Nickel Dichloride

Metals -> Nickel Compounds, Inorganic

Carcinogens

3.55 at 59 °F (USCG, 1999) - Denser than water; will sink

3.51

3.51 @25 °C

Yellow scales; ... golden yellow

Brown scales

Golden yellow

Green, deliquescent crystals or crystal powder, monoclinic, structure reported to be trans-(NiCl2(H2O)4.2H2O, sol in about one part water, in alcohol /Hexahydrate/

Green scales, sol in water, alcohol, and ammonium hydroxide /Hexahydrate/

Soluble in ethanol and ammonium hydroxide, insoluble in ammonia

64.2 g/100 cc water @ 20 °C

87.6 g/100 cc water @ 100 °C

SOL IN ETHANOL & AMMONIUM HYDROXIDE

When heated to decomp it emits very toxic fumes of /hydrogen chloride/.

Toxic gases and vapors (such as nickel carbonyl) may be released ... in the decomp of nickel cmpd. /Nickel & sol nickel cmpd/

Nickel chloride appears as a brown or green colored solid. Denser than water. Contact may irritate skin, eyes and mucous membranes. May be toxic by ingestion. Used to make other chemicals.

Liquid; Large Crystals; Dry Powder

Yellow, deliquescent solid; [Merck Index] Water soluble; [ACGIH]

Golden-yellow, sublimable in absence of air, readily absorbs NH3. /Anhydr salt/

Aq soln is acid; pH about 4. /Hexahydrate/

Heat of Solution: 8.8 Btu/lb= 4.9 cal/g= 0.21x10+5 J/kg

Heat of fusion: 142.5 cal/g

Danger

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

P203, P233, P260, P261, P264, P270, P271, P272, P273, P280, P284, P301+P316, P302+P352, P304+P340, P316, P318, P319, P321, P330, P332+P317, P333+P317, P342+P316, P362+P364, P391, P403, P403+P233, P405, and P501 (click each P-code to see the statement)

Danger

H301+H331 (18.2%): Toxic if swallowed or if inhaled [Danger Acute toxicity, oral; acute toxicity, inhalation]

P203, P233, P260, P261, P264, P270, P271, P272, P273, P280, P284, P301+P316, P302+P352, P304+P340, P316, P318, P319, P321, P330, P332+P317, P333+P317, P342+P316, P362+P364, P391, P403, P403+P233, P405, and P501 (click each P-code to see the statement)

Chemical: Nickel chloride (NiCl2)

Hazard Traits - Carcinogenicity

Hazard Traits - Carcinogenicity; Reproductive Toxicity; Respiratory Toxicity

Nickel chloride (NiCl2) is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Nickel chloride (NiCl2) are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Status: Active Update: 24-06-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/15947

Restricted substance: Nickel dichloride

Vacated 1989 OSHA PEL TWA 0.1 mg/cu m is still enforced in some states. /Nickel metal and other compounds (as Ni), soluble/

Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 1 mg/cu m. /Nickel, soluble cmpd, as Ni/

NICKEL CHLORIDE is a yellow, crystalline material, mildly toxic, carcinogenic. On contact with strong acids or acid fumes it produces highly toxic and corrosive hydrogen chloride gas. When heated to decomposition it emits toxic chloride fumes [Lewis, 3rd ed., 1993, p. 915].

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. Nickel chloride is included on this list.

If material involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty). Use foam, dry chemical, or carbon dioxide. Keep run-off water out of sewers and water sources.

Use ambient storage temp and open venting.

KEEP WELL CLOSED.

Nickel is removed from waste water containing nickel chloride by using membrane electrodialysis with a cell thickness 0.77 mm and flow rate 1.18 ml/min.

/Precipitator is/ effective for controlling ... /nickel chloride/ discharged on the ground or into water.

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.

Personnel protection: Keep upwind. Avoid breathing dusts and fumes from burning material. ... Avoid contact with the material.

If material not involved in fire: Keep material out of water sources and sewers.

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.

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

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

0.1 [mg/m3], inhalable fraction, as Ni

8 hr Time Weighted Avg (TWA) 0.1 mg/cu m (inhalable fraction). /Nickel, soluble inorganic compounds (NOS), as Ni/

A4: Not classifiable as a human carcinogen. /Nickel, soluble inorganic compounds (NOS), as Ni/

Excursion Limit Recommendation: Excursions in worker exposure levels may exceed 3 times the TLV-TWA for no more than a total of 30 minutes during a work day, and under no circumstances should they exceed 5 times the TLV-TWA, provided that the TLV-TWA is not exceeded. /Nickel, soluble inorganic compounds (NOS), as Ni/

The effect of complexans (NTA; EDTA) on the toxicity of nickel chloride ... to carp (Cyprinus carpio), and the accumulation of metals in fish at lethal level concentrations was studied. The toxicity of nickel salts to carp was relatively lower ... /and/ the inhibition of nickel accumulation by the presence of complexans was recognized throughout the fish, but no significant decrease of mortality was seen.

Nickel chloride induction of /metallothionein/ in liver and kidneys /of male Fischer rats/ was inhibited by cycloheximide (2 mg/kg, ip).

Synergistic induction /of microsomal heme oxygenase activity/ was observed in liver and kidneys of rats killed after administration of sodium diethyldithiocarbamate and nickel chloride (NiCl2) at all dosage combinations (diethyldithiocarbamate dosages: 0.33 to 1.33 mmol/kg, im, 17 hr before death; NiCl2 dosages: 0.125 and 0.25 mmol/kg, sc, 17 hr before death). At the highest dosages ... the dual treatments induced heme oxygenase activity 11 fold in liver and 16 fold in kidneys ... at the same dosage given /alone/ ... NiCl2 induction was 1.3 fold in liver and 6 fold in kidneys.

Sodium diethyldithiocarbamate caused a retention and redistribution of (63)nickel chloride in the tissues /and/ DL-penicillamine decreased the (63)nickel ion concn in the tissues ... of mice injected with (63)nickel chloride.

For more Interactions (Complete) data for NICKEL CHLORIDE (11 total), please visit the HSDB record page.

The most common harmful health effect of nickel in humans is an allergic reaction. This usually manifests as a skin rash, although some people experience asthma attacks. Long term inhahation of nickel causes chronic bronchitis and reduced lung function, as well as damage to the naval cavity. Ingestion of excess nickel results in damage to the stomach, blood, liver, kidneys, and immune system, as well as having adverse effects on reproduction and development. (L41)

LC50 (Philodina acuticornus) rotifer static unmeasured 2,900 ug/l 96 hr (in water hardness of calcium carbonate 25 mg/l)

LC50 Daphnia magna (cladoceran) static unmeasured 510 ug/l 48 hr (in water hardness of calcium carbonate 45 mg/l)

LC50 Daphnia magna 0.13 mg/l 3 week. /Conditions of bioassay not specified/

Reproductive impairment Daphnia magna 30-95 ug/l/64 hr. /Conditions of bioassay not specified/

For more Ecotoxicity Values (Complete) data for NICKEL CHLORIDE (15 total), please visit the HSDB record page.

... Nickel chloride is a water soluble salt. ... Respiratory absorption with secondary GI absorption of nickel (insoluble & soluble /salts/) is the major route of entry during occupational exposure. A significant quantity of inhaled material is swallowed following mucocillary clearance from the respiratory tract. Poor personal hygiene & work practices can contribute to GI exposure. Percutaneous absorption is negligible, quantitatively, but is important in the pathogenesis of contact hypersensitivity. Absorption is related to the solubility of the compound, followed the general relationships nickel carbonyl > soluble nickel compounds > insoluble nickel compounds. ... Studies in which nickel was administered via inhalation are limited. Studies on hamsters & rats ... /with/ soluble nickel chloride ... /absorption was/ rapid. ... Nickel chloride injected ip into mice & rats caused a rapid decr in body temperature. Nickel chloride given orally, or by inhalation, has been reported to decr iodine uptake by the thyroid /gland/. ... Nickel chloride affects the T-cell system & suppresses the activity of natural killer cells. Parenteral administration of nickel chloride ... has been reported to cause interuterine mortality & decr weight gain in rats & mice. ... Nickel chloride /did not/ induce tumors of the peritoneal cavity in rats after repeated administration. /Another study reported that/ ... nickel chloride which had not induced local tumors in im studies, were tested using repeated ip administration, ... elicited a carcinogenic response. ... Cases of nickel poisoning ... /have been reported/ in electroplaters who accidentally ingested water contaminated with ... nickel chloride.

Nickel is known to substitute for other essential elements in certain enzmes, such as calcineurin. It is genotoxic, and some nickel compounds have been shown to promote cell proliferation. Nickel has a high affinity for chromatin proteins, particularly histones and protamines. The complexing of nickel ions with heterochromatin results in a number of alterations including condensation, DNA hypermethylation, gene silencing, and inhibition of histone acetylation, which have been shown to disturb gene expression. Nickel has also been shown to alter several transcription factors, including hypoxia-inducible transcription factor, activating transcription factor, and NF-KB transcription factor. There is also evidence that nickel ions inhibit DNA repair, either by directly inhibiting DNA repair enzymes or competing with zinc ions for binding to zinc-finger DNA binding proteins, resulting in structural changes in DNA that prevent repair enzymes from binding. Nickel ions can also complex with a number of cellular ligands including amino acids, peptides, and proteins resulting in the generation of oxygen radicals, which induce base damage, DNA strand breaks, and DNA protein crosslinks. (L41, A40)

Nickel chloride (NiCl2) produces a dose dependent depression of proliferation and mitotic rate ... in 2 human cell lines, HeLa and diploid embryonic fibroblasts ... /Additional effects included/ ... increasing release of intracellular lactic dehydrogenase ...; /increased/ lactic acid production; /reduced/ plating efficiency, DNA synthesis, protein synthesis, RNA synthesis. ... Serum constituents, notably albumin, bind the metal effectively and inhibit cellular uptake.

Cells from the CHO-K1-Chinese hamster fibroblast line and human lymphocytes from the peripheral blood of a male subject were used to evaluate subtoxic doses of insoluble metal compounds in the sister chromatid exchange assay. While NTA did not induce sister chromatid exchange in the CHO cell line, soluble compounds of cadmium chloride, potassium dichromate, mercury chloride, and nickel chloride significantly increased sister chromatid exchange in CHO cells, establishing a clear dose effect relationship. Equimolar concentrations of NTA did not enhance sister chromatid exchange induction by metals. The NTA/metal complexes, once formed, were genetically active at extremely low concentrations. The enhancement of the genetic activity was not pH dependent. These effects were also demonstrated in the presence of sodium, magnesium and calcium ions in concentrations largely exceeding those of the genotoxic metal cationic and anionic forms.

Thirty-two workers in an electroplating plant accidentally drank water contaminated with nickel sulfate and nickel chloride (1.63 g nickel/l). Twenty workers rapidly developed symptoms (e.g., nausea, vomiting, abdominal discomfort, diarrhoea, giddiness, lassitude, headache, cough, shortness of breath) that typically lasted a few hours, but persisted for 1-2 days in 7 cases. The nickel doses in workers with symptoms were estimated to range from 0.5 to 2.5 g. In 15 exposed workers, who were investigated on day 1 after exposure, serum-nickel concentrations ranged from 12.8 to 1340 ug/l (average 286 ug/l) with urinary nickel concentrations ranging from 0.23 to 37.1 mg/l (average 5.8 mg/l) compared with control values for nickel-plating workers of 2.0-6.5 ug/l (average 4.0 ug/l) for serum nickel and 22-70 ug/l (average 50 ug/l) for urinary nickel. Laboratory tests showed transiently elevated levels of blood reticulocytes (7 workers), urine-albumin (3 workers), and serum-bilirubin (2 workers) ... .

When aqueous solutions of nickel chloride were applied to the back, the threshold concentrations for irritancy were 1% with occlusion and 10% without occlusion ... .

... NICKEL CHLORIDE IS LETHAL TO DOGS WHEN IV ADMIN IN A SINGLE DOSE OF 10-20 MG/KG, THE CARDIAC & RESPIRATORY NERVE CENTERS ARE AFFECTED; GROSS CHANGES CONSIST OF EDEMA, HEMORRHAGE, & DEGENERATION OF THE HEART MUSCLE, BRAIN, LUNG, LIVER, & KIDNEY.

... CHLORIDE OF INHALED NICKEL ... GREATLY INCREASED THE VISCOSITY OF LUNG WASHINGS /IN RATS/, @ APPROXIMATELY THE SAME EXPOSURE LEVEL (100 UG NICKEL/CU M). MOST PROMINENT EFFECT OF ... THE CHLORIDE WAS HYPERPLASIA OF THE BRONCHIOLAR & BRONCHIAL EPITHELIUM WITH PERIBRONCHIAL LYMPHOCYTIC INFILTRATION.

... NICKEL CHLORIDE, NICKEL SULFATE, & NICKEL NITRATE /WERE NOT/ ... MUTAGENIC IN A STUDY OF MUTATION IN STREPTOMYCIN DEPENDENT E COLI STRAIN ... SIMILAR NEGATIVE RESULTS WERE FOUND ON TESTING BACTERIOPHAGE T4 WITH NISO4 DURING PHAGE REPLICATION IN T4 INFESTED E COLI ...

FISCHER FEMALE RATS HAD PROTEINURIA AFTER SINGLE IP DOSE OF NICKEL CHLORIDE (34-85) MOLES/KG & ALPHA-AMINOACIDURIA AFTER IP DOSE OF 68 & 85 MOLES/KG. RETURNED TO NORMAL BY DAY 5.

For more Non-Human Toxicity Excerpts (Complete) data for NICKEL CHLORIDE (35 total), please visit the HSDB record page.

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. Nickel 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 100 lb or 45.4 kg. The toll free number of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

(CA) CALIFORNIA 100 ug/L /Nickel/

(CT) CONNECTICUT 100 ug/L /Nickel/

(DE) DELEWARE 100 ug/L /Nickel/

(FL) FLORIDA 100 ug/L /Nickel/

(WI) WISCONSIN 100 ug/L /Nickel/

(AZ) ARIZONA 150 ug/L /Nickel/

(MA) MASSACHUSETTS 100 ug/L /Nickel/

(ME) MAINE 140 ug/L /Nickel/

(MN) MINNESOTA 100 ug/L /Nickel/

... Cell growth was selectively blocked in S-phase by ... 1-60 uM ... nickel chloride.

SC INJECTION OF NICKEL(II) CHLORIDE INTO RABBITS (5 MG METAL/KG) INHIBITED ADP INDUCED PLATELET AGGREGATION IN PLASMA SAMPLES TAKEN @ VARIOUS TIMES AFTER INJECTION.

The mechanism of nickel mediated increases in hepatic lipid peroxidation was studied. Eighteen female albino rats were administered a single subcutaneous dose of 200 nickel chloride. A second group of 24 rats was divided into four subgroups and given 50, 100, 200, and 400 uM/kg nickel chloride. Increased lipid peroxidation and glutathione and iron concentrations were proportional to dose at 16 and 24 hr. Glutathione peroxidase activity decreased at the low dose but rose at higher nickel chloride concentrations. Lipid peroxidation was inhibited by exogenous ethylenediaminetetraacetic acid, sodium azide, ethanol, sodium benzoate, and histidine, but was unaffected by superoxide benzoate, and histidine, but was unaffected by superoxide-dismutase and catalase. The administration of Ni resulted in the accumulation of hepatic iron and glutathione peroxidase activity.

The effects of nickel on hepatic glutathione and the enzymes glutathione reductase, glutathione-peroxidase, glutathione-S-transferase, and gamma-glutamyl-transpeptidase were investigated in female albino rats. Three groups of rats were sacrificed 16, 24, or 72 hr after a subcutaneous injection of nickel as nickel chloride at a level of 200 micromol/kg. Four groups of rats were sacrificed 16 hr after a single subcutaneous injection of either 50, 100, 200, or 400 micromol/kg nickel chloride. The single dose of 200 micromol/kg nickel chloride increased glutathione levels and glutathione reductase and glutathione-S-transferase activity at 16 and 24 hr post treatment. Glutathione peroxidase and gamma-glutamyl-transpeptidase activity were reduced at 16 and 24 hr. The effect on enzyme activity was dose dependent at all levels of nickel chloride. Glutathione levels were decreased at 50 micromol/kg relative to the control values but increased with increasing nickel levels.

Induction of heme oxygenase in liver, kidney, and other organs of rodents is a nonspecific, toxic response to parenteral administration of numerous metal compounds. Cobalt and cadmium ions are especially potent inducers of heme oxygenase in rat liver; tin ion, nickel ion, and arsenic ion, are potent inducter of enzyme in rat adrenal. Rat spleen testis, and brain are relatively refractory to metal induction of heme oxygenase activity; in testicular microsomes from cadmium ion-treated rats, heme oxygenase activity is markedly inhibited. Metal induction of heme oxygenase requires de novo synthesis of mRNA and protein, based on 1) experiments with metabolic inhibitrors (actinomycin d, puromyci, and cycloheximide) and 2) translation assays of heme oxygenase mRNa. Heme oxygenase induction by metals is generally suppressed by treatments with SH compounds (for example, cysteine and glutathione) and enhanced by agents that deplete tissue SH levels (for example, diethyl maleate). Administration of DDC exerts a pronounced synergistic effect on Ni2+ induction of heme oxygenase activity in rat tissues, attributable in part to enhanced cellular uptake of nickel. Induction of heme oxygenase activity in rat tissues, attributable in part to enhanced cellular uptake of nickel. Induction of heme oxygenase is not sustained during repeated daily treatments of rats with nickel chloride.

Nickel is absorbed mainly through the lungs and gastrointestinal tract. Once in the body it enters the bloodstream, where it binds to albumin, L-histidine, and _2-macroglobulin. Nickel tends to accumulate in the lungs, thyroid, kidney, heart, and liver. Absorbed nickel is excreted in the urine, wherease unabsorbed nickel is excreted in the faeces. (L41)

THE KIDNEYS SHOWED LARGEST AMT OF NICKEL/G IN MALE RATS 6 HR AFTER INTRATRACHEAL INJECTION OF 1 MG NICKEL AS NICKEL CHLORIDE, FOLLOWED BY LUNG, ADRENAL, LIVER, PANCREAS, SPLEEN, HEART, & TESTIS IN ORDER.

TETA, 0.75 MMOL/KG IM ADMIN TO FISCHER RATS IMMEDIATELY PRIOR TO (63)NICKEL CHLORIDE, 0.068 OR 0.10 MMOL/KG IP OR IM. RENAL CLEARANCE WAS EST TO BE GREATER THAN 20 TIMES NONCHELATED-(63)NICKEL.

AFTER SINGLE IP INJECTION OF NICKEL CHLORIDE (17 OR 816 UG NICKEL/ANIMAL, RESP) INTO RATS OR RABBITS, (63)NICKEL ION RAPIDLY CLEARED PLASMA OR SERUM FIRST 2 DAYS & SLOWER NEXT 5 DAYS.

SOL NICKEL CHLORIDE ... RAPIDLY CLEARED AFTER INTRATRACHEAL INJECTION /IN RATS/. BY 72 HR, 90% OF INJECTED NICKEL ... EXCRETED, MAINLY (75%) IN THE URINE. ... 6 HR AFTER /ONE/ INTRATRACHEAL INJECTION OF 1 MG NICKEL CHLORIDE, KIDNEYS SHOWED GREATEST AMT OF NI/G. /THEN/ ... LUNG, KIDNEYS ... PANCREAS, SPLEEN, HEART, TESTES.

For more Absorption, Distribution and Excretion (Complete) data for NICKEL CHLORIDE (14 total), please visit the HSDB record page.

Used in nickel plating cast zinc, electrolytic refining of nickel, producing nickel catalysts and nickel salts, absorbing of ammonia gas in respirators, electrodeless plating of nickel, tin-nickel alloy plating, and fungicides; [HSDB]

Electroplating [Category: Plate]

For nickel plating cast zinc; mfr sympathetic ink; absorbent for NH3 in gas masks

Used for nickel plating cast zinc; agent in electrolytic refining of nickel; chemical intermediate for nickel catalysts and complex nickel salts; absorber of ammonia gas in industrial gas masks; catalyst in diarylamine and silicon tetrachloride production; agent in electrodeless plating of nickel; agent in tin-nickel alloy plating. Fungicide; control of rust and rustlike disease /SRP: former use/.

Electroplated nickel coatings, reagent chemical

... /has/ been used successfully for control of rust and rust-like diseases. /SRP: former use/

2023: 1,000,000 - <2,500,000 lb

(1977) AT LEAST 5.09X10+8 G

Prepn: nickel chloride may be prepared from nickel oxide by chlorination or by reaction with hydrogen chloride.

REACTION OF NICKEL POWDER OR NICKEL OXIDE WITH HYDROCHLORIC ACID FOLLOWED BY EVAPORATION; PASSAGE OF CHLORINE GAS OVER HEATED NICKEL

Action of hydrochloric acid on nickel

Technical, 99+%.

-10 mesh and -60 mesh, 99.5 and 99.999% purity grades; 6 lb/gal electrodeless nickel grade; high purity soln suitable for printed circuit and other plating and metal treating applications; liquid grades; crystal & powder grades

All Other Chemical Product and Preparation Manufacturing

Nickel chloride (NiCl2): ACTIVE