with all other racial/ethnic groups included in the total). The gastroschisis case definition was based on the British Pediatric Association Classification of Diseases code (756.71) or the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) code for gastroschisis (756.73, or before 10/1/2009, 756.79, with verification to confirm cases of gastroschisis, because the previous code was shared with omphalocele). Gastroschisis cases included live births, fetal deaths, † and elective terminations. § Data were pooled at CDC, and gastroschisis prevalence was calculated for each year, maternal age group, and race/ethnicity. Prevalence was calculated as number of gastroschisis cases among all birth outcomes divided by the total number of live births. The denominators of total number of live births in the same catchment area as the birth defects surveillance program were reported by states or obtained from public use data files. Poisson exact methods were used to calculate 95% CIs for each prevalence estimate. Prevalence ratios were calculated by dividing the prevalence during 2006-2012 by the prevalence during 1995-2005, and CIs for the prevalence ratios were calculated using Poisson regression.Because the comparison of prevalence between the two study periods involved an artificial breakpoint during the 18-year data span and only examined pooled prevalence within those periods, joinpoint regression analysis was used to identify statistically significant changes in the annual prevalence of gastroschisis over the course of the entire study period (1995)(1996)(1997)(1998)(1999)(2000)(2001)(2002)(2003)(2004)(2005)(2006)(2007)(2008)(2009)(2010)(2011)(2012). Joinpoint regression initially models annual trend data by fitting a straight line (i.e., zero joinpoints). Then, joinpoints are added, one at a time, and a Monte Carlo permutation test is used to determine the optimal number of joinpoints. Each joinpoint in the final model corresponds to a significant change in the trend, and an AAPC and its 95% CI are calculated to describe how the rate changes within each time interval (3). The estimated overall percent change was calculated by first converting the AAPC to the projected single year change in prevalence and then exponentiating to the number of years studied minus one to estimate the total increase throughout the 18 years. This gives the magnitude of the increase, which

Rates of neural tube defects have decreased since folic acid fortification of the food supply in the United States. The authors' objective was to evaluate the associations between neural tube defects and maternal folic acid intake among pregnancies conceived after fortification. This is a multicenter, case-control study that uses data from the National Birth Defects Prevention Study, 1998-2003. Logistic regression was used to compute crude and adjusted odds ratios between cases and controls assessing maternal periconceptional use of folic acid and intake of dietary folic acid. Among 180 anencephalic cases, 385 spina bifida cases, and 3, 963 controls, 21.1%, 25.2%, and 26.1%, respectively, reported periconceptional use of folic acid supplements. Periconceptional supplement use did not reduce the risk of having a pregnancy affected by a neural tube defect. Maternal intake of dietary folate was not significantly associated with neural tube defects. In this study conducted among pregnancies conceived after mandatory folic acid fortification, the authors found little evidence of an association between neural tube defects and maternal folic acid intake. A possible explanation is that folic acid fortification reduced the occurrence of folic acid-sensitive neural tube defects. Further investigation is warranted to possibly identify women who remain at increased risk of preventable neural tube defects.

Background: Epidemiologic literature suggests that exposure to air pollutants is associated with fetal development.Objectives: We investigated maternal exposures to air pollutants during weeks 2–8 of pregnancy and their associations with congenital heart defects.Methods: Mothers from the National Birth Defects Prevention Study, a nine-state case–control study, were assigned 1-week and 7-week averages of daily maximum concentrations of carbon monoxide, nitrogen dioxide, ozone, and sulfur dioxide and 24-hr measurements of fine and coarse particulate matter using the closest air monitor within 50 km to their residence during early pregnancy. Depending on the pollutant, a maximum of 4,632 live-birth controls and 3,328 live-birth, fetal-death, or electively terminated cases had exposure data. Hierarchical regression models, adjusted for maternal demographics and tobacco and alcohol use, were constructed. Principal component analysis was used to assess these relationships in a multipollutant context.Results: Positive associations were observed between exposure to nitrogen dioxide and coarctation of the aorta and pulmonary valve stenosis. Exposure to fine particulate matter was positively associated with hypoplastic left heart syndrome but inversely associated with atrial septal defects. Examining individual exposure-weeks suggested associations between pollutants and defects that were not observed using the 7-week average. Associations between left ventricular outflow tract obstructions and nitrogen dioxide and between hypoplastic left heart syndrome and particulate matter were supported by findings from the multipollutant analyses, although estimates were attenuated at the highest exposure levels.Conclusions: Using daily maximum pollutant levels and exploring individual exposure-weeks revealed some positive associations between certain pollutants and defects and suggested potential windows of susceptibility during pregnancy.Citation: Stingone JA, Luben TJ, Daniels JL, Fuentes M, Richardson DB, Aylsworth AS, Herring AH, Anderka M, Botto L, Correa A, Gilboa SM, Langlois PH, Mosley B, Shaw GM, Siffel C, Olshan AF, National Birth Defects Prevention Study. 2014. Maternal exposure to criteria air pollutants and congenital heart defects in offspring: results from the National Birth Defects Prevention Study. Environ Health Perspect 122:863–872; http://dx.doi.org/10.1289/ehp.1307289

Less acculturated Hispanic parents seemed to be at highest risk of NTDs. For anencephaly, U.S.-born and English-speaking Hispanic parents were also at increased risk. Finally, from an etiologic standpoint, spina bifida and anencephaly appeared to be etiologically heterogeneous from these analyses.

IntroductionWe assessed the relationship between hypospadias and proximity to agricultural pesticide applications using a GIS-based exposure method.MethodsWe obtained information for 354 cases of hypospadias born between 1998 and 2002 in eastern Arkansas; 727 controls were selected from birth certificates. We classified exposure on pounds of pesticides (estimated by crop type) applied or persisting within 500 m of each subject’s home during gestational weeks 6 to 16. We restricted our analyses to 38 pesticides with some evidence of reproductive, developmental, estrogenic, and/or antiandrogenic effects. We estimated timing of pesticide applications using crop phenology and published records.ResultsGestational age at birth [odds ratio (OR) = 0.91; 95% confidence interval (CI), 0.83–0.99], parity (OR = 0.79; 95% CI, 0.65–0.95), and delaying prenatal care until the third trimester (OR = 4.04; 95% CI, 1.46–11.23) were significantly associated with hypospadias. Risk of hypospadias increased by 8% for every 0.05-pound increase in estimated exposure to diclofop-methyl use (OR = 1.08; 95% CI, 1.01–1.15). Pesticide applications in aggregate (OR = 0.82; 95% CI, 0.70–0.96) and applications of alachlor (OR = 0.56; 95% CI, 0.35–0.89) and permethrin (OR = 0.37; 95% CI, 0.16–0.86) were negatively associated with hypospadias.ConclusionsExcept for diclofop-methyl, we did not find evidence that estimated exposure to pesticides known to have reproductive, developmental, or endocrine-disrupting effects increases risk of hypospadias. Further research on the potential effects of exposure to diclofop-methyl is recommended.