Cadmium acetate

Metals -> Cadmium Compounds, Inorganic

Carcinogens

2.34 at 68 °F (USCG, 1999) - Denser than water; will sink

2.34 g/cu cm

Becomes anhydrous at about 130 °C; density 2.01 g/cu cm; pH of 0.2 molar aq soln 7.1; colorless crystals; freely soluble in water; soluble in alcohol /Cadmium acetate dihydrate/

2.34 g/cm³

2.341 @25 °C

Colorless crystals

Monoclinic, colorless crystals

Soluble in water, ethanol

Solubility in water: very good

255 °C

255 °C

255 °C

Cadmium acetate is an odorless colorless solid. Sinks and mixes with water. (USCG, 1999)

Colorless solid; [HSDB] White powder; [MSDSonline]

COLOURLESS CRYSTALS WITH CHARACTERISTIC ODOUR.

Warning

H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]

P261, P264, P270, P271, P273, P280, P301+P317, P302+P352, P304+P340, P317, P321, P330, P362+P364, P391, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 74 reports by companies from 8 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Danger

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

Chemical: Acetic acid, cadmium salt

Restricted substance: Cadmium di(acetate)

Cadmium acetate: Does not have an individual approval but may be used under an appropriate group standard

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

Special Hazards of Combustion Products: Toxic cadmium oxide fumes may form in fires. (USCG, 1999)

Not combustible. Gives off irritating or toxic fumes (or gases) in a fire.

An eye and respiratory tract irritant; May cause damage to lungs, liver, and kidneys; [HSDB] Cadmium compounds are potential carcinogens that are toxic to the kidneys, bone, and respiratory tract. [ICSC] An irritant; May be absorbed through skin; [MSDSonline] See Cadmium and the linked diseases.

The major hazards encountered in the use and handling of cadmium acetate stem from its toxicologic properties. Toxic primarily by ingestion and inhalation, exposure to this colorless, crystalline substance may occur in its use in electroplating, in dyeing and printing textiles, in manufacturing cadmium halides, and in finishing porcelains and pottery. Effects from exposure may include headache, nausea, shortness of breath, chest pain, kidney damage, liver damage, emphysema, intense pulmonary edema (possibly resulting in death). Processes and operations which may release cadmium fumes or dust should be enclosed and fitted with exhaust ventilation to maintain exposure at or below recommended levels. 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, including eye, face, and hand protection. All clothing 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 acetate 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 acetate, extinguish with dry chemical, CO2, Halon, water spray or standard foam, and for large fires, use water spray, or standard foam. Cadmium acetate fires may produce irritating or poisonous gases. Wear a self-contained breathing apparatus and protective clothing when fighting such fires. Cadmium acetate should be stored in cool, well-ventilated areas, out of direct rays of the sun, and away from fire hazards. Small spills of cadmium acetate may be placed in containers for latter disposal (solutions are first taken up with sand or other noncombustible absorbent). Large liquid spills are contained in excavated pits or other holding areas that have been sealed with an impermeable flexible membrane liner. Runoff should be diked to prevent cadmium acetate from entering water sources or sewers. Solids should be covered with a plastic sheet. Liquid spills are neutalized with agricultural lime, crushed limestone, or sodium bicarbonate, and mechanical dredges or lifts used to remove immobilized masses. Before implementing land disposal of waste cadmium acetate, 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/

Salts, basic, such as CADMIUM ACETATE, are generally soluble in water. The resulting solutions contain moderate concentrations of hydroxide ions and have pH's greater than 7.0. They react as bases to neutralize acids. These neutralizations generate heat, but less or far less than is generated by neutralization of the bases in reactivity group 10 (Bases) and the neutralization of amines. They usually do not react as either oxidizing agents or reducing agents but such behavior is not impossible. Special Hazards of Combustion Products: Toxic cadmium oxide fumes may form in fires (USCG, 1999).

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.

Remove contaminated clothes. Rinse skin with plenty of water or shower.

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

Rinse mouth. Give one or two glasses of water to drink.

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]

If material on fire or involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) Use water in flooding quantities as fog. Use "alcohol" foam, dry chemical or carbon dioxide. /Cadmium compounds, NOS/

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.

Precipitate /cadmium/ from solutions /of cadmium acetate/ as sulfides, and return to supplier.

Peer-review: Soluble cadmium cmpd are converted to insoluble form, the sludge filtered, solidified and deposited in a suitable /SRP: hazardous waste/ landfill. Incineration of cadmium cmpd is not recommended because of the high sublimability of the oxide. (Peer-review conclusions of an IRPTC expert consultation (May 1985))

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. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Do NOT let this chemical enter the environment. Carefully collect remainder. Then store and dispose of according to local regulations.

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.

Few studies have characterized the molecular and biochemical mechanisms involved in ovarian steroidogenesis disruption by heavy metals, such as lead and cadmium coexposure, on F1 generation offspring. In this study, adult pregnant female rats were treated subcutaneously (0.05 mg/kg of body weight per day) with sodium acetate (control), lead acetate, and cadmium acetate separately and in combination throughout gestational and lactational period, and all animals from each of the experimental groups were sacrificed by decapitation on postnatal day 56 for various assays. The activities of key steroidogenic enzymes (17-hydroxysteroid dehydrogenase and 3-hydroxysteroid dehydrogenase) decreased in all the metal-treated groups. But the most significant decrease in the activities was observed in the cadmium-treated group, whereas the combined exposure group showed an intermediate effect. Serum estradiol and progesterone levels were also significantly altered in all the metal-treated groups, with the cadmium-exposed group showing maximum reductions as compared with the control group. The inhibitory effects of lead and cadmium on ovarian steroidogenic acute regulatory protein (StAR) mRNA levels along with CYP11 mRNA levels were also observed. Ovarian cholesterol content measured also showed significant depletion in all the metal-treated groups, with the cadmium-exposed group showing the maximum depletion. The activities of ovarian enzymatic antioxidants, such as superoxide dismutase, catalase, and glutathione peroxidase, were all significantly diminished along with significant depletion in nonenzymatic antioxidants. Lipid peroxidation was elevated significantly in all the metal-treated groups. In conclusion, lead and cadmium inhibit ovarian steroidogenesis by downregulating StAR gene expression along with inhibiting activities of steroidogenic enzymes and antioxidant system.

Effects of lead (Pb) and cadmium (Cd) both alone or in combination on the binding of LH and FSH on isolated granulosa cells were studied. Granulosa cells isolated from proestrous rats were incubated (in vitro) with lead acetate and/or cadmium acetate (0.03 uM of Pb or Cd) for 1 hr. LH binding was dropped to 84% in Pb treated cells, 72.5% in Cd treated cells and 74.8% in combined metal treated cells compared to control. FSH binding dropped to 85.5% in Pb treated cells, 71.16% in Cd treated cells and 72.5% in combined metal treated cells compared to control. Activity of 17beta Hydroxy Steroid Dehydrogenase (17betaHSDH), a key steroidogenic enzyme was reduced by 52% in Cd and 37% in combined metal exposed cells whereas Pb exposed cells showed 31% reduction in the enzyme activity. Pretreatment with SH groups protectants (glutathione [GSH], dithiothretol [DTT]) and zinc caused an ameriolation in enzyme activity whereas Zn pretreatment showed an increase in gonadotropin binding in metal exposed cells. These results suggest that both Pb and Cd can cause a reduction in LH and FSH binding, which significantly alters steroid production in vitro and exerts a direct influence on granulosa cell function

Heavy metals tend to occur in increasingly many aspects of human activities. Studies of cadmium (Cd) have revealed that it is extremely toxic in its effects. It is known that selenium (Se) may suppress deleterious effects of Cd. We investigated the effects of dietary Cd-intoxication on the incorporation of precursors of RNA, protein and ANP (atrial natriuretic peptide) granule synthesis in mouse cardiocytes and compared them with the results of Se interaction with Cd-intoxication. Functional condition of the heart was evaluated on the basis of the number of ANP granules synthesized in cardiocytes of the right atrium in the mice exposed to the tested elements. The experiment was conducted on 100 male white Balby mouse during the period of three months. The animals were divided into four groups. The control group I (C) was fed a standard Murigran diet. Group II (Cd)--received 50 ppm Cd as cadmium acetate in drinking water. Group III (Se) received a standard diet supplemented with 5.0 mg Se /per/kg /of dry matter per/24 hr as acid sodium selenate. The experimental animals in group IV (Cd + Se)--were fed a diet supplemented with Cd and Se in the same amounts as the above groups. Our results revealed that after 3 months long intoxication with Cd, (3)H-uridine and (3)H-alanine uptakes to cardiomyocytes were decreased by 33% and 40%, respectively, and fewer ANP granules were synthesized when compared with the controls. Ultrastructure of myocytes proved slightly distorted. Se-intoxicated cardiomyocytes indicated diminished incorporation of RNA synthesis precursors by 17% and 27% in the ventricle and atrium, respectively, in comparison with the controls. Some Se-induced structural changes were observed. Finally, after Se in interaction with Cd intoxication, the uptake of 3H-uridine and 3H-alanine to cardiocytes was higher and the number of ANP granules increased. The values approximated those in the controls. We concluded that: prolonged Cd intoxication disturbed intercellular metabolism by damaging ultrastructural elements and suppressing the incorporation of precursors of RNA, protein and ANP granule synthesis. Se in interaction with Cd revealed protective effects against Cd toxicity. After /combined/ Cd-Se-intoxication neither metabolic activity nor cardiocyte ultrastructure showed significant differences from those in the controls.

Adult female rats were treated subcutaneously (0.05 mg/kg body wt/day) with lead acetate and cadmium acetate separately and in combination during the gestational and lactational periods with a pre-exposure before mating. No change in the reproductive cyclicity was observed in any of the treated groups. The number of pregnancies was similar in all groups and no effect was observed on reproductive performance. The litter size, placental weights, pup weights, pup liver weights, maternal weights or maternal liver weights did not differ significantly. The activities of hepatic steroid metabolising enzyme 17-beta-hydroxy steroid oxidoreductase and of UDP glucoronyl transferase were decreased and the hepatic cytochrome P450 (CYP450) content was reduced by the metal exposure. Hepatic DNA and glycogen content were decreased in the cadmium and the combined treated groups in both lactating mother and pups at post-natal day 21 (PND 21). Lead and cadmium accumulated in the liver of the metal treated pregnant and lactating rats. The accumulation of the metals was also observed in fetal and pups (PND 21). Hepatic zinc content was increased in the cadmium and the combined treated pregnant and lactating mothers whereas fetal and neonatal livers showed a decrease in the zinc as compared to control. The results of the study indicate that despite the ability of lead and cadmium to alter various biochemical parameters the effect in the liver is not intensified at combined exposure to both lead and cadmium. The observed biochemical alterations in the liver of rats co-exposed to lead and cadmium may result from an independent effect of lead and/or cadmium and also from their interaction. However, these results suggest that when lead and cadmium are administered together in similar concentrations, the major effects are mediated by cadmium.

For more Interactions (Complete) data for CADMIUM ACETATE (18 total), please visit the HSDB record page.

LC50; Species: Daphnia magna (Water flea ); Conditions: freshwater, 25 °C; Concentration: 980 ug/L for 24 hr (95% confidence interval: 820-1100 ug/L) /Other conditions of bioassay not specified in source examined/

LC50; Species: Barbus ticto (Two-Spot Or Tic Tac Toe Barb) length 3.6-4.7 cm, weight 325-331 mg; Conditions: freshwater, static, 25 (23-26) °C, pH 8.0 (7.9-8.2), hardness 175 mg/L CaCO3 (170-180 mg/L CaCO3), alkalinity 145 mg/L CaCO3 (140-152 mg/L CaCO3), dissolved oxygen 5.3 mg/L (5.2-6.0 mg/L); Concentration: 35,000 ug/L for 24 hr

LC50; Species: Barbus ticto (Two-Spot Or Tic Tac Toe Barb) length 3.6-4.7 cm, weight 325-331 mg; Conditions: freshwater, static, 25 (23-26) °C, pH 8.0 (7.9-8.2), hardness 175 mg/L CaCO3 (170-180 mg/L CaCO3), alkalinity 145 mg/L CaCO3 (140-152 mg/L CaCO3), dissolved oxygen 5.3 mg/L (5.2-6.0 mg/L); Concentration: 30,000 ug/L for 48 hr

LC50; Species: Barbus ticto (Two-Spot Or Tic Tac Toe Barb) length 3.6-4.7 cm, weight 325-331 mg; Conditions: freshwater, static, 25 (23-26) °C, pH 8.0 (7.9-8.2), hardness 175 mg/L CaCO3 (170-180 mg/L CaCO3), alkalinity 145 mg/L CaCO3 (140-152 mg/L CaCO3), dissolved oxygen 5.3 mg/L (5.2-6.0 mg/L); Concentration: 26,000 ug/L for 96 hr

For more Ecotoxicity Values (Complete) data for CADMIUM ACETATE (23 total), please visit the HSDB record page.

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

Oral (L6) ; inhalation (L6) ; dermal (L6)

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)

/AQUATIC SPECIES/ With their increased use, engineered nanomaterials (ENMs) will enter the environment where they may be altered by bacteria and affect bacterial processes. Metallic ENMs, such as CdSe quantum dots (QDs), are toxic due to the release of dissolved heavy metals, but the effects of cadmium ions versus intact QDs are mostly unknown. Here, planktonic Pseudomonas aeruginosa PG201 bacteria were cultured with similar total cadmium concentrations as either fully dissolved cadmium acetate (Cd(CH3COO)2) or ligand capped CdSe QDs, and cellular morphology, growth parameters, intracellular reactive oxygen species (ROS), along with the metal and metalloid fates were measured. QDs dissolved partially in growth media, but dissolution was less in biotic cultures compared to sterile controls. Dose-dependent growth effects were similar for low concentrations of either cadmium salts or QDs, but effects differed above a concentration threshold of 50 mg/L(total cadmium basis) where (1) the growth of QD-treated cells was more impaired, (2) the membranes of QD-grown cells were damaged, and (3) QD-grown cells contained QD-sized CdSe cytoplasmic inclusions in addition to Se0 and dissolved cadmium. For most concentrations, intracellular ROS were higher for QD-versus cadmium salts-grown bacteria. Taken together, QDs were more toxic to this opportunistic pathogen than cadmium ions, and were affected by cells through QD extracellular stabilization, intracellular enrichment and cell-associated decay.

/PLANTS/ Cadmium sulfate was more toxic than cadmium nitrate or cadmium acetate when tested on garlic (Allium sativum) root meristems. Exposure to cadmium sulfate induced mitostasis within 24 hr and cellular death in 48 hr. The other two salts caused the same reaction but at concentration 5X higher than cadmium sulfate.

Cough.

Redness.

Abdominal pain. 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)

/SIGNS AND SYMPTOMS/ INHALATION CAUSES COUGHING, SNEEZING, SYMPTOMS OF LUNG DAMAGE. INGESTION PRODUCES SEVERE TOXIC SYMPTOMS /OF NAUSEA, VOMITING & LOSS OF CONSCIOUSNESS/ BOTH KIDNEY & LIVER DAMAGE MAY OCCUR. CONTACT WITH EYES CAUSES IRRITATION.

/GENOTOXICITY/ Although cadmium still represents a public health problem and despite the fact that it has been classified as an IARC Group-I carcinogen, the molecular and cellular mechanisms responsible for the toxicity and the carcinogenicity of cadmium compounds are poorly known. Since unrepaired DNA double-strand breaks (DSBs) are considered to be key-lesions in cell lethality, and because misrepaired DSBs are a source of genomic instability leading to cancer proneness, the activity of the major DSB-repair pathways, i.e. non-homologous end-joining (NHEJ) and recombination, has been evaluated in human endothelial cells exposed to cadmium chloride and cadmium diacetate. Exposure to cadmium results in the production of DSBs a few hours after incubation. These breaks trigger the phosphorylation of H2AX proteins, which was used as an indirect measure of DSB in this study. The presence of cadmium in cells decreases the repair rate of X-ray-induced DSBs, suggesting an impact of cadmium upon the reparability of DSBs. Such an interpretation was consolidated by the finding that the DNA-PK kinase activity, essential for NHEJ, is affected by the presence of cadmium. These results suggest that the toxicity of cadmium compounds may be explained by the propagation of persistent DSBs. In parallel, the presence of cadmium was also associated with an over-activation of the MRE11-dependent repair pathway that may favor genomic instability. Altogether, our data provide a first example of the impact of cadmium upon DSB repair and signalling

/ALTERNATIVE and IN VITRO TESTS/ Human XPA is a 31 kDa protein involved in nucleotide excision repair (NER), a ubiquitous, multi-enzyme pathway responsible for processing multiple types of DNA damage in the eukaryotic genome. A zinc-associated, C4-type motif (C105-X(2)-C108-X(17)-C126-X(2)-C129) located in the minimal DNA-binding region (M98-F219) of XPA (XPA-MBD) is essential for damaged DNA recognition. Cadmium is a known carcinogen and can displace the zinc in many metal-binding proteins. It has been suggested that the carcinogenic properties of cadmium may result from structural changes effected in XPA when Cd(2+) is substituted for Zn(2+) in the metal-binding site. The solution structure of XPA-MBD containing zinc(II) has recently been determined. To assess the effects of cadmium(II) substitution on the structure of XPA-MBD, XPA-MBD was expressed in minimal medium supplemented with cadmium acetate to yield a protein that was almost exclusively (>95%) associated with cadmium(II) (CdXPA-MBD). Extended X-ray absorption fine structure spectra collected on ZnXPA-MBD and CdXPA-MBD in frozen (77 K) 15% aqueous glycerol solution show that the metal is coordinated to the sulfur atoms of four cysteine residues with an average metal-sulfur bond length of 2.34 +/- 0.01 and 2.54 +/- 0.01 A, respectively. Comparison of the circular dichroism, two-dimensional H(1),N(15)-HSQC, and three-dimensional N(15)-edited HSQC-NOESY spectra of ZnXPA-MBD and CdXPA-MBD show that there are no structural differences between the two proteins. The absence of major structural changes upon substituting cadmium(II) for zinc(II) in XPA suggests that cadmium-induced mutagenesis is probably not due to structural perturbations to the zinc-binding core of XPA.

/ALTERNATIVE and IN VITRO TESTS/ A human epithelial cell line (HZR) growing with high zinc concentrations has been analyzed for its ability to sustain high cadmium concentrations. Exposure to up to 200 uM of cadmium acetate for 24 hr hardly impacted viability, whereas most of parental HeLa cells were killed by less than 10 uM of cadmium. Upon challenge by 35 fold higher cadmium concentrations than HeLa cells, HZR cells did not display increased DNA damage, increased protein oxidation, or changed intracellular cadmium localization. Rather, the main cause of resistance against cadmium was by avoiding cadmium entry into cells, which differs from that against zinc as the latter accumulates inside cells. The zinc-resistant phenotype of these cells was shown to also impair extracellular manganese uptake. Manganese and cadmium competed for entry into HeLa cells. Probing formerly identified cadmium or manganese transport systems in different animal cells did not evidence any significant change between HeLa and HZR cells. These results reveal zinc adaptation influences manganese and cadmium cellular traffic and they highlight previously unknown connections among homeostasis of divalent metals.

/OTHER TOXICITY INFORMATION/ Thirty-seven metal compounds were examined for inhibitory activities against infection with human immunodeficiency virus type 1 (HIV-1). Zinc group metal compounds, namely, zinc acetate, zinc chloride, zinc nitrate, cadmium acetate and mercury chloride, showed anti-HIV-1 activities. Cadmium and mercury compounds at 1-10 ug/mL and zinc compounds at 100 ug/mL strongly inhibited HIV-1 infection, although the cadmium, mercury and zinc compounds had severe cytotoxicities at 100, 100 and 1000 ug/mL, respectively. They inhibited transcription of HIV-1 RNA and HIV-1 production at concentrations at which they did not affect the growth of HIV-1-producing cells. They had little effect on syncytium formation resulting from cocultivation of uninfected with HIV-1-producing cells. Nor did they affect HIV-1 DNA synthesis following HIV-1 infection. The metal compounds may owe their anti-HIV-1 effects to inhibition of HIV-1 DNA to RNA transcription, rather than inhibition of the adsorption, penetration or reverse transcription step of HIV-1 infection.

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/

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 acetate 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 acetate 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/

Cadmium (Cd) is a known nephrotoxic element. In this study, the primary cultures of rat proximal tubular (rPT) cells were treated with low doses of cadmium acetate (2.5 and 5 uM) to investigate its cytotoxic mechanism. A progressive loss in cell viability, together with a significant increase in the number of apoptotic and necrotic cells, were seen in the experiment. Simultaneously, elevation of intracellular [Ca(2+)]i and reactive oxygen species (ROS) levels, significant depletion of mitochondrial membrane potential(Delta Psi) and cellular glutathione (GSH), intracellular acidification, and inhibition of Na(+), K(+)-ATPase and Ca(2+)-ATPase activities were revealed in a dose-dependent manner during the exposure, while the cellular death and the apoptosis could be markedly reversed by N-acetyl-L-cysteine (NAC). Also, the calcium overload and GSH depletion were significantly affected by NAC. In conclusion, exposure of rPT cells to low-dose cadmium led to cellular death, mediated by an apoptotic and a necrotic mechanism. The apoptotic death might be the chief mechanism, which may be mediated by oxidative stress. Also, a disorder of intracellular homeostasis induced by oxidative stress and mitochondrial dysfunction is a trigger of apoptosis in rPT cells.

Cadmium acetate (CdAc) induced apoptosis in primary alveolar type 2 cells and Clara cells from rat lung. Phosphorylation of the MAPKs ERK1/2, p38 and JNK was markedly increased in both cell types 15 min to 2 hr after start of exposure to 10 uM CdAc. The phosphorylation of all the MAPKs remained elevated or was progressively increased up to 12 hr. The p38 inhibitor SB202190 reduced the Cd-induced apoptosis, whereas the ERK and JNK inhibitors, PD98059 and JNKI1, respectively, did not have any significant effect. The activity of total PKC and the isoforms PKC(alpha) and PKC(delta) seemed initially to be high in type 2 cells and Clara cells. Exposure to 10 uM CdAc did not further increase the total PKC activity or phosphorylation levels of the specific isoforms. However, the PKC inhibitors, GF109203X and rottlerin partially reduced the Cd-induced apoptosis. Furthermore, exposure to GF109203X reduced the phosphorylation of p38 in Clara cells. In conclusion, the MAPK p38 seemed to be involved in the Cd-induced apoptosis in Clara cells and type 2 cells. The activity of PKC isoforms is suggested to have a permissive role in the apoptotic process, located upstream of p38 phosphorylation.

The aim of the current study /was/ to examine in normal and neoplastic fibroblasts culture cells the modifications induced by the Cadmium at cellular level, in particular on the cytoskeleton, responsible not only of the intracellular transport of vesicles and cell organules, but also of their positioning and of the cellular integrity. Two fibroblastic cellular strains, normal (FG) and neoplastic (SGS/3A), have been incubated in a 5 uM Cadmium acetate added medium for 1, 8, 24 hours and studied by indirect immunofluorescence methods, particularly for the following proteins: Actin, Tubulin and Vimentin. The observations show in normal and neoplastic fibroblasts comparables modifications and anomalies of cytoskeletal shape. In both the cases the cellular morphology suffers drastic modifications, gradually evolving through intermediary shapes: from triangular and spindle-shaped in the normal fibroblasts to irregular, star-shaped, and globular in the neoplastic ones. The Cadmium action on the morphology of the normal and tumoral cells changes according to the time of incubation, producing structural alterations of the cytoskeletal. The modifications that start to be observable at the first hour of incubation are more evident after the eighth hour of exposure, reaching the maximum expression at the twenty-fourth hour, often with reduction of the total volume of the cells and loss of their ability to adhere to the substratum. Such modifications can be related to great alterations of the cellular membrane, producing the change of shape and the progressive partial separation from the substratum. The intermediary filaments seem to be less sensitive, from a morphological but not functional point of view, to the action of the Cadmium in comparison to the Actin and the microtubules that, on the contrary, seem to lose their proper morphological characteristics

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)

MONGOLIAN GERBILS WERE INJECTED IP WITH TRACE QUANTITIES OF (115)CD-CADMIUM ACETATE OVER 12 WK PERIOD. AFTER 3 WK EQUILIBRATION PERIOD GERBILS WERE SACRIFICED. AS IN OTHER SPECIES, CADMIUM LEVELS WERE HIGHER IN LIVER & KIDNEYS THAN IN OTHER TISSUES.

FORTY-EIGHT & 96 HR AFTER ORAL ADMIN OF 2 MG CADMIUM AS CADMIUM ACETATE, THE TISSUES OF SOFTSHELL TURTLE RETAINED 9.43 & 4.02% OF ADMIN DOSE AS CADMIUM. LIVER RETAINED GREATEST AMT. CADMIUM CONCN PER G WET WT WAS HIGHEST IN INTESTINES AT 48 HR, & IN LIVER AT 96 HR.

Male rats treated ip with cadmium acetate (1 mg Cd/kg, daily) for 8 days, then the liver was isolated, homogenized, the supernatant fractionated on Sephadex G-75, and the fractions analyzed by atomic absorption spectroscopy for cadmium and zinc. A small amount of cadmium was bound to a high molecular weight protein fraction (fraction A) and the majority of cadmium was bound to metallothionein fraction (fraction B). In addition, to a binding to high molecular weight protein fraction and metallothionein fraction, zinc also bound to a third fraction located between high molecular weight protein fraction and metallothionein fraction. Concentrations of cadmium and zinc in all fractions remained almost unchanged when determined 3 and 8 days after termination of treatment with cadmium acetate. The zinc content in fraction B was approximately two fold that in other fractions, and the content of cadmium + zinc decreased with time (ie 3 days vs 8 days). The molar ratio of zinc/cadmium in metallothionein fraction slightly decreased (ie the ratio on day 8 was slightly lower than that on day 3 after cessation of treatment).

Used in iridescent glazes (porcelains and pottery), electroplating, colorants for glass and textiles, and as a reagent for chemical analysis; [HSDB] Used to produce acetates; [Hawley]

Electroplating [Category: Plate]

Ceramics making [Category: Hobbies]

Manufacture of acetates, assistant in dyeing and printing textiles

Producing iridescent effects on porcelains and pottery; as a reagent for determination of S, Se, and Te; in cadmium electroplating.

Colorant for glass and textiles, glaze for ceramics where it produces iridescent effects, starting material for preparation of cadmium halides, and as an alternative to the cyanide bath for cadmium electrolysis.

(1977) PROBABLY GREATER THAN 4.54X10+5 G

(1982) NOT PRODUCED COMMERCIALLY IN US

Cadmium acetate is produced by the reaction of acetic acid with cadmium metal or oxide, or by treating cadmium nitrate with acetic anhydride. The dihydrate is obtained by dissolving cadmium metal or oxide in acetic acid, followed by crystallization. Calcination of the dihydrate can be controlled to yield cadmium acetate monohydrate and the anhydrous acetate.

The anhydrous material may be prepared by treating cadmium nitrate with acetic anhydride or by very careful heating and drying the dihydrate at about 130 °C.

Reagent grade; 99.999%.

Cadmium acetate is usually available as the hydrate Cd(CH3COO)2.2H2O in technical or reagent grades.