American Journal of Epidemiology Vol. 143, No. 1: 12-24
Copyright © 1996 by The Johns Hopkins University School of Hygiene and Public Health
other |
Hispanic Origin and Neural Tube Defects in Houston/Harris County, Texas
II. Risk Factors
1Texas Birth Defects Monitoring Division, Bureau of Epidemiology, Texas Department of Health Austin, TX
2Health Services Department, School of Public Health, University of Texas Houston, TX
3Southwest Center for Occupational and Environmental Health, School of Public Health, University of Texas Houston, TX
4Department of Molecular and Human Genetics, Baylor College of Medicine Houston, TX
Reprint requests to Dr. Mark A. Canfield, Texas Birth Defects Monitoring Division, Bureau of Epidemiology, Texas Department of Health, 1100 West 49th Street, Austin, TX 78756
Several investigators have reported Hispanics to be at elevated risk for neural tube defects (anencephaly and spina bifida). Factors contributing to this risk have not been established. The authors conducted a case-control study of neural tube defects (NTDs) among births occurring in Harris County, Texas, from April 1, 1989, through December 31, 1991. Through the use of multiple ascertainment methods, 59 cases of anencephaly and 32 cases of spina bifida were detected. Controls (n = 451) were sampled for the same time period from Harris County vital records. Regardless of how Hispanic ethnicity was classified, having a Hispanic parent was a risk factor for both anencephaly and spina bifida. The primary etiologic question was whether increased NTD risk in Hispanics is explained by maternal diabetes or by other factors (e.g., maternal birthplace, prenatal care, reproductive history, age, socioeconomic status). Mexico-bom Hispanics were no more likely than Texas-bom Hispanics to deliver a fetus or infant with an NTD. Having a Hispanic mother was a risk factor for anencephaly among infants bom to women with early prenatal care (odds ratio (OR) = 4.54 95% confidence interval (Cl) 2.219.40) but not for those bom to latecomers. Earlier prenatal care seemed "protective" for non-Hispanics (OR = 0.18, 95% Cl 0.060.65) but not for Hispanics. After simultaneous adjustment for eight variables in multivariate analysis, having a Hispanic (versus non-Hispanic) mother remained a strong risk factor for both anencephaly (OR = 2.58,95% Cl 1.195.61) and spina bifida (OR = 3.71, 95% Cl 1.489.31). Any previous pregnancy termination/fetal loss was also associated with anencephaly in a final logistic regression model (OR = 2.48, 95% Cl 1.205.10), and having a teenage mother (aged <20 years) approached significance (OR = 2.21, 95% Cl 0.925.31). "Hispanic mother" was the only study variable significantly associated with spina bifida in multivariate analysis. Results for diabetes suggested no association with anencephaly (OR = 1.24, 95% Cl 0.256.17). An increased risk of NTDs among Hispanics remained after controlling for other factors. For anencephaly, this risk might be partially explained by economic and cultural differences between Hispanics and non-Hispanics, and the effect of these factors on rates of prenatal diagnosis and elective pregnancy termination. Am J Epidemiol 1996;143:1224
anencephaly; case-control studies; diabetes mellitus; Hispanic Americans; neural tube defects; prenatal care; prenatal diagnosis; spina bifida cystica
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
C. Olesen, N. Thrane, A.-M. Ronholt, J. Olsen, and T. B Henriksen Association between social position and congenital anomalies: A population-based study among 19,874 Danish women Scand J Public Health, May 1, 2009; 37(3): 246 - 251. [Abstract] [PDF] |
||||
![]() |
K. A. Bol, J. S. Collins, R. S. Kirby, and for the National Birth Defects Prevention Network Survival of Infants With Neural Tube Defects in the Presence of Folic Acid Fortification Pediatrics, March 1, 2006; 117(3): 803 - 813. [Abstract] [Full Text] [PDF] |
||||
![]() |
V. L. Stevens and J. Tang Fumonisin B1-induced Sphingolipid Depletion Inhibits Vitamin Uptake via the Glycosylphosphatidylinositol-anchored Folate Receptor J. Biol. Chem., July 18, 1997; 272(29): 18020 - 18025. [Abstract] [Full Text] [PDF] |
||||


