Chromic acid (H2CrO4), chromium salt

167.99 g/mol

167.860668 g/mol

DTXSID20194177

80.3 Ų

Freeze-dried dichromium tris(chromate) is a dark purple/black granular solid, with an amorphous non-crystalline structure. The substance melts above 300 °C. Relative density: 2.269 g/cu cm at 20 °C. Water solubility: 96.6 g/L at 20 °C /Dichromium trischromate (CAS 24613-89-6)/

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D007, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste. /Chromium/|SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.|The following wastewater treatment technology has been investigated for chromium: Concentration process: Biological Treatment. /Chromium/|The following wastewater treatment technology has been investigated for chromium: Concentration process: Chemical Precipitation. /Chromium/|For more Disposal Methods (Complete) data for CHROMIUM CHROMATE (9 total), please visit the HSDB record page.

Combustible, organic, or other readily oxidizable materials (paper, wood, sulfur, aluminum, plastics, etc.); corrosive to metals. /Chromic acid and chromates/|Hydrazine is decomposed explosively by chromates and chromic anhydride. /Chromates/

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

Impervious gloves, aprons, and footwear shall be worn at operations where solutions of chromium (VI) may contact the skin. Protective gloves shall be worn at operations where dry compounds of chromium (VI) are handled and may contact the skin. /Cr(VI)/|Protective clothing: Coveralls or other full-body protective clothing shall be worn in areas where there is occupational exposure to chromium (VI). Protective clothing shall be changed at least daily at the end of the shift and more frequently if it should become grossly contaminated. /Cr(VI)/|Respirator Recommendations: At concentrations above NIOSH REL, or where there is no REL, at any detectable concentration: /Chromic acid and chromates/[Table#4328]|Eyewash fountains should be provided in areas where there is any possibility that workers could be exposed to the substance; this is irrespective of the recommendation involving the wearing of eye protection. /Chromic acid and chromates/|For more Personal Protective Equipment (PPE) (Complete) data for CHROMIUM CHROMATE (8 total), please visit the HSDB record page.

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

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/

SRP: Contaminated protective clothing should be segregated in a manner such that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. The completeness of the cleaning procedures should be considered before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at the end of shift, but should remain at employee's place of work for cleaning.|Workers whose clothing may have become contaminated should change into uncontaminated clothing before leaving the work premises. /Chromic acid and cromates/|Work clothing that becomes wet or significantly contaminated should be removed and replaced. /Chromic acid and cromates; Chromium(II) compounds (as Cr); Chromium(III) compounds/|The worker should immediately wash the skin when it becomes contaminated. /Chromic acid and chromates; Chromium(II) compounds (as Cr); Chromium(III) compounds/

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/

... 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/

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: Applications for chromium chromate coating are extensive. Aircraft components, aluminum castings, zinc castings, magnesium castings, galvanized steel passivation, and aluminum sheet passivation are example applications for chromium chromates. HUMAN EXPOSURE AND TOXICITY: A hospital-based case-control study of 531 male and 144 female matched pairs was conducted to analyze the role of nonoccupational and occupational risk factors in the etiology of tumors of the lower urinary tract. With regard to occupational history, significantly elevated risks were found for exposure to chromium/chromate. ANIMAL STUDIES: There is no data available.

/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/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist respirations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. Activated charcoal is not effective. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Do not attempt to neutralize because of exothermic reaction. Cover skin burns with dry, sterile dressings after decontamination ... . /Inorganic acids and related compounds/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Early intubation, at the first sign of upper airway obstruction, may be necessary. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's(LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Inorganic acids and related compounds/

/HUMAN EXPOSURE STUDIES/ Addition of iron sulfate to cement means transformation of water-soluble hexavalent chromium into nonwater-soluble trivalent chromium. This has been the basis for preventive measures concerning sensitization to hexavalent chromium (chromate) in cement. For some years, iron sulfate has been added to cement manufactured in the Scandinavian countries. In the present in vivo study, cements with and without iron sulfate were compared concerning their capacity to elicit allergic patch-test reactions in eight chromate-hypersensitive individuals. No patch-test reactions were obtained from a water extract of cement with iron sulfate when appropriately buffered.|/EPIDEMIOLOGY STUDIES/ A hospital-based, case-control study of 531 male and 144 female matched pairs was conducted in Germany to analyze the role of nonoccupational and occupational risk factors in the etiology of tumors of the lower urinary tract (bladder cancer). Smoking of cigarettes was associated with an odds ratio (OR) of 3.6 for men and 3.2 for women, compared with not smoking and showed a significant dose- and time-response relationship for both sexes. Heavy pipe smoking significantly increased the risk (OR = 1.9 in men), and smoking of cigars did not alter the risk of bladder cancer. Controlling for smoking, a significantly twofold or more increase in risk was found for heavy consumption of coffee in both sexes and for heavy intake of beer in males. Increasing levels of total fluid intake were associated with increasing, smoking-adjusted risks in men. Significant associations were found for chronic infection of the lower urinary tract (OR = 1.8), familial history of bladder cancer (OR = 2.5), and frequent consumption of high fat meals (OR = 1.4) among men and for frequent consumption of canned food in both sexes (OR = 1.7 for males, 2.4 for females). With regard to occupational history, significantly elevated odds ratios were found for ever-employment in the printing (5.0), plastics and synthetics (2.6), rubber (2.5), mining (2.0), and dyestuffs (1.9) industries, for exposure to spray paints (2.9), zinc (2.3), chromium/chromate (2.2), oils (1.5), petroleum (1.4), stone dust (1.4) and metal dust/fumes (1.3), and for occupation as mining worker (2.0) and truck driver (1.8) among men. Multivariate logistic regression analysis showed significant contribution of coffee and beer drinking, ingestion of canned food, and familial occurrence of urothelial tumors to the risk of bladder cancer in men after accounting for the effects of tobacco smoking, occupational exposures, and a history of bladder infection. These other variables did not influence the risk attributable to occupational exposures.|/EPIDEMIOLOGY STUDIES/ Data from a hospital-based matched case-control study with 531 male pairs were analyzed for risks of cancer of the lower urinary tract associated with previous employment and particular occupational exposures. Statistically significant odds ratios were obtained for ever-employment as mining workers (2.0), turners (2.3), tailors (2.7), truck drivers (1.8), locomotive drivers (3.0) and janitors (3.5), whereas odds ratios of 3.0 or more, found for rubber and plastics workers, printing workers, gas workers, artists and chemists were not statistically significant. When adjusted for smoking, there was a trend toward increasing relative risks with increasing duration of employment as truck drivers and as turners, and relative risks rose 3-fold for 30 or more years of employment. With regard to a priori high-risk industries, ever-employment in the rubber, plastics and synthetics, dyestuff and paints, mining, and printing industries and secondary processing was associated with significantly higher relative risks, and a statistically significant trend in risk with increasing duration of employment was found for the first 3 industries mentioned. With regard to job-related exposures to specified substances, the relative risks observed for increasing duration of exposure suggest that exposures to petroleum, oils, chromium/chromate, spray paints, and zinc, which correspond to exposures involved in the occupations showing a higher relative risk in this study, are associated with a higher risk for cancer of the lower urinary tract.|/GENOTOXICITY/ Cultured human cells are invaluable biological models for mechanistic studies of genotoxic chemicals and drugs. Continuing replacement of animals in toxicity testing will further increase the importance of in vitro cell systems, which should accurately reproduce key in vivo characteristics of toxicants such as their profiles of metabolites and DNA lesions. In this work, we examined how a common severe deficiency of cultured cells in ascorbate (Asc) impacts the formation of oxidative DNA damage by hexavalent chromium (chromate). Cr(VI) is reductively activated inside the cells by both Asc and small thiols but with different rates and spectra of intermediates and DNA adducts. We found that Cr(VI) exposure of H460 human lung epithelial cells in standard culture (<0.01 mM cellular Asc) induced biologically significant amounts of oxidative DNA damage. Inhibition of oxidative damage repair in these cells by stable XRCC1 knockdown strongly enhanced cytotoxic effects of Cr(VI) and led to depletion of cells from G(1) and accumulation in S and G(2) phases. However, restoration of physiological levels of Asc (apporoximately 1 mM) completely eliminated Cr(VI) hypersensitivity of XRCC1 knockdown. The induction of chromosomal breaks assayed by the micronucleus test in Asc-restored H460, primary human lung fibroblasts, and CHO cells was also unaffected by the XRCC1 status. Centromere-negative (clastogenic) micronuclei accounted for 80-90% of all Cr(VI)-induced micronuclei. Consistent with the micronuclei results, Asc-restored cells also showed no increase in the levels of poly(ADP-ribose), which is a biochemical marker of single-stranded breaks. Asc had no effect on cytotoxicity of O(6)-methylguanine, a lesion produced by direct DNA alkylation. Overall, our results indicate that the presence of physiological levels of Asc strongly suppresses pro-oxidant pathways in Cr(VI) metabolism and that the use of standard cell cultures creates a distorted profile of its genotoxic properties.