promoting the sustainable and responsible use of cobalt in all forms

Red Blood Cells

One effect of systemic cobalt exposure is an increase in the number of red blood cells produced by the body.

Cobalt is known to be a potent inducer of hypoxia (a response normally associated with low oxygen levels), in the presence of normal oxygen levels.

Cobalt induces hypoxia which promotes the body to produce more red blood cells.

As a consequence of a hypoxic condition, the body responds by increasing erythropoietin (EPO) production. EPO is a hormone which controls the production of red blood cells (RBCs). EPO acts on immature red blood cells in the bone marrow, causing maturation and release into the blood.

Cobalt treatment of anaemia

A historic use for cobalt was in the treatment of certain types of anaemia, which was achieved by oral administration of inorganic cobalt chloride. Adult doses of cobalt chloride were typically in the range of 40-140 µg Co/kg body weight/day (in a 70 kg adult, this corresponds to 9,800 µg/day)[1]. Higher doses (2,700 µg Co/kg body weight/day) of cobalt were utilised to treat sickle cell anaemia in children[1]. These higher doses were associated with adverse thyroid effects (goitres) due to a decreased uptake of iodine. Both goitre and increase in red blood cells were reversible upon cessation of oral cobalt treatment. Doses lower than 1,800 µg Co/kg body weight in children were not associated with thyroid effects[1].

The clinical use of cobalt in treating anaemia has been replaced with the use of synthetic EPO.

Cobalt and doping

Blood doping is an illegal practice of enhancing athletic performance through increasing the oxygen-carrying capacity of the blood. EPO has been used in the past as a doping agent[2], due to the role of EPO in increasing the number of red blood cells, thereby increasing oxygen-carrying capacity in the body. As cobalt-induced RBC production involves the increase in natural EPO without having to use synthetic EPO, cobalt could potentially be used as a doping agent[3].

The press has published several articles about the use of cobalt chloride in racehorses to improve performance.

Occupational exposure studies

Two occupational exposure studies have included an assessment of blood parameters of cobalt workers in both a cobalt refinery and a cobalt dye factory (painting of plates). Both studies mentioned slight but statistically significant decreases in RBC parameters between control and cobalt-exposed groups[4]. This is in direct opposition to the increased RBC findings in animals. Authors of both studies have stated that this effect was hard to interpret and did not correlate with cobalt levels in the body.


This summary is intended to provide general information about the topic under consideration. It does not constitute a complete or comprehensive analysis, and reflects the state of knowledge and information at the time of its preparation. This summary should not be relied upon to treat or address health, environmental, or other conditions.

[1] Finley et al. 2012. Derivation of a chronic oral reference dose for cobalt. Regulatory Toxicology and Pharmacology 64, 491-503.
[2] Debeljak and Sytokowski 2012. Erythropoietin and erythropoiesis stimulating agents. Drug Testing and Analysis 4, 805-812.
[3] Lippi et al. 2005. Cobalt chloride administration in athletes: A new perspective in blood doping? British Journal of Sports Medicine 39, 872-873.
Duh et al. 2008 Management of anaemia: A critical and systematic review of the cost effectiveness of erythropoiesis-stimulating agents. Pharmacoeconomics 26, 99-120.
[4] Swennen, B et al. 1993. Epidemiological survey of workers exposed to cobalt oxide, cobalt salts and cobalt metal. Br J Ind Med 50:835-842.
Raffn E, et al. 1988. Health effects due to occupational exposure to cobalt blue dye among plate painters in a porcelain factory in Denmark. Scan J Work Environ health 14: 378-384.