Accumulating exposure to quality green space over time is posited to influence child health, yet longitudinal studies are scarce. This study aimed to examine the associations between trajectories of perceived green space quality and child health-related outcomes. We used data from 1874 childrenin the B-cohort of the Longitudinal Study of Australian Children who participated in the Child Health Checkpoint module at 11–12 years. Data on caregiver perceived green space quality measured biennially was assessed using discrete trajectory mixture models to group children by contrasting distributions in green space quality over time. Examination of associations between trajectory groups of perceived green space quality and child biomarkers (i.e., albumin-to-creatinine ratio, total, cholesterol, total triglycerides, and glucose), physical health and behavioural assessments (i.e., anthropometric measurements, blood pressure, sedentary behaviour, physical activity, sleep, aerobic work capacity, and general wellbeing), and health care use were assessed using multilevel models, adjusted for sociodemographic variables. Four perceived green space quality trajectories were identified: “decreasing quality from high to moderate”; “increasing quality from low to high”; “consistently high quality”; “consistently low quality”. Compared with consistently low levels of quality green space, adjusted models indicated consistently high-quality green space was associated with lower total triglycerides (β −0.13; 95%CI -0.25, −0.01). Lower odds of hospital admission was observed among children who accumulated quality green space over time (OR 0.45; 95%CI 0.23, 0.87). These associations were observed in boys only in sex-stratified analyses. Moreover, boys accumulating quality green space through time tended to have lower diastolic blood pressure (β −2.76; 95%CI -5.17, −0.35) and girls who experienced loss in quality green space tended to have a higher percentage of body fat (β 2.81; 95%CI 0.43, 5.20). Accumulating quality green space over time is important for various aspects of child health, with contrasting benefits by sex.

The adverse effects of plastic waste and nanoplastics on the water environment have become a focus of global attention in recent years. In the present study, using adult Chinese mitten crabs (Eriocheir sinensis) as an animal model, the bioaccumulation and the in vivo and in vitro toxicity of polystyrene nanoplastics (PS NPs), alone or in combination with the bacteria, were investigated. This study aimed to investigate the effects of PS NPs on apoptosis and glucose metabolism in Chinese mitten crabs, and whether PS NPs could synergistically affect the antibacterial immunity of crabs. We observed that NPs were endocytosed by hemocytes, which are immune cells in crustaceans and are involved in innate immunity. The RNA sequencing data showed that after hemocytes endocytosed NPs, apoptosis and glucose metabolism-related gene expression was significantly induced, resulting in abnormal cell apoptosis and a glucose metabolism disorder. In addition, exposure to NPs resulted in changes in the antimicrobial immunity of crabs, including changes in antimicrobial peptide expression, survival, and bacterial clearance. In summary, NPs could be endocytosed by crab hemocytes, which adversely affected the cell apoptosis, glucose metabolism, and antibacterial immunity of Eriocheir sinensis. This study revealed the effects of NPs on crab immunity and lays the foundation for further exploration of the synergistic effect of NPs and bacteria.

The link between zinc exposure and glucose metabolism or the development of type 2 diabetes (T2D) is controversial, and underlying mechanisms are unclear. This study aimed to explore the associations of zinc exposure with glucose-insulin homeostasis traits and the long-term effects of zinc on the development of T2D, and further to estimate the potential roles of inflammation and oxidative damage in such relationships. We investigated 3890 urban adults from the Wuhan-Zhuhai cohort, and followed up every three years. Mixed linear model was applied to estimate dose-response associations between urinary zinc and glycemia traits [fasting plasma insulin (FPI), fasting plasma glucose (FPG), insulin resistance (homeostasis model assessment of insulin resistance, HOMA-IR), and β-cell dysfunction (homeostasis model assessment of β-cell function, HOMA-B)], as well as zinc and biomarkers for systemic inflammation (C-reactive protein) and oxidative damage (8-isoprostane and 8-hydroxy-2′-deoxyguanosine). Logistic regression model and Cox regression model were conducted to evaluate the relationships between urinary zinc and prevalence and incidence of T2D, respectively. We further performed mediation analysis to assess the roles of inflammation and oxidative damage biomarkers in above associations. At baseline, we observed significant dose-response relationships of elevated urinary zinc with increased FPI, FPG, HOMA-IR, and T2D prevalence and decreased HOMA-B, and such associations could be strengthened by increased C-reactive protein, 8-isoprostane, and 8-hydroxy-2′-deoxyguanosine. Elevated C-reactive protein significantly mediated 9.09% and 17.67% of the zinc-related FPG and HOMA-IR increments, respectively. In longitudinal analysis, a significantly positive association between urinary zinc and T2D incidence was observed among subjects with persistent high urinary zinc levels when compared with those with persistent low zinc levels. Our results suggested that high levels of zinc exposure adversely affected on glucose-insulin homeostasis and further contributed to increased risk of T2D cross-sectionally and longitudinally. Moreover, inflammatory response might play an important role in zinc-related glucose metabolic disorder.

The decreasing ocean pH seems to adversely affect marine organisms, including crustaceans, which leads to potential threats to seafood safety. The present investigation evaluated the effect of seawater acidification on the edible marine mud crab Scylla serrata instars. The experimental setup was designed using a multi-cell cage based system assembled with 20 pre holed PVC pipes containing 20 individual crabs to avoid cannibalism. The crab instars were exposed to CO₂ driven acidified seawater at pH 7.8 (IPCC forecast pH at the end of the 21ˢᵗ century), 7.6, 7.4, 7.2, and 7.0 for 60 days. The crabs reared in seawater without acidification at pH 8.2 served as control. The present study revealed a notable decrease in survival, feed intake, growth, molting, tissue biochemical constituents, minerals, chitin, and alkaline phosphatase in S. serrata instar reared in acidified seawater, denotes the adverse effect of seawater acidification on crabs. The significant elevations in antioxidants, lipid peroxidation, and metabolic enzymes in all acidified seawater compared to ambient pH indicates the physiological stress of the crabs' instars. The changes in the metabolic enzymes reveal the metabolism of protein and glucose for additional energy required by the crabs to tolerate the acidic stress. Hence, the present study provides insight into the seawater acidification can adversely affect the crab S. serrata.

2,4,6-trinitrotoluene (TNT) is a highly toxic explosive that contaminates soil and water and may interfere with the degradation of co-occurring compounds, such as hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX). We proposed that TNT may influence RDX-degrading bacteria via either general toxicity or a specific effect on the |RDX degradation mechanisms. Thus, we examined the impact of TNT on RDX degradation by Rhodococcus strains YH1, T7, and YY1, which were isolated from an explosives-polluted environment. Although partly degraded, TNT did not support the growth of any of the strains when used as either sole carbon or sole nitrogen sources, or as carbon and nitrogen sources. The incubation of a mixture of TNT (25 mg/l) and RDX (20 mg/l) completely inhibited RDX degradation. The effect of TNT on the cytochrome P450, catalyzing RDX degradation, was tested in a resting cell experiment, proving that TNT inhibits XplA protein activity. A dose-response experiment showed that the IC50/trans values for YH1, T7, and YY1 were 7.272, 5.098, and 9.140 (mg/l of TNT), respectively, illustrating variable sensitivity to TNT among the strains. The expression of xplA was also strongly suppressed by TNT. Cells that were pre-grown with RDX (allowing xplA expression) and incubated with ammonium chloride, glucose, and TNT, completely transformed into their amino dinitrotoluene isomers and formed azoxy toluene isomers. The presence of oxygen-insensitive nitroreductase that enable reduction of the nitro group in the presence of O2 in the genomes of these strains suggests that they are responsible for TNT transformation in the cultures. The experimental results concluded that TNT has an adverse effect on RDX degradation by the examined strains. It inhibits RDX degradation due to the direct impact on cytochrome P450, xplA, or its expression. The tested strains can transform TNT independently of RDX. Thus, degradation of both compounds is possible if TNT concentrations are below their IC50 values.

Although the hazards of microplastics (MPs) have been quite well explored, the aberrant metabolism and the involvement of the autophagy pathway as an adverse response to environmental MPs in benthic organisms are still unclear. The present work aims to assess the impact of different environmental MPs collected from the south coast of the Mediterranean Sea, composed by polyethylene (PE), polyethylene vinyl acetate (PEVA), low-density polyethylene (LDPE), high-density polyethylene (HDPE), polypropylene (PP) and polyamide (PA) on the metabolome and proteome of the marine polychaete Hediste diversicolor. As a result, all the microplastic types were detected with Raman microspectroscopy in polychaetes tissues, causing cytoskeleton damage and induced autophagy pathway manifested by immunohistochemical labeling of specific targeted proteins, through Tubulin (Tub), Microtubule-associated protein light chain 3 (LC3), and p62 (also named Sequestosome 1). Metabolomics was conducted to further investigate the metabolic alterations induced by the environmental MPs-mixture in polychaetes. A total of 28 metabolites were differentially expressed between control and MPs-treated polychaetes, which showed elevated levels of amino acids, glucose, ATP/ADP, osmolytes, glutathione, choline and phosphocholine, and reduced concentration of aspartate. These novel findings extend our understanding given the toxicity of environmental microplastics and unravel their underlying mechanisms.

Denitrification, as both origins and sinks of N₂O, occurs extensively, and is of critical importance for regulating N₂O emissions in acidified soils. However, whether soil acidification stimulates N₂O emissions, and if so for what reason contributes to stimulate the emissions is uncertain and how the N₂O fractions from fungal (ffD) and bacterial (fbD) denitrification change with soil pH is unclear. Thus, a pH gradient (6.2, 7.1, 8.7) was set via manipulating cropland soils (initial pH 8.7) in North China to illustrate the effect of soil acidification on fungal and bacterial denitrification after the addition of KNO₃ and glucose. For source partitioning, we used and compared SP/δ¹⁸O mapping approach (SP/δ¹⁸O MAP) and acetylene inhibition technique combined isotope two endmember mixing model (AIT-IEM). The results showed significantly higher N₂O emissions in the acidified soils (pH 6.2 and pH 7.1) compared with the initial soil (pH 8.7). The cumulative N₂O emissions during the whole incubation period (15 days) ranged from 7.1 mg N kg⁻¹ for pH 8.7–18.9 mg N kg⁻¹ for pH 6.2. With the addition of glucose, relative to treatments without glucose, this emission also increased with the decrement of pH values, and were significantly stimulated. Similarly, the highest N₂O emissions and N₂O/(N₂O + N₂) ratios (rN₂O) were observed in the pH 6.2 treatment. But the difference was the highest cumulative N₂O + N₂ emissions, which were recorded in the pH 7.1 treatment based on SP/δ¹⁸O MAP. Based on both approaches, ffD values slightly increased with the acidification of soil, and bacterial denitrification was the dominant pathway in all treatments. The SP/δ¹⁸O MAP data indicated that both the rN₂O and ffD were lower compared to AIT-IEM. It has been known for long that low pH may lead to high rN₂O of denitrification and ffD, but our documentation of a pervasive pH-control of rN₂O and ffD by utilizing combined SP/δ¹⁸O MAP and AIT-IEM is new. The results of the evaluated N₂O emissions by acidified soils are finely explained by high rN₂O and enhanced ffD. We argue that soil pH management should be high on the agenda for mitigating N₂O emissions in the future, particularly for regions where long-term excessive nitrogen fertilizer is likely to acidify the soils.

A pre-diabetes syndrome induced by endocrine disruptors (ED) was recently demonstrated in the model amphibian Silurana (Xenopus) tropicalis and was suggested to be a potential cause of amphibian population decline. However, such effects have not been found in wild type frogs exposed to ED and the capacity of amphibians to physiologically develop diabetes under natural conditions has not been confirmed. This study showed that a high fat diet (HFD) model displaying the important characteristics of mammal HFD models including glucose intolerance, insulin resistance and nonalcoholic fatty liver disease (NAFLD) can be developed with green frogs (Pelophylax spp.). Wild green frogs exposed to 10 μg L⁻¹ benzo [a]pyrene (BaP) for 18 h also displayed several characteristics of the pre-diabetes phenotype previously observed in Xenopus including glucose intolerance, gluconeogenesis activation and insulin resistance. The study results confirmed that metabolic disorders induced by ED in wild green frogs are typical of the pre-diabetes phenotype and could serve as a starting point for field studies to determine the role of ED in the decline of amphibian populations. From an environmental perspective, the response of wild green frogs to different ED (10 μg L⁻¹) suggests that a simple glucose-tolerance test could be used on wild anurans to identify bodies of water polluted with metabolic disruptors that could affect species fitness.

Whether propylene oxide (PO) exposure is associated with hyperglycemia were rarely explored. We aimed to determine the relationship between PO exposure and glucose metabolism, and potential role of oxidative stress. Among 3294 Chinese urban adults, urinary PO metabolite (N-Acetyl-S-(2-hydroxypropyl)-L-cysteine, 2HPMA), biomarkers of oxidative DNA damage (8-oxo-7,8-dihydro-20-deoxyguanosine, 8-OHdG) and lipid peroxidation (8-isoprostane, 8-iso-PGF₂α) in urine were determined. The associations of 2HPMA with 8-OHdG, 8-iso-PGF₂α, fasting plasma glucose (FPG), and risk of diabetes were explored. The roles of 8-OHdG and 8-iso-PGF₂α on association of 2HPMA with FPG and risk of diabetes were detected. After adjusted for potential confounders, each 1-unit increase in log-transformed concentration of 2HPMA was associated with a 0.15-mmol/L increase in FPG level, and the adjusted OR (95% CI) of diabetes by the associations of log-transformed urinary 2HPMA concentrations was 1.47 (95% CI: 1.03–2.11). Combination effects of 2HPMA with 8-OHdG or 8-iso-PGF₂α on risk of diabetes were detected, and elevated 8-iso-PGF₂α significantly mediated 34.5% of the urinary 2HPMA-associated FPG elevation. PO exposure was positively associated with FPG levels and risk of diabetes. PO exposure combined with DNA oxidative damage or lipid peroxidation may increase the risk of diabetes, and lipid peroxidation may partially mediate the PO exposure-induced FPG elevation.

The emerging endocrine disruption chemicals organophosphate esters (OPEs) pose high risk of metabolic disruption. However, limited information is available on physiological disturbance of OPEs on adipose, a major endocrine and metabolic organ. In this study, physiological change was investigated after exposing 3T3-L1fully differentiated adipocytes to six OPEs at non-cytotoxic concentrations. We found two chlorinated-OPEs (tris-(2-chloro-1-(chloromethyl) ethyl) phosphate (TDCPP) and tris(2-chloroisopropyl) phosphate (TCPP)) and two alkyl-OPEs (tributyl phosphate (TBP) and tris (2-butoxyethyl) phosphate (TBEP)) induced inflammation-like adipokines (chemoattractant protein 1 and interleukin-6), respectively. Increment of insulin-resistance-related hormones (resistin and leptin) were observed under TDCPP, TCPP, and TBP exposure. Functional and mechanistic investigation revealed that all of the compounds inhibited lipolysis at basal level through dephosphorylated HSLˢᵉʳ⁵⁶³, the rate limiting enzyme of lipolysis. Triphenyl phosphate (TPhP), tricresyl phosphate (TCP), TDCPP, TBP and TBEP enhanced glucose uptake at both basal and insulin-stimulated status. We evidenced that impact was independent of the classical pIRSˢᵉʳ⁶³⁹/pAKTˢᵉʳ⁴⁷³ nor the insulin-independent AMPK pathway. The elevated mRNA of slc2a4 and its transcriptional factor LXRα may, at least partially, explain for the increase of glucose uptake. Given the focus within the endocrine disruption on glands, it would be prudent not to ignore endocrinal impact on adipocytes.