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Persistence and Emergence of Anemia in Children During Participation in the Special Supplemental Nutrition Program for Women, Infants, and Children
Jennifer L. Kahn, MD;
Helen J. Binns, MD, MPH;
Tianyue Chen, MS;
Robert R. Tanz, MD;
Robert Listernick, MD
Arch Pediatr Adolesc Med. 2002;156:1028-1032.
ABSTRACT
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Context The prevalence of iron-deficiency anemia in children has decreased owing
to the provision of iron-containing infant formula and cereal and food vouchers
to children enrolled in the Special Supplemental Nutrition Program for Women,
Infants, and Children (WIC).
Objective To determine the prevalence of anemia and changes in anemia status in
children receiving WIC supplementation.
Design Retrospective cross-sectional and longitudinal analysis of information
on WIC participants. Two definitions of anemia were condisered separately:
Anemia1 and Anemia2, the latter using a more stringent definition of anemia
to avoid misclassification.
Participants Consecutive cohort of 7053 infants and children aged 6 to 59 months.
Main Outcome Measures Prevalence of anemia by age and race or ethnicity and relationship between
anemia and sex, birth weight, and weight-for-height z
score.
Results Infants aged 6 to 8 months were 3.3 times more likely to be anemic than
children aged 36 to 59 months. There was no association between anemia and
race, birth weight, sex, or weight-for-height z score.
Anemia rates were approximately halved in the more stringently defined Anemia2
group. Among children seen for at least 3 visits (n = 2926), 8.5% developed
anemia and 19.1% of initially anemic children remained anemic; an additional
6.6% developed anemia at a third visit after having had 2 normal hemoglobin
measurements.
Conclusions Anemia was common in WIC participants, with infants at highest risk.
The diagnosis of anemia in black children depends on the cutoff value used.
Despite ongoing receipt of WIC benefits, many children develop anemia or remain
anemic. Implementation of mandatory follow-up of all anemic infants by WIC
or health care providers may be warranted.
INTRODUCTION
IRON-DEFICIENCY ANEMIA occurs most commonly in children aged 9 to 18
months and can have lasting effects on cognitive development.1-4
The prevalence of iron-deficiency anemia has decreased dramatically during
the past few decades, likely because of a national increase in breastfeeding,
standardization of the composition of iron-fortified formulas, and delay in
the introduction of whole milk until age 1 year. By providing participants
with iron-fortified formula and cereal and vouchers for iron-containing foods
the Special Supplemental Nutrition Program for Women, Infants, and Children
(WIC) has also played a substantial role in this decline.5
Infants and children 5 years and younger are eligible for enrollment
in WIC if family income is below 185% of the US Poverty Income Guidelines
and if they are at nutritional risk. Nutritional risk may be medically based,
such as being anemic or underweight, or diet based, such as an inadequate
diet. To prove nutritional risk, participants must provide a 24-hour diet
history, recent weight and height, and a recent hemoglobin or hematocrit level.
There is national variability in the frequency of blood tests required for
WIC participation. In 1998, the US Department of Agriculture, which oversees
the WIC program, recommended that all state WIC agencies follow the Centers
for Disease Control and Prevention (CDC) recommendation to screen for anemia
once between ages 9 and 12 months, once 6 months later, and then annually
from ages 2 to 5 years.6 Illinois requires
anemia screening every 6 months for WIC recertification.
Using a computer database of WIC participants from 3 Chicago sites,
we examined the prevalence and persistence of anemia. We sought to identify
factors, such as sex, age, race or ethnicity, birth weight, and weight for
height, that could be used to focus anemia screening in this population. In
addition, we hypothesized that anemic children identified by the WIC program
would develop normal hemoglobin concentrations over time.
METHODS
In 1995, Illinois implemented Project Cornerstone, a computer database
used to maintain WIC participant visit information, including demographics,
anthropometric data, and laboratory test results. We analyzed Project Cornerstone
data for all infants and children aged 6 months to 5 years who visited any
of 3 Chicago WIC sites between March 3, 1997, to March 2, 1999. The Illinois
Department of Public Health and the administrators of the WIC sites from which
the data were obtained made this anonymous data set available to us.
The analytic data set included the following variables: date of birth,
date of visit, race, ethnicity, hemoglobin level, hematocrit level, date of
hemoglobin and hematocrit measurement, weight, height, and birth weight. For
each child, a race or ethnicity variable was determined: Hispanic, non-Hispanic
black, non-Hispanic white, or other. Only visits with a hemoglobin measurement
when the child was aged 6 to 59 months were considered in analyses. Only hemoglobin
values were used (rather than hemoglobin and hematocrit levels) because most
visits did not have a recorded hematocrit value. Furthermore, visit data were
excluded if the date of the hemoglobin test reported for that visit was after
the visit date or if the hemoglobin value was outside an extreme range (<5.0
and >20.0 g/dL). Data from a subsequent visit that was within 3 months of
a previous visit were excluded. Extreme birth weight values (<500 or >6000
g) were considered suspect and were excluded from analysis.
Height and weight measurements were taken at health care provider visits
and were recorded on forms presented at the time of the WIC visits. Measurement
percentiles and z scores were determined using Epi
Info software.7 Computed weight-for-height z scores for each child were compared across visits. Anthropometric
data on children with a z score change greater than
1 between consecutive visits (suggesting a spurious measurement) were excluded.
Anthropometric data on children who had only 1 visit were not considered in
the analyses.
Data were grouped by age at first measurement in the study using 2 methods.
The first grouping method, 6 to 23 and 24 to 59 months, follows the age separation
used by WIC and the CDC to define their cutoff values for anemia. The second
grouping method, 6 to 8, 9 to 23, 24 to 35, and 36 to 59 months, was used
to examine age trends that might affect the development of anemia. In analyses
involving race or ethnicity, only 3 race or ethnicity groups were considered:
Hispanic, non-Hispanic black, and non-Hispanic white. Initial analyses examined
data cross-sectionally and included only a first visit for each child in the
data period.
The data were analyzed using 2 definitions of anemia. First, the national
WIC hemoglobin cutoff values of less than 11.0 g/dL for children aged 6 to
23 months and less than 11.1 g/dL for children aged 24 to 59 months were used
for all children. In addition, non-Hispanic black children were evaluated
using the CDC recommended cutoff value for non-Hispanic black children (<10.6
g/dL for children aged 6-23 months and <10.7 g/dL for those aged 24-59
months). These data sets were designated Anemia1. Second, a more stringent
hemoglobin cutoff value to define anemia was used for each group of children
(Hispanic and non-Hispanic white children: <10.5 g/dL at 6-23 months and
<10.6 g/dL at 24-59 months; and non-Hispanic black children: <10.1 g/dL
at 6-23 months and <10.2 g/dL at 24-59 months) to avoid misclassification
of patients.5 These data sets were designated
Anemia2. The binomial proportion test was used to evaluate the change in percentage
of anemia between the 2 definitions.  2 Tests were used to
investigate associations between categorical variables. The Mantel-Haenszel
test was used to examine an association between anemia and the 4 age groups
because age group was an ordinal variable in the analyses. For all analyses,
statistical significance was defined as P<.05.
Logistic regression models were used to determine the relationship between
anemia and the following independent variables: sex, race or ethnicity (Hispanic,
non-Hispanic black, and non-Hispanic white), age group (6-8, 9-23, 24-35,
and 36-59 months), birth weight (<2500 vs  2500 g), and weight-for-height z score. Data were also evaluated longitudinally to determine
the incidence of anemia over multiple visits and the utility of anemia at
the first visit to predict anemia at later visits. Approval for this study
was obtained from the institutional review board of Children's Memorial Hospital.
RESULTS
The initial data set included 7065 infants and children aged 6 to 59
months who had 17 283 visits for which a hemoglobin measure (valid or
not) was recorded. After review of the data, 243 visits were excluded for
the following reasons: extreme hemoglobin values (n = 68), an inappropriately
short interval (<3 months) between visits (n = 107), and the date of the
laboratory test was reported to be after the WIC visit (n = 68). Thus, 7053
children with 17 040 visits were included in the analysis. The demographics
of the children and the characteristics of the visits are given in Table 1.
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Demographic and Visit Characteristics of 7053 Infants and Children
Receiving WIC Supplementation*
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CROSS-SECTIONAL ANALYSES
Figure 1 demonstrates the
distribution of the hemoglobin values of the non-Hispanic black children compared
with those of all the Hispanic and non-Hispanic white children. When the CDC
cutoff value for anemia for black children was used, the percentage of non-Hispanic
black children defined as anemic decreased statistically significantly to
8.0%, compared with 15.8% using the WIC cutoff value (binomial proportion
test, P<.001). In the univariate analyses, only
age was statistically significantly associated with Anemia1 (2, P = .01); sex, race or ethnicity, birth weight, and weight-for-height z score were not associated with anemia. Anthropometric
data for 2.2% of the children were excluded from analysis owing to changes
in the weight-for-height z scores in excess of 1
SD between 2 visits.
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Figure 1. Distribution of the hemoglobin
values of non-Hispanic black children vs all other children.
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Anemia1 Group
Using the less restrictive definition, anemia was more common in the
6- to 23-month-old children than those aged 24 to 59 months (17.9% vs 11.7%; 2, P = .001). The prevalence of anemia at the
first visit in the 4 previously defined age groups is shown in Figure 2; there was an inverse relationship between anemia and age
(Mantel-Haenszel, P<.001). Children aged 6 to
8 months were 3.3 times more likely than children aged 36 to 59 months to
be anemic (95% confidence interval [CI], 2.4-4.5). Children aged 9 to 23 months
and 24 to 35 months were each at 2.0 times greater risk than 36- to 59-month-old
children (9-23 months: 95% CI, 1.4-2.8; 24-35 months: 95% CI, 1.3-2.8).
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Figure 2. Prevalence of anemia in the Anemia1
and Anemia2 groups stratified by age using the first hemoglobin value in the
study. For definitions of the Anemia1 and Anemia2 groups, see the "Methods"
section.
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Anemia2 Group
Using the more restrictive definition, anemia at the first visit was
more common in 6- to 23-month-old children than in those aged 24 to 59 months
(9.0% vs 5.2%; 2, P = .001). The
prevalence of anemia in the 4 previously defined age groups is shown in Figure 2; an inverse relationship between
anemia and age existed in this subgroup of patients as well (Mantel-Haenszel, P<.001). Children aged 6 to 8 months were 3.3 times
more likely than those aged 36 to 59 months to be anemic (95% CI, 2.4-4.7).
Children aged 9 to 23 months and 24 to 35 months were each at 2.0 times greater
risk than 35- to 59-month-old children (9-23 months: 95% CI, 1.4-2.9; and
24-35 months: 95% CI, 1.3-2.9).
LONGITUDINAL ANALYSES
We next examined the longitudinal changes in the incidence and persistence
of anemia by age and race using only data from children who had at least 3
visits during the study (n = 2926). Figure
3 displays these longitudinal changes using both the less and more
stringent definitions of anemia for children aged 6 to 23 months; Figure 4 displays similar data for children
aged 24 to 59 months. The 6- to 23-month-old children were more likely than
those aged 24 to 59 months to remain anemic or to develop anemia at a second
visit after having had an initial normal hemoglobin concentration using either
definition (P = .001). However, there was a great
deal of crossover between the anemic and nonanemic states in both age groups
regardless of the definition of anemia used. Race was not a significant factor
in predicting which children would either remain anemic or develop anemia
during the study.
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Figure 3. Crossover between normal and anemic
states during 3 visits in 6- to 23-month-olds. Only children who had at least
3 visits are included. Anemia1 data are listed first and Anemia2 data are
listed in parentheses. For definitions of the Anemia1 and Anemia2 groups,
see the "Methods" section.
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Figure 4. Crossover between normal and anemic
states during 3 visits in 24- to 59-month-olds. Only children who had at least
3 visits are included. Anemia1 data are listed first and Anemia2 data are
listed in parentheses. For definitions of the Anemia1 and Anemia2 groups,
see the "Methods" section.
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Anemia1 Group
In the 6- to 23-month age group, anemia developed in 11.5% of the children
at the second visit and in an additional 7.1% (113 of 1585 children) at the
third visit. Approximately one third of the children who were anemic at either
the first or second visit remained anemic at the subsequent visit. Moreover,
6.6% of the children (113 of 1402 in the 6- to 23-month-old group and 35 of
807 in the 24- to 59-month-old group) who had 2 previous normal hemoglobin
measurements developed anemia at a third visit, and 1.8% (40 of 1927 in the
6- to 23-month-old group and 6 of 999 in the 24- to 59-month-old group) remained
anemic for 3 consecutive visits.
Anemia2 Group
Using the more stringent definition, anemia developed in 6.4% of the
nonanemic 6- to 23-month-old children at the second visit and in an additional
3.9% (68 of 1757 children) at the third visit. Nearly 19% of initially anemic
children in both age groups remained anemic at the second visit, and nearly
one third of these children were still anemic at the third visit.
The mean (SD) time between the first and second visits was 6.9 (2.5)
months; the mean (SD) time between the second and third visits was 6.8 (1.7)
months. Using Anemia1 definitions, we looked at the changes in hemoglobin
concentration for children who had at least 2 visits (n = 6103). Children
who had a normal hemoglobin measurement at a first visit and who were anemic
at a second visit had a mean (SD) decrease in hemoglobin concentration of
1.6 (1.2) g/dL; they were below the WIC cutoff value by a mean (SD) of 0.7
(0.7) g/dL. Of 505 children who had a normal hemoglobin level at the first
visit and who became anemic at any subsequent visit, 77.4% were less than
1.0 g/dL below the WIC cutoff value. Of children who were first anemic at
the third or fourth visit after having had a normal hemoglobin level at the
previous visit, 78.9% and 86.7%, respectively, were still within 1.0 g/dL
of the cutoff value.
COMMENT
The prevalence of anemia in this population was as high as 17.9% in
selected subgroups. By a second visit, 10.7% of children had developed anemia,
and 30.5% of initially anemic children remained anemic while participating
in WIC. Most anemic children, however, were below the cutoff value by less
than 1.0 g/dL of hemoglobin. Although their anemia may represent iron deficiency,
this can only be an assumption without further assessment of iron status.
Factors that have been thought to contribute to WIC's success in lowering
anemia in the past include (1) improved iron intake owing to the receipt of
vouchers for iron-containing foods, (2) extensive nutrition counseling, and
(3) frequent screening for anemia.5 Contrary
to our hypothesis, many children in the longitudinal analyses either developed
anemia or remained anemic over time, indicating that participation in WIC
may be less effective in preventing and treating anemia than previously reported.
Several potential reasons for these findings exist. First, although
WIC participants are encouraged to attend 2 nutrition education sessions in
each 6-month period to be recertified, the efficacy of this education has
not been well established. Second, children in WIC who are anemic are encouraged,
but not required, to seek medical attention for appropriate treatment. Although
health care providers perform hemoglobin testing, there is no system in place
that ensures that families return to a physician for needed therapy. Finally,
the choice of an appropriate definition of anemia may partly explain its high
prevalence in our population. We chose a conservative approach and used the
WIC cutoff value for anemia for Hispanic and non-Hispanic white children and
the CDC's lower definition of anemia for non-Hispanic black children. Because
most of the children who became anemic in this study had levels less than
1.0 g/dL below the WIC cutoff value, many may have been only transiently anemic
and misclassified as such. In addition, the relationship between anemia and
iron deficiency in this cohort is unknown. Intercurrent illnesses may have
contributed to the anemia in some children.8
Determining an effective screening test for iron deficiency in children
has proved to be difficult. Screening for iron-deficiency anemia in high-risk
children using dietary and health history, as recommended by the Institute
of Medicine and the CDC, has been shown to have only modest sensitivity and
poor specificity.9 As anemia is a late manifestation
of iron deficiency, children may be iron deficient and have normal hemoglobin
or hematocrit values.10 Although hemoglobin
and hematocrit measurements are well standardized and easily performed, they
are not ideal screening tests for iron deficiency, especially if used alone
without the aid of other red blood cell indices such as the mean cell volume
or the red blood cell distribution width.
New strategies need to be implemented to ensure follow-up and treatment
of anemia. One such strategy could be to require proof of physician awareness
and treatment of anemia for WIC recertification. Alternatively, formation
of a multistep screening process might be developed in which recertification
of an anemic child would require measurement of either serum ferritin or complete
red blood cell indices. A recent position paper by the Provisional Section
on Breastfeeding of the American Academy of Pediatrics11
highlighted the need to establish uniform procedures within WIC that would
ensure the medical follow-up and treatment of anemic children. Perhaps even
more controversial would be relocation of the WIC program out of the Department
of Agriculture and into the Department of Health and Human Services, where
mandatory linkages between WIC sites and health clinics might ensure closer
follow-up and treatment.
In conclusion, despite frequent screening, food supplementation, and
nutritional counseling, the prevalence of anemia among infant and child WIC
participants was high. Very young children were at highest risk. A significant
percentage of WIC recipients either developed anemia or remained anemic while
enrolled in the program. These data support the use of a frequent screening
strategy, such as that recommended by the CDC, in this high-risk population.
Consideration should be given to implementation of mandatory follow-up by
WIC or health care providers of all anemic infants to ensure accuracy of the
diagnosis and, for most, repletion of their iron stores and resolution of
their anemia.
| What This Study Adds
Previous studies have shown that the prevalence of iron-deficiency anemia
has decreased substantially because of the provision of iron-containing infant
formula and cereal to children enrolled in WIC. The utility of repeated measurements
of hemoglobin concentrations while receiving WIC supplementation has not been
addressed. This study shows that many children either develop anemia or remain
anemic while receiving WIC benefits. This highlights the need for mandatory
follow-up by WIC.
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AUTHOR INFORMATION
Accepted for publication May 29, 2002.
This study was presented in part at the Midwest Society for Pediatric
Research Annual Meeting, Chicago, Ill, September 17, 1999, and at the Pediatric
Academic Societies Annual Meeting, Boston, Mass, May 15, 2000.
We thank Erlinda Binghay, RD, MPH, of the Near North Health Corp in
Chicago for assistance in obtaining the data set.
Corresponding author: Robert Listernick, MD, Division of General
Academic Pediatrics, Children's Memorial Hospital, Box 16, 2300 Children's
Plaza, Chicago, IL 60614 (e-mail: boblist{at}northwestern.edu).
From the Department of Pediatrics, Feinberg School of Medicine, Northwestern
University (Drs Kahn, Binns, Tanz, and Listernick), and the Division of General
Academic Pediatrics (Drs Binns, Tanz, and Listernick) and the Children's Memorial
Institute for Education and Research, Child Health Research Core (Dr Binns
and Ms Chen), Children's Memorial Hospital, Chicago, Ill.
REFERENCES
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1. Walter T, Kovalskys J, Stekel A. Effect of mild iron deficiency on infant mental development scores. J Pediatr. 1983;102:519-522.
FULL TEXT
|
ISI
| PUBMED
2. Pollitt E. Nutrition and intellectual performance. Clin Nutr. 1986;5:219-225.
3. Lozoff B, Jimenez E, Wolf A. Long-term development outcome of infants with iron deficiency. N Engl J Med. 1991;325:687-694.
ABSTRACT
4. Pollitt E. Iron deficiency and cognitive function. Annu Rev Nutr. 1993;13:521-537.
FULL TEXT
|
ISI
| PUBMED
5. Yip R, Binkin NJ, Fleshood L, Trowbridge FL. Declining prevalence of anemia among low-income children in the United
States. JAMA. 1987;258:1619-1623.
FREE FULL TEXT
6. Special Supplemental Nutrition Program for Women, Infants, and Children
(WIC): bloodwork requirements. 63. Federal Register 64211-64215 (1998).
7. Dean AG, Dean JA, Coulombier D, et al. Epi Info, Version 6: A Word-Processing, Database,
and Statistics Program for Public Health on IBM-Compatible Microcomputers. Atlanta, Ga: Centers for Disease Control and Prevention; 1995.
8. Abshire TC. The anemia of inflammation: a common cause of childhood anemia. Pediatr Clin North Am. 1996;43:623-637.
FULL TEXT
|
ISI
| PUBMED
9. Bogen DL, Duggan AK, Dover GJ, Wilson MH. Screening for iron deficiency anemia in a high-risk population. Pediatrics. 2000;105:1254-1259.
FREE FULL TEXT
10. Kazal LA Jr. Failure of hematocrit to detect iron deficiency in infants. J Fam Pract. 1996;42:237-240.
ISI
| PUBMED
11. American Academy of Pediatrics, Provisional Section on Breastfeeding. WIC program. Pediatrics. 2001;108:1216-1217.
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