PGDM was associated with a wide range of birth defects; GDM was associated with a limited group of birth defects.

To our knowledge, this is the first population-based study of its scale to examine prepregnancy obesity and a range of structural birth defects. These results suggest a weak to moderate positive association of maternal obesity with 7 of 16 categories of birth defects and a strong inverse association with gastroschisis. The mechanisms underlying these associations are not yet understood but may be related to undiagnosed diabetes.

No abstract

There have been no large population-based studies of the prevalence of achondroplasia and thanatophroic dysplasia in the United States. This study compared data from seven population-based birth defects monitoring programs in the United States. We also present data on the association between older paternal age and these birth defects, which has been described in earlier studies. The prevalence of achondroplasia ranged from 0.36 to 0.60 per 10,000 livebirths (1/27,780-1/16,670 livebirths). The prevalence of thanatophoric dysplasia ranged from 0.21 to 0.30 per 10,000 livebirths (1/33,330-1/47,620 livebirths). In Texas, fathers that were 25-29, 30-34, 35-39, and > or =40 years of age had significantly increased rates of de novo achondroplasia among their offspring compared with younger fathers. The adjusted prevalence odds ratios were 2.8 (95% CI; 1.2, 6.7), 2.8 (95% CI; 1.0, 7.6), 4.9 (95% CI; 1.7, 14.3), and 5.0 (95% CI; 1.5, 16.1), respectively. Using the same age categories, the crude prevalence odds ratios for de novo cases of thanatophoric dysplasia in Texas were 5.8 (95% CI; 1.7, 9.8), 3.9 (95% CI; 1.1, 6.7), 6.1 (95% CI; 1.6, 10.6), and 10.2 (95% CI; 2.6, 17.8), respectively. These data suggest that thanatophoric dysplasia is one-third to one-half as frequent as achondroplasia. The differences in the prevalence of these conditions across monitoring programs were consistent with random fluctuation. Birth defects monitoring programs may be a good source of ascertainment for population-based studies of achondroplasia and thanatophoric dysplasia, provided that diagnoses are confirmed by review of medical records.

Many studies of environmental exposures and birth defects use mothers' addresses at delivery as a proxy for the exposure. The validity of these studies is questionable because birth defects generally occur within 8 weeks of conception and the mother's address at delivery may differ from her address early in pregnancy. In order to assess the extent of this bias, we examined the pattern of maternal residential mobility over the span of 3 months prior to conception through delivery, and associated maternal socio-demographic characteristics. We linked Texas subjects from a national case-control study of birth defects with their corresponding records from the Texas Birth Defects Registry and the Texas live birth certificates. Logistic regression analyses were conducted to assess maternal socio-demographic factors related to mobility during pregnancy. Overall, 33% of case and 31% of control mothers changed residence between conception and delivery. The pattern of mobility was similar for both case and control mothers for each pregnancy period. Multivariate analyses indicated that for case mothers, older age (OR ¼ 0.39, 95% CI ¼ 0.21-0.70), higher household income (OR ¼ 0.35, 95% CI ¼ 0.18-0.68), Hispanic ethnicity (OR ¼ 0.64, 95% CI ¼ 0.44-0.92), and higher parity (OR ¼ 0.59, 95% CI ¼ 0.38-0.94) were indicators of lower mobility during pregnancy. For control mothers, the same pattern of association was present, however, only older age was significantly associated with low rates of mobility. Studies of birth defects using maternal address at delivery as a proxy for maternal environmental exposures during pregnancy may be subject to considerable nondifferential exposure misclassification due to maternal mobility during pregnancy.