The body content of iron in the normal individual is regulated primarily by absorptive processes. Relatively small amounts of iron are absorbed when body stores of iron are high, and relatively large amounts when body stores are low. This regulation of iron absorption is faulty in individuals with the metabolic disorder, hemochromatosis.
Although hemochromatosis is generally considered a rare, genetically transmitted disorder, several investigators believe that a latent form of hemochromatosis may be much more common. In Sweden, where food fortification with iron is at a higher level than in the United States, and where medicinal iroin supplements are widely consumed, investigators reported several cases of hemochromatosis and iron overload in a sparsely populated district. The significance of these findings suggest that it is possible that a significant number of apparently normal and unidentified individuals might be at risk of developing liver damage from intakes of iron which are innocuous and, in fact, probably beneficial for the population at large.
It should be noted that in the United States (and probably inother industrialized countries), individuals ingesting large amounts of iron may achieve these intakes through regular consumption or iron supplements. For these individuals, food fortification contributes a relatively small fraction of total intake. The question of total intake of iron by the U.S. population and its relation to chronic iron toxicity merit further study. Monitoring of the population with respect to iron nutritional status is essential. The estimated per capita intake of 5 mg per day obtained from food fortification comprises more than one-third the total iron intake for much of the population.
Iron deficiency is a leading nutritional problem in the United States. Intakes of iron are below recommended levels for a large fraction of the population. Hence, it is evident that an increase in iron fortification of selected foods could be an important public health measure.
The form of iron utilized to fortify foods should be of adequate bioavailability. Iron forms evaluated in this report which appear to be adequately bioavailable are elemental iron (reduced, electrolytic, carbonyl), ferrous ascorbate, ferrous citrate, ferrous fumarate, ferrous gluconate, ferrous lactate, ferrous sulfate, ferric ammonium citrate, ferric chloride, and ferric citrate. In contrast, the bioavailability of ferrous carbonate, ferrous oxide, ferric oxide, ferric phosphate, ferric pyrophosphate, or ferric sodium pyrophosphate is relatively low compared with ferrous sulfate. Insufficient data are available to judge the relative bioavailability of the other iron preparations considered in this report.
Experimental data are sparse for most of the forms of iron considered in this report. Animal studies have been largely confined to determination of the acute toxicity and bioavailability of specific iron forms. Such studies have limited relevance in evaluating the possible hazards of the addition of iron to foods. Few reports are available on the effects of long-term feeding experiments. An extensive literature exists on the use of certain forms given as hematinics, but the reports are largely anecdotal and their interpretation is of questionable value. Certain compounds have been employed extensively for many years both as additions to food and in the treatment of iron deficiency with no reported adverse effects. In view of the need for, and wide use of, iron compounds, it would appear prudent to place this historical and anecdotal experience on a scientifically rigorous basis in the reasonably near future. The Select Committee emphasizes the need for well-controlled chronic feeding studies with most of the individual compounds, before confident appraisal can be made of their relative merits or hazards.
Serious deficiences exist in the experimental data or clinical experience with a number of iron compounds employed or suggested as iron fortifying agents for foods.