Monitoring beach plastic contamination across space and time is necessary for understanding its sources and ecological effects, and for guiding mitigation. This is logistically and financially challenging, especially for microplastics. Citizen science represents an option for sampling accessible sites to support long term monitoring, but challenges persist around data validation. Here we test a simple citizen science methodology to monitor visible microplastic contamination on sandy beaches using a standard quadrat unit (50 cm × 50 cm x 5 cm depth) sieved to 1 mm, to support the analysis of microplastic on two islands within the marine protected area of the Galápagos Archipelago, Ecuador (San Cristóbal and Santa Cruz islands). High school and university students undertook supervised sampling of two beaches in 2019–2020 collecting over 7000 particles. A sub-sample of the suspected microplastics collected (n = 2,213, ∼30% total) were analysed using FTIR spectrometry, confirming 93% of particles >1 mm visually identified by students were microplastics or rubber, validating this method as a crowd-sourced indicator for microplastic contamination. These data provide important insights into the plastic contamination of Galápagos, revealing plastic abundances of 0–2524 particles m⁻² over the two beaches (the highest reported in Galápagos). Strong accumulation gradients were measured parallel to the waterline at Punta Pitt (San Cristobal island) and perpendicular to the waterline at Tortuga Bay (Santa Cruz island), where four-fold higher concentrations were recorded at the sea turtle nesting habitat on the back-beach dune. No significant seasonal trends were measured during one year. These results demonstrate the value of citizen science in filling spatiotemporal knowledge gaps of beach contamination to support intervention design and conservation.

β-lactams are large group of antibiotics widely used to suppress the bacterial growth by inhibiting cell wall synthesis. Bacterial resistance against β-lactam antibiotics is primarily mediated through the production of Temoneria (TEM) β-lactamase (BLs), with almost 474 variants identified in Lactamase Engineering Database (LacED). The present study aims to develop a model to track the evolution of TEM BLs and their interactions with β-lactam and BLs inhibitors through data mining and computational approaches. Further, the model will be used to predict the effective combinations of β-lactam and BLs inhibitors to treat the bacterial infection harbouring emerging variants of β-lactamase. The molecular docking study results demonstrated that most TEM mutants recorded the least binding energy to penicillin and cephalosporin (I/II/III/IV/V generations) class of antibiotics. On the contrary, the same mutants recorded higher binding energy to carbapenem and Monobactam class of antibiotics. Among the BLs inhibitors, tazobactam recorded the least binding energy against most of the TEM mutants, indicating that it can lower the catalytic activity of TEM BLs, thereby potentiating antibiotic action. Similarly, data mining work has assisted us in creating a database of TEM mutants that has comprehensive data on mutations, bacterial diversity, Km, MIC, and IRT types. It has been noted that earlier released antibiotics like amoxicillin and ampicillin had lower Km and higher MIC values, which indicates the prevalence of bacterial resistance. By analysing the differential binding energy (ΔBE) of the selected TEM mutants against β-lactam and BLs inhibitors, the most effective combination of β-lactam (carbapenem and monobactam class of antibiotics) and BLs inhibitors (tazobactam) was identified, to cure bacterial diseases/infections and to prevent similar antibiotic resistance outbreaks. Therefore, our study opens a new avenue in developing strategies to manage antibiotic resistance in bacteria.

Bisphenol A (BPA) is pervasive in the environment, and exposure to BPA may increase the incidence of noncommunicable diseases like autoimmune diseases and cancer. Although BPA causes immunological problems at the cellular level, no system-level research has been conducted on this. Hence, in this study, we aimed to gain a better understanding of the biological response to BPA exposure and its association with immunological disorders. For that, we explored the transcriptome and the proteomic modifications at the systems and cellular levels following BPA exposure. Our integrated multi-omics data showed the alteration of the T cell receptor (TCR) signaling pathway at both levels. The proportion of enlarged T cells increased with upregulation of CD69, a surface marker of early T cell activation, even though the number of T cells reduced after BPA exposure. Additionally, on BPA exposure, the levels of pLCK and pSRC increased in T cells, while that of pLAT decreased. Following BPA exposure, we investigated cytokine profiles and discovered that chitinase 3 Like 1 and matrix metalloproteinase 9 were enriched in T cells. These results indicated that T cells were hyperactivated by CD69 stimulation, and phosphorylation of SRC accelerated on BPA exposure. Hence, alteration in the TCR signaling pathway during development and differentiation due to BPA exposure could lead to insufficient and hasty activation of TCR signaling in T cells, which could modify cytokine profiles, leading to increased environmental susceptibility to chronic inflammation or diseases, increasing the chance of autoimmune diseases and cancer. This study enhances our understanding of the effects of environmental perturbations on immunosuppression at molecular, cellular, and systematic levels following pubertal BPA exposure, and may help develop better predictive, preventative, and therapeutic techniques.

The lockdown measures caused by the COVID-19 pandemic substantially affected air quality in many cities through reduced emissions from a variety of sources, including traffic. The change in PM₂.₅ and its chemical composition in downtown Toronto, Canada, including organic/inorganic composition and trace metals, were examined by comparing with a pre-lockdown period and respective periods in the three previous years. During the COVID-19 lockdown, the average traffic volume reduced by 58%, whereas PM₂.₅ only decreased by 4% relative to the baselines. Major chemical components of PM₂.₅, such as organic aerosol and ammonium nitrate, showed significant seasonal changes between pre- and lockdown periods. The changes in local and regional PM₂.₅ sources were assessed using hourly chemical composition measurements of PM₂.₅. Major regional and secondary PM₂.₅ sources exhibited no clear reductions during the lockdown period compared to pre-lockdown and the previous years. However, cooking emissions substantially dropped by approximately 61% due to the restrictions imposed on local businesses (i.e., restaurants) during the lockdown, and then gradually increased throughout the recovery periods. The reduction in non-tailpipe emissions, characterized by road dust and brake/tire dust, ranged from 37% to 61%, consistent with the changes in traffic volume and meteorology across seasons in 2020. Tailpipe emissions dropped by approximately 54% and exhibited even larger reductions during morning rush hours. The reduction of tailpipe emissions was statistically associated with the reduced number of trucks, highlighting that a small fraction of trucks contributes disproportionally to tailpipe emissions. This study provides insight into the potential for local benefits to arise from traffic intervention in traffic-dominated urban areas and supports the development of targeted strategies and regulations to effectively reduce local air pollution.

A large amount of disposable plastic face masks (DPFs) is produced and used during the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, which results in an inevitable consequence of the dramatic increase of DPFs waste. However, the impact of DPFs exposure to the environment on their toxicity is rarely considered. In this study, a range of 76–276 items/L microplastics (MPs) was detected in the DPFs leachates, and fibrous (> 80.3%) and polypropylene (PP, > 89.2%) MPs were dominant. Co, Cu, Ni, Sr, Ti and Zn, were commonly detected in all leachates of the tested DPFs. Organics, such as acetophenone, 2,4-Di-tert-butylphenol, benzothiazole, bisphenol-A and phthalide, were found in the DPFs leachate, which were including organic solvents and plasticizer. Besides, we first found an emerging environmental risk substance, namely environmentally persistent free radicals (EPFRs), was generated in the DPFs leachates. The characteristic g-factors of the EPFRs was in a range of 2.003–2.004, identified as mixture of carbon- and oxygen-centered radicals. By means of in vitro toxicity assay, the DPFs leachate were confirmed to cause cytotoxicity and oxidative stress. Significantly, it is found that the formed EPFRs could contribute more toxic effects. Furthermore, when compared to N95 respirators, the tested surgical masks tend to release more MPs, leach more metals and organics, and generate more EPFRs. Surgical masks were thus showed higher risk than N95 respirators after exposure to water. This work highlights the importance of understanding the chemical complexity and possible toxicity of DPFs for their risk assessment.

The health risks of triphenyl phosphate (TPhP) have increased since its widespread application. Using placental trophoblast cell line JEG-3, we demonstrated that TPhP could induce endoplasmic reticulum stress (ERS) and cell apoptosis through PPARγ-mediated lipid metabolism. However, the developmental toxicity of TPhP through the placenta is not known. In this study, prenatal TPhP exposure to mice was investigated. Pregnant mice were orally exposed to TPhP (1 and 5 mg/kg) from embryonic day 0 (E0) until delivery. The results showed that TPhP could accumulate in placenta and impair pregnancy outcomes. After exposure, at E18, placental hormone chorionic gonadotrophin and testosterone levels were significantly decreased, but progesterone and estradiol levels were significantly increased, and placental angiogenesis was activated in the low-dose exposure group. While, in the high-dose exposure group, only estradiol levels were significantly increased. Different with the effect on hormone level or angiogenesis, TPhP significantly increased PPARγ and its regulated lipid transport proteins FABP, FATP, and CD36, and induced lipid accumulation in placental trophoblasts of both low- and high-exposure group. RNA-seq analysis of the placenta identified differentially expressed genes that were mainly involved in the ERS and MAPK signaling pathways. Western blot analysis verified that the protein levels related to ERS stress and apoptosis were significantly increased. To further confirm the role of PPARγ in TPhP mediated placental toxicity, pregnant mice were orally exposed to TPhP (1 mg/kg) or TPhP (1 mg/kg) + GW9662 (PPARγ inhibitor, 2 mg/kg) from E0 until delivery. The results showed that GW9662 could ameliorate the effect of TPhP on placental lipid accumulation, ERS and cell apoptosis, suggesting that PPARγ mediated the placental toxicity of TPhP. Overall, our results indicated that prenatal TPhP exposure impaired pregnancy outcomes, at least partly through PPARγ regulated function of trophoblast.

Effective immobilization of industrial waste into biochar development could be one of the most promising technologies for solid waste management to achieve circular economy. In this study, post-industrial cotton textile waste (PICTW), a cellulose rich industrial waste, was subjected to slow pyrolysis to develop a surface engineered biochar through phosphoric acid impregnation. Biochar produced at 500 °C designated as PICTWB500 showed a maximum methylene blue number (240 mg g⁻¹) with remarkable specific surface area of 1498 m² g⁻¹. FESEM, FTIR, XRD and Raman spectra analysis were performed to investigate the surface texture and functionalities developed in the biochar. Adsorption efficiency of the biochar was assessed using drimarene red, blue, violet, and black dyes as model dye pollutants in batch mode at different biochar dose, pH and contact time. The maximum monolayer adsorption capacity was obtained in the range 285–325 mg g⁻¹ for different dyes, determined from Langmuir adsorption model. The kinetic behaviour was more favourable with the pseudo second-order model. The recycling ability of PICTWB500 was proven to be effective up to 6th cycle without compromising its adsorption efficiency significantly. This study demonstrated an excellent adsorption capability of the biochar in dye laden real textile effluent and recycling of spent biochar as a precursor of bio compost. Hence, this study established a dual win strategy for waste utilization in textile industry using a closed loop approach with substantial techno-economic feasibility that may have potential applications.

Antibiotics are emerging contaminants in aquatic environments which pose serious risks to the ecological environment and human health. Advanced oxidation processes (AOPs) based on ultraviolet (UV) light have good application prospects for antibiotic degradation. As new and developing UV-AOPs, UV/chlorine and derived UV/chloramine processes have attracted increasing attention due to the production of highly reactive radicals (e.g., hydroxyl radical, reactive chlorine species, and reactive nitrogen species) and also because they can provide long-lasting disinfection. In this review, the main reaction pathways of radicals formed during the UV/chlor (am)ine process are proposed. The degradation efficiency, influencing factors, generation of disinfection by-products (DBPs), and changes in toxicity that occur during antibiotic degradation by UV/chlor (am)ine are reviewed. Based on the statistics and analysis of published results, the effects caused by energy consumption, defined as electrical energy per order (EE/O), increase in the following order: UV/chlorine < UV/peroxydisulfate (PDS)< UV/H₂O₂ < UV/persulfate (PS) < 265 nm and 285 nm UV-LED/chlorine (EE/O). Some inherent problems that affect the UV/chlor (am)ine processes and prospects for future research are proposed. The use of UV/chlor (am)ine AOPs is a rich field of research and has promising future applications, and this review provides a theoretical basis for that.

We investigated the biological response of soluble organic fraction (SOF) and water-soluble fraction (WSF) extracted from particulate matter (PM) emitted by an automotive diesel engine operating in a representative urban driving condition. The engine was fueled with ultra-low sulfur diesel (ULSD), and its binary blends by volume with 13% of butanol (Bu13), and with hydrotreated vegetable oil (HVO) at 13% (HVO13) and 20% (HVO20). Cytotoxicity, genotoxicity, oxidative DNA damage and ecotoxicity tests were carried out, and 16 polycyclic aromatic hydrocarbons (PAH) expressed as tbenzo(a)pyrene total toxicity equivalent (BaP-TEQ) were also analyzed. The Hepatocarcinoma epithelial cell line (HepG2) was exposed to SOF for 24 h and analyzed using comet assay, with the inclusion of formamidopyrimidine DNA glycosylase (FPG) and endonuclease III (Endo III) to recognize oxidized DNA bases. The WSF was evaluated through acute ecotoxicity tests with the aquatic microcrustacean Daphnia pulex (D. Pulex). Results showed that there was no cytotoxic activity for all tested SOF concentrations. Genotoxic responses by all the SOF samples were at same level, except for the HVO13 which was weaker in the absence of the enzymes. The addition of the FPG and Endo III enzymes resulted in a significant increase in the comet tail, indicating that the DNA damage from SOF for all tested fuel blends involves oxidative damage including a higher level of oxidized purines for ULSD and Bu13 in comparison with HVO blends, but the oxidized pyrimidines for HVO blends were slightly higher compared to Bu13. The WSF did not show acute ecotoxicity for any of the fuels. Unlike other samples, Bu13-derived particles significantly increase the BaP-TEQ. The contribution to the genotoxic activity and oxidative DNA from SOF was not correlated to BaP-TEQ, which means that the biological activity of PM might be affected also by other toxic compounds present in particulate phase.