Enhanced photocatalytic performance of milkvetch-derived biochar via ZnO-Ce nanoparticle decoration for reactive blue 19 dye removal.

In this research, the photocatalytic removal of reactive blue 19 (RB19) dye is investigated employing zinc oxide/cerium (ZnO@Ce) nanoparticles decorated with biochar under LED irradiation. Synthesis of ZnO@Ce nanoparticles decorated with biochar was performed utilizing the co-precipitation procedure and, then, the texture and morphology of the fabricated nanocomposite were analyzed using energy dispersive X-ray (EDX), field emission scanning electron microscopy (FE-SEM), X-ray powder diffraction (XRD), transmission electron microscopy (TEM), Brunauer-Emmett-Teller (BET), and Fourier transform infrared (FTIR) spectroscopy techniques. Moreover, FE-SEM images demonstrate that ZnO-Ce nanoparticles were successfully decorated on the surface of biochar. The specific surface areas of biochar and biochar/ZnO-Ce were 519.75 and 636.52 m2/g, respectively. To achieve the maximum yield in the removal of RB19 dye, the effects of operating variables including dye concentration, LED lamp power, biochar@ZnO-Ce catalyst dose, pH and H2O2 dose were explored. Besides, the maximum percentage of RB19 dye removal was 96.47% under optimal conditions, i.e. catalyst dosage of 100 mg, H2O2 dosage of 1 mL, pH of 9, initial dye concentration of 5 ppm, LED power of 50 W, and reaction time of 140 min. Furthermore, the kinetic analysis reveals that the removal of RB19 dye follows the pseudo-first order kinetic model, with calculated values of a reaction rate constant of 0.045 min-1 and a correlation coefficient of R2 = 0.99, respectively. Moreover, the reusability and recyclability of biochar@ZnO/Ce nanocatalyst was promising over five runs, with only a 6.08% decrease in RB19 dye removal efficiency. Therefore, it can be concluded that the biochar @ZnO/Ce photocatalyst can be promisingly applied for the removal of azo dyes in aqueous solutions.

An updated systematic review on the maternal exposure to environmental pesticides and involved mechanisms of autism spectrum disorder (ASD) progression risk in children.

Autism spectrum disorder (ASD) increased dramatically over the past 25 years because of genetic and environmental factors. This systematic review (SR) aimed to determine the association between maternal exposure during pregnancy to environmental pesticides and other associations with the risk of ASD progression in children. PubMed (MEDLINE), Scopus (Elsevier) and the Institute for Scientific Information (ISI) Web of Science were searched using appropriate keywords up to March 2021. Twenty-four studies met the inclusion/exclusion criteria and were selected. Most studies reported that ASD increases the risk of offspring after prenatal exposure to environmental pesticides in pregnant mother's residences, against offspring of women from the same region without this exposure. The main potential mechanisms inducing ASD progressions are ROS and prostaglandin E2 synthesis, AChE inhibition, voltage-gated sodium channel disruption, and GABA inhibition. According to the included studies, the highest rates of ASD diagnosis increased relative to organophosphates, and the application of the most common pesticides near residences might enhance the prevalence of ASD.

The role of polybrominated diphenyl ethers in the induction of cancer: a systematic review of insight into their mechanisms.

Environmental pollution caused by persistent organic pollutants (POPs) has increased the challenge for the scientific communities. Polybrominated diphenyl ethers (PBDEs), classified as POPs, are widely applied in various materials as brominated flame retardants (BFRs). Because of the nature of these chemical compounds including toxicity, stability, and capability to bioaccumulate and biomagnify, PBDEs have posed a great challenge and risk to human health and wildlife. Therefore, the side effects of exposure to PBDEs as ubiquitous pollutants in the environment on cancer progression were investigated using a systematic review (SR) survey. To achieve this goal, forty studies were considered after defining the search terms and inclusion criteria, and/or exclusion criteria; the eligible records were collected from the international bibliographic databases. Based on the findings of the reviewed records, environmental exposure to the BFRs including PBDEs has a positive association with different mechanisms that induce cancer progression. However, the findings of the reviewed studies were not totally consistent with the mode of action and side effects are yet to be fully elucidated. Several articles have reported that BFRs can be carcinogenic and induce epithelial to mesenchymal transition via different mechanisms. The main mode of action involved in the environmental exposure to BFRs and the risk of cancer progression is endoplasmic reticulum and oxidative stress (OS). Generally, the imbalance of antioxidant mechanisms, reactive nitrogen species (RNSs) and reactive oxygen species (ROSs), during damage in cells, and stress caused OS, which increases tumorigenesis via multiple mechanisms, such as DNA damage, inflammation, and angiogenesis.

Environmental exposure to nonylphenol and cancer progression Risk-A systematic review.

Environmental exposure to nonylphenol (NP) can adversely affect human and wildlife health. A systematic review was conducted to evaluate the relationship between environmental NP exposure and cancer progression risk. Literature surveys were conducted within several international databases using appropriate keywords. A comprehensive search yielded 58 eligible studies involving a wide range of adverse effects, exposure assessment methods, study designs, and experimental models. Most studies reported that NP strongly induced breast cancer progression in intended experiments. Positive associations between NP exposure and ovarian, uterine, pituitary, and testicular cancers were also reported. Although some studies reported no relation between environmental NP exposure and tumour and/or cancer progression, NP (a known endocrine disrupting chemical) induced action mechanisms in multiple experimental models and may interfere with/hyper-activate oestrogen signalling. Secretion of oestrogen and development of reproductive tissues like breasts, uteruses, and ovaries showed strong associations with possible neoplasia (i.e., uncontrolled development of tumours and/or malignant cancers). Findings of this study are important for informing policymakers to pass legislation limiting the use of environmental contaminants such as NP before all adverse effects of exposure have been determined.

The possible DNA damage induced by environmental organic compounds: The case of Nonylphenol.

Human impact on the environment leads to the release of many pollutants that produce artificial compounds, which can have harmful effects on the body's endocrine system; these are known as endocrine disruptors (EDs). Nonylphenol (NP) is a chemical compound with a nonyl group that is attached to a phenol ring. NP-induced H2AX is a sensitive genotoxic biomarker for detecting possible DNA damage; it also causes male infertility and carcinogenesis. We attempt to comprehensively review all the available evidence about the different ways with descriptive mechanisms for explaining the possible DNA damage that is induced by NP. We systematically searched several databases, including PubMed, Scopus, Web of Science, and gray literature, such as Google Scholar by using medical subheading (MeSH) terms and various combinations of selected keywords from January 1970 to August 2017. The initial search identified 62,737 potentially eligible studies; of these studies, 33 were included according to the established inclusion criteria. Thirty-three selected studies, include the topics of animal model (n = 21), cell line (n = 6), human model (n = 4), microorganisms (n = 1), solid DNA (n = 1), infertility (n = 4), apoptosis (n = 6), and carcinogenesis (n = 3). This review highlighted the possible deleterious effects of NP on DNA damage through the ability to produce ROS/RNS. Finally, it is significant to observe caution at this stage with the continued use of environmental pollutants such as NP, which may induce DNA damage and apoptosis.