Selenium toxicity

Selenium toxicity is (rarely: hyperselenaemia) is caused by excessive intake of the metalloidnon-metallic element selenium (Se) in the diet.

Epidemiology

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

Acute selenium toxicity

• cardiac dysfunction: hypotension, tachycardia, pulmonary oedema
  • ECG: long QT, flattening/inversion of T-waves ⁴
• lassitude
• nausea and vomiting
• diarrhoea
• abdominal pain
• neurological dysfunction e.g. ataxia, tremor, confusion, loss of consciousness
• fetor oris: distinctive garlicky odour

Chronic selenium toxicity (selenosis(selenosis)

Chronic toxicity may present with features of acute toxicity plus:

• dermatological sequelae: often the initial symptoms/signs
  • nails e.g. brittleness, leuconychia, etc.
  • rash
  • alopecia
• hepatic dysfunction
• haematopoietic impairment
• dermatological sequelae e.g. brittle nails, rash, alopecia
• loss of fertility
• fetor oris: distinctive garlicky odour
• neurotoxicity e.g. hyperreflexia, paraesthesia, seizures, paresis
• hypothyroidism

Pathology

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 neurones themselves, and enzymes ².