Selenium toxicity (rarely: hyperselenemia) is caused by excessive intake of the non-metallic element selenium (Se) in the diet.
It is less common than selenium deficiency. It is most frequently seen in some parts of India, in which there are naturally high levels of selenium in the soil, which becomes incorporated into the plants that are farmed there. Less commonly seen are people who intentionally/accidentally overdose on dietary supplements or rarely in certain occupations (e.g. metal processing industry) 2.
Clinical presentation is dependent on whether poisoning is acute or chronic, with some overlap:
Acute selenium toxicity
- cardiac dysfunction: hypotension, tachycardia, pulmonary edema
- ECG: long QT, flattening/inversion of T-waves 4
- nausea and vomiting
- abdominal pain
- neurological dysfunction e.g. ataxia, tremor, confusion, loss of consciousness
- fetor oris: distinctive garlicky odor
Chronic selenium toxicity (selenosis)
Chronic toxicity may present with features of acute toxicity plus:
- dermatological sequelae: often the initial symptoms/signs
- nails e.g. brittleness, leuconychia, etc.
- hepatic dysfunction
- hematopoietic impairment
- loss of fertility
- neurotoxicity e.g. hyperreflexia, paraesthesia, seizures, paresis
Selenosis may result if the daily selenium intake exceeds 400-700 μg per day (cf. advice from the National Academy of Science in the US that adult males should aim for 40–70 μg and females 45–55 μg per day).
The level of excessive supplementation leading to selenosis is contentious, a study from China suggested at least 850 μg daily 1.
Laboratory studies demonstrate that excessive selenium can have a potentially broad range of activity against components of the CNS, including neurotransmitters, enzymes and the neurons themselves 2.
The characteristic garlicky aroma of selenium toxicity is primarily due to dimethylselenide, a volatile substance produced by cells 4.
Treatment and prognosis
Treatment is primarily supportive. Chelation is not recommended as animal research suggests that it may paradoxically increase overall toxicity 4.
Most of the toxic effects are reversible. Untreated acute/chronic toxicity may be fatal 4.
- 1. Stuss M, Michalska-Kasiczak M, Sewerynek E. The role of selenium in thyroid gland pathophysiology. (2017) Endokrynologia Polska. 68 (4): 440-465. doi:10.5603/EP.2017.0051 - Pubmed
- 2. Vinceti M, Mandrioli J, Borella P, Michalke B, Tsatsakis A, Finkelstein Y. Selenium neurotoxicity in humans: bridging laboratory and epidemiologic studies. (2014) Toxicology letters. 230 (2): 295-303. doi:10.1016/j.toxlet.2013.11.016 - Pubmed
- 3. Kurokawa S, Berry MJ. Selenium. Role of the essential metalloid in health. (2013) Metal ions in life sciences. 13: 499-534. doi:10.1007/978-94-007-7500-8_16 - Pubmed
- 4. Nuttall KL. Evaluating selenium poisoning. (2006) Annals of clinical and laboratory science. 36 (4): 409-20. Pubmed