Ó 2006 Wiley-Liss, Inc.

Birth Defects Research (Part A) 76:706–713 (2006)

Racial Differences in Infant Mortality Attributable

to Birth Defects in the United States, 1989–2002
Quanhe Yang,1 Huichao Chen,2 Adolfo Correa,1 Owen Devine,1 T.J. Mathews,3 and Margaret A. Honein1
1
National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention (CDC), Atlanta, Georgia
2
Department of Biostatistics, Emory University, Atlanta, Georgia
3
National Center for Health Statistics, Centers for Disease Control and Prevention (CDC), Hyattsville, Maryland
Received 13 February 2006; Revised 24 June 2006; Accepted 30 June 2006

BACKGROUND: The objective is to study racial differences in infant mortality attributable to birth defects
(IMBD) in the United States. METHODS: We analyzed 1989–1991 and 1995–2002 linked birth/death files for
trends and racial differences in IMBD by selected categories of birth defects for infants of non-Hispanic white,
non-Hispanic black, and Hispanic mothers. RESULTS: In 1989–2002, the IMBD rates declined. However, the
decline in postneonatal mortality attributable to birth defects (PMBD) rate was significantly slower than that
of overall postneonatal mortality. The adjusted rate ratio for non-Hispanic black and Hispanic versus non-His-
panic white for neonatal mortality attributable to birth defects (NMBD) remained unchanged from 1989–1991
through 2000–2002. For PMBD, it increased from 0.97 (95% confidence interval [CI], 0.90–1.13) in 1989–1991 to
1.12 (95% CI, 1.04–1.21) in 2001–2002 and from 1.08 (95% CI, 1.00–1.16) to 1.18 (95% CI, 1.10–1.27) for non-His-
panic black and Hispanic, respectively. Infant mortality due to cardiovascular and central nervous system
defects were the main contributors to the increased racial disparities in PMBD rates. CONCLUSIONS: The dis-
parity in PMBD between infants of non-Hispanic black and Hispanic mothers and infants of non-Hispanic
white mothers increased significantly from 1989–1991 to 2000–2002. Further studies are needed to assess the
extent to which delays in care or lack of access to care for infants with birth defects might be contributing to
the disparity in IMBD. Birth Defects Research (Part A) 76:706–713, 2006. Ó 2006 Wiley-Liss, Inc.

Key words: birth defects; infant mortality; racial disparity

INTRODUCTION in racial disparities between non-Hispanic black, His-

Birth defects account for approximately 23.4% of infant
mortality among infants of non-Hispanic white and His-
panic mothers and 12.3% of infant mortality among
infants of non-Hispanic black mothers (Mathews et al.,
2004). Infant mortality rates declined in the United States
every year from 1958 through 2001 (Luke et al., 1993;
Singh and Yu, 1995; Mathews et al., 2004). However,
infant mortality attributable to birth defects (IMBD)
declined at a slower pace compared with the overall
decline in infant mortality rate since 1970 (Centers for Dis-
ease Control and Prevention, 1998; Lee et al., 2001). The
slower decline in IMBD has made birth defects an increas-
ingly important component of infant mortality in the
United States (Lee et al., 2001; MacDorman et al., 2005).
Racial differences in overall infant mortality between
infants of non-Hispanic black and non-Hispanic white
mothers have persisted and remained largely unchanged
since 1990, with an average infant mortality rate approxi-
mately 2.4 times higher among infants of non-Hispanic
black mothers than among infants of non-Hispanic white
mothers (Mathews et al., 2004). However, temporal trends
panic, and non-Hispanic white in IMBD have not been
studied, nor have the major categories of birth defects
contributing to these disparities been described. This
study focused on: 1) examining the trend for the neonatal
and postneonatal IMBD rate for 1989–2002 and the major
birth defects categories that contributed to the changes in
the IMBD rate by racial groups, and 2) examining the
trend of racial differences in neonatal and postneonatal
IMBD and the major birth defects categories that contrib-
uted to the changes in the racial differences in IMBD for
1989–2002.
The findings and conclusions in this report are those of the authors and do
not necessarily represent the views of the CDC.
Correspondence to: Quanhe Yang, National Center on Birth Defects and De-
velopmental Disabilities, Centers for Disease Control and Prevention (CDC),
1600 Clifton Road, Mail-Stop E-86, Atlanta, GA 30333. E-mail: qay0@cdc.gov
Published online 4 October 2006 in Wiley InterScience (www.interscience.
wiley.com).
DOI: 10.1002/bdra.20308

Birth Defects Research (Part A): Clinical and Molecular Teratology 76:706–713 (2006)
 RACIAL DIFFERENCES IN BIRTH DEFECT MORTALITY
MATERIALS AND METHODS
Data
For this study, we used linked infant birth/death data for
the periods 1989–1991 and 1995–2002 produced and main-
tained by the Centers for Disease Control and Prevention
(CDC)’s National Center for Health Statistics (Kochanek
et al., 2004; Mathews et al., 2004). The linked infant birth/
death data were not available for the 1992–1994 period. In-
formation on all live births and the underlying cause-of-
death of all infants (children aged less than 1 year) was
obtained from the linked files. We restricted our analysis to
birth defects coded as the underlying cause-of-death on the
linked files (National Center for Health Statistics, 2006). For
the linked infant birth/death data (1995–2002), a small per-
centage of infant death records (approximately 1–3%)
could not be linked to their corresponding birth certificates.
A weight was applied for all infant deaths to compensate
for unlinked records to obtain national estimates of infant
mortality and IMBD rates (Mathews et al., 2004).
From 1989 through 1998, birth defects were classified ac-
cording to the Manual of the International Statistical Classi-
fication of Diseases, Injuries, and Causes of Death, Ninth
Revision (ICD-9) (World Health Organization, 1977) codes
740–759. From 1999 onward, the International Statistical
Classification of Diseases and Related Health Problems,
Tenth Revision (ICD-10) (World Health Organization, 1992)
was implemented and the corresponding birth defects
codes were Q00-Q99. Using 1996 mortality data, National
Center for Health Statistics carried out a comparability, or
‘‘bridge-coding,’’ study by dual-coding deaths to both the
ICD-9 and ICD-10. The results of this exercise were used to
generate comparability ratios; these ratios measure the net
effect of the new revision, with ratios above 1.0 indicating a
net increase in deaths classified to a cause of death, and
ratios below 1.0 indicating a net decrease (Anderson et al.,
2001). To account for this coding change, we calculated
birth defect–specific ICD-9 and ICD-10 comparability ratios
for the 3 largest racial/ethnic groups (non-Hispanic white,
non-Hispanic black, and Hispanic) and the 3 largest birth
defect categories (Hoyert, 2003). These comparability ratios
were applied to the 1989–1991 and 1995–1998 trend data
using the same method as in Anderson et al. (2001).
We present IMBD analysis by race, Hispanic origin, and
state of residence of mother. For the linked files, the race
of the mother from the birth certificate was used in both
the numerator (deaths) and denominator (births) files. The
race/ethnicity information reported on birth certificates
was considered to be more accurate than that on the death
certificate (Rosenberg et al., 1999). Only births and deaths
to United States residents were included in the analyses.
We present IMBD analysis by neonatal and postneona-
tal mortality separately. Neonatal mortality is defined as
death from birth to 27 days of age and postneonatal mor-
tality from 28 days to less than 1 year of age. The rates of
IMBD were calculated by dividing the number of birth de-
fects deaths (underlying cause of death) by the total num-
ber of live births. We restricted our trend analysis to the
total IMBD rate and the 3 most common categories of birth
defects: cardiovascular system (ICD-9, 745–747; ICD-10,
Q20-Q28), central nervous system (CNS) (ICD-9, 740–742;
ICD-10, Q00-Q07), and chromosomal abnormalities (ICD-9,
758; ICD-10, Q90-Q99). Among all infant deaths, we ex-
cluded conditions that are considered normal conditions of
prematurity: patent ductus arteriosus (747.0, Q25.0), persis-
707
tent foramen ovale (745.5, Q21.1), and lung hypoplasia
(748.5, Q33.6).
Statistical Analysis
Poisson regression was used to examine the time trend
of the IMBD rate during the 1989–1991 and 1995–2002 peri-
ods. To measure time trends, log infant mortality and
IMBD rates were represented as a function of calendar
year. The model used for the time trend had the basic form:
log (rate) ¼ b0 þ b1* (year-1989), where b0 was the log
infant mortality or IMBD rate in 1989, the first year of the
study, and b1 the annual time trend parameter. The de-
pendent variable in the Poisson regression was the log of
the count of infant deaths with the log of the number of
live births used as an offset variable. The estimated annual
percentage change (EAPC) of neonatal and postneonatal
mortality rates and IMBD rate was obtained by 100*
(exp(b1)
1).
To quantify the racial differences in IMBD, we used
Poisson regression to estimate adjusted race-specific rate
ratios (and 95% CI). The Poisson regression model to esti-
mate the adjusted rate ratios was similar to that of the
time trend model, except for replacing the calendar year
variable with the race/ethnicity variable (non-Hispanic
black, Hispanic, and non-Hispanic white; non-Hispanic
white served as reference category) and adjusting for birth
weight (<1500 gm, 1500–2499 gm, and 2500 gm), ade-
quacy of prenatal care (with adequate prenatal care vs.
without adequate care), and plurality (singleton vs. multi-
ple births); the rate ratio was obtained by exp(b1)
(Rothman and Greenland, 1998). A rate ratio of greater
than 1 indicated that the rate of IMBD among non-His-
panic blacks or Hispanics was greater than that among
non-Hispanic whites and vice-versa. To examine the
changes in rate ratios during the period of study, we cal-
culated and presented the adjusted rate ratios for 1989–
1991 and 2000–2002, pooling the first and the last 3 years
to provide stable estimates. We also examined the trend in
race-specific adjusted rate ratios for IMBD from 1989–1991
to 1995–2002. In this analysis, we pooled 2 years of data
(i.e., 1990–1991, 1995–1996, and so on) to obtain stable esti-
mates. For 1992–1994, for which the linked infant birth/
death data were not available, we used linear interpola-
tion to connect 1990–1991 and 1995–1996 rate ratio for
illustrating the trend for the figures only. Finally, to assess
the possible effect of changes from ICD-9 to ICD-10 on
adjusted rate ratios, we presented data in both unadjusted
and comparability ratio adjusted forms to account for possi-
ble differences in classification between ICD-9 and ICD-10.
RESULTS
For the periods 1989–1991 and 1995–2002, the linked in-
fant birth/death files contained 44,024,960 live births and
70,450 IMBD deaths. We deleted 6.8% of live births and
5.7% of IMBD because of: 1) missing information on race/
ethnicity; 2) nonreporting of Hispanic origin for New
Hampshire (NH), Oklahoma (OK), and Louisiana (LA) in
1989, NH and OK in 1990, and NH in 1991; 3) mother’s
race/ethnicity not 1 of the 3 categories being studied; or 4)
non-U.S. resident at the time of delivery. We also excluded
13.5% of IMBD deaths with conditions coded as the under-
lying cause of death that are considered normal conditions
of prematurity. Of the 41,040,346 live births remaining for
Birth Defects Research (Part A) 76:706–713 (2006)
708 YANG ET AL.

Table 1
Estimated Annual Percent Change (EAPC) and 95% CI of Neonatal and Postneonatal Mortality Rate and Mortality
Rate Attributable to Birth Defects (Underlying Cause-of-Deaths) (per 10,000 Live Births) by Race/Ethnicity of
Mother and Major Categories of Birth Defects 1989–1991 and 1995–2002, United States
Total neonatal mortality Total postneonatal mortality
EAPC of mortality EAPC of mortality
Birth defects by race/ethnicity rate (%) (1989–2002)* 95% CI rate (%) (1989–2002)* 95% CI
Total
2.5 (
2.7,
2.4)
4.4 (
4.6,
4.2)
Non-Hispanic White
2.3 (
2.5,
2.1)
4.3 (
4.5,
4.0)
Non-Hispanic Black
2.3 (
2.5,
2.0)
3.7 (
4.1,
3.4)
Hispanic
2.9 (
3.2,
2.6)
5.0 (
5.4,
4.5)
Total due to birth defects
2.5 (
2.8,
2.4)
2.0 (
2.5,
1.5)
Non-Hispanic White
2.7 (
3.0,
2.3)
2.8 (
3.4,
2.2)
Non-Hispanic Black
1.6 (
2.3,
0.8)
0.3 (
1.3, 0.8)
Hispanic
2.9 (
3.6,
2.2)
2.1 (
3.1,
1.0)
Cardiovascular system
6.4 (
7.0,
5.9)
3.7 (
4.3,
3.1)
Non-Hispanic White
6.7 (
7.3,
6.0)
4.6 (
5.4,
3.8)
Non-Hispanic Black
6.6 (
7.9,
5.4)
1.5 (
2.9,
0.1)
Hispanic
5.0 (
6.3,
3.7)
3.3 (
4.7,
1.8)
Central nervous system
4.2 (
4.9,
3.4)
3.0 (
4.4,
1.6)
Non-Hispanic White
4.2 (
5.2,
3.3)
3.5 (
5.4,
1.6)
Non-Hispanic Black
1.7 (
3.7, 0.3)
2.8 (
5.7,
0.2)
Hispanic
6.9 (
8.3,
5.4)
3.0 (
5.9,
0.0)
Chromosomal abnormalities 2.4 (1.7, 3.2)
1.9 (
3.0,
0.7)
Non-Hispanic White 2.8 (1.9, 3.7)
3.4 (
4.9,
1.9)
Non-Hispanic Black 3.8 (1.8, 5.8) 2.4 (
0.1, 5.0)
Hispanic 0.2 (
1.5, 1.9)
2.8 (
5.1,
0.3)
We excluded New Hampshire, Oklahoma and Louisiana in 1989, New Hampshire and Oklahoma in 1990 and New Hampshire
in 1991 because the Hispanic origin was not reported in these states.
*The annual percentage change was estimated by using data from 1989–1991 and 1995–2002 and the race–birth defects–specific
comparability ratios were applied to 1989–1991 and 1995–1998 data.

analysis, 64.6% were non-Hispanic white, 16.2% non-His-
panic black, and 19.2% Hispanic. For the remaining 57,498
IMBD deaths, 62.3% were non-Hispanic white, 19.6% were
non-Hispanic black, and 18.2% Hispanic. Neonatal mortal-
ity attributable to birth defects (NMBD) accounted for
69.3% (n ¼ 39,838) of the total IMBD. The 3 most common
categories of birth defects (cardiovascular, CNS, and chro-
mosome abnormalities) accounted for 67.0% (n ¼ 26,670) of
total NMBD and 79.3% (n ¼ 14,009) of total postneonatal
mortality attributable to birth defects (PMBD).
We present comparability ratio adjusted IMBD rates for
trend analysis because the implementation of ICD-10 cre-
ated a significant discontinuity in trends of birth defects
deaths (Hoyert, 2003). However, for racial disparity analy-
sis, we focus on rate ratio unadjusted for comparability
ratios because the rate ratio measures the association cross-
sectionally.
Neonatal Mortality Attributable to Birth Defects
During the 1989–1991 and 1995–2002 periods, the esti-
mated annual percentage decline in neonatal mortality rate
from all causes was 2.5% (95% CI, 2.7-2.4%) and in NMBD
2.5% (95% CI, 2.8-2.4%). The rate of decline varied by race/
ethnicity. Infants of non-Hispanic black mothers had a
slower annual percentage decline in NMBD (1.6%; 95% CI,
2.3-0.8%) compared with non-Hispanic white, while the
declines observed for infants of non-Hispanic white and
Hispanic mothers were similar to the total (Table 1). The
rate for chromosome abnormalities increased for non-His-
panic black and non-Hispanic whites (Table 1).
Birth defects of the cardiovascular system were the largest
group of NMBD, accounting for 27.5% of NMBD in 2000–
2002 (Table 2). Chromosomal abnormalities were the sec-
ond largest group (22.4% of NMBD), followed by deaths
affecting the CNS (15.6% of NMBD). No clear patterns of
NMBD changes emerged from the rest of the birth defects
categories, and the average annual percentage changes for
these birth defects were <0.5% (results not shown).
Among non-Hispanic blacks, the adjusted rate ratio of
NMBD compared with non-Hispanic whites was similar in
1989–1991 and 2000–2002, and was significantly lower than
that of non-Hispanic whites (Table 2). The adjusted rate
ratios for the 3 largest groups of birth defects were also
lower than that of non-Hispanic whites. For Hispanics,
birth defects of the CNS showed persistent elevated
adjusted rate ratios in the 1989–1991 and 2000–2002 periods,
though the difference was narrowed over time (Table 2).
The trends in the adjusted rate ratios from 1989–1991
through 1995–2002 among non-Hispanic blacks relative to
non-Hispanic whites remained unchanged over time and
did not vary significantly by the type of birth defect (Fig.
1a and b). Among Hispanics, the adjusted NMBD rates
were similar to the rates of non-Hispanic whites, but the
adjusted CNS rates were significantly higher through the
period of study (Fig. 1c and d).
Postneonatal Mortality Attributable to Birth
Defects
During the 1989–1991 and 1995–2002 periods, the aver-
age annual percentage decline in the postneonatal mortal-
ity rate from all causes was 4.4% (95% CI, 4.6-4.2%) and
for PMBD was 2.0% (95% CI, 2.5-1.5%). The decline in
PMBD rates among non-Hispanic black infants was not
significant (Table 1).

Birth Defects Research (Part A) 76:706–713 (2006)

 RACIAL DIFFERENCES IN BIRTH DEFECT MORTALITY 709

Table 2
Adjusted Rate Ratio and 95% CI of Neonatal Mortality Rate and Neonatal Mortality Rate Attributable to Birth
Defects (NMBDs) (per 10,000 Live Births) by Race/Ethnicity of Mother and Major Categories of Birth Defects
1989–1991 versus 2000–2002, United States
Unadjusted for comparability Comparability ratio adjusted
ratio (1989–1991) (1989–1991) 2000–2002
Birth defects by Mortality rate per Rate ratio* Mortality rate per Rate ratio* Mortality rate per Rate ratio*
race/ethnicity 10,000 live births (95% CI) 10,000 live births (95% CI) 10,000 live births (95% CI)
Total neonatal mortality 57.3 57.3 46.3
Non-Hispanic White 45.9 — 45.9 — 38.1 —
Non-Hispanic Black 111.0 1.00 (0.98–1.02) 111.0 1.00 (0.98–1.02) 91.6 1.07 (1.05–1.09)
Hispanic 48.3 0.96 (0.93–0.98) 48.3 0.96 (0.93–0.98) 37.5 0.97 (0.94–0.99)
Total NMBD 11.32 10.48 8.61
Non-Hispanic White 11.15 — 10.35 — 8.42 —
Non-Hispanic Black 11.42 0.57 (0.54–0.60) 10.15 0.54 (0.51–0.57) 8.94 0.57 (0.54–0.60)
Hispanic 11.96 0.99 (0.94–1.04) 11.41 1.02 (0.97–1.07) 8.9 0.99 (0.94–1.04)
Cardiovascular system 4.16 4.00 2.37
Non-Hispanic White 4.16 — 4.01 — 2.31 —
Non-Hispanic Black 4.63 0.87 (0.81–0.94) 4.34 0.84 (0.78–0.91) 2.56 0.80 (0.72–1.09)
Hispanic 3.63 0.84 (0.77–0.91) 3.55 0.85 (0.78–0.92) 2.41 0.99 (0.90–1.09)
Central nervous system 1.94 1.88 1.34
Non-Hispanic White 1.77 — 1.71 — 1.23 —
Non-Hispanic Black 1.68 0.43 (0.38–0.49) 1.52 0.40 (0.35–0.46) 1.28 0.50 (0.43–0.58)
Hispanic 3.00 1.49 (1.34–1.65) 2.99 1.53 (1.38–1.69) 1.68 1.27 (1.13–1.43)
Chromosomal 1.58 1.60 1.93
abnormalities
Non-Hispanic White 1.61 — 1.64 — 2.01 —
Non-Hispanic Black 1.31 0.37 (0.32–0.42) 1.30 0.36 (0.31–0.41) 1.86 0.42 (0.37–0.47)
Hispanic 1.74 1.00 (0.88–1.14) 1.79 1.01 (0.89–1.14) 1.78 0.81 (0.73–0.90)
We excluded New Hampshire, Oklahoma, and Louisiana in 1989, New Hampshire and Oklahoma in 1990, and New Hampshire in 1991
linked infant birth and death files because Hispanic origin was not reported in these states.
*Rate ratios were adjusted for birth weight, prenatal care, and plurality.

Figure 1. Adjusted rate ratios (non-Hispanic Black or Hispanic over non-Hispanic White) and 95% CIs of neonatal mortality attributable
to birth defects (NMBD) by race and selected birth defects categories (cardiovascular, CNS and chromosomal) 1989–2002, United States.
We excluded New Hampshire, Oklahoma and Louisiana in 1989, New Hampshire and Oklahoma in 1990, and New Hampshire in 1991
linked infant birth and death files because Hispanic origin was not reported in these states. The rate ratios were not adjusted for compara-
bility ratio. The dotted line of adjusted rate ratios (non-Hispanic Black or Hispanic over non-Hispanic White) for 1992–1994 was the linear
interpolation of 1990–1991 and 1995–1996 rate ratios. The linear interpolation for 1992–1994 is to illustrate the trend for the figures only.
ICD-10 was implemented in 1999.

Birth Defects Research (Part A) 76:706–713 (2006)

710 YANG ET AL.

Table 3
Adjusted Rate Ratio and 95% CI of Postneonatal Mortality Rate and Postneonatal Mortality Rate Attributable
to Birth Defects (PMBDs) (per 10,000 Live Births) by Race/Ethnicity of Mother and Major Categories
of Birth Defects 1989–1991 versus 2000–2002, United States
Unadjusted for comparability
ratio Comparability ratio adjusted
1989–1991 1989–1991 2000–2002
Mortality rate Mortality rate Mortality rate
Birth defects per 10,000 Rate ratio per 10,000 Rate ratio per 10,000 Rate ratio
Race/ethnicity live births (95% CI) live births (95% CI) live births (95% CI)
Total postneonatal mortality 32.9 32.9 23.0
Non-Hispanic White 27.3 — 27.3 — 19.3 —
Non-Hispanic Black 60.6 1.49 (1.46–1.53) 60.6 1.49 (1.46–1.53) 44.8 1.61 (1.57–1.66)
Hispanic 27.3 0.89 (0.86–0.92) 27.3 0.89 (0.86–0.92) 18.0 0.88 (0.85–0.91)
Total PMBD 4.94 4.56 3.87
Non-Hispanic White 4.53 — 4.21 — 3.35 —
Non-Hispanic Black 6.36 0.97 (0.90–1.13) 5.65 0.92 (0.86–0.99) 5.46 1.12 (1.04–1.21)
Hispanic 5.17 1.08 (1.00–1.16) 4.94 1.11 (1.03–1.20) 4.17 1.18 (1.10–1.27)
Cardiovascular system 2.69 2.59 1.90
Non-Hispanic White 2.54 — 2.45 — 1.68 —
Non-Hispanic Black 3.35 1.02 (0.93
1.12) 3.14 0.99 (0.90–1.09) 2.71 1.25 (1.12–1.39)
Hispanic 2.64 1.00 (0.90–1.10) 2.58 1.01 (0.91–1.12) 1.95 1.12 (1.01–1.25)
Central nervous system 0.54 0.52 0.42
Non-Hispanic White 0.46 — 0.45 — 0.34 —
Non-Hispanic Black 0.77 1.03 (0.84–1.26) 0.70 0.96 (0.78–1.19) 0.56 1.06 (0.83–1.35)
Hispanic 0.65 1.19 (0.96–1.48) 0.65 1.22 (0.98–1.52) 0.55 1.46 (1.18–1.80)
Chromosomal abnormalities 0.79 0.80 0.68
Non-Hispanic White 0.73 — 0.75 — 0.56 —
Non-Hispanic Black 0.86 0.67 (0.56–0.80) 0.85 0.66 (0.55–0.78) 1.05 1.05 (0.88–1.26)
Hispanic 0.94 1.24 (1.04–1.48) 0.97 1.25 (01.05–1.48) 0.76 1.27 (1.07–1.51)
We excluded New Hampshire, Oklahoma, and Louisiana in 1989, New Hampshire and Oklahoma in 1990, and New Hampshire in 1991
linked infant birth and death files because Hispanic origin was not reported in these states.
Rate ratios were adjusted for birth weight, prenatal care, and plurality.

Birth defects of the cardiovascular system were the larg-
est group of PMBD, accounting for 49.1% of total PMBD in
2001–2002 and for >70% of the PMBD rate decline. Chro-
mosomal abnormalities were the second largest group
(17.6% of total PMBD), followed by CNS (10.9%). The
changes in the cardiovascular system and CNS accounted
for >82% of PMBD rate changes in the period from 1989–
1991 through 1995–2002 (Table 3).
The adjusted rate ratio (unadjusted for the comparability
ratio) of non-Hispanic black mothers compared to infants
of non-Hispanic white mothers of PMBD was not signifi-
cantly different in 1989–1991, but increased significantly
from 1989–1991 to 2001–2002 (Table 3). The adjusted rate
ratios (unadjusted for the comparability ratio) comparing
Hispanic with non-Hispanic whites for CNS and chromo-
somal abnormalities were persistently higher during the
period of study, and increased significantly for CNS from
1989–1991 to 2001–2002 (Table 3).
The adjusted rate ratio of PMBD for infants of non-His-
panic black mothers versus infants of non-Hispanic white
mothers increased significantly in the late 1990s, from 0.96
(95% CI, 0.88–1.06) in the 1997–1998 period to 1.13 (95% CI,
1.02–1.24) during the 2001–2002, a 17.7% increase (Fig. 2a).
The change in the adjusted rate ratio for cardiovascular
system defects was the main contributor to the increased
racial disparities in the PMBD rate. The adjusted rate ratio
for the cardiovascular system increased significantly from
0.98 (95% CI, 0.88–1.11) in the 1997–1998 period to 1.34
(95% CI, 1.17–1.52) in the 2001–2002 period, a 36.7%
increase (Fig. 2b). Similarly, the significant increase in the
adjusted rate ratio of PMBD for infants of Hispanic moth-
ers versus infants of non-Hispanic white mothers also took
place in the late 1990s, from 1.04 (95% CI, 0.95–1.15) in the
1997–1998 period to 1.19 (95% CI, 1.09–1.30) during 2001–
2002, a 14.4% increase (Fig. 2c). The changes in the adjusted
rate ratios for cardiovascular system defects and CNS
defects were the main contributors to the increased racial
disparities in the PMBD rate. The adjusted rate ratio for the
cardiovascular system increased significantly from 0.93
(95% CI, 0.82–1.06) in the 1997–1998 period to 1.20 (95% CI,
1.06–1.36) in the 2001–2002 period, a 29.0% increase, and
the adjusted rate ratio for the CNS increased significantly
from 1.00 (95% CI, 0.75–1.32) in the 1997–1998 period to
1.64 (95% CI, 1.26–2.12) in the 2001–2002 period, a 64.0%
increase (Fig. 2d).
DISCUSSION
During 1989–2001, the infant mortality rate in the United
States declined 25.5%, from 9.4 deaths per 1000 live births
to 6.8, and then increased to 7.0 in 2002. During 1989–2002,
the rate of IMBD declined 18.8%, from 1.54 deaths per 1000
live births in 1989 to 1.25 in 2002 for the full time period.
The NMBD rate declined at a similar pace as the rate of
neonatal mortality. The decline in the PMBD rate was
much slower than that of postneonatal mortality, which
made the PMBD an increasingly important component of
postneonatal mortality in the United States.
For NMBD, the adjusted rate ratio was significantly
lower comparing infants of non-Hispanic black mothers

Birth Defects Research (Part A) 76:706–713 (2006)

 RACIAL DIFFERENCES IN BIRTH DEFECT MORTALITY 711

Figure 2. Adjusted rate ratios (non-Hispanic Black or Hispanic over non-Hispanic White) and 95% CI of postneonatal mortality attribut-
able to birth defects (PMBDs) by race and selected birth defects categories (cardiovascular, CNS, and chromosomal), 1989–2002, United
States. We excluded New Hampshire, Oklahoma, and Louisiana in 1989, New Hampshire and Oklahoma in 1990, and New Hampshire in
1991 linked infant birth and death files because Hispanic origin was not reported in these states. The rate ratios were not adjusted for com-
parability ratio. The dotted line of rate ratios (non-Hispanic Black or Hispanic over non-Hispanic White) for 1992–1994 was the linear inter-
polation of 1990–1991 and 1995–1996 rate ratios. The linear interpolation for 1992–1994 is to illustrate the trend for the figures only. ICD-10
was implemented in 1999.

with infants of non-Hispanic white mothers. This racial dis-
parity remained unchanged from 1989 through 2002 and
was evident for the 3 selected birth defects groups. Possible
reasons for the lower NMBD for infants of non-Hispanic
black mothers compared to that of infants of non-Hispanic
white mothers include: differences in prevalence at birth,
severity, probability of ascertainment, timely access to
quality health services, or an inherent susceptibility to neo-
natal mortality. For the birth defects groups accounting for
a substantial fraction of IMBD and examined in this study
(cardiovascular defects, CNS defects, and chromosomal
disorders), there is little evidence to suggest that there is a
difference in the occurrence of total birth defects at birth
between these 2 race/ethnicity groups (Carmichael et al.,
2004). We had no information to assess a possible variation
in severity, probability of reporting or ascertainment,
timely access to quality health care, or an inherent suscepti-
bility to mortality of the defect groups by race/ethnicity,
and are not aware of any evidence to suggest that such var-
iation exists. Worth noting was the reversal of the adjusted
rate ratio compared to the crude NMBD mortality rate
between non-Hispanic blacks and non-Hispanic whites,
reflecting the significant impact of covariates, especially
birth weight on NMBD (Davidoff et al., 2002; Berger et al.,
2003; Bol et al., 2004). Further study is underway to exam-
ine in detail the effect of covariates on racial disparity
between non-Hispanic blacks and non-Hispanic whites in
NMBD.
For PMBD, increased race/ethnicity disparities in the
rate of IMBD were evident between infants of non-His-
panic black and Hispanic mothers and infants of non-His-
panic white mothers. The increased racial differences over
time were mainly attributed to the slower decline in mor-
tality due to birth defects of the cardiovascular system
and increased PMBD rate due to chromosomal abnormal-
ities among infants of non-Hispanic black mothers. For
infants of Hispanic mothers, the increased racial differen-
ces over time were mainly attributed to the slower decline
in mortality due to birth defects of the cardiovascular sys-
tem and CNS. Both the decline in deaths among infants
with birth defects of the cardiovascular system and the
non-Hispanic black versus non-Hispanic white disparity
among infants with birth defects of the cardiovascular sys-
tem were found in a 1979–1997 analysis (Boneva et al.,
2001), and our data confirm that the same trend of infant
mortality due to birth defects of the cardiovascular system
has persisted through 2002.
An increase in the number of babies born with a birth
weight <750 gm led to the increase in infant mortality that
occurred in 2002 in the United States. The increase was
mainly for neonatal mortality, while postneonatal mortal-
ity remained unchanged (MacDorman et al., 2005). The
distinction is important because the factors affecting mor-
tality in these 2 time periods were quite different. Postneo-
natal mortality was more likely to have been influenced
by issues of access to care and associated with differential
survival (Kirby, 1993; Centers for Disease Control and Pre-
vention, 2001; Wise, 2003). Recent studies of the survival
of infants with birth defects in Atlanta, Colorado, Georgia,
and Michigan have reported a poorer survival for black
infants compared with infants of other races (Wong and
Paulozzi, 2001; Berger et al., 2003; Siffel et al., 2003; Bol

Birth Defects Research (Part A) 76:706–713 (2006)

712
et al., 2004). While the reasons for this differential in sur-
vival by race/ethnicity are not clear, presumably timely
access to quality health care plays a major role in survival
among infants with life-threatening birth defects (Chang
et al., 2000; Gonzalez et al., 2003). Differential underre-
porting of certain types of birth defects is a potential
source of the observed racial disparity in IMBD. One possi-
ble source of differential IMBD reporting might be differen-
ces in autopsy rates by race/ethnicity. If autopsies were
less likely to be performed on minority infants, then fewer
birth defects may be identified and reported for these
infants. However, studies suggested that the autopsy rates
for infant deaths did not differ by race/ethnicity (Manis-
calco and Clarke, 1982; Scott et al., 1998). The possible
impact of differential reporting is difficult to assess using
the information available in the linked files. Differential
changes in birth prevalence of selected birth defects (for
example, neural tube defects (NTDs) pre- and postfortifica-
tion with folic acid (1998) in the United States), could
also contribute to the observed racial disparity in IMBD
(Williams et al., 2005; Bol et al., 2006).
Birth defects of the cardiovascular system were the larg-
est group of IMBD. For cardiovascular defects, the observed
decline in neonatal mortality is consistent with previous
reports reflecting improvements in treatment (Morris and
Menashe, 1991; Boneva et al., 2001). This decline was simi-
lar for infants of non-Hispanic white mothers and infants of
non-Hispanic black mothers, but less apparent for infants of
Hispanic mothers. In the postneonatal period, declines in
mortality from cardiovascular defects were less apparent
for both infants of non-Hispanic black and Hispanic moth-
ers, supporting the hypothesis of disparities in access to
quality health care.
For CNS defects, both neonatal and postneonatal mor-
tality rates (NMBD and PMBD) showed persistently
higher adjusted rate ratios among infants of Hispanic
mothers compared with infants of non-Hispanic white
mothers. The adjusted rate ratios for both neonatal and
postneonatal mortality seemed to increase in 2001–2002.
The observed patterns might reflect, in part, the higher
prevalence of NTDs among Hispanic live births (Hen-
dricks et al., 1999; Centers for Disease Control and Preven-
tion, 2000). Infants of non-Hispanic black mothers had a
significantly lower adjusted rate ratio of neonatal mortal-
ity from defects of the CNS compared with non-Hispanic
white, which is consistent with the previously reported
findings (Davidoff et al., 2002).
For chromosomal abnormalities, the adjusted rate ratio
for postneonatal mortality comparing non-Hispanic black
with non-Hispanic white was significantly lower in 1989–
1991 and the racial disparity disappeared in 2000–2002.
Infants of Hispanic mothers had higher postneonatal mor-
tality compared with infants of non-Hispanic white moth-
ers. The most prevalent chromosomal abnormality is
Down syndrome (National Birth Defects Prevention Net-
work, 2003), which is often associated with defects of the
cardiovascular system (such as atrioventricular septal
defects) (Ferencz et al., 1989). The adjusted rate ratios of
postneonatal mortality of cardiovascular system for both
non-Hispanic black and Hispanic increased significantly
from 1989–1991 through 2000–2002. Whether differences in
access to appropriate health services might explain some
of the observed disparities and changes in disparities in
mortality from chromosomal abnormalities remains to be
determined.
Birth Defects Research (Part A) 76:706–713 (2006)
YANG ET AL.
Our analyses were limited by the completeness and accu-
racy of birth defect recording as an underlying cause-of-
death on infants’ death certificates (Kochanek et al., 2004;
National Center for Health Statistics, 2006). We included
deaths only when a birth defect was listed as the underlying
cause of death, and excluded deaths for which a birth defect
was listed as a cause but not the underlying cause. While
conservative, this approach might have underestimated the
true IMBD because the presence of a birth defect could
make an infant more likely to die of another cause (e.g.,
injury/trauma) that might not be directly attributed to the
birth defect (Stevenson and Carey, 2004; Redelings et al.,
2006).
Another potential limitation of our analysis relates to
the change in coding of causes of death from ICD-9 to
ICD-10 that occurred in the United States in 1999. A recent
study indicated that the implementation of ICD-10 created
a significant discontinuity in trends by decreasing the
number of birth defects deaths (Hoyert, 2003). In order to
examine the trends in IMBD rates across the entire period
of study, we calculated the comparability ratios for each
selected birth defects category of the 3 largest race/ethnic-
ity groups. The race–birth defects–specific comparability
ratios were substantially different than the combined com-
parability ratio; therefore, we applied the race–birth
defects–specific comparability ratios to 1989–1991 and
1995–1998 data for the trend analysis (Anderson et al.,
2001).
For rate ratio analysis, we presented both comparability
ratio adjusted and unadjusted rate ratios to assess the effect
of changes in ICD-9 to ICD-10 coding. Because the compa-
rability ratio adjusted rate ratio (adjusted for covariates
also) was a cross-sectional measure of racial disparity in
IMBD, the nondifferential comparability ratio with respect
to race/ethnicity would not have affected the rate ratio esti-
mate. The race-specific comparability ratios of IMBD were
substantially different; for example, the comparability ratio
was 0.93 (95% CI, 0.92–0.94) and 0.89 (95% CI, 0.87–0.91)
for non-Hispanic whites and non-Hispanic blacks, respec-
tively, suggesting a larger racial disparity if a comparabil-
ity-adjusted rate ratio had been used to assess the racial
disparity in IMBD for the periods 1989–1991 and 2000–
2002. However, we used the comparability ratio unad-
justed rate ratio (but adjusted for other covariates), a more
conservative approach.
In summary, from 1989 through 2002, the rate of IMBD
declined. The significant disparity in NMBD between
infants of non-Hispanic black mothers and infants of non-
Hispanic white mothers persisted and was unchanged
overtime. However, the overall disparity in PMBD be-
tween infants of non-Hispanic black, Hispanic mothers
and non-Hispanic white mothers increased significantly
Further studies are warranted to assess the extent to
which delays in care or lack of access to care for infants
with birth defects might be contributing to the continuing
and growing disparity in IMBD.
ACKNOWLEDGMENTS
We thank Marian MacDorman, Robert Anderson, and
Stephanie Ventura, from the National Center for Health
Statistics, Centers for Disease Control and Prevention, for
their helpful comments on the manuscript. We also thank
Jian Xing for helping with reanalysis of the data.
 RACIAL DIFFERENCES IN BIRTH DEFECT MORTALITY
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