크롬산바륨

Fresh air, rest.

Rinse and then wash skin with water and soap.

Rinse with plenty of water for several minutes (remove contact lenses if easily possible).

Rinse mouth.

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.

Use water spray to cool unopened containers.

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

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust; Environmental precautions: Do not let product enter drains; 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.

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/

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; Contaminated packaging: Dispose of as unused product.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

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

For more Disposal Methods (Complete) data for BARIUM CHROMATE (10 total), please visit the HSDB record page.

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Then store and dispose of according to local regulations.

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

Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.

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.

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.

For more Preventive Measures (Complete) data for BARIUM CHROMATE (8 total), please visit the HSDB record page.

The health effects of the different barium compounds depend on how well the compound dissolves in water or the stomach contents. At low doses, barium acts as a muscle stimulant, while higher doses affect the nervous system, causing cardiac irregularities, tremors, weakness, anxiety, dyspnea, paralysisand possibly death. Barium may also cause gastrointestinal disturbances, damage the kidneys and cause decreases in body weight. 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, L214)

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

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

IDENTIFICATION AND USE: Barium chromate is a heavy, pale-yellow crystalline powder. It is used as pigment, almost entirely in anticorrosion jointing pastes, to prevent electro-chemical corrosion at junctions of dissimilar metals; some use in artists' colors and in coloring glass, ceramics, porcelain. Also used in metal primers, pyrotechnic compositions. HUMAN EXPOSURE AND TOXICITY: Barium chromate is cytotoxic and genotoxic to human lung cells. Genotoxicity may not be solely mediated by Cr ions, but also involve some clastogenic activity of barium ions. The clastogenic effects of barium chromate and zinc chromate were similar. ANIMAL STUDIES: No implantation site tumors were seen in 35 rats given intramuscular implantation of 25 mg barium chromate or in their controls; no implantation tumors were observed in 34 rats given intramuscular implants and observed for 27 months; controls were also negative. Thirty-one rats implanted with intrapleural barium chromate revealed only one tumor in treated rats and none in the 34 control rats. Barium chromate produced a significant level of mutations in a transgenic, V79-derived, mammalian cell line (G12).

Barium is a competitive potassium channel antagonist that blocks the passive efflux of intracellular potassium, resulting in a shift of potassium from extracellular to intracellular compartments. The intracellular translocation of potassium results in a decreased resting membrane potential, making the muscle fibers electrically unexcitable and causing paralysis. Some of these barium's effects may also be due to barium induced neuromuscular blockade and membrane depolarization. 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, L214)

Cough. Sore throat.

Redness.

Redness. Pain.

Burning sensation.

Ingesting excess barium may cause vomiting, abdominal cramps, diarrhea, difficulties in breathing, increased or decreased blood pressure, numbness around the face, and muscle weakness. High levels may result in changes in heart rhythm or paralysis and possibly death. 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, L214)

Barium chromate was tested for carcinogenicity in Porton Wistar rats (52 females/48 males) exposed for up to 2 years to 2 mg of the test compound in stainless steel mesh pellets surgically implanted in the left inferior bronchiolus. Control rats (25-50/sex/treatment group) received a similar treatment with 2 mg of cholesterol (negative control) or 2 mg of 20-methylcholanthrene (positive control) or calcium chromate (positive control). Treatment with the test compound had no adverse effects with respect to mortality rate, body weights, or incidences of bronchial carcinomas or non-lung tumors. Both groups of positive control rats had an increased incidence (25-46%) of bronchial carcinomas, as compared to the negative control group (0%).

/GENOTOXICITY/ Hexavalent chromium (Cr(VI)) compounds are widely accepted as human lung carcinogens. However, there have been few investigations of the genotoxicity of Cr(VI) in human lung cells. Moreover, our knowledge of the effects of Cr(VI) in human lung cells is further limited because the available data generally focus on the effects of only lead chromate (PbCrO(4)) and sodium chromate (Na(2)CrO(4)). To fully understand these carcinogenic compounds, the genotoxic effects to its target cells need to be evaluated for additional Cr(VI) salts. Accordingly, we investigated the cytotoxicity and clastogenicity of barium chromate (BC) in a human lung cell culture model (WTHBF-6 cells). We found that BC induced concentration-dependent cytotoxicity in WTHBF-6 cells, with relative survival of 88%, 74%, 67%, 12%, 3%, and 0.1% after exposure to 0.01, 0.05, 0.1, 0.5, 1, and 5 ug/sq cm BC, respectively. Similarly, the amount of chromosomal damage also increased with concentration after a 24-hr exposure. Specifically, 0.01, 0.05, 0.1, and 0.5 ug/sq cm BaCrO(4) damaged 5%, 9%, 22%, and 49% of metaphase cells, with the total damage reaching 5, 10, 28, and 65 aberrations per 100 metaphases, respectively. Concentrations of 1 and 5 ug/sq cm BC induced a profound cell cycle delay, and no metaphases were observed. The spectrum of damage included chromatid and chromosome-type lesions consistent with mechanistic events associated with the activation of oncogenes and inactivation of tumor suppressor genes. Overall the data indicate that BC is cytotoxic and genotoxic to human lung cells.

/GENOTOXICITY/ Particulate hexavalent chromium [Cr(VI)] compounds are well-established human lung carcinogens. However, their carcinogenic mechanisms are poorly understood as most investigators have used soluble Cr(VI) compounds. Recent work from our laboratory has found that barium chromate (BC) is also cytotoxic and clastogenic. To understand how BC relates to existing data on other particulate Cr(VI) compounds, we compared its cytotoxicity and clastogenicity with lead chromate (LC), which has been used as a prototypical particulate Cr(VI) compound, in WTHBF-6 cells, a near-normal human lung cell line. We found that BC is a more potent cytotoxicant, inducing 67%, 12%, 3%, and 0% relative survival at concentrations of 0.1, 0.5, 1, and 5 ug/sq cm, respectively, while LC induced 90%, 71%, 43%, and 15% survival at these same concentrations. We found that BC was also more clastogenic, damaging 22% and 49% of metaphase cells at 0.1 and 0.5 ug/sq cm, and causing complete cell cycle arrest at 1 and 5 ug/sq cm. By contrast, 0.1, 0.5, and 1.0 ug/sq cm LC damaged 10%, 27%, and 37% of metaphase cells, respectively, and complete cell cycle arrest was not observed until a concentration of 5 ug/sq cm was reached. We found that BC and LC both partially dissolved in complete medium in the presence of cells, producing similar extracellular concentrations. Both compounds were also comparable with respect to particle uptake and the amount of intracellular Cr ions. Considering previous reports showing that lead ions were inactive and that sodium chromate and LC have similar clastogenic potencies, these data suggest that BC genotoxicity may not be solely mediated by Cr ions, but also involve some clastogenic activity of barium ions.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ No implantation site tumors were seen in 35 rats given intramuscular implantation of 25 mg barium chromate (VI) in 75 mg sheep fat or in their controls; no implantation tumors observed in 34 rats given intramuscular implants and observed for 27 months; controls also negative. /From table/

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Thirty one rats implanted with intrapleural barium chromate(VI) in sheep fat revealed only one tumor in treated rats and none in the 34 control rats. /From table/

/GENOTOXICITY/ Epigenetic gene silencing by aberrant DNA methylation of gene promoter regions is a nonmutagenic but heritable epigenetic mechanism that may mistakenly cause the silencing of important cancer-related tumor suppressor genes. Using a transgenic, V79-derived, mammalian cell line (G12) that contains a bacterial gpt reporter gene in its DNA, we can study carcinogen-induced gene inactivation by mutagenic as well as epigenetic DNA methylation mechanisms. Whereas numerous carcinogens have previously been shown to be mutagenic in these cells, a few carcinogens, including nickel, diethylstilbestrol, and X-rays, are also capable of silencing the G12 cell gpt transgene by aberrant DNA methylation. Here we report for the first time that carcinogenic potassium chromate salts can also induce aberrant DNA methylation in this system. In contrast insoluble barium chromate produced significant level of mutations in these cells but did not cause DNA methylation changes associated with transgene expression.

/IMMUNOTOXICITY/ Soluble and insoluble hexavalent chromium (Cr6+) agents are concomitantly released with ozone (O3) during welding. Although pulmonary/immunologic implications from exposure to each agent individually have been investigated, the effects from simultaneous exposure, as occurs under actual working conditions, are unclear. To investigate immunomodulatory effects of inhaled Cr6+, F-344 rats were exposed for 5 hr/day, 5 days/week for 2 or 4 weeks to atmospheres containing soluble potassium chromate (K2CrO4) or insoluble barium chromate (BaCrO4), each alone at 360 micrograms Cr/cu m or in combination with 0.3 ppm O3. One day after the final exposure, rats were euthanized, their lungs were lavaged, and pulmonary macrophages (PAM) were recovered for assessment of basal and inducible functions. Rats inhaling K2CrO4-containing atmospheres had greater levels of total recoverable cells, neutrophils, and monocytes in bronchopulmonary lavage compared to rats exposed to insoluble Cr6+ atmospheres, O3 alone, or air; these rats also had a reduced percentage of PAM, although total PAM levels remained unaffected. Although Cr exposure-related changes in PAM functionality were evident, any dependence upon Cr solubility was variable. K2CrO4-containing atmospheres modulated PAM-inducible interleukins-1 and -6, and tumor necrosis factor-alpha production to a greater degree than those containing BaCrO4. Conversely, BaCrO4-containing atmospheres affected PAM basal nitric oxide production and interferon-gamma-primed/zymosan-stimulated reactive oxygen intermediate production to a greater extent than did those containing K2CrO4. In none of the PAM assays did co-inhalation of O3 result in a modulation of the effects obtained with either Cr6+ compound itself. The results indicate that, while immunomodulatory effects of inhaled Cr6+ upon PAM are related to particle solubility, the co-inhalation of O3 apparently does not cause further modifications of the metal-induced effects.

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)/

D005; A solid waste containing barium (such as barium chromate) 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.

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/

... 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/

(AZ) ARIZONA 1500 ug/l /Barium/

(ME) MAINE 1500 ug/l /Barium/

(MN) MINNESOTA 2000 ug/l /Barium/

(ME) MAINE 35 ug/L /Cr VI)

Maximum contaminant level for inorganic contaminants: Contaminant: Chromium; MCL 0.1 mg/L. /Chromium/

Maximum contaminant level for inorganic contaminants: Contaminant: Barium; MCL 2 mg/L. /Barium/

EPA 2000 ug/L /Barium/

Maximum contaminant level goal for inorganic contaminants: Contaminant: Chromium; MCLG 0.1 mg/L. /Chromium/

Maximum contaminant level goal for inorganic contaminants: Contaminant: Barium; MCLG 2 mg/L. /Barium/

EPA 2000 ug/L /Barium/