Introduction
The element cobalt (Co) is a gray, magnetic, ductile metal with an atomic weight of 58.9 Da (Dalton) and an atomic number of 27. Cobalt is a naturally occurring element that is found in association with other elements like copper, nickel, manganese, arsenic, sulfur, and oxygen in the environment.
Cobalt is commonly utilized in industry to create hard metals and superalloys because of its ferromagnetic characteristics, high melting point (1495.05 C), and high boiling point (2927 C). For instance, the permanent magnetic characteristics of the alloy Alnico, which is a combination of iron, aluminum, nickel, and cobalt. The manufacturing of tungsten carbide, which is valued for its toughness, heat resistance, and strength, is a typical source of long-term cobalt exposure.
Due to its capacity to encourage erythropoiesis (a process of making red blood cells), cobalt chloride (CoCl2) has historically been employed in medicine as a therapy for anemia. However, the use of cobalt to treat anemia has become less popular due to its negative effects on thyroid dysfunction and the emergence of goiters. Cyanocobalamin (vitamin B12), which has a Co3+-ion, is a cobalt molecule with significant biological significance.
Foods of animal origin, including dairy, eggs, fish, chicken, and meat, naturally contain the necessary component of vitamin B12. Peripheral neuropathy (nerve damage) and pernicious anemia may result from vitamin B12 deficiency. In addition to being utilized as a cyanide poisoning antidote, the precursor Hydroxocobalamin may also be used to treat vasoplegic shock (distributive shock). Oral, respiratory, and cutaneous exposure to cobalt are all potential pathways.
What Is the Etiology of Cobalt Toxicity?
Pure organic, inorganic salt, and elemental forms of cobalt (Co) are all found in nature. Artist's pigment (cobalt blue), dyes, porcelain, cement, rubber, super alloys, drill production, cutting tools, catalysts, orthopedic implants, dental hardware, vitamin supplementation, electroplating, old-fashioned anemia treatments, and widia-steel production are some sources of common cobalt exposure.
It is stated how occupational exposure to pure elemental cobalt causes poisoning by way of the respiratory system. In general, inorganic cobalt salts like cobaltous chloride (CoCl2) and cobaltous sulfate (CoSO4) are thought to be more hazardous than organic cobalt. Because cyanocobalamin (Vitamin B12) has limited oral bioavailability, it is generally thought to have low toxicity, which leads to organic cobalt exposure.
It is unknown what the single hazardous dose of cobalt and its salts is. It was discovered that patients were taking an average of 6 to 8 mg (milligrams) of CoSO4 per day for weeks or months in the cohort of people with "beer drinker's cardiomyopathy." These patients later developed severe toxicity, which led to numerous fatalities. However, when given 40 mg (milligrams) of CoCl2 every day for three months to treat anemia in babies, there was no harm. This implies that there are additional elements involved in the growth of cobalt poisoning.
What Happens in Cobalt Toxicity?
Cobalt toxicity has an impact on various organ systems, just like other transition metals. Excessive cobalt exposure causes acute toxicity and affects the endocrine, cardiovascular (heart), metabolic, central, and peripheral neurological (nerve) systems, as well as the gastrointestinal and hematologic (circulatory) systems. Diseases of the pulmonary (lung) system, such as occupational asthma and hard metal illness, are brought on by prolonged inhalational exposures.
-
Divalent cobalt (Co2+ or cobaltous) and common intracellular cations like Ca2+ and Mg2+ are quite similar. The metal cobalt inhibits a number of enzymes involved in the production of proteins and RNA, including α-lipoic acid, α-ketoglutarate dehydrogenase, and dihydrolipoic acid. This is most likely the pathophysiology that underlies cardiomyopathy (heart muscle disease).
-
Tyrosine iodinase is inhibited by CoCl2, which results in hypothyroidism and reduced thyroid hormone (T3, T4).
-
There are several theories regarding how CoCl2 encourages erythropoiesis. Through the stimulation of hypoxia-inducible factor-1 alpha and presumably increased iron availability for erythropoiesis, cobaltous ions may bind to transferrin and hinder oxygen delivery to renal (kidney) cells. As a result, polycythemia (abnormal increase in red blood cells) and reticulocytosis (abnormal increase in immature red blood cells) develop.
-
Finally, cobalt can engage in redox cycling, producing an excess of free radicals that might harm tissue. This is the mechanism most likely to cause lung toxicity.
-
Cobalt dermatitis is probably a type IV hypersensitive reaction like nickel.
What Are the Clinical Manifestations of Cobalt Toxicity?
Clinical signs and symptoms of cobalt toxicity, an uncommon diagnosis, heavily resemble those of more widespread illnesses. Cobalt toxicity must be diagnosed based on clinical suspicion. Consuming cobalt salts or elemental cobalt may result in gastrointestinal (GI) distress, most likely as a result of GI tract inflammation.
A thorough history is necessary to assist in determining the possible source of cobalt exposure. This history should include information about employment, diet, and surgical procedures. Heart failure symptoms like tachycardia (increased heartbeat), dyspnea (shortness of breath), and indicators of fluid overload are common in people with cobalt-induced cardiomyopathy.
Hard metal lung disease (HMLD), for instance, will be significantly more likely to develop in jobs producing hard metals and polishing diamonds. These patients will complain of dyspnea, coughing, and wheezing when they first arrive.
In addition to neurologic dysfunction, such as peripheral neuropathy, ocular (eye) toxicity, and cognitive decline, arthroprosthetic-associated cobalt poisoning may also show signs of hypothyroidism and cardiomyopathy. These patients may experience general complaints of pain, swelling, and trouble walking before the start of acute toxicity, usually sometime after the initial surgery.
Patients may also exhibit dermatitis (skin inflammation), especially in an occupational situation where cobalt is a known sensitizer. Cobalt does not seem to induce kidney toxicity, teratogenicity (ability to cause defects in developing fetuses), or decreased fertility based on case reports and current research.
How Is Cobalt Toxicity Evaluated?
Early consultation with a medical toxicologist or the Poison Control Center will aid in directing workup and care. The use of cobalt testing in body fluids is restricted in the acute context since it is not widely available. Acute care should be guided by the use of supplementary tests, such as the complete blood count (CBC), reticulocyte count, erythropoietin levels, and thyroid stimulating hormone (TSH) levels, which may indicate toxicity-related signs or symptoms. Metabolic acidosis and increased lactate levels have been observed in patients with more severe diseases. Patients with cardiomyopathy may be recognized using troponin, echocardiograms, and electrocardiograms.
Although pulmonary toxicity can be identified in the context of different exposure routes, chest radiographs, and computed tomography scans will aid in identifying patients with lung disease, especially in the context of industrial exposures. Pulmonary function tests performed in an outpatient setting may reveal decreased vital capacity.
Imaging may be helpful in patients whose arthroprosthetic failure is a concern to identify those who are at high risk of developing toxicity. Studies using ultrasound and MRI are more accurate and sensitive for cobalt-containing implants. It is significant to highlight that imaging can detect local tissue responses and implant failure but cannot diagnose cobalt toxicity.
Most frequently, occupational monitoring involves measuring urine cobalt levels. The range of normal serum cobalt concentrations is 0.1 to 1.2 mcg/L. Cobalt in urine should be within the standard range of 0.1 to 2.2 mcg/L. In order to interpret urine levels correctly, it is crucial to know the dose and duration of exposure due to the typical difference in elimination kinetics. The best indicator of the burden carried by the entire body is regarded to be whole blood levels.
More recently, cobalt-induced cardiomyopathy in metal-on-metal hip prostheses has been identified using cardiac magnetic resonance imaging.
How Is Cobalt Toxicity Treated?
Supportive care is the cornerstone of treatment for cobalt poisoning. Patients who present suddenly need aggressive decontamination and care. On gastrointestinal (GI) decontamination in cobalt toxicity, there is no particular research. It is likely that standard cleaning techniques, like whole bowel irrigation, used in other metal toxicities will work for cobalt, especially if radioopaque bodies are detected on radiography. Ingestion of liquid cobalt may benefit from gastric lavage. If the ingested substance is solid, the likelihood of it being useful is lower. Vomiting and nausea should be treated with antiemetics.
The majority of the available data on chelation therapy in humans comes from case reports and animal studies. N-acetylcysteine (NAC) and calcium disodium ethylenediaminetetraacetic acid (CaNa2EDTA) are potentially acceptable options for chelation, according to current research. NAC is not typically used for chelation, although the thiol group on the molecule acts as a cobalt binding site.
Prior to removing the cobalt source, which includes removing the arthroplasty, chelation is expected to play a minor part in the course of treatment. End-organ toxicity, like severe acidosis or heart failure, is a sign that chelation is necessary.
The main approach to limiting occupational exposure is prevention. Improvements to ventilation systems, for example, have considerably reduced the toxicity linked to exposures. In addition to being removed from the exposure source, patients with cobalt-induced asthma or hard metal lung disease may benefit from corticosteroids.
Conclusion
Cobalt toxicity most frequently occurs in the context of a metal-on-metal arthroplasty or in the workplace. In order to reduce exposure to cobalt and tungsten carbide powders and debris, it is crucial to wear the proper personal protective equipment and abide by working regulations. Ultimately, lowering exposure will lower the likelihood of developing a disease. Talk to the doctor about concerns if one has a metal-on-metal hip replacement, especially if they start to have any new pain, swelling, or difficulty walking, as this could increase the possibility of experiencing implant toxicity.
