Background: Congenital heart disease (CHD) is one of the most prevalent birth defects. Housing renovations are a newly recognized source of indoor environmental pollution that is detrimental to health. A growing body of research suggests that maternal occupational exposure to renovation materials may be associated with an increased risk of giving birth to fetuses with CHD. However, the effect of indoor housing renovation exposure on CHD occurrence has not been reported. Methods: A multi-hospital case–control study was designed to investigate the association between maternal periconceptional housing renovation exposure and the risk of CHD for offspring. In total, 346 cases and 408 controls were enrolled in this study from four hospitals in China. Exposure information was based on a questionnaire given to women during pregnancy. The association between housing renovation exposure and CHD occurrence was assessed by estimating odds ratios (OR) with logistic regression models adjusted for potential confounders. Results: The risk for CHD in offspring was significantly associated with maternal exposure to housing renovations (AOR: 1.89, 95% CI: 1.29-2.77). There were similar risks for cardiac defects with or without extra-cardiac malformation (AOR of 2.65 and 1.76, respectively). Maternal housing renovation exposure may increase the fetus’ risk of suffering from conotruncal defect or anomalous venous return. There were significant risks for cardiac defects if the pregnant woman moved into a new house within one month after decoration at either 3 months before pregnancy (AOR: 2.38, 95% CI: 1.03 to 5.48) or during first trimester (AOR: 4.00, 95% CI: 1.62 to 9.86). Conclusions: Maternal exposure to housing renovations may have an increased risk of giving birth to fetuses with some selected types of CHD. This relationship was stronger for women who moved into a newly decorated house. However, considering the limited number of subjects and the problem of multiple exposures, more research is needed to clarify the effects seen here.

To determine the disease-causing mutation in a Chinese patient with Apert syndrome (AS). Genomic DNA was extracted from peripheral blood samples of the AS patient and his parents. Polymerase chain reaction (PCR) was used to amplify the exons 7 and 9 of fibroblast growth factor receptor 2 (FGFR2) gene. Then PCR products were sequenced bi-directionally. A heterozygous 934C to G transversion in exon 7 of the FGFR2 gene was detected in the patient, which resulted in the substitution of tryptophan residue for serine at position 252 of FGFR2 protein (S252W). This mutation has been reported in AS patients previously. This Chinese AS results from the 934 C to G mutation in exon 7 of FGFR2 gene.