Background: Previous research has suggested an association between maternal exposure to ambient air pollutants and the risk of congenital heart defects (CHDs). However, the effect of individual prenatal exposure to indoor air pollutants on CHD occurrence has not been reported.Methods: We carried out a hospital-based case-control study to investigate the association between personal air pollution exposure during pregnancy and the risk of CHDs in offspring. A total of 32 cases and 74 controls were included in this study from two hospitals in East China. We investigated maternal and residential environmental characteristics using a questionnaire and obtained personal indoor air samples to assess particulate matter (PM) and volatile organic compounds (VOCs) from 22–30 gestational weeks; formaldehyde, benzene, toluene, xylene, total VOCs (TVOCs), PM10, and PM2.5 were assessed. Logistic regression was performed to assess associations and interactions among individual indoor air pollutants and CHDs after adjusting for confounders. The potential residential environmental factors affecting the risks of indoor air pollutants on CHDs were also assessed.Results: Median TVOC (0.430 vs. 0.005 mg/m3, P < 0.001), PM2.5 (12.00 vs. 8.00 µg/m3, P=0.037) and PM10 (13.50 vs. 8.00 µg/m3, P=0.028) exposure levels in cases were significantly higher than those in controls. In a regression model adjusted for confounders, exposure to high levels of indoor TVOCs, PM2.5 and PM10 during pregnancy was associated with risks for CHDs and the occurrence of some major CHD subtypes in offspring. These risk effects were enhanced among pregnant woman living in a newly renovated house or near heavy-traffic roads but were mitigated by household usage of smoke ventilators when cooking. We observed a positive interaction of maternal exposure to TVOCs and PM2.5 in regard to the risk for CHDs.Conclusions: Maternal exposure to indoor VOCs and PMs may increase the risk of giving birth to foetuses with CHDs.

Objectives. Hyperhomocysteinemia (HHcy) is an easily neglected disease, which can be hidden in the body for many years without signs or symptoms. We want to explore the causes of HHcy, the correlation of HHcy with micronutrients, lifestyle, dietary habits and HHcy related genes, preventing the occurrence of HHcy.Methods. 800 subjects (M/F, 403/397) were divided into normal Hcy and HHcy group according to the plasma levels of Hcy, compared essential characteristics by questionnaires, genetic polymorphism tested by Realtime PCR and micronutrients detected by mass spectrometry. The statistical analysis methods were Chi - square tests, ANOVA, logistic regression. This trial has been registered with the trial number ChiCTR1900025136. Results. 42.66% of 143 HHcy cases were aged from 10 to 18, with higher levels of zinc (Zn), vitamin A, Uric acid (P < 0.05) and a lower level of 25-OH-D3, VB12, folic acid (Fol) (P < 0.05) compared to the normal group. The multivariate logistic regression significantly predicted HHcy development containing higher level of Zinc (Exp(B) = 1.042; 95% CI, 1.000 - 1.086), higher Uric (Exp(B) = 1.014; 95% CI, 1.008 - 1.019), lower B12 (Exp(B) = 0.993; 95%CI, 0.989 - 0.997), lower Folic acid (Exp(B) = 0.772; 95% CI, 0.657 - 0.907), and polymorphism of MTHFR C677T (Exp(B) = 2.923; 95% CI, 1.399–6.107).Conclusion. Pay more attention to those students who were facing great pressure because they are very likely to be potential HHcy patients with high levels of uric acid and zinc and anxiety.