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Maternal inflammation has been proposed as a possible pathway connecting prenatal environmental adversity (PEA), which includes maternal overweightness or obesity, diabetes, hypertensive disorders, and mood or anxiety disorders, to child neurodevelopmental delay. However, effective preventive measures have not yet been reported. Herein, we aimed to investigate whether a maternal anti-inflammatory diet reduced the risk of PEA-induced neurodevelopmental delay, by inhibiting inflammation. This prospective study included 7438 mother–child pairs. Maternal overweightness or obesity, diabetes, and hypertensive disorders were diagnosed before 28 week gestation. Maternal depression disorders were identified using the Edinburgh postnatal depression survey (EPDS) during mid-pregnancy. During mid- and late pregnancy, maternal high-sensitivity C-reactive protein (hs-CRP) levels were measured to evaluate systemic inflammation. The inflammatory potential of the diet was evaluated using the food-based empirical dietary inflammatory pattern (EDIP) score during mid-pregnancy. Pregnant women were classified into high- or low-score groups based on the median EDIP score. The outcomes of neurodevelopmental delay at 6–36 month postpartum were extracted from the Register of Child Healthcare. Among the 7438 mother–child pairs, 2937 (39.5%) were exposed to PEA, and neurodevelopmental delay occurred in 540 (7.3%). Children exposed to PEA had a higher risk of neurodevelopmental delay than those not exposed. PEA exposure was associated with increased hs-CRP during pregnancy in a PEA monotonic manner, an interquartile range increase in hs-CRP in mid- and late pregnancy was associated with an increased risk of child neurodevelopmental delay. Higher maternal persistent inflammation partially mediated the effect of PEA exposure on child neurodevelopmental delay by 17.19%. An increased risk of PEA-related neurodevelopmental delay was observed only in the children of mothers with high-EDIP rather than low-EDIP. These results suggest that increased systemic inflammation through mid- and late pregnancy mediates the association between PEA and child neurodevelopmental delay. A maternal anti-inflammatory diet may improve PEA-induced neurodevelopmental delay, by inhibiting inflammation. [ABSTRACT FROM AUTHOR]

Thallium (Tl), a ubiquitous environmental toxicant, can cross the placental barrier during pregnancy. However, the effects of prenatal Tl exposure on placental function are currently unclear. Based on the Ma'anshan Birth Cohort study, we examined whether long-term prenatal Tl exposure was associated with placental inflammation. Tl concentrations were quantified in serum samples (n = 7050) from 2515 pregnancy during each trimester, placental inflammatory cytokine mRNA expression was assessed in 2519 placenta tissues. Geometric mean values of serum Tl concentrations were 63.57, 63.63 and 48.71 ng/L for the first, second and third trimesters, respectively. After adjustment for potential confounders, serum Tl concentration was positively associated with CD68 (β: 0.30; 95% CI: 0.05, 0.56) in the first trimester and TNF-α (β: 0.12; 95% CI: 0.01, 0.23), IL-6 (β: 0.15; 95% CI: 0.05, 0.25) and CD68 (β: 0.25; 95% CI: 0.10, 0.39) in the third trimester, however was negatively associated with IL-4 (β: −0.21; 95% CI: −0.41, −0.01) and CD206 (β: −0.23; 95% CI: −0.45, −0.02) in the first trimester. Repeated measures analysis showed that TNF-α, IL-6 and CD68 increased by 0.11 (95% CI: 0.01, 0.21), 0.12 (0.15, 95% CI: 0.05, 0.25), 0.22 (95% CI: 0.10, 0.39), respectively, with each 1ln-transformed Tl increase in total samples. Gender-specific analyses revealed that these associations were largely driven by male offspring. In addition, immunohistochemistry revealed that nuclear NF-κB p65 expression increased in placenta tissue. The results of this prospective cohort study provide longitudinal evidence that prenatal Tl exposure induces a placental inflammatory response in the Chinese population. Image 1 • We measured 11 inflammatory cytokine mRNAs expression to observe local immune activation in the placenta. • Elevated Tl concentrations were associated with increased placental TNF-α, IL6 and CD68 mRNA expression in longitudinal analysis. • Our findings suggest that prenatal Tl exposure may induce the placenta inflammation response via NF-κB activation. [ABSTRACT FROM AUTHOR]

This study enrolled 3266 pregnant women, to explore the relationship of prenatal phthalate exposure with the risk of preterm birth and gestational age. All participants filled questionnaires and provided with up to three urine samples during three trimesters. Seven phthalate metabolites in urines were measured. The incidences of very preterm, late preterm, early-term, late-term and postterm births were 0.58%, 3.52%, 24.22%, 10.53%, and 0.34%, respectively. Non-linear relationships were shown between phthalate metabolites and gestational age. Except for monomethyl phthalate (OR = 1.65, 95%CI = 1.17–2.34), the average concentrations of phthalate metabolites were associated with a slightly and insignificantly increased risk of overall preterm birth (<37+0 gestational weeks). Through a restricted cubic spline regression, phthalate metabolites were found to be related to the risk of overall preterm birth in a linear manner (p -value >0.05) or a non-linear manner (p -value <0.05). All curves indicated the overall preterm birth risk rose with the increase of phthalate metabolite concentrations. Finally, compared with full-term birth (39+0 to 40+6 gestational weeks), phthalate metabolites were associated with the elevated risks of very preterm, late preterm and postterm births, although some relationships were not statistically significant. In conclusion, these findings suggested non-linear associations between phthalate metabolites and gestational age. Exposure to some phthalate metabolites was associated with increased risks of overall preterm birth and postterm birth. • Rates of very preterm, late preterm, early-term and late-term births were 0.58%, 3.52%, 24.22% and 10.53%, respectively. • Non-linear relationship was observed between certain phthalate metabolites and the odds ratio of overall preterm birth. • Some phthalates were associated with increased risks of very preterm, late preterm and postterm births. • Non-linear curves for associations between phthalates and gestational age were revealed. Capsule: Based on a cohort study with large sample size, the levels of phthalate metabolites in urine at 3 time points during pregnancy were analyzed in relation to gestational age and preterm birth, which aimed to confirm the previous findings in this topic. [ABSTRACT FROM AUTHOR]