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Co-pyrolysis of sewage sludge and plastics have been utilized for producing biochars as a strategy to fix plastic pollution. However, comparative studies on the characteristics and environmental risk of heavy metals in biochars obtained by the co-pyrolysis of sludge and microplastic with/without metal additives are seldom. Here we demonstrated the effects of simulated co-pyrolysis (at 400 °C) of sewage sludge and metal-free or metal-loaded polyvinyl chloride (PVC) microplastics at different mass ratios (1:0, 19:1, 3:1, 1:3, sewage sludge: PVC (w/w)) respectively. Results revealed that co-pyrolysis of metal-loaded PVC and sewage sludge resulted in higher electrical conductivity, ash content, and an acidic pH of biochars as compared to the co-pyrolysis of metal-free PVC and sewage sludge. Addition of metal-loaded PVC increased total concentrations of calcium (Ca), magnesium (Mg), cadmium (Cd), and lead (Pb) in biochars, but reduced the bioavailability of Cd, chromium (Cr), nickel (Ni), and zinc (Zn) in biochars. Analysis of chemical speciation showed that heavy metals (except Pb) in biochars derived from co-pyrolysis of sewage sludge and metal-loaded PVC had higher percentage of more stable fraction (residual fraction) and lower potential ecological risk index (RI) value. S1AP3 (sludge: metal-loaded PVC = 1:3) biochar had the lowest environmental risk based on RI value (14.41). To sum up the present study suggests that the addition of metal-loaded PVC microplastic in sewage sludge had a positive impact on the immobilization of heavy metals during co-pyrolysis process. [Display omitted] • Sewage sludge was co-pyrolyzed with metal-free/metal-loaded PVC to produce biochar. • Addition of metal-loaded PVC changed the acidic pH of sludge-PVC biochars to alkaline. • Addition of metal-loaded PVC increased total Ca, Mg, Cd, and Pb contents in biochars. • Addition of metal-loaded PVC reduced biochar bioavailable Cd, Cr, Ni, and Zn contents. • Co-pyrolysis of sewage sludge and metal-loaded PVC had a lower ecological risk index. [ABSTRACT FROM AUTHOR]

Air pollution has side effects on human health. Epidemiology studies indicate a positive association between ambient fine particle (PM 2.5 , or particles less than 2.5 μm in diameter) concentration and lung cancer. However, how fine particles affect lung cancer at the molecular level and related therapeutic methods to address these diseases are unclear. Here, the multi-omics analysis (DNA methylation and transcriptomic) was used to detect human bronchial epithelial cells (HBE), that were exposed to PM 2.5 using a quantified, small, portable, and organ-level air-liquid interface microfluidic system that mimics lung functions. The results indicate that 36,838 differentially methylated genes were detected. Of these 33,796 genes were hypomethylated (beta < 0), and 2862 genes were hypermethylated (beta > 0). RNA-Seq analysis demonstrated that 19,489 genes were upregulated (log 2 FC > 0), and 16,659 were downregulated. Furthermore, the calcium and apoptosis pathways were activated according to multi-omics analysis. The change in EGFR gene expression after PM 2.5 exposure was the result of alterations of the cellular DNA methylome in the promoter. Inhibition or down-regulation of EGFR could result in the regulation of the downstream intracellular Ca2+ concentration and apoptosis via the EGFR/PLCγ and EGFR/STAT/Bcl-XL pathways after PM 2.5 exposure. EGFR inhibitors decrease the Ca2+ concentration of cells, thereby strengthening the effects of fine particles on apoptosis. In short, the Ca2+ concentration and the apoptosis of cells can be regulated via EGFR related pathway after PM 2.5 exposure. The EGFR may be a potentially promising therapeutic target for the treatment of air pollution-induced lung cancer through regulation of the intracellular Ca2+ concentration and apoptosis. Unlabelled Image • A small air–liquid interface microfluidic system that mimics lung functions for cells exposure • EGFR gene expression change after PM 2.5 exposure was the result of the alteration of DNA methylome. • EGFR gene regulates calcium flux via the EGFR/PLCγ pathways after PM 2.5 exposure. • EGFR gene regulates apoptosis via the EGFR/STAT/Bcl-XL pathways after PM 2.5 exposure. [ABSTRACT FROM AUTHOR]

• An automated microfluidic system for rapid quantitative detection of chloramphenicol in milk was presented. • Ten samples could be assayed simultaneously in a single microfluidic chip less than 20 min. • The limit of detection was 0.05 μg L−1 with the recovery rate in milk of 91.3%–105.5%. Chloramphenicol (CAP) is a toxic substance for human health, and detection of CAP residues in milk is necessary. However, most of the traditional CAP detection methods including high performance liquid chromatography-tandem mass spectrometry (HPLC-MS) and enzyme-linked immunosorbent assay (ELISA) are time-consuming and complicated. Herein, an automated microfluidics system for CAP detection in milk was developed. The residual CAP of multiple milk samples was quantitatively detected via competitive immunoassay in a single microfluidic chip simultaneously and automatically, and the reliability of the method was confirmed by flow cytometry. Completion of the detection by the system required less than 20 min and the cost for the detection of ten samples was about US$2.5. The limit of detection was 0.05 µg L−1, and the recovery rate of CAP in milk ranged from 91.3% to 105.5%. The microfluidic system developed in this study exhibited considerable potential in the point-of-care testing (POCT) of CAP in milk. [ABSTRACT FROM AUTHOR]