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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.

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.

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.

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.

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

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.

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.

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.

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

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.

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.

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.

Whether propylene oxide (PO) exposure is associated with hyperglycemia were rarely explored. We aimed to determine the relationship between PO exposure and glucose metabolism, and potential role of oxidative stress. Among 3294 Chinese urban adults, urinary PO metabolite (N-Acetyl-S-(2-hydroxypropyl)-L-cysteine, 2HPMA), biomarkers of oxidative DNA damage (8-oxo-7,8-dihydro-20-deoxyguanosine, 8-OHdG) and lipid peroxidation (8-isoprostane, 8-iso-PGF2α) in urine were determined. The associations of 2HPMA with 8-OHdG, 8-iso-PGF2α, fasting plasma glucose (FPG), and risk of diabetes were explored. The roles of 8-OHdG and 8-iso-PGF2α on association of 2HPMA with FPG and risk of diabetes were detected. After adjusted for potential confounders, each 1-unit increase in log-transformed concentration of 2HPMA was associated with a 0.15-mmol/L increase in FPG level, and the adjusted OR (95% CI) of diabetes by the associations of log-transformed urinary 2HPMA concentrations was 1.47 (95% CI: 1.03–2.11). Combination effects of 2HPMA with 8-OHdG or 8-iso-PGF2α on risk of diabetes were detected, and elevated 8-iso-PGF2α significantly mediated 34.5% of the urinary 2HPMA-associated FPG elevation. PO exposure was positively associated with FPG levels and risk of diabetes. PO exposure combined with DNA oxidative damage or lipid peroxidation may increase the risk of diabetes, and lipid peroxidation may partially mediate the PO exposure-induced FPG elevation.

Heavy metal exposures have been reported to be associated with increased risk for liver injury. However, the potential mechanisms of the association remain unclear. A repeated-measure study of 9367 observations was conducted to quantify the associations of urinary heavy metals with serum alanine aminotransferase (ALT), a biomarker for liver injury, and assess the mediating role of systemic inflammation in such associations among general Chinese adults. In single-metal models, positive dose-response relationships between urinary vanadium (V), chromium (Cr), copper (Cu), arsenic (As), cadmium (Cd), tungsten (W), and lead (Pb) and serum ALT were observed. In the multiple-metal model containing the seven metals mentioned above, V and Cu remained positively associated with ALT. In longitudinal analyses of 3-6 years, each 1-unit increase in log-transformed levels of V and Cu was associated with an additional rate of annual ALT increase (95% CI) for 1.3% (0.7-1.8%) and 1.3% (0.7-2.0%), respectively. Plasma CRP concentrations were not only positively associated with urinary Cu and Cd, but also positively related with ALT. Furthermore, mediation analyses showed that CRP mediated 4.70% and 7.03% of urinary Cu- and Cd-associated ALT elevations. Our study provides clues for the prevention of heavy metal-induced liver injury.

Background: Phthalates have been largely used for years in varieties of products worldwide. However, research on the joint toxic effect of various phthalates exposure on the liver is lacking. Objectives: We aimed to assess exposure to phthalates on liver function tests (LFTs). Methods: This analysis included data on 6046 adults (≥20 years old) who participated in a National Health and Nutrition Examination Survey (NHANES) in 2007–2016. We employed linear regression and Bayesian kernel machine regression (BKMR), to explore the associations of urinary phthalate metabolites with 8 indicators of LFTs. Results: Di(2-ethylhexyl) phthalate (ΣDEHP) was found to be positively associated with serum alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT) and alkaline phosphatase (ALP) (all P FDR

About 339 million people worldwide are suffering from asthma. We aimed to investigate whether exposure to formaldehyde (FA) is associated with asthma, which could provide clues for preventive and mitigation actions. This article provides a systematic review and meta-analysis of observational studies to assess the association between indoor FA exposure and the risk of asthma in children and adults. An electronic search of PubMed, Embase, and Web of Science was performed to collect all relevant studies published before January 1, 2020, and a total of 13 papers were included in this meta-analysis. A random-effect model was conducted to calculate the pooled odds ratio (OR) between FA exposure and asthma. We found that each 10 µg/m3 increase in FA exposure was significantly associated with a 10% increase in the risk of asthma in children (OR = 1.10, 95% confidence interval = 1.00-1.21). We sorted the FA concentrations reported in the selected articles and categorized exposure variables into low (FA ≤ 22.5 µg/m3 ) and high exposure (FA > 22.5 µg/m3 ) according to the median concentration of FA. In the high-exposure adult group, FA exposure may also be associated with an increased risk of asthma (OR = 1.81, 95% CI = 1.18-2.78).

Widespread occupational and environmental exposure to benzene is unavoidable and poses a public health threat. Studies of potential interventions to prevent or relieve benzene toxicity are, thus, essential. Research has shown l-carnitine (LC) has beneficial effects against various pathological processes and diseases. LC possesses antioxidant activities and participates in fatty acid oxidation (FAO). In this study, we investigated whether 1,4-benzoquinone (1,4-BQ) affects LC levels and the FAO pathway, as well as analyzed the influence of LC on the cytotoxic effects of 1,4-BQ. We found that 1,4-BQ significantly decreased LC levels and downregulated Cpt1a, Cpt2, Crat, Hadha, Acaa2, and Acadvl mRNA expression in K562 cells. Subsequent assays confirmed that 1,4-BQ decreased cell viability and increased apoptosis and caspase-3, -8, and -9 activities. It also induced obvious oxidative stress and DNA damage, including an increase in the levels of reactive oxygen species and malondialdehyde, tail DNA%, and olive tail moment. Additionally, the mitochondrial membrane potential was significantly reduced. Cotreatment with LC (500 μmol/L) relieved these alterations by reducing oxidative stress and increasing the protein expression levels of Cpt1a and Hadha, particularly in the 20 μmol/L 1,4-BQ group. Thus, our results demonstrate that 1,4-BQ causes cytotoxicity, reduces LC levels, and downregulates the FAO genes. In contrast, LC exhibits protective effects against 1,4-BQ-induced apoptosis and DNA damage by decreasing oxidative stress and promoting the FAO pathway.

Carbon disulfide (CS2) has been reported to induce disorder of glucose metabolism. However, the associations of CS2 exposure with plasma glucose levels and risk of diabetes have not been explored in general population, and the underlying mechanisms remain unclear. We aim to examine the relationships between CS2 exposure and fasting plasma glucose (FPG) levels, as well as diabetes, and assess the potential role of oxidative stress among the abovementioned relationships in Chinese general adults. The concentrations of urinary biomarkers of CS2 exposure (2-thiothiazolidin-4-carboxylic acid, TTCA), and biomarkers for lipid peroxidation (8-isoprostane, 8-iso-PGF2α) and DNA oxidative damage (8-oxo-7,8-dihydro-20-deoxyguanosine, 8-OHdG) were measured among 3338 urban adults from the Wuhan-Zhuhai cohort. Additionally, FPG levels were tested promptly. Generalized linear models and logistic regression models were used to quantify the associations among urinary TTCA, oxidative damage markers, FPG levels and diabetes risk. Mediation analysis was employed to estimate the role of oxidative damage markers in the association between urinary TTCA and FPG levels. We discovered a significant relationship between urinary TTCA and FPG levels with regression coefficient of 0.080 (95% CI: 0.002,0.157). Besides, the risk of diabetes was positively related to urinary TTCA (OR:1.282, 95% CI: 1.055,1.558), particularly among those who did not exercise regularly. Each 1% increase of urinary TTCA concentration was associated with a 0.096% and 0.037% increase in urinary 8-iso-PGF2α and 8-OHdG, respectively. Moreover, we found an upward trend of FPG level as urinary 8-iso-PGF2α gradually increased (Ptrend

Zn

Fibrillogenesis of amyloid β-protein (Aβ) in human brain has been implicated as the main cause of Alzheimer’s disease. A few small molecules from natural sources have been discovered for their inhibition effects on Aβ fibrillation, of which (−)-epigallocatechin-3-gallate (EGCG) is one of the most broadly investigated compounds for its potent inhibitory activity. However, in vivo applicability of the inhibitors is largely limited by their low transmembrane efficiency. Hence, it is of great significance to develop inhibition systems that function at low concentrations. In this work, a dual-inhibitor system containing EGCG and negatively charged polymeric nanoparticles (NP10), which was also demonstrated effective on the inhibition of Aβ aggregation, was developed and comprehensively studied by extensive biophysical and biological assays. It was found that the dual-inhibitor system at low concentrations was more effective on the inhibition and detoxification of Aβ (Aβ 42 and Aβ 40 ) fibrillation than the additive effects of these two agents working individually. Namely, there was a synergistic effect of the two inhibitors. The synergism factor reached 1.25 with 5 μM EGCG and 5 μg/mL NP10. Kinetic studies with Aβ 40 revealed that the two inhibitors functioned in different Aβ assembling stages: NP10 mainly inhibited primary nucleation, while EGCG suppressed fibril elongation and changed the fibril structure to make it show less seeding activities in the secondary nucleation. NP10 might also help EGCG binding to Aβ, leading to its enhanced inhibitory effects on fibril elongation and secondary nucleation. The synergistic effect observed in the dual-inhibitor system offered new insight into the development of potent inhibitor systems against amyloid neurotoxicity.