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.

Emergency responses to the COVID-19 pandemic led to major changes in travel behaviours and economic activities in 2020. Machine learning provides a reliable approach for assessing the contribution of these changes to air quality. This study investigates impacts of health protection measures upon air pollution and traffic emissions and estimates health and economic impacts arising from these changes during two national ‘lockdown’ periods in Oxford, UK. Air quality improvements were most marked during the first lockdown with reductions in observed NO₂ concentrations of 38% (SD ± 24.0%) at roadside and 17% (SD ± 5.4%) at urban background locations. Observed changes in PM₂.₅, PM₁₀ and O₃ concentrations were not significant during first or second lockdown. Deweathering and detrending analyses revealed a 22% (SD ± 4.4%) reduction in roadside NO₂ and 2% (SD ± 7.1%) at urban background with no significant changes in the second lockdown. Deweathered-detrended PM₂.₅ and O₃ concentration changes were not significant, but PM₁₀ increased in the second lockdown only. City centre traffic volume reduced by 69% and 38% in the first and second lockdown periods. Buses and passenger cars were the major contributors to NO₂ emissions, with relative reductions of 56% and 77% respectively during the first lockdown, and less pronounced changes in the second lockdown. While car and bus NO₂ emissions decreased during both lockdown periods, the overall contribution from buses increased relative to cars in the second lockdown. Sustained NO₂ emissions reduction consistent with the first lockdown could prevent 48 lost life-years among the city population, with economic benefits of up to £2.5 million. Our findings highlight the critical importance of decoupling emissions changes from meteorological influences to avoid overestimation of lockdown impacts and indicate targeted emissions control measures will be the most effective strategy for achieving air quality and public health benefits in this setting.

The increasingly serious surface ozone (O₃) pollution in North China Plain (NCP) has received wide attention. However, the contribution of the changes for each emission source to the elevated O₃ concentration, as well as the direct and indirect effect of meteorological condition variation on increased O₃ level have not been comprehensively analyzed. This study applied the Community Multiscale Air Quality (CMAQ) model coupled with the integrated source apportionment method (ISAM) to quantify changes in daily maximum 8–h average O₃ concentration (MDA8 O₃) under different air pollutants emissions and meteorological conditions during summertime 2012–2017. The results showed that incoordinate NOx/VOC emission control sustainably increased MDA8 O₃ by 2.2–36.2 μg/m³ in the NCP, of which emission changes from industrial and transportation sectors were the predominant contributors (−0.6–19.5 μg/m³ for industrial sector and 1.2–18.1 μg/m³ for transportation, respectively). In contrast, MDA8 O₃ decreased by 2.5–9.2 μg/m³ for the power plants. The effect of changes in meteorological condition on MDA8 O₃ exhibited significantly spatial and temporal variation and unfavorable meteorological fields were shown in 2014, 2016, and 2017, which enhanced MDA8 O₃ by −2.5–23.1, −5.3–20.7, and −7.2–25.8 μg/m³, respectively. In addition, the changed meteorological factors indirectly affected the biogenic emission thus prompting the increases of MDA8 O₃ by −3.9–4.9 μg/m³ in the NCP during 2012–2017. The sensitive simulations suggested that more aggressive control measures about VOC reduction in industrial and transportation sectors should be implemented to further mitigate the O₃ pollution under unfavorable meteorological condition.

The decay of algal biomass and aquatic plants in freshwater lakes leads to the overproduction of autochthonous organic matter (OM) and the exhaustion of dissolved oxygen, impacting the microbial community and subsequent biodegradation of emerging contaminants in sediment. This study explored how the microbial processing of aquatic plant- and algal-derived OM (POM and AOM) mediates 17α-ethinylestradiol (EE2) biodegradation in the anoxic sediments of Lake Taihu in China. In four months of microcosm incubations, the increased concentrations of protein-like substances in AOM and POM exhibited temporary activation on microbial metabolic enzyme activity (fluorescein diacetate hydrolase and dehydrogenase) and significantly promoted the carbon mineralization with iron reduction (P < 0.001). These in turn increased the EE2 biodegradation efficiency to 77–90 ng g⁻¹ in the anoxic sediment. However, a higher EE2 biodegradation of 109 ng g⁻¹ was achieved with the humic acid augmentation containing more quinone-like compounds, showing a weaker substrate-priming effect but accelerated redox cycling of iron and organic substrates in the later period of incubation. The microbial analysis further revealed that the quinone-like compounds in OM were more closely associated with microbial electron transfer and strengthened their interspecies syntrophic cooperation favorable to contaminant biodegradation, even though the connective members exposed to protein-like components upregulated more functional genes related to organic carbon and xenobiotics metabolism and biodegradation. Our findings will help predict the fate of estrogens in various sedimentary environments under increasing eutrophication and further climate change scenarios.

Early life environmental influences such as exposure to cigarette smoke (CS) can disturb molecular processes of lung development and thereby increase the risk for later development of chronic respiratory diseases. Among the latter, asthma and chronic obstructive pulmonary disease (COPD) are the most common. The airway epithelium plays a key role in their disease pathophysiology but how CS exposure in early life influences airway developmental pathways and epithelial stress responses or survival is poorly understood. Using Drosophila melanogaster larvae as a model for early life, we demonstrate that CS enters the entire larval airway system, where it activates cyp18a1 which is homologues to human CYP1A1 to metabolize CS-derived polycyclic aromatic hydrocarbons and further induces heat shock protein 70. RNASeq studies of isolated airways showed that CS dysregulates pathways involved in oxidative stress response, innate immune response, xenobiotic and glutathione metabolic processes as well as developmental processes (BMP, FGF signaling) in both sexes, while other pathways were exclusive to females or males. Glutathione S-transferase genes were further validated by qPCR showing upregulation of gstD4, gstD5 and gstD8 in respiratory tracts of females, while gstD8 was downregulated and gstD5 unchanged in males. ROS levels were increased in airways after CS. Exposure to CS further resulted in higher larval mortality, lower larval-pupal transition, and hatching rates in males only as compared to air-exposed controls. Taken together, early life CS induces airway epithelial stress responses and dysregulates pathways involved in the fly's branching morphogenesis as well as in mammalian lung development. CS further affected fitness and development in a highly sex-specific manner.

The increased frequency and intensity of short-term extreme warming phenomena have been associated to harsh biological and ecosystem outcomes (i.e., mass mortalities in marine organisms). Marine heatwaves (MHWs), occurring when seasonal temperature threshold is exceeded for at least 5 consecutive days, may reduce the tolerance of coastal species toward additional pressures, but interactions between such multiple stressors are virtually unexplored. The present study aimed to characterize in Mytilus galloprovincialis the influence of a simulated MHW scenario on the toxicological effects of the pharmaceutical carbamazepine (CBZ), ubiquitously detected in the marine environment and chosen as model compound for this relevant class of emerging contaminants. The bioaccumulation of CBZ and responsiveness of various biological parameters, including immune system, antioxidant status, lipid metabolism and cellular integrity, were analyzed in exposed mussels both during and after the end of the heatwave. MHW appeared to strongly modulate accumulation of CBZ, paralleled by weakened immunocompetence and onset of oxidative disturbance that finally evolved to cellular damages and lipid metabolism disorders. Elaboration of the overall results through a quantitative Weight of Evidence model, revealed the highest hazard in organisms exposed to both the stressors 10 days after the end of the heatwave, suggesting that MHWs could leave a footprint on the capability of mussels to counteract CBZ toxicity, thus affecting their vulnerability and predisposition to adverse effects toward multiple stressors.

The present study aims to determine the associations of multiple plasma metal levels and plasma microRNAs (miRNAs) with diabetes risk, and further explore the mediating effects of plasma miRNAs on the associations of plasma metal with diabetes risk. We detected plasma levels of 23 metals by inductively coupled plasma mass spectrometry (ICP-MS) among 94 newly diagnosed and untreated diabetic cases and 94 healthy controls. The plasma miRNAs were examined by microRNA Array screening and Taqman real-time PCR validation among the same study population. The multivariate logistic regression models were employed to explore the associations of plasma metal and miRNAs levels with diabetes risk. Generalized linear regression models were utilized to investigate the relationships between plasma metal and plasma miRNAs, and mediation analysis was used to assess the mediating effects of plasma miRNAs on the relationships between plasma metals and diabetes risk. Plasma aluminum (Al), titanium (Ti), copper (Cu), zinc (Zn), selenium (Se), rubidium (Rb), strontium (Sr), barium (Ba), and Thallium (Tl) levels were correlated with elevated diabetic risk while molybdenum (Mo) with decreased diabetic risk (P < 0.05 after FDR multiple correction). MiR-122–5p and miR-3141 were positively associated with diabetes risk (all P < 0.05). Ti, Cu, and Zn were positively correlated with miR-122–5p (P = 0.001, 0.028 and 0.004 respectively). Ti, Cu, and Se were positively correlated with miR-3141 (P = 0.003, 0.015, and 0.031 respectively). In addition, Zn was positively correlated with miR-193b-3p (P = 0.002). Ti was negatively correlated with miR-26b-3p (P = 0.016), while Mo and miR-26b-3p were positively correlated (P = 0.042). In the mediation analysis, miR-122–5p mediated 48.0% of the association between Ti and diabetes risk. The biological mechanisms of the association are needed to be explored in further studies.

Evaluating ozone levels at high resolutions and accuracy is crucial for understanding the spatiotemporal characteristics of ozone distribution and assessing ozone exposure levels in epidemiological studies. The national models with high spatiotemporal resolutions to predict ground ozone concentrations are limited in China so far. In this study, we aimed to develop a random forest model by combining ground ozone measurements from fixed stations, ozone simulations from the Community Multiscale Air Quality (CMAQ) modeling system, meteorological parameters, population density, road length, and elevation to predict ground maximum daily 8-h average (MDA8) ozone concentrations at a daily level and 1 km × 1 km spatial resolution. The model cross-validation R² and root mean squared error (RMSE) were 0.80 and 20.93 μg/m³ at daily level in 2013–2019, respectively. CMAQ ozone simulations and near-surface temperature played vital roles in predicting ozone concentrations among all predictors. The population-weighted median concentrations of predicted MDA8 ozone were 89.34 μg/m³ in mainland China in 2013, and reached 100.96 μg/m³ in 2019. However, the long-term temporal variations among regions were heterogeneous. Central and Eastern China, as well as the Southeast Coastal Area, suffered higher ozone pollution and higher increased rates of ozone concentrations from 2013 to 2019. The seasonal pattern of ozone pollution varied spatially. The peak-season ozone pollution with the highest 6-month ozone concentrations occurred in different months among regions, with more than half domain in April–September. The predictions showed that not only the annual mean concentrations but also the percentages of grid-days with MDA8 ozone concentrations higher than 100/160 μg/m³ have been increasing in the past few years in China; meanwhile, majority areas in mainland China suffered peak-season ozone concentrations higher than the air quality guidelines launched by the World Health Organization in September 2021. The proposed model and ozone predictions with high spatiotemporal resolution and full coverage could provide health studies with flexible choices to evaluate ozone exposure levels at multiple spatiotemporal scales in the future.

Anticoagulant rodenticides (ARs) are widespread environmental contaminants that pose risks to scavenging birds because they routinely occur within their prey and can cause secondary poisoning. However, little is known about AR exposure in one of the rarest avian scavengers in the world, the California condor (Gymnogyps californianus). We assessed AR exposure in California condors and surrogate turkey vultures (Cathartes aura) to gauge potential hazard to a proposed future condor flock by determining how application rate and environmental factors influence exposure. Additionally, we examined whether ARs might be correlated with prolonged blood clotting time and potential mortality in condors. Only second-generation ARs (SGARs) were detected, and exposure was detected in all condor flocks. Liver AR residues were detected in 42% of the condors (27 of 65) and 93% of the turkey vultures (66 of 71). Although concentrations were generally low (<10 ng/g ww), 48% of the California condors and 64% of the turkey vultures exposed to ARs exceeded the 5% probability of exhibiting signs of toxicosis (>20 ng/g ww), and 10% and 13% exceeded the 20% probability of exhibiting signs toxicosis (>80 ng/g ww). There was evidence of prolonged blood clotting time in 16% of the free-flying condors. For condors, there was a relationship between the interaction of AR exposure index (legal use across regions where condors existed) and precipitation, and the probability of detecting ARs in liver. Exposure to ARs may complicate recovery efforts of condor populations within their current range and in the soon to be established northern California experimental population. Continued monitoring of AR exposure using plasma blood clotting assays and residue analysis would allow for an improved understanding of their hazard to condors, particularly if paired with recent movement data that could elucidate exposure sources on the landscape occupied by this endangered species.