Boron

The essentiality of boron for plants and animals has long been established and recent evidence (1) suggests it may also be essential for humans. Possible roles for boron include the stabilisation of connective tissue and the mediation of membrane function, both via the condensation products of boric acid with saccharide moieties. The neutral molecule boric acid, B(OH)3, diffuses freely across membranes where it is readily trapped by cis-diols, probably to specific polysaccharides, to form moderately labile condensation products which may influence membrane function (2). In humans, dietary boron has been shown to exert a modest positive effect on erythropoiesis and haematopoiesis (3) and it is also reported to affect steroid hormone metabolism. Current clinical interest in boron includes the use of 10B labelled compounds in boron neutron capture therapy of malignant brain tumours (4).
Average daily intakes of dietary boron in the UK are variable, (2.8 + 1.5 mg) and higher than in the USA (1.5 + 0.4 mg). Dietary boron is efficiently absorbed and also efficiently excreted into urine with about 85 – 100% of an oral dose of borate appearing in urine over a 5-7 day period5. The oral toxicity of boron is relatively low and it has been estimated that safe population mean intakes are <13 mg/day1 and that individuals are at risk of toxicity when intakes exceed 100 mg/day6. The richest food sources of boron are: nuts and dried fruits, 15-30 mg/kg and wine 8.5 mg/l. The use of boric acid food additives are now prohibited except for caviar at 4000 mg/kg7. Thus a toxic intake of boron could be provided by 200 g nuts plus 20 g caviar, or 25 g low fat crisps plus 12 L of wine.

Toxicity
Most reports of boron toxicity are concerned with the earlier use of borates as weak germicides or with deliberate self-poisoning5. Nowadays, aqueous solutions of borate are no longer used as antiseptic agents nor is boric acid used in skin powders or ointments, because of the toxicity of these preparations. It is however still possible to purchase boric acid.
Chronic boron toxicity in infants whose ‘dummies’ were dipped in a preparation of borax and honey was manifest by scanty hair, patchy dry erythema, anaemia and seizure disorders. These features were alleviated when the use of the borax/honey preparation was stopped1. Skin absorption of boron, via a borax dusting powder is very high and has, in infants, produced a severe erythema with weeping skin plus vomiting and diarrhoea with blue/green stools5,6. Features of acute boron toxicity are profound shock, depressed circulation, convulsions and coma. The fatal oral toxic doses for infants, adolescents and adults are respectively: 2-3 g, 5-6 g and 15-20 g (5,6).

Laboratory Indices of Boron Status
Acute and chronically excessive uptakes of boron are indicated by elevated concentrations in plasma, whole blood and urine. There are a few reliable data which define the minimum concentrations associated with toxic effects.
Because of the risk of contamination of specimens e.g. from borosilicate glassware, one must be wary when assessing published data.
See references 8,9,10 for the reference concentrations quoted in the ‘yellow pages’.
Extremely high concentrations reported to be associated with non-fatal poisonings were 3 to 30 mmol/L and 1.9 to 14 mmol/L in sera of infants and 126-215 mmol/L in serum from an adult. Similarly high levels, 20-150 mmol/L were seen in five infants who died following the ingestion of 4.5-14 g boric acid (7).

References:
World Health Organisation (1996). In: Trace Elements in Human Nutrition and Health. WHO Geneva, Chapter 13, pp 175-9
Frausto da Silva JJR and Williams RJP (1993. “The biological Chemistry of The Elements” Oxford University Press, Oxford UK, pp58: 63: 451
Hielsen FH, Mullen LM, Neilsen EJ (1991). Dietary Boron Affects Blood Cell Counts and Hemoglobin Concentrations in Humans.” J Trace E Exper Med, 4, 211-23.
Hatanaka H, Nakagawa Y (1994). “Clinical results on long surviving brain tumour patients who underwent boron neutron capture therapy”. Int J Rad Oncol Bio Phys, 28, 1061-6.
Baselt RC, Cravey RH. (1989) Disposition of Toxic Drugs and Chemicals in Man. Yearbook Medical Publications Inc, Chicago, USA, pp 91-3.
Mervyn L (1985). The Dictionary of Minerals. Thorsons, Wellingborough, UK pp 23-4
Commission of European Communities (1995). Food Regulations EC Directive No XXX.
Iyengar V and Woitties J (1988). ‘Trace elements in human clinical specimens. Evaluation of literature data to identify reference values”, Clin Chem,34, 474-81.
Sabbioni E (1996). In: Trace Elements in Human Nutrition and Health, Chapter 21 WHO, Geneva, pp 231-644
Delves HT. Unpublished observations 1994-199

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