Cobalt (Co) metal is a ductile, grey, magnetic element with an atomic weight of 58.9 Da and an atomic number of 27. Cobalt is found in the environment as a constituent of minerals that occur naturally, along with copper, manganese, nickel, sulfur, arsenic & oxygen. Cobalt is commonly utilized in industry to manufacture hard metals and superalloys due to its ferromagnetic characteristics, the high point of melting (1495.05 C), & high point of boiling (2927 C). Alnico, for example, is a permanent magnetic alloy composed of iron, nickel, aluminum, & cobalt.
The manufacturing of tungsten carbide used because of its heat resistance; hardness, & strength is a common cause of chronic cobalt exposure. Because of its potential to induce erythropoiesis, cobalt chloride (CoCl2) has traditionally been used in medicine to treat anemia. However, because of the risk of thyroid problems and the formation of goiters, the usage of cobalt in the treatment of anemia has declined. Cyanocobalamin (vitamin B12), which includes a Co3+-ion, is a biochemically significant cobalt molecule.
Vitamin B12 is an important element found in animal products such as eggs, dairy, fish, meat, and chicken. Vitamin B12 deficiency can cause pernicious anemia as well as peripheral neuropathy. The progenitor hydroxocobalamin is an antidote for acute poisoning and can be useful in the treatment of vasoplegic syndrome. Cobalt contact may take place through the respiratory, oral, & cutaneous routes.
Epidemiology
Traditionally, cobalt exposure happened through the use of cobalt chloride to cure anemia and by the consumption of beer containing cobalt sulphate as a foam stabilizer. Cobalt is currently found in chemical sets, mining, dyes, & orthopedic devices. The manufacture of the thick metal tungsten carbide is the major potential driver of cobalt poisoning. Between the 1950s & 1970s, several outbreaks of “cobalt-induced goiter & cardiomyopathy” were found.
The first occurrences of cardiomyopathy were discovered in Nebraska in 1966, including 64 patients & 30 casualties. A further 48 instances with a fatality rate of 46 percent were discovered in Quebec, while another twenty instances with a fatality rate of 43 percent were discovered in Minneapolis between 1964 and 1967. All of the cases were linked to beer that had cobalt sulphate added as a froth stabilizer, according to the researchers.
In these situations, the affected populations were mostly men who drank alcohol on a daily basis, typically up to 24 pints each day, and then were malnourished. The most prevalent source of cobalt in the overall population is likely to be dietary supplements. Improper disposal techniques by cobalt and tungsten carbide industries can result in ecological contamination & exposure of persons in the surrounding regions.
Tungsten carbide is made by sintering granulated cobalt & tungsten in the hydrogen environment at high temperatures (1550 C). According to studies, the concentrations of cobalt & tungsten in the atmosphere inside industries might be five times higher than in the surrounding environment. Some potential occupational hazards include hard-metal blade maintenance & diamond polish.
Inhaling aerosolized dissociated & ionized cobalt from polishing and cutting causes HMD (hard metal sickness). Occupational asthma is also frequently connected with cobalt poisoning, either alone or in conjunction with tungsten carbide. The real prevalence of HMD is unknown. In one case report, 5 of 320 individuals who visited an occupational respiratory center over a three-year period were detected as having HMD.
Additional case studies show 11 of 290 workers exposed who developed interstitial infiltrates on chest radiographs & 22 incidences of cobalt-induced asthma during a 36-year period. Recently, there has been some worry that athletic people may be using cobalt salts for “blood doping” in order to improve athletic performance by stimulating erythropoiesis. Despite this, the potential side effects make it a less-than-ideal form of doping.
Anatomy
Pathophysiology
Cobalt toxicity, like that of other transition metals, affects various organ systems. Excessive cobalt poisoning has cardiovascular, metabolic, endocrine, peripheral, & central nervous system, hematologic, & gastrointestinal consequences in acute poisoning. Persistent inhalational exposure causes respiratory illnesses such as occupational asthma & hard metal sickness. Divalent cobalt (cobaltous or Co2+) resembles frequent intracellular metal ions like Ca2+ & Mg2+.
Cobalt suppresses several enzymes involved in protein & RNA synthesis, including alpha-lipoic acid, alpha-ketoglutarate dehydrogenase, & dihydrolipoic acid. This is the most plausible etiology causing cardiomyopathy. CoCl2 suppresses tyrosine iodine, producing low levels of thyroid hormone (T3 & T4) & hypothyroidism. There are several theories about how CoCl2 promotes erythropoiesis.
Cobalt ions may attach to transferrin, impairing oxygen delivery to kidney cells by inducing hypoxia-inducible factor-1 alpha & possibly increasing iron access for erythropoiesis. As a result, reticulocytosis & polycythemia develop. Finally, cobalt can engage in redox cycling, which might result in an excess of free radicals & tissue injury. This is the possible mechanism causing pulmonary poisoning. Cobalt dermatitis is likely a type IV hypersensitivity reaction comparable to nickel dermatitis.
Etiology
Cobalt (Co) is found in elemental form, inorganic salts, & organic compounds. Artist’s pigmentation (cobalt blue), porcelain, dyes, cement, super alloys, rubber, cutting tools, drill production, orthopedic implants, catalysts, dental hardware, electroplating, vitamin supplementation, outdated anemia treatments, & widia-steel manufacturing are all common sources of cobalt exposed. Elemental form cobalt poisoning in the workplace is regarded as harmful via airborne secretions.
Inorganic salts of cobalt, such as cobaltous chloride and cobaltous sulfate, are thought to be more hazardous than organic cobalt. Natural cobalt poisoning is typically caused by cyanocobalamin (Vitamin B12) consumption, which is actually considered a hazard because of its modest absorption and bioavailability.
It is unknown what the single hazardous dosage of cobalt & its salts is. It was discovered that sufferers with “beer drinker’s cardiomyopathy” were taking an average of between six and eight mg of CoSO4 every day for weeks & months. Some patients developed serious toxicity, resulting in multiple fatalities. Infants diagnosed with anemia got 40 mg of CoCl2 daily for 3 months and experienced no harm. This shows that there are other factors that contribute to the development of cobalt poisoning.
Genetics
Prognostic Factors
Acute cobalt poisoning can result in serious sickness. Cardiomyopathy is connected with a significant death rate in patients. There is minimal research on the use of chelation to treat non-arthroplastic cobalt overdose. According to case reports in individuals with arthroplastic cobalt poisoning, chelation is likely to aid rehabilitation from cardiomyopathy.
Early detection & subsequent arthroplasty repair are critical for the outcome of arthroprosthetic cobalt poisoning. Arthroplasty revision reduces cobalt levels in blood & serum and is linked to medical recovery.
The extent of recovery is most likely determined by the duration of exposure to increased levels. In certain circumstances, individuals receive chelation after removal and do not recover completely. Persistent symptoms vary from tinnitus & loss of hearing to cardiomyopathy necessitating the insertion of a left-ventricular assist device.
Clinical History
Clinical history
Taking a clinical history is an important part of the diagnostic process for cobalt toxicity. Here are some key elements that might be included in a clinical history for cobalt toxicity:
Occupational exposure: Cobalt is often used in industrial settings, so the doctor may ask about the patient’s occupation and any potential exposure to cobalt in the workplace.
Medical history: The doctor may ask about the patient’s medical history, including any previous diagnoses or treatments for conditions that could be related to cobalt toxicity.
Symptoms: The doctor will ask about any symptoms the patient is experiencing, such as respiratory problems, skin irritation, heart palpitations, or neurological symptoms.
Medications: Cobalt toxicity can be caused by certain medications or medical devices that contain cobalt, so the doctor will ask about any current or previous use of such items.
Dietary habits: Cobalt is found in certain foods, such as seafood and organ meats, so the doctor may ask about the patient’s dietary habits to assess any potential sources of exposure.
Family history: The doctor may ask about any family history of cobalt toxicity or related conditions.
Environmental exposure: Cobalt can be found in the environment, such as in soil or water, so the doctor may ask about any potential environmental exposure.
Overall, a clinical history for cobalt toxicity will involve a thorough assessment of the patient’s potential sources of exposure and symptoms. Depending on the severity of the condition, additional tests or imaging studies may be necessary to confirm the diagnosis and determine the best course of treatment.
Physical Examination
Physical examination
Cobalt toxicity can cause a variety of symptoms and health problems, and a physical examination can help diagnose the condition. Here are some key elements that might be involved in a physical examination for cobalt toxicity:
General observation: The doctor will observe the patient for any visible signs of illness or distress, such as pallor, sweating, or difficulty breathing.
Skin examination: Cobalt toxicity can cause a rash or hives, so the doctor may examine the skin for any signs of irritation or inflammation.
Neurological examination: Cobalt toxicity can affect the nervous system, so the doctor may perform a neurological examination to assess the patient’s reflexes, coordination, and mental status.
Cardiac examination: Cobalt toxicity can cause heart problems, so the doctor may listen to the patient’s heart for any abnormal sounds or rhythms.
Respiratory examination: Cobalt toxicity can cause respiratory problems, so the doctor may listen to the patient’s lungs for any wheezing or crackling sounds.
Abdominal examination: Cobalt toxicity can affect the liver and kidneys, so the doctor may palpate the abdomen to check for any signs of enlargement or tenderness.
Blood tests: The doctor may order blood tests to check for elevated levels of cobalt or other metals in the blood.
Overall, a physical examination for cobalt toxicity will involve a thorough assessment of the patient’s overall health and specific symptoms. Depending on the severity of the condition, additional tests or imaging studies may be necessary to confirm the diagnosis and determine the best course of treatment.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential diagnosis
Acute cobalt poisoning is uncommon and is most often caused by ingestion. As with other heavy metals, the initial symptoms are typically Gastrointestinal distress, with a large differential. Detection of cobalt toxicity may be easier without an adequate history. Furthermore, other metal poisonings might cause identical symptoms, emphasizing the significance of a thorough history.
When a patient presents for examination of respiratory problems in a suitable work situation, including tungsten carbide manufacture, pneumoconiosis should be prominent on the differential. Cobalt and hard metal sickness should be mentioned in the list of possible causes. The occupational background will aid in quickly narrowing down the possible causes.
Consumption of cobalt salts should be evaluated in patients with polycythemia and goiter. Cardiomyopathy has a wide differential diagnosis; however, a background of hip arthroplasty would raise the possibility of cobalt poisoning. To aid in the diagnosis, further inquiry into the sort of implant the individual has should be conducted.
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Supportive care is the cornerstone of cobalt poisoning treatment. Acute patients will require extensive decontamination & treatment. There have been no particular investigations on GI decontamination in cobalt poisoning. Typical cleaning procedures employed in other metal overdoses, such as whole intestine irrigation, are likely to be appropriate for cobalt, especially if radioopaque materials are detected on radiography.
If the cobalt consumed is a liquid, gastric evacuation may be advantageous. If the ingested item is solid, it is less likely to be useful. Vomiting and nausea should be treated with antiemetics. The majority of the information regarding chelation therapy in humans comes from animal research & case reports. According to existing evidence, calcium disodium ethylenediaminetetraacetic acid (CaNa2EDTA) & N-acetylcysteine (NAC) are probable viable chelation options.
While NAC is not a common chelation agent, the thiol atom on the molecule functions as a cobalt binding site. Chelation is unlikely to have an impact on therapy until the cobalt supply is eliminated, which includes the removal of the arthroplasty. End-organ poisonings, such as severe acidosis and heart failure, are an indication of chelation.
The basic technique for avoiding workers’ exposure is prevention. Improved ventilation systems, for example, have greatly reduced the toxicity associated with encounters. Corticosteroids, in conjunction with removal from the source of exposure, may help patients with hard metal pulmonary disease and cobalt-induced respiratory disease.
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
Future Trends
Media Gallary
References
https://www.ncbi.nlm.nih.gov/books/NBK587403/
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Cobalt (Co) metal is a ductile, grey, magnetic element with an atomic weight of 58.9 Da and an atomic number of 27. Cobalt is found in the environment as a constituent of minerals that occur naturally, along with copper, manganese, nickel, sulfur, arsenic & oxygen. Cobalt is commonly utilized in industry to manufacture hard metals and superalloys due to its ferromagnetic characteristics, the high point of melting (1495.05 C), & high point of boiling (2927 C). Alnico, for example, is a permanent magnetic alloy composed of iron, nickel, aluminum, & cobalt.
The manufacturing of tungsten carbide used because of its heat resistance; hardness, & strength is a common cause of chronic cobalt exposure. Because of its potential to induce erythropoiesis, cobalt chloride (CoCl2) has traditionally been used in medicine to treat anemia. However, because of the risk of thyroid problems and the formation of goiters, the usage of cobalt in the treatment of anemia has declined. Cyanocobalamin (vitamin B12), which includes a Co3+-ion, is a biochemically significant cobalt molecule.
Vitamin B12 is an important element found in animal products such as eggs, dairy, fish, meat, and chicken. Vitamin B12 deficiency can cause pernicious anemia as well as peripheral neuropathy. The progenitor hydroxocobalamin is an antidote for acute poisoning and can be useful in the treatment of vasoplegic syndrome. Cobalt contact may take place through the respiratory, oral, & cutaneous routes.
Traditionally, cobalt exposure happened through the use of cobalt chloride to cure anemia and by the consumption of beer containing cobalt sulphate as a foam stabilizer. Cobalt is currently found in chemical sets, mining, dyes, & orthopedic devices. The manufacture of the thick metal tungsten carbide is the major potential driver of cobalt poisoning. Between the 1950s & 1970s, several outbreaks of “cobalt-induced goiter & cardiomyopathy” were found.
The first occurrences of cardiomyopathy were discovered in Nebraska in 1966, including 64 patients & 30 casualties. A further 48 instances with a fatality rate of 46 percent were discovered in Quebec, while another twenty instances with a fatality rate of 43 percent were discovered in Minneapolis between 1964 and 1967. All of the cases were linked to beer that had cobalt sulphate added as a froth stabilizer, according to the researchers.
In these situations, the affected populations were mostly men who drank alcohol on a daily basis, typically up to 24 pints each day, and then were malnourished. The most prevalent source of cobalt in the overall population is likely to be dietary supplements. Improper disposal techniques by cobalt and tungsten carbide industries can result in ecological contamination & exposure of persons in the surrounding regions.
Tungsten carbide is made by sintering granulated cobalt & tungsten in the hydrogen environment at high temperatures (1550 C). According to studies, the concentrations of cobalt & tungsten in the atmosphere inside industries might be five times higher than in the surrounding environment. Some potential occupational hazards include hard-metal blade maintenance & diamond polish.
Inhaling aerosolized dissociated & ionized cobalt from polishing and cutting causes HMD (hard metal sickness). Occupational asthma is also frequently connected with cobalt poisoning, either alone or in conjunction with tungsten carbide. The real prevalence of HMD is unknown. In one case report, 5 of 320 individuals who visited an occupational respiratory center over a three-year period were detected as having HMD.
Additional case studies show 11 of 290 workers exposed who developed interstitial infiltrates on chest radiographs & 22 incidences of cobalt-induced asthma during a 36-year period. Recently, there has been some worry that athletic people may be using cobalt salts for “blood doping” in order to improve athletic performance by stimulating erythropoiesis. Despite this, the potential side effects make it a less-than-ideal form of doping.
Cobalt toxicity, like that of other transition metals, affects various organ systems. Excessive cobalt poisoning has cardiovascular, metabolic, endocrine, peripheral, & central nervous system, hematologic, & gastrointestinal consequences in acute poisoning. Persistent inhalational exposure causes respiratory illnesses such as occupational asthma & hard metal sickness. Divalent cobalt (cobaltous or Co2+) resembles frequent intracellular metal ions like Ca2+ & Mg2+.
Cobalt suppresses several enzymes involved in protein & RNA synthesis, including alpha-lipoic acid, alpha-ketoglutarate dehydrogenase, & dihydrolipoic acid. This is the most plausible etiology causing cardiomyopathy. CoCl2 suppresses tyrosine iodine, producing low levels of thyroid hormone (T3 & T4) & hypothyroidism. There are several theories about how CoCl2 promotes erythropoiesis.
Cobalt ions may attach to transferrin, impairing oxygen delivery to kidney cells by inducing hypoxia-inducible factor-1 alpha & possibly increasing iron access for erythropoiesis. As a result, reticulocytosis & polycythemia develop. Finally, cobalt can engage in redox cycling, which might result in an excess of free radicals & tissue injury. This is the possible mechanism causing pulmonary poisoning. Cobalt dermatitis is likely a type IV hypersensitivity reaction comparable to nickel dermatitis.
Cobalt (Co) is found in elemental form, inorganic salts, & organic compounds. Artist’s pigmentation (cobalt blue), porcelain, dyes, cement, super alloys, rubber, cutting tools, drill production, orthopedic implants, catalysts, dental hardware, electroplating, vitamin supplementation, outdated anemia treatments, & widia-steel manufacturing are all common sources of cobalt exposed. Elemental form cobalt poisoning in the workplace is regarded as harmful via airborne secretions.
Inorganic salts of cobalt, such as cobaltous chloride and cobaltous sulfate, are thought to be more hazardous than organic cobalt. Natural cobalt poisoning is typically caused by cyanocobalamin (Vitamin B12) consumption, which is actually considered a hazard because of its modest absorption and bioavailability.
It is unknown what the single hazardous dosage of cobalt & its salts is. It was discovered that sufferers with “beer drinker’s cardiomyopathy” were taking an average of between six and eight mg of CoSO4 every day for weeks & months. Some patients developed serious toxicity, resulting in multiple fatalities. Infants diagnosed with anemia got 40 mg of CoCl2 daily for 3 months and experienced no harm. This shows that there are other factors that contribute to the development of cobalt poisoning.
Acute cobalt poisoning can result in serious sickness. Cardiomyopathy is connected with a significant death rate in patients. There is minimal research on the use of chelation to treat non-arthroplastic cobalt overdose. According to case reports in individuals with arthroplastic cobalt poisoning, chelation is likely to aid rehabilitation from cardiomyopathy.
Early detection & subsequent arthroplasty repair are critical for the outcome of arthroprosthetic cobalt poisoning. Arthroplasty revision reduces cobalt levels in blood & serum and is linked to medical recovery.
The extent of recovery is most likely determined by the duration of exposure to increased levels. In certain circumstances, individuals receive chelation after removal and do not recover completely. Persistent symptoms vary from tinnitus & loss of hearing to cardiomyopathy necessitating the insertion of a left-ventricular assist device.
Clinical history
Taking a clinical history is an important part of the diagnostic process for cobalt toxicity. Here are some key elements that might be included in a clinical history for cobalt toxicity:
Occupational exposure: Cobalt is often used in industrial settings, so the doctor may ask about the patient’s occupation and any potential exposure to cobalt in the workplace.
Medical history: The doctor may ask about the patient’s medical history, including any previous diagnoses or treatments for conditions that could be related to cobalt toxicity.
Symptoms: The doctor will ask about any symptoms the patient is experiencing, such as respiratory problems, skin irritation, heart palpitations, or neurological symptoms.
Medications: Cobalt toxicity can be caused by certain medications or medical devices that contain cobalt, so the doctor will ask about any current or previous use of such items.
Dietary habits: Cobalt is found in certain foods, such as seafood and organ meats, so the doctor may ask about the patient’s dietary habits to assess any potential sources of exposure.
Family history: The doctor may ask about any family history of cobalt toxicity or related conditions.
Environmental exposure: Cobalt can be found in the environment, such as in soil or water, so the doctor may ask about any potential environmental exposure.
Overall, a clinical history for cobalt toxicity will involve a thorough assessment of the patient’s potential sources of exposure and symptoms. Depending on the severity of the condition, additional tests or imaging studies may be necessary to confirm the diagnosis and determine the best course of treatment.
Physical examination
Cobalt toxicity can cause a variety of symptoms and health problems, and a physical examination can help diagnose the condition. Here are some key elements that might be involved in a physical examination for cobalt toxicity:
General observation: The doctor will observe the patient for any visible signs of illness or distress, such as pallor, sweating, or difficulty breathing.
Skin examination: Cobalt toxicity can cause a rash or hives, so the doctor may examine the skin for any signs of irritation or inflammation.
Neurological examination: Cobalt toxicity can affect the nervous system, so the doctor may perform a neurological examination to assess the patient’s reflexes, coordination, and mental status.
Cardiac examination: Cobalt toxicity can cause heart problems, so the doctor may listen to the patient’s heart for any abnormal sounds or rhythms.
Respiratory examination: Cobalt toxicity can cause respiratory problems, so the doctor may listen to the patient’s lungs for any wheezing or crackling sounds.
Abdominal examination: Cobalt toxicity can affect the liver and kidneys, so the doctor may palpate the abdomen to check for any signs of enlargement or tenderness.
Blood tests: The doctor may order blood tests to check for elevated levels of cobalt or other metals in the blood.
Overall, a physical examination for cobalt toxicity will involve a thorough assessment of the patient’s overall health and specific symptoms. Depending on the severity of the condition, additional tests or imaging studies may be necessary to confirm the diagnosis and determine the best course of treatment.
Differential diagnosis
Acute cobalt poisoning is uncommon and is most often caused by ingestion. As with other heavy metals, the initial symptoms are typically Gastrointestinal distress, with a large differential. Detection of cobalt toxicity may be easier without an adequate history. Furthermore, other metal poisonings might cause identical symptoms, emphasizing the significance of a thorough history.
When a patient presents for examination of respiratory problems in a suitable work situation, including tungsten carbide manufacture, pneumoconiosis should be prominent on the differential. Cobalt and hard metal sickness should be mentioned in the list of possible causes. The occupational background will aid in quickly narrowing down the possible causes.
Consumption of cobalt salts should be evaluated in patients with polycythemia and goiter. Cardiomyopathy has a wide differential diagnosis; however, a background of hip arthroplasty would raise the possibility of cobalt poisoning. To aid in the diagnosis, further inquiry into the sort of implant the individual has should be conducted.
Supportive care is the cornerstone of cobalt poisoning treatment. Acute patients will require extensive decontamination & treatment. There have been no particular investigations on GI decontamination in cobalt poisoning. Typical cleaning procedures employed in other metal overdoses, such as whole intestine irrigation, are likely to be appropriate for cobalt, especially if radioopaque materials are detected on radiography.
If the cobalt consumed is a liquid, gastric evacuation may be advantageous. If the ingested item is solid, it is less likely to be useful. Vomiting and nausea should be treated with antiemetics. The majority of the information regarding chelation therapy in humans comes from animal research & case reports. According to existing evidence, calcium disodium ethylenediaminetetraacetic acid (CaNa2EDTA) & N-acetylcysteine (NAC) are probable viable chelation options.
While NAC is not a common chelation agent, the thiol atom on the molecule functions as a cobalt binding site. Chelation is unlikely to have an impact on therapy until the cobalt supply is eliminated, which includes the removal of the arthroplasty. End-organ poisonings, such as severe acidosis and heart failure, are an indication of chelation.
The basic technique for avoiding workers’ exposure is prevention. Improved ventilation systems, for example, have greatly reduced the toxicity associated with encounters. Corticosteroids, in conjunction with removal from the source of exposure, may help patients with hard metal pulmonary disease and cobalt-induced respiratory disease.
https://www.ncbi.nlm.nih.gov/books/NBK587403/
medtigo
Cobalt Toxicity
Updated :
September 5, 2023
Cobalt (Co) metal is a ductile, grey, magnetic element with an atomic weight of 58.9 Da and an atomic number of 27. Cobalt is found in the environment as a constituent of minerals that occur naturally, along with copper, manganese, nickel, sulfur, arsenic & oxygen. Cobalt is commonly utilized in industry to manufacture hard metals and superalloys due to its ferromagnetic characteristics, the high point of melting (1495.05 C), & high point of boiling (2927 C). Alnico, for example, is a permanent magnetic alloy composed of iron, nickel, aluminum, & cobalt.
The manufacturing of tungsten carbide used because of its heat resistance; hardness, & strength is a common cause of chronic cobalt exposure. Because of its potential to induce erythropoiesis, cobalt chloride (CoCl2) has traditionally been used in medicine to treat anemia. However, because of the risk of thyroid problems and the formation of goiters, the usage of cobalt in the treatment of anemia has declined. Cyanocobalamin (vitamin B12), which includes a Co3+-ion, is a biochemically significant cobalt molecule.
Vitamin B12 is an important element found in animal products such as eggs, dairy, fish, meat, and chicken. Vitamin B12 deficiency can cause pernicious anemia as well as peripheral neuropathy. The progenitor hydroxocobalamin is an antidote for acute poisoning and can be useful in the treatment of vasoplegic syndrome. Cobalt contact may take place through the respiratory, oral, & cutaneous routes.
Traditionally, cobalt exposure happened through the use of cobalt chloride to cure anemia and by the consumption of beer containing cobalt sulphate as a foam stabilizer. Cobalt is currently found in chemical sets, mining, dyes, & orthopedic devices. The manufacture of the thick metal tungsten carbide is the major potential driver of cobalt poisoning. Between the 1950s & 1970s, several outbreaks of “cobalt-induced goiter & cardiomyopathy” were found.
The first occurrences of cardiomyopathy were discovered in Nebraska in 1966, including 64 patients & 30 casualties. A further 48 instances with a fatality rate of 46 percent were discovered in Quebec, while another twenty instances with a fatality rate of 43 percent were discovered in Minneapolis between 1964 and 1967. All of the cases were linked to beer that had cobalt sulphate added as a froth stabilizer, according to the researchers.
In these situations, the affected populations were mostly men who drank alcohol on a daily basis, typically up to 24 pints each day, and then were malnourished. The most prevalent source of cobalt in the overall population is likely to be dietary supplements. Improper disposal techniques by cobalt and tungsten carbide industries can result in ecological contamination & exposure of persons in the surrounding regions.
Tungsten carbide is made by sintering granulated cobalt & tungsten in the hydrogen environment at high temperatures (1550 C). According to studies, the concentrations of cobalt & tungsten in the atmosphere inside industries might be five times higher than in the surrounding environment. Some potential occupational hazards include hard-metal blade maintenance & diamond polish.
Inhaling aerosolized dissociated & ionized cobalt from polishing and cutting causes HMD (hard metal sickness). Occupational asthma is also frequently connected with cobalt poisoning, either alone or in conjunction with tungsten carbide. The real prevalence of HMD is unknown. In one case report, 5 of 320 individuals who visited an occupational respiratory center over a three-year period were detected as having HMD.
Additional case studies show 11 of 290 workers exposed who developed interstitial infiltrates on chest radiographs & 22 incidences of cobalt-induced asthma during a 36-year period. Recently, there has been some worry that athletic people may be using cobalt salts for “blood doping” in order to improve athletic performance by stimulating erythropoiesis. Despite this, the potential side effects make it a less-than-ideal form of doping.
Cobalt toxicity, like that of other transition metals, affects various organ systems. Excessive cobalt poisoning has cardiovascular, metabolic, endocrine, peripheral, & central nervous system, hematologic, & gastrointestinal consequences in acute poisoning. Persistent inhalational exposure causes respiratory illnesses such as occupational asthma & hard metal sickness. Divalent cobalt (cobaltous or Co2+) resembles frequent intracellular metal ions like Ca2+ & Mg2+.
Cobalt suppresses several enzymes involved in protein & RNA synthesis, including alpha-lipoic acid, alpha-ketoglutarate dehydrogenase, & dihydrolipoic acid. This is the most plausible etiology causing cardiomyopathy. CoCl2 suppresses tyrosine iodine, producing low levels of thyroid hormone (T3 & T4) & hypothyroidism. There are several theories about how CoCl2 promotes erythropoiesis.
Cobalt ions may attach to transferrin, impairing oxygen delivery to kidney cells by inducing hypoxia-inducible factor-1 alpha & possibly increasing iron access for erythropoiesis. As a result, reticulocytosis & polycythemia develop. Finally, cobalt can engage in redox cycling, which might result in an excess of free radicals & tissue injury. This is the possible mechanism causing pulmonary poisoning. Cobalt dermatitis is likely a type IV hypersensitivity reaction comparable to nickel dermatitis.
Cobalt (Co) is found in elemental form, inorganic salts, & organic compounds. Artist’s pigmentation (cobalt blue), porcelain, dyes, cement, super alloys, rubber, cutting tools, drill production, orthopedic implants, catalysts, dental hardware, electroplating, vitamin supplementation, outdated anemia treatments, & widia-steel manufacturing are all common sources of cobalt exposed. Elemental form cobalt poisoning in the workplace is regarded as harmful via airborne secretions.
Inorganic salts of cobalt, such as cobaltous chloride and cobaltous sulfate, are thought to be more hazardous than organic cobalt. Natural cobalt poisoning is typically caused by cyanocobalamin (Vitamin B12) consumption, which is actually considered a hazard because of its modest absorption and bioavailability.
It is unknown what the single hazardous dosage of cobalt & its salts is. It was discovered that sufferers with “beer drinker’s cardiomyopathy” were taking an average of between six and eight mg of CoSO4 every day for weeks & months. Some patients developed serious toxicity, resulting in multiple fatalities. Infants diagnosed with anemia got 40 mg of CoCl2 daily for 3 months and experienced no harm. This shows that there are other factors that contribute to the development of cobalt poisoning.
Acute cobalt poisoning can result in serious sickness. Cardiomyopathy is connected with a significant death rate in patients. There is minimal research on the use of chelation to treat non-arthroplastic cobalt overdose. According to case reports in individuals with arthroplastic cobalt poisoning, chelation is likely to aid rehabilitation from cardiomyopathy.
Early detection & subsequent arthroplasty repair are critical for the outcome of arthroprosthetic cobalt poisoning. Arthroplasty revision reduces cobalt levels in blood & serum and is linked to medical recovery.
The extent of recovery is most likely determined by the duration of exposure to increased levels. In certain circumstances, individuals receive chelation after removal and do not recover completely. Persistent symptoms vary from tinnitus & loss of hearing to cardiomyopathy necessitating the insertion of a left-ventricular assist device.
Clinical history
Taking a clinical history is an important part of the diagnostic process for cobalt toxicity. Here are some key elements that might be included in a clinical history for cobalt toxicity:
Occupational exposure: Cobalt is often used in industrial settings, so the doctor may ask about the patient’s occupation and any potential exposure to cobalt in the workplace.
Medical history: The doctor may ask about the patient’s medical history, including any previous diagnoses or treatments for conditions that could be related to cobalt toxicity.
Symptoms: The doctor will ask about any symptoms the patient is experiencing, such as respiratory problems, skin irritation, heart palpitations, or neurological symptoms.
Medications: Cobalt toxicity can be caused by certain medications or medical devices that contain cobalt, so the doctor will ask about any current or previous use of such items.
Dietary habits: Cobalt is found in certain foods, such as seafood and organ meats, so the doctor may ask about the patient’s dietary habits to assess any potential sources of exposure.
Family history: The doctor may ask about any family history of cobalt toxicity or related conditions.
Environmental exposure: Cobalt can be found in the environment, such as in soil or water, so the doctor may ask about any potential environmental exposure.
Overall, a clinical history for cobalt toxicity will involve a thorough assessment of the patient’s potential sources of exposure and symptoms. Depending on the severity of the condition, additional tests or imaging studies may be necessary to confirm the diagnosis and determine the best course of treatment.
Physical examination
Cobalt toxicity can cause a variety of symptoms and health problems, and a physical examination can help diagnose the condition. Here are some key elements that might be involved in a physical examination for cobalt toxicity:
General observation: The doctor will observe the patient for any visible signs of illness or distress, such as pallor, sweating, or difficulty breathing.
Skin examination: Cobalt toxicity can cause a rash or hives, so the doctor may examine the skin for any signs of irritation or inflammation.
Neurological examination: Cobalt toxicity can affect the nervous system, so the doctor may perform a neurological examination to assess the patient’s reflexes, coordination, and mental status.
Cardiac examination: Cobalt toxicity can cause heart problems, so the doctor may listen to the patient’s heart for any abnormal sounds or rhythms.
Respiratory examination: Cobalt toxicity can cause respiratory problems, so the doctor may listen to the patient’s lungs for any wheezing or crackling sounds.
Abdominal examination: Cobalt toxicity can affect the liver and kidneys, so the doctor may palpate the abdomen to check for any signs of enlargement or tenderness.
Blood tests: The doctor may order blood tests to check for elevated levels of cobalt or other metals in the blood.
Overall, a physical examination for cobalt toxicity will involve a thorough assessment of the patient’s overall health and specific symptoms. Depending on the severity of the condition, additional tests or imaging studies may be necessary to confirm the diagnosis and determine the best course of treatment.
Differential diagnosis
Acute cobalt poisoning is uncommon and is most often caused by ingestion. As with other heavy metals, the initial symptoms are typically Gastrointestinal distress, with a large differential. Detection of cobalt toxicity may be easier without an adequate history. Furthermore, other metal poisonings might cause identical symptoms, emphasizing the significance of a thorough history.
When a patient presents for examination of respiratory problems in a suitable work situation, including tungsten carbide manufacture, pneumoconiosis should be prominent on the differential. Cobalt and hard metal sickness should be mentioned in the list of possible causes. The occupational background will aid in quickly narrowing down the possible causes.
Consumption of cobalt salts should be evaluated in patients with polycythemia and goiter. Cardiomyopathy has a wide differential diagnosis; however, a background of hip arthroplasty would raise the possibility of cobalt poisoning. To aid in the diagnosis, further inquiry into the sort of implant the individual has should be conducted.
Supportive care is the cornerstone of cobalt poisoning treatment. Acute patients will require extensive decontamination & treatment. There have been no particular investigations on GI decontamination in cobalt poisoning. Typical cleaning procedures employed in other metal overdoses, such as whole intestine irrigation, are likely to be appropriate for cobalt, especially if radioopaque materials are detected on radiography.
If the cobalt consumed is a liquid, gastric evacuation may be advantageous. If the ingested item is solid, it is less likely to be useful. Vomiting and nausea should be treated with antiemetics. The majority of the information regarding chelation therapy in humans comes from animal research & case reports. According to existing evidence, calcium disodium ethylenediaminetetraacetic acid (CaNa2EDTA) & N-acetylcysteine (NAC) are probable viable chelation options.
While NAC is not a common chelation agent, the thiol atom on the molecule functions as a cobalt binding site. Chelation is unlikely to have an impact on therapy until the cobalt supply is eliminated, which includes the removal of the arthroplasty. End-organ poisonings, such as severe acidosis and heart failure, are an indication of chelation.
The basic technique for avoiding workers’ exposure is prevention. Improved ventilation systems, for example, have greatly reduced the toxicity associated with encounters. Corticosteroids, in conjunction with removal from the source of exposure, may help patients with hard metal pulmonary disease and cobalt-induced respiratory disease.
https://www.ncbi.nlm.nih.gov/books/NBK587403/
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