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CAS 7782-49-2

Selenium

metalloidessential nutrient/toxic at excessHAP

Selenium is an essential trace mineral required for the function of selenoproteins including glutathione peroxidase and thioredoxin reductase — but with one of the narrowest margins between beneficial and toxic intake of any essential nutrient, making deficiency and toxicity both real public health concerns across different populations and geographies.

Where It Comes From

Selenium was discovered in 1817 by Swedish chemist Jöns Jacob Berzelius, who named it after the moon goddess Selene because of its association with tellurium (named for Earth) [1]. Its essentiality to mammals wasn't established until 1957, when Klaus Schwarz showed it prevented liver necrosis in vitamin E-deficient rats. The dramatic demonstration of selenium's geographic variation came from contrasting Chinese provinces: Keshan disease (a fatal cardiomyopathy affecting children) was endemic in low-selenium soil regions, while Kashin-Beck disease (a disabling joint disease) was linked to selenium deficiency in separate regions — and industrial selenosis with hair loss and nerve damage occurred in selenium-rich areas of China [2]. The United States has similar geographic variation: Great Plains soils are selenium-rich (supporting cattle health but capable of causing selenosis in livestock), while Pacific Northwest soils are relatively selenium-poor [1]. Industrial selenium sources include copper and lead smelting (selenium is a byproduct), electronics manufacturing (selenium rectifiers, photoelectric cells), and glass decolorization [2].

How You Are Exposed

Dietary intake from food grown in selenium-sufficient soils is the primary healthy exposure route — the U.S. RDA is 55 µg/day and the tolerable upper limit is 400 µg/day [1]. Brazil nuts from the Amazon basin are extraordinarily selenium-rich, with a single nut often containing 50-90 µg — multiple daily Brazil nuts can approach or exceed the upper limit [2]. Selenium supplements, widely marketed for cancer prevention (following the Nutritional Prevention of Cancer trial in the 1990s), have been a source of inadvertent excess — the SELECT trial showed high-dose selenium supplements failed to prevent prostate cancer and potentially increased risk in some groups [1]. Occupational inhalation occurs in copper smelting, electronics manufacturing, and glass production. Contaminated groundwater from mining or industrial areas is an environmental exposure pathway [2].

Why It Matters

Selenium functions primarily through selenoproteins — proteins containing the unusual amino acid selenocysteine encoded by UGA codons [1]. Glutathione peroxidase (GPx) uses selenium to reduce peroxides and oxidized lipids, playing a central role in antioxidant defense. Thioredoxin reductase uses selenium in the reduction of thioredoxin, critical for ribonucleotide reductase activity in DNA synthesis [2]. At deficient levels: impaired thyroid hormone activation (selenoenzyme iodothyronine deiodinase), impaired antioxidant defense, and at severe deficiency, Keshan disease cardiomyopathy. At toxic levels (selenosis): hair and nail loss, peripheral neuropathy, garlic-smelling breath (dimethylselenide), and at extreme doses, acute respiratory distress and liver failure [1]. The therapeutic window is narrow: the difference between the recommended dietary intake (55 µg/day) and the tolerable upper intake level (400 µg/day) is roughly 7-fold [2].

Who Is at Risk

Populations in low-selenium soil regions (parts of China, New Zealand, Finland before food fortification, some Pacific Northwest areas) are at risk of deficiency [1]. People taking high-dose selenium supplements (>200 µg/day) risk selenosis over time [2]. Residents in selenium-hyperaccumulator plant regions or near selenium-rich agricultural drainage (e.g., Kesterson Reservoir contamination in California) face elevated environmental exposure [1]. Workers in copper smelting and electronics manufacturing face occupational exposure via inhalation [2]. Patients with chronic kidney disease on dialysis often become selenium-deficient [1].

How to Lower Your Exposure

1. Do not exceed selenium supplement doses of 200 µg/day — the tolerable upper limit is 400 µg/day and chronic toxicity (hair loss, neuropathy) occurs with regular excess [1]. 2. Limit Brazil nut intake to 1-3 per day maximum given their highly variable and potentially very high selenium content [2]. 3. Test your groundwater for selenium if you live near mining operations, fly ash ponds, or selenium-rich agricultural drainage areas [1]. 4. For selenium deficiency: increase intake of seafood, Brazil nuts (1/day), meat, whole grains, and dairy — selenium content depends heavily on soil selenium where food was grown [2].

References

  1. [1]Institute of Medicine (2000). Dietary Reference Intakes: Selenium. National Academies Press. https://www.nap.edu/read/9810/
  2. [2]Rayman MP (2012). Selenium and human health. The Lancet. https://doi.org/10.1016/S0140-6736(11)61452-9

Recovery & Clinical Information

Body Half-Life

Selenium in blood has a half-life of approximately 65-77 days [1]. Urine selenium reflects recent intake (prior 1-2 days), while serum selenium and whole blood selenium reflect steady-state body burden [2].

Testing & Biomarkers

Serum or plasma selenium is the standard clinical test — optimal range 120-160 µg/L for general health [1]. Whole blood selenium for longer-term assessment. Selenoprotein P is a more informative functional biomarker [2]. Urine selenium for occupational monitoring [1].

Interventions

For deficiency: selenium supplementation (selenomethionine is better absorbed than selenite) and selenium-rich foods [1]. For selenosis (toxicity): remove selenium source immediately; hair and nail changes are reversible over months after stopping excess intake [2]. For acute high-dose poisoning: supportive care; acetylcysteine has been used [1].

Recovery Timeline

Blood selenium rises to new equilibrium within 4-8 weeks of dietary or supplement changes [1]. Hair and nail changes from selenosis reverse over 3-6 months after stopping excess intake [2].

Recovery References

  1. [1]ATSDR (2003). Toxicological Profile for Selenium. https://www.atsdr.cdc.gov/toxprofiles/tp92.pdf
  2. [2]Rayman MP (2012). Selenium and human health. The Lancet. https://doi.org/10.1016/S0140-6736(11)61452-9

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