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The discharge of antibiotics evokes environmental health crisis, and is also a waste of organic energy. Currently, heterogeneous Fenton for antibiotics removal has attracted growing attentions due to wide pH range and no iron sludge production, however, it often suffers from a low formation rate of Fe(II), resulting in difficult application of heterogeneous Fenton technology in sewage treatment. To overcome this drawback, bamboo biochar (BB) is coupled with schwertmannite (Sch) through Acidithiobacillus ferrooxidans- mediated Fe(II) oxidation reaction to obtain a heterogeneous catalyst (Sch/BB) with high adsorption performance and Fenton activity. According to the analysis of experimental results, electrons around C (from BB) can easily transfer to Fe by Fe–O–C bonds to expedite ≡Fe(III)/≡Fe(II) cycle, while electrons of antibiotics adsorbed on Sch/BB surface are effectively utilized to maintain the efficient regeneration of ≡Fe(II) through BB electron shuttle or Fe–O–C bonds between Sch/BB and pollutants, further causing a superior Fenton activity (98% antibiotics removal) of Sch/BB. Moreover, due to its excellent adsorption performance, Sch/BB as filter materials can effectively remove dye pollutants in flow wastewater. These findings provided a high-activity and practical heterogeneous Fenton catalyst for pollutants degradation, while a new perspective for efficient utilization of the electrons of organic pollutants was given. • Sch/BB shows excellent Fenton activity for antibiotics degradation. • The electron energy of pollutants is utilized for promoting Fe redox cycling. • Well-structured Fe–O–C bridge is a key factor for the Fe(II) regeneration. • Bamboo biochar remarkably promotes the adsorption performance of schwertmannite. • Sch/BB can develop into a filter material for flowing dye water treatment. [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]

Regarding the association between the sensitive time-windows of air pollution (AP) exposure and gestational diabetes mellitus (GDM), epidemiological findings are inconsistent. The dietary inflammatory potential has been implicated in the development of GDM, but it is unclear whether an anti-inflammatory diet during pregnancy reduces the association between AP and GDM. We aimed to characterize the sensitive time-windows of AP to GDM risk. Further, to verify whether a maternal anti-inflammatory diet can reduce the risk of AP-induced GDM, by inhibiting inflammation. A total of 8495 pregnant women were included between 2015 and 2021 in the Maternal & Infants Health in Hefei study. Weekly mean AP exposure to fine particles (PM 2.5 and PM 10), SO2, and NO 2 was estimated from the data of Hefei City Ecology and Environment Bureau. High-sensitivity C-reactive protein (hs-CRP) concentrations were measured to evaluate systemic inflammation. The empirical dietary inflammatory pattern (EDIP) score based on a validated food frequency questionnaire was used to assess the dietary inflammatory potential of pregnant women. Logistic regression models with distributed lags were used to identify the sensitive time-window for the effect of AP on GDM. Mediation analysis estimated the mediated effect of hs-CRP, linking AP with GDM. Stratified analysis was used to investigate the potential effect of anti-inflammatory diet on GDM risk. The increased risks of GDM were found to be positively associated with exposure to PM 2.5 (OR = 1.11, 95% CI :1.07–1.15), PM 10 (OR = 1.12, 95% CI :1.09–1.16), and SO 2 (OR = 1.42, 95% CI :1.25–1.60) by distributed lag models, and the critical exposure windows were 21st to 28th weeks of preconception. The proportion of association between PM 2.5, PM 10, and SO 2 with GDM mediated by hs-CRP was 25.9%, 21.1%, and 19.4%, respectively, according to mediation analysis. In the stratified analyses by EDIP, the association between AP and GDM was not statistically significant among women those with anti-inflammatory diets. Exposure to AP, especially in 21st to 28th week of preconception, is associated with risk of GDM, which is partly mediated by hs-CRP. Adherence to the anti-inflammatory dietary pattern may reduce the risk of AP-induced GDM. • Exposure to air pollution during preconception is associated with the risk of GDM. • Time windows of exposure occur between the 21st and 28th week of preconception. • The association between air pollutants with GDM is partly mediated by hs-CRP. • Anti-Inflammatory diets reduced GDM risk related to air pollutants. [ABSTRACT FROM AUTHOR]

Prenatal air pollutant exposure has been linked to impaired fetal growth. However, its special vulnerability windows and biological mechanisms remain unclear. A prospective birth cohort study including 7419 mother-newborn pairs was conducted from 2015 to 2020 to determine critical exposure windows and examine whether cortisol mediates the relationship between air pollutant exposure and fetal growth. Air pollutant data for PM 2.5 , PM 10 , SO 2 , and CO were obtained from the Hefei City Ecology and Environment Bureau. Data on fetal ultrasound measurements and birth size were collected. Maternal and cord blood samples were used for measuring cortisol. Prenatal air pollutant (PM 2.5 , PM 10 , SO 2 , and CO) exposure, particularly in the first trimester, was associated with reduced fetal size from later pregnancy to birth. An IQR increase in PM 2.5 (β = 0.082, 95% CI : 0.029, 0.135), PM 10 (β = 0.086, 95% CI : 0.036, 0.136), SO 2 (β = 0.086, 95% CI : 0.028, 0.144), and CO (β = 0.063, 95% CI : 0.017, 0.109) exposure in the first trimester was associated with higher cord blood cortisol levels. Significant relationships were observed between air pollutant exposure in the first trimester and increased ratio of cord to maternal blood cortisol levels. Exposure to high levels of cord blood cortisol significantly reduced the Z scores of birth weight (β = −0.17, 95% CI : −0.23, −0.10), length (β = −0.09, 95% CI : −0.16, −0.03), and head circumference (β = −0.33, 95% CI : −0.42, −0.25). Mediation analysis showed that the association of air pollutant exposure in the first trimester with neonatal parameters mediated by cord blood cortisol was 20.62%. These results indicated that air pollutant exposure during pregnancy could reduce fetal growth by the increased fetal cortisol levels due to placental barrier impairment, with the critical window of exposure occurring in the first trimester. • Prenatal air pollutant exposure impaired fetal growth from late pregnancy to birth. • Exposure to air pollutants was associated with higher cord blood cortisol levels. • Air pollutant exposure increased the ratio of cord to maternal blood cortisol levels. • The critical windows of air pollutant exposure were in the first trimester. • Cord blood cortisol mediated the effect of air pollutant exposure on fetal growth. [ABSTRACT FROM AUTHOR]