IPCS INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY
Health and Safety Guide No. 62
NICKEL, NICKEL CARBONYL, AND SOME NICKEL COMPOUNDS
HEALTH AND SAFETY GUIDE
UNITED NATIONS ENVIRONMENT PROGRAMME
INTERNATIONAL LABOUR ORGANISATION
WORLD HEALTH ORGANIZATION
WORLD HEALTH ORGANIZATION, GENEVA 1991
This is a companion volume to Environmental Health Criteria 108:
Nickel
Published by the World Health Organization for the International
Programme on Chemical Safety (a collaborative programme of the United
Nations Environment Programme, the International Labour Organisation,
and the World Health Organization)
This report contains the collective views of an international group of
experts and does not necessarily represent the decisions or the stated
policy of the United Nations Environment Programme, the International
Labour Organisation, or the World Health Organization
WHO Library Cataloguing in Publication Data
Nickel, nickel carbonyl, and some nickel compounds : health and safety
guide.
(Health and safety guide ; no. 62)
1.Nickel - adverse effects 2.Nickel - standards
3.Environmental exposure
4.Environmental pollutants I.Series
ISBN 92 4 151062 5 (NLM Classification: QV 290)
ISSN 0259-7268
(c) World Health Organization 1991
Publications of the World Health Organization enjoy copyright
protection in accordance with the provisions of Protocol 2 of the
Universal Copyright Convention. For rights of reproduction or
translation of WHO publications, in part or in toto, application
should be made to the Office of Publications, World Health
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products does not imply that they are endorsed or recommended by the
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that are not mentioned. Errors and omissions excepted, the names of
proprietary products are distinguished by initial capital letters.
CONTENTS
INTRODUCTION
1. PRODUCT IDENTITY AND USES
1.1. Identity
1.2. Physical and chemical properties
1.3. Analytical methods
1.4. Uses
2. SUMMARY AND EVALUATION
2.1. Sources of nickel
2.2. Behaviour in the environment
2.3. Human exposure
2.4. Metabolism
2.5. Effects on organisms in the environment
2.6. Effects on experimental animals and in vitro test systems
2.7. Effects on human beings
3. CONCLUSIONS AND RECOMMENDATIONS
3.1. Conclusions
3.2. Recommendations
4. HUMAN HEALTH HAZARDS, PREVENTION AND PROTECTION, EMERGENCY ACTION
4.1. Main human health hazards, prevention and protection,
first aid
4.1.1. Advice to physicians
4.1.2. Health surveillance advice
4.2. Explosion and fire hazards
4.2.1. Explosion hazards
4.2.2. Fire hazards
4.2.3. Prevention
4.2.4. Fire extinguishing agents
4.3. Storage
4.4. Transport
4.5. Spillage and disposal
4.5.1. Spillage
4.5.2. Disposal
5. HAZARDS FOR THE ENVIRONMENT AND THEIR PREVENTION
6. SUMMARY OF CHEMICAL SAFETY INFORMATION
7. CURRENT REGULATIONS, GUIDELINES, AND STANDARDS
7.1. Previous evaluations by international bodies
7.2. Exposure limit values
7.3. Specific restrictions
7.4. Labelling, packaging, and transport
7.5. Waste disposal
BIBLIOGRAPHY
INTRODUCTION
The Environmental Health Criteria (EHC) documents produced by the
International Programme on Chemical Safety include an assessment of
the effects on the environment and on human health of exposure to a
chemical or combination of chemicals, or physical or biological
agents. They also provide guidelines for setting exposure limits.
The purpose of a Health and Safety Guide is to facilitate the
application of these guidelines in national chemical safety
programmes. The first three sections of a Health and Safety Guide
highlight the relevant technical information in the corresponding EHC.
Section 4 includes advice on preventive and protective measures and
emergency action; health workers should be thoroughly familiar with
the medical information to ensure that they can act efficiently in an
emergency. Within the Guide is a Summary of Chemical Safety
Information which should be readily available, and should be clearly
explained, to all who could come into contact with the chemical. The
section on regulatory information has been extracted from the legal
file of the International Register of Potentially Toxic Chemicals
(IRPTC) and from other United Nations sources.
The target readership includes occupational health services, those in
ministries, governmental agencies, industry, and trade unions who are
involved in the safe use of chemicals and the avoidance of
environmental health hazards, and those wanting more information on
this topic. An attempt has been made to use only terms that will be
familiar to the intended user. However, sections 1 and 2 inevitably
contain some technical terms. A bibliography has been included for
readers who require further background information.
Revision of the information in this Guide will take place in due
course, and the eventual aim is to use standardized terminology.
Comments on any difficulties encountered in using the Guide would be
very helpful and should be addressed to:
The Manager
International Programme on Chemical Safety
Division of Environmental Health
World Health Organization
1211 Geneva 27
Switzerland
THE INFORMATION IN THIS GUIDE SHOULD BE CONSIDERED AS A STARTING POINT
TO A COMPREHENSIVE HEALTH AND SAFETY PROGRAMME
1. PRODUCT IDENTITY AND USES
1.1 Identity
Common name: Nickel
Chemical symbol: Ni
CAS registry number: 7440-02-0
1.2 Physical and Chemical Properties
1.2.1 Nickel
Nickel is a naturally occurring, shiny, light-coloured metal with high
electrical and thermal conductivities. It is resistant to corrosion
by air, water, and alkalis, but reacts with dilute oxidizing agents.
1.2.2 Some nickel salts
Nickel carbonate hydroxide tetrahydrate (2NiCO3.3Ni(OH)2.4H2O)
The composition of basic nickel carbonate varies. The most common
forms range from 2NiCO33Ni(OH)2.XH2O to NiCO3Ni(OH)3.XH20.
Nickel carbonate hydroxide is insoluble in water, but soluble in
ammonia and in dilute acids.
Nickel carbonyl (Ni(CO)4)
Nickel carbonyl is a colourless, volatile liquid that is formed when
nickel powder is treated with carbon monoxide at about 50°C. It is
insoluble in water, but soluble in most organic solvents.
Nickel chloride (NiCl2) and nickel chloride hexahydrate (NiCl2.6H2O)
Nickel chloride and nickel chloride hexahydrate are soluble in both
water and ethanol.
Nickel hydroxide (Ni(OH)2)
Nickel hydroxide is insoluble in water, but soluble in acids. It
forms complexes with ammonia.
Nickel nitrate (Ni(NO3)2)
Nickel nitrate is readily soluble in both water and alcohol.
Nickel oxide (NiO)
The name "nickel oxide" covers several nickel-oxygen compounds that
differ in stoichiometry, and chemical and physical properties.
Nickel oxide (NiO) exists in two forms. Black nickel oxide is
chemically reactive and forms simple salts in the presence of acids.
Green nickel oxide is an inert and refractory material. Nickel oxide
is insoluble in water. The solubility in acids and other properties
depend on the method of preparation of the nickel oxide.
Nickel sulfate (NiSO4)
Nickel sulfate exists as a hexahydrate, initially in the alpha-form,
which changes into the ß-form at 53.3°C. Nickel sulfate is soluble in
water, ethanol, and methanol.
Nickel sulfide (NiS)
Nickel sulfide is insoluble in water.
Nickel subsulfide (Ni3S2)
At high temperatures, nickel subsulfide exists in a bronze-yellow form
(beta-Ni3S2). At lower temperatures, it changes to a green ß-form,
which is stable at normal temperature. alpha-Nickel subsulfide occurs
naturally as the grey mineral heazlewoodite. Nickel subsulfide is
insoluble in water.
1.3 Analytical Methods
The most commonly used analytical methods for biological and
environmental samples are atomic absorption spectroscopy and
voltammetry. In order to obtain reliable results, especially in the
ultratrace range, specific procedures have to be followed to minimize
the risk of contamination during sample collection, storage,
processing, and analysis. Depending on sample pretreatment,
extraction, and enrichment procedures, detection limits of
1-100 ng/litre can be achieved in biological samples and water.
For water, electrothermal atomic absorption spectroscopy (EAAS) has a
detection limit of 10 ng nickel/litre. Voltammetry is more sensitive
and the use of differential pulse voltammetry (DPV) can achieve a
detection limit of 1 ng/litre.
DPV can also be used for the determination of the nickel contents of
foodstuffs.
Flame atomic absorption spectroscopy (FAAS) is a commonly used method
for measuring nickel concentrations in air. Inductively coupled
plasma atomic emission spectroscopy (ICP-AES) can also be used for the
analysis of air samples.
Atomic absorption spectroscopy is a sensitive method for nickel
determination in blood, serum, urine, other biological samples, and
soil.
Electron microscopy and X-ray microanalysis can be used for the
determination of nickel levels in dust particles, such as grinding
dust and welding fumes.
1.4 Uses
Nickel is mined from sulfide or oxide ores (laterites). Production of
nickel metal is performed by pyro- and hydrometallurgical methods.
Final refining can be achieved by electrolytic techniques or by
passing carbon monoxide gas over nickel powder to form nickel
carbonyl, which is decomposed to yield pure nickel.
A major use of nickel is as an alloying element for steel and cast
iron, yielding alloys and steels with increased strength and
resistance to corrosion and temperature. Nickel compounds are used in
nickel-cadmium batteries, in electronic and computer equipment, and as
constituents of pigments in the glass and ceramics industries. Other
important applications include the use of nickel sulfate and nickel
chloride in electroplating, and of nickel compounds as catalysts in
the manufacture of organic chemicals, petroleum refining, and edible
oil hardening. Nickel carbonyl is used in nickel refining.
2. SUMMARY AND EVALUATION
2.1 Sources of Nickel
Nickel is a ubiquitous trace metal and occurs in soils, water, air,
and in the biosphere. The average content of the earth's crust is
about 0.008%. Farm soils contain between 3 and 1000 mg nickel/kg.
Levels in natural waters have been found to range from 2 to
10 µg/litre (fresh water) and from 0.2 to 0.7 µg/litre (marine).
Atmospheric nickel concentrations in remote areas range from <0.1 to
3 ng/m3.
Nickel ore deposits are accumulations of nickel sulfide minerals
(mostly pentlandite) and laterites. Nickel is extracted from the
mined ore by pyro- and hydro-metallurgical refining processes. Global
mining production of nickel was approximately 67 million kg in 1985.
Most of the nickel is used for the production of stainless steel and
other nickel alloys with high corrosion and temperature resistance.
Nickel alloys and nickel plating are used in vehicles, processing
machinery, armaments, tools, electrical equipment, household
appliances, and coinage. Nickel compounds are also used as catalysts,
pigments, and in batteries. The primary sources of nickel emissions
into the ambient air are the combustion of coal and oil for heat or
power generation, the incineration of waste and sewage sludge, nickel
mining and primary production, steel manufacture, electroplating, and
miscellaneous sources, such as cement manufacturing. In polluted air,
the predominant nickel compounds appear to be nickel sulfate, oxides,
and sulfides, and, to a lesser extent, metallic nickel.
Nickel from various industrial processes and other sources finally
reaches waste water. Residues from waste-water treatment are disposed
of by deep well injection, ocean dumping, land treatment, and
incineration. Effluents from waste-water treatment plants have been
reported to contain up to 0.2 mg nickel/litre.
2.2 Behaviour in the Environment
Nickel is introduced into the environment from both natural and
man-made sources and is circulated throughout all environmental
compartments by means of chemical and physical processes, as well as
by being biologically transported by living organisms.
Atmospheric nickel is considered to exist mainly in the form of
particulate aerosols containing different concentrations of nickel,
depending on the source. The highest nickel concentrations in ambient
air are usually found in the smallest particles. Nickel carbonyl is
unstable in air and decomposes to form nickel oxide.
The transport and distribution of nickel particles to, or between,
different environmental compartments is strongly influenced by
particle size and meteorological conditions. Particle size
distribution is primarily a function of the emitting sources. In
general, particles from man-made sources are smaller than natural dust
particles.
Nickel is introduced into the hydrosphere by removal from the
atmosphere, by surface runoff, by discharge of industrial and
municipal waste, and also following natural erosion of soils and
rocks. In rivers, nickel is mainly transported in the form of a
precipitated coating on particles, and in association with organic
matter; in lakes, it is transported in the ionic form, predominantly
in association with organic matter. Nickel may also be absorbed on
clay particles and via uptake by biota. Absorption processes can be
reversed leading to the release of nickel from the sediment. Part of
the nickel is transported via rivers and streams to the ocean.
Riverine suspended particulate input is estimated to be
135 × 107 kg/year.
Depending on the soil type, nickel may exhibit a high mobility within
the soil profile, finally reaching ground water and, thus, rivers and
lakes. Acid rain has a pronounced tendency to mobilize nickel from
the soil. Terrestrial plants take up nickel from soil, primarily via
the roots. The amount of nickel uptake from soil depends on various
geochemical and physical parameters including the type of soil, soil
pH, humidity, the organic matter content of the soil, and the
concentration of extractable nickel. The best known example of nickel
accumulation is the increased nickel levels, in excess of 1 mg/kg dry
weight, found in a number of plant species ("hyperaccumulators")
growing on relatively infertile serpentine soils. Nickel levels
exceeding 50 mg/kg dry weight are toxic for most plants. Accumulation
and toxic effects have been observed in vegetables grown on sewage
sludge-treated soils and in vegetation near nickel-emitting sources.
High concentration factors have been observed in aquatic plants.
Laboratory studies showed that nickel had little capacity for
accumulation in all the fish studied. In uncontaminated waters, the
concentrations reported in whole fish, on a wet-weight basis, ranged
from 0.02 to 2 mg/kg. These values could be up to 10 times higher in
fish from contaminated waters. However, there is no evidence for the
biomagnification of nickel in the food chain.
In wildlife, nickel is found in many organs and tissues, due to
dietary uptake by herbivorous animals and their carnivorous predators.
2.3 Human Exposure
Typical atmospheric nickel levels for human exposure range from about
5 to 35 ng/m3 at rural and urban sites, leading to a nickel uptake
via inhalation of 0.1-0.7 µg/day. Drinking-water generally contains
less than 10 µg nickel/litre, but, occasionally, nickel may be
released from the plumbing fittings resulting in concentrations of up
to 500 µg nickel/litre.
Nickel concentrations in food are usually below 0.5 mg/kg fresh
weight. Cocoa, soybeans, some dried legumes, various nuts, and
oatmeal contain high concentrations of nickel. Daily intake of nickel
from food varies widely, according to different dietary habits, and
can range from 100 to 800 µg/day; the mean dietary nickel intake in
most countries is 100-300 µg/day. Release of nickel from kitchen
utensils may contribute significantly to oral intake. Pulmonary
intake of 2-23 µg nickel/day can result from smoking 40 cigarettes a
day.
Daily skin contact with nickel-plated objects or nickel-containing
alloys (e.g., jewellery, coins, clips) is an important factor in the
induction and maintenance of contact hypersensitivity.
Iatrogenic exposure to nickel results from implants and prostheses
made from nickel-containing alloys, from intravenous or dialysis
fluids, and from radiographic contrast media. An estimated average
intravenous nickel uptake from dialysis fluids is 100 µg per
treatment.
In the working environment, airborne nickel concentrations can vary
from a few µg/m3 to, occasionally, a few mg/m3, depending on the
process involved and the nickel content of the material being handled.
Globally, millions of workers are exposed to nickel-containing dusts
and fumes during welding, plating, grinding, mining, nickel refining,
and in steel plants, foundries, and other metal industries.
Dermal exposure to nickel may occur in a wide range of jobs, either by
direct exposure to dissolved nickel, e.g., in the refining,
electroplating, and electroforming industries, or by handling
nickel-containing tools. Wet cleaning work may involve exposure to
nickel, because of the nickel that becomes dissolved in the washing
water.
2.4 Metabolism
Nickel can be absorbed by humans and animals via inhalation,
ingestion, or percutaneously. Respiratory absorption with secondary
gastrointestinal absorption of nickel (insoluble and soluble) is the
major route of entry during occupational exposure. A significant
quantity of inhaled material is swallowed following mucociliary
clearance from the respiratory tract. Thus, poor personal hygiene and
work practices can contribute to gastrointestinal exposure.
Percutaneous absorption is negligible, quantitatively, but is
important in the pathogenesis of contact hypersensitivity. Absorption
is related to the solubility of the compound, following the general
relationships nickel carbonyl >soluble nickel compounds >insoluble
nickel compounds. Nickel carbonyl is the most rapidly and completely
absorbed nickel compound in both animals and man. Studies in which
nickel was administered via inhalation are limited. Studies on
hamsters and rats, exposed to insoluble nickel oxide, showed poor
absorption with retention of much of the material in the lung after
several weeks. In contrast, absorption of soluble nickel chloride or
amorphous nickel sulfide was rapid. Nickel is transported in the
blood principally bound to albumin.
Gastrointestinal absorption of nickel is variable and depends on the
composition of the diet. In a recent study on human volunteers,
absorption of nickel was 27% from water versus less than 1% from food.
All body secretions are potential routes of excretion including urine,
bile, sweat, tears, milk, and mucociliary fluid. Non-absorbed nickel
is eliminated in the faeces.
Transplacental transfer has been demonstrated in rodents.
Following parenteral administration of nickel salts, the highest
nickel accumulation occurs in the kidney, endocrine glands, lung, and
liver: high concentrations are also observed in the brain following
administration of nickel carbonyl. Data on nickel excretion suggest a
two-compartment model. Nickel concentrations in the serum and urine
of healthy non-occupationally exposed adults are 0.2 µg/litre (range:
<0.05-1.1µg/litre) and 2 µg/litre (range: 0.5-6.0 µg/litre)
equivalent to 2 µg/g creatinine (range: 0.4-6.0 µg/g creatinine),
respectively. Increased concentrations of nickel are noted in both of
these fluids following occupational exposure. The body burden of
nickel in a non-exposed, 70 kg adult is 0.5 mg.
2.5 Effects on Organisms in the Environment
In microorganisms, growth was generally inhibited at nickel
concentrations in the medium of 1-5 mg/litre in the case of
actinomycetes, yeast, and marine and non-marine eubacteria, and at
concentrations of 5-1000 mg/litre in the case of filamentous fungi.
In algae, no growth was observed at approximately 0.05-5 mg
nickel/litre. Abiotic factors, such as the pH, hardness, temperature,
and salinity of the medium, and the presence of organic and inorganic
particles, influence the toxicity of nickel.
Nickel toxicity in aquatic invertebrates varies considerably,
according to species and abiotic factors. A 96-h LC50 of 0.5 mg
nickel/litre was found for Daphnia spp. while, in molluscs, 96-h
LC50 values of around 0.2 mg/litre were found for two freshwater
snail species and of 1100 mg/litre for a bivalve.
In fish, the 96-h LC50 values generally fall within the range
4-20 mg nickel/litre, but they can be higher in some species.
Long-term studies on fish and fish development demonstrated some
effects on rainbow trout in soft water at levels as low as
0.05 mg nickel/litre. In terrestrial plants, nickel levels exceeding
50 mg/kg dry weight are usually toxic. Copper was found to act
toxicologically in a synergistic way, whereas calcium reduced the
toxicity of nickel. Data on the effects of nickel on terrestrial
animals are limited. Earthworms seem to be relatively insensitive to
nickel, when the medium is rich in microorganisms and organic matter,
thus making nickel less available to earthworms. Nickel has not been
considered as a wide-scale global contaminant; however, ecological
changes, such as decreases in the number and diversity of species,
have been observed near nickel-emitting sources. Microecosystem
studies have shown that the addition of nickel to soil disturbs the
nitrogen cycle.
2.6 Effects on Experimental Animals and In vitro Test Systems
Nickel is essential for the catalytic activity of some plant and
bacterial enzymes. Slow weight gain, anaemia, and decreased viability
of offspring have been described in some animal species, after dietary
deprivation of nickel.
The most acutely toxic nickel compound is nickel carbonyl, the lung
being the target organ; pulmonary oedema may occur within 4 h
following exposure. The acute toxicity of other nickel species is
low.
Though contact allergy to nickel is very common in humans,
experimental sensitization in animals is only successful under special
conditions. Long-term inhalation exposure to metallic nickel, nickel
oxide, or nickel subsulfide caused mucosal damage and an inflammatory
reaction in the respiratory tract in rats, mice, and guinea-pigs.
Epithelial hyperplasia was observed in rats after inhalation exposure
to nickel chloride or nickel oxide aerosols.
High-level, long-term exposure to nickel oxide led to gradually
progressive pneumoconiosis in rats. Inflammatory reaction, sometimes
accompanied by slight fibrosis, was observed in rabbits after
high-level exposure to nickel-graphite dust. Pulmonary fibrosis was
seen in rats exposed to nickel subsulfide.
Nickel salts induced a rapid transistory hyperglycaemia in rats,
rabbits, and chickens, after parenteral administration. These changes
may be associated with effects on alpha and beta cells in the islets
of Langerhans. Nickel also decreased the release of prolactin.
Nickel chloride, given orally or by inhalation, has been reported to
decrease iodine uptake by the thyroid.
Nickel salts, given intravenously, decreased blood flow in the
coronary arteries in the dog; high concentrations of nickel decreased
the contractility of the dog myocardium in vitro.
Nickel chloride affects the T-cell system and suppresses the activity
of natural killer cells. Parenteral administration of nickel chloride
and nickel subsulfide has been reported to cause intrauterine
mortality and decreased weight gain in rats and mice. Inhalation
exposure to nickel carbonyl caused fetal death and decreased weight
gain, and was teratogenic in rats and hamsters. No information on
maternal toxicity was given in these studies. Nickel carbonyl has
been reported to cause dominant lethal mutations in rats.
Several inorganic nickel compounds were tested for mutagenicity in
various test systems. Nickel compounds were generally inactive in
bacterial mutagenesis assays, except where fluctuation tests were
used. Mutations were observed in several cultured mammalian cell
types. Nickel compounds inhibited DNA synthesis in a wide variety of
organisms. In addition, nickel compounds induced chromosomal
aberrations and sister chromatid exchange (SCE) in both mammalian and
human cultured cells. Chromosomal aberrations, but not SCE (except in
one study on electrolysis workers), were observed in humans
occupationally exposed to either insoluble or soluble nickel
compounds. Nickel induced cell transformation in vitro.
Nickel subsulfide induced benign and malignant pulmonary tumours in
rats in an inhalation study. A few pulmonary tumours were seen in
rats in a series of inhalation studies with nickel carbonyl. There
was no significant increase in lung tumours in rats in an adequate
inhalation study with metallic nickel. Inhalation exposure to black
nickel oxide did not induce lung tumours in Syrian golden hamsters (a
species resistant to lung carcinogenesis). Adequate carcinogenicity
studies using inhalation exposure were not available for other nickel
compounds. However, nickel subsulfide, metallic nickel powder, and an
unspecified nickel oxide induced benign and malignant lung tumours in
rats after repeated intratracheal instillations.
Nickel carbonyl, nickelocene, and a large number of slightly soluble
or non-soluble nickel compounds, including nickel subsulfide,
carbonate, chromate, hydroxide, sulfides, selenides, arsenides,
telluride, antimonide, various unidentified oxide preparations, two
nickel-copper oxides, metallic nickel, and various nickel alloys,
induced local mesenchymal tumours in a variety of experimental animals
after intramuscular, subcutaneous, intraperitoneal, intrapleural,
intraocular, intraosseous, intrarenal, intra-articular,
intratesticular, or intra-adipose administration. No local
carcinogenic response was seen in single-dose studies with some nickel
alloys, colloidal nickel hydroxide, or with two specimens of nickel
oxide, especially prepared for carcinogenicity testing by calcining at
735°C or 1045°C.
Nickel sulfate and nickel acetate, but not nickel chloride, induced
tumours of the peritoneal cavity in rats after repeated
intraperitoneal administration.
Metallic nickel and a very large number of nickel compounds have been
tested for carcinogenicity by the parenteral route of administration;
with few exceptions, they caused local tumours.
Only nickel subsulfide has been shown convincingly to cause cancer
after inhalation exposure. However, the number of adequate inhalation
studies is very small.
In studies using repeated intratracheal instillation, nickel powder,
nickel oxide, and nickel subsulfide caused pulmonary tumours.
When three different soluble nickel salts, which had not induced local
tumours in earlier studies, were tested using repeated intraperitoneal
administration, two of the salts elicited a carcinogenic response.
The International Agency for Research on Cancer concluded, in 1989,
that there was:
a) sufficient evidence in experimental animals for the
carcinogenicity of metallic nickel, nickel monoxides, nickel
hydroxides, and crystalline nickel sulfides;
b) limited evidence in experimental animals for the
carcinogenicity of nickel alloys, nickelocene, nickel carbonyl,
nickel salts, nickel arsenides, nickel antimonide, nickel
selenides, and nickel telluride;
c) inadequate evidence in experimental animals for the
carcinogenicity of nickel trioxide, amorphous nickel sulfide, and
nickel titanate.
2.7 Effects on Human Beings
In terms of human health effects, nickel carbonyl is the most acutely
toxic nickel compound. The effects of acute nickel carbonyl poisoning
include frontal headache, vertigo, nausea, vomiting, insomnia, and
irritability, followed by pulmonary symptoms similar to those of a
viral pneumonia. Pathological pulmonary lesions include haemorrhage,
oedema, and cellular derangement. Liver, kidneys, adrenal glands,
spleen, and brain are also affected. Cases of nickel poisoning have
also been reported in patients dialysed with nickel-contaminated
dialysate and in electroplaters who accidentally ingested water
contaminated with nickel sulfate and nickel chloride.
Chronic effects, such as rhinitis, sinusitis, nasal septal
perforations, and asthma, have been reported in nickel refinery and
nickel plating workers. Some authors have reported pulmonary changes
with fibrosis in workers inhaling nickel dust. In addition, nasal
dysplasia has been reported in nickel refinery workers. Nickel
contact hypersensitivity has been documented extensively in both the
general population and in a number of occupations, including those in
which workers were exposed to soluble nickel compounds. In several
countries, it has been reported that 10% of the female population and
1% of the male population are sensitive to nickel; 40-50% of these
have vesicular hand eczema, which, in some cases, may be very severe
and lead to loss of working ability. Oral nickel intake may aggravate
vesicular hand eczema and possibly eczema arising on other parts of
the body where there has been no skin contact with nickel.
Prostheses or other surgical implants made from nickel-containing
alloys have been reported to cause nickel sensitization or to
aggravate existing dermatitis.
Nephrotoxic effects, such as renal oedema with hyperaemia and
parenchymatous degeneration, have been reported in cases of accidental
industrial exposure to nickel carbonyl. Transient nephrotoxic effects
have been recorded after accidental ingestion of nickel salts.
Very high lung and nasal cancer risks have occurred in nickel refinery
workers employed in the high-temperature roasting of sulfide ores,
involving substantial exposure to nickel subsulfide, nickel oxide, and
perhaps nickel sulfate. Similar risks have been reported in processes
involving exposure to soluble nickel (electrolysis, copper sulfate
extraction, hydrometallurgy), often combined with some nickel oxide
exposure, but with low nickel subsulfide exposure. The risk to miners
and other refinery workers has been much lower. Cancer rates have
generally been close to normal in workers in stainless steel welding
and in the nickel-using industries, except where exposure to chromium
has been involved, particularly electroplating. However, the risk of
lung cancer may have been slightly increased in nickel/cadmium battery
workers exposed to high levels of both nickel and cadmium. Excesses
of various cancers, other than lung and nasal cancers (e.g.,renal,
gastric, or prostatic cancers), have occasionally been reported in
nickel workers, but none has been found consistently.
There is evidence of a cancer risk in workers who had been exposed to
soluble nickel concentrations of the order of 1-2 mg/m3, both in
electrolysis and in the preparation of soluble salts. These workers
were also exposed to other nickel compounds, but often at lower levels
than in other high-risk processes. In the absence of historical
exposure measurements, it is impossible to draw unequivocal
conclusions, but the evidence that soluble nickel is carcinogenic is
certainly strong. Refinery dust sometimes contains a substantial
proportion of nickel sulfate, in addition to nickel subsulfide. This
raises the possibility that the very high cancer risk observed in
workers employed in the high-temperature oxidation of nickel
subsulfide may partly be due to soluble nickel.
In refinery areas where cancer risks were high, exposure to nickel
subsulfide almost always occurred together with exposure to the oxide
and perhaps the sulfate (see above). Therefore, it is difficult to
demonstrate that nickel subsulfide is carcinogenic on the basis of
epidemiological data alone, though this seems likely.
Nickel oxide was present in almost all circumstances in which cancer
risks were elevated, together with one or more other forms of nickel
(nickel subsulfide, soluble nickel, metallic nickel). As for nickel
subsulfide, it is difficult either to demonstrate or to disprove its
suspected carcinogenicity from epidemiological data alone.
No increased cancer risk has been demonstrated in workers exposed
exclusively to metallic nickel. The combined data on nickel alloy
workers and gaseous diffusion workers, who were exposed to average
concentrations of the order of 0.5 mg nickel/m3, show no excess
risk, though the total number of lung cancers in these cohorts is too
small to exclude a small increase in risk at this level.
The International Agency for Research on Cancer concluded, in 1989,
that nickel compounds are carcinogenic to humans (Group 1) and
metallic nickel is possibly carcinogenic to humans (Group 2B).
3. CONCLUSIONS AND RECOMMENDATIONS
3.1 Conclusions
(a) Exposure
Nickel is an ubiquitous element and has been detected in different
media in all parts of the biosphere.
Nickel is introduced into the environment from both natural and
man-made sources and is circulated throughout all environmental
compartments by means of chemical and physical processes, as well as
by the biological transport mechanisms of living organisms.
Acid rain may leach nickel as well as other metals from plants and
soil.
Atmospheric nickel is considered to exist mainly in the form of
particulate aerosols.
Nickel is introduced into the hydrosphere by removal from the
atmosphere, by surface run-off, by the discharge of industrial and
municipal wastes, and also following natural erosion of soils and
rocks.
A major source of nickel in the environment is the combustion of
fossil fuels, particularly coal.
Uncontrolled emissions and disposal of wastes may impact the
environment and have adverse effects.
The chemical and physical forms of nickel and its salts strongly
influence their bioavailability and toxicity.
Nickel from soil and water is absorbed and metabolized by plants and
microorganisms and these small quantities of nickel are widely present
in all foods and water.
Some foods, such as pulses and cocoa products, contain relatively high
amounts of nickel, but these quantities have not been correlated with
adverse health effects.
(b) Human health effects
Nickel is normally present in human tissues and, under conditions of
high exposure, these levels may increase significantly.
The general population is exposed to nickel via the diet and objects
containing nickel, especially jewellery and coins.
Occupational exposure to nickel is important.
Inhalation is an important route of exposure to nickel and its salts
with regard to health risks. The gastrointestinal route is of lesser
importance.
Nickel absorption from the gastrointestinal tract is poor, though, in
an empty stomach, nickel in drinking-water is absorbed to a greater
extent. This may be a risk for sensitized persons.
Smoking tobacco may contribute to nickel intake, but there is no
agreement on the chemical nature of nickel or on its health
significance in tobacco smoke.
Target organs are the respiratory system, especially the nasal
cavities and sinuses, and the immune system.
The percutaneous absorption of nickel is minor, but important in
sensitization.
Nickel and its salts are potent skin sensitizers and possible
respiratory sensitizers in man. Nickel dermatitis is a common result
of nickel exposure, especially in women.
Primary skin and eye irritation reactions to high concentrations of
soluble nickel salts have also been reported.
Acute nickel toxicity is a minor risk, except in the case of nickel
carbonyl.
There is no convincing evidence that nickel salts produce point
mutations in bacterial systems. However, some nickel salts are
clastogenic in vitro, producing chromosome aberrations
(transformation), and sister chromatid exchanges, in mammalian cells.
Evidence for a carcinogenic risk from oral nickel exposure is lacking,
but the possibility that nickel acts as a promoter has been raised.
There is evidence of a carcinogenic risk in association with the
inhalation of nickel metal dusts and some nickel compounds.
Only very high concentrations of nickel induce teratogenic or
genotoxic effects.
The effects of nickel on the immune system are not clear.
(c) Environmental effects
Nickel is accumulated by plants. Growth retardation has been reported
in some species exposed to high nickel concentrations.
There is no evidence that nickel undergoes biotransformation, though
it does undergo complexation.
Nickel has been shown to be essential for the nutrition of many
microorganisms, a variety of plants, and for some vertebrate animals.
3.2 Recommendations
The use of nickel in consumer products that may release nickel in
contact with skin should be regulated. The specification and testing
requirements should be standardized.
Priority should be given to improving industrial hygiene in
occupations where exposure to high levels of soluble nickel compounds
may occur.
4. HUMAN HEALTH HAZARDS, PREVENTION AND PROTECTION, EMERGENCY ACTION
4.1 Main Human Hazards, Prevention and Protection, First Aid
The human health hazards associated with exposure to nickel and nickel
compounds, preventive and protective measures, and first aid are
listed in the Summary of Chemical Safety Information in section 6.
4.1.1 Advice to physicians
In cases of suspected poisoning by inhalation, attention should be
paid to the lungs and upper respiratory tract for irritant effects.
Acute poisoning can be associated with heart failure. Admit to
hospital as soon as possible. Obtain detailed advice on diagnosis and
treatment from the nearest Poisons Information Centre.
Nickel carbonyl is the only nickel compound that causes acute
poisoning by inhalation. If breathing stops, apply artificial
respiration and administer oxygen. Measurement of urinary nickel will
assist in assessing the severity of poisoning. Inhaled steroids will
help to prevent lung damage and oedema. When poisoning is the result
of ingestion, gastric lavage can be performed, providing precautions
are taken to prevent accidental aspiration into the respiratory tract.
4.1.2 Health surveillance advice
Workers occupationally exposed to nickel and its compounds should
undergo periodic health checks, with emphasis on the condition of the
skin, lungs, and upper respiratory tract. Cases of dermatitis should
be patch tested (usually with 0.5% nickel sulfate) by a qualified
dermatologist; in case of positive results they should be given
alternative employment, where available. Since nickel exposure can
interfere with immune defence mechanisms, careful attention should be
given to persistent infective diseases.
The physician should be aware of the carcinogenic potential of nickel
and nickel compounds.
4.2 Explosion and Fire Hazards
4.2.1 Explosion hazards
The vapour of nickel carbonyl is heavier than air. It can react
violently with atmospheric oxygen, with risk of explosion at about
60°C.
4.2.2 Fire hazards
With the exception of nickel carbonyl, most nickel compounds of
commercial interest do not normally constitute a fire hazard. Liquid
nickel carbonyl is extremely flammable and autoignition is possible at
its boiling point (42.2°C). Nickel carbonyl vapour can ignite
spontaneously at room temperature.
4.2.3 Prevention
For nickel carbonyl, use closed systems, suitable ventilation,
non-sparking tools, explosion-protected electrical equipment and
lighting. Do not use nickel carbonyl near sources of ignition. Do
not use compressed air for filling, discharging, or handling nickel
carbonyl. In case of fire, keep containers with nickel carbonyl cool
by spraying with water. Fire fighters should use self-contained
breathing apparatus.
4.2.4 Fire extinguishing agents
Suitable agents include: carbon dioxide, powder, or water.
4.3 Storage
Nickel compounds should be stored in tightly closed and correctly
labelled containers. In the case of nickel carbonyl, these should be
kept in a cool, ventilated area away from heat and oxidizing agents,
such as nitric acid and chlorine.
4.4 Transport
In case of accident during the road transport of nickel carbonyl, stop
the engine. Remove all sources of ignition. Evacuate the danger
area. Keep bystanders at a distance, put warning signs on the road,
and keep upwind. Notify the police and fire brigade immediately. If
self-contained breathing apparatus is available, use it. In case of
spillage or fire, follow the advice given in sections 4.7 and 4.4,
respectively. In case of poisoning, follow the advice in the Summary
of Chemical Safety Information (section 6).
4.5 Spillage and Disposal
4.5.1 Spillage
In case of spillage of nickel carbonyl, remove all ignition sources
and evacuate the danger area. Wear full protective clothing and a
self-contained breathing apparatus. Collect and put leaking liquid in
sealable containers. Cover smaller quantities of spilled liquid with
water and slowly add nitric acid to convert nickel carbonyl into
nickel nitrate. In case of larger spillage, absorb the spilled liquid
in a absorbent and remove in a sealable container to a safe place. Do
not allow nickel carbonyl to runoff into sewers and ditches. To avoid
water contamination, do not allow spilled nickel compounds (especially
soluble nickel salts) to run into soil and ground water.
4.5.2 Disposal
Large quantities of nickel carbonyl should be collected and atomized
in a suitable combustion chamber equipped with an efficient effluent
gas-cleaning device. Other nickel compounds should also be treated as
hazardous wastes.
5. HAZARDS FOR THE ENVIRONMENT AND THEIR PREVENTION
Nickel circulates throughout all environmental compartments (air,
soil, and water), and can be accumulated by microorganisms and higher
aquatic and terrestrial organisms. Nickel is toxic for many
organisms, but problems arise only when it is present in high
concentrations as a result of man-made contamination.
Contamination of soil, water, and air can be minimized by proper
methods of storage, transport, handling, and waste disposal. In case
of spillage, apply methods recommended in section 4.7.1.
6. SUMMARY OF CHEMICAL SAFETY INFORMATION
This summary should be easily available to all health workers
concerned with, and users of, nickel and nickel compounds. It should
be displayed at, or near, entrances to areas where there is potential
exposure to nickel and nickel compounds, and on processing equipment
and containers. The summary should be translated into the
appropriate language(s). All persons potentially exposed to the
chemical should also have the instructions in the summary clearly
explained.
Space is available for insertion of the National Occupational
Exposure Limit, the address and telephone number of the National
Poison Control Centre, and for local trade names.
NICKEL CARBONYL
Ni(C0)4,: CAS Registry No. 13463-39-3
PHYSICAL PROPERTIES OTHER CHARACTERISTICS
Melting point (°C) -19.3 Nickel carbonyl is a colourless liquid that
Boiling point (°C) 43 autoignites at its boiling point (42.2°C);
Water solubility insoluble its vapour can ignite spontaneously
Specific density (g/cm3) (25°C) 1.318 at room temperature.
Relative vapour density (25°C) 1.2983
Vapour pressure (kPa) (20°C) 4.28
Flash-point (°C) -20
HAZARDS/SYMPTOMS PREVENTION AND PROTECTION FIRST AID
SKIN: nickel carbonyl may enter Wear effective, impervious Wash skin immediately with plenty of water;
body through skin clothing, gloves and remove contaminated clothing
boots; change clothing
daily, maintain high standard
of personal hygiene
EYES: nickel carbonyl may enter Wear safety goggles or Rinse eyes with plenty of water for at least
body through mucous membranes face-shield 15 minutes; obtain medical advice
INHALATION: fatigue, nausea, Use closed systems with Fresh air, rest; keep victim warm, conscious
vomiting, headache, dyspnoea; after automatic devices and victim may inhale steroid spray; if breathing
a latency period of 12-36 h: alarm systems; apply has stopped, apply artificial respiration; obtain
chest pain, difficulty in breathing, exhaust ventilation; medical attention and hospital admission
coughing, elevated temperature, wear self-contained urgently
lung oedema, cyanosis, death in breathing apparatus for
severe cases non-routine operations
INGESTION: effects on Do not drink, eat, or Give plenty of water to drink; administer
gastro-intestinal and respiratory smoke when working activated charcoal if available; obtain medical
system; in severe cases: death with nickel carbonyl attention and hospital admission
REPEATED EXPOSURE
INHALATION: excitement, Avoid exposure
sleeplessness, headache, dizziness,
weakness, poor memory, tightness
in chest, polyidrosis, loss of hair,
sexual frigidity, increased risk of
nasal and lung cancer
SPILLAGE STORAGE FIRE AND EXPLOSION
Remove ignition sources; Store in tightly closed Nickel carbonyl is extremely flammable; no open
evacuate area; collect containers; store fires, no sparks; extinguish with carbon-dioxide,
leaking liquid in sealable containers with nickel powder, fluorocarbons, or water; nickel carbonyl
containers carbonyl in a cool, vapour can react violently with air
ventilated area away
from oxidizers
WASTE DISPOSAL
Atomization in a combustion
chamber with appropriate
effluent gas-cleaning device
NICKEL, NICKEL ALLOYS AND NICKEL COMPOUNDS
Ni: CAS Registry No. 7440-02-0
PHYSICAL PROPERTIES OTHER CHARACTERISTICS
Melting point (°C) 1555 Nickel is a naturally occurring, lustrous,
Boiling point (°C) 2837 light-coloured metal, very resistant to
Water solubility insoluble corrosion by air, water, and non-oxidizing
Specific density (g/cm3) (25°C) 8.90 acids; most nickel compounds do not constitute
Relative vapour density (25°C) - a fire or explosion hazard
Vapour pressure (kPa) (20°C) -
Flash-point (°C) -
HAZARDS/SYMPTOMS PREVENTION AND PROTECTION FIRST AID
(Nickel is a possible human carcinogen: nickel compounds are carcinogenic)
SKIN: irritation, dermatitis Wear effective, impervious Wash skin immediately with plenty of water;
(eczema) clothing, gloves and remove contaminated clothing; obtain medical
boots; change clothing advice
daily; maintain high
standard of personal hygiene
EYES: irritation by dust and Wear safety goggles or Rinse eyes with plenty of water for at least
aerosols face shield 15 minutes; obtain medical advice
INHALATION (powders, dusts, Use closed system with automatic Remove victim to fresh air; keep
aerosols): irritation of respiratory monitoring devices and alarm victim warm and quiet; obtain medical
tract; carcinogenicity systems; apply exhaust ventilation; advice
use self-contained breathing
apparatus for non-routine operations
INGESTION (solids, solutions): Do not drink, eat, or Keep victim warm and quiet; give
vomiting, diarrhoea, tremor, smoke when working plenty of water to drink; administer
respiratory problems, death; and in with nickel compounds activated charcoal, if available;
case of nickel salts solutions: obtain medical attention and hospital
nausea, headache, giddiness,
lassitude admission
REPEATED EXPOSURE
SKIN: Dermatitis (eczema) Wear clean impervious clothing,
gloves, and boots; change clothing
daily and maintain high standard
of personal hygiene
HAZARDS/SYMPTOMS PREVENTION AND PROTECTION FIRST AID
INHALATION: Chronic irritation Avoid exposure or keep exposure
of upper respiratory tract, loss of as low as possible
sense of smell, bronchial asthma,
pulmonary fibrosis, pneumoconiosis;
increased risk of nasal and lung
cancer
SPILLAGE STORAGE FIRE AND EXPLOSION
Remove larger spillages of Store in tightly closed Not flammable
dusts or solutions containing containers
nickel by special vacuum
cleaners or with water
WASTE DISPOSAL
Recycle, if possible; otherwise use
hazardous waste disposal site; highly
toxic nickel salts, e.g., arsenide,
antimonide, selenide, should be
encapsulated before disposal
7. CURRENT REGULATIONS, GUIDELINES, AND STANDARDS
The information given in this section has been extracted from the
International Register of Potentially Toxic Chemicals (IRPTC) legal
file and other United Nations sources. Its intention is to give the
reader a representative, but not an exhaustive, overview of current
regulations, guidelines, and standards. When no effective date
appears in the IRPTC legal file, the year of the reference from which
the data are taken is indicated by (r).
The reader should be aware that regulatory decisions about chemicals,
taken in a certain country, can only be fully understood in the
framework of the legislation of that country. Furthermore, the
regulations and guidelines of all countries are subject to change and
should always be verified with the appropriate regulatory authorities
before application.
7.1 Previous Evaluations by International Bodies
No information available.
7.2 Exposure Limit Values
Some exposure limit values are given in the table on pages 38-44.
7.3 Specific Restrictions
In the Federal Republic of Germany, the concentration of respirable
dusts and aerosols of nickel metal, nickel sulfide and sulfidic ores,
nickel oxide, nickel carbonate, and nickel carbonyl in air emissions,
may not exceed 1 mg nickel/m3 at a mass flow (= mass of emitted
compound related to time) of 5 g/h or more. In the European Economic
Community (EEC), nickel emissions in waste gas, resulting from the
combustion of waste oils, may not exceed 1.0 mg/m3 (plants with
thermal input of 3 MW or more). The USSR has set daily, average,
maximum allowable concentrations in ambient air of 0.0002 mg/m3 for
water-soluble nickel salts and 0.001 mg/m3 for metallic nickel.
The EEC, Sweden, and the USA regulate nickel waste. In the EEC,
member states must limit the introduction of nickel and its compounds
into ground and marine waters by controlling direct and indirect
discharges. Nickel in titanium dioxide waste discharged on to soil
can result in the migration of nickel to surface and ground waters.
The use of sludge as an agricultural fertilizer is prohibited, if the
concentration of nickel exceeds 400 mg/kg (dry matter) and the limit
for the amount of nickel that can be added annually to agricultural
land is 3 kg/ha per year (10-year average). Sweden requires reporting
of the composition of nickel wastes, and authorization for transport,
handling, and export. The United Kingdom treats waste consisting of
nickel and nickel compounds as "special waste", with specified
disposal procedures. In the USA, nickel and its compounds are
classified as toxic pollutants and permits are required for discharges
into water.
7.4 Labelling, Packaging, and Transport
The United Nations classifies dry nickel catalyst as:
Hazard Class 4.2 - Substance liable to spontaneous combustion;
Packing Group 1 - Very dangerous substance.
Czechoslovakia classifies nickel in nickel ore processing and nickel
production and refining as a carcinogenic substance; requirements are
listed for handling, labelling, packing, storing, and transport.
7.5 Waste Disposal
The International Registry of Potentially Toxic Chemicals advises
"Recycling; Precipitation, Solidification, Landfill. Sort, classify
and put in a box properly labelled. Salvage profitably for reuse by
local shop or sell as scrap metal. Nickel antimonide, nickel
arsenide, nickel selenide - encapsulation followed by disposal in a
chemical waste landfill. However, nickel from various industrial
wastes may also be recovered and recycled. Insoluble nickel compounds
may be landfilled. Soluble nickel compounds should be treated to
precipitate an insoluble nickel compound, solidified and landfilled".
EXPOSURE LIMIT VALUES
Medium Specification Country/ Exposure limit descriptiona Value Effective
organization date
AIR Occupational Australia Threshold limit value (TLV) 1985 (r)
- Time-weighted average (TWA)
Metallic nickel 1.0 mg/m3
- Time-weighted average (TWA)
Soluble nickel compounds 0.1 mg/m3 (as Ni)
- Short-term exposure limit (STEL)
Soluble nickel compounds 0.3 mg/m3 (as Ni)
Belgium Threshold limit value (TLV) 1989 (r)
- Time-weighted average (TWA) (metal) 1 mg/m3
- Time-weighted average (TWA) 0.1 mg/m3 (as Ni)
(soluble compounds)
Bulgaria Maximum permissible concentration (MPC) 0.5 mg/m3 1985 (r)
Canada Threshold limit value (TLV) 1980
- Time-weighted average (TWA) 1 mg/m3
- Time-weighted average (TWA) 0.1 mg/m3
(soluble compounds as Ni)
Czechoslovakia Maximum allowable concentration (MAC) 1985
- Time-weighted average (TWA) 0.05 mg/m3
- Ceiling value (CLV) (calculated as Ni) 0.25 mg/m3
(applies to nickel and its compounds)
Medium Specification Country/ Exposure limit description Value Effective
organization date
AIR Occupational Germany, Federal No maximum allowable concentration (MAK) carcinogenic 1989 (r)
Republic of value established (applies to dusts/aerosols working
from nickel metal, nickel sulfide and sulfidic material
ores, nickel oxide and nickel carbonate
arising in production and processing)
Technical reference concentration (TRK)
(nickel and compounds except nickel carbonyl)
- Time-weighted average (TWA) 0.5 mg/m3 (as Ni)
respirable dusts and
fumers, except dusts
from nickel alloys
(calculated as nickel in
total inhalable dust)
0.05 mg/m3 (as Ni)
respirable droplets
(calculated as Ni sensi-
tization in entire
respirable portion)
Japan Maximum allowable concentration (MAC) 1988 (r)
- Time-weighted average (TWA) 1 mg/m3
working material) (carcinogenic)
Netherlands Maximum limit (MXL) 1987 (r)
- Time-weighted average (TWA), metal 1 mg/m3
- Time-weighted average (TWA), 0.1 mg/m3 (as Ni)
(water soluble nickel compounds)
Romania Maximum permissible concentration (MPC) Nickel salts as 1985 (r)
hydroaerosols
- Time-weighted average (TWA) (as Ni) 0.5 mg/m3
- Ceiling value (CLV) (as Ni) 1.5 mg/m3
Medium Specification Country/ Exposure limit description Value Effective
organization date
AIR Occupational Sweden Threshold limit value (TLV)
- Time-weighted average (TWA), 1 day 1988
metallic nickel 0.5 mg/m3
- Time-weighted average (TWA), 1 day
(soluble nickel compounds, 0.1 mg/m3 (as Ni)
nickel oxide and nickel carbonate) carcinogenic
sensitization
Switzerland Maximum work-site concentration (MAK) 1985 (r)
- Time-weighted average (TWA) 0.5 mg/m3 (as Ni)
metal dust, sulfide, oxide and carbonate
Switzerland - Time-weighted average (TWA) 0.05 mg/m3 (as Ni)
dust of water soluble nickel sensitizer
compounds carcinogenic
United Kingdom Recommended limit (RECL) 1987 (r)
- Time-weighted average (TWA)
elemental nickel 1 mg/m3
- Time-weighted average (TWA)
soluble nickel compounds 0.1 mg/m3 (as Ni)
insoluble nickel compounds 1.0 mg/m3 (as Ni)
- Short-term exposure limit (STEL),
(10-min time-weighted average)
soluble nickel compounds 3 mg/m3 (as Ni)
insoluble nickel compounds 0.3 mg/m3 (as Ni)
USA (ACGIH) Threshold limit value (TLV) 1987
- Time-weighted average (TWA), metal 1 mg/m3 (as Ni)
- Time-weighted average (TWA), 0.1 mg/m3
soluble compounds (as Ni)
Medium Specification Country/ Exposure limit description Value Effective
organization date
AIR Occupational USA (OSHA) Permissible exposure limit (PEL) 1987 (r)
- Time-weighted average (TWA), metal 1 mg/m3
and soluble compounds (as Ni)
USSR Maximum allowable concentration (MAC) 1989
- Ceiling value (CLV), metal, oxides, 0.05 mg/m3
sulfide and mixtures of these compounds (as Ni)
- Ceiling value (CLV), nickel salts, 0.005 mg/m3
aerosols (as Ni)
AIR Ambient USSR Maximum allowable concentration (MAC) 1984
Metallic nickel (daily average) 0.001 mg/m3 (as Ni)
Water soluble nickel salts, 0.0002 mg/m3
(daily average) (as Ni)
WATER Surface Czechoslovakia Maximum allowable concentration (MAC) 1975
Nickel and its compounds 0.1 mg/litre
USSR Maximum allowable concentration (MAC) 1983
Nickel and its inorganic compounds 0.1 mg/litre (as Ni)
- Surface water for fishing 0.01 mg/litre 1982 (r)
Nickel and its compounds (as Ni)
WATER Drinking European Maximum allowable concentration (MAC) 0.05 mg/litre 1982
Economic
Community
United Kingdom Maximum residue limit (MRL) 0.05 mg/litre 1985
Water Drinking USA (EPA) 10-day health advisory (HA) - child 1.0 mg/litre 1985
10-day health advisory (HA) - adult 3.5 mg/litre
Acceptable daily intake (ADI) 0.35 mg/litre
Medium Specification Country/ Exposure limit description Value Effective
organization date
SOIL Agricultural European Maximum limit (MXL) 30-75 mg/kg 1989 (r)
Economic dry matter in soil sample with pH=6
Community
SOIL General USSR Maximum allowable concentration (MAC) 4 mg/kg 1985
mobile forms of nickel extractable by
ammonium acetate buffer solution pH=4.6
SEWAGE Agriculture European Maximum limit (MXL) 300-400 mg/kg 1989
SLUDGE Economic dry matter
Community Annual limit value 3 kg/ha/yr
(10 year average)
FOOD CMEA Maximum permissible concentration (MPC) 1983
Nickel and its compounds (as Ni)
- Milk products 0.1 mg/kg
- Meat products 0.5 mg/kg
- Fish products (as Ni) 0.5 mg/kg
- Cereals 3.0 mg/kg
- Vegetables, fruits 0.5 mg/kg
- Other products 0.2-8.0 mg/kg
- Beverages 0.3 mg/kg
Czechoslovakia Maximum permissible concentration (MPC) 1986
Nickel and its compounds
(due to production, packing, transport and
storage of food products)
- Specified food products 0.1-8.0 mg/kg
- Beverages, general 0.3 mg/kg
Medium Specification Country/ Exposure limit description Value Effective
organization date
FOOD USSR Maximum permissible concentration (MPC) 1981
Nickel and its compounds (as Ni)
- Fish products 0.5 mg/kg
- Meat products 0.5 mg/kg
- Milk products (as Ni) 0.1 mg/kg
- Cereals 0.5 mg/kg
- Vegetables, fruits 0.5 mg/kg
- Beverages 0.3 mg/kg
a TWA = time-weighted average over one working day (usually 8 h).
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