Background Antecedents for infantile hypertrophic pyloric stenosis (IHPS) vary across studies; therefore, we conducted a multistate, population‐based retrospective study of the prevalence and descriptive epidemiology of IHPS in the United States (US). Methods Data for IHPS cases (n = 29,554) delivered from 1999–2010 and enumerated from 11 US population‐based birth defect surveillance programs, along with data for live births (n = 14,707,418) delivered within the same birth period and jurisdictions, were analyzed using Poisson regression to estimate IHPS prevalence per 10,000 live births. Additional data on deliveries from 1999–2005 from seven of these programs were analyzed using multivariable logistic regression to estimate adjusted prevalence ratios (aPR)s and 95% confidence intervals (CI)s for selected infant and parental characteristics. Results Overall, IHPS prevalence from 1999–2010 was 20.09 (95% CI = 19.87, 20.32) per 10,000 live births, with statistically significant increases from 2003–2006 and decreases from 2007–2010. Compared to their respective referents, aPRs were higher in magnitude for males, preterm births, and multiple births, but lower for birth weights <2,500 g. The aPRs for all cases increased with decreasing parental age, maternal education, and maternal parity, but decreased for parental race/ethnicity other than non‐Hispanic White. Estimates restricted to isolated cases or stratified by infant sex were similar to those for all cases. Conclusions This study covers one of the largest samples and longest temporal period examined for IHPS in the US. Similar to findings reported in Europe, estimates suggest that IHPS prevalence has decreased recently in the US. Additional analyses supported associations with several infant and parental characteristics.

This study examined associations for maternal reports of drinking water filtration and consumption and maternal DBP exposure from drinking water with OFCs in offspring. Associations observed were near or below unity and mostly nonsignificant. Continued, improved research using maternal individual-level exposure data will be useful in better characterizing these associations.

Nonsyndromic orofacial clefts are common birth defects. Reported risks for orofacial clefts associated with parental occupational pesticide exposure are mixed. To examine the role of parental pesticide exposure in orofacial cleft development in offspring, this study compared population-based case-control data for parental occupational exposures to insecticides, herbicides, and fungicides, alone or in combinations, during maternal (1 month before through 3 months after conception) and paternal (3 months before through 3 months after conception) critical exposure periods between orofacial cleft cases and unaffected controls. Multivariable logistic regression was used to estimate odds ratios, adjusted for relevant covariables, and 95% confidence intervals for any (yes, no) and cumulative (none, low [

Background: Arsenic is widely distributed in the environment in both inorganic and organic forms. Evidence from animal studies suggests that maternal inorganic arsenic may lead to the development of orofacial clefts (OFC)s in offspring. This evidence, together with the limited epidemiologic data available, supports the need for a comprehensive examination of major sources of arsenic exposure and OFCs in humans. Methods: Using interview data collected in the National Birth Defects Prevention Study, public and well water arsenic sampling data, and dietary arsenic estimates, we compared expert-rater assessed occupational arsenic exposure, individual-level exposure to arsenic through drinking water, and dietary arsenic exposure between mothers of OFC cases (N = 435) and unaffected controls (N = 1267). Associations for each source of exposure were estimated for cleft lip ± palate (CL/P) and cleft palate (CP) using unconditional logistic regression analyses. Results: Associations for maternal drinking water arsenic exposure and CL/P were near or below unity, whereas those for dietary arsenic exposure tended to be positive. For CP, positive associations were observed for maternal occupational arsenic and inorganic arsenic exposures, with confidence intervals that excluded the null value, whereas those for drinking water or dietary arsenic exposures tended to be near or below unity. Conclusions: Positive associations were observed for maternal occupational arsenic exposure and CP and for maternal dietary arsenic exposure and CL/P; the remainder of associations estimated tended to be near or below unity. Given the exploratory nature of our study, the results should be interpreted cautiously, and continued research using improved exposure assessment methodologies is recommended.

To our knowledge, this is the first study to specifically examine maternal occupational cadmium exposure and OFCs, using expert rater exposure assessment. The small numbers of exposed mothers observed, however, led to imprecise estimates. Continued research using more detailed occupational exposure assessment and increased sample sizes is recommended.

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Objectives: To explore associations between maternal pre-pregnancy exposure to arsenic in diet and non-cardiac birth defects. Design: Population-based, case-control study using maternal responses to a dietary assessment and published arsenic concentration estimates in food items to calculate average daily total and inorganic arsenic exposure during the year before pregnancy. Assigning tertiles of total and inorganic arsenic exposure, logistic regression analysis was used to estimate odds ratios for middle and high tertiles, compared to the low tertile. Setting: US National Birth Defects Prevention Study, 1997-2011. Participants: Mothers of 10,446 children without birth defects and 14,408 children diagnosed with a non-cardiac birth defect. Results: Maternal exposure to total dietary arsenic in the middle and high tertiles was associated with a threefold increase in cloacal exstrophy, with weak positive associations (1.2-1.5) observed either in both tertiles (intercalary limb deficiency) or the high tertile only (encephalocele, glaucoma/anterior chamber defects, bladder exstrophy). Maternal exposure to inorganic arsenic showed mostly weak, positive associations in both tertiles (colonic atresia/stenosis, esophageal atresia, bilateral renal agenesis/hypoplasia, hypospadias, cloacal exstrophy, gastroschisis), or the high (glaucoma/anterior chamber defects, choanal atresia, intestinal atresia stenosis) or middle (encephalocele, intercalary limb deficiency, transverse limb deficiency) tertiles only. The remaining associations estimated were near the null or inverse. Conclusions: This exploration of arsenic in diet and non-cardiac birth defects produced several positive, but mostly weak associations. Limitations in exposure assessment may have resulted in exposure misclassification. Continued research with improved exposure assessment is recommended to identify if these associations are true signals or chance findings.

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