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Protein powder has attracted attention due to its possible adverse effects.

The relationships of exposures to volatile organic compounds (VOCs) with vitamin D and kidney function remain unclear. Our analyses included 6070 adults from 2003 to 2010 survey cycles of the National Health and Nutrition Examination Survey to explore associations of six VOCs with serum vitamin D, albumin-to-creatinine ratio (ACR), and estimated glomerular filtration rate (eGFR). The results suggested that dibromochloromethane was positively associated with ACR, and chloroform was inversely associated with ACR. U-shaped associations of toluene, m-/p-xylene, bromodichloromethane, and 1,4-dichlorobenzene with ACR were observed. Toluene, m-/p-xylene, and 1,4-dichlorobenzene were associated with eGFR in U-shaped manners, while bromodichloromethane and chloroform were inversely associated with eGFR. Elevation in 1,4-dichlorobenzene was associated with decrease in vitamin D, while chloroform and m-/p-xylene were in U-shaped associations with vitamin D. VOCs mixture was U-shaped associated with ACR, inversely associated with eGFR, and inversely associated with vitamin D. Vitamin D was in a U-shaped association with ACR. Vitamin D significantly interacted with VOCs on the two kidney parameters. In the US adult population, exposures to VOCs were associated with kidney function and serum vitamin D level decline, and the serum vitamin D may have interaction effects with VOCs exposures on kidney function.

Objective To investigate potential causal pathways and temporal relationships of glucose metabolism and diabetes with heart rate variability (HRV). Methods The cohort study was developed in 3858 Chinese adults. At baseline and 6 years follow-up, participants underwent HRV measurement (low frequency [LF], high frequency [HF], total power [TP], standard deviation of all normal-to-normal intervals [SDNN], and square root of the mean squared difference between adjacent normal-to-normal intervals [r-MSSD]) and determination of glucose homeostasis (fasting plasma glucose [FPG] and insulin [FPI], homeostatic model assessment for insulin resistance [HOMA-IR]). Cross-lagged panel analysis was used to examine the temporal relationships of glucose metabolism and diabetes with HRV. Results FPG, FPI, HOMA-IR, and diabetes were cross-sectionally negatively associated with HRV indices at baseline and follow-up (P Conclusions The findings provide strong evidence that elevated FPG and diabetes may be the causes rather than the consequences of HRV reduction over time.

Sustainable and efficient production of chiral amines was realized with an oriented co-immobilized dual-enzyme system via SiBP-tag.

Toxicological studies have reported propylene oxide (PO) exposure may harm the respiratory system, but the association between PO exposure and lung function and potential mechanism remain unclear.How are the association between PO exposure and lung function and potential mediating mechanism?Urinary PO metabolite (N-Acetyl-S-(2-hydroxypropyl)-L-cysteine, 2HPMA) as PO internal exposure biomarker and lung function were measured for 3692 community residents at baseline and repeated at 3-year follow-up. Cross-sectional and longitudinal associations between urinary 2HPMA and lung function were assessed by linear mixed model. Urinary 8-hydroxy-deoxyguanosine (8-OHdG), urinary 8-iso-prostaglandin-F2α (8-iso-PGF2α), and plasm protein carbonyls (PC) as biomarkers of oxidative DNA damage, lipid peroxidation, and protein carbonylation, respectively, were measured for all participants to explore their potential roles in 2HPMA-associated lung function decline by mediation analysis.After adjustment for potential covariates, each 3-fold increase in urinary 2HPMA was cross-sectionally associated with a 26.18 mL (95% confidence interval: -50.55, -1.81) and a 21.83 mL (-42.71, -0.95) decrease in forced vital capacity (FVC) and forced expiration volume in 1s (FEVPO exposure was associated with lung function decline among community residents, and oxidative DNA damage and protein carbonylation partially mediated PO exposure-associated lung function decline. Further attention on respiratory damage caused by PO exposure is warranted.

BackgroundThe impact of birth weight on lung function and risk of asthma remains contentious. Our aim was to investigate the specific association of birth weight with lung function and the risk of asthma in children.MethodsWe performed cross-sectional analyses of 3,295 children aged 6–15 years who participated in the 2007–2012 National Health and Nutrition Examination Survey (NHANES). After controlling for potential covariates other than gestational diabetes, maternal asthma and obesity, the linear and non-linear associations of birth weight with lung function metrics and the risk of asthma were evaluated by a generalized linear model and generalized additive model, respectively.ResultsWe observed a non-linear association of birth weight with FEV1 %predicted, FEV1/FVC %predicted and FEF25 − 75 %predicted (P for non-linearity was 0.0069, 0.0057, and 0.0027, respectively). Further threshold effect analysis of birth weight on lung function detected the turning point for birth weight was 3.6 kg. When the birth weight was < 3.6 kg, birth weight was significantly positively associated with all pulmonary function metrics. However, negative associations were found in FEV1 %predicted, FEV1/FVC %predicted and FEF25 − 75 %predicted when the birth weight was ≥3.6 kg. These results were consistent in the stratified and sensitivity analyses. Additionally, a possible non-linear relationship was also detected between birth weight and the risk of asthma.ConclusionAlthough not all maternal factors were accounted for, our findings provided new insight into the association of birth weight with lung function. Future studies are warranted to confirm the present findings and understand the clinical significance.

1-bromopropane is a US Environmental Protection Agency-identified significant hazardous air pollutant with concerned adverse respiratory effect. We aimed to investigate the relationship between 1-bromopropane exposure and pulmonary function and the underlying role of oxidative damage, which all remain unknown. Pulmonary function and urinary biomarkers of 1-bromopropane exposure (N-Acetyl-S-(n-propyl)-L-cysteine, BPMA) and oxidative damage to DNA (8-hydroxy-deoxyguanosine, 8-OHdG) and lipid (8-iso-prostaglandin-F2α, 8-iso-PGF2α) were measured for 3259 Chinese urban adults from the Wuhan-Zhuhai cohort. The cross-sectional relationship of BPMA with pulmonary function and the joint relationship of BPMA and 8-OHdG or 8-iso-PGF2α with pulmonary function were investigated by linear mixed models. The mediating roles of 8-OHdG and 8-iso-PGF2α were evaluated by mediation analysis. Additionally, a panel of 138 subjects was randomly convened from the same cohort to evaluate the stability of BPMA repeatedly measured in urine samples collected over consecutive three days and intervals of one, two, and three years, and to estimate the longitudinal relationship of BPMA with pulmonary function change in three years. We found each 3-fold increase in BPMA was cross-sectionally related to FVC and FEV

High fasting plasma glucose (HFPG) is an independent risk factor for several adverse health outcomes and has become a serious public health problem. We aimed to evaluate the spatial pattern and temporal trend of disease burden attributed to HFPG from 1990 to 2019 using data from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019.Using data from GBD 2019, we estimated the numbers and age-standardized rates of deaths and disability-adjusted life years (DALYs) attributed to HFPG by calendar year, age, gender, country, region, Socio-demographic Index (SDI), and specific causes. The joinpoint regression analysis was used to assess the temporal trends of deaths and DALYs from 1990 to 2019.In 2019, globally, the numbers of deaths and DALYs attributable to HFPG were approximately 6.50 million and 172.07 million, respectively, with age-standardized rates of 83.00 per 100,000 people and 2104.26 per 100,000 people, respectively. From 1990 to 2019, the global numbers of deaths and DALYs attributed to HFPG have over doubled. The age-standardized rate of DALYs showed an increasing trend, particularly in males and in regions with middle SDI or below. The leading causes of the global disease burden attributable to HFPG in 2019 were diabetes mellitus, ischaemic heart disease, stroke, and chronic kidney disease.HFPG is an important contributor to increasing the global and regional disease burden. Necessary measures should be taken to curb the growing burden attributed to HFPG, particularly in males and in regions with middle SDI or below.

The adverse health effects of pyrethroids exposure have attracted wide concern. We aimed to assess the associations of bifenthrin, a widely used pyrethroid, with glucose homeostasis and risk of type 2 diabetes mellitus (T2DM) and to explore the underlying mechanism. Serum bifenthrin, fasting plasma glucose (FPG), fasting plasma insulin (FPI), and plasma protein carbonyl (PCO) were determined among 3822 participants from the Wuhan-Zhuhai cohort. Glucose homeostasis was evaluated by FPG, FPI, homeostasis model assessment of insulin resistance (HOMA-IR), impaired fasting glucose (IFG), and abnormal glucose regulation (AGR). The associations of serum bifenthrin with glucose homeostasis and risk of T2DM were assessed by generalized linear models and logistic regression models. The role of PCO in the above associations was evaluated by mediation analyses. After adjusting for covariates, each 2-fold increase in serum bifenthrin was associated with a 0.21 mmol/L increase in FPG and a 5.19%, 10.49%, and 12.18% increase in FPI, HOMA-IR, and PCO levels, respectively. Monotonically elevated ORs of IFG and AGR (all P and P for trend0.05), but not T2DM (P 0.05) were detected to be associated with increased bifenthrin. Compared with the participants with low bifenthrin and low PCO, participants with high bifenthrin exposure and high PCO showed a 0.40 mmol/L, 11.07%, and 22.50% increase in FPG, FPI, and HOMA-IR, as well as a 119.97% and 48.88% increase in risks of IFG and AGR, respectively (P for trend0.05). Moreover, PCO mediated 13.61%-24.98% of the serum bifenthrin-associated glucose dyshomeostasis. The study suggested that bifenthrin exposure was dose-dependently associated with glucose dyshomeostasis in the general Chinese urban adults, and these associations were exacerbated and partly mediated by PCO. Given that other pollutants were not included in this study, the effect of co-exposure of pyrethroids with multiple pollutants is necessary to be considered in future studies.

Oriented immobilization of antibodies is important for the effective recognition of target antigens. In this paper, a heptapeptide ligand, HWRGWVC (HC7), was modified onto non-porous monosized poly(glyceryl methacrylate) (pGMA) microspheres (named pGMA-HC7) to explore the antibody immobilization behaviors. Characterization of the microspheres by particle size analyzer, scanning electron microscopy, Fourier transform infrared spectroscopy, and reversed-phase chromatography proved the success of each fabrication step. The capacity and activity of antibody immobilization through HC7 were studied using immunoglobulin G (IgG) as a model antibody and horseradish peroxidase (HRP) as a model antigen. Additionally, IgG immobilizations on pGMA microspheres by nonspecific adsorption and covalent coupling through carbodiimide chemistry were conducted for comparison. pGMA-HC7 exhibited an IgG adsorption capacity of 3-4 mg/g in 10 min by the specific binding of HC7 without nonspecific interactions. Notably, the ligand HC7 showed a by two orders of magnitude stronger affinity for IgG than its original hexapeptide ligand HWRGWV. Moreover, the capacity and activity of the immobilized anti-HRP antibody on pGMA-HC7 were 1.6-fold and 3-fold higher than those of the covalent coupling, respectively. The results proved the superior role of HWRGWVC in the affinity binding of antibody and the potential of pGMA-HC7-25 in immunoassay and immunodiagnostic applications.

The link between zinc exposure and glucose metabolism or the development of type 2 diabetes (T2D) is controversial, and underlying mechanisms are unclear. This study aimed to explore the associations of zinc exposure with glucose-insulin homeostasis traits and the long-term effects of zinc on the development of T2D, and further to estimate the potential roles of inflammation and oxidative damage in such relationships. We investigated 3890 urban adults from the Wuhan-Zhuhai cohort, and followed up every three years. Mixed linear model was applied to estimate dose-response associations between urinary zinc and glycemia traits [fasting plasma insulin (FPI), fasting plasma glucose (FPG), insulin resistance (homeostasis model assessment of insulin resistance, HOMA-IR), and β-cell dysfunction (homeostasis model assessment of β-cell function, HOMA-B)], as well as zinc and biomarkers for systemic inflammation (C-reactive protein) and oxidative damage (8-isoprostane and 8-hydroxy-2'-deoxyguanosine). Logistic regression model and Cox regression model were conducted to evaluate the relationships between urinary zinc and prevalence and incidence of T2D, respectively. We further performed mediation analysis to assess the roles of inflammation and oxidative damage biomarkers in above associations. At baseline, we observed significant dose-response relationships of elevated urinary zinc with increased FPI, FPG, HOMA-IR, and T2D prevalence and decreased HOMA-B, and such associations could be strengthened by increased C-reactive protein, 8-isoprostane, and 8-hydroxy-2'-deoxyguanosine. Elevated C-reactive protein significantly mediated 9.09% and 17.67% of the zinc-related FPG and HOMA-IR increments, respectively. In longitudinal analysis, a significantly positive association between urinary zinc and T2D incidence was observed among subjects with persistent high urinary zinc levels when compared with those with persistent low zinc levels. Our results suggested that high levels of zinc exposure adversely affected on glucose-insulin homeostasis and further contributed to increased risk of T2D cross-sectionally and longitudinally. Moreover, inflammatory response might play an important role in zinc-related glucose metabolic disorder.

Alveolar macrophage (AM) injury and inflammatory response are key processes in pathological damage caused by silica. However, the role of triiodothyronine (T3) in silica-induced AM oxidative stress, inflammation, and mitochondrial apoptosis remained unknown. To investigate the possible effects and underlying mechanism of T3 in silica-induced macrophage damage, differentiated human acute monocytic leukemia cells (THP-1) were exposed to different silica concentrations (0, 50, 100, 200, and 400 μg/mL) for 24 h. Additionally, silica-activated THP-1 macrophages were treated with gradient-dose T3 (0, 5, 10, 20, and 40 nM) for 24 h. To illuminate the potential mechanism, we used short hairpin RNA to knock down the thyroid hormone receptor α (TRα) in the differentiated THP-1 macrophages. The results showed that T3 decreased lactate dehydrogenase and reactive oxygen species levels, while increasing cell viability and superoxide dismutase in silica-induced THP-1 macrophages. In addition, silica increased the expression of interleukin 1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor-α (TNF-α), and T3 treatment reduced those pro-inflammatory cytokines secretion. Compared with silica-alone treated groups, cells treated with silica and T3 restored the mitochondrial membrane potential loss and had reduced levels of cytochrome c and cleaved caspase-3 expressions. Lastly, we observed that TRα-knockdown inhibited the protective effects of T3 silica-induced THP-1 macrophages. Together, these findings revealed that T3 could serve as a potential therapeutic target for protection against silica-induced oxidative stress, inflammatory response, and mitochondrial apoptosis, which are mediated by the activation of the T3/TRα signal pathway.

In our previous work, a series of polyethylenimine (PEI)-derived cation exchangers were synthesized using PEI-grafted resin FF-PEI-L740 (ionic capacity, 740 mmol·L−1) as the basic resin to study lysozyme adsorption and chromatographic behavior. It was found that the resin with an ionic capacity of 630 mmol·L−1 (FF-PEI-CR630) possessed high adsorption performance towards lysozyme at 0–100 mmol·L−1 NaCl. Therefore, in this work, FF-PEI-CR630 was selected to study the influences of pH and ionic strength (IS) on protein adsorption and chromatographic behavior towards lysozyme. The increase of lysozyme adsorption capacity in the pH range of 6 to 10 was observed. However, the uptake rate decreased in the pH range of 6 to 8 and then remained essentially unchanged from pH 8 to pH 10. Increasing IS led to decreased protein adsorption capacity and increased uptake rate in different pH ranges. Besides, FF-PEI-CR630 maintained dynamic binding capacity as high as over 150 mg·ml−1 at pH 8–10 without NaCl. The research has thus provided insight into the selection of proper pH and IS conditions for protein purification by using FF-PEI-CR630.

Styrene and ethylbenzene (S/EB) are the monomers of polystyrene (PS) and polyethylene (PE), respectively, and have been identified as significant hazardous air pollutants by the U.S. Environmental Protection Agency. However, the adverse effects of S/EB on human health, especially cardiovascular health, have not been well established. Urinary biomarker of S/EB exposure and heart rate variability (HRV) were measured in urban adults from the Wuhan-Zhuhai cohort and were repeated after 3-year and 6-year follow-ups. Linear mixed models were used to estimate associations of S/EB exposure biomarker with HRV and longitudinal additional annual change of HRV. The mediating role of transforming growth factor (TGF)-β1 was tested by using mediation analysis. A total of 2842 general adults were included at baseline analysis, and 4748 observations were included in the repeated measurement study. In the cross-sectional analysis, each 1% increment in urinary S/EB exposure biomarker was significantly associated with a 0.106 % (95 % CI: -0.160, -0.052), 0.109 % (-0.169, -0.049), 0.099 % (-0.145, -0.053), 0.040 % (-0.060, -0.020), and 0.031 % (-0.054, -0.007) decrement in low frequency (LF), high frequency (HF), total power (TP), standard deviation of all normal-to-normal intervals (SDNN), and square root of the mean squared difference between adjacent normal-to-normal interval, respectively. Smoking status modified the relationships of urinary S/EB exposure biomarker with TP and SDNN. TGF-β1 mediated 3.09-5.16 % of the association between urinary S/EB biomarker and lower HRV. The follow-up analyses detected a negative association between urinary S/EB exposure biomarker and the additional annual change of LF (β: -0.016; 95 % CI: -0.028, -0.004), HF (-0.014; -0.026, -0.001), and TP (-0.011; -0.021, -0.001). Our findings demonstrated that S/EB exposure was associated with HRV reduction among the general urban adults and the TGF-β pathway may play a part of the mediating role in this association.

Environmental risk factors have been implicated in adverse health effects. Previous epidemiological studies on environmental risk factors mainly analyzed the impact of single pollutant exposure on health, while in fact, humans are constantly exposed to a complex mixture consisted of multiple pollutants/chemicals. In recent years, environmental epidemiologists have sought to assess adverse health effects of exposure to multi-pollutant mixtures based on the diversity of real-world environmental pollutants. However, the statistical challenges are considerable, for instance, multicollinearity and interaction among components of the mixture complicate the statistical analysis. There is currently no consensus on appropriate statistical methods. Here we summarized the practical statistical methods used in environmental epidemiology to estimate health effects of exposure to multi-pollutant mixture, such as Bayesian kernel machine regression (BKMR), weighted quantile sum (WQS) regressions, shrinkage methods (least absolute shrinkage and selection operator, elastic network model, adaptive elastic-net model, and principal component analysis), environment-wide association study (EWAS), etc. We sought to review these statistical methods and determine the application conditions, strengths, weaknesses, and result interpretability of each method, providing crucial insight and assistance for addressing epidemiological statistical issues regarding health effects from multi-pollutant mixture.

The factors that lead to coronavirus disease 2019 (COVID-19) vaccine hesitancy among health-care workers (HCWs) are unclear. We aimed to identify the factors that influence HCWs’ hesitancy, especially the influence of their social network. Using an online platform, we surveyed HCWs in Chongqing, China, in January 2021 to understand the factors that influence the COVID-19 vaccine hesitancy among HCWs. Proportional allocation stratified sampling method was used to recruit respondents. Multivariable logistic regression and social network analysis (SNA) were used to analyze the influence factors. A total of 5247 HCWs were included and 23.3% of them were vaccine-hesitant. Participants were more hesitant if they had chronic diseases (OR = 1.411, 95% CI: 1.146–1.738), worked in tertiary hospitals (OR = 1.546, 95% CI: 1.231–1.942), and reported a history of vaccine hesitancy (OR = 1.637, 95% CI: 1.395–1.920) and refusal toward other vaccines (OR = 2.433, 95% CI: 2.067–2.863). The participants with a social network to communicate COVID-19 immunization were less hesitant (OR = 0.850, 95% CI: 0.728–0.993). Several influential members with social networks were found in SNA. Most of these influential members in the networks were department leaders who were willing to get COVID-19 vaccines (P

Laccases are multicopper oxidases of significant importance for the degradation of phenolic pollutants. Because of the inherent defects of natural laccases in practical applications, herein, we discovered highly effective and non-cytotoxic laccase-like metallo-nanofibers based on the supramolecular assembly of single unnatural amino acid, benzophenone-alanine (BpA), in combination with copper ions. Structural analysis revealed that the catalytic BpA-Cu nanofibers possess a Cu(I)-Cu(II) electron transfer system similar to that in natural laccase. Our BpA-Cu nanofibers exhibit 4 times higher substrate affinity and 24% higher catalytic efficiency than the well-known high-performance industrialized laccase (Novozym 51003) in 2,4-dichlorophenol degradation. In addition, the BpA-Cu nanofibers were demonstrated to be stable (gt;75% residual activity) in long-term storage at a wide range of pH, ionic strength, temperature, ethanol, and water sample, and to be readily recovered for pollutant degradation, keeping 83% of the laccase activity after 10 catalytic recycles. Remarkably, the nanofibers displayed a wide substrate spectrum, detecting and degrading a variety of phenolic pollutants with high activity than other laccase mimics reported in the literature. Furthermore, the biocompatibility of the material was proved with cultured cells. These findings demonstrated the potential of BpA-Cu nanofibers in mimicking laccases for environmental remediation.

The effect of caffeine exposure on children's health remains poorly understood. We aimed to characterize the associations of caffeine and caffeine metabolites with adiposity outcomes among children and adolescents. We performed cross-sectional analyses of 1,447 children and adolescents aged 6-19 years from the 2009-2014 National Health and Nutrition Examination Survey. The linear regression and weighted quantile sum (WQS) regression were used to explore the associations of urinary caffeine and 14 caffeine metabolites with adiposity outcomes, including body mass index (BMI) z-score, waist circumference (WC), obesity, and overweight. In linear regression models, compared with the participants who consumed low caffeine, higher BMI z-score, WC, and risks of obesity and overweight were more likely among those who consumed high caffeine (P 0.05). In WQS regression models, an interquartile range increase in the weighted caffeine index was significantly associated with increased BMI z-score (β = 0.10, 95% CI = 0.01, 0.17) and WC (β = 1.20, 95% CI = 0.31, 2.09), and risks of obesity (OR = 1.09, 95% CI = 1.02, 1.17). Totally, no modification effect of age or gender was observed in the linear regression model. Nonetheless, in WQS models, the positive associations of caffeine exposure with WC and risks of obesity and overweight were significant in children aged 6-11 years rather than 12-19 years. When stratified by gender, caffeine exposure was significantly associated with BMI z-score and WC in both boys and girls. These results add novel evidence that caffeine exposure might be associated with adverse adiposity outcomes among children and adolescents.

This study aimed to investigate the diagnostic value of MRI in serous borderline ovarian tumor (SBOT), and to determine the MRI features of SBOT and their correlations with clinicopathological characteristics.A total of 121 patients suspected of SBOT by preoperative MRI and then underwent surgery at our hospital were retrospectively reviewed. The accuracy of MRI in diagnosing SBOT was assessed. MRI features of the SBOT subtypes were compared and their correlations with clinicopathological characteristics were evaluated.SBOT was confirmed by postoperative pathology in 95 patients, including 77 patients with conventional SBOT (SBOT-C) and 18 patients with micropapillary SBOT (SBOT-MP). The accuracy of MRI in diagnosing SBOT was 87.6%. Three MRI morphological patterns of SBOT were identified: (i) mainly solid, (ii) mainly cystic, and (iii) mixed. Branching papillary architecture and internal branching (PAIB) structures corresponding to multiple branching papillary projections and internal fibrous stalks in tumors were observed in 69.7% of SBOTs on T2-weighted images. MRI findings were consistent with postoperative pathology. Compared with SBOT-C, patients with SBOT-MP were more likely to display elevated cancer antigen 125, bilateral tumors, peritoneal implantation, lymph node metastasis, and advanced tumor staging. No significant differences were observed in MRI features between SBOT-C and SBOT-MP groups.MRI has good performance in diagnosing SBOT. MRI findings of SBOT are consistent with clinicopathological characteristics. The PAIB structure is the characteristic MRI finding of SBOT. Compared to SBOT-C, SBOT-MP tends to display more aggressive clinical behavior, but their MRI features are similar.

The topic of cardiovascular hazards from multiple metal (loid)s exposures has attracted widespread attention. Here, we measured concentrations of twenty-three urinary metal (loid)s and mean platelet volume (MPV), an early cardiovascular damage biomarker, for 3396 Chinese adults. We aimed to comprehensively assess the associations of single metal (loid) and multiple metal (loid)s (as a mixture) with MPV by combined use of five statistical methods, including general linear models, Bayesian kernel machine regression (BKMR), weight quartile sum (WQS) regression, quantile g-computation (QGC), and adaptive elastic network regression (AENR). And based on that, we hope to provide insight into assessing the health effect of multipollutant exposure. After adjustment for potential covariates, at least three methods jointly suggested that of twenty-three metal (loid)s, iron, arsenic, and antimony were positively while aluminum, tungsten, and thallium were inversely associated with MPV. The environmental risk score of metal (loid)s construed by AENR was significantly positively associated with MPV, while the association between overall twenty-three metal (loid)s mixture and MPV was neutralized to be insignificant in QGC and BKMR. Conclusively, single metal (loid) may be inversely (iron, arsenic, and antimony) and positively (aluminum, tungsten, and thallium) associated with early cardiovascular damage, while the association of overall twenty-three metal (loid)s mixture with MPV was insignificant when concurrent exposures exist. It is crucial to select appropriate statistical methods based on study purpose and principles/characteristics of statistical methods, and combined employment of multimethod is insightfully suggested when assessing health effects of multipollutant exposure.

One of the main challenges of transmucosal drug delivery is that of enabling particles and molecules to move across the mucosal barrier of the mucosal epithelial surface. Inspired by nanovehicles and mucus-penetrating nanoparticles, a magnetically driven, mucus-inert Janus-type nanovehicle (Janus-MMSN-pCB) was fabricated by coating the zwitterionic polymer poly(carboxybetaine methacrylate) (pCB) on the mesoporous silica nanorod, which was grown on one side of superparamagnetic Fe3O4 nanoparticle using the sol–gel method. X-ray diffraction, transmission electron microscopy, vibrating sample magnetometry, and Fourier infrared spectroscopy were used to characterize the structure and morphology of the nanovehicles, proving the success of each synthesis step. The in vitro cell viability assessment of these composites using Calu-3 cell lines indicates that the nanovehicles are biocompatible in nature. Furthermore, the multiparticle tracking, Transwell® system, and cell imaging experimental results demonstrate that both the modification of pCB and the application of a magnetic field effectively accelerated the diffusion of the nanovehicles in the mucus and improved the endocytosis through Calu-3. The favorable cell uptake performance of Janus-MMSN-pCB in mucus systems with/without magnetic driving proves its potential role in the diagnosis, treatment, and imaging of mucosal-related diseases.

Acrolein is a significant high priority hazardous air pollutant with pulmonary toxicity and the leading cause of most noncancer adverse respiratory effects among air toxics that draws great attention. Whether and how acrolein exposure impacts pulmonary function remain inconclusive.To assess the association of acrolein exposure with pulmonary function and the underlying roles of oxidative DNA damage, inflammation, and pulmonary epithelium integrity.Among 3,279 Chinese adults from the Wuhan-Zhuhai cohort, associations of urinary acrolein metabolites (N-Acetyl-S-(2-carboxyethyl)-L-cysteine, CEMA; N-Acetyl-S-(3-hydroxypropyl)-L-cysteine, 3HPMA) as credible biomarkers of acrolein exposure with pulmonary function were analyzed by linear mixed models. Joint effects of biomarkers of oxidative DNA damage (8-hydroxy-deoxyguanosine), inflammation (C-reactive protein, CRP), and pulmonary epithelium integrity (Club cell secretory protein, CC16) with acrolein metabolites on pulmonary function and the mediating roles of these biomarkers were assessed. Besides, a subgroup (N = 138) was randomly recruited from the cohort to assess the stabilities of acrolein metabolites and their longitudinal associations with pulmonary function change in three years.Significant inverse dose-response relationships between acrolein metabolites and pulmonary function were found. Each 10-fold increment in CEMA, 3HPMA, or ΣUACLM (CEMA + 3HPMA) was cross-sectionally related to a 68.56-, 40.98-, or 46.02-ml reduction in FVC and a 61.54-, 43.10-, or 50.14-ml reduction in FEVAcrolein exposure of general adults was cross-sectionally and longitudinally related to pulmonary function decline, which was aggravated and/or partly mediated by oxidative DNA damage, inflammation, and pulmonary epithelium injury.

Polychlorinated biphenyls (PCBs) exposure has been related to the abnormal glucose metabolism and the risk of diabetes. However, the joint effects of various PCBs are uncertain and the potential mechanisms remain unclear. Our objectives were to evaluate the associations of serum PCBs with fasting plasma glucose (FPG) and the risk of diabetes among a general Chinese population, and to estimate the mediating effects of oxidative stress in the above associations. Serum levels of seven indicator-PCBs (PCB-28, 52, 101, 118, 138, 153, and 180) and FPG values were determined among 4498 subjects from the Wuhan-Zhuhai cohort. Oxidative DNA damage biomarker (urinary 8-hydroxy-2'-deoxyguanosine, 8-OHdG) and lipid peroxidation biomarker (urinary 8-isoprostane, 8-iso-PGF

Few study has revealed spatial transmission characteristics of COVID-19 in Wuhan, China. We aimed to analyze the spatiotemporal spread of COVID-19 in Wuhan and its influence factors. Information of 32,682 COVID-19 cases reported through March 18 were extracted from the national infectious disease surveillance system. Geographic information system methods were applied to analysis transmission of COVID-19 and its influence factors in different periods. We found decrease in effective reproduction number (Rt) and COVID-19 related indicators through taking a series of effective public health measures including restricting traffic, centralized quarantine and strict stay-at home policy. The distribution of COVID-19 cases number in Wuhan showed obvious global aggregation and local aggregation. In addition, the analysis at streets-level suggested population density and the number of hospitals were associated with COVID-19 cases number. The epidemic situation showed obvious global and local spatial aggregations. High population density with larger number of hospitals may account for the aggregations. The epidemic in Wuhan was under control in a short time after strong quarantine measures and restrictions on movement of residents were implanted.

Microplastics (MPs) are currently a global environmental pollutants and health hazards that caused by MPs cannot be ignored. However, studies on MP toxicity in mammals are scare. Here, we investigated the effects of two doses (0.1 mg and 0.5 mg) of 5 µm polystyrene microplastic (PS-MP) particles on the hematological system of mice through traditional toxicology experiments and assessed the related potential biological mechanisms using transcriptome sequencing analysis. The toxicological examinations showed that the 0.5 mg dose significantly decreased white blood cell count, increased Pit count, and inhibited the growth of colony-forming unit CFU-G, CFU-M and CFU-GM. Compared with the control group, there were 41 differentially expressed genes (DEGs) in the 0.1 mg-treated group and 32 significantly changed genes in 0.5 mg-treated group. Of note, eight genes were found to be significantly altered in both the PS-MP-treated groups. Gene ontology analysis showed that DEGs were mainly involved in T cell homeostasis, response to osmotic stress, extracellular matrix and structure organization, and metabolic process of NADP and nucleotides. In addition, pathway analysis revealed that the Jak/Stat pathway, pentose and glucuronate interconversions, nicotinate and nicotinamide metabolism, biosynthesis of unsaturated fatty acids, and the pentose phosphate pathway were involved in PS-MP-induced toxicity in mice. These results indicated that PS-MP exposure can cause hematotoxicity to some extent, impact gene expression, and disturb related molecular and biological pathways in mouse bone marrow cells. Our study provides fundamental data on the hematotoxicity of PS-MPs in terrestrial mammals that will help to further assess the corresponding health risks in these mammals.

Background: Lung function decline and miRNAs are known to involve in the pathogenesis process of respiratory diseases. However, the association between miRNA profiles and lung function decline was rarely elucidated. This study aimed to compare the expression pattern of plasma miRNAs among people with rapid lung function decline and healthy controls. Methods: Ten controls and 10 cases with rapid lung function decline in last 3 years were enrolled from the Wuhan-Zhuhai cohort. The miRNA sequencing and bioinformatics analysis were carried out to explore miRNAs expression and possible signal pathways. Pearson correlation analysis was carried out to assess the associations between lung function and miRNAs expression levels.Results: A total of 1209 detected miRNAs were differently expression in the reaseach participants. Among them, 17 miRNAs (miR-6749-5p, miR-6797-3p, miR-4468, miR-4301, miR-629-3p, miR-4713-3p, miR-486-3p, miR-450a-1-3p, miR-4732-5p, miR-514a-5p, miR-193b-5p, miR-6749-5p, miR-3168, miR-4691-5p, miR-6730-5p, miR-184, miR-486-5p) were significantly down-regulated in cases with reduced lung function. The expression levels of these miRNAs, except miR-514a-5p and miR-3168, were significantly correlated with lung function parameters. Through bioinformatics analysis, the Wnt signaling pathway, FoxO signaling pathway, MAPK signaling pathway, Pathway in cancer, inflammatory mediator regulation of TRP channels, and TGF-β signaling pathway maybe involved in mediating the association between 17 identified miRNAs and lung function decline.Conclusions: The plasma miRNA profile of people with rapid lung function decline are different when compared with healthy controls. These miRNAs might become research candidates or biomarkers in the early progression of respiratory diseases.

Benzene, a known occupational and environmental contaminant, has been recognized as the hematotoxin and human carcinogen. Lipids have a variety of important physiological functions and the abnormal lipid metabolism has been reported to be closely related to the occurrence and development of many diseases. In the present study, we aim to utilize LC–MS/MS lipidomic platform to identify novel biomarkers and provide scientific clues for mechanism study of benzene hematotoxicity. Results showed that a total of 294 differential metabolites were obtained from the comparison of benzene-treated group and control group. The glycerophospholipid pathway was altered involving the down-regulation of the levels of phosphatidylcholine and phosphatidylserine. In addition, phosphatidylethanolamine (PE) and 1-Acyl-sn-glycero-3-phosphocholine levels were increased in benzene-treated group. Based on the relationship between PE and autophagy, we then found that effective biomarker of autophagy, Beclin1 and LC3B, were increased remarkably. Furthermore, following benzene treatment, significant decreases in glucosylceramide (GlcCer) and phytosphingosine (PHS) levels in sphingolipid pathway were observed. Simultaneously, the levels of proliferation marker (PCNA and Ki67) and apoptosis regulator (Bax and Caspase-3) showed clear increases in benzene-exposed group. Based on our results, we speculate that disturbances in glycerophospholipid pathway play an important role in the process of benzene-induced hematopoietic toxicity by affecting autophagy, while sphingolipid pathway may also serve as a vital role in benzene-caused toxicity by regulating proliferation and apoptosis. Our study provides basic study information for the future biomarker and mechanism research underlying the development of benzene-induced blood toxicity.

Global incidence and temporal trends of asbestosis are rarely explored. Using the detailed information on asbestosis from the Global Burden of Disease (GBD) 2017, we described the age-standardised incidence rate (ASIR) and its average annual percentage change. A Joinpoint Regression model was applied to identify varying temporal trends over time. Although the use of asbestos has been completely banned in many countries, the ASIR of asbestosis increased globally from 1990 to 2017. Furthermore, the most pronounced increases in ASIR of asbestosis were detected in high-income North America and Australasia. These findings indicate that efforts to change the asbestos regulation policy are urgently needed.

Chinese biochemical engineering is committed to supporting the chemical and food industries, to advance science and technology frontiers, and to meet major demands of Chinese society and national economic development. This paper reviews the development of biochemical engineering, strategic deployment of these technologies by the government, industrial demand, research progress, and breakthroughs in key technologies in China. Furthermore, the outlook for future developments in biochemical engineering in China is also discussed.

Acrylamide (ACR) exposure and consequent health hazards are alarming public health issues that attract worldwide concern. The World Health Organization urges more researches into health hazards from ACR exposure. However, whether and how ACR exposure increases cardiovascular risk remain unclear, and we sought to address these issues in this prospective cohort study conducted on 3024 general adults with 3-year follow-up (N = 871 at follow-up). Individual urinary ACR metabolites (N-Acetyl-S-(2-carbamoylethyl)-L-cysteine [AAMA] and N-Acetyl-S-(2-carbamoyl-2-hydroxyethyl)-L-cysteine [GAMA]) as credible biomarkers of ACR exposure were detected to assess their cross-sectional and longitudinal relationships with 10-year cardiovascular disease (CVD) risk, a well measure of overall cardiovascular risk. Besides, biomarkers of oxidative stress (urinary 8-hydroxy-deoxyguanosine [8-OHdG] and 8-iso-prostaglandin-F2α [8-iso-PGF2α]) and inflammation (circulating mean platelet volume [MPV] and plasma C-reactive protein [CRP]) as well as plasma transforming growth factor-β1 (TGF-β1) were measured to assess their mediating/mechanistic roles in the relationships of ACR metabolites with 10-year CVD risk. We found AAMA, GAMA, and ΣUAAM (AAMA + GAMA) were cross-sectionally and longitudinally related to increased 10-year CVD risk with odds ratios (95% confidence intervals [CIs]) of 1.32 (1.04, 1.70), 1.81 (1.36, 2.40), and 1.40 (1.07, 1.82), respectively, and risk ratios (95% CIs) of 1.99 (1.10, 3.60), 2.48 (1.27, 4.86), and 2.13 (1.15, 3.94), respectively. Furthermore, 8-OHdG, 8-iso-PGF2α, MPV, CRP, and TGF-β1 were found to significantly mediate 8.06-48.92% of the ACR metabolites-associated 10-year CVD risk increment. In summary, daily ACR exposure of general adults was cross-sectionally and longitudinally associated with increased cardiovascular risk, which was partly mediated by oxidative stress, inflammation, and TGF-β1, suggesting for the first time that ACR exposure may well increase cardiovascular risk of general adult population partly by mechanisms of inducing oxidative stress, inflammation, and TGF-β1. Our findings have important public health implications that provide potent epidemiological evidence and vital mechanistic insight into cardiovascular risk increment from ACR exposure.

Coal workers’ pneumoconiosis (CWP) is one of the most serious occupational diseases caused by long-term inhalation of coal dust (including dust from coal mining or pure coal dust) in the workplace [1]. Although prevention efforts have been taken for many decades, CWP is still a public health issue around the world [2]. Especially in developing countries where coal is the main energy source, millions of workers are exposed to coal dust during their professional activities. Published literatures reported that more than 20 million workers are exposed to coal dust in the workplace in China and India alone [3, 4]. In addition, several international or national plans and programs were conducted to control industrial coal dust and prevent CWP since 1990. However, the global incidence and disease burden of CWP and their temporal trends over time are limited. Footnotes This manuscript has recently been accepted for publication in the European Respiratory Journal . It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Please open or download the PDF to view this article. Conflict of interest: Dr. Wang has nothing to disclose. Conflict of interest: Dr. Liang has nothing to disclose. Conflict of interest: Dr. Yang has nothing to disclose. Conflict of interest: Dr. Ma has nothing to disclose. Conflict of interest: Dr. Li has nothing to disclose. Conflict of interest: Dr. Mu has nothing to disclose. Conflict of interest: Dr. Xiao has nothing to disclose. Conflict of interest: Dr. Feng has nothing to disclose. Conflict of interest: Dr. Dong has nothing to disclose. Conflict of interest: Dr. Yu has nothing to disclose. Conflict of interest: Dr. Liu has nothing to disclose. Conflict of interest: Dr. Tan has nothing to disclose. Conflict of interest: Dr. Zhou has nothing to disclose. Conflict of interest: Dr. Wang has nothing to disclose. Conflict of interest: Dr. Shi has nothing to disclose. Conflict of interest: Dr. Yuan has nothing to disclose. Conflict of interest: Dr. Chen has nothing to disclose.

Benzene is a ubiquitous, occupational, and environmental hematotoxic and leukemogen. Damage to hematopoietic stem cells (HSCs) induced by benzene and its metabolites is a key event in bone marrow (BM) depression and leukemogenesis. There are no reports on transcriptome profiles of HSCs following benzene exposure. Here, Smart-seq2 single-cell transcriptome sequencing was used to detect transcriptomic alternations in BM HSCs and peripheral blood HSCs (PBSCs) in male C57B/6 mice exposed to benzene. We found that benzene caused hematotoxicity which was confirmed by routine blood test, pathological examination, and HSCs percentage analysis. A total of 1514 differentially expressed genes (DEGs) in BM HSCs and 1703 DEGs in PBSCs were screened after treatment with benzene. Weighted gene correlation network analysis revealed that pathways in cancer, transcriptional misregulation in cancer, and hematopoietic cell lineage are vital pathways involved in benzene-induced toxicity in BM HSCs, whereas hematopoietic cell lineage and leukocyte transendothelial migration are critical pathways in PBSCs. Of note, there were 164 common DEGs in both HSCs, out of which 53 genes were co-regulated in both types of HSCs. Subsequent pathway analysis of these 53 genes indicated that the most relevant pathways involved neutrophil degranulation and CD93 localized in the core of the network of the 53 genes, which are known to regulate leukemia stem cell self-renewal and quiescence. Our results could enhance our understanding of HSC responses to benzene, facilitate the identification of potential molecular biomarkers and future studies on its mechanism of toxicity toward HSCs.

Wnt5a is a key mediator of non-canonical Wnt signaling, and an early indicator of epithelial injury and lung dysfunction. Polycyclic aromatic hydrocarbons (PAHs) could induce acute pulmonary pathogenesis, of which the underlying mechanism remains unclear. To elucidate the potential role of Wnt5a-mediated non-canonical Wnt-YAP/TAZ signaling in the lung injury induced by short-term exposure of benzo(a)pyrene (BaP, a representative PAHs), intratracheally instilled mouse model was used and further interfered with its Wnt5a level by small molecule antagonists and agonists. Our data revealed that BaP exposure induced the lung inflammatory response and reduced the expression of Clara cell secretory protein (CC16) in a dose-dependent manner. More importantly, the activation of Wnt5a and downstream YAP/TAZ were accompanied with the enhanced release of epithelial-derived thymic stromal lymphopoietin and interleukin-33, which acted as pro-inflammatory cytokines. Functionally, inhibition of Wnt5a attenuated the BaP-induced inflammation and recuperated CC16 expression, as well as suppressed the epithelial cytokines release. Whereas promoting Wnt5a expression affected the toxic effects of BaP oppositely. Our findings together suggest that Wnt5a is a potential endogenous regulator in lung inflammation and airway epithelial injury, and Wnt5a-YAP/TAZ signaling contributes to lung dysfunction in acute exposure to BaP.

Background: No study has revealed spatial transmission characteristics of COVID-19 in Wuhan, China. We aimed to analyze the spatiotemporal spread of COVID-19 in Wuhan and its influence factors.Methods: Information of 32,682 COVID-19 cases reported through March 18 were extracted from the national infectious disease surveillance system. Geographic information system methods were applied to analysis transmission of COVID-19 and its influence factors in different periods.Results: We found decrease in effective reproduction number (Rt) and COVID-19 related indicators through taking a series of effective public health measures including restricting traffic, centralized quarantine and strict stay-at home policy. The distribution of COVID-19 cases number in Wuhan showed an obvious global aggregation and a local aggregation in central urban areas, but such aggregations was decreased in the later period of the epidemic. In addition, the analysis at streets-level suggested population density and the number of hospitals were influence factors of spatial difference.Conclusions: The epidemic situation showed obvious global and local spatial aggregations. High population density and directional flow of the Population to hospitals may account for the aggregations. Strong quarantine measures and restrictions on movement of residents in Wuhan make the epidemic under control in a short time.

Background Coronavirus Disease 2019 (COVID-19) spread rapidly around the world. We aimed to describe the epidemiological characteristics and the entire evolution of COVID-19 in Wuhan, and to evaluate the effect of non-pharmaceutical intervention by the government. Methods The information of COVID-19 cases until Mar 18, 2020 in Wuhan were collected from the national infectious disease surveillance system in Hubei province. Results A total of 49,973 confirmed cases were reported until Mar 18, 2020 in Wuhan. Among whom, 2496 cases died and the overall mortality was 5.0%. Most confirmed cases (25,619, 51.3%) occurred during Jan 23 to Feb 4, with a spike on Feb 1 (new cases, 3374). The number of daily new cases started to decrease steadily on Feb 19 (new cases, 301) and decreased greatly on Mar 1 (new cases, 57). However, the mortality and the proportion of severe and critical cases has been decreasing over time, with the lowest of 2.0 and 10.1% during Feb 16 to Mar 18, 2020, respectively. The percentage of severe and critical cases among all cases was 19.6%, and the percentage of critical and dead cases aged over 60 was 70.1 and 82.0%, respectively. Conclusion The number of new cases has dropped significantly after the government taking the isolation of four types of personnel and the community containment for 14 days. Our results indicate that the mortality and proportion of severe and critical cases gradually decreased over time, and critical and dead cases are more incline to be older individuals.

The strategy of using polymer-grafted media is effective to create protein chromatography of high capacity and uptake rate, giving rise to an excellent performance in high-throughput protein separation due to its high dynamic binding capacity. Taking the scientific development and technological innovation of protein chromatography as the objective, this review is devoted to an overview of polymer-grafted media reported in the last five years, including their fabrication routes, protein adsorption and chromatography, mechanisms behind the adsorption behaviors, limitations of polymer-grafted media and chromatographic operation strategies. Particular emphasis is placed on the elaboration and discussion on the behaviors of ion-exchange chromatography (IEC) with polymer-grafted media because IEC is the most suitable chromatographic mode for this kind of media. Recent advances in both the theoretical and experimental investigations on polymer-grafted media are discussed by focusing on their implications to the rational design of novel chromatographic media and mobile phase conditions for the development of high-performance protein chromatography. It is concluded that polymer-grafted media are suitable for development of IEC and mixed-mode chromatography with charged and low hydrophobic ligands, but not for hydrophobic interaction chromatography with high hydrophobic ligands and affinity chromatography with ligands that have single binding site on the protein.