12.1 Toxic Effects
There are three basic types of selenium poisoning in livestock:
(a) acute poisoning that results from consumption (usually in a single feeding) of a sufficient quantity of highly seleniferous weeds,
(b) chronic poisoning or `blind staggers' from consumption of moderately toxic amounts of seleniferous weeds over an extended period of time, and
(c) chronic poisoning or `alkali disease' caused by the consumption of moderately seleniferous grains and forage grasses over a period of several weeks to months (Eisler 1985). The distinction between the two types of chronic poisoning is described as follows: alkali disease in cattle, horses, hogs, and poultry is said to be associated with the consumption of seleniferous forages in which Se is bound to protein (i.e., water-insoluble Se). In comparison, blind staggers that occur in cattle, and possibly sheep, is associated with the consumption of Se-indicator plants over a period of time wherein the Se is in a water-soluble form (Rosenfeld and Beath 1964).
Alkali disease has been experimentally reproduced using both inorganic Se compounds and seleniferous plants and seems to be the principal manifestation of Se poisoning. On the other hand, selenium-induced blind staggers has not been reproduced by using inorganic Se compounds and is questionable when using seleniferous plants. Therefore, it seems to be a condition of questionable etiology in which Se may or may not be involved (James et al. 1989).
The most characteristic sign of acute Se poisoning in animals is the development of the so-called `garlicky breath odour', which is due to the pulmonary excretion of volatile selenium compounds (e.g., dimethyl selenide) by animals overexposed to selenium. Other signs of acute Se poisoning in domestic livestock include abnormal movements, lowered head, drooped ears, diarrhoea, elevated temperature, rapid pulse, laboured breathing, bloating with abdominal pain, increased urination, and dilated pupils. Before death, which is due to respiratory failure, there is complete prostration and lethargy (Eisler 1985, WHO 1987).
Stowe and Herdt (1992) reported selenium toxicity in pigs and horses exposed to a diet of 8.1 mg/kg dry weight for a period of 5 weeks (pigs) and 20 mg/kg dry weight for 3 weeks (horses). Assuming that large animals consume 2-3% of food/day of their body weight, these toxic doses were expressed as 0.16-0.24 mg Se/kg body weight/d for pigs and 0.4-0.6 mg Se/kg body weight/d for horses. The maximum dietary tolerable level of 2 mg Se/kg dry-weight for livestock was recommended by NAS (1980).
MacDonald et al. (1981) reported that a single dose of 2 mg Se/kg body weight administered to neonatal calves resulted in lassitude, inappetance, dyspnea and death within 12 hours following injection. Smyth et al. (1990) reported that two of four sheep (12-week-old lambs) died within 16 hours of administration of 5 mg Se/kg body weight as sodium selenite. In another study, 2 mg Se/kg body weight produced 100% mortality in swine within 4 hours of injection. A lower dose of 1.2 mg Se/kg body weight produced 100% mortality in 5 days (Orstadins 1960).
Smyth et al. (1990) reported that a single oral dose of 5 mg Se/kg body weight/d caused edema in the skeletal muscles of the diaphragm and congestion of viscera in sheep. In a study of weaned 5-week-old pigs, a dose of 1.3 mg Se/kg body weight/d, as sodium selenite, killed all eight pigs within 10 days (Wilson et al. 1989). Pigs exposed to organic (in plants) or inorganic (sodium selenate) in the diet at the rate of 1.1 to 1.3 mg Se/kg/d exhibited diffuse swelling and vacuolar degeneration of hepatocytes, and had a mean survival of 44 days (Baker et al. 1989). However, pigs exposed to 0.47 mg Se/kg/d of sodium selenite in their feed for 35 days showed no liver damage (Mahan and Magee 1991). Mihailovic et al. (1992) reported hepatic effects in pigs exposed to 0.59 or 1.07 mg Se/kg/d, as sodium selenite, in feed for 8 weeks.
Harr and Muth (1972) reported a decreased conception rate and an increased fetal resorption rate in cattle, sheep, and horses fed natural diets containing 20-50 mg Se/kg diet. Assuming that large animals consume an amount of food equal to about 2-3% of their body weight/d, the dose would correspond to 0.5-1.5 mg Se/kg body weight/d. These levels of Se also produced other signs of toxicity including hair loss, lameness, and degenerative fibrosis of the heart, liver, and kidney.
12.2 Summary of Existing Guidelines
The CCME (CCREM 1987), recommended that the concentration of total selenium in water used for livestock watering should not exceed 0.05 mg/L. The Province of Manitoba (Williamson 1988) also recommended a maximum concentration of 0.05 mg Se/L for livestock watering. The recommended limits for livestock watering are 0.02 mg Se/L in Australia (Hart 1984), 0.05 mg Se/L in the United States (USEPA 1973), and 0.05 mg Se/L in Ontario (OMOE 1984).
12.3 Recommended Water Quality Guidelines
A water quality guideline of 0.03 mg/L selenium is recommended to protect livestock water use.
12.4 Rationale
Based upon the above review, it appears that pigs are among the most sensitive livestock species to selenium effects. Puls (1981) reported adequate7 levels of selenium ranging from 0.2 to 0.8 mg Se/kg diet for pigs, with an average value of 0.5 mg Se/kg diet. Assuming an average daily dry-matter intake of 2.5% of the body weight, the safe dose, or the total daily intake (TDI), was determined to be 0.5 x 0.025 = 0.0125 mg Se/kg body weight/d. The safe dose thus determined is nearly the same as the 0.0085 mg Se/kg body weight/d calculated using the lowest adverse observed effect level (LOAEL) of 8.1 mg Se/kg diet (Stowe and Herdt 1992)8 and the CCME protocol (1993).
Assuming an average body weight (BW) for a pig of 200 kg and a daily water intake rate (WIR) of 17 L/d (Warrington 1993), the reference concentration (RC) was calculated as follows:
RC = (TDI x BW) ÷ WIR = 0.0125 mg Se/kg/d x 200 kg ÷ 17 L/d = 0.147 mg/L
Assuming a drinking water contribution (PDWC) of 20% for the daily body burden of selenium for livestock, the recommended water quality guideline was determined to be:
Guideline = RC x PDWC = 0.147 mg/L x 0.20 0.03 mg/L.
7 Adequate levels are defined as levels sufficient for full functioning of all body mechanisms with a small margin of reserve to counteract commonly encountered antagonistic conditions.
8 Assuming an average dry-matter intake of 2.5% of body weight/day, the LOAEL, in terms of body weight, is equal to 0.203 mg Se/kg body weight/d. The no observed adverse effect level was estimated to be 0.203÷5.6 = 0.036 mg Se/kg body weight/d. Using an uncertainty factor (UF) of 10, the tolerable daily intake (TDI) was calculated to be (0.203 x 0.036)0.5 ÷10 = 0.0085 mg Se/kg body weight/d.