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I I Boron Mammals I probably encounter both types of boron exposure, during embryogenesis and posthatching development, and so these higher mortality figures are probably more relevant. I Smith and Anders found that diets containing as little as 30 mg B/kg fresh weight (fw) fed to mallard adults adversely affected the growth rate of their ducklings. In a study by Hoffman et a1. (1990), dietary levels of 100 mg B/kg fw resulted in reduced growth of female mallard ducklings. These findings indicate that concentrations greater than 30-100 mg B/kg in natural diets of ducklings could adversely affect their development. I I I I Mallards fed concentrations up to 2,000 mg B/kg did not exhibit any histological pathologies. Therefore, histology may not prove to be an adequate means of assessing boron exposure or toxicosis in mallard ducks. Boron levels in egg, liver, and brain tissues increased in proportion to dietary concentra- tions of boron; however, these tissues con- tained residues that were at least one order of magnitude lower than the dietary concentration administered. Hoffman et al. (1990) and Smith and Anders (1989) found that boron accumulation in the brain and liver was substantially greater in all boron- supplemented groups than in controls, with a greater accumulation in the brain. I I I I I I Pendleton et al. (1995) reported extremely rapid accumulation and elimination of boron in mallard tissues. Adult male mallards fed a diet containing 1,600 mg B/kg accumulated equilibrium levels of boron in liver tissue and blood within 2-15 days. After boron was removed from the diet of these mallards, it was completely cleansed from the liver and blood within 1 day. These findings are consistent with early research on cows and rats which revealed that the boron concen- tration of cow's milk could increase tenfold within the first 24 hours of dietary boron supplementation and that boric acid fed to rats is eliminated with extreme rapidity (Hove et a1. 1939). I I I I I The reported toxic effects of boron on mammals are summarized in table 7, at the end of this chapter. In general, excessive boron consumption by mammals results in a reduced growth rate and in some cases loss of body weight. Growth retardation has been reported in cattle given 150 mg B/l drinking water, in dogs consuming diets containing 1,750 mg B/kg, in rabbits eating rations equivalent to >140 mg B/kg bw daily, and in rats given 150 mg B/l in drinking water or 1,060 mg B/kg in food (Eisler 1990). In some instances, animals avoid boron-contaminated drinking water; rats reject drinking water containing as little as 1.0 mg BIL (Dixon et al. 1976), and cattle avoid water containing >29 mg B/l (Green and Weeth 1977). Adverse effects on the reproduction of laboratory mammals have been reported in sensitive species fed diets containing more than 1,000 mg B/kg or given drinking water containing 1.0 mg B/L (Eisler 1990). Boric acid caused decreased fetal body weight and increased malformations in rats, mice, and rabbits with doses in the range of 80-400 mgl kg/day, given either throughout gestation or only during major organogenesis (Heindel et al. 1994). Boron is readily transmitted into milk and eggs, as well as through the placenta (Hove et a1. 1939). Boron compounds, especially boric acid, can accumulate in animal tissues and produce a reduction in fertility, an increase in developmental abnormalities, and death (Weir and Fisher 1972; Lee et al. 1978; Landolph 1985). Boron is found at concentra- tions ranging from 0.05-0.6 mglkg fw in most animal tissues but may be several times higher in bones (Nielsen 1986). Mule deer metacarpals have been found to contain 0.8-3.6 mg B/kg dw, with younger animals having much higher bone boron concentra- tions than adults (Stetler 1980). Boron from boric acid has been shown to concentrate in the brain, spinal cord, and liver following ingestion (Beyer et al. 1983). Nontoxic concentrations of dietary boron (sodium Cf:::J