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Updated: May 14, 2026

Setup of Capillary Electrophoresis-Inductively Coupled Plasma Mass Spectrometry (CE-ICP-MS) for Quantification of Iron Redox Species (Fe(II), Fe(III))
Published on: May 4, 2020
[Neurotoxic effects of cobalt: an open question]
1Dipartimento di Medicina Sperimentale e Applicata, Sezione di Medicina del Lavoro e Igiene Industriale, Università degli Studi di Brescia, P.le Spedali. Civili 1. 25123 Brescia. catalani@med.unibs.it
Cobalt exposure can cause neurological issues like tremors and cognitive decline, alongside heart problems. This toxicity is linked to oxidative stress and mitochondrial damage.
Area of Science:
- Toxicology
- Neuroscience
- Cardiology
Context:
- Cobalt exposure is linked to various health issues, including neurological and cardiac diseases.
- Neurotoxicity from cobalt is observed in isolated cases due to occupational, iatrogenic, or prosthetic exposures.
- The mechanism involves oxidative stress and mitochondrial dysfunction.
Purpose:
- To summarize the neurological and cardiac effects of increased cobalt levels.
- To highlight the typical symptomatology of cobalt neurotoxicity.
- To underscore the role of oxidative stress and mitochondrial alterations in cobalt toxicity.
Summary:
- Elevated cobalt levels are associated with neurological disorders such as hand tremor, incoordination, cognitive decline, depression, vertigo, hearing loss, and visual changes.
- Classic cardiac conditions like arrhythmias and cardiomyopathies, as well as allergic and endocrine symptoms, are also linked to cobalt.
- Reported cases of cobalt neurotoxicity, stemming from occupational, iatrogenic, or prosthetic sources, reveal a distinct set of symptoms.
Impact:
- Understanding cobalt's neurotoxic potential is crucial for diagnosing and managing related neurological conditions.
- Identifying the link between cobalt exposure and mitochondrial dysfunction can inform therapeutic strategies.
- This information is vital for occupational health, medical device safety, and clinical toxicology.
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