Cobalt poisoning is a medical state caused by the excessive accumulation of cobalt in the body. Cobalt can enter the human organism via the respiratory tract or via ingestion.
Cobalt poisoning can manifest with symptoms of varying degrees of severity and can even cause death. An individual is exposed to this chemical element via inhalation, ingestion, or dermal exposure and, in general, chronic exposure is required for most of the adverse effects to develop.
The manifestations originating from the respiratory tract are traditionally linked to toxicity due to cobalt inhalation and comprise asthma, fibrosis, pneumonia, decreased lung function, and bronchospasm [1] [2] [3]. Cardiovascular manifestations are generally limited to cardiomyopathy accompanied with cardiomegaly and cardiac failure, while anemia with an approximate 5% decrease in hemoglobin has also been reported [4] [5] [6] [7]. Also documented are the effects of cobalt poisoning on the endocrine system, and specifically on the thyroid gland: even though reports evince a certain dissent, increased serum thyroxine (T4) or decreased concentrations of triiodothyronine (T3) have been observed [8]. In addition to the aforementioned symptomatology, persisting occupational exposure to cobalt may also lead to conjunctival congestion, weight loss in patients with the cobalt-associated pulmonary disease, and neurological sequelae which include nerve deafness, as well as memory and visual acuity impairment [9] [10] [11].
Ingesting cobalt is an important way of exposure to the element's toxic effects, with lethal cardiomyopathy having been reported as the most detrimental manifestation [12]. It develops abruptly with a clinical picture that resembles beriberi or alcoholic cardiomyopathy. Sinus tachycardia, left ventricular failure, and cardiogenic shock are some of the main manifestations, which may be preceded by nausea, diarrhea, and vomiting [13]. Ingestion of cobalt has also shown to result in polycythemia, increased hemoglobin levels, goiter, and histological changes of the thyroid gland [14].
Cobalt is known to cause dermatitis, should it come into contact with an individual's skin [15] [16].
An additional way in which cobalt poisoning is induced is metal-on-metal hip arthroplasty (MoM) [17]. The phenomenon is known as prosthetic hip-associated cobalt toxicity (PHACT) and leads to some of the manifestations that inhaled and ingested cobalt does, including cardiac, neurologic, and thyroid impairment [18]. Depression, lack of orientation and concentration, as well as aphasia, are also results of PHACT-related cobalt poisoning [19].
The diagnosis of cobalt poisoning initially requires a thorough medical history, including a history of potential exposure to toxic metals. This chemical element can be detected in the blood or urine [20] [21]. On average, an individual that has not been exposed to an excessive amount of cobalt is expected to exhibit values of the element less than 0.19 μg/dL and 2 μg/dL in the serum and urine, respectively [22]. A patient believed to have been exposed to a dangerous amount of cobalt should undergo laboratory evaluation of cobalt concentration in the urine and blood as soon as possible upon presentation, as the excretion rate is maximized within 24 hours after an occasion of exposure. Cobalt-associated allergic reactions can lead to elevated levels of IgE and IgA in the serum, which can be used both for diagnostic and monitoring purposes [23].