Hey. Thanks for stopping by. I hope everyone is healthy and safe out there.
I’m in my 5th week of being back in school and in addition to learning about the myriad of substances out there in the world that can be toxic to you or the environment, I’m also learning how to manage my study time. What worked for me in the past definitely does not work in the online learning environment but I’ll adapt 🙂 That’s one of my learning discoveries this week…management of study time. I tend to be a procrastinator (old news) but the amount of reading for PHR 7588/Toxic Substances while reasonable for this class, is not something that should be done on a Monday (this was a lesson I only needed to teach myself one time).
But enough about me. Let’s get back to an essential, yet potentially toxic metal, cobalt.
Cobalt is an essential trace element that is required for normal functioning of the mammalian body and it is not produced by the body. Cobalamin (also called vitamin B12 or cyanocobalamin) is a cobalt-containing molecule that is required for the production of red blood cells. Cobalamin is synthesized by bacteria or archaea by microbial fermentation. Good dietary sources of vitamin B12 include milk, eggs and meat and individuals with gastrointestinal absorption issues, some vegetarians and some elderly people can become deficient in this element.
Image from: https://pernicious-anaemia-society.org/conference/the-cobalamin-b12-conference/
Cobalt is found in the environment and is typically sourced as a by-product of copper mining.
Where cobalt is mined: https://www.americanexperiment.org/2018/09/wall-street-journal-mining-cobalt-congo-still-dirty-dangerous/
According to Department of the Interior data from 2020, the following states have the largest cobalt reserves: “Alaska, California, Idaho, Maine, Michigan, Minnesota, Missouri, Montana, North Carolina, New Mexico, Oregon, Pennsylvania, Puerto Rico and Tennessee.” from https://catalog.data.gov/dataset/cobalt-deposits-in-the-united-states
Cobalt is found in the environment, so mammalian exposure could be from food, water or air at low levels. Higher exposure to cobalt (via dust inhalation or skin contact, occasionally ingestion) can occur in some industries where metal grinding or cobalt containing metal production occurs or sporadically in some individuals. Cobalt is also a component of medical implants (such as hip replacement surgery). Cobalt is also a component of some blue pigments. Radioactive cobalt (cobalt 60) has medical uses in cancer radiation therapy. https://semspub.epa.gov/work/HQ/174482.pdfÂ
Here are some ways that cobalt can enter the body:
From: https://apcz.umk.pl/czasopisma/index.php/EQ/article/view/EQ.2019.016/17600
Here’s a sample of the color cobalt from Pantone:
From: https://www.pantone.com/color-finder/19-4037-TCX
Individuals employed in the cobalt industry are at risk for developing a condition called “hard metal lung disease” (also known as “hard metal pneumoconiosis”) which is a rare condition that results in permanent lung damage. As a result of this disease association, the Occupational Safety and Health Administration has set limits to reduce the level of acceptable levels of cobalt in the air. Additional information at: https://www.osha.gov/dts/sltc/methods/inorganic/id213/id213.html
Here’s an interesting article from Brazil (2016) that is a case series for Hard Metal Lung Disease: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5344095/
Cobalt can result in skin irritation or allergy. Cobalt was declared the Contact Allergen of the Year by the American Contact Dermatitis Society in 2016.
Image from:Â https://dermnetnz.org/topics/allergy-to-cobalt/
The toxicokinetics of cobalt have been studied and the form of the cobalt-containing compound affects the absorption of cobalt. Differences in oral absorption of cobalt in rodents and humans have been reported. For instance, from C&D:
Less than 5% of an oral dose of cobalt oxide is absorbed, whereas about 30% of an oral dose of cobalt chloride is absorbed in rodents. Oral absorption of cobalt varies widely in humans, and it is estimated to be between 5% and 45%. Increasing doses of cobalt results in a decreasing proportional absorption, so increased cobalt levels tend not to cause significant accumulation. Absorption of inhaled cobalt compounds appears to be relatively effective in humans and animals.
Cobalt is considered by the International Agency for Research on Cancer (IARC) to be a Group 2A (probably carcinogenic to humans) or 2B (possibly carcinogenic to humans) depending on the form (cobalt metal with or without tungsten carbide and cobalt salts).
https://oem.bmj.com/content/58/10/619
Cobalt can have toxic effects on the mitochondrial enzyme system (it inhibits aerobic metabolism), it can interfere with protein synthesis (cobalt displaces magnesium from cofactor enzyme site) and it can have effect on cell membrane lipid movement (by binding to these molecules). More can be found here: https://www.sciencedirect.com/science/article/abs/pii/S0005273620300754
As well as here: https://pubmed.ncbi.nlm.nih.gov/22732165/
Target organ/organs for cobalt poisoning include the cardiovascular system, the endocrine system, the hematologic system, the pulmonary system, effects on the nervous system, the renal system, the dermatological system as well as the reproductive system. There is quite a bit online about cobalt poisoning related to metal-on-metal prosthetic hip implants and some of the side effects that can result from this condition (called arthroplasty cobaltism). This is a particularly interesting syndrome that results in symptoms of heart disease, hypothyroidism, polycythemia and effects on both the peripheral and nervous system.
Signs/symptoms of cobalt poisoning can include the following:
From: https://www.sciencedirect.com/science/article/pii/S2451993620300104
Cobalt cardiomyopathy in hip arthroplasty article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6728440/
Here’s an image from an echocardiogram showing the depressed systolic function of the left ventricle:
From: https://www.nejm.org/doi/10.1056/NEJMcps1213196
There may be a genetic differences in an individual’s ability to metabolize and detoxify metals, including cobalt.
From: https://www.sciencedirect.com/science/article/pii/S0753332218374407
The most interesting historical aspect I found regarding cobalt poisoning is a syndrome called “beer drinker’s cardiomyopathy”. This was a historical issue in the 1960’s in Nebraska and Quebec where cobalt was added to beer to restore and stabilize the foam that can be destroyed by agents used to clean glassware. This syndrome was characterized by some differences from a typical alcoholic cardiomyopathy (the acute cobalt cardiomyopathy that resulted from this syndrome tended to show an abrupt onset of biventricular heart failure, pericardial effusion as well as polycythemia).
One of the implicated brands:
From: https://www.macleans.ca/general/of-meat-beer-disease-and-death/
Quebec historical article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1923410/?page=2
Nebraska historical article: https://www.amjmed.com/article/0002-9343(72)90136-2/pdf
Cobalt effects on heart: https://www.ahajournals.org/doi/10.1161/CIRCHEARTFAILURE.116.003604
Cobalt could potentially be used as an athletic (in both humans, and race horses) performance enhancing substance, by increasing the production of red blood cells (the hypoxia that can be caused by cobalt results in a compensatory increase in red blood cell production).
From: https://www.cobaltinstitute.org/cobalt-and-red-blood-cells.html
Treatment of cobalt poisoning depends on the body system involved and the degree of exposure but if there is an acute cobalt intoxication, then decontamination of the patient should be performed as well as aggressive medical management. Gastric decontamination methods have not been studied but if radiopaque solid forms of cobalt are noted in the gastrointestinal tract, whole-bowel irrigation can be considered. After any remaining cobalt has been irrigated from the gastrointestinal tract, then chelation therapy can be considered. Chelators, such as CaNa2EDTA and NAC can be used to enhance urinary or fecal elimination of cobalt based on a single human case report and several animal studies. Sulfur-containing proteins (NAC, L-histidine and L-cysteine) are administered to reduce mortality by reducing the tissue cobalt burden and tissue injury in the liver and spleen. For arthroplasty cobaltism, revision of the surgery is also an important part of therapy. Specific cardiac therapy for cobalt cardiomyopathy would be appropriate. Thiamine should be administered as well.
Are there any biomarkers are ways to measure cobalt concentration in the body?
From: https://www.mctlaw.com/joint-replacement/cobalt-chromium-poisoning/
Cobalt is excreted primarily via the urine, with a lesser extent in the feces, so urine cobalt testing is available.
Here’s an example of a US laboratory that performs urine cobalt testing: https://www.labcorp.com/tests/071514/cobalt-urine
Blood testing is also available (appears to be in combination with chromium): https://www.labcorp.com/tests/738770/chromium-and-cobalt-whole-blood
It appears that the testing is the easy part, but the interpretation of these results can be difficult because of a variable elimination pattern in the urine. Cobalt is present in the urine after inhalation, and can be rapidly found in the urine after exposure, but if there is a prolonged exposure to cobalt, the elimination of cobalt is reduced in rate. Vitamin supplementation or a diet high in vitamin B12 can also affect the blood or urine cobalt test results. The toxic level of cobalt appears to be not well-defined and can vary whether there is an acute exposure or a chronic lower level exposure.
References and resources:
Fang, H., Kang, J., & Zhang, D. (2017). Microbial production of vitamin B12: a review and future perspectives. Microbial cell factories, 16(1), 15. https://doi.org/10.1186/s12934-017-0631-y.