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Ambient fine particulate matter (PM 2.5) exposure increases local and systemic interleukin-6 (IL-6). However, the pathogenic role of IL-6 signalling following PM 2.5 exposure, particularly in the development of pulmonary dysfunction and abnormal glucose homeostasis, has hardly been investigated. In the study, IL-6 receptor (IL-6R)-deficient (IL-6R-/-) and wildtype littermate (IL-6R+/+) mice were exposed to concentrated ambient PM 2.5 (CAP) or filtered air (FA), and their pulmonary and metabolic responses to these exposures were analyzed. Our results demonstrated that IL-6R deficiency markedly alleviated PM 2.5 exposure-induced increases in lung inflammatory markers including the inflammation score of histological analysis, the number of macrophages in bronchoalveolar lavage fluid (BALF), and mRNA expressions of TNFα, IL-1β and IL-6 and abnormalities in lung function test. However, IL-6R deficiency did not reduce the hepatic insulin resistance nor systemic glucose intolerance and insulin resistance induced by PM 2.5 exposure. Our findings support the crucial role of IL-6 signalling in the development of pulmonary inflammation and dysfunction due to PM 2.5 exposure but question the putative central role of pulmonary inflammation for the extra-pulmonary dysfunctions following PM 2.5 exposure, providing a deep mechanistic insight into the pathogenesis caused by PM 2.5 exposure. [Display omitted] • IL-6R deficiency alleviates PM 2.5 exposure-induced pulmonary dysfunction. • IL-6R deficiency aggravates PM 2.5 -induced glucose intolerance and insulin resistance. • PM 2.5 induces adipose hypertrophy and inflammation in WT and IL-6R deficient mice. • IL-6R deficiency reduces PM 2.5 -induced pulmonary but not extra-pulmonary inflammation. [ABSTRACT FROM AUTHOR]

Splenomegaly is a symptom characterized by the presence of an enlarged spleen. The impact of environmental factors on splenomegaly is largely unknown. In this study, C57BL/6 mice were treated with 125 ppm or 1250 ppm lead (Pb) via drinking water for 8 wk, and the process of splenomegaly was evaluated. Treatment with 1250 ppm Pb, but not 125 ppm Pb, caused splenomegaly, which was associated with increased capacity for erythrocyte clearance. Intriguingly, Pb-caused splenomegaly was independent of lymphoid tissue inducer (LTi) cells, which produce lymphotoxins α and β (LTα/β) to activate endothelial cells and LT organizer (LTo) cells and drive the development of spleen physiologically. A direct action of Pb on endothelial cells and LTo cells did not impact their proliferation. On the other hand, during steady state, a tonic level of interferon (IFN)γ acted on endothelial cells and LTo cells to suppress splenomegaly, as IFNγ receptor (IFNγR)-deficient mice had enlarged spleens relative to wild-type mice; during Pb exposure, splenic IFNγ production was suppressed, thus leading to a loss of the inhibitory effect of IFNγ on splenomegaly. Mechanically, Pb acted on splenic CD4+ T cells to suppress IFNγ production, which impaired the Janus kinase (Jak)1/ signal transducer and activator of transcription (STAT)1 signaling in endothelial cells and LTo cells; the weakened Jak1/STAT1 signaling resulted in the enhanced nuclear factor-κB (NF-κB) signaling in endothelial cells and LTo cells, which drove their proliferation and caused splenomegaly. The present study reveals a previously unrecognized mechanism for the immunotoxicity of Pb, which may extend our current understanding for Pb toxicology. [Display omitted] • Lead suppresses the production of IFNγ from CD4 T cells in the spleen. • The decreased IFNγ impairs the Jak1/STAT1 signaling in endothelial and LTo cells. • The weakened Jak1/STAT1 signaling activates the NF-κB signaling. • The enhanced NF-κB signaling in endothelial and LTo cells drives splenomegaly. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is a highly toxic heavy metal in our living environment. Hematopoietic stem cells (HSC) are ancestors for all blood cells. Therefore understanding the impact of Cd on HSC is significant for public health. The aim of this study was to investigate the impact of Cd2+ on energy metabolism of HSC and its involvement in hematopoiesis. Wild-type C57BL/6 mice were treated with 10 ppm of Cd2+ via drinking water for 3 months, and thereafter glycolysis and mitochondrial (MT) oxidative phosphorylation (OXPHOS) of HSC in the bone marrow (BM) and their impact on hematopoiesis were evaluated. After Cd2+ treatment, HSC had reduced lactate dehydrogenase (LDH) activity and lactate production while having increased pyruvate dehydrogenase (PDH) activity, MT membrane potential, ATP production, oxygen (O 2) consumption and reactive oxygen species (ROS), indicating that Cd2+ switched the pattern of energy metabolism from glycolysis to OXPHOS in HSC. Moreover, Cd2+ switch of HSC energy metabolism was critically dependent on Wnt5a/Cdc42/calcium (Ca2+) signaling triggered by a direct action of Cd2+ on HSC. To test the biological significance of Cd2+ impact on HSC energy metabolism, HSC were intervened for Ca2+, OXPHOS, or ROS in vitro, and thereafter the HSC were transplanted into lethally irradiated recipients to reconstitute the immune system; the transplantation assay indicated that Ca2+-dependent MT OXPHOS dominated the skewed myelopoiesis of HSC by Cd2+ exposure. Collectively, we revealed that Cd2+ exposure activated Wnt5a/Cdc42/Ca2+ signaling to reprogram the energy metabolism of HSC to drive myelopoiesis at the expense of lymphopoiesis. • Cd2+ suppresses glycolysis in hematopoietic stem cells. • Cd2+ drives mitochondrial oxidative phosphorylation in hematopoietic stem cells. • Cd2+ activates non-canonical Wnt signaling to impact energy metabolism in HSC. • Cd2+ switches the style of energy metabolism in HSC to skew toward myelopoiesis. [ABSTRACT FROM AUTHOR]

Polybrominated diphenyl ethers (PBDEs) exist extensively in the environment. Toxicological studies suggested PBDEs may interfere with adipogenic pathways. However, few human evidence addressed PBDE exposures in utero related to childhood adiposity. We assessed associations between PBDEs concentrations in cord serum and childhood adiposity measures at 7 years. Among 318 mother-child pairs from Sheyang Mini Birth Cohort Study (SMBCS) in China, nine PBDE congener concentrations were quantified in umbilical cord serum using gas chromatography-negative chemical ionization mass spectrometry (GC-NCI-MS). Anthropometric indicators of children aged 7 years were measured, including weight, height and waist circumference. Age and sex-specific body mass index (BMI) z scores were calculated based on World Health Organization (WHO)'s child growth standards. Multivariate linear and logistic regression models adjusted for putative confounders were performed to examine associations between PBDE congeners and adiposity parameters. BDE-209 was the most abundant congener of PBDEs with a median value of 19.5 ng/g lipid. The geometric mean values of nine PBDE congeners ranged from below limit of detection (LOD) to 18.1 ng/g lipid, and the detection rates were 46.5%~96.5%. Cord serum BDE-153 and BDE-154 concentrations were associated with lower childhood BMI z score (regression coefficient, β=-0.15, 95% confidence interval: -0.29, −0.02; p =0.02; β=-0.23, 95%CI: -0.43, −0.03; p =0.03, respectively) and lower waist circumference (β=-0.75 cm, 95%CI: -1.43, −0.06; p =0.03; β=-1.22 cm, 95%CI: -2.23, −0.21; p =0.02, respectively), after controlling for potential confounders. Moreover, prenatal BDE-154 exposure was related to a decreased obesity risk of children aged 7 years (odds ratio, OR=0.46, 95%CI: 0.22, 0.94; p =0.03). These effects were only observed among boys in sex-straitified analyses. Cord serum BDE-153 and BDE-154 concentrations were related to reduced adiposity measures at 7 years of age. Further evidence regarding the impacts of prenatal PBDE exposures on childhood development is warranted. • BDE-209 was the most predominant PBDE congener with a median value of 19.5 ng/g lipid. • BDE-153 and BDE-154 exposures were related to decreased adiposity measures. • Cord serum BDE-154 concentrations predicted a lower risk of obesity at 7 years. • Sex-specific effects of PBDE exposures on childhood adiposity were observed. [ABSTRACT FROM AUTHOR]

Paraquat (1,1′-dimethyl-4,4′-bipyridium dichloride, PQ), a non-selective and efficient herbicide, causes neuroinflammation, neurodegeneration and memory dysfunction. However, adverse effects of PQ on the neuroimmune interactions have rarely been investigated. Female adult C57/BL6 mice were divided into 3 groups and treated with PQ (intraperitoneal injection, 1 mg/kg or 5 mg/kg) or the vehicle (an equivalent volume of 0.9% saline) every two days, at day 1, 3, 5, 7, 9, 11, 13, 15, 17, 19, 21, 23, 25, 27, for a total of 14 doses. We evaluated blood-brain barrier (BBB) integrity and PQ concentrations during the course of PQ exposure and tested interleukin-1β (IL-1β) concentrations in dentate gyrus (DG) after 28 days PQ exposure. In addition, memory function, neural stem cells (NSCs) proliferation, neurogenesis and microglia polarization were analyzed after PQ exposure. Furthermore, mice were intraperitoneal injections of anti-IL-1β during 5 mg/kg PQ exposure to test the rule of IL-1β. Blood-brain barrier (BBB) permeability and PQ concentrations increased gradually during PQ exposure (n = 6). Moreover, memory function, NSCs proliferation and neurogenesis were impaired after 5 mg/kg PQ exposure (n = 6). Further analyses revealed that 'classically' activated (M1) microglia and IL-1β concentrations in DG were increased after 5 mg/kg PQ treatment (n = 6). Moreover, we found that neutralization of IL-1β partly restored PQ-induced NSCs impairments and memory dysfunction (n = 6). In conclusion, our results revealed that PQ induced NSCs impairments and memory dysfunction in adult mice, which was related to the release of IL-1β by M1-polarized microglia in DG. These findings may help understand the neurotoxic effect of PQ. • Paraquat induced memory dysfunction and neural stem cells impairments. • Paraquat increased microglia M1 polarization and IL-1β in DG. • Anti-IL-1β treatment rescued paraquat-induced memory dysfunction of mice. • IL-1β mediated paraquat-induced the impairments of neural stem cells. [ABSTRACT FROM AUTHOR]

Interleukin-6 (IL-6) signaling is critical for cardiomyocyte hypertrophy, while the role of IL-6 in the pathogenesis of myocardium hypertrophy remains controversial. To determine the essential role of IL-6 signaling for the cardiac development during AngII-induced hypertension, and to elucidate the mechanisms, wild-type (WT) and IL-6 knockout (IL-6 KO) mice were infused subcutaneously with either vehicle or AngII (1.5 μg/h/mouse) for 1 week. Immunohistological and serum studies revealed that the extents of cardiac fibrosis, inflammation and apoptosis were reduced in IL-6 KO heart during AngII-stimulation, while cardiac hypertrophy was obviously induced. To investigate the underlying mechanisms, by using myocardial tissue and neonatal cardiomyocytes, we observed that IL-6/STAT3 signaling was activated under the stimulation of AngII both in vivo and in vitro . Further investigation suggested that STAT3 activation enhances the inhibitory effect of EndoG on MEF2A and hampers cardiomyocyte hypertrophy. Our study is the first to show the important role of IL-6 in regulating cardiac pathogenesis via inflammation and apoptosis during AngII-induced hypertension. We also provide a novel link between IL-6/STAT3 and EndoG/MEF2A pathway that affects cardiac hypertrophy during AngII stimulation. [ABSTRACT FROM AUTHOR]

CoFe-LDH after cyclic voltammetry is a kind of high efficiency supercapacitor and electrocatalytic multifunctional electrode material. [Display omitted] • The morphology of the CoFe-LDH-X can be regulated by electrochemical activation strategy. • Abundant grain boundaries not only provide more chemical active sites, but also reduce the energy barrier of OER. • The optimal CoFe-LDH exhibits superior performance for supercapacitor and OER. Regulating the intrinsic properties of the transition-metal layered double hydroxide (LDH) material is a promising strategy to improve the performance of oxygen evolution reaction (OER) and supercapacitor. Herein, a facile, low-cost and convenient electrochemical cyclic voltammetry (CV) activation strategy is reported. We demonstrate that electrochemical activation could regulate the morphology, crystal structure and electronic states of the Co-Fe layered double hydroxides (CoFe-LDH), thus significantly increasing the active site and electron transfer rate. As a result, in 1 M KOH, after 200 cycles CV activation CoFe-LDH (CoFe-LDH-200) has extremely low overpotential (360 mV at 100 mA cm−2) and Tafel slope (38.6 mV dec-1). Meanwhile, the CoFe-LDH-200 has the specific capacitance of 4662.2 mF cm−2 and good cycle stability (133.8 % after 10,000 cycles). Therefore, this method opens a novel insight for developing LDH in the field of supercapacitor and electrochemical water splitting. [ABSTRACT FROM AUTHOR]

Acute pneumonia induced by Pseudomonas aeruginosa is characterized by massive infiltration of inflammatory cell and the production of reactive oxygen species (ROS), which lead to severe and transient pulmonary inflammation and acute lung injury. However, P.aeruginosa infection is resistant to multiple antibiotics and causes high mortality in clinic, the search for alternative prophylactic and therapeutic strategies is imperative. This study was aimed to investigate the anti-inflammatory and antioxidant effects of DMB, a novel derivative of berberine, and explore the role of AIM2 inflammasome in P. aeruginosa -induced acute pneumonia. Acute pneumonia mice were established by tracheal injection of P. aeruginosa suspension. Pathological changes of lung tissue were observed by its appearance and H&E staining. The lung coefficient ratio was measured to evaluate pulmonary edema. Inflammatory factors were detected by qRT-PCR, western blotting and immunohistochemistry. ROS and other indicators of oxidative damage were analyzed by flow cytometry and specific kit. Proteins related to AIM2 inflammasome were detected by western blotting. Compared with the P. aeruginosa -induced group, DMB ameliorated pulmonary edema, hyperemia, and pathological damage based on its appearance and H&E staining in DMB groups. First, DMB attenuated the inflammatory response induced by P.aeruginosa. Compared with the P. aeruginosa -induced group, the lung coefficient ratio was decreased by 31.5%, the MPO activity of lung tissue was decreased by 44.0%, the mRNA expression levels of TNF-α, IL-1β and IL-6 were decreased by 64.8%, 51.2% and 64.0% respectively, and those protein expression levels were decreased by 40.1%, 42.8% and 47.8% respectively, and the number of white blood cells, neutrophils and monocytes were decreased by 53.5%, 29.4% and 13.7% in high dose (200 mg/kg) DMB group. Second, DMB alleviates oxidative stress in the lung tissue during P. aeruginosa -induced acute pneumonia. Compared with the P. aeruginosa -induced group, the level of GSH was increased by 42.5% and MDA was decreased by 49.5% in high dose DMB group. Moreover, the western blotting results showed that DMB markedly suppressed the expression of AIM2, ASC, Cleaved caspase1 and decreased the secretion of IL-1β. Additionally, these results were also confirmed by in vitro experiments using MH-S and BEAS-2B cell lines. Taken together, these results indicated that DMB ameliorates P. aeruginosa -induced acute pneumonia through anti-inflammatory, antioxidant effects, and inhibition of AIM2 inflammasome activation. [ABSTRACT FROM AUTHOR]

Abstract To date, the connection between inorganic mercury (Hg) and social behavior remains incompletely understood. The aim of this study was to investigate the influence of maternal autoimmunity by inorganic Hg (Hg2+) exposure on social behavior of offspring. Wild-type (WT) and immunoglobulin deficient (Ig−/−) B10.S dams fertilized by male WT B10.S or SJL mice were treated with 50 μM Hg chloride (HgCl 2). Non-pregnant female WT B10.S mice were used to investigate factors regulating HgCl 2 -induced autoimmunity to brain. HgCl 2 selectively impaired social behavior in male offspring, but not female offspring from WT B10.S dams × male SJL, in that only male offspring displayed reduced time distribution with the stranger mouse, decreased sniffing to the stranger mouse and increased self-grooming. HgCl 2 did not disrupt social behavior of male or female offspring from WT B10.S dams × male WT B10.S or Ig−/− B10.S dams × male SJL. The offspring from WT and Ig−/− B10.S dams × male SJL had equivalent autoimmunity to brain antigens during HgCl 2 exposure, indicating that maternal, but not offspring-derived anti-brain antibodies (Ab) impaired social behavior of the offspring. Non-pregnant WT B10.S mice treated with HgCl 2 had increased anti-brain Ab dependent on increase in CD4 T cell activation and IFNγ signaling to macrophages. IFNγ interaction with macrophages drove B cells and plasma cells to produce IgG. Therefore, HgCl 2 selectively impaired social behavior in males with certain genetic background via maternally derived anti-brain Ab production, thus providing a novel insight into our current understanding of Hg toxicity. Highlights • HgCl 2 impairs social behavior in male offspring of B10.S dams × male SJL mice. • HgCl 2 -impaird social behavior depends on maternal anti-brain Ab production. • HgCl 2 -induced anti-brain Ab requires increased CD4 T cell activation and IFNγ. • IFNγ acts on macrophages to drive anti-brain Ab production during HgCl 2 exposure. [ABSTRACT FROM AUTHOR]

Protein kinase B2 (AKT2) is implicated in diverse process of cardiomyocyte signaling including survival and metabolism. However, the role of AKT2 in myocardium development and the signaling pathway is rarely understood. Therefore, we sought to determine the effect of AKT2 deletion on heart development and its downstream targets. By using experimental animal models and neonatal rat cardiomyocytes (NRCMs), we observed that AKT2 deficiency induces retardation of heart development and increased systemic blood pressure (BP) without affecting cardiac function. Further investigation suggested that deficiency of AKT2 in myocardium results in diminished MEF2A abundance, which induced decreased size of cardiomyocytes. We additionally confirmed that EndoG, which is also regulated by AKT2, is a suppressor of MEF2A in myocardium. Finally, our results proved that AKT2 deficiency impairs the response to β-adrenergic stimuli that normally causes hypertrophy in cardiomyocytes by downregulating MEF2A expression. Our data are the first to show the important role of AKT2 in determining the size of myocardium, its deficiency causes retardation of cardiomyocyte development. We also proved a novel pathway of heart development involving EndoG and MEF2A regulated by AKT2. [ABSTRACT FROM AUTHOR]

The heavy metal cadmium (Cd) is known to modulate immunity and cause osteoporosis. However, how Cd influences on hematopoiesis remain largely unknown. Herein, we show that wild-type C57BL/6 (B6) mice exposed to Cd for 3 months had expanded bone marrow (BM) populations of long-term hematopoietic stem cells (LT-HSCs), common myeloid progenitors (CMPs) and granulocyte-macrophage progenitors (GMPs), while having reduced populations of multipotent progenitors (MPPs) and common lymphoid progenitors (CLPs). A competitive mixed BM transplantation assay indicates that BM from Cd-treated mice had impaired LT-HSC ability to differentiate into mature cells. In accordance with increased myeloid progenitors and decreased lymphoid progenitors, the BM and spleens of Cd-treated mice had more monocytes and/or neutrophils and fewer B cells and T cells. Cd impaired the ability of the non-hematopoietic system to support LT-HSCs, in that lethally irradiated Cd-treated recipients transplanted with normal BM cells had reduced LT-HSCs after the hematopoietic system was fully reconstituted. This is consistent with reduced osteoblasts, a known critical component for HSC niche, observed in Cd-treated mice. Conversely, lethally irradiated control recipients transplanted with BM cells from Cd-treated mice had normal LT-HSC reconstitution. Furthermore, both control mice and Cd-treated mice that received Alendronate, a clinical drug used for treating osteoporosis, had BM increases of LT-HSCs. Thus, the results suggest Cd increase of LT-HSCs is due to effects on HSCs and not on osteoblasts, although, Cd causes osteoblast reduction and impaired niche function for maintaining HSCs. Furthermore, Cd skews HSCs toward myelopoiesis. [ABSTRACT FROM AUTHOR]

Non-alcoholic fatty liver disease (NAFLD) has reached an epidemic level globally, which is recognized to form non-alcoholic steatohepatitis (NASH) by the “two-hit” model, including oxidative stress and inflammation. AMP-activated protein kinase (AMPK) has long been regarded as a key regulator of energy metabolism, which is recognized as a critical target for NAFLD treatment. Here we introduce a natural product, demethyleneberberine (DMB), which potentially ameliorated NAFLD by activating AMPK pathways. Our study showed that the intraperitoneal injection of DMB (20 or 40 mg/kg body weight) decreased hepatic lipid accumulation in methionine and choline deficient (MCD) high-fat diet feeding mice and db/db mice. The further investigation demonstrated that DMB activated AMPK by increasing its phosphorylation in vitro and in vivo . Accompanied with AMPK activation, the expression of lipogenic genes were significantly reduced while genes responsible for the fatty acid β-oxidation were restored in DMB-treated NAFLD mice. In addition, the remarkable oxidative damage and inflammation induced by NAFLD were both attenuated by DMB treatment, which is reflected by decreased lipid oxidative product, malonaldehyde (MDA) and inflammatory factors, tumor necrosis factor α (TNFα) and interleukin 1β (IL-1β). Based on all above, DMB could serve as a novel AMPK activator for treating NAFLD and preventing the pathologic progression from NAFLD to NASH by inhibiting the oxidative stress and inflammation. [ABSTRACT FROM AUTHOR]

Abstract: The plasma kinetics of ciprofloxacin (CF) were investigated in the eels after administration by oral gavage and bath treatment. Plasma concentrations of CF were determined by high-performance liquid chromatography with fluorescence detection. The mean concentration time data after oral gavage of a single dose (10.0mg/kg CF) and after bath treatment by exposure (10μg/ml CF) to medicated water for 48h were both best fitted by a one-compartment model. After oral gavage in eels, the half-time of absorption was 0.10h, the half-time of elimination was 51.87h, and the maximum plasma concentration (Cmax) was 0.4552μg/ml at Tmax 0.88h. After bath treatment, the was 0.02h, the was 15.46h, and the Cmax was 0.1175μg/mL at Tmax 0.22h. [Copyright &y& Elsevier]

Parabens, suspected as endocrine-disrupting chemicals, are nearly ubiquitous in the human body and exposure to these chemicals during pregnancy may disrupt thyroid hormones homeostasis and even affect fetal growth, although the impacts are still unclear. We aimed to estimate associations of maternal urinary paraben concentrations with cord serum thyroid hormones and birth weight. A subset of 437 mother-newborn pairs were included from a prospective birth cohort with five parabens quantified in maternal urine and seven thyroid function indicators measured in cord serum samples. Multivariable linear regression models and elastic net regression (ENR) models were applied to explore associations between individual and mixtures of prenatal urinary paraben concentrations and thyroid hormones and birth weight, respectively. Maternal urinary ethyl-paraben (EtP) concentrations were associated with increased cord serum total triiodothyronine levels (TT3) [percent change: 1.51%; 95% confidence interval (CI): 0.20%, 2.74%; p =0.017]. Urinary propyl-paraben (PrP) levels predicted higher thyroid peroxidase antibodies (percent change: 4.19%, 95%CI: 0.20%, 8.44%; p =0.041). Maternal urinary EtP and butyl-paraben (BuP) concentrations were significantly positively associated with birth weight [regression coefficient, (β)=40.9g, 95%CI: 3.99, 76.6; p =0.030; β=62.1g, 95%CI: 8.70, 115; p =0.023, for EtP and BuP, respectively]. In sex-stratified analyses, positive relationship between EtP levels and birth weight was observed in boys. Urinary EtP concentrations predicted higher TT3 levels in cord serum samples, assessing parabens as a chemical mixture with ENR models. Prenatal exposure to parabens may affect thyroid hormone indicators with increased serum TT3 levels and associate with higher birth weight, especially in boys. The underlying biological mechanisms and effects of prenatal paraben exposures on disruption of thyroid function homeostasis and potential impacts of childhood growth and development needed to be further investigated. Image 1 • Maternal urinary EtP levels were associated with increased cord serum TT3 levels. • Urinary PrP levels were positively related to TPOAb levels in cord serum. • Prenatal exposure to EtP and BuP was associated with higher birth weight. • Sex-specific effects of EtP and BuP exposure on neonatal birth weight were observed. • EtP exposure contributes to higher serum TT3 levels with adjustment for other parabens. [ABSTRACT FROM AUTHOR]

Carbamate pesticides exposure have been linked with adverse health effects during developmental period. Based on 377 mother-child pairs from Sheyang Mini Birth Cohort Study, the present study aimed to assess carbofuranphenol exposure of three-year-old children and explore the associations between prenatal or postnatal carbofuranphenol exposures and neurodevelopmental indicators. Urinary carbofuranphenol concentrations were measured by gas chromatography-tandem mass spectrometry. Neural developmental quotient (DQ) of children was evaluated using Gesell Developmental Schedules. Generalized linear models were used to examine the associations between carbofuranphenol concentrations and neurodevelopment. Geometric mean, geometric standard deviation, median, inter quartile range of postnatal urinary carbofuranphenol concentrations were 0.653 μg/L, 9.345 μg/L, 0.413 μg/L, 0.150–1.675 μg/L, respectively. Postnatal carbofuranphenol level showed negatively significant trend in language DQ [beta (β) = -0.121; 95% confidence interval (95% CI): 0.212, −0.031; p value (p) = 0.008] and total average DQ (β = −0.059, 95% CI: 0.115, −0.003; p = 0.035). Prenatal carbofuranphenol level showed negative correlations with children's adaptive DQ (β = −0.755; 95% CI: 1.257, −0.254; p = 0.003), social DQ (β = −0.341; 95% CI: 0.656, −0.027; p = 0.032) and total average DQ (β = −0.349; 95% CI: 0.693, −0.005; p = 0.047). The results of the present study supposed children in agricultural region of China are widely exposed to carbamate pesticides, and both prenatal and postnatal exposure to carbamate pesticides may lead to neurodevelopmental effect. • Carbofuranphenol was detected in most of postnatal urine samples using GC-MS/MS. • Associations between prenatal and postnatal carbofuranphenol and neurodevelopment were explored in 377 3-year-old children. • Both prenatal and postnatal carbofuranphenol exposures were significantly associated with neurodevelopmental quotients. [ABSTRACT FROM AUTHOR]