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Cobalt Toxicology



Cobalt (Co)-atomic weight 58.9, density
8.9 g/cm3, and melting point 1495 0C, is water- insoluble, but
soluble in acids.

It is a bluish-white metal, shiny, very
hard, with magnetic properties.

The most important ores are the
arsenides, sulfides and oxides. Zaire is the world largest
producer with 58% of the production.

The commercially significant cobalt
compounds are the oxides, hydroxide, chloride, phosphate,
carbonate, acetate, oxalate, and other carboxylic acid

Compounds used by ceramicists are the
carbonate and the oxide.


Uses and Sources of
Exposure :


About 75% of its consumption is used in
production of steel and alloys.


It is used :

- in the production of very resistant
alloys. One employs the alloy aluminium-nickel-cobalt for the
manufacture of magnets;

-in the industry of hard metal or
fritted metals. The cobalt-carbide of tungsten mixture is
particularly resistant (hardness from 90% to 95% of that of
diamond). It is used to manufacture teeth of saws, drilling
machines, drills, bits for drills;

- in the ceramic and glass industry
cobalt salts are used for the preparation of glazes and colouring

-in cobalt plating of metals by
electrolysis, it covers them with a shiny finish more resistant
than nickel;

-in the body of certain tools as a union
material with their tungsten ends.


The grinding of surgical and dental
prostheses (alloy with nickel, chromium and molybdenum) can
involve exposure to cobalt as well as the polishing of diamonds
using discs made up of microdiamonds whose binding agent is

Cobalt is present in trace amounts in
some cements.


Experimental Toxicology


In the rat, the oral lethal dose 50
(LD50) of different inorganic cobalt compounds (cobalt fluoride,
oxide, phosphate, bromide, chloride, sulphate, nitrate, and
acetate) varies from 150 to 500 mg/kg body weight.

Animals given cobalt chloride perorally
or via injections show higher concentrations in the liver, with
somewhat lower concentrations in the kidney and spleen.


Cobalt salts inhalation causes
respiratory irritation possibly leading to pulmonary oedema
(chemical pneumonia) in animals. Inhalation studies in hamsters
did not show any increase in tumors from cobalt oxide.

Its polycythemic action resembles the
human essential variety. This action would result from its
in vivo COLOR="#004080"> unstable action on renal lysosomes causing the
secretion of a factor stimulating the production of

Pancreatic lesions have been observed in
animals but, the pancreatic cells effects are reversible by

Cobalt may cause myocardial

Cancers (lung cancer,
rhabdomyofibrosarcoma) may be caused in animals, at least when
cobalt (oxide dust, chloride) is administered parenterally or

In procaryotic cells COLOR="#004080">in vitro,
divalent cobalt compounds (CoII) do not cause any mutagenic

In vitro COLOR="#004080"> ,in mammalian cells, cobalt compounds induce DNA
strand breaks and an increase in sister-chromatid exchanges and
micronuclei. Cobalt sulfide (CoS), insoluble, induces breaks in
ovarian cells of the chinese hamster.

Cobalt chloride COLOR="#004080"> in vivo, does
not seem to be foetotoxic nor teratogenic in the rat; but at high
doses, it may cause testicular degeneration in rodents which is
partly reversible with the administration of zinc.

In vivo COLOR="#004080">, cobalt inhibits microsomal enzymes oxidizing
foreign substances and lowers the concentration of P 450


Clinical Toxicology



I-General Information :


For the general population, food and
beverages represent the main source of cobalt exposure. Traces of
cobalt are also present in various household products.

One atom of cobalt comprises the central
and necessary core in the vitamin B12, or cyanocobalamin, molecule
which is an essential vitamin.

Its deficiency may cause anemia.

Polycythemia has been reported in heavy
drinkers of cobalt fortified beer.

Cobalt per se is not essential for
humans or other mammals.


II-Routes of Absorption and Exposure


The usual routes of absorption are
ingestion and inhalation.

Absorption through the skin can occur
for certain compounds but is low.

The main source of absorption during
occupational exposure is via the respiratory tract.


III-Biochemokinetics :


Cobalt is not a cumulative toxin.

The normal daily intake by ingestion is
estimated at 20-40µg.

The total body burden is about 1.5

After absorption, cobalt is mainly
distributed to the liver.


Cobalt is mainly excreted in urine and
to a lesser extent via faeces.

Gastrointestinal absorption of
radioactive cobalt chloride in humans has been estimated to be
about 18%. Eight days after parenteral administration, 56% and 11%
of the given dose is eliminated via urine and feces,

Following initial rapid elimination, the
remaining 10% usually clears slowly with a biologic half-time of
about 2 years.

Relatively high concentrations are also
found in the myocardium (heart).

The major proportion of parenterally
administered cobalt is rapidly cleared from the body, mainly via
the urine.

Cobalt concentrations of 90µg/m3 in
air have been reported to give cobalt concentration of about
100µg/L urine after a work shift, decreasing to less than
half this concentration within 1 day.


The normal concentrations of cobalt in
blood and urine from non-occupationally exposed persons are about
0.1 to 2µg/L. The levels of cobalt in blood, and particularly
in urine, increase in proportion to the level of occupational
exposure and may be used for biologic monitoring in order to
assess individual exposure.

Elimination of cobalt is considerably
slower in uremic patients.



IV-Symptoms and Signs :


A-Acute Toxicity :


Possible irritation of :



-respiratory tract


If ingested or inhaled in large amounts




-epigastric pain.


B-Chronic Toxicity


1-Non-Occupational Intoxication


Endemic outbreaks of cardiomyopathy with
mortality rates up to 50% have been described among heavy
consumers (up to 10L/day) of cobalt-contaminated beer giving an
exposure of a few milligrams per day.

It has been suggested that the
cardiomyopathy had a multicausal origin, since cobalt exposure
from beer was considerably lower than the doses prescribed to
patients with anemia.

Other factors of importance are high
alcool intake combined with a generally poor nutritional

This practice of fortifying beer with
cobalt chloride in order to improve the stability of the foam has
now been abandoned.

The disease may be reproduced in the




The two main target organs are the
respiratory tract and the skin.


Respiratoty Symptoms


Concomitant exposure to tungsten carbide
increases the pulmonary absorption rate of metallic cobalt.


a-Transitory symptoms :


Shortness of breath, pharyngeal
irritation, sneezing and dry cough are only encountered during the
work shift and disappear with job change. Exposure at a
concentration near 40µg/m3 for a few hours would be
sufficient to cause these effects.

It has been demonstrated that an
exposure mainly above 50µg/m3 causes an increase in the
prevalence of exertional shortness of breath in a refinery where
workers were exposed to metallic cobalt, oxides and salts.


b-Spasmodic Rhinitis or Occupational
Asthma :


The clinical picture may be one of
spasmodic rhinitis or typical, true, classical occupational asthma
with a probable immunologic origin. Antibodies (IgE) against the
cobalt-albumin complex have been found in the serum of patients
suffering from cobalt asthma.

A cobalt chloride challenge test may be

In the hard metal industry, cobalt
asthma may occur at levels of exposure lower than

In one report, the syndrome did not
develop until after 6 to 18 months of exposure.

On screening 1039 tungsten carbide
workers work-related wheezing occurred in 10.9%

There is no evidence that this type of
disease progresses to interstitial fibrosis.


c-Allergic Alveolitis :


Symptoms may ressemble those of allergic
alveolitis (shortness of breath, chills, fever).

Cases have been described among workers
exposed to cobalt in cutting oils used to polish hard metals.
Symptoms disappear when workers are away from work for 1 month
but, come back when work resumes. The alveolitis may be associated
with a bronchoconstrictive reaction.


d-Desquamative Alveolitis


Desquamative alveolitis with
multinuclear giant cells (type II alveolar cells and macrophages)
evolving progressively towards diffuse interstitial fibrosis,
characterized clinically by shortness of breath and weight loss,
may develop.

On clinical grounds, functionnal and
radiologic, this syndrome in its acute phase resembles the
previous one and we may ask ourselves if a distinction between the
two syndromes is justified.

At the beginning of the disease,
symptomatogy may be very scarce (dry cough, exertional shortness
of breath) and the chest X-ray may seem normal. If exposure
persists, general health state may deteriorate and a rapidly fatal
alveolitis may occur.

This disease has been observed mainly in
hard metal and diamond industries.

Lung physiology testing shows a
restrictive pattern with a lowered CO diffusing capacity.

Chest X-ray shows reticulo-nodular

Giant multinuclear cells may be found
following bronchoalveolar lavage.

An allergic origin is suspected.

On screening 1039 tungsten carbide
workers, interstitial lung disease was observed in 0.7%.

Experiments in animals tend to
incriminate cobalt as the main cause of desquamative alveolitis
but, its pulmonary toxicity would be enhanced by the presence of
tungsten carbide and other substances

Analogous results have been encountered
in studies in workers exposed to a mixture of cobalt dust and
other substances such as carbides.

But, some authors believe that exposure
to cobalt dusts alone without a concomitant exposure to tungsten
carbide (diamond polishing) may cause fibrosing alveolitis with
giant mononuclear cell interstitial infiltrate or diffuse
interstitial fibrosis.


Cutaneous effects :


Cobalt may cause allergic dermatitis
with positive skin patch tests( urticaria and/or exzema). Cobalt
itself is a sensitizer as well as different salts and oxides.

This allergic dermatitis of an
erythematous papular type usually occurs in the skin areas
subjected to friction, such as the ankle, elbow flexures, and
sides of the neck.

Even if there is no cross allergy
between metals, sensitization to cobalt is often encountered in
patients already allergic to chromium and/or nickel.


Other effects :


-Cobalt cardiomyopathy has been
described in workers exposed to cobalt in different

-Polycythemia could be encountrered
among workers exposed to cobalt in the production of fritted
metallic carbides.

-One case of progressive deafness and
optic nerve atrophy has been attributed to a severe exposure to
powdered metallic cobalt for 20 months.

-Sub-clinical hypothyroidism has been
described among workers exposed exclusively to cobalt in a
refinery of this metal.

-Ocular effects have included congestion
of conjunctiva.




In man, it has been suggested that
cobalt was carcinogenic(lung cancer); it is most probable that it
is due to its association with other particles such as tungsten
carbide, or concomitant exposure to arsenic and nickel as
suggested among workers employed in cobalt recycling in nickel
extraction firms.

A significant increase in lung cancer
has been observed among workers of some hard metal industries, but
not in others.

It is agreed that human data are
insufficient to conclude that cobalt per se is carcinogenic in

Cobalt has been designated as being
possibly carcinogenic to humans, group 2B, by IARC.

Taking into account data from
epidemiologic studies, it is possible that exposure to dusts from
hard metals may increase the risk of lung cancer but this requires


Medical Surveillance


Cobalt in blood and urine mainly
reflects recent exposure.

Among workers exposed to cobalt-tungsten
carbide dust, a good correlation was found between the severity of
exposure to cobalt and its concentration in urine at the end of
the work week. Taking into account the biologic half-life of
urinary cobalt, its concentration at the end of the work week
reflects mostly the average exposure of previous days. Under these
circumstances, an average exposure of 0.1 mg/m3 would lead to a
urinary concentration of 60 µg/L at the end of the work

End of shift blood and urine cobalt also
eflects severity of exposure.


ACGIH proposed in 1996 :

-Urine :15 µg/ L as a biological
limit (end of work week) corresponding to an atmospheric TLV of 20

-Blood : a maximal permissible
concentration of 0.1 µg/100 ml (end of work week).


When occupational exposure has ceased
for a long period of time, these measurements are not reliable
anymore to assert previous exposure but, measurements in hair and
nails could.

Those who were subjected to hip
arthroplasty ( hip prosthesis) may have elevated levels of urinary
cobalt, chromium and nickel.


Periodical examination :


For workers exposed to cobalt and hard

It should comprise :

-Specific medical history taking

-Physical examination with special
attention to the skin and lungs;

-A chest X-ray every 2 years;

-Spirometry once a year and CO diffusion
capacity every 2-3 years;

-Urinary cobalt measurement.


Exposure Limits


In Quebec, the VEMP ( Valeur
d'Exposition Moyenne Pondérée) is set at 0.02 mg/m3
(as Co) for metallic cobalt and inorganic compounds.

It has a C3 designation, which means it
is a carcinogen in animals and the results of animal studies are
not necessarily applicable to man,


Summary :


Certain cobalt compounds skin absorb but
the absorption is low.

If skin contact occurs, protection
should be used to avoid skin sensitization.

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

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-Chemical Hazards of the Workplace,
Proctor & Hughes, last edition.

2-Occupational & Environmental
Medicine, Ladou J., last edition

3-Sax's Dangerous Properties of
Industrial Materials, Lewis C., last edition.

4-Occupational Medicine, Zenz Carl,
last edition.

5-Toxicologie Industrielle et
Intoxications Professionnelles, Lauwerys R.R.

last 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 Cobalt Oxide
Materials Cobalt Carbonate
Hazards Cobalt Oxide and Carbonate

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