10108-64-2[Cl][Cd][Cl]YKYOUMDCQGMQQO-UHFFFAOYSA-LCadmium chloride is a white crystalline solid. It is soluble in water. It is noncombustible. The primary hazard of this material is that it poses a threat to the environment. Immediate steps should be taken to limit its spread to the environment. Cadmium chloride is used in photography, in fabric printing, in chemical analysis, and in many other uses.
10108-64-2CHEBI:35456Metals -> Cadmium Compounds, Inorganic
Carcinogens
4.05 at 77 °F (USCG, 1999) - Denser than water; will sink
4.08 g/cu cm
Density: 4.05 (CdCl2); 3.327 (CdCl2.2.5H2O)
Efflorescent granules or rhombohedral leaflet; density, 3.33; freely soluble in water /Cadmium chloride hemipentahydrate/
Colorless crystals, density 3.33 g/mL /Cadmium chloride pentahydrate/
4.1 g/cm³
Rhombohedral crystals
Small, white crystals
Hexagonal, colorless crystals
greater than or equal to 100 mg/mL at 68 °F (NTP, 1992)
Soluble in acetone; practically insoluble in ether.
Slightly soluble in ethanol
In water, 120 g/100 g water at 25 °C
Solubility in water: good
1760 °F at 760 mmHg (NTP, 1992)
960 °C
960 °C
964 °C @760 [mm Hg]
안전 정보는 참고용이며, 공급업체의 물질안전보건자료(SDS), 관련 법규 및 전문가 평가를 대체하지 않습니다.
Danger
H301: Toxic if swallowed [Danger Acute toxicity, oral]
P203, P260, P264, P270, P271, P273, P280, P284, P301+P316, P304+P340, P316, P318, P319, P320, P321, P330, P391, P403+P233, P405, and P501 (click each P-code to see the statement)
Danger
H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]
P203, P260, P264, P270, P271, P273, P280, P284, P301+P316, P304+P340, P316, P318, P319, P320, P321, P330, P391, P403+P233, P405, and P501 (click each P-code to see the statement)
Chemical: Cadmium chloride (CdCl2)
Hazard Traits - Carcinogenicity; Genotoxicity; Reproductive Toxicity
REACH registered substance: Cadmium chloride (EC: 233-296-7)
Restricted substance: Cadmium chloride
Substance: Cadmium chloride
Cadmium chloride: HSNO Approval: HSR004389 Approved with controls
Literature sources indicate that this chemical is nonflammable. (NTP, 1992)
Not combustible. Gives off irritating or toxic fumes (or gases) in a fire.
Metallothioneins (MTs) have a low molecular weight and have been considered to be important metal-binding proteins in defense from cadmium (Cd) toxicity in animals. These proteins are known to be induced by the injection of heavy metals such as Cd. Previously, we developed the measurement of the MT mRNA expression by the RT-PCR method. In this study, to clarify the relation between Cd-induced MT-I mRNA expression and female sex hormones in liver, we investigated the influences of the ovariectomy and female sex hormones on hepatic MT-I mRNA expression after Cd injection, and also investigated the effects of aging on hepatic MT-I mRNA expression in mice after Cd injection. We analysed the MT-I mRNA expression by the RT-PCR method. Cd-induced MT-I mRNA expression in ovariectomized mice was more than that in sham-operated mice (9 weeks old). Both 17 beta-estradiol and progesterone reduced the Cd-induced MT-I mRNA expression in ovariectomized mice (9 weeks old). Moreover, the MT-I mRNA expression in male mice was more than that of females (9 weeks old). However, the sex difference in the gene expression was not found in younger (4 weeks old) or older (46 weeks old) mice. These results suggest that the expression of hepatic MT-I mRNA after Cd injection is influenced by female sex hormones.
Acute administration of cadmium results in hepatotoxicity. Recent reports indicate that Kupffer cells, the resident macrophages of the liver, participate in the manifestation of chemical-induced hepatotoxicity. Tumor necrosis factor-alpha (TNF-a) is a proinflammatory cytokine that is a major product of Kupffer cells and mediates the hepatotoxic effects of lipopolysaccharide (LPS). It has been speculated that cadmium also may exert its hepatotoxicity via the production of TNF-a by the Kupffer cells. Therefore, this study was undertaken to determine whether mice deficient in TNF-a are resistant to CdCl2-induced hepatotoxicity. TNF-a-null (TNF-KO) and wild-type (WT) mice were dosed ip with saline, LPS (0.1 mg/kg)/Gln (L-galactosamine, 700 mg/kg), or CdCl2 (2.2, 2.8, 3.4, and 3.9 mg Cd/kg). Serum alanine aminotransferase (ALT) and sorbitol dehydrogenase (SDH) activities were quantified to assess liver injury. Caspase-3 activity was quantified to assess hepatocellular apoptosis. LPS/Gln treatment increased ALT (17-fold) and SDH (21-fold) in WT mice. In contrast, LPS/Gln-treatment did not significantly increase ALT or SDH in TNF-KO mice. LPS/Gln-treatment caused a 7.8-fold increase in caspase-3 activity in WT mice but did not increase caspase-3 in TNF-KO mice. Cadmium caused a dose-dependent increase in liver injury in both WT and TNF-KO mice. However, the liver injury produced by Cd in the TNF-KO mice was not different from that in WT at any dose. No significant increase in caspase-3 activity was detected in any of the Cd-treated mice. These data indicate that, in contrast to LPS/Gln-induced hepatotoxicity, TNF-a does not appear to mediate Cd-induced hepatotoxicity.
현재 필터 조건에 해당하는 반응 기록이 없습니다.
불러오는 중…
1054 °F (NTP, 1992)
568 °C
568 °C
568 °C
10 mmHg at 1213 °F ; 0 mmHg at 68 °F (NTP, 1992)
VP: 1 Pa at 412 °C (sublimes); 10 Pa at 471 °C (sublimes); 100 Pa at 541 °C (sublimes); 1 kPa at 634 °C; 10 kPa at 768 °C; 100 kPa at 959 °C
10 mm Hg at 656 °C
10 [mm Hg] @656 °C
Cadmium chloride is a colorless, odorless, crystalline solid, or powder.
A severe skin, eye, and respiratory tract irritant; Inhalation may effects on the kidneys and lungs; [ICSC] An irritant; [MSDSonline] See Cadmium and the linked diseases.
The major hazards encountered in the use and handling of cadmium chloride stem from its toxicologic properties. Toxic primarily by ingestion and inhalation, exposure to this odorless, colorless-to-white, crystalline substance may occur from its use in fungicides, electroplating baths, dyeing and printing of textiles. Effects from exposure may include contact burns to the skin, headace, shortness of breath, chest pain, kidney damage, liver damage, and pulmonary edema (possibly resulting in death). While the OSHA PEL has been set at a TWA of 0.2 mg Cd/cu m for cadmium dust, NIOSH recommends that cadmium dust be treated as a potential human carcinogen. Processes and operations which may release cadmium fumes or dust should be enclosed and fitted with exhaust ventilation. In activities where over-exposure is possible, workers should wear a high efficiency particulate filter respirator or self-contained breathing apparatus. Protective clothing also should be worn. Preferably this should include disposable one-piece suits (close-fitting at the ankles and wrists), gloves, hair covering, and overshoes. These should be removed before leaving work. If contact should occur, immediately wash contaminated skin with large amounts of water. Do not eat, smoke, or drink in work areas. Cadmium chloride presents only a moderate fire hazard (when in the form of dust) if exposed to heat, flame, or by chemical reaction with oxidizing agents, metals, hydrogen azide, zinc, selenium, or tellurium. For small fires involving cadmium chloride, extinguish with dry chemical, CO2, Halon, water spray, or standard foam, and for large fires, use water spray, fog, or standard foam. Wear a self-contained breathing apparatus when fighting such fires. Cadmium chloride should be stored in cool, well-ventilated areas, out of direct rays of the sun, and away from fire hazards. If small amounts cadmium chloride are released, remove all ignition sources, ventilate the area, and collect the released material in closed containers for latter disposal. For large spills on land, contain material in excavated pits or other holding areas (preferably lined with an impermeable flexible membrane liner). Cover solids with a plastic sheet. Dike far ahead of liquids to prevent the substance from entering water sources or sewers. For large spills into bodies of water, first neutralize with agricultural lime, crushed limestone, or sodium bicarbonate, then use mechanical dredges or lifts to remove immobilized masses and precipitates. Before implementing land disposal of waste cadmium chloride, consult environmental regulatory agencies for guidance.
National Toxicology Program. Eleventh Report on Carcinogens (2005). The Report on Carcinogens is an informational scientific and public health document that identifies and discusses substances (including agents, mixtures, or exposure circumstances) that may pose a carcinogenic hazard to human health. Cadmium and Cadmium Compounds are listed as known to be human carcinogens. /Cadmium and Cadmium Compounds/[Available from, as of July 31, 2009: http://ntp.niehs.nih.gov/ntp/roc/eleventh/profiles/s028cadm.pdf]
D006; A solid waste containing cadmium 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. /Cadmium/
Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:
In case of fire in the surroundings, use appropriate extinguishing media.
Fresh air, rest. Half-upright position. Artificial respiration may be needed. Refer for medical attention.
Remove contaminated clothes. Rinse skin with plenty of water or shower.
First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.
Rinse mouth. Give one or two glasses of water to drink. Refer for medical attention .
EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.
Biological Exposure Indices (BEI) [ACGIH] - Cd in urine = 5 ug/g creatinine; Cd in blood = 5 ug/L; sampling time not critical; Monitoring in blood should be preferred during the initial year of exposure and whenever changes in the degree of exposure are suspected. [ACGIH]
Environmental considerations: Land Spill: Dig a pit, pond, lagoon, or holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Cover solids with a plastic sheet to prevent dissolving in rain or fire fighting water.
Environmental considerations: Water Spill: neutralize with agricultural lime, crushed limestone, or sodium bicarbonate. Add ferric chloride. Adjust pH to neutral (pH= 7).
Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D006, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.
Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D006, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste. /Cadmium/
SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.
Personal protection: chemical protection suit including self-contained breathing apparatus. Do NOT let this chemical enter the environment. Sweep spilled substance into covered sealable containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.
An eye wash fountain should be provided within the immediate work area where cadmium chloride is being used. /Cadmium chloride dust/
If material not involved in fire: Keep material out of water sources and sewers. Build dikes to contain flow as necessary.
Personnel protection: Keep upwind. Avoid breathing vapors or dusts. ... Wash away any material which may have contacted the body with copious amounts of water or soap and water.
Notify local health and wildlife officials; notify operators of nearby water intakes.
SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. Quality assurance to ascertain the completeness of the cleaning procedures should be implemented before the decontaminated protective clothing is returned for reuse by the workers. All contaminated clothing should not be taken home at end of shift, but should remain at employee's place of work for cleaning.
THE RELATIVE EFFICACY OF A NUMBER OF CHELATING AGENTS WHEN ACTING AS ANTAGONISTS FOR ORAL CADMIUM CHLORIDE INTOXICATION IN MICE WAS STUDIED. THE CMPD WERE ADMINISTERED ORALLY AFTER THE ORAL ADMINISTRATION OF CADMIUM CHLORIDE AT 1 MMOL/KG. BY FAR THE MOST EFFECTIVE IN BOTH ENHANCING SURVIVAL AND LEAVING MINIMAL RESIDUAL LEVELS OF CADMIUM IN THE LIVER AND THE KIDNEY, WAS MESO-2,3-DIMERCAPTOSUCCINIC ACID. SEVERAL POLYAMINOCARBOXYLIC ACIDS ALSO ENHANCED SURVIVAL. THE MOST EFFECTIVE OF THESE IN REDUCING LIVER AND KIDNEY LEVELS OF CADMIUM WERE DIETHYLENETRIAMINEPENTAACETIC ACID, TRANS-1,2-DIAMINOCYCLOHEXANE-N,N,N',N'-TETRAACETIC ACID, AND TRIETHYLENETETRAMINEHEXAACETIC ACID. D-PENICILLAMINE PROMOTED SURVIVAL BUT ALSO LED TO KIDNEY CADMIUM LEVELS HIGHER THAN THOSE FOUND IN THE CONTROLS. SODIUM 2, 3-DIMERCAPTOPROPANE-1-SULFONATE WAS AS EFFECTIVE IN PROMOTING SURVIVAL AS MESO-2,3-DIMERCAPTOSUCCINIC ACID BUT LEFT LEVELS OF CADMIUM IN THE KIDNEY AND LIVER THAT WERE APPROXIMATELY 4 TIMES GREATER THAN THOSE FOUND WITH MESO-2,3-DIMERCAPTOSUCCINIC ACID.
Quinamic acid, bis-(3-carboxy-5-N-dicarboxymethyl-aminomethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinolinyl-8)-5,8 -dimethyl-6,7-dihydroxyl-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid, is a new chelating agent. Quinamic acid iv 500 mg/kg markedly reduced the mortality of acute ip poisoning of zinc sulfate, nickel chloride, cadmium chloride and uranyl nitrate in mice (p < 0.01). ... Within two weeks, treated rats showed less toxic reactions and renal /damage/ than the control rats. The activity of urinary catalase in treated rats was significatly lower than in controls.
the seeds of Cicer arietinum (L.) cv. Uday were inoculated with specific Rhizobium grown in sandy loam soil and were allowed to grow for 15 days. At this stage, the seedlings were supplied with 0, 50, 100 or 150 uM of cadmium in the form of cadmium chloride and sprayed with 0.01 uM of 28-homobrassinolide (HBL) at 30-day stage. The data indicated that plant fresh and dry mass, number of nodules, their fresh and dry mass, leghemoglobin content, nitrogen and carbohydrate content in the nodules, leaf chlorophyll content, nitrate reductase and carbonic anhydrase activities decreased proportionately with the increasing concentrations of cadmium but the content of proline and the activities of catalase, peroxidase and superoxide dismutase increased. The ill effect, generated by cadmium, was overcome if the stressed plants were sprayed with HBL. The cadmium toxicity can be overcome by the foliar application of 28-homobrassinolide.
Several observations, both in humans and laboratory animals, have suggested that proanthocyanidins exhibit a broad spectrum of pharmacological, therapeutic and chemoprotective properties. Specifically, some of our earlier studies have shown that IH636 grape seed proanthocyanidin extract (GSPE, commercially known as ActiVin) provides excellent concentration- and dose-dependent protection against toxicities induced by diverse agents, such as acetaminophen, hydrogen peroxide, 12-O-tetradecanoylphorbol-13-acetate (TPA), smokeless-tobacco extract, idarubicin and 4-hydroxyperoxycyclophosphamide in both in vitro and in vivo models. In some models, GSPE proved to be a better cytoprotectant than vitamins C, E and beta-carotene. The purpose of this investigation was three fold: (i) to indirectly assess the bioavailability of GSPE in multiple target organs, (ii) quantify GSPE's capacity to avert cadmium chloride (CdCl2)-induced nephrotoxicity, dimethylnitrosamine (DMN)-induced splenotoxicity and O-ethyl-S,S-dipropyl phosphorodithioate (MOCAP)-induced neurotoxicity, and lastly (iii) to evaluate possible mechanisms of protection in mice. In order to determine all these, three separate experiments were designed and each experiment consisted of four groups, such as vehicle control, GSPE alone, toxicant alone and GSPE + toxicant. GSPE was administered orally (100 mg/kg) for 7-8 days prior to the toxicant exposure. Parameters of the analyses included evaluation of serum chemistry changes (ALT, BUN and CK), histopathology and integrity of genomic DNA, both quantitatively and qualitatively. Results indicate that GSPE preexposure prior to cadmium chloride and DMN provided near complete protection in terms of serum chemistry changes (ALT, BUN and CK) and inhibition of both forms of cell death. e.g., apoptosis and necrosis. DNA damage, a common denominator usually associated with both apoptosis and necrosis was significantly reduced by GSPE treatment. Histopathological examination of organs correlated strongly with the changes in serum chemistry and the DNA modification data. Surprisingly, MOCAP exposure showed symptoms of neurotoxicity coupled with serum chemistry changes in the absence of any significant genomic DNA damage or brain pathology. Although, GSPE appeared to partially protect the neural tissue, it powerfully antagonized MOCAP-induced mortality. Taken together, this study suggests that in vivo GSPE-preexposure may protect multiple target organs from a variety of toxic assaults induced by diverse chemical entities.
For more Interactions (Complete) data for CADMIUM CHLORIDE (30 total), please visit the HSDB record page.
LC50; Species: Coturnix japonica (Japanese quail) 14 days old, oral 2584 ppm for 5 days (95% confidence limit: 2165-3083 ppm)
LC50; Species: Coturnix japonica (Japanese quail) 14 days posthatch, oral, ad libitum (chemical incorporated into the food) 2400 ppm for 5 days (95% confidence limit: 1807-3294 ppm)
LC50; Species: Phasianus colchicus (Ring-necked Pheasant) 10 days old, oral 767 ppm for 5 days (95% confidence limit: 651-898 ppm)
LC50; Species: Anas platyrhynchos (Mallard duck) 10 days old, oral >5000 ppm (no mortality to 1580 ppm, 8% at 5000 ppm)
For more Ecotoxicity Values (Complete) data for CADMIUM CHLORIDE (136 total), please visit the HSDB record page.
Nephrotoxin - The chemical is potentially toxic to the kidneys in the occupational setting.
Compound with “fair evidence” of ototoxicity (suspected ototoxic substance).
The substance can be absorbed into the body by inhalation of its aerosol and by ingestion.
Oral (L6) ; inhalation (L6) ; dermal (L6)
IN LACTATING COWS FED 3 G CADMIUM AS CADMIUM CHLORIDE DAILY, CADMIUM ACCUMULATED IN THE MAMMARY GLAND, AND MILK PRODUCTION WAS DECREASED DRASTICALLY, BUT CADMIUM WAS NOT INCORPORATED INTO MILK PROTEINS AND COULD BE FOUND ONLY IN TRACE AMOUNTS, LESS THAN 0.1 PPM, IN THE MILK.
Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (L8, A18, A19, A28)
/BIRDS and MAMMALS/ Mechanism of testicular toxicity induced by dietary cadmium (Cd) has been less investigated than that following acute Cd injection. In the present study ... testicular injury in a small rodent, the bank vole, exposed subchronically to dietary Cd in a quantity of 0.9 mol/g /was characterized/, and ... the importance of some factors (Cd accumulation, metallothionein (MT), oxidative stress, and zinc (Zn)) /was determined/ in the injury. Dietary Cd induced moderate histopathological changes (hemorrhage in interstitium, necrosis and apoptosis in seminiferous tubule epithelium) in young (1 month old) bank voles fed, for 6 weeks, Fe-adequate (1.1-1.4 mol/g) and Fe-enriched (4.5-4.8 mol/g) diets. In contrast, adult (5 months old) bank voles appeared to be resistant to the toxic effects of dietary Cd, despite the fact that testicular Cd contents were higher and MT levels lower than those in the young animals. The Cd-induced histopathological changes and apoptosis were accompanied by increased testicular lipid peroxidation, decreased testicular Zn concentration and elevated levels of hepatic and renal MT and Zn. Supplemental dietary Zn (1.7-1.8 mol/g) prevented the Cd-induced testicular Zn depletion and injury. The data indicate that dietary Cd produces testicular lesions indirectly, through decreasing testicular Zn, which seems to be due to the sequestration of this element by the Cd-induced hepatic and renal MT.
/BIRDS and MAMMALS/ Pairs of adult black ducks (Anas rubripes) were fed a diet containing 0, 4 or 40 ppm cadmium as cadmium chloride. One-week-old ducklings that had been fed the same dietary concentrations of cadmium as had their parents were tested for avoidance of a fright stimulus. Ducklings fed 4 ppm cadmium ran significantly farther from the stimulus than did controls or ducklings fed 40 ppm cadmium. Such an alteration in behavior could have harmful effects on wild birds.
/BIRDS and MAMMALS/ The effects of in vitro exposure of beluga whale splenocytes and thymocytes to different concentrations of mercury chloride (HgCl2), cadmium chloride (CdCl2), and lead chloride (PbCl2) were evaluated. The cells were cultured for 66 hr with either concanavalin A (Con-A), phytohemagglutinin-P, or without mitogen, after which percentage of cell death and proliferation were evaluated. Increased percentage of cell death was observed in Con-A-stimulated thymocytes cultured with HgCl2, while the viability of splenocytes was not affected by exposure to metals. Decreased splenocyte and thymocyte proliferation was observed with the highest concentration of HgCl2 and CdCl2 (10-5 M), while lower concentrations of these metals (10-6 and 10-7 M) as well as all the different concentrations of PbCl2 (10-4, 10-5, and 10-6 M) did not significantly influence cell proliferation. Concentrations of metals that were found to affect the proliferation of beluga lymphocytes are similar to those found in the liver of beluga whales from wild populations.
/AQUATIC SPECIES/ Common carp (Cyprinus carpio), Prussian carp (Carassius gibelio) and Peppered cory (Corydoras paleatus) were evaluated as target species to perform genotoxicity tests for heavy metals. Fishes were exposed to different doses of cadmium (0.005-0.1 mg/L) and copper (0.01-0.25 mg/L) for 21 days. Hexavalent chromium at a single dose of 5 mg/L was used as a positive control. Frequencies of micronuclei and binuclei were evaluated comparatively in peripheral blood erythrocytes, gill epithelial cells and liver cells. As a result it was observed that, fish species and their tissues showed differential sensitivity to the heavy metal treatment. In general, frequencies of micronucleated and binucleated cells significantly increased following the exposure for 21 days to copper, cadmium and chromium. On the other hand, gill and liver cells showed higher frequencies of micronuclei and binuclei than erythrocytes. Our results indicated the formation of micronuclei and binuclei in fish cells caused by their exposure to cadmium, copper and chromium, thus verifying results obtained earlier on mammals, which indicated that these heavy metals have cytotoxic and genotoxic effects. The suitability of the micronucleus assay in native fish species for the screening of aquatic genotoxicants is highlighted and the importance of target tissue selection in the piscine micronucleus test is emphasized.
Cough. Laboured breathing. Symptoms may be delayed.
Redness.
Redness. Pain.
Abdominal pain. Burning sensation. Diarrhoea. Nausea. Vomiting.
Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (L6)
D006; A solid waste containing cadmium 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. /Cadmium/
As the federal pesticide law FIFRA direct, EPA is conducting a comprehensive review of older pesticides to consider their health and environmental effects and make decisions about their future use. Under this pesticide reregistration program, EPA examines health and safety data for pesticide active ingredients initially registered before November 1, 1984, and determines whether they are eligible for reregistration. In addition, all pesticides must meet the new safety standard of the Food Quality Protection Act of 1996. Pesticides for which EPA had not issued Registration Standards prior to the effective date of FIFRA 88 were divided into three lists based upon their potential for human exposure and other factors, with List B containing pesticides of greater concern and List D pesticides of less concern. Cadmium chloride is found on List B. Case No: 2085; Pesticide type: Fungicide; Case Status: Cancelled - No products containing the pesticide are actively registered. Therefore, we are characterizing the case as cancelled. Under FIFRA, pesticide producers may voluntarily cancel their registered products. EPA also may cancel pesticide registrations if registrants fail to pay required fees or make/meet certain reregistration commitments, or if EPA reaches findings of unreasonable adverse effects. Active ingredient (AI): Cadmium chloride; AI Status: Cancelled - The active ingredient is no longer contained in any registered pesticide product. Thus, we characterize it as cancelled.
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. Cadmium chloride is included on this list.
Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 10 lb or 4.54 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).
Cadmium chloride is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.
Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /Cadmium and compounds/
(AZ) ARIZONA 5 ug/L /Cadmium/
(ME) MAINE 3.5 ug/L /Cadmium/
(MN) MINNESOTA 4 ug/L /Cadmium/
Whether translation initiation factor 4E (eIF4E), the mRNA cap binding and rate-limiting factor required for translation, is a target for cytotoxicity and cell death induced by cadmium, a human carcinogen, was investigated. Exposure of human cell lines, HCT15, PLC/PR/5, HeLa, and Chang, to cadmium chloride resulted in cytotoxicity and cell death, and this was associated with a significant decrease in eIF4E protein levels. Similarly, specific silencing of the expression of the eIF4E gene, caused by a small interfering RNA, resulted in significant cytotoxicity and cell death. On the other hand, overexpression of the eIF4E gene was protective against the cadmium-induced cytotoxicity and cell death. Further studies revealed the absence of alterations in the eIF4E mRNA level in the cadmium-treated cells despite their decreased eIF4E protein level. In addition, exposure of cells to cadmium resulted in enhanced ubiquitination of eIF4E protein while inhibitors of proteasome activity reversed the cadmium-induced decrease of eIF4E protein. Exposure of cells to cadmium, as well as the specific silencing of eIF4E gene, also resulted in decreased cellular levels of cyclin D1, a critical cell cycle and growth regulating gene, suggesting that the observed inhibition of cyclin D1 gene expression in the cadmium-treated cells is most likely due to decreased cellular level of eIF4E. Taken together, our results demonstrate that the exposure of cells to cadmium chloride resulted in cytotoxicity and cell death due to enhanced ubiquitination and consequent proteolysis of eIF4E protein, which in turn diminished cellular levels of critical genes such as cyclin D1.
A POSSIBLE MECHANISM OF THE PRESSOR EFFECT OF CADMIUM (AS CADMIUM CHLORIDE) WAS INVESTIGATED BY USING THE ISOLATED THORACIC AORTA FROM RATS. CADMIUM PRODUCED CONTRACTION IN THE LOW CONCN & RELAXATION AT THE HIGH CONCN. THE CONTRACTION BY CADMIUM IS DEPENDENT ON THE EXTERNAL CALCIUM & THE LOW CONCN OF CADMIUM ACCELERATES THE CALCIUM RELEASE FROM THE CALCIUM STORE, THE HIGH CONCN INHIBITING THE CALCIUM RELEASE &/OR THE FUNCTION OF CONTRACTILE PROTEINS.
For more Mechanism of Action (Complete) data for CADMIUM CHLORIDE (8 total), please visit the HSDB record page.
Cadmium is absorbed from oral, inhalation, and dermal routes. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (L6)
To investigate the relationship between cadmium (Cd) toxicity, intestinal absorption, and its distribution to various tissues in rats treated orally with minimum amounts of Cd, 14 female rats per dose group per time point were given diets consisting of 28% purified diet and 72% ordinary rice containing Cd-polluted rice (0.02, 0.04, 0.12, or 1.01 ppm of Cd) or CdCl2 (5.08, 19.8, or 40.0 ppm of Cd) for up to 8 months. At 1, 4, and 8 months after the commencement of Cd treatment, seven rats per group were euthanized for pathological examinations to determine the Cd concentrations in the liver and kidneys and metallothionein (MT) in the liver, kidneys, intestinal mucosa, serum, and urine. One week before each period of 1, 4, and 8 months, the remaining seven rats in each group were administered a single dosage of Cd(109), a tracer, to match the amounts of the designated Cd doses (about 1.2 to 2400 ug/kg body wt). They were euthanized 5 days later to determine the distribution of Cd to various tissues. No Cd-related toxic changes were observed. The concentrations of Cd in the liver and kidneys at any time point and MT in the liver, kidney, serum, and urine at 4 and 8 months increased dose-dependently, whereas MT in the intestinal mucosa did not alter markedly at any time point. The distribution rates of Cd to the liver increased dose-dependently (40% at lower doses to 60% at higher doses), whereas those to the kidney decreased dose-dependently (20% at lower doses to 10% at higher doses). The Cd retention rates 5 days after Cd(109) administration (amounts of Cd in various tissues/amounts of Cd administered) ranged from 0.2 to 1.0% at any time point. These results suggest that the distribution of Cd to the liver and kidneys after the oral administration vary depending on the dosage levels of Cd. The difference of the distribution pattern of Cd to the liver and kidney is probably due to the difference in the form of the absorbed Cd, i.e., free ion or Cd-MT complex, although not closely related to the MT in the intestinal mucosa.
An increased body retention of Cd in rats orally pretreated with Cd or Zn is explained by induction of hepatic and renal metallothionein. Whether intestinal absorption of Cd increases after such treatments is not clear yet. To approach this problem we measured jejunal transfer rates of Cd(109) in vitro and in vivo in pretreated rats (0.44 mmol Cd/L or 4.6 mmol Zn/L in the drinking water for 10 days) and compared them with those of untreated controls. Isolated jejunal segments were used for in vitro perfusion. In vivo perfusion was performed in anaesthetized rats with blood collected from mesenteric venules substituting corresponding losses by reinfusion of rat blood. Water and glucose transfer did not differ between controls and pretreated rats. At a luminal concentration of 5 umol Cd(109)Cl2/L, Cd and Zn pretreatment significantly increased the transfer rate of Cd(109) in vitro and in vivo similarly. The Cd(109) transfer rates in controls in the final perfusion intervals (80-120 min) were 0.06 (pmol/cm/min) in vivo and 0.05 in vitro; the corresponding rates in Cd or Zn pretreated rats were significantly higher (P<0.05) and amounted to 0.11 and 0.18 or 0.15 and 0.23, respectively. Mucosal concentrations of Cd(109) measured at the end of the perfusion period tended to be lower in the pretreated animals than in the controls. This suggests that pretreatment with Cd or Zn reduces the amount of Cd(109) bound to the tissue leaving more Cd(109) for the transfer step. As compared to a level of mucosal metallothionein of 8 ug/g wet weight in controls, increased amounts of 67 or 52 ug/g wet weight in the Cd or Zn pretreated rats, respectively, thus did not decrease but increased transfer rates of Cd(109). Therefore, increased small intestinal transfer rates of Cd can contribute to increase the body retention of Cd seen after oral pretreatment with Cd or Zn.
ADULT RATS WERE INJECTED INTRAVENOUSLY WITH (109)CADMIUM CHLORIDE AND THE DISTRIBUTION OF THE ISOTOPE WITHIN THE BRAIN AND NEIGHBORING NERVOUS STRUCTURES WAS SUBSEQUENTLY STUDIED BY AUTORADIOGRAPHY. CADMIUM ACCUMULATED IN REGIONS OUTSIDE THE BLOOD-BRAIN BARRIER SUCH AS THE CHOROID PLEXUS, PINEAL GLAND AND AREA POSTREMA, BUT DID NOT APPEAR IN THE BRAIN PARENCHYMA. UPTAKE OF CADMIUM WAS OBSERVED IN THE TRIGEMINAL GANGLIA CLOSE TO THE NERVE CELLS AND IN THE OLFACTORY BULBS. IN ADDITION, CADMIUM ACCUMULATED IN THE IRIS, CILIARY BODY AND CHOROID OF THE EYE, BUT NOT IN THE OPTIC NERVES. THE DEPOSITION OF CADMIUM IN THE OLFACTORY BULBS MAY BE RELATED TO THE ANOSMIA REPORTED IN WORKERS EXPOSED TO THIS METAL.
CADMIUM CHLORIDE ADMIN TO RATS BY SC INJECTION OR DIRECTLY INTO LIVER IS TRANSPORTED TO TESTES. ... /ALSO, WHEN/ GIVEN SC TO RATS /IT/ APPEARED IMMEDIATELY IN PLASMA & THEN DISAPPEARED RAPIDLY; AFTER 6 DAYS ONLY 2% OF DOSE ... EXCRETED IN FECES.
For more Absorption, Distribution and Excretion (Complete) data for CADMIUM CHLORIDE (18 total), please visit the HSDB record page.
Used in photography; textile dyeing, galvanoplasty, mirror manufacturing, lubricants; fungicides, pyrotechnics, and electroplating; [Merck Index] Used in tinning solution and to make cadmium sulfide (cadmium yellow); [Hawley]
No longer used as fungicide in the US; EPA cancelled status; [HSDB]
Electroplating [Category: Plate]
For Cadmium chloride (USEPA/OPP Pesticide Code: 012902) there are 0 labels match. /SRP: Not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./
The use of cadmium soaps as components of PVC stabilizers is decreasing because of their toxic properties. Solid PVC stabilizers contain cadmium soaps of saturated fatty acids, whereas liquid stabilizers contain soaps of unsaturated or branched, short-chain fatty acids. The soaps act as heat and light stabilizers, and soaps of saturated fatty acids are used as lubricants in the processing of PVC. Unlike other metallic soaps used in the PVC sector, cadmium soaps do not affect transparency and are suitable for hard, transparent PVC products. However, for safety reason their use is nowadays being replaced by mixtures of calcium-zinc stearate plus other stabilizers. /Cadmium metallic soaps/
Intermediate in the production of cadmium-containing stabilizers and pigments.
Insoluble matter: 0.01%; substances not precipitated by H2S: 0.3%; nitrate and nitrite as NO3: 0.003%; sulfate as (SO4): 0.005%; ammonium (NH4): 0.002%; copper: 0.001%; iron: 0.001%; lead: 0.005%; zinc: 0.1%.
Cadmium chloride, 2.5 hydrate, crystal: insoluble matter: 0.005%; substances not precipitated by hydrogen sulfide (as sulfate): 0.2%; nitrate and nitrite as NO3: 0.003%; sulfate as SO4: 0.005%; ammonium (NH4): 0.002%; lead: 0.005; zinc: 0.1%; maximum limits of trace impurities: copper: 5 ppm; iron: 5 ppm. /Cadmium chloride, 2.5 hydrate, crystal/
Cadmium chloride is produced by reaction of molten cadmium and chlorine gas at 600 °C or by dissolving cadmium metal or the oxide in hydrochloric acid, subsequently vaporizing the solution.
Preparation of cadmium chloride (anhydrous): the hydrate is refluxed with thionyl chloride, or calcined in a hydrogen chloride atmosphere.
It may be formed by the addition of dry cadmium acetate to a mixture of glacial acetic acid and acetyl chloride.
Dissolving the metal, the carbonate, oxide, sulfide, or hydroxide in hydrochloric acid and evaporating the solution. /Pentahydrate/
Anhydrous material may be drived from /the pentahydrate/ ... by heating in a stream of dry HCl.
USEPA/OPP Pesticide Code 012902; Trade Names: Vi-cad, Caddy.
Commercial cadmium chloride is mixture of hydrates that approximates to dihydrates (CdCl2.2H2O). Commercial grade ... available in USA typically contains about 51% cadmium & 0.005% each of iron and copper. Higher purity grades /are/ available for specialized applications ...
/FORMER/ LIQUID. CADDY CONTAINS 20.1% EQUIVALENT TO 12.3% ELEMENTAL CADMIUM. CAD-TRETE IS A COMBINATION OF THIRAM AND CADMIUM CHLORIDE COMPLEX.
Purities: 99.0 - >99.99%; American Chemical Society reagent grade, 95 - >99%; anhydrous, 99.99 - 99.999%.
For more Formulations/Preparations (Complete) data for CADMIUM CHLORIDE (6 total), please visit the HSDB record page.
Cadmium chloride (CdCl2): ACTIVE
Fungicide (Status: Cancelled)
개요Cadmium chloride is a colourless and odourless crystal. It is used for the preparation of cadmium sulphide, used as ‘cadmium yellow’, a brilliant-yellow pigment, which is stable to heat and sulphide fumes. Cadmium chloride has a high solubility in water and is a non-combustible solid, but the dust can be a moderate fire hazard when exposed to heat or flame or when reacted with oxidising agents. It is incompatible with bromine trifluoride, potassium oxidisers, zinc, selenium, tellurium, and hydrogen azide.
용도Cadmium Chloride is used in the preparation of the stable inorganic pigment cadmium sulfide (Cadmium Yellow). Cadmium Chloride treatment of thin film CDTe solar cells is used to produce high-efficienc y solar cells.. Cadmium Chloride is also used in the preparation of organocadmium compounds.
일반 설명Cadmium chloride is a white crystalline solid. Cadmium chloride is soluble in water. Cadmium chloride is noncombustible. The primary hazard of Cadmium chloride is that Cadmium chloride poses a threat to the environment. Immediate steps should be taken to limit its spread to the environment. Cadmium chloride is used in photography, in fabric printing, in chemical analysis, and in many other uses.
Cadmium chloride may be prepared by heating the metal with chlorine or hydrogen chloride gas. In the solution, it is formed by treating the metal or its salts, such as oxide, hydroxide, carbonate, or sulfide with hydrochloric acid:Cd + 2HCl → CdCl2 + H2CdO + 2HCl → CdCl2 + H2OCdCO3 + 2HCl → CdCl2+ H2O + CO2The solution is evaporated and crystallized to yield a hydrated salt. The hydrated salt yields anhydrous cadmium chloride upon heating under hydrogen chloride or when refluxed with thionyl chloride.Cadmium chloride also may be prepared by adding dry cadmium acetate to acetyl chloride in glacial acetic acid.
생산 방법Cadmium chloride is manufactured in reaction of cadmium metal, carbonate, sulfide, oxide, or hydroxide with hydrochloric acid, followed by evaporation; it forms hydrated salt. Commercial cadmium chloride is amixture of hydrates that approximates to dihydrates. The commercial grade available in the United States typically contains about 51% of cadmium. Liquid caddy contains 20.1% cadmium chloride.
For more Ecotoxicity Excerpts (Complete) data for CADMIUM CHLORIDE (17 total), please visit the HSDB record page.