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Inconsistent evidence exists about whether exposure to greenspace benefits childhood asthma. Previous studies have only focused on residential or school greenspace, and no research has combined greenspace exposures at both homes and schools to determine their link with childhood asthma. A population-based cross-sectional study was conducted among 16,605 children during 2019 in Shanghai, China. Self-reported questionnaires were used to collect information on childhood asthma and demographic, socioeconomic and behavioural factors. Environmental data including ambient temperature, particulate matter with aerodynamic diameter less than 1 µm (PM 1), enhanced vegetation index (EVI), and normalized difference vegetation index (NDVI) were collected from satellite data. Binomial generalized linear models with a logit link were carried out to evaluate the association between greenspace exposure and children's asthma, as well as the effect modifiers. An interquartile range increment of whole greenspace (NDVI 500 , NDVI 250 , EVI 500 , and EVI 250) exposure was associated with a reduced odds ratio of children's asthma (0.88, 95% CI: 0.78, 0.99; 0.89, 95% CI: 0.79, 1.01; 0.87, 95% CI: 0.77, 0.99; and 0.88, 95% CI: 0.78, 0.99, respectively) after controlling potential confounders. Low temperature, low PM 1 , males, vaginal delivery, suburban/rural area, and without family history of allergy appeared to enhance the greenspace-asthma association. Increased greenspace exposure was associated with a lower risk of childhood asthma, and the association was modified by a range of socio-environmental factors. These findings add to the body of evidence on the benefits of biodiversity and supporting the promotion of urban greenspace to protect children's health. • It's the first study on whole greenspace near home and school and children's asthma. • Higher greenspace exposure was associated with lower risks of childhood asthma. • A range of socio-environmental factors modified the greenspace-asthma association. [ABSTRACT FROM AUTHOR]

Prenatal single and combined exposure to lead (Pb) and stress (Ps) impairs neurodevelopment. Prenatal single exposure to Pb or Ps affects the composition of intestinal microbiota, and bidirectional communication between gut microbiota and central nervous system has been well recognized. However, whether gut microbiota mediated the effects of prenatal Pb+Ps co-exposure on neurodevelopmental deficits remains unclear. This study established rat models with prenatal single and combined exposure to Ps and Pb. We investigated the effects of such prenatal single and combined exposure on hippocampal structures using morphological analyses, on learning/memory using the Morris-water-maze test, and on fecal microbiota using 16S rRNA sequencing. The mediating roles of gut microbiota were analyzed using the bootstrap method. The study found both single and combined exposure affected hippocampal ultra-structures and spatial learning/memory, and the most significant impairments were observed in the Pb+Ps group. Prenatal Pb+Ps co-exposure decreased fecal microbial alpha/beta-diversity. Significantly lower levels of B/F-ratio, class-Bacteroidia, order-Bacteroidales, and family-S24–7, and significantly higher levels of class-Bacilli, order-Lactobacillales, family-Lactobacillaceae, and genus- Lactobacillus were observed in the co-exposure group, compared with the controls. Increased relative abundances of genus- Helicobacter mediated the detrimental effect of prenatal Ps+Pb co-exposure on learning/memory [ β (95%CI) for the total and indirect effects: − 10.70 (−19.19, −2.21) and − 4.65(−11.07, −1.85)], accounting for 43.47% of the total effect. As a result, increased relative abundances of genus- Lactobacillus alleviated the adverse effects of the co-exposure on learning/memory, and the alleviation effect accounted for 44.55% of the direct effect [ β (95%CI) for the direct and indirect effects: − 0.28(−0.48, −0.08) and 0.13(0.01, 0.41)]. This study suggested that prenatal combined exposure to Pb and Ps induced more impairments in offspring gut microbiota and neurodevelopment than single exposure, and alterations in fecal microbiome may mediate the developmental neurotoxicity induced by such prenatal co-exposure. • Pregnant women can hardly avoid the risk of concurrent exposure to lead and stress. • Prenatal exposure to lead and stress alone both affects gut microbiota in offspring. • Prenatal Pb-stress co-exposure (vs. single) induced more neurobehavioral deficits. • Increased Helicobacter abundance may mediate the co-exposure-induced memory deficits. [ABSTRACT FROM AUTHOR]

Emerging evidence suggests that prenatal exposure to ambient SO 2 or NO 2 induces fetal brain-damage. However, effects of prenatal exposure to SO 2 or NO 2 on toddler neurodevelopment and the effect-modification by ambient temperature remain unclear. Therefore, a prospective birth-cohort study was conducted from 2010 to 2012 in Shanghai, and 225 mother-child pairs were followed-up from mid-to-late pregnancy until 24–36 months postpartum. During the whole pregnancy, daily SO 2 /NO 2 and temperature levels were obtained for each woman. Gesell-Development-Schedule was used to assess toddler neurodevelopment in the domains of gross-motor, fine-motor, adaptive-behavior, language and social-behavior. Distributed-lag-nonlinear-models simultaneously accounting for exposure-response and lag-response associations were applied to assess the impacts of prenatal SO 2 /NO 2 exposure on neurodevelopment. Each 10-μg/m3 increase in weekly average SO 2 concentrations had adverse associations with gross-motor in gestational-weeks 1–6, with adaptive-behavior in weeks 26–30, and with language in weeks 30–36 (developmental-quotient changes: − 1.17% to − 0.12%, P- values < 0.05). Each 10-μg/m3 increase in weekly average NO 2 concentrations had adverse associations with gross-motor in gestational-weeks 33–36, with fine-motor in weeks 26–36 and with social-behavior in weeks 31–36 (developmental-quotient changes: − 0.91% to − 0.20%, P -values < 0.05). The cumulative effects for the whole pregnancy showed that each 10-μg/m3 increase in SO 2 induced significant deficits in gross-motor and adaptive-behavior (developmental-quotient changes: − 4.71% and − 4.06%, respectively, P < 0.05). We found prenatal cumulative SO 2 exposure induced more deficits in low temperature in language and adaptive-behavior than in high/moderate temperature. Thus, prenatal ambient SO 2 /NO 2 exposure in specific time-windows (1st and 3rd trimesters for SO 2 ; 3rd trimester for NO 2) could impair toddler neurodevelopment and low temperature may aggravate the SO 2 -induced neurotoxicity. [Display omitted] • Prenatal SO 2 /NO 2 exposure was associated with toddler neurodevelopmental deficits. • Windows of vulnerability to prenatal SO 2 exposure were in the 1st and 3rd trimesters. • Windows of vulnerability to prenatal NO 2 exposure were in the 3rd trimester. • The neurotoxicity of prenatal SO 2 exposure was aggravated by low temperature. [ABSTRACT FROM AUTHOR]

As common environmental pollutants, persistent organic pollutants (POPs) that are widely applied in industry and agriculture have adverse effects on neurodevelopment. However, evidence on the neurotoxicity of POPs in neural development of offspring is limited. This study explored the relationship between prenatal exposure to POPs and neurodevelopment of 18-month-old toddlers in a mother-child cohort in Shanghai, China. In this study, we determined exposure levels of 37 POPs in cord blood serum collected at the time of delivery. The detection rate of pollutants HCB, β-HCH, and p,p′-DDE was higher than 60%, so these will be discussed in the following analysis. From birth to approximately 18 months, we followed up infants to longitudinally explore whether POPs influenced their language, motor, and cognitive development according to a Bayley-Ⅲ assessment. Based on multivariable regression analyses, the β-HCH concentration in cord serum was negatively related to motor development scores in children at 18 months by adjusting for the covariates, but there was no change in language and cognition. Further piecewise linear regression analysis showed that a cord serum β-HCH concentration greater than 0.2 μg/L had a significantly negative correlation with the motor development scores. p,p′-DDE was positively associated with language development at 18 months before and after adjusting for covariates. But prenatal HCB levels were not associated with any of the Bayley-Ⅲ subscales at 18 months. We concluded that prenatal exposure to β-HCH might have adverse effects on infants' motor development. The minimum harmful concentration of β-HCH was estimated at 0.2 μg/L in cord serum. The unexpected positive association between p,p′-DDT and language development could be due to live birth bias. ga1 • Cord serum β-HCH level was negatively associated with toddlers' motor development. • The inflection point was found in non-linear relationship between β-HCH and motor. • HCB, p,p′-DDE were not associated with toddlers' cognitive and motor development. • Prenatal DHA status may modify the effects of POPs on toddlers' motor development. [ABSTRACT FROM AUTHOR]

To explore the impacts of Pb exposure and the dimercaptosuccinic acid (DMSA) chelation therapy on bone metabolisms in young rats of different ages, as well as the potential mechanisms. Young rats were exposed to 0.05%–0.1% Pb acetate for 19 days, during infanthood (postnatal day, PND2-20), childhood (PND21-39) and adolescenthood (PND40-58) respectively. In each developmental stage, rats were further divided into three subgroups: lead-exposed, one-course and two-course DMSA chelation therapy subgroups. Blood/bone lead concentrations, serum calciotropic hormones concentrations, and mRNA and protein expressions of bone turnover markers in the serum and bones were measured. Bone microstructures were analyzed using Micro-CT. Compared with lead-exposed during childhood and adolescenthood, increases in blood/bone lead levels, and the changes of blood/bone lead and trabecular bone microstructures after one-course DMSA chelation were most significant in rats lead-exposed during infanthood (P <.05). The serum osteocalcin (OC) concentrations, mRNA/protein expressions of OC and runt-related transcription factor 2 (RUNX2) in bones all decreased after Pb exposure, along with significant increases in serum C-terminal telopeptide of type I collagen (CTX) concentrations (P <.05). These effects were accompanied by changes of serum parathormone (PTH) and 1,25-dihydroxyvitamin D 3 (1,25-(OH 2)-D 3) concentrations. DMSA chelation partially reversed the changes of bone microarchitectures, bone formation and resorption markers, and calciotropic-hormones, and the efficiency was greatest when the therapy was provided during infanthood. Developmental Pb exposure impaired bone microstructures and interfered bone metabolism, and the exposure effect was more obvious during infanthood than during childhood and adolescenthood. Lead effects were partially reversed by chelation therapy, and the efficacy may be most significant when the therapy was provided at younger ages. Inf: infanthood ; chd: childhood; adol: adolescenthood; Control group: receiving double distilled water; PbN: rats were lead exposed but not treated ; PbT1: one-course chelation therapy treatment groups ; PbT2: two-course chelation therapy treatment groups * P ：<0.05. Image 1 • Higher blood/bone lead were induced by developmental lead-exposure at younger age. • Lead-exposure at a younger age may induce more injuries in bone metabolisms. • Lead-exposure at a younger age may induce more injuries in bone microstructures. • The chelation therapy partially reversed effects due to developmental lead exposure. • The efficacy was more significant if chelation therapy was provided at younger age. [ABSTRACT FROM AUTHOR]

Subclinical hypothyroidism (SCH) is a very common preclinical condition during pregnancy. The adverse effect of maternal clinical hypothyroidism (CH) on the nervous system development of offspring is beyond doubt, but it is still controversial in SCH. The aim of this study was to investigate whether spatial learning and memory ability of offspring is inhibited in SCH rat model and its possible mechanism. 45 Wistar female rats were randomly divided into SCH, CH and control (CON) groups, which were induced by semi-thyroid electrocauterization, total thyroidectomy and sham operation, respectively. Rat pups were sacrificed at embryonic day 14 (E14), E18, postnatal day 1 (P1), P3, and P10, and pups' cerebellar tissues were collected. The proliferation, differentiation and migration of cerebellar cells were observed, and RNA level of the thyroid hormone receptor α (TRα) and TRβ in the cerebellum was detected by real-time PCR, respectively. Morris Water Maze (MWM) test was performed to detect the spatial learning and memory ability of pups at P40. Our data indicated that maternal SCH will significantly extend the offspring's escape latency time, and pups perform worse in the spatial probe test compared with the CON group. Except for E14, the proliferation of pups' cerebellar granule cells (GCs), and the migration of pups' Purkinje cells (PCs) in the SCH group was significantly inhibited compared with that in the CON group at other time points (P < 0.05 or P < 0.01), and the differentiation of cerebellar astrocytes (As) in SCH group was higher than that in CON group at P3 and P10. Except for E14, the expression of TRα mRNA in SCH group was significantly lower than that in CON group (P < 0.05 or P < 0.01). And the difference of the differentiation of As and the spatial learning and memory between SCH and CH groups was not statistically significant. Our findings suggested that SCH during pregnancy nuisances the offspring's spatial learning and memory. It may be related to the decrease of the expression of TRα in cerebellum, which may further inhibit the proliferation of GCs and the migration of PCs, and increase the differentiation of As. • Maternal SCH significantly extended the offspring's escape latency time. • Maternal SCH decreased proliferation of cerebellar granule cells of pups. • Maternal SCH slower migration of Purkinje cells (PCs) of pups. • The expression of TRα mRNA in SCH group was lower than that in CON group. • No difference in AS differentiation between SCH & CON group, indicating SCH is very harmful. [ABSTRACT FROM AUTHOR]

Arsenic (As) and lead (Pb) are toxins found in the natural surroundings, and the harmful health outcomes caused by the co-exposure of such toxins have become a considerable problem. However, the joint neurotoxicity of As and Pb to neurodevelopment and the underlying mechanisms remain unclear. Pluripotent stem cell-derived human brain organoids are emerging animal model alternatives for understanding neurological-related diseases. Therefore, we utilized brain organoids with optic vesicles (OVB-organoids) to systematically analyze the neurotoxicity of As and Pb. After 24 h of As and/or Pb exposure, hematoxylin-eosin staining revealed that As and Pb exposure could cause disorders in the structure of the ventricular zone and general cell disarrangement in OVB-organoids. Immunostaining displayed that OVB-organoids are more susceptible to As and Pb co-exposure than independent exposure in apoptosis, proliferation, and cell differentiation. Meanwhile, even though As and Pb could both hinder cell proliferation, contrary to Pb, As could induce an increasing proportion of mitotic (G2/M) cells. The proteome landscape of OVB-organoids illustrated that Pb synergized with As in G2/M arrest and the common role of As and Pb in carcinogenesis. Besides, proteomics analyses suggested the consequential role of autophagy and Wnt pathway in the neurotoxicity of As and Pb co-exposure. Overall, our findings provide penetrating insights into the cell cycle, carcinogenesis, autophagy, and Wnt pathway underlying the As and Pb binary exposure scenarios, which could enhance our understanding of the mixture neurotoxicity mechanisms. • We constructed an animal model alternative to conduct environmental research. • Exposure to arsenic and lead can induce structural disorders and carcinogenesis in brain organoids. • Autophagy, Wnt pathway and cell cycle arrest contribute to the neurotoxicity of arsenic and lead. [ABSTRACT FROM AUTHOR]

Background Maternal psychological stress during pregnancy has essentially been conceptualized as a teratogen. However, little is known about the effect of temperature on maternal stress during pregnancy. The aim of this study is to investigate the relationship between temperature and maternal stress during pregnancy. Methods In 2010, a total of 1931 eligible pregnant women were enrolled across Shanghai from four prenatal-care clinics during their mid-to-late pregnancy. Maternal life-event stress and emotional stress levels during pregnancy were assessed by the "Life Event Scale for Pregnant Women" (LESPW) and "Symptom Checklist-90-Revised Scale" (SCL-90-R), respectively. Exposure to ambient temperature was evaluated based on daily regional average in different moving average and lag days. The generalized estimating equations were used to evaluate the relationship between daily average temperature/temperature difference and maternal stress. Results After adjusting for relevant confounders, an U-shaped relationship was observed between daily average temperature and maternal Global-Severity-Index (GSI) of the SCL-90-R. Cumulative exposures to extremely low temperatures ( < P5, 1.4–10.5 ℃, lag 0–1 days, 0–2 days and 0–5 days) and extremely high temperatures (≥ P95, 31.2–34.1 ℃, lag 0–1 days and 0–2 days), and acute exposures to extremely low (lag day 0, 1, 2 and 3) and high (lag day 0, 1) temperatures, all induced higher risks of high GSI (the highest tertile), compared to the risk induced by exposed to an optimal temperature range (20–25 ℃) ( P < 0.05). Increased temperature difference was associated with high maternal GSI ( P < 0.05). However, non-significant associations were observed between daily average temperatures/temperature differences and maternal log-transferred LESPW scores. Conclusions Cumulative and acute exposures to extremely low/high temperatures may both induce emotional stress during pregnancy. [ABSTRACT FROM AUTHOR]

Short-term temperature variability (TV) is associated with the exacerbation of asthma, but little is known about the relative effects of intra- and inter-day TV. We aimed to assess the relative impacts of intra- and inter-day TV on childhood asthma and to explore the modification effects by season. A quasi-Poisson generalized linear regression model combined with a distributed lag nonlinear model was adopted to evaluate the nonlinear and lagged effects of TV on childhood asthma in Shanghai from 2009 to 2017. Intra- and inter-day TV was measured with diurnal temperature range (DTR) and temperature changes between neighboring days (TCN), respectively. Increased DTR was associated with the elevated relative risk (RR) of daily outpatient visits for childhood asthma (DOVCA) in both the whole year (RR lag0-14 for the 99th percentile: 1.264, 95% confidence interval (CI): 1.052, 1.518) and cold season (RR lag0-12 for the 99th percentile: 1.411, 95% CI: 1.053, 1.889). Higher TCN in the warm season was associated with the increased RR of DOVCA (RR lag0-14 for the 99th percentile: 2.964, 95% CI: 1.636, 5.373). The number and fraction of DOVCA attributed to an interquartile range (IQR) increase of TCN were higher than those attributed to DTR in both the whole year period and warm season. However, the number and fraction of DOVCA attributed to an IQR increase of DTR were greater than those attributed to TCN in the cold season. Our results provide novel evidence that both intra- and inter-day TV might be a trigger of childhood asthma. Higher DTR appeared to have greater impacts on childhood asthma in the cold season while an increase in TCN seemed to have bigger effects in the warm season. [ABSTRACT FROM AUTHOR]