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Currently, there is limited knowledge regarding occupational exposure of traditional and emerging organophosphate esters (OPEs) from e-waste and automobile dismantling activities, and their distribution within the human blood. In the present study, we collected dust and urine samples from e-waste (ED) (n = 91 and 130, respectively) and automobile dismantling (AD) plants (n = 93 and 94, respectively), as well as serum-plasma-whole blood samples (sets from 128 participants) within ED areas for analyzing traditional and emerging organophosphate tri-esters (tri-OPEs) and organophosphate di-esters (di-OPEs). Median concentration of ∑tri-OPEs and ∑di-OPEs in dust (37,400 and 9,000 ng/g in ED, and 27,000 and 14,700 ng/g in AD areas, respectively) and urine samples (11.8 and 21.9 ng/mL in ED areas, and 17.2 and 15.0 ng/mL in AD areas, respectively) indicated that both e-waste and automobile dismantling activities served as important pollution source for OPEs. Dust ingestion has been evidenced to be the main exposure pathway compared to dermal absorption and inhalation. The median concentration (ng/mL) of OPEs in blood matrices descended order as follow: whole blood (13.1) > serum (11.6) > plasma (10.4) for ∑tri-OPEs, and plasma (3.51) > serum (0.36) > whole blood (0.23) for ∑di-OPEs. Concentration ratios of OPEs varied across blood matrices, depending on the compounds, suggesting that the essentiality of appropriate biomonitoring matrix for conducting comprehensive exposure assessments.

Acute myeloid leukemia (AML), a highly heterogeneous myeloid malignancy, remains a challenge in terms of proper risk stratification. In this study, we developed a novel pyroptosis prognostic model based on pyroptosis-related gene pairs, which exhibited excellent prognostic performance across multiple cohorts (N = 1506) and accurately predicted both adult and pediatric AML prognosis. Additionally, we integrated the pyroptosis risk model with other clinical risk factors to construct a highly operational nomogram. Moreover, our findings indicate a significant correlation between elevated pyroptosis risk scores and increased stemness of AML. Using CIBERSORT immune analysis, we found a decreased proportion of resting NK cells and activated mast cells in the high-risk group. Through analyzing the correlation between chemotherapy drug response sensitivity and risk scores, we found that AZD1332 and BPD-0008900 were extremely sensitive in the high-risk group.

Automotive interiors have been identified as significant sources of various chemicals, yet their occupational hazards for end-of-life vehicle (ELV) dismantlers remain poorly characterized. Herein, eight classes of plasticizers, including 11 phthalates esters (PAEs) and 16 non-phthalates esters (NPAEs), were detected in dust samples from inside and outside ELV dismantling workshops. Moreover, indoor dust from ordinary households and university dormitories was compared. The indoor dust from the ELV dismantling workshops contained the highest concentrations of plasticizers (median: 594 μg/g), followed by ordinary households (296 µg/g), university dormitories (186 µg/g), and outdoor dust (157 µg/g). PAEs remained the dominant plasticizers, averaging 11.7-fold higher than their NPAE alternatives. Specifically, diisononyl phthalate and trioctyl trimellitate were notably elevated in workshop dust, being 15.5 and 4.78 times higher, respectively, than in ordinary household dust, potentially indicating their association with ELV dismantling activities. The estimated daily intake of occupational ELV dismantling workers was up to five times higher than that of the general population. Moreover, certain dominant NPAEs demonstrated nuclear receptor interference abilities comparable to typical PAEs, suggesting potential toxic effects. This study is the first to demonstrate that ELV dismantling activities contribute to the co-emission of PAEs and NPAEs, posing a substantial risk of exposure to workers, which warrants further investigation.

Recently, evidence of aromatic amine antioxidants (AAs) existence in the dust of the electronic waste (e-waste) dismantling area has been exposed. However, there are limited studies investigating occupational exposure and toxicity associated with AAs and their transformation products (p-phenylenediamines-quinones, i.e., PPD-Qs). In this study, 115 dust and 42 hand wipe samples collected from an e-waste recycling industrial park in central China were analyzed for 19 AAs and 6 PPD-Qs. Notably, the median concentration of ∑6PPD-Qs (1,110 ng/g and 1,970 ng/m2) was significantly higher (p

5-methylcytosine modifications play a significant role in carcinogenesis; however, studies exploring 5-methylcytosine-related genes in diffuse large B-cell lymphoma patients are lacking. In this study, we aimed to understand the potential role and clinical prognostic impact of 5-methylcytosine regulators in diffuse large B-cell lymphoma and identify a prognostic biomarker based on 5-methylcytosine-associated genes. Gene expression profiles and corresponding clinical information of diffuse large B-cell lymphoma patients and normal controls were obtained from The Cancer Genome Atlas, Gene Expression Omnibus, and Genotype-Tissue Expression databases. Diffuse large B-cell lymphoma was divided into three clusters according to the 5-methylcytosine regulators, and differentially expressed genes were screened among the three clusters. Univariate Cox and Lasso-Cox regression analyses were used to screen prognostic genes and construct a prognostic risk model. Kaplan-Meier curve analysis, univariate and multivariate Cox regression analyses, and time-dependent receiver operator characteristic curve analysis were used to evaluate prognostic factors. GSVA was used to enrich potential pathways associated with 5-methylcytosine modification patterns. SsGSEA and CIBERSORT were used to assess immune cell infiltration. Six 5-methylcytosine-related genes (TUBB4A, CD3E, ZNF681, HAP1, IL22RA2, and POSTN) were used to construct a prognostic risk model, which was proved to have a good predictive effect. In addition, univariate and multivariate Cox regression risk scores were independent prognostic factors for diffuse large B-cell lymphoma. Further analysis showed that the 5-methylcytosine risk score was significantly correlated with immune cell infiltration and immune checkpoint of diffuse large B-cell lymphoma. Our study reveals for the first time a potential role for 5-methylcytosine modifications in diffuse large B-cell lymphoma, provides novel insights for future studies on diffuse large B-cell lymphoma, and offers potential prognostic biomarkers and therapeutic targets for patients with diffuse large B-cell lymphoma.

Bisphenol A and its structural analogues (BPs) are widely used chemicals in electronics devices. To get insight into the occupational exposure to the full-time employees compared with the residents, urinary BPs in workers dismantling e-waste and in nearby residents were compared. Only 4 BPs among the tested 8 congeners, bisphenol AF (BPAF), bisphenol A, bisphenol S (BPS), and bisphenol F (BPF), were extensively detected with the detection frequencies of 100%, 99%, 98.7%, 51.3%. The median concentration of bisphenol A was 8.48 ng/mL, followed by BPAF (1.05 ng/mL), BPS (0.115 ng/mL), and BPF (0.110 ng/mL). The 4 detected BPs had a median concentration (Σ4BPs) ranging from 0.950 to 64.5 ng/mL in all volunteers, with a median value of 10.2 ng/mL. Result indicated the median concentration of ∑4BPs in worker’s urine was significantly higher (14.2 ng/mL) than those in residents in nearby towns (4.52 ng/mL and 5.37 ng/mL) (p

Melamine (MEL) and its derivatives are increasingly applied as nitrogenous flame retardants in consumer products. Nevertheless, limited information is available on their environmental occurrence and subsequent human exposure via multiple exposure pathways. In this study, we analysed MEL and its derivatives in dust (indication of the dust ingestion route) and hand wipe samples (indication of the hand-to-mouth route) collected in various microenvironments. The levels of ∑MELs in both dust (median: 24,100 ng/g) and participant hand samples (803 ng/m2) collected in e-waste dismantling workshops were significantly higher than those in samples collected in homes (15,600 ng/g and 196 ng/m2, respectively), dormitories (13,100 ng/g and 227 ng/m2, respectively) and hotel rooms (11,800 ng/g and 154 ng/m2, respectively). Generally, MEL dominated in dust samples collected in e-waste dismantling workshops, whereas cyanuric acid dominated in hand wipe samples. This may occur partly because the latter is an ingredient in disinfection products, which are more frequently employed in daily lives during the COVID-19 pandemic. Exposure assessment suggests that dust ingestion is an important exposure pathway among dismantling workers and the general population, whereas hand-to-mouth contact could not be overlooked in certain populations, such as children and dismantling workers not wear gloves at work.

Single-use or disposable facemasks have been widely used by the public for personal protection against the spread of COVID-19. The majority of disposable facemasks are made of synthetic polymers such as polypropylene, polyethylene terephthalate (as polyester), and polystyrene, and could therefore be a source of human exposure to plasticizers that are incorporated into these polymers during production. Little is known, however, about the occurrence of plasticizers in facemasks. In this study, we determined the concentrations of nine phthalate diesters and six non-phthalate plasticizers in 66 facemasks purchased in the United States. Among phthalate diesters, dibutyl phthalate, di(2-ethylhexyl)phthalate, di-iso-butyl phthalate, and butyl benzyl phthalate were found in all facemask samples, at median concentrations of 486, 397, 254, and 92 ng/g, respectively. Among non-phthalate plasticizers, dibutyl sebacate (median: 3390 ng/g) and di(2-ethylhexyl)adipate (352 ng/g) were found at notable concentrations. Inhalation exposure to select phthalate and non-phthalate plasticizers from the use of facemasks was estimated to range from 0.1 to 3.1 and 3.5 to 151 ng/kg-bw/d, respectively. To our knowledge, this is the first study to report the occurrence of phthalate and non-phthalate plasticizers in facemasks collected from the United States.

Air pollution is a serious global environmental problem, especially in developing countries. PM2.5 is a major air pollutant that poses critical risks in urban areas. In this study, we identified the influence of comprehensive urbanization on regional PM2.5 in the Yangtze River Delta (YRD), the largest metropolitan region in China, from 1998 to 2015. The impacts of four urbanization subsystems (Economic, Spatial, Demographic, and Social) on the spatiotemporal evolution of PM2.5 were investigated at the city level using a linear mixed effect model (LME). The annual average concentration of PM2.5 over the YRD increased during the study period, with rapid growth in the northern plains and slow growth in the mountainous south. The LME model showed good performance between the predicted and observed PM2.5, with an R2 value for 10-fold cross-validation reaching 0.87 and a regression coefficient of 0.88. Urban population, GDP ratio of secondary industry, built-up area, total road area, number of students in colleges and universities, and total retail sales of consumer goods all had positive associations with PM2.5 concentration, while the proportion of tertiary industry employment, GDP ratio of primary industry, forest area, and number of hospital beds all had negative associations. Economic had the strongest effect (44%) on PM2.5 early on (1998–2003), but over time the contribution of other subsystems gradually increased. The overall contributions of urbanization type to PM2.5 in the YRD were Spatial (33.10%) > Economic (26.76%) > Demographic (16.85%) > Social (12.72%). Our results help deepen the understanding of regional air pollution in China as well as its correlation with urbanization and its subsystems.

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental pollutants. Urinary concentrations of mono-hydroxylated metabolites of PAHs (OH-PAHs) have been used as biomarkers of these chemicals’ exposure in humans. Little is known, however, with regard to intra- and inter-individual variability in OH-PAH concentrations and their association with oxidative stress. We conducted a longitudinal study of measurement of urinary concentrations of 15 OH-PAHs and 7 oxidative stress biomarkers (OSBs) of DNA damage [8-hydroxy-2′-deoxyguanosine (8-OHdG)], lipid [malondialdehyde (MDA) and F2-isoprostanes (PGF2α)] and protein [o,o′-dityrosine (diY)] peroxidation in 19 individuals for 44 consecutive days. Metabolites of naphthalene (OHNap), fluorene (OHFlu), phenanthrene (OHPhe), and pyrene (OHPyr) were found in >70% of 515 urine samples analyzed, at sum concentrations (∑OH-PAH) measured in the range of 0.46–60 ng/mL. After adjusting for creatinine, OHNap and ∑OH-PAH concentrations exhibited moderate predictability, with intra-class correlation coefficients (ICCs) ranging from 0.359 to 0.760. However, ICC values were low (0.001–0.494) for OHFlu, OHPhe, and OHPyr, which suggested poor predictability for these PAH metabolites. Linear mixed-effects analysis revealed that an unit increase in ∑OH-PAH concentration corresponded to 4.5%, 5.3%, 20%, and 21% increase in respective urinary 8-OHdG, MDA, PGF2α, and diY concentrations, suggesting an association with oxidative damage to DNA, lipids, and proteins. The daily intakes of PAHs, calculated from urinary concentrations of OH-PAHs, were 10- to 100-fold below the current reference doses. This study provides valuable information to design sampling strategies in biomonitoring studies and in assigning exposure classifications of PAHs in epidemiologic studies.

Melamine is used extensively in household products, such as furniture, dinnerware, and food utensils. Several studies have shown that melamine adversely affects kidney function. Nevertheless, little is known about urinary melamine concentrations, and its temporal variability. In this study, 213 first-morning-void urine samples were collected from 19 volunteers for over a month to assess longitudinal variability in concentrations of melamine and its three structural analogues, i.e., cyanuric acid, ammeline, and ammelide. Target analytes were found in all urine samples at mean concentrations of 3.3, 16, 0.99, and 0.62 ng/mL, for melamine, cyanuric acid, ammelide, and ammeline, respectively. Cyanuric acid was the major compound found in all urine samples, accounting for 74–80% of the total concentrations, followed by melamine (12–20%), ammelide (4–6%), and ammeline (2–4%). Gender- and age-related differences in melamine concentrations were observed, although no such pattern was found for cyanuric acid. After adjusting for creatinine, melamine and cyanuric acid concentrations were moderately predictable with inter-day intraclass correlation coefficients (ICCs) in the range of 0.541–0.763. Nevertheless, substantial inter-individual variation in melamine levels existed even after creatinine adjustment, as evidenced by low ICCs (0.008–0.108). Cumulative daily intake of melamine and cyanuric acid was calculated on the basis of urinary concentrations and the mean values were found to be at least 10-fold below the current tolerable daily intake. Keywords: Melamine, Cyanuric acid, Human urine, Variability, Exposure assessment

Per- and polyfluoroalkyl substances (PFAS), polybrominated diphenyl ethers (PBDEs), and organophosphate esters (OPEs) are found in building materials and associated with thyroid disease, infertility, and impaired development. This study’s objectives were to (1) compare levels of PFAS, PBDEs, and OPEs in dust from spaces with conventional versus “healthier” furniture and carpet, and (2) identify other product sources of flame retardants in situ. We measured 15 PFAS, 8 PBDEs, and 19 OPEs in dust from offices, common areas, and classrooms having undergone either no intervention (conventional rooms in older buildings meeting strict fire codes; n = 12), full “healthier” materials interventions (rooms with “healthier” materials in buildings constructed more recently or gut-renovated; n = 7), or partial interventions (other rooms with at least “healthier” foam furniture but more potential building contamination; n = 28). We also scanned all materials for bromine and phosphorus as surrogates of PBDEs and OPEs respectively, using x-ray fluorescence. In multilevel regression models, rooms with full “healthier” materials interventions had 78% lower dust levels of PFAS than rooms with no intervention (p

Plant foliar uptake is an essential part of the overall biogeochemical cycling of semivolatile organic compounds. Chambers were therefore designed to expose wheat to polybrominated diphenyl ethers (PBDEs) via various combinations of exposure routes (i.e., soil, air and particle). Under the simulated scenarios, most of PBDEs in wheat leaves originated from foliar uptake (including gaseous and particle-bound depositions) rather than translocation from root uptake. Our results further revealed that higher brominated PBDEs (h-PBDEs; i.e. hepta- through deca-BDEs) were inclined to enter wheat leaves via particle-bound deposition while gaseous deposition could not be ignored for less-brominated PBDEs (l-PBDEs; i.e., tri- through hexa-BDEs). Sequential extraction of wheat leaf displayed that the transfer velocities of h-PBDEs were lagged behind l-PBDEs during their deposition to leaf cuticle and subsequent erosion to mesophyll, where a large fraction of the target chemicals were ultimately stored (29–93% of total PBDEs burden). Applying McLachlan’s framework to our data suggested that the uptake of PBDEs was controlled primarily by kinetically limited gaseous deposition for l-PBDEs and by particle-bound deposition for h-PBDEs. The combined use of exposure chamber measurement and framework provides a robust tool for interpreting the behaviors of PBDEs between the atmosphere and plant foliage.

Bisphenol A (BPA) and its alternatives are suspected endocrine disruptors. However, prenatal exposure and transplacental transfer of bisphenols (BPs is still limited. Therefore, BPA and its six alternatives in maternal serum (MS), maternal urine (MU), cord serum (CS), and amniotic fluid (AF) samples collected from 106 maternal-fetal pairs in an e-waste dismantling site in Southern China were determined. Bisphenol AF (BPAF) and bisphenol S (BPS) were the dominant BPA alternatives observed in MS and CS, and the geometric mean (GM) concentration of BPAF (0.013 ng/mL in MS, 0.097 ng/mL in CS) and BPS (0.01 ng/mL in MS, 0.03 ng/mL in CS) in MS and CS was lower than that of BPA (0.5 ng/mL in MS, 1.2 ng/mL in CS). The ratios of BPA concentrations between MU and MS (MU:MS ratio) were over three times higher than those of AF and CS (AF:CS ratio), thereby suggesting low biotransformation/metabolism of BPA in fetuses. The placental transfer rates of BPs (i.e., CS:MS ratio) were compound-specific (BPAF 3.26, BPA 1.94, BPS 1.11). Results suggest that BPA and its alternatives can pass through the placental barrier. The placental transfer rates of BPs are positively related to molecular weight or log Kow values. This finding indicates that an active transport is responsible for the placental transfer of BPs. Keywords: Bisphenol A, BPA alternatives, E-waste, Placental transfer

We determined the concentrations of melamine, ammeline, ammelide, and cyanuric acid in meat, fish and seafood, cereal products, beverages, cooking oil, and vegetables (n = 121) collected from Albany, New York, United States. In addition, food packaging (n = 24) and animal feed (n = 12) were analyzed to determine the sources of melamine and its derivatives in foods. Among the six categories of foods analyzed, median concentrations of ∑melamine (sum of melamine and its three derivatives) in meat (23.6 ng/g fresh weight; fw) and cereal products (20.9 ng/g fw) were significantly (p

Objectives: The impact of N7-methylguanosine (m7G) on tumor progression and the regulatory role of microRNAs (miRNAs) in immune function significantly influence breast cancer (BC) prognosis. Investigating the interplay between m7G modification and miRNAs provides novel insights for assessing prognostics and drug responses in BC. Materials and methods: RNA sequences (miRNA and mRNA profiles) and clinical data for BC were acquired from the Cancer Genome Atlas (TCGA) database. A miRNA signature associated with 15 m7G in this cohort was identified using Cox regression and LASSO. The risk score model was evaluated using Kaplan-Meier and time-dependent ROC analysis, categorizing patients into high-risk and low-risk groups. Functional enrichment analyses were conducted to explore potential pathways. The immune system, including scores, cell infiltration, function, and drug sensitivity, was examined and compared between high-risk and low-risk groups. A nomogram that combines risk scores and clinical factors was developed and validated. Single-sample gene set enrichment analysis (ssGSEA) was employed to explore m7G-related miRNA signatures and immune cell relationships in the tumor microenvironment. Additionally, drug susceptibility was compared between risk groups. Results: Fifteen m7G-related miRNAs were independently correlated with overall survival (OS) in BC patients. Time-dependent ROC analysis yielded area under the curve (AUC) values of 0.742, 0.726, and 0.712 for predicting 3-, 5-, and 10-year survival rates, respectively. The Kaplan-Meier analysis revealed a significant disparity in OS between the high-risk and low-risk groups (p = 1.3e-6). Multiple regression identified the risk score as a significant independent prognostic factor. An excellent calibration nomogram with a C-index of 0.785 (95 % CI: 0.728–0.843) was constructed. In immune analysis, low-risk patients exhibited heightened immune function and increased responsiveness to immunotherapy and chemotherapy compared to high-risk patients. Conclusion: This study systematically analyzed m7G-related miRNAs and revealed their regulatory mechanisms concerning the tumor microenvironment (TME), pathology, and the prognosis of BC patient. Based on these miRNAs, a prognostic model and nomogram were developed for BC patients, facilitating prognostic assessments. These findings can also assist in predicting treatment responses and guiding medication selection.

Background: Although some improvements in the management of pancreatic cancer (PC) have been made, no major breakthroughs in terms of biomarker discovery or effective treatment have emerged. Here, we applied artificial intelligence (AI)-based methods to develop a model to diagnose PC and predict survival outcome. Methods: Multiple bioinformatics methods, including Limma Package, were performed to identify differentially expressed genes (DEGs) in PC. A Back Propagation (BP) model was constructed, followed by Genetic Algorithm (GA) filtering and verification of its prognosis capacity in the TCGA cohort. Furthermore, we validated the protein expression of the selected DEGs in 92 clinical PC tissues using immunohistochemistry. Finally, intro studies were performed to assess the function of SLC6A14 and SPOCK1 on pancreatic ductal adenocarcinoma (PDAC) cells proliferation and apoptosis. Results: Four candidate genes (LCN2, SLC6A14, SPOCK1, and VCAN) were selected to establish a four-gene signature for PC. The gene signature was validated in the TCGA PC cohort, and found to show satisfactory discrimination and prognostic power. Areas under the curve (AUC) values of overall survival were both greater than 0.60 in the TCGA training cohort, test cohort, and the entire cohort. Kaplan-Meier analyses showed that high-risk group had a significantly shorter overall survival and disease-free survival than the low-risk group. Further, the elevated expression of SLC6A14 and SPOCK1 in PC tissues was validated in the TCGA + GETx datasets and 92 clinical PC tissues, and was significantly associated with poor survival in PC. In PDAC cell line, SLC6A14 or SPOCK1 knockdown inhibited cells proliferation, migration and promoted cells apoptosis. Conclusions: Using Limma Package and GA-ANN, we developed and validated a diagnostic and prognostic gene signature that yielded excellent predictive capacity for PC patients' survival. In vitro studies were further conducted to verify the functions of SLC6A14 and SPOCK1 in PC progression.