard is the threat to the environment. Immediate steps should be taken to limit its spread to the environment. It is used in chemical analysis, in making pigments for paints and inks, as a fungicide, and to make other chromium compounds.

Lemon-yellow solid; Soluble in water; [Merck Index] Yellow crystalline solid; [MSDSonline]

YELLOW CRYSTALS.

Yellow orthorhombic crystals

Lemon-yellow crystals

Odorless

Disagreeable bitter taste

In water, 65.0 g/100 g water at 25 °C

In water, 39.96 wt% at 20 °C; 45.0 wt% at 100 °C

62.9 g/100 cc water at 20 °C; 79.2 g/100 cc water at 100 °C

Insoluble in alcohol, acetone, phenyl cyanide

Solubility in water, g/100ml at 20 °C: 62.9 (good)

2.73 at 64.4 °F (USCG, 1999) - Denser than water; will sink

Density (at 18 °C): 2.73 g/cm³

2.73 @25 °C

Vapor pressure at 20 °C: negligible

Stable under recommended storage conditions.

When heated to decomposition it emits toxic fumes of /potassium oxide/.

... decomposition at 500 °C

Corrosive

Aqueous solution is alkaline to litmus or phenolphthalein

Index of refraction: beta 1.74

pH: 8.5 - 10.0 at 50 g/L at 20 °C

Heat of fusion: 35.6 cal/g; Strong oxidizing agent

Non-hygroscopic; occurs as the stable beta-modification; heat of solution: -71.3 kJ/kg; Standard enthalpy of formation: -1383 kJ/mol

dielectric constant

crystal structure

enthalpy

effective mass

isothermal section

molar conductivity

Gibbs energy

enthalpy change

phase diagram

unit cell parameter

melting temperature

heat capacity

Schoenflies notation

sound velocity

excitation energy

Soluble in water.

Salts, Basic

Oxidizing Agents, Strong

Strong Oxidizing Agent

Oxidizing agents, such as POTASSIUM CHROMATE, can react with reducing agents to generate heat and products that may be gaseous (causing pressurization of closed containers). The products may themselves be capable of further reactions (such as combustion in the air). The chemical reduction of materials in this group can be rapid or even explosive, but often requires initiation (heat, spark, catalyst, addition of a solvent). Explosive mixtures of inorganic oxidizing agents with reducing agents often persist unchanged for long periods if initiation is prevented. Such systems are typically mixtures of solids, but may involve any combination of physical states. Some inorganic oxidizing agents are salts of metals that are soluble in water; dissolution dilutes but does not nullify the oxidizing power of such materials. Organic compounds, in general, have some reducing power and can in principle react with compounds in this class. Actual reactivity varies greatly with the identity of the organic compound. Inorganic oxidizing agents can react violently with active metals, cyanides, esters, and thiocyanates.

Incompatible materials: Organic materials, powdered metals, strong oxidizing agents

Contact with hydrazine causes explosion.

Violent reactions with combustibles, organics, powdered metals, or easily oxidizable substances.

Combustible, organic, or other readily oxidizable materials (paper, wood, sulfur, aluminum, plastics, etc.); corrosive to metals. /Chromic acid and chromates/

Hydrazine is decomposed explosively by chromates and chromic anhydride. /Chromates/

IDENTIFICATION AND USE: Potassium chromate forms lemon-yellow crystals. It has a limited application in enamels, finishing leather, and rustproofing of metals. Oxidizing agent in analytical chemistry. HUMAN EXPOSURE AND TOXICITY: If ingested, violent gastroenteritis, severe circulatory collapse and toxic nephritis may ensue, or peripheral vascular shock. Eye contact can cause severe damage with possible loss of vision. Evaluation of genotoxic effects of potassium chromate (K2CrO4) and was carried out in human blood lymphocytes in vitro as measured by the electron microscopy in situ end-labeling (EM-ISEL). EM-ISEL was used to assess DNA single-strand breaks (SSBs) expressed as number of immunogold particles per sq um of chromatin at both chromosomal and nuclear DNA levels. Quantification of SSBs by EM-ISEL showed that potassium chromate is genotoxic agent at non-cytotoxic concentrations. Potassium chromate quadrupled frequency of sister-chromatid exchanges in cultured human fibroblasts. Potassium chromate induced DNA damage and unscheduled DNA synthesis in cultured human fibroblasts. ANIMAL STUDIES: The embryotoxic and teratogenic potential of potassium chromate was evaluated by the teratological analysis of mouse fetuses. The test chemical was administered intraperitoneally to mice of both sexes for 30 days. Teratological scanning of the fetuses born to treated animals revealed a reduction in the number of live implants and litter size. Higher incidence of resorption and dead litter indicated the embryotoxic effect of the test chemical. Malformations, both skeletal and morphological, suggest the possibility of potassium chromate being fetotoxic. Potassium chromate induced significant and dose-related increase in micronucleated polychromatic erythrocytes (micronuclei) in bone marrow of mice following 2 ip injections of doses ranging from 12-48 mg/kg body wt. Potassium chromate was tested for its potential to induce forward mutations at the thymidine kinase locus in L5178Y mouse lymphoma cells. Strong positive responses at survivals greater than 10% were observed. ECOTOXICITY STUDIES: 90 Days after hatching, young carp were reared for 75 wk in test waters of pH 7 & 5 containing 0.1 ppm potassium chromate. This pollutant caused deformation in the bone by chronic leaching of calcium, and the low pH hastened the leaching.

Hexavalent chromium's carcinogenic effects are caused by its metabolites, pentavalent and trivalent chromium. The DNA damage may be caused by hydroxyl radicals produced during reoxidation of pentavalent chromium by hydrogen peroxide molecules present in the cell. 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)

WEIGHT OF EVIDENCE CHARACTERIZATION: Under the current guidelines (1986), Cr(VI) is classified as Group A - known human carcinogen by the inhalation route of exposure. Carcinogenicity by the oral route of exposure cannot be determined and is classified as Group D. Under the proposed guidelines (1996), Cr(VI) would be characterized as a known human carcinogen by the inhalation route of exposure on the following basis. Hexavalent chromium is known to be carcinogenic in humans by the inhalation route of exposure. Results of occupational epidemiological studies of chromium-exposed workers are consistent across investigators and study populations. Dose-response relationships have been established for chromium exposure and lung cancer. Chromium-exposed workers are exposed to both Cr(III) and Cr(VI) compounds. Because only Cr(VI) has been found to be carcinogenic in animal studies, however, it was concluded that only Cr(VI) should be classified as a human carcinogen. Animal data are consistent with the human carcinogenicity data on hexavalent chromium. Hexavalent chromium compounds are carcinogenic in animal bioassays, producing the following tumor types: intramuscular injection site tumors in rats and mice, intrapleural implant site tumors for various Cr(VI) compounds in rats, intrabronchial implantation site tumors for various Cr(VI) compounds in rats and subcutaneous injection site sarcomas in rats. In vitro data are suggestive of a potential mode of action for hexavalent chromium carcinogenesis. Hexavalent chromium carcinogenesis may result from the formation of mutagenic oxidatitive DNA lesions following intracellular reduction to the trivalent form. Cr(VI) readily passes through cell membranes and is rapidly reduced intracellularly to generate reactive Cr(V) and Cr(IV) intermediates and reactive oxygen species. A number of potentially mutagenic DNA lesions are formed during the reduction of Cr(VI). Hexavalent chromium is mutagenic in bacterial assays, yeasts and V79 cells, and Cr(VI) compounds decrease the fidelity of DNA synthesis in vitro and produce unscheduled DNA synthesis as a consequence of DNA damage. Chromate has been shown to transform both primary cells and cell lines. HUMAN CARCINOGENICITY DATA: Occupational exposure to chromium compounds has been studied in the chromate production, chromeplating and chrome pigment, ferrochromium production, gold mining, leather tanning and chrome alloy production industries. Workers in the chromate industry are exposed to both trivalent and hexavalent compounds of chromium. Epidemiological studies of chromate production plants in Japan, Great Britain, West Germany, and the United States have revealed a correlation between occupational exposure to chromium and lung cancer, but the specific form of chromium responsible for the induction of cancer was not identified ... Studies of chrome pigment workers have consistently demonstrated an association between occupational chromium exposure (primarily Cr(VI)) and lung cancer. Several studies of the chromeplating industry have demonstrated a positive relationship between cancer and exposure to chromium compounds. ANIMAL CARCINOGENICITY DATA: Animal data are consistent with the findings of human epidemiological studies of hexavalent chromium ... /Chromium (VI)/

Evaluation: There is sufficient evidence in humans for the carcinogenicity of chromium(VI) compounds. Chromium(VI) compounds cause cancer of the lung. Also positive associations have been observed between exposure to Chromium(IV) compounds and cancer of the nose and nasal sinuses. There is sufficient evidence in experimental animals for the carcinogenicity of chromium(VI) compounds. Chromium(VI) compounds are carcinogenic to humans (Group 1). /Chromium(VI) compounds/

Chromium Hexavalent Compounds: known to be human carcinogens. /Chromium hexavalent compound/

A1; Confirmed human carcinogen. /Water-soluble Cr(VI) inorganic compounds/

A1; Confirmed human carcinogen. /Insoluble Cr(VI) inorganic compounds/

1, carcinogenic to humans. (L135)

Hexavalent chromium is a known carcinogen. Chronic inhalation especially has been linked to lung cancer. Hexavalent chromium has also been know to cause reproductive and developmental defects. (A12)

The substance can be absorbed into the body by inhalation of its vapour or dust, through the skin and by ingestion.

Inhalation (L16) ; oral (L16) ; dermal (L16)

Burning sensation. Sore throat. Cough. Wheezing. Laboured breathing.

Redness. Pain. Skin burns.

Redness. Pain. Blurred vision. Severe deep burns.

Nausea. Vomiting. Abdominal pain. Burning sensation. Diarrhoea. Shock or collapse.

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)

Occupational hepatotoxin - Secondary hepatotoxins: the potential for toxic effect in the occupational setting is based on cases of poisoning by human ingestion or animal experimentation.

Nephrotoxin - The chemical is potentially toxic to the kidneys in the occupational setting.

Dermatotoxin - Skin burns.

Skin Sensitizer - An agent that can induce an allergic reaction in the skin.

Asthma - Reversible bronchoconstriction (narrowing of bronchioles) initiated by the inhalation of irritating or allergenic agents.

IARC Carcinogen - Class 1: International Agency for Research on Cancer classifies chemicals as established human carcinogens.

NTP Carcinogen - Known to be a human carcinogen.

ACGIH Carcinogen - Confirmed Human.

LD50: 180 mg/kg (Oral, Rat) (T14)

LD50: 32 mg/kg (Intraperitoneal, Mouse) (T14)

LD50: 11 mg/kg (Intramuscular, Rabbit) (T14)

LD50 Mouse oral 180 mg/kg

LD50 Mouse ip 32 mg/kg

LD50 Rabbit intramuscular 11 mg/kg

There is no know antidote for chromium poisoning. Exposure is usually handled with symptomatic treatment. (L16)

Tumor promoters such as phorbol esters, teleocidin and okadaic acid increase the numbers of multilayered, transformed foci produced by BPV DNA-transfected C3H/10T1/2 cells. We questioned whether arsenic and chromium, which are known human carcinogens also enhance transformation of BPV DNA-transfected C3H/10T1/2 cells. Cr(III) potassium sulfate at 100 uM enhanced transformation by 1.4-fold, but Cr(VI) as potassium chromate did not enhance transformation, although toxicity of potassium chromate may have prevented enhancement of transformation. Sodium arsenite (As(III) at 5 uM and sodium arsenate (As(V)) at 25 uM both enhanced neoplastic transformation by 6-fold. By comparison, in previous studies, sodium orthovanadate (V(IV)) or vanadyl sulfate (V(IV)) at 4 uM enhanced numbers of transformed foci by 25-50-fold. The comparatively strong enhancement of transformation by vanadium and phorbol esters suggests that neoplastic transformation may occur by mechanisms that are common to these compounds including alteration of tyrosine phosphorylation.

In an attempt to develop biomarkers of chromate and nickel exposure, we have used a rapid, simple and sensitive (125)I-postlabelling assay to detect the formation of DNA-protein crosslinks (DPCs) in different tissues from male Sprague-Dawley rats exposed i.p. to potassium chromate (K2CrO4) and nickel chloride (NiCl2). The results demonstrated that 20 hr after rats were injected i.p. with these agents, DPCs were observed in WBC, liver and kidney of rats treated with K2CrO4 in doses ranging from 10 to 40 mg/kg body wt. There was a dose-dependent relationship between chromate exposure and DPCs in WBC and liver, but no DPC increase was shown in lung. In the same way, DPCs were found in WBC and lung of rats treated with NiCl2 in doses ranging from 10 to 30 mg/kg in a dose-dependent manner. The formation of DPCs in different tissues was also observed following repeated exposure of rats to K2CrO4 and NiCl2 (10 mg/kg, i.p.) for 3 weeks. These results were similar with the single dose. It is indicated that chromate and nickel compounds possibly cause DNA or protein damage to form DPCs, suggesting DPCs might be useful as a biomarker for quantitative K2CrO4 and NiCl2 exposure and genotoxic lesions. In addition, WBC were shown to be more sensitive to chromate(VI) and nickel(II) induced DPCs than other targets. There were significant correlations between DPCs induced by K2CrO4 in WBC and liver, and by NiCl2 generated DPCs in WBC and lung, indicating that DPCs in WBC may be a good surrogate for some internal organs of humans exposed to chromate(VI) and nickel(II) compounds.

In a previous report chromate potentiated the mutagenicity of sodium azide, apparently by affecting repair and/or replication of DNA. Further evidence in support of such a mechanism for chromate potentiation is reported here. Chromate does not react directly with azide or its major mutagenic metabolite, azidoalanine, eliminating such reactions as possible mechanisms for potentiation. Further, azide was unable to potentiate the mutagenicity of chromate in Salmonella typhimurium strain TA104, which is sensitive to chromate mutagenicity but not to azide. Thus, it appears that the potentiation is not due to an action of azide in modulating chromate mutagenicity. Finally, the interaction was not altered by deficiency in recA gene product in S typhimurium GW19, nor by enhancement of SOS repair in the pKM101 containing strain TA100. Thus, induction of recA-dependent functions seems to play no role in the comutagenic actions of chromate. The simplest explanation for potentiation seems to be that chromate is able either to limit error-free recovery from azide-induced DNA damage or to promote error-prone repair or error-prone processing at sites of lesions.

A fluctuation test using Salmonella typhimurium strain 1535 has been used in an experimental protocol to assess biological effects of interactions between chromium (VI), such as K2CrO4, and two DNA-damaging agents, ethyl methanesulfonate (EMS), and sodium azide. Mutagenicity, expressed as the average number of mutations induced over a parallel control, was determined for the compounds alone and in combination. The significance of the differences between the "expected" response, calculated by simple addition of the responses from the individual tests, and the observed response when the combination was tested, were estimated by chi square. For the combination of K2CrO4 and NaN3, the response was significantly greater than expected suggesting a possible potentiation of mutagenesis. The opposite (a less-than-additive response) was found for the K2CrO4/EMS combination. Both effects were found to be dose related to the concentration of potassium chromate used. Toxicity of the compounds or their combinations to the bacteria could not explain the results.

Twenty-three rabbits were fed for 8 weeks with standard diet to which was added a 1.5% cholesterol supplement. After this the cholesterol supplement was discontinued, but 11 rabbits received a daily intraperitoneal injection of 20 micrograms of potassium chromate while the remaining 12 received distilled water. The aortas were examined after a further 30 weeks; their mean weight per unit length was 1.27 g (SE +/- 0.17) in the control group and 0.81 g (SE +/- 0.08) in the chromium treated group (t = 2.36; P < 0.05). The percentage area of intimal surface covered by plaques was 94.8% (SE +/- 1.7) and 62.6% (SE +/- 10.4), respectively (t = 3.53; P < 0.005), and the total cholesterol content per unit length of aorta was 729 mg/100 ml (SE +/- 44.0) and 457.8 mg/100 ml (SE +/- 117.1), respectively (t = 23; P < 0.05). The results show a significant effect of chromium on the regression of cholesterol-induced atherosclerotic plaques in rabbits.

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Inorganic Acids and Related Compounds/

Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist respirations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. Activated charcoal is not effective. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Do not attempt to neutralize, because of exothermic reaction. Cover skin burns with dry, sterline dressings after decontamination ... . /Ammonia and Related Compounds/

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Early intubation, at the first sign of upper airway obstruction, may be necessary. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W TKO. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid colume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Inorganic Acids and Related Compounds/

/SIGNS AND SYMPTOMS/ If ingested, violent gastroenteritis, severe circulatory collapse & toxic nephritis may ensue. ... /As may/ peripheral vascular shock ...

/SIGNS AND SYMPTOMS/ Eye contact can cause severe damage with possible loss of vision.

/GENOTOXICITY/ Evaluation of genotoxic effects of potassium chromate (K2CrO4) and cadmium chloride (CdCl2) was carried out in human blood lymphocytes in vitro as measured by the electron microscopy in situ end-labeling (EM-ISEL). EM-ISEL was used to assess DNA single-strand breaks (SSBs) expressed as number of immunogold particles per sq um of chromatin at both chromosomal and nuclear DNA levels. Human lymphocytes were cultured in supplemented RPMI medium for 72 hr including treatment for 2 hr with K2CrO4 (0-150 microM), CdCl2 (0-150 microM) or methyl methanesulfonate (500 microM) as a positive control. Quantification of SSBs by EM-ISEL showed that both compounds are genotoxic agents at non-cytotoxic concentrations. This study brings new information on the utility of EM-ISEL for the evaluation of genotoxicity and confirms the genotoxic effects induced by chromium and cadmium.

EC50; Species: Daphnia magna (Cladoceran) 19.2 and 7.39 ug/L as chromium for 48 and 96 hr, respectively; Both with a water hardness of 50 mg/L as calcium carbonate. Effect: immobilization.

LC50; Species: Physa heterostropha (snail); Conditions: static, water hardness as 171 mg/L as calcium carbonate; Concentration: 31,600 ug/L as chromium, unmeasured

EC50; Species: Chlorella vulgaris (Green Algae) Exponential Growth Phase, 5x10+4 cells/mL; Conditions: freshwater, static, 20 °C; Concentration: 548 ug/L for 96 hr; Effect: growth, increased whole organism size

EC50; Species: Chlorella vulgaris (Green Algae) Exponential Growth Phase, 5x10+4 cells/mL; Conditions: freshwater, static, 20 °C; Concentration: 414 ug/L for 96 hr; Effect: growth, increased whole organism volume

For more Ecotoxicity Values (Complete) data for POTASSIUM CHROMATE (10 total), please visit the HSDB record page.

/AQUATIC SPECIES/ 90 Days after hatching, young carp were reared for 75 wk in test waters of pH 7 and 5 containing 0.1 ppm potassium chromate. This pollutant caused deformation in the bone by chronic leaching of calcium, and the low pH hastened the leaching.

/AQUATIC SPECIES/ The coastal teleost species, Periophthalmus dipes, commonly known as the mudskipper, was exposed to three sublethal concentrations (5, 10 and 15 mg/L) of potassium chromate for three exposure durations (2, 4 and 6 days). The study compares the dose- and duration-dependent effects of Cr(VI), as potassium chromate, on the ATPase systems in various organs of this fish species. In this study, effects of Cr(VI) stress on total ATPase, (Na+,K+)-ATPase, (Ca+2)-ATPase, (Mg+2)-ATPase, (Ca+2, HCO3-)-ATPase and (Mg+2,HCO3-)-ATPase in gills, kidney and intestine were estimated. A general dose- and duration-dependent inhibitory trend was observed. However, it is evident that exposure duration is more important than dose in the inhibition of the activity of the enzymes. At some concentrations, initial stimulation of the activity of some enzymes were also noticed. However, maximum inhibition was observed in higher Cr(VI) concentrations exposed for the longest time. It is possible that this inhibition of the ATPases by Cr(VI) blocked the active transport system of the gill epithelial as well as chloride cells, glomerular and epithelial cells of the tubules and thus altered the osmoregulatory mechanism of the fish. It appears that this heavy metal ion alters the membrane permeability of the intestinal epithelial cells and other layer of cells by altering the activity of ATPases, resulting in a breakdown of the active transport mechanism needed for the absorption of nutrients, ions and metabolites.

The substance is very toxic to aquatic organisms. The substance may cause long-term effects in the aquatic environment. It is strongly advised not to let the chemical enter into the environment.

Using potassium chromate as the source for chromium, a BCF of 1.0 (based on chromium) was determined for the whole body of Salmo gairdneri (rainbow trout) over a 30 days duration period(1). According to a classification scheme(2), this BCF range suggests that bioconcentration in aquatic organisms is low(SRC).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 25,511 workers (5,985 of these are female) are potentially exposed to potassium chromate in the US(1).

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/

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D002, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

Product: Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Offer surplus and non-recyclable solutions to a licensed disposal company; Contaminated packaging: Dispose of as unused product.

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 POTASSIUM CHROMATE (11 total), please visit the HSDB record page.

49 633 64; Potassium chromate

Oxidizer Corrosive

Do not transport with food and feedstuffs.

Symbol: T, N; R: 49-46-36/37/38-43-50/53; S: 53-45-60-61; Note: 3

UN Hazard Class: 6.1; UN Pack Group: III