Sodium Dichromate

H272: May intensify fire; oxidizer [Danger Oxidizing liquids; Oxidizing solids]

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

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

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

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

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

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

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

H350: May cause cancer [Danger Carcinogenicity]

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

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

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, P210, P220, 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, P370+P378, P391, P403, P403+P233, P405, and P501 (click each P-code to see the statement)

This chemical does not meet GHS hazard criteria for < 0.1% (1 of 2584) of reports.

H272 (98.5%): May intensify fire; oxidizer [Danger Oxidizing liquids; Oxidizing solids]

H301 (> 99.9%): Toxic if swallowed [Danger Acute toxicity, oral]

H312 (98.5%): Harmful in contact with skin [Warning Acute toxicity, dermal]

H314 (> 99.9%): Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]

H317 (> 99.9%): May cause an allergic skin reaction [Warning Sensitization, Skin]

H330 (> 99.9%): Fatal if inhaled [Danger Acute toxicity, inhalation]

H334 (> 99.9%): May cause allergy or asthma symptoms or breathing difficulties if inhaled [Danger Sensitization, respiratory]

H340 (> 99.9%): May cause genetic defects [Danger Germ cell mutagenicity]

H350 (99.1%): May cause cancer [Danger Carcinogenicity]

H360 (94%): May damage fertility or the unborn child [Danger Reproductive toxicity]

H372 (98.5%): Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]

H400 (> 99.9%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

H410 (> 99.9%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

Aggregated GHS information provided per 2584 reports by companies from 24 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Reported as not meeting GHS hazard criteria per 1 of 2584 reports by companies.

There are 23 notifications provided by 2583 of 2584 reports by companies with hazard statement code(s).

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.

P203, P280, P318, P405, and P501 (click each P-code to see the statement)

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

H311: Toxic in contact with skin [Danger Acute toxicity, dermal]

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

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

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, P262, P264, P264+P265, P270, P271, P272, P280, P284, P301+P316, P301+P330+P331, P302+P352, P302+P361+P354, P304+P340, P305+P354+P338, P308+P316, P316, P317, P318, P319, P320, P321, P330, P333+P317, P342+P316, P361+P364, P362+P364, P363, 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 .

INGESTION: have victim drink water or milk; do NOT induce vomiting; call a doctor.

SKIN OR EYE CONTACT: treat like acid burns; flush eyes with water for at least 15 min.; external lesions can be scrubbed with a 2% solution of sodium thiosulfate. (USCG, 1999)

Excerpt from ERG Guide 141 [Oxidizers - Toxic]:

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: 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. /Sodium Dichromate Dihydrate/

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary. /Sodium Dichromate Dihydrate/

Use water spray to cool unopened containers. /Sodium Dichromate Dihydrate/

Use flooding amount of water. Extinguish fire using agent suitable for types of surrounding fire (material itself does not burn or burn with difficulty). Use water in flooding quantities as fog. Cool all affected containers with flooding quantities of water. Apply water from as great a distance as possible. /Chromic acid solution/

For more Fire Fighting Procedures (Complete) data for SODIUM DICHROMATE (6 total), please visit the HSDB record page.

Excerpt from ERG Guide 141 [Oxidizers - Toxic]:

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. (ERG, 2024)

Personal protection: complete protective clothing including self-contained breathing apparatus. Do NOT let this chemical enter the environment. Sweep spilled substance into covered non-combustible containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations. Do NOT absorb in saw-dust or other combustible absorbents.

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: Sweep up and shovel. Contain spillage, and then collect with an electrically protected vacuum cleaner or by wetbrushing and place in container for disposal according to local regulations. Keep in suitable, closed containers for disposal. /Sodium Dichromate Dihydrate/

Cr(VI) cmpd in waste sludge are completely removed by redn by carbon at 600 °C. /Chromium VI/

Persons not wearing protective equipment and clothing should be restricted from areas of spills until cleanup has been completed. If chromic acid or chromates are spilled, the following steps should be taken: 1. Ventilate area of spill. 2. Collect spilled material in the most convenient and safe manner and deposit in sealed containers for reclamation or for disposal in a secured sanitary landfill. Liquid containing chromic acid or chromates should be absorbed in vermiculite, dry sand, earth, or a similar material. /Chromic acid and chromates/

PRECAUTIONS FOR "CARCINOGENS": A high-efficiency particulate arrestor (HEPA) or charcoal filters can be used to minimize amt of carcinogen in exhausted air ventilated safety cabinets, lab hoods, glove boxes or animal rooms ... Filter housing that is designed so that used filters can be transferred into plastic bag without contaminating maintenance staff is avail commercially. Filters should be placed in plastic bags immediately after removal ... The plastic bag should be sealed immediately ... The sealed bag should be labelled properly ... Waste liquids ... should be placed or collected in proper containers for disposal. The lid should be secured & the bottles properly labelled. Once filled, bottles should be placed in plastic bag, so that outer surface ... is not contaminated ... The plastic bag should also be sealed & labelled. ... Broken glassware ... should be decontaminated by solvent extraction, by chemical destruction, or in specially designed incinerators. /Chemical Carcinogens/

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: Burn in a chemical incinerator equipped with an afterburner and scrubber but exert extra care in igniting as this material is highly flammable. 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. /Sodium Dichromate Dihydrate/

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.

The following wastewater treatment technology has been investigated for chromium: Concentration process: Biological Treatment. /Chromium/

For more Disposal Methods (Complete) data for SODIUM DICHROMATE (15 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. /Sodium Dichromate Dihydrate/

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. Keep away from sources of ignition - No smoking. Keep away from heat and sources of ignition. /Sodium Dichromate Dihydrate/

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

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. /Sodium Dichromate Dihydrate/

For more Preventive Measures (Complete) data for SODIUM DICHROMATE (20 total), please visit the HSDB record page.

Excerpt from ERG Guide 141 [Oxidizers - Toxic]:

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.

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

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

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

Keep container tightly closed in a dry and well-ventilated place. Storage class (TRGS 510): Oxidizing hazardous materials /Sodium Dichromate Dihydrate/

PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practical to lab in which carcinogens are to be used, so that only small quantities required for ... expt need to be carried. Carcinogens should be kept in only one section of cupboard, an explosion-proof refrigerator or freezer (depending on chemicophysical properties ...) that bears appropriate label. An inventory ... should be kept, showing quantity of carcinogen & date it was acquired ... Facilities for dispensing ... should be contiguous to storage area. /Chemical Carcinogens/

0.015 [mg/m3]

0.61 [mg/m3]

3.7 [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 SODIUM DICHROMATE (11 total), please visit the HSDB record page.

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

(as Cr): 0.005 mg/m

(inhalable fraction): skin absorption (H); sensitization of skin (SH); carcinogen category: 1; germ cell mutagen group: 2

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.

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.

Approved dust mask; protective gloves; goggles or 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). /Sodium Dichromate Dihydrate/

Skin protection: Handle with gloves. /Sodium Dichromate Dihydrate/

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. /Sodium Dichromate Dihydrate/

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). /Sodium Dichromate Dihydrate/

For more Personal Protective Equipment (PPE) (Complete) data for SODIUM DICHROMATE (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.

Sodium dichromate appears as a red or red-orange crystalline solid. May be strongly irritating to skin, eyes and mucous membranes. Used as a corrosion inhibitor, and in the manufacture of other chemicals.

CBI; Other Solid; Liquid; Other Solid; Large Crystals; Liquid; Liquid

Red to orange hygroscopic solid; Soluble in water; [ICSC] Dark red aqueous solution; Deliquescent; [CAMEO]

RED-TO-ORANGE HYGROSCOPIC CRYSTALS.

Light-brown to orange-red plates which are strongly hygroscopic

Monoclinic prisms

Red or red-orange crystalline solid

Red hydroscopic crystals

Odorless

400 °C (decomposes)

675 °F (USCG, 1999)

356.7 °C

Solubility in water: 77.09 wt% at 40 °C; 82.04 wt% at 60 °C; 88.39 wt% at 80 °C

In water, 187 g/100 g water at 25 °C

In water, 70.6 wt% at 0 °C; 73.18 wt% at 20 °C

513.2 g/L methanol at 19.4 °C

Solubility in water, g/100ml at 20 °C: 236 (very good)

2.35 at 77 °F (USCG, 1999) - Denser than water; will sink

2.52 g/cu cm at 13 °C

Bulk density: 1 g/cu cm; heat of solution: -33.5 kJ/kg

Density: 2.35 g/cu cm /Sodium chromate dihydrate/

2.5 g/cm³

2.35 @ 13°C

Stable under recommended storage conditions. /Sodium Dichromate Dihydrate/

Considered stable

Not flammable (USCG, 1999)

Decomposition at about 400 °C

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

Corrosive because of oxidizing potency. /Chromate salts/

Solutions are acidic, pH of 1% soln 4.0 and pH of 10% soln 3.5.

Becomes anhydrous on prolonged heating at about 100 °C

Decomposes above 400 °C with the formation of sodium monochromate(VI), chromium(III) oxide, and oxygen

Powerful oxidizing agent

Mol wt: 298.00; red, monoclinic prism; loses 2 water at 100 °C; insol in alcohol; solubility: 180 g/100 cc cold water & 433 g/100 cc at 98 °C; index of refraction: 1.661, 1.699, 1.751 /Dihydrate/

Orange-red crystals /Sodium dichromate dihydrate/

Metals -> Chromium Compounds, Inorganic

Carcinogens

Reactive agents - 1st degree

Deliquescent. Soluble in water.

Salts, Basic

Oxidizing Agents, Strong

Strong Oxidizing Agent

SODIUM DICHROMATE 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). The well known "chromic acid mixture" of dichromate and sulfuric acid with organic residue led to violent exothermic reaction. This mixture in combination with acetone residue also led to violent reaction. The combination of the dichromate and sulfuric acid with alcohols, ethanol and 2-propanol, led to violent exothermic reaction. Because of the occurrence of many incidents involving the dichromate-sulfuric acid mix with oxidizable organic materials, it is probably best to avoid such interactions. The combination of the dichromate with hydrazine is explosive (one may expect the reaction of the dichromate to be vigorous with amines in general), [Mellor, 1943, Vol. 11, 234]. The addition of the dehydrated dichromate salt to acetic anhydride led to an exothermic reaction which eventually exploded. An induction period proceeded the explosion event [Bretherick, 5th Ed., 1995]. Boron, silicon, and dichromates form pyrotechnic mixtures. A mixture of acetic acid, 2-methyl-2-pentenal and the dichromate led to a runaway reaction and eruption of the reactor contents, [J. Haz. Mat., 1987, 233-239].

Incompatible materials: Strong reducing agents, alcohols. /Sodium Dichromate Dihydrate/

Addition of the dihydrated salt to acetic anhydride caused an exothermic reaction which accelerated to explosion. Presence of acetic acid (including that produced by hydrolysis of the anhydride by the hydrate water) has a delaying effect on the onset of violent reaction, which occurs when the proportion of anhydride to acid (after hydrolysis) exceeds 0.37:1, with an initial temperature above 35 °C. Mixtures of dichromate (30 g) with mixtures of anhydride-acid (70 g, to give ratios of 2:1, 1:1, 0.37:1) originally at 40 °C accelerated out of control after 18, 43 & 120 min, to 160, 155 & 115 °C, respectively.

During preparation of acetic acid by acid dichromate oxidation of ethanol according to a published procedure, minor explosions occurred on two occasions after refluxing had been discontinued.

A powerful oxidizer. Potentially explosive reaction with acetic anhydride, ethanol + sulfuric acid + heat, hydrazine. Violent reaction or ignition with boron + silicon (pyrotechnic), organic residues + sulfuric acid, 2-propanol + sulfuric acid, sulfuric acid + trinitrotoluene. Incompatible with hydroxylamine.

For more Hazardous Reactivities and Incompatibilities (Complete) data for SODIUM DICHROMATE (8 total), please visit the HSDB record page.

IDENTIFICATION AND USE: Sodium dichromate is a red or red-orange crystalline solid. It is used as oxidizing agent in the manufacture of dyes, many other synthetic organic chemicals, and inks; in chrome-tanning of hides; in electric batteries; bleaching fats, oils, sponges, resins; refining petroleum; in corrosion-inhibitors, corrosion-inhibiting paints; in many metal treatments; electroengraving of copper; mordant in dyeing; for hardening gelatin; for the defoliation of cotton plants and other plants and shrubs. It is also used as veterinary medication. HUMAN EXPOSURE AND TOXICITY: Eye contact can cause severe damage with possible loss of vision. In clinical course and toxicological findings in 18 patients intoxicated with ingested chromium salts, 17 patients ingested potassium and sodium dichromate while the remaining patients ingested chromic acid. The first stage of 6-valent chromium is characterized by its irritating effect on the gastrointestinal mucous membrane manifested by diarrhea, vomiting often with blood, leading to severe water-electrolyte disorders, acidosis and shock. Lesions to kidneys, liver and myocardium may develop in the next stage. Probably endothelium is also in injured with resulting increase in its permeability. Acute renal failure is not seen even with high levels of chromium in the urine provided, that the recovery from the shock is prompt, and adequate diuresis induced with mannitol and/or furosemide is maintained. All patients with blood chromium concentration exceeding 1 mg/100 g died. This level is of prognostic and diagnostic value indicating an ingestion and absorption of the high doses of this metal. Increased chromosome aberrations were detected in human peripheral lymphocytes cultured in vitro for 72 hr in water soluble compounds containing chromium (6+) (as sodium dichromate). Nanomolar concentrations of sodium dichromate cause DNA base oxidation in human white blood cells. ANIMAL STUDIES: In the rat, a single subcutaneous injection of sodium dichromate (20 mg/kg) causes acute renal injury and significant polyuria, proteinuria, and glycosuria (peaking 2-3 days after treatment, and returning to normal by day 5) without any changes in the plasma levels of protein, glucose, and glycated hemoglobin. Groups of 20 male and 19 female rats received 16 monthly intrapleural injections of 2 mg sodium dichromate(VI) in gelatin and were observed for up to 2 yr. One Adenocarcinoma of lung was observed, and no tumors at injection site were observed in 60 control rats. Chronic ingestion of high concentrations of sodium dichromate in drinking water induced intestinal tumors in mice. Sister chromatid exchanges and chromosome aberrations increased in CHO cells. Salmonella typhimurium strain TA102, particularly suited to the detection of oxidative mutagens, was the most sensitive out of 9 strains of S. typhimurium his- in revealing the mutagenicity of Cr(VI) compounds (sodium dichromate, calcium chromate and chromium trioxide). The rank of sensitivity was the following: TA102, TA100, TA97, TA92, TA1978, TA98, TA1538 and TA1537, TA1535 being the only insensitive strain. ECOTOXICITY STUDIES: Sodium dichromate (25 uM) increased the frequency of chromosome aberrations in the root cells using Allium anaphase-telophase test.

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)

Cancer Classification: Group A Human Carcinogen by Inhalation; Group D Not Classifiable as to Human Carcinogenicity by Oral Route

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/

For more Evidence for Carcinogenicity (Complete) data for SODIUM DICHROMATE (6 total), please visit the HSDB record page.

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 aerosol, 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.

LC50 (rat) = 124.42 mg/m3/4h

LD50: 51.10 mg/kg (Oral, Rat) (L16)

LD50: 1000 mg/kg (Dermal, Rabbit) (L16)

LC50: 124.42 mg/m3 over 4 hours (Inhalation, Rat) (L16)

LD50 Rat oral 50 mg/kg

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

The injection to rats of glycerol, cisplatin, uranyl acetate, sodium dichromate, and mercuric chloride is followed on the third day by acute renal failure. A new approach for quantitative estimation of disturbance of excretory renal function is presented. The decrease in renal function due to uranyl acetate was 77%; sodium dichromate, 71%; mercuric chloride, 52%; cisplatin, 25%; and glycerol, 10%. The kidneys still maintained serum ion concentration close to normal values. Injection of nephrotoxic drugs increased kidney wet weight by 24-57%. This was caused by swelling of renal tissue and increases in dry weight of the kidneys. The sodium content increased in the renal cortex and decreased in the papilla. The potassium content of the renal cortex is increased. The effect of some nephrotoxic drugs is suggested to depend on an increased number of cells in the renal cortex (probably due to hemostasis and inflammation) and a decrease of renal medulla function. The above drugs induce disturbance of kidney tissue but have no effect on the ion and water content in liver and m. gastrocnemius.

Cactus (Opuntia ficus-indica) is a xerophyte plant that belongs to the Cactaceae family. The present study was designed to investigate the possible protective effects of cactus cladodes extract (CCE) on sodium dichromate-induced testis damage in adult male Wistar rats. For this purpose, CCE at a dose of 100 mg/kg was orally administrated, followed by 10 mg/kg sodium dichromate (intraperitoneal injection). After 40 days of treatment, the rats were sacrificed, and the testes were excised for histological, lipid peroxidation (LPO), and antioxidant enzyme analyses. Sodium dichromate treatment significantly (P<0.01) decreased the body, testis, and accessory sex organ weights, sperm count and motility, and serum testosterone level. In addition, histological analysis revealed pronounced morphological alterations with tubular necrosis and reduction in the number of gametes in the lumen of the seminiferous tubules of sodium dichromate-intoxicated rats. Furthermore, exposure to sodium dichromate significantly (P<0.01) increased LPO level and decreased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in testis. Interestingly, pretreatment with CCE significantly (P<0.01) restored the serum testosterone level, sperm count, and motility to the levels of the control group. Moreover, CCE administration was capable of reducing the elevated level of LPO and significantly (P<0.01) increased SOD, CAT, and GPx activities in testis. Cactus cladodes supplementation minimized oxidative damage and reversed the impairment of spermatogenesis and testosterone production induced by sodium dichromate in the rat testis.

Antioxidants of the vitamin E family have protective effects against metal toxicity. We examined the protective effect of racemic LLU-alpha [2,7,8-trimethyl-2-(carboxyethyl)-6-hydroxychroman] a metabolite of gamma-tocopherol, in comparison to the effect of alpha- and gamma-tocopherol in rats treated with sodium dichromate (Cr) or thallium sulfate (Tl). We measured metal nephrotoxicity based on urinary protein excretion and discussed it with respect to the metal concentration in renal tissue. The ranking of antioxidant activity (iron stimulated lipid peroxidation, luminol and lucigenin amplified chemiluminescence) was determined in the following order: alpha-tocopherol<gamma-tocopherol<LLU-alpha. Pretreatment with LLU-alpha produced lower chromate nephrotoxicity than alpha- or gamma-tocopherol, but did not influence Cr concentration in renal tissue. The protective effect of LLU-alpha against Cr toxicity seemed to be caused by its stronger antioxidant activity in comparison to alpha- and gamma-tocopherol. Pretreatment with LLU-alpha resulted in lower thallium-induced proteinuria, a lower concentration of Tl in the renal medulla, and higher urinary Tl excretion. Unlike LLU-alpha, which has been shown to inhibit K(+) channels in the apical membrane of the thick ascending limb of Henle's loop, we found that gamma-tocopherol did not. This finding reaffirmed the similarity between K(+) and Tl(+) and also explained the significantly decreased Tl concentration in the renal medulla in rats treated with LLU-alpha. We speculate that the protective effect of LLU-alpha against Tl nephrotoxicity is caused both by its antioxidant effect and, at least in part, by its ability to decrease Tl concentration as a consequence of inhibited Tl(+) uptake through K(+) channels. This finding confirmed the similarity between K(+) and Tl(+) and also explained the significantly decreased Tl concentration in the renal medulla in rats treated with LLU-alpha.

Genotoxic effects of xenobiotics are a possible step in tumor initiation in the mucosa of the upper aerodigestive tract. Using the comet assay, detecting genotoxicity in human tissue has been restricted to single incubations in vitro, but in vivo most xenobiotics harm their target in a repetitive or chronic manner. Therefore, we propose a model, which provides repetitive incubations in human upper aerodigestive tract mucosa cultures. Samples of human inferior nasal turbinate mucosa (n = 25) were cultured according to a modified version of a technique originally described by Steinsvag. On day 1 fresh samples and on days 7, 9 and 11 organ cultures were incubated with N-nitrosodiethylamine (NDEA), sodium dichromate (Na2Cr2O7) and N'-methyl-N-nitro-N-nitrosoguanidine (MNNG). Mucosa samples and organ cultures, respectively, underwent a modified comet assay on days 1, 7 and 11. Genotoxicity could be shown for NDEA, Na2Cr2O7 and MNNG on days 1, 7 and 11. Duration of tissue culture and repetitive incubations did not significantly influence the results for NDEA. Nevertheless, Na2Cr2O7 and MNNG caused higher genotoxic effects on cultures subjected to the comet assay on day 11. This model may help to assess genotoxic hazards posed by environmental pollutants that have a cumulative character in repetitive or chronic exposure in vivo.

For more Interactions (Complete) data for SODIUM DICHROMATE (14 total), please visit the HSDB record page.

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/

A 22-month-old infant died after ingesting sodium dichromate his father had brought from work. Treatment included folic acid and dimercaprol administration, hemodialysis, and exchange transfusion. To evaluate this treatment, four dogs were hemodialyzed after receiving intravenous sodium dichromate: their dialyzer chromate clearance was similar to their renal chromate clearance and their dialyzer chromate clearance was not significantly different before or after dimercaprol administration. This and other cases in the literature indicate that although chromate poisoning is often fatal, supportive care, forced diuresis, and chelating agents may be helpful. Hemodialysis may be required if renal failure occurs. Awareness of toxicity and prevention remain the most important approaches.

For more Antidote and Emergency Treatment (Complete) data for SODIUM DICHROMATE (8 total), please visit the HSDB record page.

PRECAUTIONS FOR "CARCINOGENS": Whenever medical surveillance is indicated, in particular when exposure to a carcinogen has occurred, ad hoc decisions should be taken concerning ... /cytogenetic and/or other/ tests that might become useful or mandatory. /Chemical Carcinogens/

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

LC50; Species: /Oncorhynchus mykiss/ (rainbow trout); Conditions: flow through, measured, water hardness 45 mg/L as calcium carbonate; Concentration: 69,000 ug/L for 96 hr

LC50; Species: Salvelinus fontialis (brook trout); Conditions: flow-through, measured, water hardness 45 mg/L as calcium carbonate; Concentration: 59,000 ug/L for 96 hr

LC50; Species: Carassius auratus (goldfish); Conditions: static, unmeasured, water hardness 100 mg/L as calcium carbonate; Concentration: 249,000 ug/L for 96 hr

LC50; Species: Lepomis macrochirus (bluegill); Conditions: static, unmeasured, water hardness of 120 mg/L as calcium carbonate; Concentration: 213,000 ug/L for 96 hr

For more Ecotoxicity Values (Complete) data for SODIUM DICHROMATE (21 total), please visit the HSDB record page.

/AQUATIC SPECIES/ Little information is available on the responses of lower animals to genotoxic chemicals or on their sensitivity for detecting genotoxic chemicals, especially at different life-stages, despite the established use of the water flea Daphnia magna in ecotoxicity testing. Comet assay methodology was developed and applied to daphnid cells but only limited, non-statistically significant responses to the genotoxicants sodium dichromate (0.2-1 uM), chrysoidine (0.1-2 uM), and mixtures of benzo-a-pyrene (BaP) and sodium dichromate were found (from 0.01 uM BaP & 0.1 uM sodium dichromate to 0.25 uM BaP & 0.75 uM sodium dichromate). Transcriptomic analyses using Agilent D. magna oligonucleotide microarrays were undertaken to assess the effect of a mixture of sodium dichromate and BaP (designed to produce both adducted and oxidized DNA) on gene transcription. Neonates (<24hr) and adults (day 7) were exposed for 6 hr and 24 hr at two combination concentration levels (0.02 uM BaP & 0.15 uM sodium dichromate and 0.1 uM BaP & 0.75 uM sodium dichromate). The greatest differences in transcriptional profile occurred between adults and neonates. Subsets of the transcriptional profiles distinguished genotoxicant-exposed animals from controls, both for neonates and adults. Higher transcript levels of DNA repair genes were found in adults and adults also displayed significant induction of DNA repair gene transcripts in response to exposure whereas neonates did not. Transcriptional changes in response to genotoxicant exposure proved more sensitive than measurement of DNA strand breaks by the Comet assay and the extensive differences in transcription between adults and neonates emphasized the importance of life stage in toxicant testing with Daphnia.

/AQUATIC SPECIES/ The oxidation of DNA and lipid was analyzed in the marine mussel (Mytilus edulis) in response to exposure (10 ug/L and 200 ug/L) to cadmium (Cd) and chromium [Cr(VI)]. Concentration dependent uptake of both metals into mussel tissues was established and levels of gill ATP were not depleted at these exposure levels. DNA strand breakage in gill cells (analyzed by the comet assay) was elevated by both metals, however, DNA oxidation [measured by DNA strand breakage induced by the DNA repair enzyme formamidopyrimidine glycosylase (FPG)] was not elevated. This was despite a statistically significant increase in both malondialdehyde and 4-hydroxynonenal - indicative of lipid peroxidation - following treatment with Cd. In contrast, both frank DNA stand breaks and FPG-induced DNA strand breaks (indicative of DNA oxidation) were increased following injection of mussels with sodium dichromate (10.4 ug Cr(VI)/mussel). The metals also showed differential inhibitory potential towards DNA repair enzyme activity with Cd exhibiting inhibition of DNA cutting activity towards an oligonucleotide containing 8-oxo-7,8-dihydro-2'-deoxyguanosine and Cr(VI) showing inhibition of such activity towards an oligonucleotide containing ethenoadenosine, both at 200 ug/L. The metals thus show DNA damage activity in mussel gill with distinct mechanisms involving both direct and indirect (oxidative) DNA damage, as well as impairing different DNA repair capacities. A combination of these activities can contribute to adverse effects in these organisms.

/AQUATIC SPECIES/ As a result of a widespread application in numerous industrial processes, chromium is a contaminant of many environmental systems. Chromium and their compounds are toxic to both invertebrates and vertebrates and, for this reason, there has been a search for suitable and less toxic alternatives. Molybdenum compounds have been studied as alternative to chromium compounds for some industrial applications. The toxicity of chromium is well known but the effects of molybdenum and molybdenum mining on natural populations and communities of freshwater invertebrates have not often been studied. However, chromium, and molybdenum (and their compounds) are included in the same list (List II) of European Union dangerous substances. In this study, the acute and chronic effects of sodium molybdate and sodium dichromate to Daphnia magna Straus were evaluated. Furthermore, in vitro and in vivo effects of these two metals on acetylcholinesterase (AChE) activity of D. magna Straus were investigated. LC(50) values determined at 48 hr were 0.29 and 2847.5 mg/L for chromium (as sodium dichromate) and molybdenum (as sodium molybdate), respectively. No significant in vitro effects of both metals on AChE were found. However, both toxicants inhibited AChE in vivo at concentrations under the respective 48-hr LC(50) values. Both sodium dichromate and sodium molybdate inhibited the reproduction and growth of D. magna, but the concentrations inducing significant effects were different for the two chemicals. Sodium molybdate had significant lower toxicity to D. magna Straus than sodium dichromate.

/AQUATIC SPECIES/ To stimulate a potential field situation in which seaward-migrating juvenile coho salmon, Oncorhynchus kisutch, pass through Cr-polluted freshwater (FW) before being exposed to seawater (SW), the effects of sublethal FW exposure to Cr (as sodium dichromate) on salinity tolerance and serum osmolality after transfer to SW were investigated. SW survival was significantly decreased in salmon exposed in FW to 0.23 mg Cr/L for four weeks or to 0.5 mg Cr/L for two weeks and transferred to 20 or 30 parts per thousand (%) salinity, respectively. Serum osmolality, measured after two weeks of FW exposure to 0.0 or 0.5 mg Cr/L and after transfer to 20 or 30% SW, was significantly higher in Cr-exposed fish from one-half to two days after SW transfer but not at the end of the FW exposure period or at seven days after SW transfer. These effects in SW occurred at Cr exposure concentrations which had no effect on survival or serum osmolality in FW. It is suggested that Cr acted non-specifically on osmoregulatory epithelia to cause excessive dehydration in SW, and that measurement of salinity tolerance and serum osmolality may be sensitive and ecologically realistic indicators of sublethal toxicity in aquatic animals.

/PLANTS/ The Allium anaphase-telophase test was evaluated to find out if it could be recommended in the screening of wastewater for genotoxicity. Five mutagenic or carcinogenic chemicals usually found in wastewater were tested in the Allium anaphase-telophase test. Sodium dichromate (25 uM), benzene (100 uM), dichloromethane (175 uM) and 1,1,1-trichloromethane (175 uM) increased the frequency of chromosome aberrations in the root cells, whereas formaldehyde (1 mM) was found to be non-mutagenic in this test system. Other studies where chemicals were tested in the Allium test were reviewed. For 15 chemicals the results were compared with results from the Ames test, the Microscreen assay, and carcinogenicity tests in rodents. The sensitivity of the Allium test was calculated to be 82%. In conclusion the Allium test is recommended for the screening of wastewater because it has a high sensitivity, is cheap, rapid, easy to handle, and because it can be used on wastewater without pretreatment of the sample.

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.

Sodium dichromate is reported to be non-biodegradable based on results of the Japanese MITI test(1); however, BOD values and test protocols were not reported(SRC).

Using carp (Cyprinus carpio) which were exposed over a 4-week period to sodium dichromate dihydrate concentrations of 1 and 0.1 mg/L, the BCF ranged from <3.6 to <36(1). According to a classification scheme(2), this BCF range suggests that bioconcentration in aquatic organisms is low(SRC).

DRINKING WATER: Sodium dichromate dihydrate is one of a number of inorganic compounds containing hexavalent chromium (CrVI) found in drinking water source supplies as a contaminant resulting from various industrial processes including electroplating operations, leather tanning, and textile manufacturing(1).

According to the 2012 TSCA Inventory Update Reporting data, 2 reporting facilities estimate the number of persons reasonably likely to be exposed during the manufacturing, processing, or use of Chromic acid (H2Cr2O7), sodium salt (1:2) (10588-01-9) may be as low as <10 workers up to the range of 100-499 workers per plant; the data may be greatly underestimated due to confidential business information (CBI) or unknown values(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 136,313 workers (24,542 of these are female) were potentially exposed to sodium dichromate in the US(1). Occupational exposure to sodium dichromate may occur through inhalation and dermal contact with this compound at workplaces where sodium dichromate is produced or used(2).

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: Burn in a chemical incinerator equipped with an afterburner and scrubber but exert extra care in igniting as this material is highly flammable. 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. /Sodium Dichromate Dihydrate/

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.

The following wastewater treatment technology has been investigated for chromium: Concentration process: Biological Treatment. /Chromium/

For more Disposal Methods (Complete) data for SODIUM DICHROMATE (15 total), please visit the HSDB record page.

49 411 70; Sodium dichromate

PRECAUTIONS FOR "CARCINOGENS": Procurement ... of unduly large amt ... should be avoided. To avoid spilling, carcinogens should be transported in securely sealed glass bottles or ampoules, which should themselves be placed inside strong screw-cap or snap-top container that will not open when dropped & will resist attack from the carcinogen. Both bottle & the outside container should be appropriately labelled. ... National post offices, railway companies, road haulage companies & airlines have regulations governing transport of hazardous materials. These authorities should be consulted before ... material is shipped. /Chemical Carcinogens/

PRECAUTIONS FOR "CARCINOGENS": When no regulations exist, the following procedure must be adopted. The carcinogen should be enclosed in a securely sealed, watertight container (primary container), which should be enclosed in a second, unbreakable, leakproof container that will withstand chem attack from the carcinogen (secondary container). The space between primary & secondary container should be filled with absorbent material, which would withstand chem attack from the carcinogen & is sufficient to absorb the entire contents of the primary container in the event of breakage or leakage. Each secondary container should then be enclosed in a strong outer box. The space between the secondary container & the outer box should be filled with an appropriate quantity of shock-absorbent material. Sender should use fastest & most secure form of transport & notify recipient of its departure. If parcel is not received when expected, carrier should be informed so that immediate effort can be made to find it. Traffic schedules should be consulted to avoid ... arrival on weekend or holiday ... /Chemical Carcinogens/

Oxidizer Poison

Do not transport with food and feedstuffs.

Symbol: T+, N, O; R: 45-46-60-61-8-21-25-26-34-42/43-48/23-50/53; S: 53-45-60-61; Note: E

UN Hazard Class: 6.1; UN Pack Group: II