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.

Most amyotrophic lateral sclerosis (ALS) cases are sporadic (∼90%) and environmental exposures are implicated in their etiology. Large industrial facilities are permitted the airborne release of certain chemicals with hazardous properties and report the amounts to the US Environmental Protection Agency (EPA) as part of its Toxics Release Inventory (TRI) monitoring program. The objective of this project was to identify industrial chemicals released into the air that may be associated with ALS etiology. We geospatially estimated residential exposure to contaminants using a de-identified medical claims database, the SYMPHONY Integrated Dataverse®, with ∼26,000 nationally distributed ALS patients, and non-ALS controls matched for age and gender. We mapped TRI data on industrial releases of 523 airborne contaminants to estimate local residential exposure and used a dynamic categorization algorithm to solve the problem of zero-inflation in the dataset. In an independent validation study, we used residential histories to estimate exposure in each year prior to diagnosis. Air releases with positive associations in both the SYMPHONY analysis and the spatio-temporal validation study included styrene (false discovery rate (FDR) 5.4e-5), chromium (FDR 2.4e-4), nickel (FDR 1.6e-3), and dichloromethane (FDR 4.8e-4). Using a large de-identified healthcare claims dataset, we identified geospatial environmental contaminants associated with ALS. The analytic pipeline used may be applied to other diseases and identify novel targets for exposure mitigation. Our results support the future evaluation of these environmental chemicals as potential etiologic contributors to sporadic ALS risk.

A vast amount of evidence indicates that bisphenol A (BPA) and phthalates are widely distributed in the environment since these compounds are mass-produced for the manufacture of plastics and plasticizers. These compounds belong to a large group of substances termed endocrine-disrupting chemicals (EDC). It is well known that humans and living organisms are unavoidably and unintentionally exposed to BPA and phthalates from food packaging materials and many other everyday products. BPA and phthalates exert their effect by interfering with hormone synthesis, bioavailability, and action, thereby altering cellular proliferation and differentiation, tissue development, and the regulation of several physiological processes. In fact, these EDC can alter fetal programming at an epigenetic level, which can be transgenerational transmitted and may be involved in the development of various chronic pathologies later in the adulthood, including metabolic, reproductive and degenerative diseases, and certain types of cancer.In this review, we describe the most recent proposed mechanisms of action of these EDC and offer a compelling selection of experimental, epidemiological and clinical studies, which show evidence of how exposure to these pollutants affects our health during development, and their association with a wide range of reproductive, metabolic and neurological diseases, as well as hormone-related cancers. We stress the importance of concern in the general population and the urgent need for the medical health care system to closely monitor EDC levels in the population due to unavoidable and involuntary exposure to these pollutants and their impact on human health.

The COVID-19 pandemic has exerted great shocks and challenges to the environment, society and economy. Simultaneously, an intractable issue appeared: a considerable number of hazardous medical wastes have been generated from the hospitals, clinics, and other health care facilities, constituting a serious threat to public health and environmental sustainability without proper management. Traditional disposal methods like incineration, landfill and autoclaving are unable to reduce environmental burden due to the issues such as toxic gas release, large land occupation, and unsustainability. While the application of clean and safe pyrolysis technology on the medical wastes treatment to produce high-grade bioproducts has the potential to alleviate the situation. Besides, medical wastes are excellent and ideal raw materials, which possess high hydrogen, carbon content and heating value. Consequently, pyrolysis of medical wastes can deal with wastes and generate valuable products like bio-oil and biochar. Consequently, this paper presents a critical and comprehensive review of the pyrolysis of medical wastes. It demonstrates the feasibility of pyrolysis, which mainly includes pyrolysis characteristics, product properties, related problems, the prospects and future challenges of pyrolysis of medical wastes.

Triclocarban (TCC), a broad-spectrum lipophilic antibacterial agent, is the main ingredient of personal and health care products. Nonetheless, its ubiquitous presence in the environment has been established to negatively affect the reproduction in humans and animals. In this work, we studied the possible toxic effects of TCC on mouse oocytes maturation in vitro. Our findings revealed that TCC-treated immature mouse oocytes had a significantly reduced rate of polar body extrusion (PBE) compared to that of control. Further study demonstrated that the cell cycle progression and cytoskeletal dynamics were disrupted after TCC exposure, which resulted in the continuous activation of spindle assembly checkpoint (SAC). Moreover, TCC-treated oocytes had mitochondrial damage, reduced ATP content, and decreased mitochondrial membrane potential (MMP). Furthermore, TCC exposure induced oxidative stress and subsequently triggered early apoptosis in mouse oocytes. Besides, the levels of histone methylation were also affected, as indicated by increased H3K27me2 and H3K27me3 levels. In summary, our results revealed that TCC exposure disrupted mouse oocytes maturation through affecting cell cycle progression, cytoskeletal dynamics, oxidative stress, early apoptosis, mitochondria function, and histone modifications in vitro.

Benzene is widely employed in the field of production, and its toxicity on biological systems has received increasing attention. Cell proliferation is a major life characteristic of living organisms. KLF15 and NOTCH1 are mature and classical genes in cell proliferation studies, particularly in the area of tumor investigation. The aim of this study was to investigate the effect and mechanism of VNN3 on cell proliferation induced by 1,4-benzoquinone (1,4-BQ), an important metabolite of benzene, and obtain a sensitive biomarker for the hazard screening and health care of benzene exposure. Normally growing AHH-1 cells were cultured in vitro and were incubated with different concentrations of 1,4-BQ (0, 10, 20, and 40 μM) for 24 h. A CCK-8 assay was used to assess the cell viability, whereas EdU was used to detect the cell proliferation of AHH-1 cells. The expression of VNN3, KLF15 and NOTCH1 was detected by real-time PCR. Moreover, a lentiviral model was constructed in AHH-1 cells to interfere with VNN3 expression. The results showed that 1,4-BQ clearly increased the expression of VNN3. Moreover, 1,4-BQ dose-dependently inhibited cell proliferation and caused increased KLF15 expression; in contrast, the NOTCH1 expression decreased in AHH-1 cells. Furthermore, following interference with the VNN3 expression, the cell proliferation inhibition and the expression of KLF15 and NOTCH1 were rescued. To further investigate the action of VNN3 in benzene hematotoxicity, we assessed it in benzene-exposed workers. The results showed that there was a remarkable correlation between the VNN3 expression and hemogram, which included RBC, NEUT and HGB. In addition, analysis of the KLF15 and NOTCH1 expression showed that the VNN3 expression was related to cell proliferation, which was consistent with the in vitro results. In conclusion, VNN3 influences cell proliferation induced by 1,4-BQ by regulating the expression of KLF15 and NOTCH1. VNN3 may represent a potential biomarker of benzene toxicity.

There is an increasing body of evidence illustrating the negative health effects of air pollution including increased risk of respiratory, cardiac and other morbid conditions. During March and April 2014 there were two air pollution episodes in England that occurred in close succession. We used national real-time syndromic surveillance systems, including general practitioner (GP) consultations, emergency department attendances, telehealth calls and ambulance dispatch calls to further understand the impact of these short term acute air pollution periods on the health seeking behaviour of the general public. Each air pollution period was comparable with respect to particulate matter concentrations (PM10 and PM2.5), however, the second period was longer in duration (6 days vs 3 days) and meteorologically driven ‘Sahara dust’ contributed to the pollution. Health surveillance data revealed a greater impact during the second period, with GP consultations, emergency department attendances and telehealth (NHS 111) calls increasing for asthma, wheeze and difficulty breathing indicators, particularly in patients aged 15–64 years. Across regions of England there was good agreement between air quality levels and health care seeking behaviour. The results further demonstrate the acute impact of short term air pollution episodes on public health and also illustrate the potential role of mass media reporting in escalating health care seeking behaviour.

This study evaluated whether short term exposures to NO2, O3, particulate matter <10 mm in diameter (PM10) were associated with higher risk of mortality. A total of 223,287 hypertensive patients attended public health-care services and newly prescribed at least 1 antihypertensive agent were followed-up for up to 5 years. A time-stratified, bi-directional case-crossover design was adopted. For all-cause mortality, significant positive associations were observed for NO2 and PM10 at lag 0–3 days per 10 μg/m3 increase in concentration (excess risks 1.187%–2.501%). Significant positive associations were found for O3 at lag 1 and 2 days and the excess risks were 1.654% and 1.207%, respectively. We found similarly positive associations between these pollutants and respiratory disease mortality. These results were significant among those aged ≥65 years and in cold seasons only. Older hypertensive patients are susceptible to all-cause and respiratory disease-specific deaths from these air pollutants in cold weather.

Antibiotic resistance is a growing problem for ecosystem health and public healthcare. Hence, the transmission of antibiotic resistance from human and animal origins to natural environments requires careful investigation. In this study, nine antibiotic resistance genes (ARGs), three mobile genetic elements (MGEs), and their relations with antibiotics, heavy metals, and microbiota were investigated in 16 sample sites (Xinxiang, China). Fluoroquinolones (0.13–14.22 μg/L) were most abundant in hospital effluent and oxytetracycline (251.86–5817.47 μg/kg) in animal manure. Animal manure showed the highest levels of zinc (80.79–2597.14 mg/kg) and copper (32.47–85.22 mg/kg), possibly affecting the prevalence of intI1 and aac(6′)-Ib genes. Aminoglycoside and sulfonamide resistance genes (aac(6’)-Ib, aadA, and sul1) were the main ARGs in this area. In addition, the detected ARGs and MGEs were higher in animal manure than in hospital effluent, except for the sul1 gene. On the other hand, the incomplete removal of antibiotics (29.76–100%), heavy metals (31.25–100%), and ARGs (1–3 orders of magnitude) in MWWTPs resulted in the accumulation of these contaminants in the receiving river. Network analysis suggested that the potential hosts (Jeotgalibaca, Atopostipes, Corynebacterium_1, etc.) of ARGs were more predominant in animal manure rather than hospital effluent, indicating a higher ARG transfer potential in animal manure compared with hospital sources. These results provide useful insights into the different migration and dissemination routes of antibiotics, heavy metals, ARGs, and microbiota from anthropogenic and animal origins to their receiving environments via MWWTP discharge and manure fertilization.