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Cobalt Toxicology


Introduction :
 
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 derivatives.
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 materials;
-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.
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 unstable action on renal lysosomes causing the secretion of a factor stimulating the production of erythropoetin.
Pancreatic lesions have been observed in animals but, the pancreatic cells effects are reversible by hyperglycemia.
Cobalt may cause myocardial degeneration.
Cancers (lung cancer, rhabdomyofibrosarcoma) may be caused in animals, at least when cobalt (oxide dust, chloride) is administered parenterally or intratracheally.
In procaryotic cells in vitro, divalent cobalt compounds (CoII) do not cause any mutagenic action.
In vitro ,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 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, cobalt inhibits microsomal enzymes oxidizing foreign substances and lowers the concentration of P 450 cytochrome
 
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 mg.
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, respectively.
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 :
-skin;
-eyes;
-respiratory tract
 
If ingested or inhaled in large amounts :
-nausea;
-vomiting;
-diarrhoea;
-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 status.
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 animal.
 
2-Occupational Intoxication :
 
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 positive.
In the hard metal industry, cobalt asthma may occur at levels of exposure lower than 50µg/m3.
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 lesions.
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 situations.
-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.
 
Carcinogenesis :
 
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 man.
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 confirmation.
 
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 week.
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 µg/m3.
-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 metals.
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 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-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

Out Bound Links

In Bound Links

  • (Hazards) Cobalt Oxide and Carbonate

    The use of cobalt in ceramics and its hazards.

  • (Materials - General) Cobalt Carbonate - CoCO3

    Spherocobaltite, CoCO3, Cobalt(II) carbonate

  • (Materials - General) Cobalt Oxide - CoO

    Cobalt(II) oxide, Cobaltosic Oxide, CoO, cobaltous oxide




Edouard Bastarache M.D.
Occupational & Environmental Medicine
Author of "Substitutions for Raw Ceramic Materials"
Tracy, Québec, CANADA

edouardb@sorel-tracy.qc.ca
http://www.sorel-tracy.qc.ca/~edouardb/




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