Dipotassium chromate (K2CrO4)

194.19

193.84800

232-140-5

5P0R38CN2X

1770

3085|3288|9142

DTXSID8064858

C45889

Yellow orthorhombic crystals|Lemon-yellow crystals

28415000

80.26000

-0.47520

Yellow Solid

2.73 g/cm³

975 °C

1000°C

Index of refraction: beta 1.74

H2O: 640 g/L (20 ºC)

2-8°C

Zero

6.7 (vs air)

Odorless

Disagreeable bitter taste

Aqueous solution is alkaline to litmus or phenolphthalein

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

Soluble in water.

Salts, Basic

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.

Corrosive

III

5.1

UN 3288 6.1/PG 3

3

49-46-43-51/53-8-50/53-36/37/38-22-45-52/53-25-42/43-20

53-45-60-61-36/37-26-23

GB2940000

T,N,O

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.

Stable. Strong oxidizing agent - contact with combustible materials may lead to fire or violent reaction. Incompatible with strong reducing agents, combustible materials.

P201-P273-P280-P301 + P310 + P330-P304 + P340 + P312-P308 + P313

H301-H315-H317-H319-H335-H340-H350i-H410

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.

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/

DHHS/ATSDR; Toxicological profile for chromium (September 2012).[DHHS/ATSDR; Toxicological profile for chromium (September 2012); Available from, as of February 8, 2016: ww.atsdr.cdc.gov/toxprofiles/tp7.pdf]

Behavior in Fire: May increase intensity of fire if in contact with combustible materials. Cool containers and spilled material with plenty of water. (USCG, 1999)|Not combustible but enhances combustion of other substances.

|Danger|H315: Causes skin irritation [Warning Skin corrosion/irritation]|P201, P202, P261, P264, P271, P272, P273, P280, P281, P302+P352, P304+P340, P305+P351+P338, P308+P313, P312, P321, P332+P313, P333+P313, P337+P313, P362, P363, P391, P403+P233, P405, and P501|H315 (99.83%): Causes skin irritation [Warning Skin corrosion/irritation]|Aggregated GHS information provided by 589 companies from 17 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H301: Toxic if swallowed [Danger Acute toxicity, oral]|P201, P202, P260, P261, P264, P270, P271, P272, P273, P280, P281, P284, P285, P301+P310, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P304+P341, P305+P351+P338, P308+P313, P310, P312, P314, P320, P321, P322, P330, P333+P313, P342+P311, P363, P391, P403+P233, P405, and P501|P201, P202, P261, P264, P270, P271, P272, P273, P280, P281, P301+P310, P302+P352, P304+P340, P305+P351+P338, P308+P313, P312, P321, P330, P332+P313, P333+P313, P337+P313, P362, P363, P391, P403+P233, P405, and P501|P201, P202, P260, P261, P264, P270, P272, P273, P280, P281, P285, P301+P310, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P304+P341, P305+P351+P338, P307+P311, P308+P313, P310, P314, P321, P330, P333+P313, P342+P311, P363, P391, P405, and P501|H314: Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]|P201, P202, P260, P261, P264, P272, P280, P281, P285, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P304+P341, P305+P351+P338, P308+P313, P310, P321, P333+P313, P342+P311, P363, P405, and P501

Excerpt from ERG Guide 140 [Oxidizers]: As an 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 car or tank truck 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. (ERG, 2016)

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. Following product recovery, flush area with water. (ERG, 2016)

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.

Non-combustible

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/

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.

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.

Irritation of nose, throat, and bronchial tubes can occur, with cough and/or wheezing. Skin contact can cause severe irritation, deep ulcers, or an allergic skin rash.|Chromic acid mist & chromate dusts may cause severe irritation of the nose, throat, bronchial tubes, and lung. /Chromic acid mist & chromate dusts/

Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 1 mg/cu m. /Chromium metal and insoluble salts, as Cr/|Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 0.5 mg/cu m. /Chromium(II) compounds, as Cr/|Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 0.5 mg/cu m. /Chromium(III) compounds, as Cr/|Permissible Exposure Limit: Table Z-2 Acceptable Ceiling Concentration: 1 mg/10 cu m. /Chromic acid and chromates (as CrO3)/

Recommended Exposure Limit: 8-hour Time-Weighted Average: 0.5 mg Cr/cu m. /Chromium metal, chromium(II) and chromium(III) compounds/|Recommended Exposure Limit: 8-hour Time-Weighted Average: 0.0002 mg Cr(VI)/cu m. NIOSH considers all Cr(VI) compounds (including chromic acid, tert-butyl chromate, zinc chromate, and chromyl chloride) to be potential occupational carcinogens. /All hexavalent chromium (Cr(VI) compounds/|NIOSH usually recommends that occupational exposures to carcinogens be limited to the lowest feasible concentration. /Chromic acid and chromates/

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.

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.

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.

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.

... Substances for which a Federal Register notice has been published that included consideration of the serious health effects, including cancer, from ambient air exposure to the substance. Chromium is included on this list. /Chromium/|Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Chromium compounds is included on this list. /Chromium compounds/

D002; A waste containing potassium chromate may (or may not) be characterized a hazardous waste following testing for corrosivity characteristics as prescribed by the Resource Conservation and Recovery Act (RCRA) regulations.|D007; A 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/

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 10 lb or 4.54 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV.D.3.b).

D002; A solid waste containing potassium chromate may become characterized as a hazardous waste when subjected to testing for corrosivity as stipulated in 40 CFR 261.22, and if so characterized, must be managed as a hazardous waste.|D007; A 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/

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.

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.

LD50 Mouse oral 180 mg/kg|LD50 Mouse ip 32 mg/kg|LD50 Rabbit intramuscular 11 mg/kg

/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.

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).

Chromium compounds are known to be associated with cytotoxicity and carcinogenicity when applied via a skin route. The aim of this study was to evaluate the skin permeability and toxicological profiles of four chromium species. Chromium permeation across the skin, as determined by an in vitro Franz cell, decreased in the order of sodium chromate>potassium chromate>potassium dichromate>chromium nitrate. The uptake of chromium species within the skin generally showed a contrary trend to the results of permeation, although differences among the various compounds were not large. Levels of in vivo skin deposition of the four compounds showed no statistically significant differences. Potassium chromate produced the greatest disruption of the skin structure as determined by HE staining, followed in order by sodium chromate, potassium dichromate, and chromium nitrate. This indicates that hexavalent chromium elicited greater toxicity to the skin compared to trivalent chromium. A similar result was observed for the viability of skin fibroblasts. To improve our understanding of the molecular mechanisms leading to functional changes in proteins, proteomic tools, including 2-DE and MS techniques combined with sequence database correlations, were applied to identify target proteins altered by pathologic states. Eight protein spots, corresponding to cutaneous enzymes involved in energy metabolism and chaperon proteins, which were identified and discussed in this study, were associated with skin cytotoxicity, immunity, and carcinogenesis. In addition, functional proteomics of skin tissues may provide a promising tool for developing therapeutic strategies and can serve as the basis for further research.|After exposure of growing chicks to different concentrations of dietary chromium (Cr) as potassium chromate (K2CrO4) for a period of 3 wk, the Cr uptake by different internal organs was determined. More Cr was accumulated in the kidney, liver, pancreas and spleen than in the blood, muscle, heart and lung. A very small amount was found in the brains of the birds given different concentrations of Cr.

Inhalation causes local irritation of mucous membranes; continuing nose irritation can result in perforation of nasal septum. Ingestion may cause violent gastroenteritis, circulatory collapse, vertigo, coma, and toxic nephritis; ingestion of excessive quantities can be fatal. Contact with eyes causes severe irritation and conjunctivitis. Repeated or prolonged exposure to dust, mist, or solutions may cause dermatitis; contact with breaks in the skin may cause ``chrome sores'' appearing as slow-healing, hard-rimmed ulcers which leave the area vulnerable to infection. (USCG, 1999)|Carcinogens, Mutagens

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)

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.

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.|/GENOTOXICITY/ We are trying to understand individual differences in susceptibility to chromate toxicity by comparing three different lymphoblastic cell lines derived from three different individuals. We have compared the uptake of CrO4(2-), the release of LDH from cells, the proliferation ability of the cells, and the DNA-protein crosslinks in these lymphoblastic cell lines exposed to chromate. We report here that one lymphoblastic cell line, GM0922B, appears to be considerably less sensitive than the other two cells lines to the cytotoxic effects of hexavalent chromium. The diminished sensitivity is almost twofold and can be accounted for by the decreased uptake of hexavalent chromium, which results in less lactate dehydrogenase release, and greater tolerance to chromate inhibition of cell proliferation and less DNA-protein crosslinking. This lower uptake of chromate combined with interindividual differences in extracellular Cr(VI) reducing capacity are probably the two most important determinants of genetic susceptibility to chromate toxicity. /Hexavalent chromium/|For more Human Toxicity Excerpts (Complete) data for POTASSIUM CHROMATE (11 total), please visit the HSDB record page.

bipotassium chromate

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

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

Redness. Pain. Skin burns.

Redness. Pain. Blurred vision. Severe deep burns.

Analytical reagent-grade potassium chromate (crystals) is available at a purity of 99.0%.

Chromic acid (H2CrO4), potassium salt (1:2): ACTIVE|R - indicates a substance that is the subject of a TSCA section 6 risk management rule.|... /potassium chromate/ has been supplanted nearly completely by the cheaper sodium chromate and is used only for very specific purposes such as in the photographic industry.

Health Hazards -> Carcinogens, Mutagens