Cadmium Nitrate

H302: Harmful if swallowed [Warning Acute toxicity, oral]

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

H332: Harmful if inhaled [Warning Acute toxicity, inhalation]

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

H350: May cause cancer [Danger Carcinogenicity]

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

H400: Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

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

P203, P260, P261, P264, P270, P271, P273, P280, P301+P317, P302+P352, P304+P340, P317, P318, P319, P321, P330, P362+P364, P391, P405, and P501 (click each P-code to see the statement)

H301 (90%): Toxic if swallowed [Danger Acute toxicity, oral]

H302+H312+H332 (31.4%): Harmful if swallowed, in contact with skin or if inhaled [Warning Acute toxicity, oral; acute toxicity, dermal; acute toxicity, inhalation]

H302 (10%): Harmful if swallowed [Warning Acute toxicity, oral]

H312 (42.9%): Harmful in contact with skin [Warning Acute toxicity, dermal]

H330 (90%): Fatal if inhaled [Danger Acute toxicity, inhalation]

H332 (10%): Harmful if inhaled [Warning Acute toxicity, inhalation]

H340 (90%): May cause genetic defects [Danger Germ cell mutagenicity]

H350 (92.9%): May cause cancer [Danger Carcinogenicity]

H360 (88.6%): May damage fertility or the unborn child [Danger Reproductive toxicity]

H372 (90%): Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]

H400 (100%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

H410 (100%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

P203, P260, P261, P264, P270, P271, P273, P280, P284, P301+P316, P301+P317, P302+P352, P304+P340, P316, P317, P318, P319, P320, P321, P330, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 70 reports by companies from 8 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

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

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

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

H361: Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

H370: Causes damage to organs [Danger Specific target organ toxicity, single exposure]

P203, P260, P264, P270, P280, P301+P316, P308+P316, P318, P319, P321, P330, P405, and P501 (click each P-code to see the statement)

P203, P264, P270, P280, P301+P316, P318, P321, P330, P405, and P501 (click each P-code to see the statement)

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

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

P203, P260, P264, P270, P271, P273, P280, P284, P301+P316, P302+P352, P304+P340, P316, P317, P318, P319, P320, P321, P330, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

INHALATION: remove patient to fresh air; seek medical attention.

INGESTION: give large amounts of water and induce vomiting; give milk or egg whites; seek medical attention.

EYES: flush with copious amounts of water for 15 min.; consult a physician.

SKIN: wash with soap and water. (USCG, 1999)

Excerpt from ERG Guide 141 [Oxidizers - Toxic]:

SMALL FIRE: Use water. Do not use dry chemicals or foams. CO2 or Halon® may provide limited control.

LARGE FIRE: Flood fire area with water from a distance. Do not move cargo or vehicle if cargo has been exposed to heat. If it can be done safely, move undamaged containers away from the area around the fire.

FIRE INVOLVING TANKS, RAIL TANK CARS OR HIGHWAY TANKS: Fight fire from maximum distance or use unmanned master stream devices or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. ALWAYS stay away from tanks in direct contact with flames. For massive fire, use unmanned master stream devices or monitor nozzles; if this is impossible, withdraw from area and let fire burn. (ERG, 2024)

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/

Cadmium nitrate will increase the intensity of fire when in contact with combustible material. /Tetrahydrate/

Mixtures with wood or other combustibles may catch fire. /Tetrahydrate/

Excerpt from ERG Guide 141 [Oxidizers - Toxic]:

IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.

LARGE SPILL: Consider initial downwind evacuation for at least 100 meters (330 feet).

FIRE: If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2024)

Stop discharge if possible, isolate and remove discharged material. /Tetrahydrate/

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.

May be dangerous if it enters water intakes; notify local health and wildlife officials; notify operators of nearby water intakes. /Tetrahydrate/

In case of spill: notify local ... pollution control agencies. /Tetrahydrate/

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.

Excerpt from ERG Guide 141 [Oxidizers - Toxic]:

Keep combustibles (wood, paper, oil, etc.) away from spilled material. Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk.

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

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

Keep cadmium nitrate /tetrahydrate/ well closed in a cool place. /Tetrahydrate/

Ambient temperature with open venting. /Tetrahydrate/

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]

TIH (Toxic Inhalation Hazard) - Term used to describe gases and volatile liquids that are toxic when inhaled. Some are TIH materials themselves, e.g., chlorine, and some release TIH gases when spilled in water, e.g., chlorosilanes. [ERG 2016].

0.90 [mg/m3]

9.9 [mg/m3]

59 [mg/m3]

0.005 [mg/m3], as Cd, see 29 CFR 1910.1027

9.0 [mg/m3], as Cd

0.01 [mg/m3], as Cd ( 0.002 mg/m3, as Cd, respirable fraction)

8 hr Time Weighted Avg (TWA): 0.01 mg/cu m /Cadmium and compounds, as Cd/

8 hr Time Weighted Avg (TWA): 0.002 mg/cu m (respirable fraction) /Cadmium and compounds, as Cd/

A2; Suspected human carcinogen. /Cadmium and compounds, as Cd/

Biological Exposure Index (BEI): Determinant: Cadmium in urine; Sampling Time: not critical; BEI: 5 ug/g creatinine. The determinant may be present in biological specimens collected from subjects who have not been occupationally exposed, at a concentration which could affect interpretation of the result. Such background concentrations are incorporated in the BEI value. /Cadmium and inorganic compounds/

For more Threshold Limit Values (TLV) (Complete) data for CADMIUM NITRATE (6 total), please visit the HSDB record page.

Acute Inhalation: 0.00003 mg/m3 (L134)

Chronic Inhalation: 0.00001 mg/m3 (L134)

Intermediate Oral: 0.0005 mg/kg/day (L134)

Chronic Oral: 0.0001 mg/kg/day (L134)

Rubber gloves; safety goggles; dust mask (USCG, 1999)

Cadmium nitrate is an odorless white solid. Sinks in water. (USCG, 1999)

White solid; [HSDB] White odorless crystals; [MSDSonline] There are 3 hydrates that form at temperatures <56 deg C; [Ullmann]

White cubic crystals

White, amorphous pieces or hygroscopic needles

White, prismatic needles

132 °C @760 [mm Hg]

138 °F (USCG, 1999)

Soluble in ammonia, alcohol

Sol in ethanol

Soluble in ether, acetone

In water, 156 g/100 g water at 25 °C

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

3.6 g/cu cm

3.6 @25 °C

Stable during transport. /Tetrahydrate/

When heated to decomp, emits very toxic fumes of /cadmium and nitrogen oxides/.

Strongly hygroscopic

Enthalpy of Fusion: 18.3 kJ/mol at 360 °C

Specific gravity 2.455; bp 132 °C /Tetrahydrate/

... forms both a dihydrate and a tetrahydrate

For more Other Experimental Properties (Complete) data for CADMIUM NITRATE (9 total), please visit the HSDB record page.

Metals -> Cadmium Compounds, Inorganic

Carcinogens

Potential endocrine disrupting compound

Water soluble.

Nitrate and Nitrite Compounds, Inorganic

Strong Oxidizing Agent

Mixtures of metal/nonmetal nitrates with alkyl esters may explode, owing to the formation of alkyl nitrates; mixtures of a nitrate with phosphorus, tin (II) chloride, or other reducing agents may react explosively [Bretherick 1979 p. 108-109].

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. Nitrate's toxicity is a result of it's conversion to nitrite once in the body. Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (A2450, L1613, L8, A18, A19, A28)

Evaluation: There is sufficient evidence in humans for the carcinogenicity of cadmium and cadmium compounds. There is sufficient evidence in experimental animals for the carcinogenicity of cadmium compounds. There is limited evidence in experimental animals for the carcinogenicity of cadmium metal. In making the overall evaluation, the Working Group took into consideration the evidence that ionic cadmium causes genotoxic effects in a variety of types of eukaryotic cells, including human cells. Overall evaluation: Cadmium and cadmium compounds are carcinogenic to humans (Group 1). /Cadmium and cadmium compounds/

CLASSIFICATION: B1; probable human carcinogen. BASIS FOR CLASSIFICATION: Limited evidence from occupational epidemiologic studies of cadmium is consistent across investigators and study populations. There is sufficient evidence of carcinogenicity in rats and mice by inhalation and intramuscular and subcutaneous injection. Seven studies in rats and mice wherein cadmium salts (acetate, sulfate, chloride) were administered orally have shown no evidence of carcinogenic response. HUMAN CARCINOGENICITY DATA: Limited. /Classification based on former EPA guidelines/

A2; Suspected human carcinogen. /Cadmium and compounds, as Cd/

Cadmium and Cadmium Compounds: known to be human carcinogens.

1, carcinogenic to humans. (L135)

Chronic exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. Nitrate and nitrite poisoning causes methemoglobinemia. Nitrites may cause pregnancy complications and developmental effects. They may also be carcinogenic. (L1137, L6)

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

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. Nitrate and nitrite poisoning causes methemoglobinemia. Symptoms include cyanosis, cardiac dysrhythmias and circulatory failure, and progressive central nervous system (CNS) effects. CNS effects can range from mild dizziness and lethargy to coma and convulsions. (L1137, L6)

Nephrotoxin - The chemical is potentially toxic to the kidneys in the occupational setting.

Reproductive Toxin - A chemical that is toxic to the reproductive system, including defects in the progeny and injury to male or female reproductive function. Reproductive toxicity includes developmental effects. See Guidelines for Reproductive Toxicity Risk Assessment.

LD50: 100 mg/kg (Oral, Rat) (L449)

LC50: 1925 ppm over 4 hours (Inhalation, Mouse) (L449)

LD50 Rat oral 300 mg/kg

LD50 Mouse oral 100 mg/kg

Cadmium poisoning is treated by removal from exposure and supportive care. If ingested, induced vomiting or gastric lavage may be performed. Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution administered intravenously slowly over five minutes followed by IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. (L1613, L139)

In order to test the potential effect of prior exposure to different Cd concentrations on Cd uptake and accumulation, plants of Arabidopsis thaliana, including a phytochelatin-deficient mutant, cad1-3, and the wild type, were compared. For Cd uptake experiments, plants were grown for 1 week in nutrient solution containing different Cd concentrations (0, 0.05, 0.1, 0.25, 0.5, and 1.0 uM Cd(NO3)2). Thereafter they were subjected to 0.5 uM Cd labelled with (109)Cd for 2 hr. Uptake experiments with (109)Cd showed that the phytochelatin-deficient mutant cad1-3, accumulated less Cd than the wild type. Both a lower proportion and lower total amount of absorbed Cd were translocated to the shoot in cad1-3 plants compared to wild-type plants. Cadmium exposure also influenced the amounts of nutrients found, whereby after exposure to high Cd concentrations (0.5, 1.0 uM) during growth, cad1-3 roots contained less Fe, K, Mg, P, and S compared to roots of the wild type. In cad1-3 these elements decreased with increasing Cd concentration. The total Cd content in roots and shoots increased significantly with increasing Cd concentration during growth, although the increase was much less in cad1-3 plants. In time-dependent experiments of Cd uptake carried out between 15 and 120 min on plants not previously exposed to Cd, no significant difference in Cd accumulation between the mutant and wild type were found, although a smaller amount of Cd was translocated to the shoot in cad1-3 plants. The possibility that the differences in Cd accumulation in mutant and wild-type lines may be due to the cytosolic Cd regulation, which is inhibited by the complexation of Cd by phytochelatins, is discussed

The interaction between selenium and cadmium was studied in relation to cellular uptake and expressions of selenium-cadmium interaction. Human K-562 cells were pre-treated or simultaneously treated with (5 or 50 uM) selenite or (10 or 50 uM) selenomethionine and with (60 or 75 uM) cadmium nitrate. Cells pre or simultaneously treated with selenite revealed increased cadmium concentration with increased doses of selenite, particularly pronounced in the simultaneous treatments. In both treatments, selenium protection was observed during the exposure period, but not during the growth period. In cells simultaneously treated with selenomethionine and 60-uM cadmium, an increase in cadmium concentration was observed after increased selenium dose. In addition, it was found that simultaneous selenomethionine treatment with 60-uM cadmium resulted in selenium protection during the exposure period, although protection was not observed during the growth period.

Plants that hyperaccumulate metals are ideal subjects for studying the mechanisms of metal and mineral nutrient uptake in the plant kingdom. Indian Mustard (Brassica juncea) has been shown to accumulate moderate levels of Cd, Pb, Cr, Ni, Zn, and Cu. In this experiment, 10 levels of Cd concentration treatments were imposed by adding 10-190 mg Cd /per/ kg to the soils as cadmium nitrate [Cd(NO3)2]. The effect of Cd on phosphorus (P), potassium (K), calcium (Ca), magnesium (Mg), and the micronutrients iron (Fe), manganese (Mn), copper (Cu), and zinc (Zn) in B. juncea was studied. Plant growth was affected negatively by Cd, root biomass decreased significantly at 170 mg Cd /per/ kg dry weight soils treatment. Cadmium accumulation both in shoots and roots increased with increasing soil Cd treatments. The highest concentration of Cd was up to 300 mg /per/ kg dw in the roots and 160 mg /per/ kg dw in the shoots. The nutrients mainly affected by Cd were P, K, Ca, Fe, and Zn in the roots, and P, K, Ca, and Cu in the shoots. K and P concentrations in roots increased significantly when Cd was added at 170 mg /per/ kg, and this was almost the same level at which root growth was inhibited. Zn concentrations in roots decreased significantly when added Cd concentration was increased from 50 to 110 mg /per/ kg, then remained constant with Cd treatments from 110 to 190 mg /per/ kg. However, Zn concentrations in the shoots seemed less affected by Cd. It is possible that Zn uptake was affected by the Cd but not the translocation of Zn within the plant. Ca and Mg accumulation in roots and shoots showed similar trends. This result indicates that Ca and Mg uptake is a non-specific process.

We examined the influences of three trace metals on the accumulation of a major nutrient (NO3-) in Scenedesmus quadricauda. A comparative study on metal-nutrient interaction in free and immobilized states of algal cells was conducted. The effect due to interaction between different variables (cell state type, metal type, and metal dose) was studied to assess the variation in the nitrate uptake by free and immobilized cells. The results analyzed by ANOVA (three-way) (components: cell state type, metal type, and metal dose) confirmed that the inhibition of nitrate uptake by test metals was highly significant (P<0.001). Free and immobilized states of S. quadricauda responded differently (P<0.05, ANOVA) to the types of metal added. Uptake kinetics was studied by monitoring short-term uptake rates at different nutrient levels. Free and immobilized cells of the organism displayed noncompetitive modes of inhibition for Ni and Zn while a competitive mode of inhibition by Cd was observed in both free and immobilized states of the organism.

For more Interactions (Complete) data for CADMIUM NITRATE (6 total), please visit the HSDB record page.

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Cadmium and Related Compounds/

Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Administer activated charcoal ... . /Cadmium and Related Compounds/

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... .... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Cadmium and Related Compounds/

/ALTERNATIVE and IN VITRO TESTS/ Effects of some metals on the growth of cultured human erythroleukemia K-562 cells were investigated when grown in two different types of media based upon RPMI-1640 or Ham's F-10. The study on proliferation, using RPMI-1640 supplemented with sodium selenite, selenomethionine, mercuric chloride, methylmercuric chloride and cadmium nitrate showed no inhibition of growth at concentrations of 2.5, 25, 25, 2.5 and 25 uM, while at 75, 250, 50, 5 and 50 uM toxicity was apparent. Selenite at 5-50 uM and selenomethionine at 50-100 uM inhibited the growth. In Ham's F-10 supplemented with the same compounds no inhibition was found at concentrations of 5, 10, 25, 1 and 50 uM, while at 50, 100, 50, 5 and 75 uM toxic effects were noted. Selenite 10 uM and selenomethionine 25-50 uM inhibited the proliferation. Measurements of trace element levels in pellets of K-562 cells grown in RPMI-1640 or Ham's F-10 unveiled higher cell contents of cadmium and selenium in cells grown in RPMI-1640, being consistent with higher concentrations of these elements in that medium. Manganese and mercury concentrations were higher in cells grown in Ham's F-10 correlating with a higher medium concentration of these elements. The growth responses and cellular uptake differed between the metals and the selenocompounds and although extrapolating the results to humans is difficult the selenium exposures were in approximately the same order of magnitude as in human exposures. The compounds could be ranked according to decreasing toxicity as: methylmercuric chloride > mercuric chloride, cadmium nitrate, sodium selenite > selenomethionine.

/ALTERNATIVE and IN VITRO TESTS/ Recent reports, highlighting the relationships of cadmium exposure and vascular diseases, indicated that vascular endothelial cell was the target of cadmium (Cd) toxicity. However, the underlying mechanisms have not been fully elucidated. ...this study...evaluated the internalization of Cd(2+) into human umbilical vein endothelial cells (HUVECs) by a novel Cd(2+)-selective sensor suitable for living cells. Then, we detected apoptosis in the treated cells. Our results showed that Cd(2+) at low concentrations (< 10 umol/L) inhibited apoptosis induced by deprivation of serum and basic fibroblast growth factor (bFGF). To investigate the corresponding molecular mechanisms, we employed acridine orange staining and Western blotting of /microtubule-associated protein 1 light chain 3 alpha/ MAP1 LC3 to detect autophagy, and analyzed the levels of integrin beta4, caveolin-1 and activity of /phosphatidylcholine-specific phospholipase/ PC-PLC. Our results showed that low concentrations of Cd(2+) promoted autophagy and depressed the levels of integrin beta4, caveolin-1 and PC-PLC activity. The data suggested that autophagy played a key role in Cd(2+) induced endothelial dysfunction; integrin beta4, caveolin-1 and PC-PLC might be the targets of Cd(2+) in vascular endothelial cells

/LABORATORY ANIMALS: Acute Exposure/ Cadmium nitrate Cd(NO3)2 (CdN) is commonly used in Ni-Cd battery factories. The possibility of accidental exposure to CdN is great. CdN is very soluble in water compared to other Cd compounds. Therefore, acute toxicity would be expected to be quick due to rapid absorption after exposure. However, the mechanisms of CdN toxicity have not been fully elucidated. We investigated the acute lethal toxicity and harmful systemic effects of acute exposure to large doses of CdN. The lethal dose and dose-response study of the liver and kidney were determined after intravenous administration of CdN in rats. The LD50 of CdN was determined to be 5.5 mg/kg. Doses of 2.1, 4.2, 6.3 mg/kg were selected for the dose-response study. Liver injury was induced at doses greater than 4.2 mg/kg. Severe hepatic injury occurred in the 6.3 mg/kg group, which would have been caused by acute exposure to the high concentration of Cd that exceeded the critical concentration in hepatic tissue. A remarkable decrease in urine volume in the 6.3 mg/kg group indicated acute renal failure. A decrease in creatinine clearance suggested acute glomerular dysfunction at doses greater than 4.2 mg/kg. Increases in urinary N-acetyl-beta-D-glucosaminidase/creatinine, beta(2)-microglobulin and glucose in the 6.3 mg/kg group indicated proximal tubular injury. Secretion of K ion was also severely affected by proximal tubular injury and severe decreases in urine volume, and an increase in serum K ion was identified at doses greater than 4.2 mg/kg. Thus severe hyperkalemia might be associated with the cardiac-derived lethal toxicity of CdN.

/LABORATORY ANIMALS: Acute Exposure/ Cadmium is a potent carcinogen in rodents and has recently been accepted by the International Agency for Research on Cancer as a category 1 (human) carcinogen, but the molecular mechanism of its action remains largely unclear. It has however been suggested that cadmium-induced carcinogenesis may involve either direct or indirect interaction of Cd(2+) with DNA. Cd(2+) is believed to bind covalently with N7 centers of adenine and guanine. At low concentrations (< or =50 mM), Cd(2+) is found to react with plasmid DNA to produce a mixture of Form I and Form II bands whereas at higher concentrations (> or =100 mM), Cd(2+) causes extensive damage to DNA at a pH 5.8 solution of cadmium nitrate. Within the range 0-100 mM (when pH is adjusted to 7.4 by adding NaOH) an increase in concentration of Cd(2+) is found to cause a decrease in the gel mobility rate of plasmid and an increase in the intensity of the Form II band. When plasmid DNA is digested with BamH1, only the Form III band is observed both in the presence and absence of Cd(2+). However, the mobility of the band is found to decrease with the increase in the concentration of Cd(2+). When the enzyme Ssp1 which cuts plasmid DNA at the AT sites is used instead of BamH1, two bands are observed in the presence of cadmium as against one band in the absence of cadmium. These results suggest that Cd(2+) binds covalently with DNA (possibly at G, A and T centres) and can form intrastrand bifunctional AT adducts but not the GG adducts. It may also be that neither GG nor AT adducts are formed and yet Ssp1 digestion is prevented because of a structural modification introduced in adenine by its interaction with Cd(2+). In the presence of antioxidants such as cysteine, glutathione and ascorbate (especially cysteine and ascorbate), DNA damage is found to be greater than expected for the combined effects of the antioxidant and Cd(2+). The increased DNA damage is believed to be due to the formation of reactive oxygen species (ROS).

/LABORATORY ANIMALS: Acute Exposure/ Studies were conducted /in mice/ to determine the effects of inhalation exposure to particulate and gaseous air pollutants on the resistance to experimental bacterial pneumonia. Changes in resistance to this respiratory infection, expressed as mortality rates and survival time served as the most sensitive and consistent indicators of damage produced by the exposure. Using these parameters it was possible to rank the effects of single 3 hr inhalation exposure to the particulate pollutants. Among the pollutants included in these studies, cadmium sulfate, and cadmium nitrate were most toxic, followed in decreasing order of toxicity by copper, aluminum, and magnesium sulfate or magnesium nitrate aerosols. The metallic cation appeared to be most important in altering the resistance to infection. ...

/LABORATORY ANIMALS: Acute Exposure/ The effect of a single intravenous injection of cadmium nitrate was investigated in livers of male Wistar rats. A significant increase in liver weight, accompanied by an elevation of total hepatic DNA content was observed. DNA synthesis as measured by the incorporation of (3)H thymidine, was found to be 6 times greater than the control, at 24 hr after treatment, and remained elevated over a period of 72 hr.

For more Non-Human Toxicity Excerpts (Complete) data for CADMIUM NITRATE (13 total), please visit the HSDB record page.

EC50; Species: Folsomia candida (Springtail) adults Reading strain; Conditions: direct application in artificial soil (70% sand, 20% clay, pH 5.84, 10% organic matter, 30% moisture); Concentration: 590 ug/g soil for 28 days; Effect: progeny counts/numbers

EC50; Species: Folsomia candida (Springtail) adults Reading strain; Conditions: direct application in artificial soil (70% sand, 20% clay, pH 5.08, 10% organic matter, 30% moisture); Concentration 780 ug/g soil for 28 days; Effect: progeny counts/numbers

EC50; Species: Folsomia candida (Springtail) adults Reading strain; Conditions: direct application in artificial soil (70% sand, 20% clay, pH 4.54, 10% organic matter, 30% moisture); Concentration: 480 ug/g soil for 28 days; Effect: progeny counts/numbers

EC50; Species: Folsomia candida (Springtail) adults Reading strain; Conditions: direct application in artificial soil (70% sand, 20% clay, pH 6.0, 10% organic matter, 30% moisture), 20 °C; Concentration: 590 ug/g soil for 28 days; Effect: progeny counts/numbers

For more Ecotoxicity Values (Complete) data for CADMIUM NITRATE (52 total), please visit the HSDB record page.

/AQUATIC SPECIES/ Daphnia magna (cladoceran) 0.17 ug/L/21 days in water hardness of 45 mg/L calcium carbonate, toxic effect: reproductive impairment.

/AQUATIC SPECIES/ Chilomonas paramecium (protozoan) exposed to 160 ug/L/48 hr, toxic effect: incipient inhibition.

/AQUATIC SPECIES/ Uronema parduezi (protozoan) exposed to 26 ug/L/20 hr, toxic effect: incipient inhibition.

/AQUATIC SPECIES/ Entosiphon sulcatum (protozoan) exposed to 11 ug/L/72 hr, toxic effect: incipient inhibition.

For more Ecotoxicity Excerpts (Complete) data for CADMIUM NITRATE (14 total), please visit the HSDB record page.

EC50; Species: Folsomia candida (Springtail) adults Reading strain; Conditions: direct application in artificial soil (70% sand, 20% clay, pH 5.84, 10% organic matter, 30% moisture); Concentration: 590 ug/g soil for 28 days; Effect: progeny counts/numbers

EC50; Species: Folsomia candida (Springtail) adults Reading strain; Conditions: direct application in artificial soil (70% sand, 20% clay, pH 5.08, 10% organic matter, 30% moisture); Concentration 780 ug/g soil for 28 days; Effect: progeny counts/numbers

EC50; Species: Folsomia candida (Springtail) adults Reading strain; Conditions: direct application in artificial soil (70% sand, 20% clay, pH 4.54, 10% organic matter, 30% moisture); Concentration: 480 ug/g soil for 28 days; Effect: progeny counts/numbers

EC50; Species: Folsomia candida (Springtail) adults Reading strain; Conditions: direct application in artificial soil (70% sand, 20% clay, pH 6.0, 10% organic matter, 30% moisture), 20 °C; Concentration: 590 ug/g soil for 28 days; Effect: progeny counts/numbers

For more Ecotoxicity Values (Complete) data for CADMIUM NITRATE (52 total), please visit the HSDB record page.

/AQUATIC SPECIES/ Daphnia magna (cladoceran) 0.17 ug/L/21 days in water hardness of 45 mg/L calcium carbonate, toxic effect: reproductive impairment.

/AQUATIC SPECIES/ Chilomonas paramecium (protozoan) exposed to 160 ug/L/48 hr, toxic effect: incipient inhibition.

/AQUATIC SPECIES/ Uronema parduezi (protozoan) exposed to 26 ug/L/20 hr, toxic effect: incipient inhibition.

/AQUATIC SPECIES/ Entosiphon sulcatum (protozoan) exposed to 11 ug/L/72 hr, toxic effect: incipient inhibition.

For more Ecotoxicity Excerpts (Complete) data for CADMIUM NITRATE (14 total), please visit the HSDB record page.

Salvinia natans (fern) exposed to cadmium nitrate for 21 days exhibited a bioconcentration factor of 960.

Mya arenaria, (soft shell clam) exposed to cadmium nitrate for 70 days exhibited a bioconcentration factor of 160.

Crassostrea virginica, (American oyster) exposed to cadmium nitrate for 98 days exhibited a bioconcentration factor of 1,220.

Lemna valdiviana (duck weed) exposed to cadmium nitrate for 21 days exhibited a bioconcentration factor of 603.

An adsorption rate of 1.22/hr in river sediments from the Nagara River, Japan, which is heavily impacted by industrial effluents and urban wastes, has been reported for cadmium nitrate; the desorption rate was reported as 0.0038/hr. These values correspond to a concentration factor of 321(1).

According to the 2006 TSCA Inventory Update Reporting data, the number of persons reasonably likely to be exposed in the industrial manufacturing, processing, and use of cadmium nitrate is 1 to 99; the data may be greatly underestimated(1).

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.

/GUIDE 154: SUBSTANCES - TOXIC AND/OR CORROSIVE (NON-COMBUSTIBLE)/ First Aid: Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. For minor skin contact, avoid spreading material on unaffected skin. Keep victim warm and quiet. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves. /Cadmium compound/

/GUIDE 154: SUBSTANCES - TOXIC AND/OR CORROSIVE (NON-COMBUSTIBLE)/ Spill or Leak: ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS. /Cadmium compound/

/GUIDE 154: SUBSTANCES - TOXIC AND/OR CORROSIVE (NON-COMBUSTIBLE)/ Fire: Small fires: Dry chemical, CO2 or water spray. Large fires: Dry chemical, CO2, alcohol-resistant foam or water spray. Move containers from fire area if you can do it without risk. Dike fire control water for later disposal; do not scatter the material. Fire involving tanks or car/trailer loads: Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Do not get water inside containers. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire. /Cadmium compound/

/GUIDE 154: SUBSTANCES - TOXIC AND/OR CORROSIVE (NON-COMBUSTIBLE)/ Evacuation: ... Fire: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. /Cadmium compound/

For more DOT Emergency Guidelines (Complete) data for CADMIUM NITRATE (8 total), please visit the HSDB record page.

UN 2570; Cadmium compounds

IMO 6.1; Cadmium compounds

Oxidizer Poison