Monthly Tech-Tip from Tony Hansen SignUp

No tracking! No ads!

Alumina Toxicology | Ammonia and Latex Toxicity | Antimony Oxide | Are colored porcelains hazardous? | Arsenic Oxide | Asbestos: A Difficult-to-Repace Material | Ball Clay | BARIUM and COMPOUNDS / Toxicology | Barium Carbonate | Bentonite Toxicity | Beryllium Monoxide Toxicology | Bismuth Trioxide Toxicology | Boron Compounds and Their Toxicity | Brown Stain | Cadmium Toxicity | Calcium Carbonate Toxicology | Carbon Monoxide Toxicity | Cesium Toxicology | Chromium Compounds Toxicology | Clay Toxicity | Cobalt Oxide and Carbonate | Cobalt Toxicology | Copper Compounds Toxicology | Copper Oxide and Carbonate | Cristobalite Toxicity | Cryolite and Ceramics | Dealing With Dust in Ceramics | Diatomaceous Earth Toxicology | Dioxins in Clays | Epsom Salts | Eye Injuries Due to Radiation | Feldspar | Fighting Micro-Organisms in Ceramics | Fluorine Gas | Gallium Oxide Toxicology | Hafnium Oxide Toxicty | Hydrofluoric Acid Toxicity | Iron oxide and Hematite | Lead Chromate | Lead in Ceramic Glazes | Lead Toxicology | Lithium Carbonate Toxicity | Lithium Toxicology | Man-Made Vitreous Fibers (MMVF) Toxicology | Man-Made Vitreous Fibers Safety Update | Manganese and Parkinsons by Jane Watkins | Manganese in Clay Bodies | Manganese Inorganic Compounds Toxicology | Manganese Toxicity by Elke Blodgett | Manganese: Creativity and Illness by Dierdre O'Reilly | Molybdenum Compounds Toxicology | Nickel Compounds Toxicity | Niobium Oxide Toxicity | Occupational Dermatoses | Overview of Material Safety by Gavin Stairs | Paraffin Toxicology | Perlite Toxicity | Plant Ash Toxicity | Potassium Carbonate Toxicity | Pregnancy and Ceramics | Propane Toxicology | Quartz Toxicity | Quartz Toxicity on Clayart | Rare Earth Compounds Toxicity | Rubidium and Cesium Toxicology | Rutile Toxicology | Silicosis and Screening | Silver Compounds Toxicology | Sodium Azide Toxicology | Sodium Carbonate Toxicology | Sodium Silicate Powder Toxicology | Stannous Chloride Toxicity | Strontium Carbonate Toxicity Note | Sulfur Dioxide Toxicity | Talc Hazards Overview | Talc Toxicology | Thallium Oxide Toxicology | The Use of Barium in Clay Bodies | Thorium Dioxide Toxicity | Tin Inorganic Compounds | Titanium Dioxide Toxicology | Toxicological Assessment of Zeolites | Tungsten Compounds Toxicology | Understanding Acronyms on MSDS's | Uranium and Ceramics | Vanadium and Compounds Toxicology | Vermiculite | Zinc Compounds Toxicology | Zirconium Compounds Toxicity | Zirconium Encapsulated Stains Toxicity

Nickel Compounds Toxicity

Chemical and Physical Forms :
Nickel (atomic number, 28; atomic weight, 58.7; boiling point, 2,732 C; specific gravity, 8.9 at 25 C), from natural sources, is a mixture of 5 stable isotopes.
9 unstable nickel isotopes have also been identified.
Major deposits of nickel ores are located in Australia, Canada, Cuba, Indonesia, New Caledonia, and Russia.
Nickel exists in 5 major forms :
- elemental nickel and its alloys;
- inorganic, water-soluble compounds;
- inorganic, water-insoluble compounds;
- organic, water-insoluble compounds;
- nickel carbonyl Ni(CO)4
Nickel is a silver-white, lustrous, hard, malleable, ductile, ferromagnetic metal that is relatively resistant to corrosion and is a fair conductor of heat and electricity.
Black NiO is chemically reactive and readily yields nickel salts on contact with mineral acids; green NiO is relatively inert and refractory to solubilization in dilute acids.
The volatility and lipid solubility of nickel carbonyl Ni(CO)4 enable it to cross cell membranes, and the redox reactivity of Ni(CO)4 contributes to its high toxicity.
Exposure sources :
I-Occupational Exposures :
Exposure to nickel is possible in:
- the production of nickel. The annual world production is estimated at 900,000 tons;
- the fabrication of alloys with copper, iron, aluminium;
- the preparation of corrosion and heat resistant special steels;
- nickel plating by electrolysis (use of nickel sulphate, chloride and nitrate);
- arc welding,
- plasma spraying and flame cutting;
- producing and processing nickel salts;
- fabricating Ni-Cd batteries;
- producing molds for the hollow-glass industry;
- chemical reactors (as a catalyst);
- the manufacture of coins, jewelry;
- the manufacture of kitchen wares;
- the manufacture of medical and dental implants;
- applying nickel glazes to ceramics;
- painting with nickel pigments;
- manufacturing electrical resistors, magnetic tapes, and computer components;
- the metallization with nickel.
- incinerating or reprocessing nickel-containing wastes
- combusting fossil fuels;
- etc.
Many cements contain small amounts of nickel (< 1000 ppm)
II-Environmental Exposures :
A-Water Sources :
Nickel enters groundwater and surface waters from dissolution of rocks and soils, biological cycles, atmospheric fallout, industrial processes, and waste disposal.
Nickel leached from dump sites can contribute to nickel contamination of the aquifer, with potential ecotoxicity.
Acid rain has a tendency to mobilize nickel from soil and increase the nickel concentration in groundwater, leading eventually to increased uptake and possible toxicity in microorganisms, plants, and animals.
Drinking water usually contains less than 20 µg of nickel per L.; much higher concentrations may occur due to pollution of the water supply or leaching from nickel-containing pipes and nickel-plated faucets.
B-Air Sources :
Nickel enters the atmosphere from natural sources such as volcanic emissions and windblown dusts produced by weathering of rocks and soils, combustion of fossil fuels, emissions of mining and refining operations, metal consumption in industrial processes, and incineration of wastes.
Substantial atmospheric concentrations of nickel are derived from fly-ash released from coal-fired power plants, nickel derived from petroleum is released into the environment in automotive exhaust fumes.
Cigarette smoking can increase the amount of inhaled nickel by as much as 4 µg per pack of cigarettes.
C-Other sources :
The dietary intake of nickel by adult persons averages approximately 165µg per day but may reach 900 µg in diets rich in oatmeal, cocoa, chocolate, nuts, and soya products.
Wearing or handling of jewelry, coins, and ustensils that are fabricated from nickel alloys or that have nickel-plated coatings can induce allergic dermatitis.
Implantation of nickel-containing prostheses or iatrogenic administration of nickel-contaminated medications or media leads to parenteral exposures, which can cause acute toxicity and immunologic disturbances.
Toxicology :
I-Absorption, Metabolism, and Elimination :
A-Absorption :
Contrary to insoluble compounds, such as NiO, soluble salts are readily absorbed by the pulmonary and digestive tracts, and less by the skin.
The alimentary absorption of nickel is greatly influenced by dietary constituents, fasting individuals absorbing more.
The respiratory, oral, and parenteral exposure routes are important for acute nickel toxicity (e.g inhalation of nickel carbonyl; ingestion of nickel-contaminated beverages and foods; implantation of nickel-containing devices; administration of nickel-contaminated medications).
Inhaled nickel carbonyl Ni(CO)4 is rapidly absorbed by the lungs and enters red blood cells where the compound undergoes conversion to Ni2+ and CO.
Respiratory exposure is of paramount importance in nickel carcinogenesis.
In nickel refinery workers, inhaled nickel dust is retained in the nasal sinuses and lungs for many years after cessation of exposure; some of the nickel is slowly absorbed, as evidenced by sustained hypernickelemia among these workers.
During hemodialysis, traces of Ni2+ in hemodialysis fluid may be absorbed into the plasma, owing to the chelating action of plasma albumin.
Dermal exposure is primarely responsible for nickel dermatitis, although oral or parenteral exposures to nickel can potentiate hand ecxema in nickel-sensitive persons.
B-Metabolism :
The metabolism and distribution of Ni2+ in humans have been fitted by a two-compartment toxicokinetic model.
In human plasma, Ni2+ is bound to ultrafilterable constituents :
-nickeloplasmin, an alpha2-macroglobulin.
The mean nickel concentrations of human tissues may be ranked in order of highest to lowest concentration as follows :
-adrenal gland,
In adult humans, the body burden of nickel is estimated to average approximately 0.5 mg per 70 kg , or approximately 7.3 µg per kg of body weight.
In tissue cytosol, nickel is bound to several proteins and peptides.
C-Elimination :
Nickel is not a cumulative toxicant. The majority of the absorbed amount is excreted rapidly.
Urine is the major route for elimination of absorbed nickel with a half-life varying from 17 to 39 hours. Therefore, urine and plasma nickel concentrations constitute valuable indicators of recent exposure to soluble nickel derivatives.
Most nickel in food remains unabsorbed in the alimentary tract and passes through into the feces.
However, biliary excretion of nickel may be quantitatively significant.
Minor routes of elimination are :
-gastric and intestinal secretions,
-dermal detritus,
-mother's milk,
II-Acute Toxicity :
A-Acute Nickel Carbonyl Poisoning :
Accidental inhalation of nickel carbonyl Ni(CO)4 generally causes acute toxic effects in 2 stages:
1-Immediate symptoms :
which usually last a few hours, followed by an asymptomatic interval of 12 hours to 5 days before the onset of :
2-Delayed symptoms :
-tightness of the chest,
-nonproductive cough,
-visual disturbances,
-weakness , lassitude.
The delayed symptoms often mimic viral pneumonia.
In cases of severe Ni(CO)4 poisonning, deaths have occurred 4-13 days after exposure.
Autopsies have revealed the following pulmonary lesions :
-proteinaceous alveolar exudate,
-interstitial pneumonitis,
-damage to alveolar lining cells,
-denudation of bronchial epithelium.
Autopsies have also revealed pathologic lesions :
-parenchymal degeneration,
-punctate hemorrhages,
in other organs :
-adrenal glands,
In survivors, the recovery period tends to be protracted, with lassitude and dyspnea persisting up to 6 months.
It is estimated that exposure to 30 ppm. nickel carbonyl for 30 minutes may be lethal to humans.
B-Acute Nickel Pneumonitis :
Accidental inhalation of metallic nickel particles can cause pneumonitis. For example, a welder died from acute respiratory distress syndrome after inhalation of a finely particulate nickel fume that was produced by a metal arc-welding process.
C-Acute Toxicity from Divalent Nickel :
Acute Ni2+ toxicity occurred when 32 electroplating workers accidently drank water contaminated with NiSO4 and NiCl2. Twenty of the workers promptly developed symptoms :
-abdominal discomfort,
-shortness of breath,
that generally ceased within a few hours, but symptoms persisted for 1-2 days in seven cases.
In the workers with symptoms, the estimated nickel doses ranged from approximately 0.5-2.5 g.
All subjects recovered rapidly, without evident sequellae, and returned to work by the 8th day after exposure.
III-Chronic Toxicity :
A-Allergic and Immunologic Effects :
One of the most common causes of contact dermatitis throughout the world is allergy to nickel alloys and nickel compounds; positive dermal patch tests to nickel occur in 7-10% of women and 1-3% of men in the general population. Dermal sensitization frequently occurs from exposures to :
-nickel-containing coins,
-watch cases,
-clothing fasteners.
Nickel dermatitis (nickel itch) typically begins as papulovesicular erythema of hands, forearms, earlobes, or other areas of skin that contact nickel alloys, and spreads secondarily to areas (usually symmetric) that are distant from the contact sites.
The erythematous lesions become eczematous and eventually undergo lichenification. Pompholyx ( i.e., dyshidrotic eczema) is the predominant type of nickel-induced dermatitis, characteristically affecting the sides of the fingers, the palms, and sometimes the soles.
Nickel itch may be prevented by the use of a ointment containing 10% sodium diethyl-
Nickel hypersensitivity can cause :
-pulmonary asthma,
-eosinophilic pneumonitis,
-inflammatory reactions around nickel-containing implants (e.g., orthopedic prostheses, dental inlays or bridges, cardiac valve prostheses, pacemaker wires),
-anaphylactoid reactions after parenteral injection of nickel-contaminated medications.
B-Respiratory Effects :
Chronic respiratory insufficiency may develop as a consequence of acute Ni(CO)4 poisonning.
In workers in nickel refineries, plating shops, or welding shops, inhalation of irritant nickel-containing dusts and aerosols may contribute to chronic respiratory diseases, including :
The workers may develop :
-hypertrophic rhinitis,
-nasal polyposis,
-nasal septal perforation,
Incidences of such non-neoplastic respiratory diseases in nickel-exposed workers have not been thoroughly studied, and the etiologic role of nickel is often unclear, as the affected workers generally are exposed to " sundry " dusts and vapors in addition to nickel compounds
C-Renal Effects :
Workers who are exposed to soluble nickel compounds may develop mild renal tubular dysfunction, as evidenced by increased urinary excretion of ß2-microglobulin and N-acetyl-glucosaminidase.
D-Reproductive effects :
1-In animals :
In experimental animals, a range of reproductive effects can be induced by nickel.
In male rats, exposure to nickel salts results in degenerative changes in the testes and epididymis and in effects on spermatogenesis.
Exposure of pregnant animals has been associated with delayed embryonic development, increased resorptions, and an increase in structural malformations. It has been noted, however, that doses used are high and may not relate at all to human exposures.
2-In man :
Increased incidences of congenital defects and spontaneous or threatened abortion were observed in a study of 758 Russian women who were employed in a nickel hydrometallurgy refining plant.
A sixfold increase in the relative risk of cardiovascular defects was noted in the infants of nickel-exposed women.
In light of these findings and those found in rodents and other animals, further investigations are needed of the adverse reproductive effects in nickel-exposed women.
D-Carcinogenesis :
Epidemiologic studies have demonstrated increased mortality from carcinomas of the lung and nasal cavities in nickel refinery workers who were chronically exposed to inhalation of nickel-containing dusts and fumes from roasting, smelting, and electrolysis processes.
The respiratory tract cancers in nickel refinery workers have been associated with inhalation exposures to nickel compounds with low aqueous solubility such as Ni3S2, NiO; as well as soluble nickel compounds like NiSO4.
A review of the whole of epidemiologic studies has demonstrated that the risk for cancer of the respiratory tract is increased when the atmospheric concentration of soluble nickel exceeds 1 mg Ni/m3 and that of insoluble derivatives exceeds 10 mg Ni/m3.
Nickel cumulates in the nasal mucosa of exposed workers, its concentration is in proportion with the lenght of exposure; since its biologic half-life is 3½ years its concentration remains high even after cessation of exposure.
An investigation of respiratory tract cancers in former workers at a Canadian nickel sinter plant demonstrated that the excess risk of death from cancers of the lung or nasal cavities continued for as long as 30-40 years after leaving the sinter plant; this reflects long-term persistence of carcinogenic nickel compounds in the respiratory tract mucosa.
The interaction between smoking and nickel exposure appears to be additive rather than multiplicative.
The mechanism by which nickel exerts its carcinogenic action is not known because its derivatives are usually of low mutagenic activitry. It is possible that divalent salts interfere with DNA reparation mechanisms.
In 1990 the IARC (International Agency for Research on Cancer) classified nickel compounds as carcinogenic to humans (Group I); and metallic nickel as possibly carcinogenic to humans (Group 2B)
Clinical management :
I-Acute Nickel Carbonyl Poisoning :
After acute exposure to Ni(CO)4, the victim should be quickly transported to a hospital; after removal of contaminated clothing, life support measures and administration of oxygen should be instituted .
Hyperglycemia and glycosuria typically develop after exposure to Ni(CO)4.
An acute exposure to Ni(CO)4 may be classified as :
A-Mild :
if the initial 8-hour urine collection reveals a nickel concentration of less than 100 µg/L.
B-Moderate :
if the nickel concentration in the initial 8-hour urine collection is between 100 µg/L.and 500 µg/L.
C-Severe :
if the nickel concentration in the initial 8-hour urine collection is greater than 500 µg/L.
Patients in the moderate and severe categories of acute Ni(CO)4 poisonning should be treated immediately with a chelating drug, sodium diethyldithiocarbamate (DDC).
The beneficial effect of DDC in acute Ni(CO)4 poisonning has been attributed to diminution of the pulmonary nickel burden.
II-Acute poisoning from Divalent Nickel :
Presumptive diagnosis of acute Ni2+ poisonning is based on the clinical history and analysis of nickel in the exposure medium.
The immediate supportive treatment is :
A- to maintain body temperature, because Ni2+ impairs thermoregulation;
B- to induce diuresis by administration of intravenous fluids, because Ni2+ is eliminated primarely via the urine.
Confirmation of the diagnosis rests on the quantative determinations of nickel in body fluids, usually serum and urine.
Hemodialysis would be the therapy of choice for patients with acute Ni2+ poisonning, if renal function fails, or if cardiotoxicity and neurotoxicity become life-threatening.
Chelation with DDC is not recommended in severe Ni2+ toxicity because DDC enhances the cerebral uptake of Ni2+ in rodents.
Biological and Medical Monitoring :
I-Biological Monitoring :
Urine is the most practical specimen for biological monitoring of occupational, environmental, or iatrogenic exposures to nickel compounds. Nickel can also be measured in serum, plasma, and whole blood.
Feces are the best specimen for monitoring oral nickel intake.
Nickel concentrations in saliva, hair, fingernails, sweat, milk, and blood lymphocytes sometimes are assayed in clinical investigations, but such tests seldom are practical for routine biological monitoring.
Analysis of expired breath may be useful to detect Ni(CO)4 after its inhalation.
In persons without occupational exposure, and based on a critical evaluation of published data for nickel determinations in body fluids, the upper limit for serum nickel concentration is approximately 1 µg/L and the upper limit for urinary nickel concentration is approximately 6 µg/L.
A-Soluble compounds :
Nickel concentrations in urine or serum specimens from workers with inhalation exposures to soluble nickel salts (e.g. NiCl2, NiSO4) are generally proportional to the exposure levels and reflect the amount of nickel absorbed during the 1 or 2 preceding days.
B-Poorly soluble nickel compounds, nickel powders, nickel alloys :
In workers with inhalation exposures, nickel concentrations in urine and serum specimens reflect the combined influences of recent exposures and long-term accumulation, as well as the bioavailability of the nickel species.
Absence of increased values does not necessarily indicate freedom from health risk (e.g. cancers of the nasal cavities and lungs) that have been associated with chronic exposure to such compounds.
II-Biological Monitoring :
A- Clinical Examination :
A special attention should be paid to the examination of the nasal mucosa, lungs, and skin.
B- Diagnostic Tests :
Certain diagnostic tests may assist in detecting the pathologic sequelae of nickel exposures. These tests include :
1-To detect nickel allergy :
- dermal patch test;
- lymphocyte transformation assay.
2-To detect nephrotoxicity :
3-To detect pneumonitis, sinusitis, and tumors :
-radiographic imaging of the lungs, mediastinum and nasal cavities
4-To detect respiratory tract dysplasia and neoplasia :
- biopsy and exfoliative cytology.
5- Pulmonary function tests.
Occupational exposure limits :
I- In Quebec, the VEMPs (Valeur d'Exposition Moyenne Pondérée) are as follows :






Insoluble compounds, as Ni


Soluble compounds, as Ni


Nickel carbonyl, as Ni


Nickel sulfide, roasted, fumes and dust, as Ni


C1 =Confirmed carcinogen to humans.
RP =Substance whose recirculation is prohibited in accordance with the law.
EM =Substance that should be kept at the lowest practicable level.
II- In the USA, ACGIH proposed the following in 2001 :

Nickel, as Ni




Soluble compounds (NOS)


Insoluble compounds (NOS)


Nickel subsulfide



Nickel carbonyl

0.05 ppm

A1=Confirmed Human Carcinogen
A4=Not Classifiable as a Human Carcinogen
A5=Not Suspected as a Human Carcinogen
Prevention :
Good housekeeping of your studio is important. Avoidance of processes generating unnecessary dust is also important.
Depending on the severity of exposure, local ventilation should be used and the aspired air should be vented outside to avoid producing dust from work tables and the floor.
The wearing of an approved dust mask when the exposure seems hazardous is mandatory.
It should be forbidden to drink, eat or smoke in the workshop.
References :
1-Occupational Medicine,Carl Zenz, last edition.
2-Clinical Environmental Health and Toxic Exposures, Sullivan & Krieger; last edition.
3-Sax's Dangerous Properties of Industrial Materials, Lewis C., last edition.
4-Toxicologie Industrielle et Intoxications Professionnelles, Lauwerys R. last edition.
5-Chemical Hazards of the Workplace, Proctor & Hughes, 4th edition.

By Edouard Bastarache

Related Information


Typecodes Article by Edouard Bastarache
Edouard Bastarache is a well known doctor that has written many articles on the subject of toxicity of ceramic materials and books on technical aspects of ceramics. He writes in both English and French.
Materials Nickel Oxide Green
Materials Nickel Oxide Black
Materials Nickel Carbonate

Got a Question?

Buy me a coffee and we can talk, All Rights Reserved
Privacy Policy