Low birthweight (< 2500 g) is a strong predictor of infant mortality.1 However, low birthweight may be the consequence of preterm birth or restricted fetal growth. During the past 2 decades, preterm birth rates have been increasing in developed countries,2–9 whereas population-based trends in small-for-gestational-age (SGA) births in the United States remain unexplored. Trends in SGA births are important because the severely growth restricted are at increased risk for infant death,10 whereas less severe cases may lead to permanent deficits in growth and neurocognitive development in later childhood11 and increased risk for adult chronic diseases.12
We performed this study to evaluate temporal trends and their determinants in singleton SGA births among term and preterm births to White and Black women in the United States between 1989 and 1998.
METHODS
The study was based on the US vital statistics data (1989 and 1998) assembled by the National Center for Health Statistics.13,14 SGA birth was defined as a sex-specific birthweight for gestational age less than the 10th percentile, based on 1989 US singleton births.15 To minimize gestational age errors, all analyses were restricted to live-born infants delivered between 28 and 41 completed weeks’ gestation. Births from California, Indiana, Louisiana, Washington, South Dakota, Oklahoma, and Tennessee were excluded because these states do not report data on several potential determinants. Infants with congenital malformations also were excluded.
We first evaluated crude temporal trends in SGA births between 1989 and 1998. We then used logistic regression to sequentially adjust for sociodemographic determinants, followed by medical and obstetrical complications of pregnancy, and finally smoking or alcohol use (because they contained more than 25% missing data). Trends in SGA birth were expressed as percent change in the SGA birth rate between 1989 and 1998 relative to that in 1989, after transforming odds ratios to relative risks.16
RESULTS
Term SGA birth rates declined by 8.2% between 1989 (9.8%) and 1998 (9.0%) among Whites and by 10.3% (19.4% in 1989 and 17.4% in 1998) among Blacks. Preterm SGA birth rates increased by 10.2% (8.8% in 1989 and 9.7% in 1998) among Whites and by 21.4% (10.3% in 1989 and 12.5% in 1998) among Blacks.
After adjusting for sociodemographic determinants, further adjustment for marital status increased the decline in SGA birth rate at term to 11.8% and 11.3% among Whites and Blacks, respectively (Table 1 ▶). Additional adjustment for smoking led to a major reduction in the decline in SGA birth rate among both races. However, none of the other determinants examined helped account for the decline in term SGA birth rates. Similar trends were noted (data not shown) for pregnancies with and without obstetrical interventions (labor induction and cesarean delivery).
TABLE 1—
Change (%) in Rates (Unadjusted and Adjusted) of Term Small-for-Gestational-Age (SGA) Births to White and Black Women, 1989 to 1998
| Potential Determinants of Term SGA Births | White Women Percentage (95% CI) | Black Women Percentage (95% CI) |
| Unadjusted | −8.2 (−8.7, −7.5) | −10.3 (−11.4, −9.5) |
| Sequentially adjusted | ||
| Maternal age | −7.0 (−7.6, −6.4) | −9.7 (−10.6, −8.8) |
| Gravidity | −7.2, (−7.8, −6.5) | −9.9 (−11.0, −9.0) |
| Education | −8.3 (−8.9, −7.6) | −9.7 (−10.6, −8.8) |
| Unmarried status | −11.8 (−12.4, −11.1) | −11.3 (−12.2, −10.4) |
| Late prenatal care | −10.6 (−11.2, −9.9) | −9.2 (−10.2, −8.2) |
| Prior preterm or SGA birth | −10.5 (−11.1, −9.8) | −9.0 (−10.1, −8.0) |
| Chronic hypertension | −10.5 (−11.1, −9.8) | −9.0 (−10.0, −8.0) |
| Pregnancy-induced hypertension | −10.7 (−11.3, −10.0) | −9.1 (−10.1, −8.1) |
| Placental abruption | −10.6 (−11.2, −9.8) | −9.0 (−10.0, −8.0) |
| Placenta previa | −10.5 (−11.1, −9.8) | −9.0 (−10.0, −7.9) |
| Unexplained bleeding | −10.5 (−11.1, −9.8) | −9.0 (−10.0, −7.9) |
| Diabetes (all classes) | −10.5 (−11.1, −9.8) | −8.8 (−9.9, −7.8) |
| Smoking and alcohol use | −2.9 (−3.7, −2.0) | −4.1 (−5.3, −3.1) |
| Missing smoking or alcohol | −3.1 (−3.8, −2.4) | −3.8 (−4.9, −2.7) |
Note. CI = confidence interval. Term SGA rates among Whites in 1989 and 1998 were 9.8% and 9.0%, respectively. Term SGA rates among Blacks in 1989 and 1998 were 19.4% and 17.4%, respectively.
Among preterm births with interventions, SGA birth rates increased by 4.3% and 13.5% among Whites and Blacks, respectively; among those without interventions, SGA birth rates were relatively unchanged for Whites (0.2%) but increased by 9.4% for Blacks (Table 2 ▶). After adjusting for the sociodemographic and behavioral determinants, the rise in SGA birth rate among pregnancies with interventions in Whites disappeared with further adjustment for pregnancy-induced hypertension and declined slightly among Blacks. Because the proportion of smokers declined between 1989 and 1998, SGA rates increased when smoking was adjusted for in the model. The corresponding data among Blacks indicated a rise in the crude preterm SGA birth rate that was not explained by any of the determinants examined.
TABLE 2—
Change (%) in Rates (Unadjusted and Adjusted) of Preterm Small-for-Gestational-Age (SGA) Births to White and Black Women With and Without Interventions, 1989 to 1998
| White Women Percentage (95% CI) | Black Women Percentage (95% CI) | |||
| Potential Determinants of Preterm SGA Births | With Interventionsa | Without Interventions | With Interventionsa | Without Interventions |
| Unadjusted | 4.3 (1.2, 7.4) | 0.2 (−3.2, 3.5) | 13.5 (8.8, 19.0) | 9.4 (5.1, 13.9) |
| Sequentially adjusted | ||||
| Maternal age | 4.8 (1.6, 7.9) | 0.3 (−3.0, 3.8) | 14.5 (10.1, 19.0) | 7.9 (3.6, 12.4) |
| Gravidity | 4.4 (1.3, 7.6) | 0.3 (−3.1, 3.7) | 14.7 (9.8, 19.9) | 7.5 (3.3, 11.9) |
| Education | 4.5 (1.4, 7.7) | 0.4 (−3.0, 3.9) | 15.5 (10.5, 20.7) | 8.0 (3.6, 12.5) |
| Unmarried status | 3.7 (0.5, 6.9) | −1.7 (−5.1, 1.8) | 15.4 (10.4, 20.6) | 7.1 (2.8, 11.6) |
| Late prenatal care | 3.5 (0.3, 6.8) | −1.2 (−4.8, 2.4) | 15.2 (9.9, 20.6) | 9.8 (5.0, 14.8) |
| Prior preterm or SGA birth | 3.7 (0.4, 7.1) | 0.3 (−3.4, 4.0) | 15.5 (10.1, 21.0) | 12.2 (7.2, 17.4) |
| Chronic hypertension | 3.3 (0.0, 6.6) | 0.2 (−3.5, 4.0) | 14.6 (9.3, 20.2) | 12.2 (7.2, 17.4) |
| Pregnancy-induced hypertension | 0.0 (−3.3, 3.3) | −0.9 (−4.5, 2.9) | 12.1 (6.8, 17.6) | 11.4 (6.5, 16.7) |
| Placental abruption | 0.7 (−2.6, 4.0) | −0.3 (−3.9, 3.5) | 12.5 (7.1, 18.0) | 11.8 (6.7, 16.9) |
| Placenta previa | 0.6 (−2.7, 3.9) | −0.2 (−3.9, 3.5) | 12.6 (7.3, 18.2) | 11.8 (6.8, 17.0) |
| Unexplained bleeding | 0.6 (−2.6, 3.9) | 0.0 (−3.7, 3.8) | 12.6 (7.3, 18.2) | 11.8 (6.8, 17.0) |
| Diabetes (all classes) | 0.6 (−2.7, 3.9) | 0.1 (−3.6, 3.9) | 13.0 (7.7, 18.6) | 12.0 (7.0, 17.3) |
| Preterm prelabor ROM | 0.9 (−2.3, 4.4) | 2.2 (−1.6, 6.1) | 14.3 (8.8, 19.9) | 13.9 (8.8, 19.2) |
| Smoking and alcohol use | 5.6 (2.2, 9.0) | 10.5 (6.3, 14.5) | 19.0 (13.3, 25.1) | 19.6 (14.1, 25.2) |
| Missing smoking or alcohol | 5.2 (1.8, 8.7) | 10.1 (6.0, 14.3) | 19.3 (13.6, 25.3) | 19.7 (14.3, 25.4) |
Note. CI = confidence interval; ROM = rupture of membranes. Preterm SGA rates among Whites with and without interventions in 1989 were 13.9% and 6.5%, respectively, and in 1998 were 14.4% and 6.5%, respectively. Preterm SGA rates among Blacks with and without interventions in 1989 were 16.0% and 8.5%, respectively, and in 1998 were 18.5% and 9.3%, respectively.
aIntervened pregnancies were those that were either induced or delivered by cesarean birth.
DISCUSSION
Results from our study indicate that the rates of term SGA births declined between 1989 and 1998 among Whites and Blacks. However, during the same period rates of preterm SGA births increased for both races. Because the preterm SGA trends varied by whether the pregnancy was terminated through an intervention, we evaluated these temporal trends separately.
Intrauterine growth restriction, which is usually defined operationally as SGA, is an indication for labor induction, especially among preterm pregnancies. Intrauterine growth restriction also can result from pathological conditions, such as pregnancyinduced hypertension (including preeclampsia) or placental abruption.17,18 Among Whites, an increase in interventions for pregnancyinduced hypertension helped explain most of the increase in preterm SGA births. However, adjustment for these determinants did not explain the puzzling increase in preterm SGA births among Blacks. Although rates of chronic hypertension, pregnancy-induced hypertension, and diabetes have increased more in Blacks than in Whites in the United States, the magnitude of the Black–White disparity in these changes was modest (data not shown). The severity of these complications also may have increased more in Blacks than in Whites, which might explain the observed trends.
A few unexplored factors also might help account for the SGA trends. Among them are changes in maternal anthropometry19 and illicit drug use during pregnancy,20 which are unavailable in vital statistics data. The presence or absence of labor is unfortunately not recorded, thereby making it difficult to separate “cold” cesarean deliveries from cesarean deliveries after a trial of labor.
Acknowledgments
This study was supported, in part, through a grant from the National Institutes of Health (R01-HD38902).
This article was presented in part at the Society for Pediatric and Perinatal Epidemiologic Research Annual Meeting, Toronto, Ontario, Canada, June 11–12 2001.
The authors are grateful to Susan Fosbre for help with the manuscript preparation.
Human Participant Protection
This study was approved by the Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey’s institutional review board.
C. V. Ananth conceived the idea for the study, assembled and analyzed the data, and drafted the brief. K. Demissie, M. S. Kramer, and A. M. Vintzileos reviewed the brief, offered comments, and helped edit the brief.
Peer Reviewed
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