7.1 Toxic Effects
Humans may be exposed to selenium through air, water and food. Those exposed to high air concentrations of selenium in industrial settings have reported dizziness, fatigue, and irritation of mucous membranes. In extreme cases, fluid in the lungs (pulmonary edema) and severe bronchitis have been reported (USDHHS 1994).
The severity of the effect of selenium in food and water depends on the amount ingested and the period of exposure. One 3-year-old boy died 1.5 hours after ingesting an unknown quantity of selenious acid contained in a gun-bluing preparation (Carter 1966). Clinical signs included excessive salivation, garlic odour of the breath, and shallow breathing. Death probably resulted from lung edema. A 15-year-old female survived ingestion of a solution of sodium selenate estimated to have provided 22.3 mg selenium/kg body weight, probably because she was forced to vomit soon after exposure (Civil and McDonald 1978). Clinical signs included garlic odour of the breath and diarrhoea.
A number of systemic effects including respiratory, cardiovascular, gastrointestinal, haematological, musculoskeletal, hepatic, renal, dermal, endocrine, and change in body weight has been reported in humans and animals exposed to selenium (USDHHS 1994). Contempre et al. (1991) reported a decrease in the level of thyroid hormone T4 in a cretin (person with marked mental deficiency) and normal schoolchildren treated with selenomethionine for 2 months. Jensen et al. (1984) reported both marked hair loss and the deformity, and loss of fingernails in a woman who had consumed super potent supplement tablets containing 31 mg total selenium (as sodium selenite and elemental selenium) per tablet for 77 days.
In an epidemiological study with a Chinese population living in an area with high selenium levels in soils and food, Yang et al. (1983) reported that the average dietary Se intake in this area of selenosis occurrence was estimated to be 3.2 mg Se/person/day (or 0.05 mg Se/kg body weight/day). In the subsequent follow-up study, Yang et al. (1989a) reported that the estimated daily dietary Se intake required to produce the selenium effects was at least 0.016 mg Se/kg body weight/day. Based on occurrence of these dermal effects, USDHHS (1994) derived a chronic minimum risk level of 0.005 mg Se/kg body weight/day. (A minimum risk level or MRL is an estimated daily human exposure to a dose of chemical that is likely to be without an appreciable risk of adverse non-cancerous effects over a specified duration of exposure).
Rosenfeld and Beath (1964) reported listlessness, a general lack of alertness, and other symptoms of selenosis in a family exposed for about three months to well water containing 9 mg Se/L (0.26 mg Se/kg body weight/day from drinking water). All symptoms disappeared after the use of seleniferous well water had been discontinued. These authors did not estimate the family's exposure to total dietary (water and food) selenium.
Roy et al. (1990) examined the concentration of selenium in sperm samples from 211 men. No significant correlation was found between the seminal plasma selenium concentration and sperm count or mobility. In a three-generation reproduction study, selenium administered as sodium selenate (0.57 mg Se/kg body weight/day) in drinking water of breeding mice produced adverse effects on reproduction. The most notable adverse effects included the failure of about half of the pairs to breed (Schroeder and Mitchener 1971b).
Little is known about the specific mechanism by which selenium and selenium compounds exert their toxic effects. The soluble compounds of sodium selenite and sodium selenate appear to be most toxic; on the other hand, elemental selenium and selenium sulphide are less toxic than most selenium compounds because of their extremely low solubility. It is generally theorized that acute toxicity is the result of selenium inactivating the sulfhydryl enzymes necessary for the oxidative reactions in respiration. Acute toxic effects such as swelling of the lung tissue result in respiratory failure and death. The lung, however, does not appear to be a target organ at lower levels of exposure (Mack 1990, USDHHS 1994).
Selenium can replace sulphur in biomolecules especially when the concentration of selenium is high and the concentration of sulphur is low in the organism. This may be a mechanism of selenium toxicity. Although selenocysteine appears to be specifically substituted for cysteine in glutathione peroxidase, selenomethionine appears randomly substituted for methionine in protein synthesis. This may be an additional mechanism for intermediate or chronic toxicity (Stadtman 1983, Tarantal et al. 1991). Skin, hair, and nail damage are the most sensitive significant indicators of chronic selenium overexposure; however, the mechanisms causing these effects are not known. It has been hypothesized that the body uses nails and hair to excrete excess selenium (Yang et al. 1989b, USDHHS 1994).
7.2 Summary of Existing Guidelines
The current Canadian drinking water quality guideline is 0.01 mg/L for selenium (Health and Welfare Canada 1993). A drinking water quality guideline of 0.01 mg Se/L is also recommended by the World Health Organisation (1994) and many states in the U.S. (USDHHS 1994). The USEPA Office of Drinking Water recommended a maximum contaminant level of 0.05 mg Se/L in drinking water, whereas the U.S. Food and Drug Administration recommended a permissible level in bottled water of 0.01 mg Se/L (USDHHS 1994).
7.3 Recommended Water Quality Guidelines
It is recommended that the maximum concentration of selenium in drinking water should not exceed 0.01 mg/L. The recommended level is based on the Health and Welfare Canada's (1993) maximum acceptable concentration of 0.01 mg/L selenium in drinking water to protect from adverse health effects.
7.4 Human Exposure
Since selenium is naturally occurring and widespread, humans are exposed to low levels of selenium daily through food, water and air. The U.S. Department of Health and Human Services (1994) reviewed data found in the literature on human exposure (see below). It is quite obvious that most of these data are old and there is lack of recent data on the subject.
In the U.S., the average intake of selenium from food was estimated to range from 0.071 to 0.153 mg Se/person/day. Most of the daily intake came from eating cereals, grains, and meat. Measured average concentrations of selenium in the foods ranged from 0.004-0.083 mg/kg wet-weight in fruits, vegetables, and dairy products, 0.063-0.66 mg/kg wet-weight in grains and wheat bread, and 0.21-2.84 mg/kg wet-weight in meat, fish, and seafood. Seafood (e.g., 2.54 -3.44 mg Se/kg wet-weight in swordfish), organ meats (1.45 - 2.32 mg Se/kg wet-weight in raw beef kidney) and Brazil nuts (0.2-253 mg Se/kg wet-weight, with an average value of 14.7 mg Se/kg wet-weight) contain the highest level of selenium (Schubert et al. 1987, Secor and Lisk 1989, USDHHS 1994).
Levels of selenium in drinking water are generally low. USDHHS (1994) estimated that less than 1% of the daily intake of selenium came from drinking water. Based on a review of selenium concentrations in different types of foods and the amounts of each type of food eaten, Schubert et al. (1987) estimated a Se uptake of 0.071 mg Se/d for the U.S. population. Certain areas of Canada and the U.S. have highly seleniferous soils, and people living in these areas may be at risk of higher selenium exposure.