Disodium chromate

161.97

161.90000

231-889-5

6A49BO6K4M

1370

3085|3288

DTXSID7032056

C45887

Yellow orthorhombic crystals

28415000

80.3

-0.47520

Yellow Solid

2.72 g/cm³

792 °C

392ºC

Solubility in water, g/100ml at 20°C: 53 (good)

Store in a secure poison location. Store in tightly closed containers in a cool, well-ventilated area away from combustibles, organics, or other easily oxidized materials. Where possible, automatically transfer materials from drums or other storage containers to process containers. A regulated, marked area should be established where this chemical is handled, used, or stored in compliance with OSHA Standard 1910.1045.

Odorless

Bitter metallic taste

Aqueous solution is alkaline

Hygroscopic, forms tetra-, hexa- or decahydrates. Deliquescent in moist air|Heat of solution: -24.5 Btu/lb = -13.6 cal/g = -0.75X10+5 J/kg|In water, 48.8 wt% at 40 °C; 53.5 wt% at 60 °C; 55.8 wt% at 80 °C; 56.1 wt% at 100 °C|The substance is a strong oxidant and reacts with combustible and reducing materials.|For more Other Experimental Properties (Complete) data for SODIUM CHROMATE (6 total), please visit the HSDB record page.|Yellow, translucent efflorescent crystals; density: 1.483; melting point: 19.92 °C /Sodium chromate decahydrate/

Water soluble.

Salts, Basic

Strong Oxidizing Agent

SODIUM CHROMATE is a strong oxidizing agent. Incompatible with strong acids. (NTP, 1992). Contact with combustible materials may lead to fires. Toxic chromium oxide fumes may form in fire (USCG, 1999).

Corrosive because of oxidizing potency. /Chromate salts/

II

6.1

UN 3288 6.1/PG 2

3

45-46-60-61-21-25-26-34-42/43-48/23-50/53

53-45-60-61

GB2955000

T+,N

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

Stable under recommended storage conditions.

P201-P260-P273-P280-P304 + P340 + P310-P305 + P351 + P338

H301-H312-H314-H317-H330-H334-H340-H350-H360FD-H372-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/|Product: Offer surplus and non-recyclable solutions to a licensed disposal company. 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; Contaminated packaging: Dispose of as unused product.|Dissolved or soluble chromium cmpd in which the chromium is more than trivalent, thus chromate waste above all, must be reduced chemically and precipitated as chromium (III) hydroxide. The precipitated sludges must be compacted by partial dewatering to enable disposal and prevent degradation of waters and ground water. Normal standards for the introduction of electroplating waste water into the sewerage system tolerate a maximum of 2 mg of chromium per l of waste water, dissolved or undissolved. Where no central detoxification, neutralization, and sludge dewatering systems are available, these waste water treatment measures must be taken in the plants. To this end, chromate-containing wastes, baths, eluates, and semiconcentrates must be collected separately. Reduction to trivalent chromium is usually accomplished with the aid of sodium bisulfate in sulfuric acid soln (pH 2-3). Under certain circumstances, agents such as sulfur dioxide from waste gases or sulfite-containing liquids obtained from the scrubbing of waste gas, iron filings, brass or aluminum chips can be profitably used for reduction. The subsequent precipitation of the chromium is accomplished by alkalizing to pH 8-9; waste alkali soln or alkaline treated waste water, for example from cyanide detoxification, can be used here. The sludge is usually dewatered through a process of sedimentation in settling basins, decanting and pressing the thin sludge in chamber filter presses, insofar as it cannot be recycled. Depending on local conditions, the compacted sludge (residual water content 60-70%) is disposed of in SRP:/hazardous waste landfill/. Recommendable methods: Reduction, solidification, & landfill. Not recommendable methods: Discharge to sewer & thermal destruction. Peer-review: The filtrate should be diluted and discharged to sewer. Chromium containing sludges cannot be disposed of in incinerators, as the trivalent chromium is reoxidized to hexavalent chromium in the heat. (Peer-review conclusions of an IRPTC expert consultation (May 1985))|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 SODIUM CHROMATE (11 total), please visit the HSDB record page.

Incompatible materials: Strong reducing agents|A powerful oxidizer.|Aqueous solution in a base. A strong oxidizer. Violent reaction with reducing agents, combustibles, strong acids, organic materials.|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/

Sodium chromate is an indirect food additive for use only as a component of adhesives.

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]

Special Hazards of Combustion Products: Toxic chromium oxide fumes may form in fire. Behavior in Fire: May increase intensity of fire when in contact with combustible material (USCG, 1999)|Not combustible but enhances combustion of other substances.

|Danger|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|H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]|Aggregated GHS information provided by 711 companies from 12 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H300: Fatal if swallowed [Danger Acute toxicity, oral]|P201, P202, P260, P261, P264, P270, P271, P272, P280, P281, P284, P285, P301+P310, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P304+P341, P305+P351+P338, P307+P311, P308+P313, P310, P312, P314, P320, P321, P322, P330, P333+P313, P342+P311, P363, P403+P233, 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)

U.S. Bu. Mines approved respirator; rubber gloves; chemical safety goggles; rubber apron and sleeves, face shield, rubber shoes, protective clothing. (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 SODIUM CHROMATE (13 total), please visit the HSDB record page.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.|Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.|Extinguish fire using agent suitable for type of surrounding fire (material itself does not burn or burns with difficulty.)|If material involved in fire: Extinguish fire using agent suitable for type of surrounding fire (Material itself does not burn or burns with difficulty.) /Sodium chromate (Environmentally hazardous substances, liquid, N.O.S.); Sodium chromate (Environmentally hazardous substances, solid, N.O.S.); Sodium chromate (Toxic solids, organic, N.O.S.); Sodium chromate (Toxic liquid, inorganic, N.O.S.); Sodium chromate (toxic solid, inorganic, N.O.S.)/|For more Fire Fighting Procedures (Complete) data for SODIUM CHROMATE (7 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; 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.|Land Spill: Dig a pit, pond, lagoon, or 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./ Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash or cement powder. /Sodium chromate soln/|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. /Sodium chromate (Environmentally hazardous substances, solid, N.O.S.); Sodium chromate (Toxic liquid, inorganic, N.O.S.); Sodium chromate (Toxic solid, inorganic, N.O.S.)/|Environmental considerations: Land Spill: Dig a pit, pond, lagoon, holding area to contain liquid or solid material. Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash or cement powder. /Sodium chromate (Environmentally hazardous substances, liquid, N.O.S.)/|For more Cleanup Methods (Complete) data for SODIUM CHROMATE (10 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 SODIUM CHROMATE (12 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 ... .|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: complete protective clothing including self-contained breathing apparatus. Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.

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

A harmful concentration of airborne particles can be reached quickly when dispersed.

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/

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).

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: Sodium chromate forms yellow orthorhombic crystals. It is used in inks, dyeing, paint pigment, leather tanning, other chromates, and protection of iron against corrosion. (51)Chromium, as sodium chromate ((51)Cr), is used to label red blood cells so that red cell survival and red cell volume can be measured. HUMAN EXPOSURE AND TOXICITY: Eye contact can cause severe damage with possible loss of vision. A 51-year-old man committed suicide by ingesting a fatal dose of sodium chromate solution. He unexpectedly lost consciousness 6 hrs after the ingestion and died approximately 20.5 hrs later. The patient's death was assumed to have been caused by circulatory collapse due to internal bleeding and the direct toxicity of chromate compounds with hepatic malfunction and possibly disseminated intravascular coagulation. None of the results showed statistically significant differences that would suggest an excess risk for malignant neoplasms, particularly lung cancer, among workers engaged in the manufacture of chromate pigment in Japan. When tested in cultured human bronchial epithelial cells, it was found that 1, 2.5, 5 and 10 uM sodium chromate induced 66, 35, 0 and 0% relative survival, respectively. The amount of chromosome damage increased with concentration after 24 hr exposure to sodium chromate. Specifically, 1, 2.5 and 5 microM damaged 25, 34 and 41% of metaphase cells with the total amount of damage reaching 33, 59 and 70 aberrations per 100 metaphases, respectively. Ten micromolar sodium chromate induced profound cell cycle delay and no metaphases were found. In other experiment, cells exposed to 1 microM sodium chromate for 24, 48 and 72 hr induced 23, 13 and 17% damaged metaphases, respectively. ANIMAL STUDIES: Rats treated ip with sodium chromate(VI) at 2 mg/kg chromium 3 times per week for up to 60 days developed liver damage. In a study examining the effects of chromium(VI) on motor activity, no effects were noted in six rats provided with drinking water containing sodium chromate at 0.07 g/L chromium(VI). A significant decrease in motor activity was noted 7 days after six rats were provided with drinking water containing sodium chromate at 0.7 g/L chromium(VI) (p< 0.02), and 1 day after six rats were given a single intraperitoneal injection of sodium chromate at 2 mg/kg body weight chromium(VI) (p< 0.01). Sodium chromate gave positive results in Escherichia coli WP2 reverse mutation test. Sodium chromate gave positive (significant increases in chromatid breaks and fragments) results in cytogenetics testing in cultured Chinese hamster CHO cells at doses of 5 to 10x10-6 molar. Treatment of chick embryo hepatocytes with sodium chromate resulted in the rapid uptake of chromate and the induction of DNA lesions in a time and concn dependent manner. DNA interstrand cross links, strand breaks and DNA-protein cross links were observed after treatment of hepatocytes with chromate concn which did not affect cell viability. Treatment of Chinese hamster ovary cells with 150 and 300 uM sodium chromate (Na2CrO4) for 2 hr decreased colony-forming efficiency by 46 and 92%, respectively. These treatments induced dose-dependent internucleosomal fragmentation of cellular DNA beyond 24 hr after chromate treatment. ECOTOXICITY STUDIES: When tested in hawksbill sea turtle cells, concentrations of 0.25, 0.5, 1, 2.5, and 5uM sodium chromate induced 84, 69, 46, 25, and 3% relative survival, respectively. Sodium chromate induced 3, 9, 9, 14, 21, and 29% of metaphases with damage, and caused 3, 10, 10, 16, 26, and 39 damaged chromosomes in 100 metaphases at concentrations of 0, 0.25, 0.5, 1, 2.5, and 5uM sodium chromate, respectively. In medaka cells, concentrations of 1, 5 and 10 uM sodium chromate damaged 17, 32 and 43% of metaphases, respectively and these same concentrations 1, 2.5, 5 and 10 uM sodium chromate damaged 14, 24 and 49% of metaphases, respectively, in North Atlantic right whale lung cells and 11, 32 and 41% of metaphases, respectively, in North Atlantic right whale testes cells.

Sodium chromate consistently stimulated organic binding of iodine & thiocyanate oxidation, & potentiated effects of submaximal concn of thyroid-stimulating hormone on these processes, in bovine thyroid slices.|The effect of vitamin B2, which is capable of reducing chromium(VI) to chromium(V), on chromosomal aberrations and mutation caused by Na2CrO4 was investigated in Chinese hamster V79 cells. Pretreatment with 200 uM vitamin B2 (riboflavin) for 24 hr prior to exposure to Na2CrO4 (2.5-5 uM) resulted in an increase of metal-induced chromosomal aberrations and mutation at the HGPRT locus. These and other previous studies suggest that vitamin B2 enhances the clastogenic and mutagenic action of chromate compounds, through its ability to directly reduce chromium(VI) in cells.|The effect of vitamin E on chromosomal aberrations and mutation caused by Na2CrO4 was investigated in Chinese hamster V79 cells. Pretreatment with 25 uM alpha-tocopherol succinate (vitamin E) for 24 hr prior to chromate exposure (2.5-5 uM) resulted in a decrease of metal-induced chromosomal aberrations. Na2CrO4 (2.5-7.5 uM) induced mutations at the HGPRT locus, but only within a very limited concentration range. This mutagenic response could also be suppressed by pretreatment with vitamin E. These results suggest that vitamin E can protect cells from the clastogenic and mutagenic action of chromate compounds, possibly through its ability to scavenge chromium(V) and/or free radicals.|The effect of pretreatment with ascorbic acid (vitamin C) on chromate-induced DNA damage, cytotoxicity, and enzyme inhibition as well as on the cellular reduction of chromium(VI) was investigated using Chinese hamster V-79 cells. Cellular pretreatment with nontoxic levels of 1 mM ascorbic acid for 24 hr prior to exposure resulted in a significant increase (1.7-fold) in cellular levels of this vitamin. Alkaline elution assays demonstrated that this pretreatment decreased cellular levels of Na2CrO4-induced alkali-labile sites while the numbers of DNA-protein crosslinks produced by chromate increased. In colony-forming assays, pretreatment with ascorbic acid enhanced the cytotoxicity of chromate. However, the inhibition of glutathione reductase attributed to Na2CrO4 was attenuated by this pretreatment. Under the same experimental condition, the uptake of chromate in pretreated cells was found to increase. ESR studies revealed that cellular pretreatment with ascorbic acid reduced the level of chromium(V) intermediate and increased the level of chromium(III) complex, indicating that cellular reduction of chromium(VI) to chromium(III) was accelerated by this vitamin. These results suggest that ascorbic acid decreases chromate-induced alkali-labile sites and chromium inhibition of glutathione reductase, but it enhances DNA-protein cross-links and cytotoxicity caused by this metal through its ability to directly reduce chromium(VI).|For more Interactions (Complete) data for SODIUM CHROMATE (8 total), please visit the HSDB record page.

LD50 Rat ip 57 mg/kg|LD50 Mouse ip 32 mg/kg|LD50 Cat iv 164 mg/kg

/AQUATIC SPECIES/ ... the cytotoxic and clastogenic effects of Cr(VI) in human (Homo sapiens) and sperm whale (Physeter macrocephalus) skin fibroblasts /were compared/. ...Data show that increasing concentrations of both particulate /lead chromate/ and soluble /sodium chromate/ Cr(VI) induce increasing amounts of cytotoxicity and clastogenicity in human and sperm whale skin cells. Furthermore, the data show that sperm whale cells are resistant to these effects exhibiting less cytotoxicity and genotoxicity than the human cells. Differences in Cr uptake accounted for some but not all of the differences in particulate and soluble Cr(VI) genotoxicity, although it did explain the differences in particulate Cr(VI) cytotoxicity. Altogether, the data indicate that Cr(VI) is a genotoxic threat to whales, but also suggest that whales have evolved cellular mechanisms to protect them against the genotoxicity of environmental agents such as Cr(VI).|/AQUATIC SPECIES/ Toxic effects were studied in rainbow trout exposed to sodium chromate solution. When survival was used as the criterion, chromium was more toxic at pH 6.5 than at pH 7.8 at all life stages studied. For trout in the embryo through juvenile exposure study, the lowest concentrations increasing mortality were 0.2 mg/L at pH 6.5 and 2.0 mg/L at pH 7.8.|/AQUATIC SPECIES/ The survival of Rhithropanopeus harrisii larvae from hatching to first crab stage occurred in sodium chromate concentrations from 1.1 to 29.1 ppm. The estimated median lethal concentration (LC50) for complete zoeal development was 17.8 ppm sodium chromate and 13.7 ppm for development to first crab stage. A concentration of 1.1 ppm sodium chromate was nontoxic, whereas concentrations of 7.2 and 14.5 ppm were sublethal, with 29.1-58.1 ppm being acutely toxic.|/AQUATIC SPECIES/ Sea turtles are a charismatic and ancient ocean species and can serve as key indicators for ocean ecosystems, including coral reefs and sea grass beds as well as coastal beaches. Genotoxicity studies in the species are absent, limiting our understanding of the impact of environmental toxicants on sea turtles. Hexavalent chromium (Cr(VI)) is a ubiquitous environmental problem worldwide, and recent studies show it is a global marine pollutant of concern. Thus, we evaluated the cytotoxicity and genotoxicity of soluble and particulate Cr(VI) in hawksbill sea turtle cells. Particulate Cr(VI) was both cytotoxic and genotoxic to sea turtle cells. Concentrations of 0.1, 0.5, 1, and 5 ug/sq cm lead chromate induced 108, 79, 54, and 7% relative survival, respectively. Additionally, concentrations of 0, 0.1, 0.5, 1, and 5ug/sq cm lead chromate induced damage in 4, 10, 15, 26, and 36% of cells and caused 4, 11, 17, 30, and 56 chromosome aberrations in 100 metaphases, respectively. For soluble Cr, concentrations of 0.25, 0.5, 1, 2.5, and 5 uM sodium chromate induced 84, 69, 46, 25, and 3% relative survival, respectively. Sodium chromate induced 3, 9, 9, 14, 21, and 29% of metaphases with damage, and caused 3, 10, 10, 16, 26, and 39 damaged chromosomes in 100 metaphases at concentrations of 0, 0.25, 0.5, 1, 2.5, and 5uM sodium chromate, respectively. These data suggest that Cr(VI) may be a concern for hawksbill sea turtles and sea turtles in general.|For more Ecotoxicity Excerpts (Complete) data for SODIUM CHROMATE (7 total), please visit the HSDB record page.

Sodium chromate's use in drilling muds(1) will result in its direct release to the environment(SRC). About one metric ton of sodium chromate has been used annually in drilling muds for an average West Texas well to combat fatigue corrosion cracking of drill strings(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 80,015 workers (3,487 of these are female) were potentially exposed to sodium chromate in the US(1). Occupational exposure to sodium chromate may occur through inhalation of dust and particulates and dermal contact with this compound at workplaces where sodium chromate is produced or used(2).

(51)Chromium, as sodium chromate ((51)Cr) sterile solution, is used to label red blood cells so that red cell survival and red cell vol can be measured.|EXP THER The effects of food supplementation with sodium chromate at concentrations of 1-500 uM on development of Drosophila melanogaster larvae and food intake, carbohydrate and lipid pools in adult fruit flies were investigated. Food supplementation with hexavalent chromium (Na2CrO4) at high concentrations delayed larval development and decreased the percentage of larvae that pupated which indicated a relatively low toxicity. The supplement decreased glucose levels in fly hemolymph, but at concentrations of 5-25 uM increased fly carbohydrate reserves: hemolymph trehalose and whole body trehalose and glycogen. The data on parameters of carbohydrate metabolism show that chromate possesses some insulin-mimetic properties. The changes in metabolism of carbohydrates under chromate exposure were also accompanied by an increase in total lipid levels and in the portion of triacylglycerides among all lipids. Chromate addition to fly food did not affect male or female body mass, but reduced food consumption by females at all concentrations used, whereas in males only 500 uM chromate decreased food consumption. The data show that: (1) Cr(6+) has many of the same effects as Cr(3+) suggesting that it might be just as effective to treat diabetic states, likely as a result of intracellular reduction of Cr(6+) ions, and (2) the Drosophila model can be used to develop new approaches to investigate the molecular mechanisms of chromium as an insulin-mimetic. Although it is usually believed that hexavalent chromium possesses higher toxicity than the trivalent ion, due to its easier penetration into the cell, application of hexavalent chromium may substantially decrease the chromium doses needed to get the desired effects.

When injected intravenously into rats, sodium chromate(VI) accumulates in the kidneys and later in the spleen.|(51)Chromium labelled sodium, zinc and lead chromates were studied. Sodium chromate and the less soluble zinc chromate were absorbed into the blood, resulting in increased urinary excretion of chromium. ... The less water soluble the chromate, the higher was its elimination via the feces. Absorbed chromium was retained in the spleen and bone marrow in all three cases, and also in the liver and kidneys in the case of sodium chromate. Chromium levels in blood and urine are not indicative of inhalation exposure to insoluble chromates.|Percutaneous absorption of labelled sodium chromate occurred in guinea pigs: a maximum of 4% of the dose applied on the skin disappeared within 5 hours, and labelled chromium was detected in a number of organs.|Following intratracheal administration of sodium chromate solution to rabbits, about 45% (as Cr) remained in the lungs 4 hours after instillation; 15% was excreted in urine. The highest concentration of chromium (IV) was reached in red cells after about 3 hours, and the corresponding plasma concentration at that time was about one-third of that in red cells.|For more Absorption, Distribution and Excretion (Complete) data for SODIUM CHROMATE (8 total), please visit the HSDB record page.

Hexavalent chromium, as sodium chromate in an aq soln, was reduced rapidly to trivalent chromium in the presence of glutathione (0.3-3.0 mM). Such glutathione-dependent redn of hexavalent chromium can take place in the cytosolic space of hexavalent chromium exposed cells, since glutathione is found in reactive concn in this compartment.|The capacity of glutathione (GSH) to reduce Cr(VI) to Cr(III) in vitro was investigated. The reaction was determined spectrophotometrically by following the absorption of Cr(VI) at 370 nm. At stoichiometric conditions (molar ratio Cr(VI)/GSH of 1:3) the reduction was strongly dependent on the solution's pH. It was much slower at pH 7.4 than at pH values below 5. An excess of GSH (100- or 1000-fold) accelerated the reaction. In any case, 3 GSH molecules were required to reduce 1 molecule of chromate. Incubation of human red blood cells (RBC) with an excess of Na2CrO4 (10 mM) decreased the GSH content of the cells to 10% of the original amount. This depletion of GSH was similar to that obtained when RBC were incubated with 62 mM diethylmaleate (DEM), a well known GSH depleting agent. Sephadex G-100 chromatography of lysates from human RBC incubated with radioactive chromate (51)Cr(VI] showed a strong affinity of (51)Cr for hemoglobin: 97% of the applied dose was bound to hemoglobin whilst only minor amounts of (51)Cr were found in the low-molecular fractions. However, incubations of prepared lysates (as opposed to intact cells) with 10 mM Na2 (51)CrO4 markedly raised the chromium content of low-molecular fractions (probably GSH-Cr-complexes), probably indicative of a role of GSH in the intra-cellular reduction of Cr(VI) to Cr(III), the latter being regarded as the ultimately toxic species of this metal.|Comparative metabolic fate of labelled chromium chloride and sodium chromate and interaction of these compounds in the rat liver and blood were investigated after their oral and intravenous administration. Gastrointestinal absorption of both compounds was below 1% of the oral dose, but trivalent chromium showed higher radioactivity than the hexavalent form in rats (biological half-life: CrCl3 91.79 days, Na2CrO4 22.24 days). The higher residual activity of the trivalent chromium was also observed after intravenous administration. Both forms of chromium were excreted more in the urine via the kidney than in the intestinal tract after intravenous administration. When (51)CrCl3 and Na2(51)CrO4 were injected into rats, in the time-distribution patterns of( 51)Cr in the organs, a significant difference was shown between oxidation states of the two compounds, especially in subcellular fractions of the liver and blood constituents. This significant difference mainly observed in the rat blood came from the fact that trivalent chromium possessed a high binding activity for transferrin in plasma, while hexavalent chromium was permeable into red cells and bound with hemoglobin.

/Rats were treated/ with (51)Cr labeled sodium chromate or chromium chloride by gavage or intravenous injection and found that, regardless of the route, (51)Cr from chromium(VI) was excreted more rapidly through the urine and feces than was (51)Cr from chromium(III). Following oral administration, the biologic half-life was 22.24 days for sodium chromate and 91.79 days for chromium chloride.|Gastrointestinal absorption of both compounds was below 1% of the oral dose, but trivalent chromium showed higher radioactivity than the hexavalent form in rats (biological half-life: CrCl3 91.79 days, Na2CrO4 22.24 days).|... Gastrointestinal absorption of /chromium chloride and sodium chromate/ was below 1% of the oral dose, but trivalent chromium showed higher radioactivity than the hexavalent form in rats (biological half-life: CrCl3 91.79 days, Na2CrO4 22.24 days). ...

The reduction of hexavalent chromium Cr(VI) in isolated liver mitochondria was studied under different redox conditions in the respiratory chain. With 25 uM sodium chromate the rates were 1.6 + or - 0.7, 13.9 + or - 0.6 and 12.7 + or - 0.7 nmole Cr(VI) reduced 15 min/mg protein with the electron transport chain oxidized, reduced and only complex 1 reduced, respectively. Electrons from succinate, bypassing complex 1, were apparently unavailable for Cr(VI) reduction. The kinetics of chromate reduction was studied with only complex 1 in a reduced state. A rapid and a slow phase were found, probably corresponding to different electron donors in the mitochondria. Blocking the free thiols with N-ethylmaleimide led to less than 10% decrease in the rapid initial Cr(VI) reduction and to about 20% decrease during the whole incubation period (15 min). The amounts of free thiols were moderately decreased (15%) in chromate treated mitochondria during the slow reduction of Cr(VI). Only SH-groups may thus participate as reductants during the slow reduction phase. The respiration rate was inhibited about 50% by 25 uM sodium chromate when the mitochondria oxidized NAD-linked substrates. In contrast, succinate stimulated respiration was inhibited 50% by 3.6 mM sodium chromate. The observed inhibition with sodium chromate in the micromolar range was therefore probably localized at complex 1 and may be coupled to the reduction of Cr(VI) at the same place. The respiration of isolated hepatocytes was also affected by sodium chromate. Five micromolar chromate caused 5-10% inhibition. The inhibitory action of chromate on the mitochondrial respiration may thus constitute an important cytotoxic mechanism.

Inhalation causes irritation and may ulcerate mucous membranes; continued irritation of the nose may lead to perforation of the septum. Ingestion causes severe circulatory collapse and toxic nephritis; may be fatal. Contact with eyes causes severe irritation and possible conjunctivitis. Irritates skin and can cause ulcers; if skin is broken, prolonged contact may cause ``chrome sores'' (slow-healing, hard-rimmed ulcers), which leave the area vulnerable to infection as a secondary effect. (USCG, 1999)|Carcinogens

INHALATION: remove victim to fresh air; get medical attention. INGESTION: get immediate medical help; if vomiting is not spontaneous, give an emetic such as soapy water followed by copious water intake. EYES: immediately flush with plenty of water for at least 15 min.; consult physician promptly. SKIN: immediately flush with plenty of water for at least 15 min.; persistent dermatitis should be referred to a physician; wash contaminated skin or clothing until chromate color disappears. (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 if 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. /Poisons A and B/|Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W 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. Watch for signs of fluid overload ... . Treat seizures with diazepam (Valium) or lorazepam (Ativan) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/|/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR 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/|For more Antidote and Emergency Treatment (Complete) data for SODIUM CHROMATE (6 total), please visit the HSDB record page.

/SIGNS AND SYMPTOMS/ A corrosive. Eye contact can cause severe damage with possible loss of vision.|/CASE REPORTS/ An interesting case of acute poisoning by chromate compounds is reported. A 51-year-old man committed suicide by ingesting a fatal dose of sodium chromate solution. He unexpectedly lost consciousness 6 hr after the ingestion and died approximately 20.5 hr later. An examination of the blood showed noticeable hepatic damage and thrombocytopenia. The postmortem examination revealed extensive bleeding in the alimentary tract and a severe hepatic lesion due to hepatocellular necrosis. However, the renal disorder was unusually light in the microscopic and clinical findings. Moreover, the renal lesion was observed mainly in the distal tubules instead of the proximal tubules which is more typical in cases of acute poisonings by diverse heavy metals including chromium. The patient's death was assumed to have been caused by circulatory collapse due to internal bleeding and the direct toxicity of chromate compounds with hepatic malfunction and possibly disseminated intravascular coagulation (DIC).|/CASE REPORTS/ A 29-year-old male welder reported systemic reactions after exposure to chromium. Inhalation challenge testing to 29 ug/cu m of sodium chromate aerosol resulted in late appearing systemic urticaria, angioedema, and severe bronchospasm that occurred at the same time as a threefold rise in plasma histamine. A direct leukocyte inhibitory factor test to 5.5 X 10(-6)mol/L Na2CrO4 was positive. Although the mechanism of this reaction is unknown, the positive leukocyte inhibitory factor and the general acceptance of hexavalent chromium as a contact skin sensitizer suggest that cell-mediated mechanisms could be involved.|/SURVEILLANCE/ In 1975, five manufacturers of chromate pigment in Japan were examined in a study of the carcinogenicity of chromates. These companies were producing lead chromate, zinc chromate, molybdate orange and/or strontium chromate. The current study covers a cohort of 666 workers involved in the manufacture of chromate pigment for at least 1 year between 1950 and 1975. The workers were followed up for 15-40 years, until 1989. Many previous reports have found an excess lung cancer risk among workers involved in the manufacture of chromate pigments and chromate chemicals. In the current study, subjects were classified on the basis of years worked, years of observation, characteristics of company, type of work engaged in for the longest period of time, and involvement in the manufacture of zinc chromate. Mortality was compared with that of all Japanese males by means of the person-year method. The route of exposure was primarily inhalation through the respiratory system. None of the results showed statistically significant differences that would suggest an excess risk for malignant neoplasms, particularly lung cancer, among workers engaged in the manufacture of chromate pigment in Japan.|For more Human Toxicity Excerpts (Complete) data for SODIUM CHROMATE (13 total), please visit the HSDB record page.

Chromitope Sodium

The substance can be absorbed into the body by inhalation of its aerosol, 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.

Technical-grade anhydrous sodium chromate available from one USA company has the following typical analysis: purity, 99.5%; sulfates (as sodium sulfate), 0.41%; chlorides (as sodium chloride), 0.02%; vanadium (as V), less than 0.001%; and water insoluble materials, less than 0.01%. Sodium chromate was also available as a chemically pure grade, as the tetrahydrate and in solutions. It is available in Japan in two grades, with 99.0 and 99.9% purity.|Grade: Pure neutral, highest purity, technical, CP, reagent

Chromic acid (H2CrO4), sodium salt (1:2): ACTIVE|R - indicates a substance that is the subject of a TSCA section 6 risk management rule.

Simultaneous analysis of ascorbic acid and chromium (VI) in soluble fractions and bronchoalveolar lavage fluids of rat lungs treated with sodium chromate in vitro and in vivo was performed by anion-exchange high-performance liquid chromatography coupled to a photodiode-array detector. Absorbances at 265 and 370 nm were used for the determination of ascorbic acid and chromium (VI), respectively. The calibration graphs of standard solutions were linear in the test ranges of ascorbic acid and chromium (VI) (below 10 and 8 ppm, respectively). The detection limits of ascorbic acid and chromium (VI) were 1 and 0.5 ng, respectively. The recovery of ascorbic acid from lung tissues homogenized at pH 7.4 was 99%, and that of chromium (VI) was 96%, when tissues were homogenized under alkaline conditions (pH 11.4). Using this method, ascorbic acid levels in the soluble fractions and lavage fluids of normal rat lungs were determined. In the lung of a rat intratracheally injected with a saline solution of sodium chromate, ascorbic acid decreased to 80% of the normal level, and ca. 90% of the chromium (VI) was reduced within 4 min after injection, indicating that the ascorbic acid-related reduction of chromium (VI) is very rapid. The present method will be useful for studies of the reduction of chromium (VI) by ascorbic acid in biological systems.

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