Circulating exosome level of indigenous fish may be a novel biomarker for the integrated ecotoxicity effect of water environment.

The deficiency of effective biomarker for the toxic effects of water pollutants greatly limits the application of biological monitoring. This study aimed to investigate the possibility of circulating exosomes of indigenous fish acting as biomarker for the ecotoxicity effect of water environment. The Helong Reservoir in Guangzhou, China, was chosen as the investigating field, of which the water quality belongs to Class V (2013) (GB 3838-2002, China). The clean drinking water source of the upper reaches of the Liuxihe Reservoir was selected as the control. Indigenous fishes including Oreochromis niloticus (Nile tilapia), Labeo rohita (Rohu), Carassius auratus (Crucian carp) were sampled during the period from July 2020 to April 2021. Circulating exosomes of fish samples were isolated by using ultracentrifugation, characterized with transmission electron microscopy (TEM) and quantified by using bicinchoninic acid (BCA) assay. Oxidative stress, DNA and chromosome damage in liver, kidney, brain, gill and blood of fish samples were measured. The results showed that there were significant differences in superoxide dismutase (SOD) activity, glutathione (GSH) and malondialdehyde (MDA) contents, DNA and chromosome damage in fish samples between the Helong Reservoir and the control. Interestingly, there were also significant differences in circulating exosome levels of fish samples between them. Our data suggested that circulating exosome level of indigenous fish may be a novel biomarker for the ecotoxicity effects of water environment.

lncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1.

BACKGROUND: Fine particle pollution, specifically pollution by fine particulate matter (PM2.5), remains a significant concern in developing countries and plays an important role in the development and progression of respiratory diseases. Increasing evidences have demonstrated that long non-coding RNAs (lncRNAs) may act as vital molecules by binding to specific RNA-binding protein (RBP); however, their relationship with PM2.5 pollution is largely unexplored. OBJECTIVE: We investigated the association between lncRNA and respiratory system inflammation caused by PM2.5. METHODS: PM2.5 components were detected by gas chromatography-mass spectrometry (GC-MS), inductively coupled plasma-mass spectrometry (ICP-MS), and ionic chromatography. We established an inflammation model of PM2.5-induced toxicity in vivo (male and female SD rats, 0, 25, 50 and 100 mg/k PM2.5, 1, 7 and 14 days, single non-invasive tracheal instillation) and in vitro (rat alveolar macrophage cell line (NR8383), 0, 50, 100, 200, 400 µM PM2.5 for 24, 48, and 72 h). lncRNA high-throughput sequencing (lncRNA-seq) was used to investigate lncRNA profiles in PM2.5-treated NR8383 cells, and RNA interference (RNAi) was applied to explore the function of the target lncRNA. The mechanisms associated with specific lncRNAs were explored using comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) and western blot. RESULTS: PM2.5-treated NR8383 cells and SD rats exhibited respiratory inflammation. lncRNA AABR07005593.1 was a pro-inflammatory factor that regulated IL-6 levels. Mechanistically, ChIRP-MS and western blot analyses revealed that highly expressed lncRNA AABR07005593.1 interacted with MCCC1 to involve in the activation of NF-κB pathway, and ultimately promoted the expression of IL-6. CONCLUSION: This study demonstrated that PM2.5 induced inflammation in vivo and in vitro. Furthermore, lncRNA AABR07005593.1 bound to MCCC1 to potentiated IL-6 expression. Therefore, lncRNA AABR07005593.1 may act as a potential biomarker for PM2.5 inflammation.

PM2.5-inducible long non-coding RNA (NONHSAT247851.1) is a positive regulator of inflammation through its interaction with raf-1 in HUVECs.

Several studies have demonstrated that PM2.5 inhalation is associated with an increased risk of cerebrovascular disease (CVD), in which inflammation plays an important role. The mechanisms of this disease are not fully understood to date. Long non-coding RNAs (lncRNAs) are involved in many pathophysiological processes, such as immune responses; however, their functions associated with inflammation are largely unexplored. High-throughput sequencing assay and obtained numerous lncRNAs that altered the expression in response to PM2.5 treatment in HUVECs. NONHSAT247851.1 was also identified, which was significantly up-regulated to control the expression of immune response genes. Mechanistically, the results indicated that NONHSAT247851.1 knockdown reduced the expression of IL1ß. In study, we investigated NONHSAT247851.1 as a promoter in regulating immune response genes via binding with raf-1 to regulate the phosphorylation level of p65 protein in HUVECs. The data collected suggests that NONHSAT247851.1 regulates inflammation via interaction with raf-1 to control the inflammatory expression in PM2.5 exposure.

Hypoxic storage of erythrocytes slows down storage lesions and prolongs shelf-life.

Conventional storage conditions of erythrocytes cause storage lesions. We propose that hypoxic storage conditions, involving removal of oxygen and replacement with helium, the changes in stored erythrocytes under hypoxic condition were observed and assessed. Erythrocytes were divided into two equal parts, then stored in conventional and hypoxic conditions, separately. Blood gas analysis, hemorheology, and hemolysis were performed once a week. Energy metabolism and membrane damage were monitored by enzyme-linked immunosorbent assay. Phosphatidylserine exposure was measured by flow cytometry. P50 was measured and the oxygen dissociation curve (ODC) plotted accordingly. Erythrocyte morphology was observed microscopically. In the 9th week of storage, the hemolysis of the hypoxia group was 0.7%; lower (p < .05) than that of the control group and still below the threshold of quality requirements. The dissolved oxygen and pO2 were only 1/4 of that in the control group (p < .01); the adenosine triphosphate, glucose, and lactic acid levels were decreased (p < .05), while the 2,3-diphosphoglycerate levels were increased relative to that in the control group (p < .01). There were no statistically significant differences in membrane damage, deformability, and aggregation between the two groups. In addition, the ODC of the two groups was shifted to the left but this difference was not statistically different. Basically similar to the effect of completely anaerobic conditions. Erythrocytes stored under hypoxic conditions could maintain a relatively stable state with a significant decrease in hemolysis, reduction of storage lesions, and an increase in shelf-life.

Induction of Inflammatory Responses in Human Bronchial Epithelial Cells by Pb2+-Containing Model PM2.5 Particles via Downregulation of a Novel Long Noncoding RNA lnc-PCK1-2:1.

Airborne particular matter (PM2.5) contains complex mixtures of pollutants, and their compositions also vary with time and location. Inhalation of PM2.5 may cause a number of diseases, such as bronchial and lung inflammation and lung cancer. So far, how different components of PM2.5 contribute to inflammation and toxicity is still not known. To identify key PM2.5 components that are responsible for inflammation, here we took a reductionism approach and synthesized a model PM2.5 library containing 20 carbon nanoparticle based members with loadings of As(III), Pb2+, Cr(VI), and BaP individually or in combination at environment relevant concentrations. We discovered that only carbon nanoparticle-Pb2+ adducts, not other pollutants or adducts, induced inflammation in human bronchial cells by suppressing the expression of a novel long noncoding RNA lnc-PCK1-2:1, while lnc-PCK1-2:1 routinely plays a regulatory role in inhibiting inflammation. This finding was further substantiated by varying Pb2+ loadings on carbon nanoparticles and overexpressing lnc-PCK1-2:1. The success of this approach opens an avenue for further elucidation of molecular mechanisms of PM2.5-induced inflammation and toxicity.

Cr(VI)/Pb2+ are responsible for PM2.5-induced cytotoxicity in A549 cells while pulmonary surfactant alleviates such toxicity.

The composition of PM2.5 is extremely complicated, making the causes of PM2.5-induced toxicity hard to understand. To identify the major toxic components of PM2.5 particles, we used reductionism approach, synthesized and investigated a model PM2.5 library containing 24 carbon nanoparticles with adsorbed pollutants including Cr(VI), Pb2+, As(III) and BaP either individually or in combinations. Our data showed that major physicochemical characteristics of model PM2.5 library members were similar to PM2.5 particles from Guangzhou city (PM2.5-GZ). Cytotoxicity of lung cells (A549) was increasing as the member of adsorbed pollutants at environment relevant concentrations. Using these model particles, we identified that co-existence of Cr(VI) and Pb2+ components contributed to the PM2.5-induced cytotoxicity in A549 cells. Besides, pulmonary surfactant reduced the PM2.5-induced cytotoxicity in A549 cells probably via enhancing cell autophagy. The findings from this study suggest that systematic investigation using model PM2.5 particle library helps identify key toxic pollutants in otherwise very complex PM2.5 particles and facilitate our understanding of the underlying biological mechanisms.

Ultrafine particle libraries for exploring mechanisms of PM2.5-induced toxicity in human cells.

Air pollution worldwide, especially in China and India, has caused serious health issues. Because PM2.5 particles consist of solid particles of diverse properties with payloads of inorganic, organic and biological pollutants, it is still not known what the major toxic components are and how these components induce toxicities. To explore this complex issue, we apply reductionism principle and an ultrafine particle library approach in this work. From investigation of 63 diversely functionalized ultrafine particles (FUPs) with adsorbed key pollutants, our findings indicate that 1) only certain pollutants in the payloads of PM2.5 are responsible for causing cellular oxidative stress, cell apoptosis, and cytotoxicity while the particle carriers are much less toxic; 2) pollutant-induced cellular oxidative stress and oxidative stress-triggered apoptosis are identified as one of the dominant mechanisms for PM2.5-induced cytotoxicity; 3) each specific toxic component on PM2.5 (such as As, Pb, Cr or BaP) mainly affects its specific target organ(s) and, adding together, these pollutants may cause synergistic or just additive effects. Our findings demonstrate that reductionism concept and model PM2.5 particle library approach are very effective in our endeavor to search for a better understanding of PM2.5-induced health effects.

[Effect of Qingluo Tongbi Compound on Osteoclast Differentiation-related mIRNA Expressions in Adjuvant Induced Arthritis Rats].

Objective To observe the effect of Qingluo Tongbi Compound (QTC) on osteoclast dif- ferentiation-related miRNA expressions in adjuvant induced arthritis (AIA) rats, and to study its mecha- nism for treating rheumatoid arthritis (RA). Methods The synovial fibroblasts and monocytes of peripher- al blood from AIA rats were co-cultured to induce osteoclast-like cells. Differently expressed miRNAs in the late stage osteoclasts differentiation were detected by miRCURY™ Array. Real-time quantitative PCR (RT- PCR) was applied to verify the reliability of miRNA array. QTC drug-containing sera and blank sera were prepared and added to the co-cultured system. The osteoclasts were randomly divided into three groups, the blank group, the blank serum group, and the QTC group. RT-PCR was applied to detect the effect of QTC on related differentially expressed miRNAs. Bioinformatics software was applied to analyze related differentially expressed miRNAs. Results miRNA array results showed that as compared with the monocytes group, there were 211 miRNAs differentially expressed in osteoclast-like cell differentiation, including 88 up-regulated miRNAs and 123 down-regulated miRNAs. Results of RT-PCR were consistent with results of the array. RT-PCR showed that the expression level of miR-140-5p was obviously up-regulated after the intervention of QTC. Results of bioinformatics analyses showed that the target gene of miR-140-5p was sig- nificantly enriched in signaling pathways such as the regulation of actin cytoskeleton, Ras signaling path- ways, cAMP signaling pathways, and Rap1 signaling pathways. Conclusions There were various dysregulated expressions of miRNAs in the anaphase of osteoclast-like cells differentiation. QTC participated the regulation of osteoclast differentiation by effecting the expression of miR-140-5p.

Simultaneous measurement of methyl tert-butyl ether and tert-butyl alcohol in human serum by headspace solid-phase microextraction gas chromatography-mass spectrometry.

The abundant production of methyl tert-butyl ether (MTBE) and its widespread use have led to an increase in the potential for human exposure. This work described a simple, fast, sensitive, reliable and low-cost method for the simultaneous measurement of MTBE and its metabolite, tert-butyl alcohol (TBA) in human serum by headspace solid-phase microextraction gas chromatography-mass spectrometry. Extraction conditions were optimized and 40 °C, 10 min, 250 rpm and 0.3 g NaCl for a 1 mL sample were the optimal conditions. This method showed good analytical performance in terms of sensitivity with limits of detection in serum (1 mL) of 0.03 µg/L for MTBE and 0.05 µg/L for TBA, accuracy (mean recovery values) from 75.8% to 85.8%, precision (relative standard deviations) <10% and sample stability (biodegradation) <10% after 28 days. A verification experiment proved the reproducibility and stability of this method as well. Finally the method was used to detect 212 specimens, and the internal dose levels for MTBE in human serum were presented in China.

Polybrominated Diphenyl Ethers (PBDEs) in paired human hair and serum from e-waste recycling workers: source apportionment of hair PBDEs and relationship between hair and serum.

Human hair has been widely used as a bioindicator for human persistent organic pollutants (POPs) exposure, but studies on the sources of hair POPs and the relationship between hair and body burden are limited. This study analyzed the possible source apportionment of hair PBDEs and examined the relationship between PBDE concentrations in paired hair and serum from e-waste recycling workers. Using the ratio of BDE 99/47 and BDE 209/207 as indices, we calculated that only 15% of the highly brominated congeners (nona- and deca-BDE congeners) comes from exogenous (external) exposure for both female and male hair, but an average of 64% and 55% of the lower-brominated congeners (tetra- to penta-BDE congeners) come from exogenous exposure for female and male hair, respectively. The higher contribution of exogenous exposure for less-brominated congeners could be related to their relatively lower log KOW and higher volatility than higher-brominated congeners, which make them more readily to evaporate from dust and then to be adsorbed on hair. Higher hair PBDE levels and higher exogenous exposure of less-brominated congeners in females than in males can be attributed to a longer exogenous exposure time for females than males. Significant positive relationships were found in tri- to hepta-BDE congeners (BDE 28, 47, 66, 85, 100, 153, 154, and 183) (R = 0.36-0.55, p < 0.05) between hair and serum, but this relationship was not found for octa- to deca-BDE. Difference in the half-lives between highly brominated congeners and less-brominated congeners could be a reason. This result also implied that we should treat the results of correlation analyses between hair and other organs cautiously.

p53-Dependent apoptosis induced in human bronchial epithelial (16-HBE) cells by PM(2.5) sampled from air in Guangzhou, China.

Epidemiological studies have shown that air pollution particulate matter (PM) is associated with increased respiratory morbidity and mortality. However, the mechanisms are not fully understood. Oxidative stress-mediated apoptosis plays an important role in the occurrence of respiratory diseases. In this study, human bronchial epithelial (16-HBE) cells were exposed to different concentrations (16-128 µg/ml) of PM(2.5) for 24 h to investigate the apoptosis induced by PM(2.5). The results showed that PM(2.5) exposure significantly induced apoptosis, DNA strand breaks, and oxidative damage in a dose-dependent manner in 16-HBE cells. The expression of p53 and p73 increased significantly along with the dose of PM(2.5) in 16-HBE cells, whereas the expression of p21(Cip1/WAF1) decreased; the expression of mdm2 increased and then decreased, but not significantly. Taken together, these observations indicate that PM(2.5) may lead to oxidative damage and induce apoptosis through the p53-dependent pathway in 16-HBE cells. p53-Dependent apoptosis mediated by DNA strand breaks may be an important mechanism of PM(2.5)-induced apoptosis in 16-HBE cells.

Virus-like structures for combination antigen protein mRNA vaccination.

Improved vaccination requires better delivery of antigens and activation of the natural immune response. Here we report a lipid nanoparticle system with the capacity to carry antigens, including mRNA and proteins, which is formed into a virus-like structure by surface decoration with spike proteins, demonstrating application against SARS-CoV-2 variants. The strategy uses S1 protein from Omicron BA.1 on the surface to deliver mRNA of S1 protein from XBB.1. The virus-like particle enables specific augmentation of mRNAs expressed in human respiratory epithelial cells and macrophages via the interaction the surface S1 protein with ACE2 or DC-SIGN receptors. Activation of macrophages and dendritic cells is demonstrated by the same receptor binding. The combination of protein and mRNA increases the antibody response in BALB/c mice compared with mRNA and protein vaccines alone. Our exploration of the mechanism of this robust immunity suggests it might involve cross-presentation to diverse subsets of dendritic cells ranging from activated innate immune signals to adaptive immune signals.

Heavy metals in food, house dust, and water from an e-waste recycling area in South China and the potential risk to human health.

Concentrations of heavy metals (Cd, Pb, Cu, Zn, and Ni) were measured in the foodstuffs, house dust, underground/drinking water, and soil from an electronic waste (e-waste) area in South China. Elevated concentrations of these potentially toxic metals were observed in the samples but not in drinking water. The health risks for metal exposure via food consumption, dust ingestion, and drinking water were evaluated for local residents. For the average residents in the e-waste area, the non-carcinogenic risks arise predominantly from rice (hazard index=3.3), vegetables (2.2), and house dust (1.9) for adults, while the risks for young children are dominated by house dust (15). Drinking water may provide a negligible contribution to risk. However, local residents who use groundwater as a water supply source are at high non-carcinogenic risk. The potential cancer risks from oral intake of Pb are 8×10(-5) and 3×10(-4) for average adults and children, and thus groundwater would have a great potential to induce cancer (5×10(-4) and 1×10(-3)) in a highly exposed population. The results also reveal that the risk from oral exposure is much higher than the risk from inhalation and dermal contact with house dust.

Mechanism of Interaction between hsa_circ_0002854 and MAPK1 Protein in PM2.5-Induced Apoptosis of Human Bronchial Epithelial Cells.

Fine particulate matter (PM2.5) pollution increases the risk of respiratory diseases and death, and apoptosis is an important factor in the occurrence of respiratory diseases caused by PM2.5 exposure. In addition, circular RNAs (circRNAs) can interact with proteins and widely participate in physiological and pathological processes in the body. The aim of this study was to investigate the mechanism of circRNA and protein interaction on PM2.5-induced apoptosis of human bronchial epithelial cells (16HBE) in vitro. In this study, we exposed human bronchial epithelial cells to a PM2.5 suspension with different concentration gradients for 24 h. The results showed that apoptosis of 16HBE cells after PM2.5 treatment was accompanied by cell proliferation. After exposure of PM2.5 to 16HBE cells, circRNAs related to apoptosis were abnormally expressed. We further found that the expression of hsa_circ_0002854 increased with the increase in exposure concentration. Functional analysis showed that knocking down the expression of hsa_circ_0002854 could inhibit apoptosis induced by PM2.5 exposure. We then found that hsa_circ_0002854 could interact with MAPK1 protein and inhibit MAPK1 phosphorylation, thus promoting apoptosis. Our results suggest that hsa_circ_0002854 can promote 16HBE apoptosis due to PM2.5 exposure, which may provide a gene therapy target and scientific basis for PM2.5-induced respiratory diseases.

A time-stratified case-crossover study of fine particulate matter air pollution and mortality in Guangzhou, China.

OBJECTIVES: Few studies in China investigate health impact of fine particulate matter (PM(2.5)) due to lack of monitoring data and the findings are controversial. The aim of this study is to examine the short-association between PM(2.5) and daily mortality in Guangzhou, the economic center of south China. METHODS: In Guangzhou, we measured daily PM(2.5) concentrations between 2007 and 2008 and conducted a time-stratified case-crossover analysis to explore the association between PM(2.5) and daily mortality, and examine potential effect modifiers including age, sex, and education. RESULTS: The averaged PM(2.5) concentration in 2007-2008 was 70.1 µg/m(3) in Guangzhou, which was approximately seven times higher than the WHO Air Quality Guidelines for PM(2.5) (annual average: 10 µg/m(3)). Regression analysis showed that ambient PM(2.5) was associated with mortality from all causes and cardiorespiratory diseases. An increase of 10 µg/m(3) in 2-day moving average (lag01) concentration of PM(2.5) corresponds to 0.90% [95% confidence interval (CI): 0.55, 1.26%] increase of total mortality, 1.22% (95% CI: 0.63, 1.68%) increase of cardiovascular mortality, and 0.97% (95% CI: 0.16, 1.79%) increase of respiratory mortality. The associations were stronger in the elderly (aged 65 years or more), in females, and in those with low education level, but the differences were statistically insignificant. After adjustment for nitrogen dioxide (NO(2)), however, the effects of PM(2.5) decreased and became statistically insignificant. CONCLUSIONS: Our findings provided new information for the adverse health effects of PM(2.5) in China, and may have some implications for environmental policy making and standard setting in Guangzhou.

[A cross-sectional study about the effects of residential exposure to power transmission line on human nervous system symptoms and hematology].

OBJECTIVE: To investigate the possible effects on nervous system and health condition under the exposure to electromagnetic field. METHODS: Take the resident around the power transmission line as the objects and were divided into 3 groups by the distance from the power transmission line 20 m, 100 m and 500 m, respectively. Some living conditions and health conditions were recorded by face-to-face the questionnaire survey, and Hematological indices of each groups were examined including IgG, IgM, leukocyte formulae, erythrocyte, hemoglobin and platelet. RESULTS: There was no significant difference in each group, according exposure of daily life, such as drinking and smoking (P > 0.05). Compared with the each distance groups, it was presented significant difference between the distance from the power transmission line and the incidence of headache or dizziness, insomnia and easy weary and so on (P < 0.05). In hematology aspect, with the horizontal distance from the power transmission line decreasing, PLT level of residents was reductive and the difference was statistically significant (P < 0.001), whereas leukocyte formulae, erythrocyte, hemoglobin, IgG and IgM had no significant difference among each group (P < 0.05). CONCLUSION: Closely exposure to electromagnetic field may induce headache and so on and decrease the level of PLT.

Indigenous Fish-Based Assessment of Genotoxic Potentials of the Helong Reservoir in Guangzhou, China.

The present study was conducted to assess the genotoxic potential of water from the Helong Reservoir, which was designated as a strategic drinking water source by the Guangdong Provincial Government of China in October 2016. Four kinds of common indigenous fish samples (Labeo rohita, Cirrhinus molitorella, red tilapia, and Oreochromis niloticus) were collected at 6 sampling sites during the period from July to November 2020. Fish from the clean drinking water source of the upper reaches of the Liuxihe Reservoir in Guangzhou were collected as the control. Both the alkaline single cell gel electrophoresis assay and the micronucleus test were used to detect DNA damage and the micronucleus rate in erythrocytes of fish samples, respectively. The results indicated that there was a significant increase in comet tail length, Olive tail moment, and micronucleus rates of all fish samples compared with those of the control (p < 0.05). The order of sensitivity to DNA damage and micronucleus formation was Labeo rohita > Cirrhinus molitorella > red tilapia > Oreochromis niloticus. The results of the 2 kinds of experiments were in perfect agreement with each other. We conclude that there are obvious genotoxic effects from the water in the Helong Reservoir. As a strategic drinking water source, the safety of the Reservoir water quality should be considered. The local government should put the restoration of the Helong Reservoir water quality on the agenda as soon as possible. Environ Toxicol Chem 2021;40:1919-1927. © 2021 SETAC.

Lithium recovery from effluent of spent lithium battery recycling process using solvent extraction.

A novel process of lithium recovery from effluent of spent lithium batteries recycling by solvent extraction was proposed. The ß-diketone extraction system used in the experiment was composed of benzoyltrifluoroacetone (HBTA), trioctylphosphine oxide (TOPO) and kerosene. The effective parameters such as solution pH value, saponification degree, initial lithium concentration and phase ratio were evaluated by experiments. More than 90% of lithium could be extracted by saponified organic phase through three-stage countercurrent extraction. The loaded organic phase was first eluted by dilute HCl solution to remove nontarget sodium, and then stripped by 6 mol/L HCl at a large phase ratio to obtain lithium-rich solution with 4.322 mol/L lithium. The lithium-rich solution from the process could be used to prepare lithium carbonate or lithium chloride. The stripped organic phase can be recycled and no crud or emulsification was observed during the process. The extraction mechanism of HBTA-TOPO was investigated via FT-IR spectroscopy, and the results indicated the two extractants showed strong synergistic effect. The thermodynamic study revealed lithium extraction is an exothermic process, which meant lower temperature promotes extraction of lithium. This work provided a novel approach to recover lithium from effluent of spent lithium battery recycling.

EDTA-functionalized magnetic chitosan oligosaccharide and carboxymethyl cellulose nanocomposite: Synthesis, characterization, and Pb(II) adsorption performance.

A novel ethylenediaminetetraacetic acid (EDTA)-functionalized magnetic chitosan oligosaccharide and carboxymethyl cellulose (Fe3O4@CMCCOS-EDTA) nanocomposite adsorbent was successfully fabricated for Pb(II) adsorption. The adsorbent was characterized by Fourier transform infrared, and X-ray photoelectron spectroscopy was used to confirm successful EDTA modification and Pb(II) adsorption. Scanning electron microscopy, transmission electron microscopy, vibrating sample magnetometer, and thermogravimetric analysis were used to study the morphology and properties of magnetic particles. EDTA modification considerably improved the capacity of the adsorbent. The batch adsorption experiment results indicated that the pseudo-second-order (PSO) model and the Langmuir isotherm model reliably described the adsorption behavior. The maximum adsorption capacity (qm) for monolayer chemical adsorption was calculated to be 432.34 mg/g at the pH of 5 and temperature of 308 K. Notably, Fe3O4@CMCCOS-EDTA exhibited a high Pb(II) removal rate of ~100% using an initial metal ion solution of 100 mg/L and 200 mg/L.

Assessment of kitchen emissions using a backpropagation neural network model based on urinary hydroxy polycyclic aromatic hydrocarbons.

Kitchen emissions are mixed indoor air pollutants with adverse health effects, but the large-scale assessment is limited by costly equipment and survey methods. This study aimed to discuss the application of backpropagation (BP) neural network models in the assessment of kitchen emissions based on the exposure marker. A total of 3686 participants were recruited for the kitchen survey, and their sleep quality was measured by the Pittsburgh sleep quality index (PSQI). After excluding the confounders, 365 participants were selected to assess their urinary hydroxy polycyclic aromatic hydrocarbons (OH-PAHs) concentrations by ultra-high-performance liquid chromatography/tandem mass spectrometry. Two BP neural network models were then set up using the survey and detection data from the 365 participants and used to predict the total urinary OH-PAHs concentrations of all participants. The total urinary OH-PAHs and 1-hydroxy-naphthalene (1-OHNap) concentrations were significantly higher among the 365 participants with poor sleep quality (global PSQI score > 5; P < 0.05). Results from internal and external validation showed that our model has high credibility (model 2). Further, the participants with higher predicted total urinary OH-PAHs concentrations were associated with the global PSQI score of >5 (odds ratio (OR) = 1.284, 95% confidence interval (CI) = 1.082-1.525 for participants with predicted total urinary OH-PAHs concentrations of over 1.897 µg/mmol creatinine in model 1, and OR = 1.467, 95% CI = 1.240-1.735 for participants with predicted total urinary OH-PAHs concentrations of over 2.253 µg/mmol creatinine in model 2) after adjusting for the confounders. Findings suggest that the BP neural network model is suitable for assessing kitchen emissions, and the urinary OH-PAHs concentrations can be taken as the model outlay.