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244 IS
2442S SUPPLEMENT
an RDA, but for which potentially toxic upper intakes tion in relation to boron intake and human boron deple
were known. There is a need to replace the ESADDI tion/repletion studies.
category because of ambiguities in interpretation of
values provided. For example, the term "safe" as used
Boron intakes of healthy people
in the ESADDI can be misinterpreted as the upper safe
limit of intake. Ambiguities are best eliminated by re Good estimates of boron intake are now available
naming the category; "provisional RDA" could be a
because of improvements in boron analytical technol
term for a category that provides dietary guidance but ogy. Recent analyses of food and personal care products
acknowledges limitations of the data used to set it. A (Anderson et al. 1994, Hunt et al. 1991, lyengar et al.
provisional RDA would be defined for a dietary sub 1990) indicate that usual adult human dietary boron
stance that meets criteria set for one of two classes consumption in the United States is in the range of 1-
of nutrients: class 1, clear evidence of essentiality but 2 mg [0.092-0.185 mmol]/d, not 10-25 mg [0.925-2.31
uncertain or limited quantitative data or endpoints to mmol]/d as calculated earlier (Ploquin 1967). However,
use for defining dietary requirements; and class 2, all recently calculated intakes are probably less than
strong evidence of essentiality and clear nutritional actual intakes by more than 10% because the calcula
benefit based on reasonably certain quantitative data, tions were based on the Food and Drug Administration
but lack of clear information on function or endpoints Total Diet Study (TDS) (Pennington 1983). Diets con
to use for defining dietary requirements. Specific ap structed from the TDS food lists for U.S. men and
proaches for assigning provisional RDAs for each of women aged 25-30 y do not provide sufficient energy
the three elements, boron, chromium and fluoride, are
Western diet (0.36 mg/d) also equalled total daily boron Adequacy of molecular function in relation to boron
intake. The women may have exhibited obligatory uri intake
nary boron loss because, in addition to urinary boron
losses, an amount of boron equal to 12% of boron in To date, five naturally occurring, well-defined, bio
take was also recovered from the feces. If plant and logical boron oxy compounds have been identified;
animal boron absorption mechanisms are analogous, they are all ionophoric macrodiolide antibiotics
the organic forms of boron per se are probably unavail (Schummer et al. 1994) produced by certain bacteria.
able to humans; the organic forms of boron in soil must There is universal agreement that vascular plants, dia
be mineralized to be available to plants (Gupta et al. toms and some species of marine algal flagellates have
1985). However, the strong association between poly-
acquired an absolute requirement for boron (Loomis
hydroxyl ligands and boron is easily and rapidly re and Durst 1992, Lovatt 1985). Although a specific bio
versed by change in pH, heat or the excess addition chemical role for the element in the metabolism of
of another low molecular polyhydroxyl ligand (Zittle higher plants remains to be elucidated, the unambigu
1951). Thus, within the intestinal tract, most ingested ous characteristics of both boron deficiency and boron
boron is probably converted to B(OH)3, the normal end-
toxicity are sufficient to define precisely the boron re
product of hydrolysis of most boron compounds quirements of many plant species (Lovatt and Dugger
(Greenwood and Earnshaw 1984) and subsequently ab 1984).
sorbed. As described below, findings from numerous studies
High boron intakes from typical natural foodstuffs indicate that animals or humans fed low boron diets
may stimulate an uncharacterized mechanism that
taken together, can be used to establish a provisional Hg [0.38-0.77 //mol] Cr/d for 6-12 mo. The ESADDI
boron RDA. established for young children was 20-80 //g [0.38-
1.54 //mol] Cr/d and for adolescents is 30-120 //g [0.58-
Suggested approaches for assigning a provisional 2.31 //mol] Cr/d.
RDA for boron
Dietary chromium sources and usual intakes
In summary, there is sufficient information to esti
mate average boron consumption by adult Americans Meat, poultry, fish and especially dairy products
(between 1 and 2 mg/d), adequate understanding of bo tend to be low in chromium. Fruits, vegetables and
ron status in relation to intake, and a clear indication grain products have variable chromium concentrations
that boron, in amounts typically consumed, affects (Anderson et al. 1992). Pulses, seeds and dark chocolate
mineral metabolism and energy substrate utilization. may contain more chromium than most other foods
Taken as a whole, the experimental boron nutrition (Jorhem and Sundstrom 1993). Certain spices such as
research data indicate an essential role for the element black pepper contain high concentrations of chromium
and a need for a provisional RDA, or similar status but contribute little to the usual diet on a per serving
category, for this element. The approach to use in the basis (Anderson et al. 1992). Loss of chromium in the
determination of a provisional RDA should include process of refining sugar has been noted (Wolf et al.
consideration of daily boron intake, boron status in 1974). However, processing also may add chromium to
relation to boron intake and the response of human the food supply. Chromium is leached from stainless
volunteers to boron supplementation after a period of steel containers particularly when contents are acidic
The first ESADDI for chromium appeared in the 9th Factors affecting chromium utilization
edition of the Recommended Dietary Allowances
(NRC 1980). The ESADDI remained at 50-200 //g Intestinal absorption of trivalent chromium is low
[0.96-3.85 //mol]/d for adults in the 10th edition (NRC with estimates in fasted rats ranging from <0.5 to 2-
1989). The ESADDI established for infants was 10-40 3% (Davis et al. 1995, Mertz 1969). In a metabolic
//g [0.19-0.77 //mol] Cr/d for the first 6 mo and 20-40 balance study, two men consuming an average of 36.8
2446S SUPPLEMENT
lower than the 50-200 //g [0.96-3.85 //mol]/d for water was demonstrated many years ago (Dean et al.
adults. 1942); this negative correlation has been confirmed by
There are very few reports that provide information a number of studies (Burt 1982). However, concerns
on which to base future recommendations. In one have surfaced recently about excessive fluoride intakes,
study, subjects were fed low chromium diets (<20 //g particularly from various dentifrices and the potential
[0.38 //mol]/d) for 14 wk. After 4 wk, 200 //g [3.85 /zmol] for fluorosis (Pendrys and Katz 1989). An additional
chromium (as CrCl3 ) or placebo was randomly assigned area of current research is evaluation of the efficacy of
for 5 wk in a crossover trial. Chromium supplementa pharmacologie doses of fluoride in the treatment of
tion had no affect in subjects with normal glucose toler osteoporosis (Hedlund and Gallagher 1989, Pak et al.
ance tests; however, the glucose tolerance test of eight 1986, Pak et al. 1994, Resch et al. 1993, Riggs et al.
subjects with initially impaired glucose tolerance dete 1994).
riorated further during the placebo period and improved
significantly during chromium supplementation (An Past recommendations for fluoride in the
derson et al. 1991). Less than 20 //g [0.38 /¿mol]chro-
Recommended Dietary Allowances
mium/d was sufficient to prevent impaired glucose tol
erance in the control group, but how long normal glu In the 10th edition of the Recommended Dietary
cose tolerance could be maintained on such a low Allowances (NRC 1989), the ESADDI established for
chromium intake is unknown. fluoride for adults was 1.5-4.0 mg [0.08-0.21 mmol]/
Based on current data, an infant consuming 750 mL d. The ESADDI established for infants was between 0.1
of human milk would receive less than 1 //g [0.019 [0.005] and 1.0 mg [0.053 mmol] F/d. For children and
bone than the adult (Ekstrand et al. 1994).The primary doses or slow-release sodium fluoride (25 mg [0.60
route of excretion of fluoride is the kidney. mmol] twice daily) combined with calcium supplemen
tation have shown lower vertebral and peripheral frac
Toxlcity ture rates (Pak et al. 1994; Prestwood et al. 1995; Resch
et al. 1993). Further research is needed to clarify the
"therapeutic window" for blood fluoride levels that is
Chronic toxicity of fluorine is called fluorosis; this
not associated with skeletal fragility or the painful
condition has increased in recent years (Pendrys and
lower extremity syndrome (Kleerekoper and Mendlovic
Katz 1989; Pendrys et al. 1994). Enamel fluorosis was
1993).
strongly associated with fluoride supplementation dur
ing the first 6 y of life and with fluoride dentifrice use
(Pendrys and Katz 1989). Fluorosis ranges from barely Suggested approaches for establishing dietary
perceptible white striations to brownish stains (Com guidance for fluoride
mittee on Nutrition 1995). The brownish mottling of
teeth is a very obvious result of excessive fluoride in Recommendations for fluoridation of the water sup
the water supply (Segreto et al. 1984). ply should consider reduction in dental caries vs. inci
Fatal fluoride intoxication was observed in hemodi- dence of enamel fluorosis. Fluoride balance data
alysis patients because of malfunction of a deionization throughout the life cycle are needed to establish opti
system used to purify dialysis solutions. With normal mal fluoride intakes.
renal function a serum fluoride of <2 //mol/L would
be expected; the hemodialysis patients who suffered
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