Prenatal vanadium exposure, cytokine expression, and fetal growth: A gender-specific analysis in Shanghai MCPC study

Increasing evidence supports that maternal exposure to vanadium (V) is associated with adverse birth outcomes including preterm birth and low birth weight. However, the effect of V exposure on intrauterine fetal growth and the underlying biological mechanism are still unclear. The present study includes 227 mother-infant pairs from the Shanghai Maternal-Child Pairs Cohort to assess the gender-specific effect of intrauterine V exposure on fetal growth and related cytokines. Maternal blood samples were collected to measure V concentration and biomarkers of growth. We used multiple linear regression to evaluate the gender-specific effect of prenatal V exposure on birth parameter and growth-related cytokines. Mixed-effect models were applied to assess the non-linear association between gestational V exposure and intrauterine fetal growth. Covariates adjusted in the regression models as potential confounders including maternal age, pre-pregnancy body mass index, gestational weeks, parity, socio-demographic status, etc. Results showed that prenatal V exposure was negatively associated with birth weight (β = -64.73) in female newborns and body length (β = -0.10) in male. During the fetal period, maternal V exposure was associated with decreased biparietal diameter (β = -0.91), head circumference (β = -2.96), femur length (β = -0.72) and humerus length (β = -0.64) in male. Trimester-specific analyses showed that serum V concentration in the second trimester was associated with significant reductions in intrauterine growth parameters. Besides, prenatal V exposure could down-regulate the expression of growth hormone (GH) in both maternal blood (β = -0.23) and umbilical cord blood (β = -1.66) in male fetuses, and the expression of brain derived neurotrophic factor (BDNF) in cord blood in females (β = -0.52). Our results suggest that prenatal V exposure has a gender-specific effect on fetal growth and the second trimester may be a sensitive window. The disruption of grow-related cytokines may potentially be the biological mechanism of these effects.