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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]

Previous epidemiologic research has shown that phthalate exposure in pregnant women is related to adverse birth outcomes in a sex-specific manner. However, the biological mechanism of phthalate exposure that causes these birth outcomes remains poorly defined. In this research, we investigated the association between phthalate exposure and placental oxidative stress in a large population-based cohort study, aiming to initially explore the relationship between phthalate exposure and gene expression in placental oxidative stress in a sex-specific manner. Quantitative PCR was performed to measure the expression of placental inflammatory mRNAs (HO-1, HIF1α, and GRP78) in 2469 placentae. The multiple linear regression models were used to investigate the associations between mRNA and urinary phthalate monoesters. Phthalate metabolites monomethyl phthalate (MMP) and mono-n-butyl phthalate (MBP) were positively correlated with higher HIF1α expression in placentae of male fetuses (p <.05). Mono-benzyl phthalate (MBzP) increased the expression of HO-1, HIF1α, and GRP78 in placentae of male fetuses, and mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) up-regulated the expression of HIF1α and GRP78. Additionally, mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP) was negatively correlated with HO-1, HIF1α, and GRP78 in placentae of female fetuses. Maternal phthalate exposure was associated with oxidative stress variations in placental tissues. The associations were closer in the placentas of male fetuses than in that of female ones. The placenta oxidative stress is worth further investigation as a potential mediator of maternal exposure-induced disease risk in children. [ABSTRACT FROM AUTHOR]

Background: The rate of autism spectrum disorder (ASD) has been rising worldwide, and therefore it is important to identify potential causes of ASD to facilitate early prevention. This study examined the role of breastfeeding and the association between caesarean delivery (CD) and children's autism spectrum disorder. Methods: The data were from the Ma'anshan birth cohort (MABC) in China, that was set up between May 2013 and September 2014. Women within 14 gestational weeks were recruited. The delivery mode was extracted from medical notes and infant feeding was obtained from questionnaire surveys. Autism-like behaviour was assessed using the Checklist for Autism in Toddlers (CHAT-23) when children were 18 months old, and 3 years of age. At 5 years of age, autism-like behaviour was assessed using the Clancy Autism Behavior Scale behavior. Structural equation models tested the mediation effects of breastfeeding between CD and children's autism spectrum disorder. Results: In all, 1520 (48.89%) women gave birth via CD, and 406 (13.86%) children were identified with autism-like behaviours at 18 months. Compared with women giving birth via vaginal delivery, those giving birth via CD were more likely to experience a higher proportion of delayed initiation of breastfeeding (p < 0.01), and delayed onset of lactogenesis (p < 0.01). CD was associated with a lower proportion of exclusive breastfeeding at 4 months after delivery (p = 0.02). Autism-like behaviour was less likely amongst infants with exclusively breastfeeding at 4 months than amongst those not exclusively breastfeeding at 4 months (p < 0.01). SEM indicated that women who gave birth by CD were more likely to stop exclusive breastfeeding in the first 4 months (standard estimations = − 0.04, p = 0.02), and those children who were not exclusively breastfed at 4 months were more likely to have autism-like behaviours (standard estimations = − 0.05, p < 0.01). The associations persisted at 3 years, but not at 5 years. Conclusions: Exclusive breastfeeding at 4 months of age mediated the association between caesarean delivery and children's autism-like behaviours. [ABSTRACT FROM AUTHOR]

Maternal prenatal depression is associated with child sleep. We investigated whether maternal depression comorbid with anxiety worsens toddler's sleep problems in a prospective cohort study. A total of 1583 mother-infant pairs from the China-Anhui Birth Cohort study were examined. The participants completed the Center for Epidemiologic Studies Depression Scale (CES-D) and Self-Rating Anxiety Scale (SAS) at 30–34 weeks of gestation, and the Edinburgh Postnatal Depression Scale (EPDS) at 3-month postpartum. Toddler's sleep was assessed by the Brief Infant Sleep Questionnaire (BISQ) at 30 months old. Logistic regression models were used to investigate the associations between prenatal depression and anxiety and toddler's sleep, while adjusting for maternal gestational age, education, family income, alcohol use, premature birth, fetal growth restriction, mode of delivery, postnatal depression, and 3-month breastfeeding. In total, 9.0% of participants reported prenatal depression comorbid with anxiety symptoms, and the prevalence of depression, anxiety was 6.7% and 7.3%, respectively. Compared with mothers without depression and anxiety, maternal depression combined with anxiety were significantly associated with shorter total sleep duration (11.16 ± 1.06 h), longer settling time (29.25 ± 23.57 min), and higher risk of toddlers' sleep problems assessed by BISQ (OR = 2.09, 95% CI: 1.22–3.57) or parental report (OR = 1.84, 95% CI: 1.22–2.77). However, there was no significant association between maternal postnatal depression and toddler sleep behaviors. Maternal prenatal depression comorbid with anxiety significantly associated with poorer toddler's sleep. Strategies to regulate prenatal mood status should be considered during prenatal health care to improve children's sleep development. [ABSTRACT FROM AUTHOR]

Background: Maternal selenium (Se) deficiency is associated with some adverse pregnant outcomes. However, it remains controversial whether maternal Se deficiency during gestation enhances the risks for low-birth-weight (LBW) and small-for-gestational-age (SGA) newborns.Methods: For our cohort study, total 3133 mother-and-infant pairs were selected. Maternal serum Se concentration was detected by graphite furnace atomic absorption spectrometry. According to international references for maternal serum Se concentration, subjects were divided into Se deficiency (<45.0 μg/L), Se insufficiency (45.0-94.9 μg/L) and Se sufficiency (≥95.0 μg/L).Results: There was a positive relation of maternal serum Se concentration in gestation and neonatal birth weight. Further analysis showed that the risks for LBW and SGA in SD group were significantly higher than that in SI and SS group, the adjusted ORs for LBW and SGA newborns were 1.87 (95%CI: 1.02, 3.45; P = 0.04) and 1.47 (95%CI: 1.07, 2.02; P = 0.02) in SI group, and 3.92 (95%CI: 2.03, 7.57; P < 0.001) and 2.77 (95%CI: 1.92, 4.02; P < 0.001) in SD group compared to SS group. In different gender subgroup, positive relations were observed between maternal Se deficiency and the risk for LBW girls, as well as the risks for both SGA girls and boys.Conclusion: Maternal Se deficiency in gestation was positively associated with the risk for LBW girls, as well as the risks for both SGA girls and boys. [ABSTRACT FROM AUTHOR]

Previous studies have shown conflicting findings regarding the relationship between maternal vitamin D deficiency (VDD) and fetal growth restriction (FGR). We hypothesised that parathyroid hormone (PTH) may be an underlying factor relevant to this potential association. In a prospective birth cohort study, descriptive statistics were evaluated for the demographic characteristics of 3407 pregnancies in the second trimester from three antenatal clinics in Hefei, China. The association of the combined status of vitamin D and PTH with birth weight and the risk of small for gestational age (SGA) was assessed by a multivariate linear and binary logistic regression. We found that declined status of 25-hydroxyvitamin D is associated with lower birth weight (for moderate VDD: adjusted β = −49·4 g, 95 % CI −91·1, −7·8, P < 0·05; for severe VDD: adjusted β = −79·8 g, 95 % CI −127·2, −32·5, P < 0·01), as well as ascended levels of PTH (for elevated PTH: adjusted β = −44·5 g, 95 % CI −82·6, −6·4, P < 0·05). Compared with the non-VDD group with non-elevated PTH, pregnancies with severe VDD and elevated PTH had the lowest neonatal birth weight (adjusted β = −124·7 g, 95 % CI −194·6, −54·8, P < 0·001) and the highest risk of SGA (adjusted risk ratio (RR) = 3·36, 95 % CI 1·41, 8·03, P < 0·01). Notably, the highest risk of less Ca supplementation was founded in severe VDD group with elevated PTH (adjusted RR = 4·67, 95 % CI 2·78, 7·85, P < 0·001). In conclusion, elevated PTH induced by less Ca supplementation would further aggravate the risk of FGR in pregnancies with severe VDD through impaired maternal Ca metabolism homoeostasis. [ABSTRACT FROM AUTHOR]

Background: The biological pathways through which vitamin D is involved in the regulation of systemic inflammation remain largely unknown. Objective: The objective of this study was to evaluate the role of vitamin D status on the relationship between lipid profile and high-sensitivity C-reactive protein (hs-CRP) in pregnant women. Design: Serum 25-hydroxyvitamin D (25(OH)D), hs-CRP, and indicators of lipid profiles (total cholesterol, TC; triglyceride, TG; high-density lipoprotein cholesterol, HDL-C; low-density lipoprotein cholesterol, LDL-C), were measured in 2479 pregnant women during the second trimester. Potential confounding including maternal sociodemographic characteristics, perinatal health status, diet, and lifestyle was prospectively collected. Multiple regression models and cubic models were used to evaluate the associations. Results: There was a significant non-linear relationship between lipid profile (TC, TG, HDL-C, LDL-C) and hs-CRP (P < 0.05). Increased serum 25(OH)D was significantly associated with decreasing TC, TG, HDL-C, LDL-C, and hs-CRP levels. Compared with medium levels of lipids group, pregnant women with higher levels of TC or TG have higher levels of hs-CRP, and pregnant women with lower levels of TC, HDL-C or LDL-C also have higher levels of hs-CRP in the vitamin D deficient group, and there was a significant correlation between low levels of TG and decreased hs-CRP (adjusted β for TG: -0.063, 95%CI: − 0.120,-0.007) in the non-vitamin D deficient group. Mediators that had appreciable shares of the associations between 25(OH)D and hs-CRP was TG (10.2% of the association; β = − 0.011; total indirect effect: 95% CI: − 0.019, − 0.002). The cubic model suggested that a steep increase in the adjusted regression coefficient of lipid with hs-CRP up to 50 nmol/L of 25(OH)D, and the highest adjusted regression coefficients were observed in pregnant women with 25(OH)D above 50 nmol/L. Conclusion: Our findings suggest that high levels of vitamin D during pregnancy may improve lipid profile levels and inhibit elevated hs-CRP induced by high lipid metabolism. [ABSTRACT FROM AUTHOR]

Objective: This study was conducted to evaluate the changes of temporomandibular joints (TMJs) through magnetic resonance imaging (MRI) scanning and the electrical changes in mandibular movement and masticatory muscle surface of mild‐to‐moderate obstructive sleep apnoea‐hypopnoea syndrome (OSAHS) patients before and after treatment with mandibular advancement device (MAD). Methods: This was a single‐centre, prospective study recruiting OSAHS patients undergoing treatment with MAD in Department of Stomatology, Yannan Hospital, Kunming, China. Patients were recruited from February 2015 to October 2015, and TMJ changes were observed in MRI scanning before and after 18 months of treatment with MAD in cohort 1. The second cohort of the patients were recruited from January 2014 to September 2015 and electrical changes in mandibular movement and masticatory muscle surface of patients before and after 6 months of treatment with MAD. Results: In the cohort 1, TMJ changes analysed through MRI scanning, before and after 18‐month treatment with MAD, there was no significant deviation in the angle of joint disc position. A minor change in the position relationship between condylar process, articular disc and articular fossa but not significant was observed. There was no significant difference in the shape and magnitude of mandibular incision edge movement, percussion movement, masticatory movement and condylar central trajectory among the recruited OSAHS patients, before and after 6 months of MAD treatment as analysed through electromyography. Conclusion: In this study, from the results it was evident that the effect of MAD on the stomatognathic system of OSAHS patients is minimal. [ABSTRACT FROM AUTHOR]

Background Previous studies have shown conflicting findings regarding the relation of vitamin D status and supplementation during pregnancy with gestational diabetes mellitus (GDM). Most of these studies hypothesized that 25-hydroxyvitamin D [25(OH)D] concentrations were associated with GDM risk and glucose metabolism based on linear association models. Objectives We aimed to estimate the associations of 25(OH)D concentrations and vitamin D supplementation with GDM risk and glucose metabolism and determine the threshold concentrations of 25(OH)D that could significantly affect glucose metabolism and GDM risk. Methods In a prospective birth cohort study, we collected information about sociodemographic characteristics, health status, and lifestyle from 4984 pregnant women. Vitamin D supplementation and 25(OH)D concentrations were assessed in the second trimester. Data from the 75-g oral-glucose-tolerance test were obtained at 24–28 weeks of gestation. Results A total of 922 (18.5%) women were diagnosed with GDM. Compared with women with 25(OH)D concentrations <25 nmol/L, the GDM risk was significantly lower in women with 25(OH)D concentrations ranging from 50 to 75 nmol/L (RR: 0.74; 95% CI: 0.58, 0.95) and >75 nmol/L (RR: 0.40; 95% CI: 0.22, 0.70). The curve-fitting models suggested a significant large reduction in GDM risk, fasting plasma glucose, and area under the curve of glucose with increasing 25(OH)D concentrations only for concentrations >50 nmol/L. Consistently, GDM risk was significantly reduced only in women who took 400–600 IU vitamin D/d (RR: 0.83; 95% CI: 0.70, 0.97) with a mean 25(OH)D concentration of 50 nmol/L but not in women taking vitamin D sometimes with a mean 25(OH)D concentration of 40 nmol/L. Conclusions GDM risk was significantly reduced only in pregnant women with 25(OH)D concentrations >50 nmol/L. Pregnant women taking 400–600 IU vitamin D/d with mean 25(OH)D concentrations of 50 nmol/L had a lower risk of GDM. [ABSTRACT FROM AUTHOR]

Objectives: This study depicts the dose-response relationship between blood pressure (BP) during pregnancy and adverse birth outcomes in different trimesters.Study Design: We used restricted cubic spline to quantify the dose-response relationship between maternal BP in different trimesters and risk of adverse birth outcomes (small for gestational age, SGA; and pre-term birth, PTB). The data were from the Ma'anshan birth cohort study in China (N = 3273).Main Outcome Measures: Risk of SGA and PTB.Results: There were dose-response associations of both systolic blood pressure (SBP) and diastolic blood pressure (DBP) with risk of SGA in the third trimester and with PTB in both second and third trimesters. In the third trimester, compared with SBP of 120 mmHg, the odds ratios (ORs) and 95% confidence intervals (CI) of SGA were 1.12 (1.01-1.19), 1.32 (1.10-1.60), 1.65 (1.20-2.27) and 2.05 (1.30-3.24) for SBP of 125, 130, 135 and 140 mmHg, respectively. The corresponding ORs and 95% CIs of PTB were 1.15 (1.00-1.32), 1.59 (1.28-1.98), 2.35 (1.66-3.33) and 3.47 (2.10-5.73), respectively. Compared with DBP of 70 mmHg, the ORs and 95% CIs of SGA were 1.44 (1.16-1.78) and 3.04 (2.06-4.50) for DBP of 80 and 90 mmHg, respectively. The corresponding ORs and 95% CIs of PTB were 1.32 (0.93-1.90) and 3.58 (2.21-5.78), respectively.Conclusions: A consistent set of dose-response relationships between maternal BP and adverse birth outcomes were observed. Most importantly, we found that moderately elevated maternal BP, even within a normal range, increased the risk of adverse birth outcomes. [ABSTRACT FROM AUTHOR]

Background: Evidence exists that maternal zinc status during pregnancy is linked to adverse pregnancy outcomes including abortion, fetal growth restriction, and neural tube defects. However, it remains unclear whether maternal serum zinc concentration (SZC) during pregnancy is associated with risk of preterm birth.Objective: This study was designed to investigate the association between maternal SZC during pregnancy and risk of preterm birth.Methods: For this substudy of the China-Anhui Birth Cohort Study, 3081 maternal-singleton pairs with detailed birth records and available serum samples were identified. The maternal SZC was determined with flame atomic absorption spectroscopy. A total of 169 preterm births were identified. In this study, the women were divided into tertiles on the basis of their SZC: low (<76.7 μg/dL), medium (76.7-99.6 μg/dL), and high (≥99.7 μg/dL). The ORs for preterm birth were estimated by using multiple logistic regression models.Results: The median SZC was 87.3 μg/dL (range: 11.1-211 μg/dL). Incidences of preterm birth were 7.3% and 6.0% among subjects with low and medium SZCs, respectively, which were significantly higher than 3.1% among subjects with a high SZC [ORs (95% CIs) for low and medium SZCs: 2.45 (1.60, 3.74), P < 0.001, and 2.00 (1.29, 3.09), P < 0.01, respectively]. After adjustment for prepregnancy body mass index, maternal age, time of serum collection, gravidity, parity, and monthly income, adjusted ORs were 2.41 (95% CI: 1.57, 3.70; P < 0.001) and 1.97 (95% CI: 1.27, 3.05; P < 0.01) among subjects with low and medium maternal SZCs.Conclusions: Maternal serum zinc concentration during pregnancy is inversely associated with risk of preterm birth in the Chinese population, and the results are driven by maternal SZC in the first trimester. [ABSTRACT FROM AUTHOR]

Objectives Higher or lower blood pressure may relate to cognitive impairment, whereas the relationship between blood pressure and cognitive impairment among the elderly is not well-studied. The study objective was to determine whether blood pressure is associated with cognitive impairment in the elderly, and, if so, to accurately describe the association. Design Cross-sectional data from the sixth wave of the Chinese Longitudinal Healthy Longevity Survey (CLHLS) conducted in 2011. Setting Community-based setting in longevity areas in China. Participants A total of 7144 Chinese elderly aged 65 years and older were included in the sample. Measures Systolic blood pressures (SBP) and diastolic blood pressures (DBP) were measured, pulse pressure (PP) was calculated as (SBP) − (DBP) and mean arterial pressures (MAP) was calculated as 1/3(SBP) + 2/3(DBP). Cognitive function was assessed via a validated Mini-Mental State Examination (MMSE). Results Based on the results of generalized additive models (GAMs), U-shaped associations were identified between cognitive impairment and SBP, DBP, PP, and MAP. The cutpoints at which risk for cognitive impairment (MMSE <24) was minimized were determined by quadratic models as 141 mm Hg, 85 mm Hg, 62 mm Hg, and 103 mm Hg, respectively. In the logistic models, U-shaped associations remained for SBP, DBP, and MAP but not PP. Below the identified cutpoints, each 1-mm Hg decrease in blood pressure corresponded to 0.7%, 1.1%, and 1.1% greater risk in the risk of cognitive impairment, respectively. Above the cutpoints, each 1-mm Hg increase in blood pressure corresponded to 1.2%, 1.8%, and 2.1% greater risk of cognitive impairment for SBP, DBP, and MAP, respectively. Conclusion A U-shaped association between blood pressure and cognitive function in an elderly Chinese population was found. Recognition of these instances is important in identifying the high-risk population for cognitive impairment and to individualize blood pressure management for cognitive impairment prevention. [ABSTRACT FROM AUTHOR]

Background: Outdoor artificial light at night (ALAN) has been linked to an elevated risk of diabetes, but the available literature on the relationships between ALAN and glucose homeostasis in pregnancy is limited. Methods: A prospective cohort study of 6730 pregnant women was conducted in Hefei, China. Outdoor ALAN exposure was estimated using satellite data with individual addresses at a spatial resolution of approximately 1 km, and the average ALAN intensity was calculated. Gestational diabetes mellitus (GDM) was diagnosed based on a standard 75-g oral glucose tolerance test. Multivariable linear regression and logistic regression were used to estimate the relationships between ALAN and glucose homeostasis. Results: Outdoor ALAN was associated with elevated glucose homeostasis markers in the first trimester, but not GDM risk. An increase in the interquartile range of outdoor ALAN values was related to a 0.02 (95% confidence interval [CI]: 0.00, 0.03) mmol/L higher fasting plasma glucose, a 0.42 (95% CI: 0.30, 0.54) μU/mL increase in insulin and a 0.09 (95% CI: 0.07, 0.12) increase in homeostatic model assessment of insulin resistance (HOMA-IR) during the first trimester. Subgroup analyses showed that the associations between outdoor ALAN exposure and fasting plasma glucose, insulin, and HOMA-IR were more pronounced among pregnant women who conceived in summer and autumn. Conclusions: The results provided evidence that brighter outdoor ALAN in the first trimester was related to elevated glucose intolerance in pregnancy, especially in pregnant women conceived in summer and autumn, and effective strategies are needed to prevent and manage light pollution. [Display omitted] • The first trimester ALAN exposure was associated with elevated glucose intolerance. • Outdoor ALAN exposure was associated with higher FPG, insulin, and HOMA-IR. • Outdoor ALAN exposure was not associated with a higher risk of GDM. [ABSTRACT FROM AUTHOR]

Background: Vitamin D has been demonstrated a "neuroprotective" effect, but it is unclear whether early-life adequate vitamin D protect adverse neurodevelopment. We aimed to examine the role of neonatal vitamin D in the association of maternal depression (MD) symptoms with toddlers ADHD.Methods: Participants included 1 125 mother-infant pairs from the China-Anhui Birth Cohort study. MD was assessed by the Center for Epidemiological Studies Depression Scale (CES-D) at 30-34 gestational weeks. Toddlers ADHD was reported by the Conners' Hyperactivity Index (CHI) at 48-54 months postpartum. Multiple logistic regression models were performed to evaluate the association of maternal depressive score and toddlers ADHD while cord blood 25(OH)D levels were stratified.Results: Toddlers of mothers with higher depression score were at higher risk of ADHD (20.1% vs 11.1%, P = 0.003; adjusted RR=1.75, 95% CI: 1.10-2.81). Among toddlers with neonatal vitamin D deficiency (VDD), ADHD risk was significantly increased with maternal MD (adjusted RR=3.74, 95% CI: 1.49-9.41), but the association was not found in toddlers with neonatal vitamin D adequacy (VDA). Compared to toddlers without MD, toddlers with both MD and neonatal VDD had higher risk of ADHD (adjusted RR=3.10, 95% CI: 1.44-6.63). But the risk did not significantly increase in toddlers with MD and neonatal VDA (adjusted RR=1.53, 95% CI: 0.86-2.72).Limitations: Maternal depressive symptoms in early pregnancy and anxious symptoms were needed to include.Conclusion: This prospective study indicated that the detrimental effect of maternal prenatal depressive symptoms on offspring's ADHD symptoms strengthened in toddlers with neonatal VDD. [ABSTRACT FROM AUTHOR]

Background: Pregnancy-related anxiety plays a major role in shaping offspring's neural development. However, its gender-specific effect on children's emotional and behavioral development is controversial and the knowledge of critical period is limited. This study aims to examine gender-specific effect of pregnancy-related anxiety on preschooler's emotional and behavioral development.Methods: This study was based on the China-Anhui Birth Cohort Study (C-ABCS). A total of 3443 mother-child pairs were included in final data analysis. Pregnancy-related anxiety was assessed by Pregnancy-Related Anxiety Questionnaire respectively in the 1st and 3rd trimester of pregnancy. Strengths and Difficulties Questionnaires (SDQ) were completed by parents to assess preschool emotional and behavioral development in boys and girls. Logistic regression models were used to examine the association between pregnancy-related anxiety and preschoolers' emotional and behavioral problems.Results: The overall prevalence of pregnancy-related anxiety was 31.6%. Compared with those whose mothers without pregnancy-related anxiety in either 1st or 3rd trimester, preschool boys born of mothers with pregnancy-related anxiety in the 1st trimester and in the 3rd trimester had an increased risk of conduct problems. Pregnancy-related anxiety in the 1st, 3rd trimester and in both trimesters all related with preschool boys' hyperactivity and total difficult problems. Pregnancy-related anxiety in the 1st trimester and in both 1st and 3rd trimester increased the risk of preschool girls' emotional problems and total difficult problems.Conclusion: Pregnancy-related anxiety may relate with preschool boys' externalizing problems in early and late of pregnancy and increase the risk of internalizing problems in girls in early pregnancy.Limitations: There was no data on pregnancy-related anxiety in the second trimester. [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]