Preventing iron deficiency in toddlers: A major public health problem

February 1, 2003

A pediatrician argues that the prevalence and consequences of iron deficiency in the second year of life warrant a new practice: daily, prophylactic iron supplementation for 1- to 2-year-olds.


Preventing iron deficiency in toddlers:
A major public health problem

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By Alvin N. Eden, MD

In this commentary, a pediatrician argues that the prevalence and consequences of iron deficiency in the second year of life warrant a new practice: daily, prophylactic iron supplementation for children 1 to 2 years old.

The striking reduction in the prevalence of iron deficiency (ID) and iron deficiency anemia (IDA) during the first year of life has been one of the major success stories of pediatrics. This reduction has largely been the result of a rise in breastfeeding and increased use of iron-fortified infant formulas. Other significant factors include the use of infant cereals fortified with iron—as required by United States law—and the popularity of citrus juices, which contain vitamin C and thereby enhance iron absorption when taken with meals.

In cases in which ID does occur during the first year of life, the infant usually was:

  • born with low iron stores (low cord-blood ferritin levels),

  • breastfed and not supplemented with dietary iron (infant cereal) or an iron supplement (iron drops or an iron-fortified vitamin) after 6 months of age,

  • fed low-iron formula, or

  • switched to cow's milk before 12 months of age.

Among children 12 to 24 months old, the story is very different: ID and IDA are significant problems in this age group. Whereas the third National Health and Nutrition Examination Survey (NHANES III), conducted between 1988 and 1994, found that only 3% of children 1 to 2 years old had IDA (and 9% of children this age had ID),1 the Third Report on Nutrition Monitoring in the United States reported a 15% rate of anemia among 1- to 3-year-olds tested between 1988 and 1991.2 Three studies conducted more recently reported an IDA rate of about 10% among children between about 9 months and 3 years of age; the studies were carried out primarily among poor and minority groups.3–5 In one of these studies, the rate for ID among 485 children age 1 to 3 years was 35%.3

The prevalence of ID and IDA during the second year of life comes as no surprise. Less-than-adequate iron intake during the first year of life and low iron stores in utero are contributing factors. Poor iron intake between 12 and 24 months is the other main reason. NHANES III confirms what many pediatricians and parents recognize—that daily iron intake in children 1 to 2 years old is lower than in any other age group throughout life.6

Certain dietary changes that commonly occur around 1 year of age make toddlers vulnerable to ID and IDA:

  • A switch from breast milk or iron-fortified formula to regular cow's milk, which is low in iron and interferes with iron absorption.

  • Use of adult-type non-iron-fortified cereal instead of iron-fortified infant cereal.

  • Decreased appetite for solid foods with increased consumption of cow's milk, often more than 24 oz a day.

Several studies have shown that IDA during the first two years of life is clearly associated with impaired mental and psychomotor development.7–13 Two large-scale, well-controlled, prospective follow-up studies demonstrated that these deficits were long lasting and, perhaps, irreversible.14,15 [Editors' note: For additional information, see "Putting a dent in iron deficiency," in the July 2002 issue.] There is, therefore, general agreement that IDA among infants and toddlers must be prevented. But while there is consensus about how best to accomplish this during the first year of life, the same cannot be said about how to prevent IDA in children ages 1 to 2.

Whether ID without anemia also is a risk factor for impaired cognition is less clear. Do the cognitive effects of ID precede the hematologic manifestations of anemia? There is, in fact, some evidence suggesting that ID alone can adversely affect behavior and mental and psychomotor performance. Lozoff found that iron status correlated highly with mental developmental test performance in a large group of 19- to 24-month-olds.13 She showed that children who were iron deficient without being anemic scored lower than a comparable group of iron-sufficient children. Oski7 and Walter8 demonstrated that iron therapy improved Bayley Mental Developmental test scores in a group of toddlers with ID.

Tamura recently reported an association between fetal iron status and mental and psychomotor development at 5 years of age.16 Umbilical cord serum ferritin concentrations were obtained and measured at delivery. The results of this study indicated that poor iron status (low ferritin) in utero appears to be associated with diminished performance in certain mental and psychomotor tests at 5 years of age. (Serum ferritin levels are the earliest markers of ID.) No information is available related to the iron status of those children after birth to age 5.

Halterman reported the results of a large scale study of 6- to 16-year-old children who were iron deficient with or without anemia.17 Both groups scored lower in math testing as compared with a group of children who were iron replete, suggesting that the brain may be vulnerable to ID of insufficient severity to effect erythropoiesis. No information was available about the iron status of these school-age children from birth to the time of testing.

Given that about three cases of ID occur for every one case of IDA,1 results of the studies of ID without anemia and its possible association with impaired cognition suggest that millions more US children than previously thought may be at risk. These risks may begin in utero or may occur during school-age years, but they appear to be greatest during the first two years of life.

Another potential danger of ID in children younger than 2 years lies in its relationship to lead poisoning. The evidence that ID increases lead absorption has been based primarily on animal data.18,19 Studies have shown that iron-deficient animals absorb a greater percentage of ingested lead than do iron-replete animals, and that ID increases lead retention. Watson studied the oral absorption of lead and iron in adults,20 and his results indicate that iron-deficient subjects absorbed two to three times more dietary lead than those who were iron sufficient.

A number of epidemiologic studies in children support a correlation between ID and higher blood lead levels.21–23 Bradman studied 319 children, ages 1 to 5, 24% of whom were iron deficient.24 Blood lead levels were found to be higher in the children with ID than in those who were iron sufficient. He states that the mechanism for the enhanced absorption of lead is likely a substitution of Fe+2 with Pb+2 and increased active transport into the body. "Similarly," he notes, "it is possible that Pb+2 may occupy vacant Fe+2 sites in the hematopoietic system, thereby reducing lead excretion." Bradman further says that ID may modify behavior and increase pica or hand-to-mouth behavior in children, thereby increasing ingestion exposure to lead in the environment. He notes that improving iron status may help reduce blood lead levels among most children, especially those living in the most contaminated environments (old housing, low income, and minority ethnicity). The Bradman study is consistent with several studies that have reported a higher percentage of children with an elevated blood lead level among those with a low iron level.21–23,25

Wright studied 3,650 children 9 to 48 months of age from an urban, low socioeconomic primary care clinic.25 He measured their iron status and lead level and concluded that ID is significantly associated with low-level lead poisoning. He states that "further study should include the investigation of dietary iron supplementation as a secondary measure for preventing lead poisoning." The primary prevention of lead poisoning—removing it from the environment—is a major health priority because lead is so prevalent in the environment that a significant reduction in exposure is difficult and not immediately feasible. Lead-contaminated house dust is the major source of lead intake, especially during the second year of life.26 Wright states that secondary preventive measures to reduce lead absorption, such as dietary intervention, should be pursued, and that "dietary iron supplementation may limit lead absorption not only in iron-deficient children but also in those who are iron replete or only marginally iron deficient."25

The relationship between ID and increased lead absorption becomes even more significant when you consider Lanphear's recent study demonstrating that lead-associated cognitive deficits occur at lead levels below 10 µg/dL27—once thought harmless. Furthermore, he found that the IQ deficits observed with each 1 µg/dL increase in the blood lead concentration were greater at blood lead levels less than 10 µg/dL. These findings, if confirmed by others, expand the playing field enormously— indicating a much greater number of young children at risk for the dangers of increased lead absorption than previously thought—and make the case for prevention of ID even more compelling.

The recommendations of the American Academy of Pediatrics (AAP)28 to screen for anemia (based on hemoglobin or hematocrit) and then treat children in whom it is detected are, in my opinion, inadequate and often unsuccessful. The prevalence rates for ID and IDA in toddlers, especially among those in lower socioeconomic groups, are unacceptably high. There are no routine screening recommendations for ID, only for anemia, and so a large number of toddlers with ID—perhaps 30%—go undetected. As discussed, these young children are doubly at risk of neurodevelopmental impairment—from the possible damage caused by ID and from the damage from increased lead absorption associated with ID. This combined effect can be devastating and may account for many lost IQ points.

In a recent, extensive review, "Iron-Deficiency Anemia: Reexamining the Nature and Magnitude of the Public Health Problem," Grantham-McGregor and Ani conclude: "It is clear that iron deficiency identifies children at [current] and future risk of poor development."29

Evidence appears to be sufficient to support the importance of preventing ID at all ages. However, the first two years of life, a period of rapid brain growth and therefore great vulnerability to psychomotor and mental impairment from ID, is of particular importance. This also is the age when ingestion of lead, primarily from house dust, appears to be greatest. Lead levels peak during the second year, and the correlation between ID and blood lead levels has been found to be strongest among 1- to 2-year-olds.21

The ideal way to prevent ID is to offer the toddler an iron-rich diet, encouraging heme iron foods, such as red meats, poultry, and fish, in particular; the food sources of heme iron are more efficiently absorbed than those of nonheme iron (see the table). Good sources of nonheme iron include green leafy vegetables, dried fruit, and beans. Because vitamin C enhances iron absorption, offering citrus fruits and juices during meals is helpful. It is also a good idea to limit milk consumption to less than 24 oz a day, thereby reserving some appetite for iron-rich foods.

Regrettably, these dietary measures are often insufficient to prevent ID and IDA during the second year of life. In our office, we routinely recommend daily iron supplementation (10 mg) for all 1- to 2-year-olds. Results from a pilot study we conducted suggest that such supplementation is a highly effective way to prevent morbidity in high-risk populations. The supplementation regimen and pilot study are described in the box.

I do not believe it is necessary to wait for the results of a larger study to confirm our finding. The evidence is that AAP "screen-and-treat" recommendations have been unsuccessful. Recent studies of toddlers primarily from lower socioeconomic groups suggest a rate of ID of about 30%.3–5 Those affected face the potential dangers of neurodevelopmental damage from both the ID itself and the resulting increased lead absorption.

I continue to advocate for the primary prevention of ID and IDA during the second year of life with routine, daily supplementation of 10 mg of elemental iron—via iron-fortified vitamins, iron drops, or an iron-fortified nutritional drink—in 1- to 2-year-olds. The risk of long-lasting, possibly permanent mental and psychomotor impairment associated with iron deficiency in this vulnerable group makes the prevention of ID and IDA an important public health problem.


1. Looker AC, Dallman PR, Carroll MS, et al: Prevalence of iron deficiency in the United States. JAMA 1997;277:973

2. Third Report on Nutrition Monitoring in the United States. Bethesda, Md: Federation of American Societies for Experimental Biology, Life Sciences Research Office;1995:2

3. Eden AN, Mir MA: Iron deficiency in 1- to 3-year-old children: A pediatric failure? Arch Pediatr Adolesc Med 1997;151:986

4. Brugnara C, Zurakowski D, DiCanzio J, et al: Reticulocyte hemoglobin content to diagnose iron deficiency anemia in children. JAMA 1999;281:2225

5. Bogen DL, Duggan AK, Dover GJ, et al: Screening for iron deficiency anemia by dietary history in a high-risk population. Pediatrics 2000;105:1254

6. McDowell MA, Briefel RR, Alaimo K, et al: Energy and macronutrient intakes of persons ages 2 months and over in the United States: Third National Health and Nutrition Examination Survey, Phase 1, 1988-91. Hyattsville, Md., U.S. Dept. of Health and Human Services; 1994. Centers for Disease Control and Prevention Advance Data No. 258

7. Oski, FA, Honig AS, Helu B, et al: Effect of iron therapy on behavior performance in non-anemic, iron- deficient infants. Pediatrics 1983;71:877

8. Walter T, Kovalsky J, Sekel A: Effect of mild iron deficiency on infant mental development scores. J Pediatr 1983;102:519

9. Lozoff B, Britteham GM, Wolf AW, et al: Iron deficiency anemia and iron therapy: Effects on infant developmental test performance. Pediatrics 1987;79:981

10. Aukett MA, Parks YA, Scott PH, et al: Treatment with iron increases weight gain and psychomotor development. Arch Dis Child 1986;61:849

11. Idjradinata P, Pollitt E: Reversal of developmental delays in iron-deficient anaemic infants treated with iron. Lancet 1993;341:1

12. Gringulis H, Scott PH, Belton NR, et al: Combined deficiency of iron and vitamin D in Asian toddlers. Arch Dis Child 1986;61:843

13. Lozoff B, Brittenham GM, Viteri FE, et al: The effects of short-term iron therapy on developmental deficits in iron deficient anemic infants. J Pediatr 1982;100:351

14. Lozoff B, Jimenez E, Wolf AW: Long-term developmental outcome of infants with iron deficiency. N Engl J Med 1991;325:687

15. Walter T, Deandraca I, Chadud MT, et al: Iron deficiency anemia: Adverse effects on infant psychomotor development. Pediatrics 1989;84:7

16. Tamura T, Goldenberg AL, Hou J, et al: Cord serum ferritin concentrations and mental and psychomotor development of children at five years of age. J Pediatr 2001;140;165

17. Halterman JS, Kaczorowski JM, Aligne CA, et al: Iron deficiency and cognitive achievement among school-aged children and adolescents in the U.S. Pediatrics 2001;107:1381

18. Mahaffey-Six K, Goyer RA: The influence of iron deficiency on tissue content and toxicity of ingested lead in the rat. J Lab Clin Med 1972;79:128

19. Barton SC, Conrad ME, Nuby S, et al: Effects of iron on the absorption and retention of lead. J Lab Clin Med 1978;92:536

20. Watson WA, Hume R, Moore MR: Oral absorption of lead and iron. Lancet 1980;2(8188):236

21. Yip R, Dallman PR: Developmental changes in erythrocyte protoporphyrin: The roles of iron deficiency and lead toxicity. J Pediatr 1984;104:710

22. Hammad T, Saxton M, Langanberg P: Relationship between blood lead and dietary iron intake in preschool children. Ann Epidemiol 1996;8:30

23. Yip R, Norris TN, Anderson AS: Iron status of children with elevated blood lead concentrations. J Pediatr 1981;98:922

24. Bradman A, Eskenazi B, Sutton P, et al: Iron deficiency associated with higher blood lead in children living in contaminated environments. Environ Health Perspect 2001;109:1079

25. Wright RO, Shannon MW, Wright RJ, et al: Association between iron deficiency and low-level lead poisoning in an urban primary care clinic. Am J Public Health 1999;89:1049

26. Lanphear BP, Hornung R, Ho M, et al: Environmental lead exposure during early childhood. J Pediatr 2001; 140:40

27. Lanphear BP, Dietrich K, Auinger P, et al: Cognitive deficits associated with blood lead concentrations <10 mcg/dL in US children and adolescents. Public Health Rep 2000; 115:521

28. Baker SS (Ed): Pediatric Nutrition Handbook, ed 4. Elk Grove Village, Ill., American Academy of Pediatrics, 1998

29. Grantham-McGregor S, Ani C: Iron-deficiency anemia. Reexamining the nature and magnitude of the public health problem. A review of studies on the effect of iron deficiency on cognitive development in children. American Society for Nutritional Sciences 2001; (supplement): 649S

DR. EDEN is chairman, department of pediatrics, Wyckoff Heights Medical Center, Brooklyn, N.Y. He has nothing to disclose in regard to affiliations with, or financial interests in, any organization that may have an interest in any part of this article.

Sources of iron at the dining table

Heme iron
Red meats

Nonheme iron
Baked potato with skin
Bread, enriched white
Breakfast cereals, enriched and fortified
Dried fruit
Green leafy vegetables
Macaroni, enriched
Peanut butter
Prune juice
Spaghetti, enriched

Prophylactic supplementation: Preliminary results are positive

Dietary measures are often insufficient to prevent ID and IDA during the second year of life. Our office has been routinely recommending a daily iron supplement of 10 mg of elemental iron (1 mL of Polyvisol with iron) for children 12 to 24 months old as a safe and easy way to prevent iron deficiency and its consequences.

To determine the effectiveness of daily supplementation, we conducted a placebo-controlled trial of iron supplementation in a group of 1- to 2-year-olds (unpublished data). This pilot study, which involved a poor and minority population, was limited in power because of the size of the sample and therefore did not provide conclusive, statistically significant effectiveness results. However, based on our findings, we estimate that prophylactic daily supplementation reduced the incidence of IDA in the treatment group by 72%. (In the group that received iron supplementation, two of 69 children had IDA at study completion; in the control group, 5 of 48 children had IDA.)

These results suggest that prophylactic daily iron supplementation in 1- to 2-year-olds could be a highly effective and economical way of preventing morbidity in populations at high risk. I believe that a larger trial would provide more convincing, statistically significant evidence of the effectiveness of supplementation for 1- to 2-year-olds at preventing ID and, perhaps, lowering blood lead levels. Plans are being made for a multicenter study.

Offering an acknowledgment (and a tribute)

My interest in ID and IDA began 20 years ago when I listened to Frank Oski, MD, give a lecture on the subject. He got my undivided attention when he said that "the least important manifestation of IDA is the anemia itself." He went on to discuss the newly found association between ID and impaired mental and psychomotor development in infants and toddlers. Dr. Oski presented data from his own study demonstrating this relationship and made a plea to redouble the effort to prevent ID during this critical period of rapid brain growth. As was usually the case, Dr. Oski was on target. Twenty years later, the prevention of iron deficiency remains a major public health problem that has not, I believe, been adequately addressed by the pediatric community.


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Alvin Eden. Preventing iron deficiency in toddlers: A major public health problem.

Contemporary Pediatrics