Foetal 25-hydroxyvitamin D moderates the association of prenatal air pollution exposure with foetal glucolipid metabolism disorder and systemic inflammatory responses
Yang Liu, Lei Li, Jun Xie, X C Jiao, Honglin Hu, Ying Zhang, Ruixue Tao, Fangbiao Tao, Peng Zhu
Abstract
BACKGROUND: Previous studies have indicated that systemic inflammation may play an important role in the association between air pollution exposure and glucolipid metabolism disorders, and vitamin D supplementation was beneficial in improving systemic inflammation and glucolipid metabolism. However, the role of foetal 25-hydroxyvitamin D (25(OH)D) and high-sensitivity C-reactive protein (hs-CRP) in the association between prenatal air pollution exposure and foetal glucolipid metabolism disorders is still not clear. OBJECTIVE: To verify whether foetal 25(OH)D can improve glucolipid metabolism disorders induced by prenatal air pollution exposure by inhibiting the systemic inflammation. METHODS: ) data from the Hefei City Ecology and Environment Bureau. Cord blood biomarkers (25(OH)D, hs-CRP, C-peptide, HDL-C, LDL-C, TC, and TG) were measured. RESULTS: , and CO was associated with 20.0% (95% confidence interval (CI): 16.9, 23.6), 20.1% (16.8, 23.3), 22.9% (20.6, 25.3), and 16.7% (14.4, 19.0) higher cord blood hs-CRP levels, respectively, and an SD increase in hs-CRP was associated with 1.4% (0.1, 2.8), 2.2% (1.6, 2.9), 1.4% (0.9, 2.0), and 3.9% (2.8, 4.9) higher C-peptide, LDL-C, TC, and TG levels in the cord blood, respectively. However, there was a monotonic decrease in βs between cord blood 25(OH)D and biomarkers (P for trend < 0.001). Furthermore, mediation analysis revealed that the association between air pollution exposure and foetal glucolipid metabolic indexes mediated by hs-CRP and 25(OH)D was 19.35%. In stratified analyses, the significant negative association between cord blood 25(OH)D with foetal hs-CRP and glucolipid metabolic indexes was observed only at low-medium levels of air pollution exposure. CONCLUSIONS: Prenatal air pollution exposure could damage foetal glucolipid metabolic function through systemic inflammation. High foetal 25(OH)D levels may improve foetal systemic inflammation and glucolipid metabolism at low-medium levels of prenatal air pollution exposure.