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Context: Daily consumption of 400 microg of folic acid before conception and during early pregnancy dramatically reduces the occurrence of neural tube defects (NTDs). Before food fortification, however, only an estimated 29% of US reproductive-aged women were taking a supplement containing 400 microg of folic acid daily. The US Food and Drug Administration authorized addition of folic acid to enriched grain products in March 1996, with compliance mandatory by January 1998., Objective: To evaluate the impact of food fortification with folic acid on NTD birth prevalence., Design, Setting, and Population: National study of birth certificate data for live births to women in 45 US states and Washington, DC, between January 1990 and December 1999., Main Outcome Measure: Birth certificate reports of spina bifida and anencephaly before fortification (October 1995 through December 1996) compared with after mandatory fortification (October 1998 through December 1999)., Results: The birth prevalence of NTDs reported on birth certificates decreased from 37.8 per 100 000 live births before fortification to 30.5 per 100 000 live births conceived after mandatory folic acid fortification, representing a 19% decline (prevalence ratio [PR], 0.81; 95% confidence interval [CI], 0.75-0.87). During the same period, NTD birth prevalence declined from 53.4 per 100 000 to 46.5 per 100 000 (PR, 0.87; 95% CI, 0.64-1.18) for women who received only third-trimester or no prenatal care., Conclusions: A 19% reduction in NTD birth prevalence occurred following folic acid fortification of the US food supply. However, factors other than fortification may have contributed to this decline.

Objective: To describe the recent trends and epidemiologic characteristics of neural tube defects in the United States., Research Design: Ongoing surveillance data., Setting: Two birth defect surveillance systems: the nationwide Birth Defects Monitoring Program and the Metropolitan Atlanta (Ga) Congenital Defects Program for 1970 through 1989 and 1968 through 1989, respectively., Participants: Between 1970 and 1989, using discharge diagnoses of approximately 1 million live-born and stillborn infants per year, the Birth Defects Monitoring Program identified 15,503 cases of spina bifida and anencephaly. Between 1968 and 1989, using discharge diagnoses and clinical records until age 1 year of 38,000 infants per year, the Metropolitan Atlanta Congenital Defects Program identified 800 cases of spina bifida and anencephaly., Interventions: None., Measurements/main Results: Nationwide, neural tube defect rates have declined from 1.3 per 1000 births in 1970 to 0.6 per 1000 births in 1989. In Atlanta, neural tube defect rates have declined from 2.0 per 1000 births in 1968 to 0.6 per 1000 births in 1989. Several changes in the epidemiologic characteristics of neural tube defects were observed: (1) the proportion of spina bifida cases has increased; (2) the proportion of neural tube defect cases compared with the proportion of other unrelated defects has increased; (3) the race ratio of whites to other races for isolated neural tube defect cases has declined in Atlanta; and (4) the rate of isolated neural tube defects in females has also decreased., Conclusions: The declining rates of neural tube defects can be partially explained by increased widespread prenatal diagnostic techniques, strongly suggesting the role of environmental factors in neural tube defects. In particular, the use of multivitamins and folic acid to prevent the occurrence of neural tube defects needs further evaluation. Nevertheless, the changing clinical and epidemiologic characteristics of cases over time points to the etiologic heterogeneity of these conditions.

Trends in postneonatal mortality (PNM) rates in the United States were analyzed for the period 1962 through 1978 using National Center for Health Statistics birth and death certificate data. The PNM rates declined from 5.5 to 3.6 per 1,000 live births for whites and from 15.6 to 7.6 per 1,000 live births for blacks. Most of the decline in PNM rates could be accounted for by a drop in mortality from infectious diseases. A dramatic increase occurred in the reported rates of unexplained sudden infant death (SID), which emerged as the leading reported cause of PNM. The second leading cause of PNM was birth defects among whites and infectious diseases among blacks. Gaps in PNM continued to exist between whites and blacks, and between metropolitan and nonmetropolitan areas. These gaps suggest that further improvement in PNM may be possible by improving access to health care. The massive increase in the rates of SID, although partially explained by coding or reporting phenomena, warrants active pursuit for a better pathophysiologic and etiologic delineation of the entity.

Vietnam veterans' risks for fathering babies with major structural birth defects were assessed using a case-control study. Information regarding military service in Vietnam was obtained from interviews with mothers and fathers of babies in case and control groups and from review of military records. Vietnam veterans, in general, did not have an increased risk of fathering babies with defects (all types combined; relative risk estimate, 0.97). Vietnam veterans who had greater estimated opportunities for Agent Orange exposure did not seem to be at greater risk for fathering babies with all types of defects combined. However, for a few specific types of defects the estimated risks were higher for subgroups of Vietnam veterans that may have had a greater likelihood of exposure to Agent Orange. These seemingly higher risks could be chance events, the result of some experience in the Vietnam service of the father, or the result of some other unidentified risk factor.

Relative to the countries of northern Europe, the United States has a high crude infant mortality rate. We compared the United States' fetal and infant mortality rates with those of Norway, a nation tht is internationally recognized for having a low infant mortality. Norwegian birth-weight-specific rates were applied to the US birth populations, yielding adjusted rates. The adjusted rates, which are the crude rates that would have resulted in the United States if the Norwegian birth-weight-specific rates had been in force, were generally higher than the US rates that were actually observed. Thus, the major reason for the United States' poor international rank is probably its unfavorable birth-weight distributions, and any major improvement in the United States' international standing will likely await a reduction in the proportion of high-risk, low-weight births.

We studied the association between multivitamin use during the periconceptional period and the occurrence of neural tube defects using data from the Atlanta Birth Defects Case-Control Study. There were 347 babies with neural tube defects who were live born or stillborn to residents of metropolitan Atlanta from 1968 through 1980. The 2829 control-babies born without birth defects were randomly selected through birth certificates. Periconceptional multivitamin use was defined as reported use for each of the three months before conception through the first three months of pregnancy. Mothers who reported not using multivitamins any time during the six-month period were defined as nonusers. Fourteen percent of mothers reported periconceptional multivitamin use and 40% reported nonuse. Multivitamin users were different from nonusers in a number of demographic, health-related, and life-style characteristics. We found an overall apparent protective effect of periconceptional multivitamin use on the occurrence of neural tube defects, with a crude estimated relative risk of 0.40 (95% confidence interval, 0.25 to 0.63). At this time, it is not possible to determine whether this apparently lower risk is the direct result of multivitamin use or the result of other characteristics of women who use multivitamins.

The crude incidence of Down's syndrome (DS) in the United States is currently about 1/1,000 births. Reduction in the proportion of births to women 35 years and older can account for a halving of the estimated percentage of DS births to this age group and a drop in the estimated crude incidence of DS from 1.33/1,000 births in 1960 to 0.99/1,000 births in 1978. Epidemiologic studies suggest that among women 35 years and older, the risk of having a child with DS has not changed. With the present distribution of maternal ages, prenatal diagnosis among women 35 years and older can result in no more than a 20% decrease in the crude incidence of DS. With continued use of prenatal diagnosis among older gravidas, upward of 80% of DS births will occur to younger mothers.