Case reports in humans have indicated neurological effects after accidental ingestion of high levels of boron (as boric acid). Newborn infants who ingested 4.5-14 g boric acid showed central nervous system involvement manifested by headache, tremors, restlessness, and convulsions followed by weakness and coma (Wong et al. 1964). Histological examination of 2 of 11 infants revealed congestion and edema of brain and meninges with perivascular hemorrhage and intravascular thrombosis at a dose >505 mg boron/kg/day (Wong et al. 1964). Seizure disorders have been associated with boron exposures (as borax) in infants who ingested 4-30 g borax for 4-10 weeks (O'Sullivan and Taylor 1983) and 9-125 g borax for 5-12 weeks (Gordon et al. 1973). Estimates of boron consumption could not be determined since the authors did not provide data on kilogram body weights. Blood boron levels in patients who ingested borax ranged from 2.6 to 8.5 mg/mL (O'Sullivan and Taylor 1983). In one infant with a seizure disorder who ingested borax for 3 months, the blood boron level was 1.64 mg/100 mL (Gordon et al. 1973).
In rats, exposure to approximately 20.8 mg boron/kg/day as borax (based on weight of 0.35 kg and average water consumption of 20.7 mL) in drinking water for up to 14 weeks caused increased cerebral succinate dehydrogenase activity after 10 and 14 weeks of exposure (Settimi et al. 1982). Increased RNA concentration and increased acid proteinase activity in brain occurred after 14 weeks (Settimi et al. 1982).
All LOAEL values for neurological effects in humans and animals are recorded in Table 2-2 and plotted in Figure 2-2.
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