Air pollution associated with incidence and progression trajectory of chronic lung diseases: a population-based cohort study.

BACKGROUND: No prior study has examined the effects of air pollution on the progression from healthy to chronic lung disease, subsequent chronic lung multimorbidity and further to death. METHODS: We used data from the UK Biobank of 265 506 adults free of chronic lung disease at recruitment. Chronic lung multimorbidity was defined as the coexistence of at least two chronic lung diseases, including asthma, chronic obstructive pulmonary disease and lung cancer. The concentrations of air pollutants were estimated using land-use regression models. Multistate models were applied to assess the effect of air pollution on the progression of chronic lung multimorbidity. RESULTS: During a median follow-up of 11.9 years, 13 863 participants developed at least one chronic lung disease, 1055 developed chronic lung multimorbidity and 12 772 died. We observed differential associations of air pollution with different trajectories of chronic lung multimorbidity. Fine particulate matter showed the strongest association with all five transitions, with HRs (95% CI) per 5 µg/m3 increase of 1.31 (1.22 to 1.42) and 1.27 (1.01 to 1.57) for transitions from healthy to incident chronic lung disease and from incident chronic lung disease to chronic lung multimorbidity, and 1.32 (1.21 to 1.45), 1.24 (1.01 to 1.53) and 1.91 (1.14 to 3.20) for mortality risk from healthy, incident chronic lung disease and chronic lung multimorbidity, respectively. CONCLUSION: Our study provides the first evidence that ambient air pollution could affect the progression from free of chronic lung disease to incident chronic lung disease, chronic lung multimorbidity and death.

High-Temperature Soup Foods in Plastic Packaging Are Associated with Phthalate Body Burden and Expression of Inflammatory mRNAs: A Dietary Intervention Study.

Plastic packaging material is widely used to package high-temperature soup food in China, but this combination might lead to increased exposure to phthalates. The health effects and potential biological mechanisms have not been well studied. This study aimed to examine urinary phthalate metabolites and the expression of inflammatory cytokines in the blood before, during, and after a "plastic-packaged high-temperature soup food" dietary intervention in healthy adults. The results showed that compared with those in the preintervention period, urinary creatinine-adjusted levels of monomethyl phthalate (MMP), mono-n-butyl phthalate (MBP), mono-isobutyl phthalate (MIBP), and total phthalate metabolites in the intervention period were significantly higher, with increases of 71.6, 41.8, 38.8, and 29.8% for MMP, MBP, MIBP, and the total phthalate metabolites, respectively. After intervention, the mean levels of IL-1ß, IL-4, and TNF-α mRNA increased by 19.0, 21.5, and 25.0%, respectively, while IL-6 and IFN-γ mRNA decreased by 24.2 and 32.9%, respectively, when compared with the preintervention period. We also observed that several phthalates were associated with the mRNA or protein expression of IL-8, TNF-α, and IL-10. Therefore, consumption of plastic-packaged high-temperature soup food was linked to increased phthalate exposure and might result in significant changes in mRNA expression of several inflammatory cytokines.

Regulation of anthocyanin accumulation via MYB75/HAT1/TPL-mediated transcriptional repression.

Anthocyanin is part of secondary metabolites, which is induced by environmental stimuli and developmental signals, such as high light and sucrose. Anthocyanin accumulation is activated by the MYB-bHLH-WD40 (MBW) protein complex in plants. But the evidence of how plants maintain anthocyanin in response to signals is lacking. Here we perform molecular and genetic evidence to display that HAT1 plays a new breaker of anthocyanin accumulation via post-translational regulations of MBW protein complex. Loss of function of HAT1 in the Arabidopsis seedlings exhibits increased anthocyanin accumulation, whereas overexpression of HAT1 significantly repressed anthocyanin accumulation. We found that HAT1 interacted with MYB75 and thereby interfered with MBW protein complex. Overexpression of HAT1 suppresses abundant anthocyanin phenotype of pap1-D plant. HAT1 is characterized as a transcriptional repressor possessing an N-terminal EAR motif, which determines to interact with TOPLESS corepressor. Repression activity of HAT1 in regulation of gene expression and anthocyanin accumulation can be abolished by deletion or mutation of the EAR motif 1. Chromatin immunoprecipitation assays revealed that MYB75 formed a transcriptional repressor complex with HAT1-TPL by histone H3 deacetylation in target genes. We proposed that HAT1 restrained anthocyanin accumulation by inhibiting the activities of MBW protein complex through blocking the formation of MBW protein complex and recruiting the TPL corepressor to epigenetically modulate the anthocyanin late biosynthetic genes (LBGs).

Association of liver and kidney functions with Klotho gene methylation in a population environment exposed to cadmium in China.

Exposure to the heavy metal cadmium has adverse effects on human health, including DNA methylation. This study aimed to investigate the effects of cadmium on liver and kidney functions and Klotho gene methylation and to explore the relationship of methylation level with indicators of liver and kidney functions. Graphite furnace atomic absorption spectrometry was conducted to determine urinary cadmium, and an automatic biochemical analyzer was used to detect indices of liver and kidney functions. PCR pyrosequencing was performed to detect the methylation rate of Klotho. One-way ANOVA was adopted to compare the differences between groups, and the linear correlation to variables was analyzed. Cadmium exposure was negatively correlated with albumin level (r=-0.143, p=0.021) and positively correlated with urinary ß2-microglobulin level (r=0.229, p<0.001). However, the methylation levels of Klotho gene was decreased and increased by low and high doses of cadmium exposure, respectively. And Klothomethylation levels were negatively correlated with albumin levels and positively correlated with ß2-microglobulin levels.In this study, cadmium exposure affects liver and kidney functions as well as Klotho methylation levels, but the effect on Klotho methylation levels is not linear. Klotho methylation levels also influence liver and kidney functions.

Sumoylation of BRI1-EMS-SUPPRESSOR 1 (BES1) by the SUMO E3 Ligase SIZ1 Negatively Regulates Brassinosteroids Signaling in Arabidopsis thaliana.

Brassinosteroids (BRs), a group of plant steroid hormones, participate in the regulation of plant growth and developmental processes. BR functions through the BES1/BZR1 family of transcription factors, however, the regulation of the BES1 activity by post-translational modifications remains largely unknown. Here, we present evidence that the SUMO E3 ligase SIZ1 negatively regulates BR signaling pathway. T-DNA insertion mutant siz1-2 shows BL (Brassinolide, the most active BR) hypersensitivity and BRZ (Brassinazole, a BR biosynthesis inhibitor) insensitivity during hypocotyl elongation. In addition, expression of BES1-dependent BR-response genes is hyper-regulated in siz1-2 seedlings. The siz1-2bes1-D double mutant exhibits longer hypocotyl than bes1-D. Moreover, SIZ1 physically interacts with BES1 in vivo and in vitro and mediates the sumoylation of BES1. A K302R substitution in BES1 blocks its sumoylation mediated by SIZ1 in plants, indicating that K302 is the principal site for SUMO conjugation. Consistently, we find that sumoylation inhibits BES1 protein stability and activity. Taken together, our data show that the sumoylation of BES1 via SIZ1 negatively regulates the BR signaling pathway.

Nitric oxide as a signaling molecule in brassinosteroid-mediated virus resistance to Cucumber mosaic virus in Arabidopsis thaliana.

Brassinosteroids (BRs) are growth-promoting plant hormones that play a crucial role in biotic stress responses. Here, we found that BR treatment increased nitric oxide (NO) accumulation, and a significant reduction of virus accumulation in Arabidopsis thaliana. However, the plants pre-treated with NO scavenger [2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-1-oxyl-3-oxide (PTIO)] or nitrate reductase (NR) inhibitor (tungstate) hardly had any NO generation and appeared to have the highest viral replication and suffer more damages. Furthermore, the antioxidant system and photosystem parameters were up-regulated in brassinolide (BL)-treated plants but down regulated in PTIO- or tungstate-treated plants, suggesting NO may be involved in BRs-induced virus resistance in Arabidopsis. Further evidence showed that NIA1 pathway was responsible for BR-induced NO accumulation in Arabidopsis. These results indicated that NO participated in the BRs-induced systemic resistance in Arabidopsis. As BL treatment could not increase NO levels in nia1 plants in comparison to nia2 plants. And nia1 mutant exhibited decreased virus resistance relative to Col-0 or nia2 plants after BL treatment. Taken together, our study addressed that NIA1-mediated NO biosynthesis is involved in BRs-mediated virus resistance in A. thaliana.

Increased oxidative stress and plasma Hsp70 levels among gasoline filling station attendants.

OBJECTIVES: Methylcyclopentadienyl manganese tricarbonyl (MMT) is an organic derivative of manganese (Mn) and is used as an antiknock agent and octane enhancer in gasoline. In this article, we tested the oxidative stress and heat stress protein (Hsp) 70 levels of gasoline station attendants to explore potential plasma biomarkers. Furthermore, the dose-response relationship was also identified. METHODS: A total of 144 workers, including 96 petrol fillers and 48 cashiers, participated in the study. Ambient concentrations of benzene, toluene, ethylbenzene, and xylene (BTEX) and Mn were monitored at nine filling stations. During the measuring process, the individual cumulative exposure index was calculated. Plasma oxidative stress and Hsp70 levels were also analysed using enzyme-linked immunosorbent assay. RESULTS: The BTEX time-weighted average in office areas was significantly lower than in refuelling areas ( p < 0.05). In refuelling areas, the content of Mn ranged from 6.44 µg/m3 to 127.34 µg/m3, which was much higher than that in office areas (3.16-7.22 µg/m3; p < 0.05). Exposed workers had significantly different plasma oxidative stress indicators compared with the control group, respectively: superoxide dismutase (SOD), 39.18 ± 6.05 U/mL versus 52.84 ± 3.87 U/mL; glutathione peroxidase (GSH-Px), 186.07 ± 15.63 U versus 194.38 ± 10.42 U; and malondialdehyde (MDA), 1.68 ± 0.52 nmol/L versus 1.43 ± 0.64 nmol/L (in all comparisons, p < 0.05). Plasma Hsp70 level in the exposed group (2.77 ± 0.64 ng/mL) was significantly higher than in the control group (2.32 ± 0.87 ng/mL; p < 0.05). Furthermore, Hsp70 levels were inversely correlated with the activities of SOD ( r = -0.305) and GSH-Px ( r = -0.302) in the exposed group ( p < 0.05). Moreover, a positive correlation ( r = 0.653) was found between plasma Hsp70 levels and plasma MDA levels ( p < 0.05). CONCLUSION: Exposure to MMT-containing gasoline may result in increasing reactive oxygen stress among filling station attendants. Plasma Hsp70 levels could be used as a sensitive responsive biomarker for exposed workers.

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

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

Manganese induces podocyte injury through regulating MTDH/ALKBH5/NLRP10 axis: Combined analysis at epidemiology and molecular biology levels.

Manganese (Mn) is an essential micronutrient required for various biological processes but excess exposure to Mn can cause neurotoxicity. However, there are few reports regarding the toxicity effect of Mn on the kidney as well as the underlying molecule mechanism. Herein, in vivo experiments were adopted to assess the toxicity effects associated with Mn, and found that chronic Mn treatment induced the injury of glomerular podocytes but not renal tubule in rats. Genome-wide CRISPR/Cas9 knockout screen was then employed to explore the biotargets of the toxic effect of Mn on podocytes. Through functional analyses of the enriched candidate genes, NLRP10 was found to be significantly up-regulated and mediated Mn-induced podocyte apoptosis. Further mechanism investigation revealed that NLRP10 expression was regulated by demethylase AlkB homolog 5 (ALKBH5) in an m6A-dependent fashion upon Mn treatment. Moreover, Mn could directly bind to Metadherin (MTDH) and promoted its combination with ALKBH5 to promote NLRP10 expression and cell apoptosis. Finally, logistic regressions, restricted cubic spline regressions and uniform cubic B-spline were used to investigate the association between Mn exposure and the risk of chronic kidney disease (CKD). A U-shaped nonlinear relationship between CKD risk and plasma Mn level, and a positive linear relationship between CKD risk and urinary Mn levels was found in our case-control study. To sum up, our findings illustrated that m6A-dependent NLRP10 regulation is indispensable for podocyte apoptosis and nephrotoxicity induced by Mn, providing fresh insight into understanding the health risk of Mn and a novel target for preventing renal injury in Mn-intoxicated patients.

Metal mixture exposure and the risk for immunoglobulin A nephropathy: Evidence from weighted quantile sum regression.

Immunoglobulin A nephropathy (IgAN) is the most common type of glomerulonephritis in adults worldwide. Environmental metal exposure has been reported to be involved in the pathogenic mechanisms of kidney diseases, yet no further epidemiological study has been conducted to assess the effects of metal mixture exposure on IgAN risk. In this study, we conducted a matched case‒control design with three controls for each patient to investigate the association between metal mixture exposure and IgAN risk. A total of 160 IgAN patients and 480 healthy controls were matched for age and sex. Plasma levels of arsenic, lead, chromium, manganese, cobalt, copper, zinc, and vanadium were measured using inductively coupled plasma mass spectrometry. We used a conditional logistic regression model to assess the association between individual metals and IgAN risk, and a weighted quantile sum (WQS) regression model to analyze the effects of metal mixtures on IgAN risk. Restricted cubic splines were used to evaluate overall associations between plasma metal concentrations and estimated glomerular filtration rate (eGFR) levels. We observed that except for Cu, all the metals analyzed were nonlinearly associated with decreased eGFR, and higher concentrations of arsenic and lead were associated with elevated IgAN risk in both single-metal [3.29 (1.94, 5.57), 6.10 (3.39, 11.0), respectively] and multiple-metal [3.04 (1.66, 5.57), 4.70 (2.47, 8.97), respectively] models. Elevated manganese [1.76 (1.09, 2.83)] levels were associated with increased IgAN risk in the single-metal model. Copper was inversely related to IgAN risk in both single-metal [0.392 (0.238, 0.645)] and multiple-metal [0.357 (0.200, 0.638)] models. The WQS indices in both positive [2.04 (1.68, 2.47)] and negative [0.717 (0.603, 0.852)] directions were associated with IgAN risk. Lead, arsenic, and vanadium contributed significant weights (0.594, 0.195, and 0.191, respectively) in the positive direction; copper, cobalt, and chromium carried significant weights (0.538, 0.253, and 0.209, respectively). In conclusion, metal exposure was related to IgAN risk. Lead, arsenic, and copper were all significantly weighted factors of IgAN development, which may require further investigation.

Household cooking oil type and risk of oral micronucleus frequency in Chinese nonsmokers.

Household animal fat has been linked to increased incidence of cancers compared with vegetable fat. However, few epidemiological studies have associated these two cooking oil types with precancerous genotoxic effects, such as occurrence of micronuclei (MN). This study aimed to explore the association between oral MN frequency and household cooking oil type and whether the association can be attributed to polycyclic aromatic hydrocarbons (PAHs). We collected information about individual cooking oil use, measured genotoxic effects by MN tests and urinary PAHs metabolites (OHPAHs) in 245 nonsmokers. The associations between household cooking oil type and MN frequency and OHPAHs were analyzed using generalized linear models (GLMs) and logistic regression models, evaluating odds ratios and coefficient (95% confidence intervals) (ORs, 95% Cls; ß, 95% Cls). The odds of animal fat consumers, rather than vegetable fat consumers, was positively associated with higher MN frequency (OR = 1.94, P < 0.05). The associations were discovered in participants only using kitchen ventilation (OR = 2.04, P < 0.05). Animal fat consumers had higher total OHPAHs than vegetable fat consumers (1.58 ± 0.22 mg/mol, Cr vs 1.20 ± 0.12 mg/mol, Cr; P = 0.028). Significant correlations were observed between total OHPAHs quartiles and increased MN frequency (ß = 0.38, P-trend = 0.026). After stratifying by household cooking oil type, sensitivity analyses showed that the positive association between total OHPAHs quartiles and increased MN frequency was only observed in animal fat consumers (ß = 0.61, P-trend = 0.030). In conclusion, usage of household animal fat was associated with an increased odds of oral MN frequency in Chinese nonsmokers and the odds correlated with increased PAHs exposure. This finding supplemented evidence associating cooking oil type with genotoxic effects and explained its association with PAHs exposure.

Influence of manganese exposure on cognitive function, plasma APP and Aß levels in older men.

BACKGROUND: Elevated manganese (Mn) exposure impairs cognition in adults and children, but the association between Mn and cognitive function in elderly people is unclear. Previous studies have linked Mn neurotoxicity in AD to Aß-dependent mechanisms. However, the association between Mn and plasma APP and Aß in the general elderly population remains unknown. This study aimed to investigate the association between Mn exposure and cognitive function, plasma APP and plasma Aß in older adults. METHODS: Cognitive abilities in 375 men aged 60 and older in Guangxi, China were assessed using the Mini-Mental State Examination (MMSE) and cognitive impairment were identified using education-stratified cut-off points of MMSE scores. Urinary Mn levels and plasma APP, and Aß levels were measured using ICP-MS and ELISA, respectively. RESULTS: A total of 109 (29.07 %) older men were identified as having cognitive impairment. The median urinary Mn level was 0.22 µg/g creatinine. Urinary Mn levels were negatively correlated with MMSE scores (ß = -1.35, 95 % CI: -2.65 to -0.06; p = 0.041). In addition, higher concentrations of urinary manganese were associated with a greater risk of cognitive impairment (OR = 2.03, 95 % CI: 1.14-3.59; comparing the highest and lowest manganese; p = 0.025). Moreover, plasma APP levels were inversely associated with urinary Mn levels (r = -0.123, p = 0.020), and positively associated with MMSE scores (r = 0.158, p = 0.002). Surprisingly, no correlations were observed between plasma Aß42, Aß40, Aß40/Aß42, or Aß42/Aß40 and urinary Mn levels and MMSE scores. CONCLUSION: These results suggested that Mn exposure is negatively associated with older men's cognition and plasma APP levels, but not plasma Aß levels.

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

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

Spatiotemporal disequilibrium and spillover effect of fine particulate matter across China.

Massive monitoring data requires effective statistical analysis methods. This paper aims to visualize the spatiotemporal characteristics and spillover effect of air pollutants. Ground-based PM2.5 data in 336 cities across China revealed a tough but improving situation. The PM2.5 average annual concentrations in 2016 and 2017 were 47 ± 18 µg/m3 and 44 ± 16 µg/m3 respectively, but a worse, or at least a not-improving PM2.5 situation happened in winter. A slight declining north-south disequilibrium and a growing east-west disequilibrium exhibited in 2017, along with an increasing weight of eastern and southern pollution in the proportion of the overall pollution level. North-south disequilibrium existed stably throughout the year but east-west disequilibrium was erratic. Nearly half of the cities exhibited significant spillover effects, presenting 2 clusters with spillover by high concentrations and 3 clusters with spillover by low concentrations. Most cities in Hebei, Shandong and Henan provinces showed a high but decreasing spillover effect, but increasing trend happened in the cities in Anhui and Shanxi provinces. A significant correlation appeared between the city population and PM2.5 concentration. Population density explained about 25% of the PM2.5 concentration change, and the explanation ability increased in 2017. A higher influence of population on PM2.5 concentration happened in the early stage of city development, and the influence exhibited spatial differences. The city population and PM2.5 spillover effect existed an overall positive correlation, but the population only addressed about 10% of the spillover effect change. Our findings provide important information for the joint prevention and control of air pollution in China, and the approach proposed in this paper is applicable to other fields.

Relation between cadmium body burden and cognitive function in older men: A cross-sectional study in China.

Cadmium (Cd) is a known neurotoxicant and its relation with cognition has been well studied in children. However, evidence linking Cd and cognitive function among older individuals is limited. To evaluate the association between Cd exposure and cognitive function in older age, we conducted a cross-sectional study involving 375 older men aged 60-74 years (mean age: 66.0 years) in Guangxi, China. Urinary Cd concentrations were measured. Cognitive function was assessed by the Chinese version of Mini-Mental State Examination (MMSE) and cognitive impairment was identified using education-specific cutoff points of MMSE scores. General linear regression and logistic regression models were applied to evaluate the associations of urinary Cd concentrations with MMSE scores and the risk of cognitive impairment, respectively. The median urinary Cd concentration of all participants was 1.58 µg/g creatinine. Urinary Cd levels were inversely associated with MMSE scores [ß = -0.76; 95% confidence interval (CI): -1.28 to -0.23 for a 2-fold increase in urinary Cd]. A 2-fold increase in urinary Cd was associated with increased risk of cognitive impairment [adjusted odds ratio (OR) = 1.46; 95% CI: 1.14 to 1.86]. When urinary Cd levels were analyzed as quartiles, higher urinary Cd levels were also significantly associated with increased risk of cognitive impairment in a dose-response manner (adjusted OR = 2.68; 95% CI: 1.33 to 5.38 for the highest vs. lowest quartile; p for trend = 0.002). Our findings suggest that long-term exposure to Cd may have adverse consequences for older men's cognitive function, but these results need further confirmation.

Potential diagnostic and prognostic value of plasma long noncoding RNA LINC00086 and miR-214 expression in gastric cancer.

BACKGROUND: Plasma carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9), and cancer antigen 72-4 (CA72-4) are common markers which are useful in the diagnosis and prognosis of GC. However, their sensitivity and specificity in GC remain unsatisfactory. Identification of cancer diagnosed-biomarkers would be of great value. OBJECTIVE: Evaluate the diagnostic and prognostic value of LINC00086 and miR-214 in GC. METHODS: In this study, we determined the expression of LINC00086 and miR-214 in GC by qRT-PCR. Additionally, we investigated the relationship between various clinicopathological features of GC patients and LINC00086 or miR-214 expression, and evaluated the diagnostic and prognostic value of LINC00086 and miR-214 in GC. RESULTS: In this study, we found that plasma LINC00086 expression was significantly lower, whereas plasma miR-214 expression was significantly higher in GC patients than in normal individuals. LINC00086 and miR-214 exhibited high sensitivity and specificity in diagnosing GC. Additionally, GC patients with low LINC00086 or high miR-214 expression were likely to have larger tumors, lymphatic metastasis, larger TNM stage, and higher CEA and CA19-9 levels. Moreover, GC patients with low LINC00086 or high miR-214 expression showed lower survival rates. Lymphatic metastasis, LINC00086, and miR-214 are independent factors affecting patient diagnosis. CONCLUSIONS: LINC00086 and miR-214 are potentially diagnostic and prognostic markers for GC.

Probiotics Ameliorate Colon Epithelial Injury Induced by Ambient Ultrafine Particles Exposure.

Diesel exhaust particles (DEPs) are common airborne ultrafine particles (UFPs); however, few studies have examined their effects on the gastrointestinal tract. To investigate the interaction of gut microbiota and DEPs-induced colonic injury, adult C57BL/6 mice are kept in whole-body inhalation chambers and exposed to filtered room air (FRA) or DEPs (300 µg m-3) 1 h per day for 28 consecutive days. DEPs exposure results in colon epithelial injury with inflammatory cell infiltration and mucus depletion. Abundance of Lactobacillus in murine feces is transiently increased following 7-day DEPs exposure and then decreased until the end of 28-day exposure. A reduction of the colonic mucus layer thickness is observed in mice receiving gut microbiota from DEPs-exposed mice. Mechanistically, RNA-sequencing suggests disruption of the nitrogen metabolism pathway in DEPs-exposed NCM460 cells. Upregulation of carbonic anhydrase 9 (CA9) expression levels is observed in epithelia following DEPs exposure both in vivo and in vitro. Oral administration of probiotics protects the mice against DEPS-induced colon epithelial injury. The results strongly suggest the involvement of gut microbiota in response to DEPs exposure and subsequently epithelial injury in vivo. Supplementation with probiotic may be a potential way to protect against UFPs-induced colon epithelial injury.

Multiple-life-stage probabilistic risk assessment for the exposure of Chinese population to PBDEs and risk managements.

Studies assessing body burden of polybrominated diphenyl ethers (PBDEs) exposure have been conducted in the United States and Europe. However, the long-term assessment that is associated with multimedia exposure of PBDEs for the Chinese population is not available. The current study estimated the health risks using large PBDEs data to quantify the contributions of various media from different regions and distinguished the most vulnerable periods in life. We summarized media-specific (soil, dust, outdoor and indoor air, human milk and food) concentration of PBDEs in China from 2005 to 2016. Probabilistic risk assessment was adopted to estimate the health risks of infants, toddlers, children, teenagers and adults through ingestion, inhalation and dermal absorption. Monte Carlo simulation and sensitivity analysis were performed to quantify risk estimates uncertainties. E-waste areas had the highest PBDEs concentration, which was at least an order of magnitude higher than in other areas. BDE209 was the primary congener, accounting for 38-99% of the estimated daily intake. The dominant exposure pathway for infants was dietary intake through human milk, whereas dust ingestion was a higher contributing factor for toddlers, children, teenagers and adults. The 95th percentile of hazard index for infants and toddlers from e-waste areas of Guangdong and Zhejiang provinces exceeded one. Our estimates also suggested that infants may have the highest body burdens of PBDEs compared to other age groups. Sensitivity analyses indicated that PBDEs concentrations and ingestion rates contributed to major variances in the risk model. In this study, e-waste was found as a significant source of PBDEs, and PBDEs-containing e-waste are likely to be a threat to human health especially during early period of life. Risk strategies for better managing environmental PBDEs-exposure and human health are needed, due to the high intake of PBDEs and their persistence in the environment.

Association of active/passive smoking and urinary 1-hydroxypyrene with poor sleep quality: A cross-sectional survey among Chinese male enterprise workers.

INTRODUCTION: Tobacco use has been implicated as an important factor for poor sleep quality. However, in most studies, the sleep quality of smokers was only assessed though a self-reported questionnaire, without measuring any internal biomarkers that reflect the levels of tobacco exposure. We examined the association of active and passive smoking with sleep quality, assessed smoking exposure using urinary 1-hydroxypyrene (1-HOP) as an internal biomarker, and further explored the relationship between 1-HOP and sleep quality. METHODS: A cross-sectional survey was conducted in Liuzhou city, Guangxi, China. A total of 1787 male enterprise workers were enrolled. The smoking attribute data were collected by self-reported questionnaire, and individual sleep quality was evaluated through the Pittsburgh Sleep Quality Index (PSQI). The concentration of urinary 1-HOP was measured by high-performance liquid chromatography. RESULTS: Compared with non-smoking, active smoking and passive smoking were significantly associated with long sleep latency (odds ratio, OR=1.84, 95% confidence interval, CI=1.28-2.64; 1.45, 1.00-2.11, respectively), short sleep duration (OR=2.72, 95% CI=1.45-5.09; 1.94, 1.01-3.71, respectively), daytime dysfunction (OR=1.54, 95% CI=1.10-2.17; 1.44, 1.02-2.03, respectively), and overall poor sleep quality with PSQI total score >5 (OR=1.41, 95% CI=1.05-1.88; 1.34, 1.00-1.79, respectively). Compared with non-smokers, active smokers had higher urinary 1-OHP concentrations that were significant (p=0.004), while passive smokers had no significant difference in urinary 1-OHP concentration (p=0.344). The high concentration group was significantly associated with daytime dysfunction and overall poor sleep quality with PSQI total score >5 (OR = 1.73, 95% CI=1.06-2.81; 1.76, 1.18-2.63, respectively). CONCLUSIONS: Both active smoking and passive smoking are risk factors for poor sleep quality among Chinese male enterprise workers. Active smokers had significantly higher levels of urinary 1-OHP than non-smokers, and high concentration of 1-OHP was associated with daytime dysfunction and overall poor sleep quality.

Relationship between shift work schedule and self-reported sleep quality in Chinese employees.

Few studies have reported on the effects of fixed and rotating shift systems on the prevalence of sleep disturbance. Thus, in this study, the relationships between different work schedules and sleep disturbance in Chinese workers were investigated. A total of 2180 workers aged 19-65 years responded to the self-report questionnaire on shift work schedule (fixed day-shift, fixed night-shift, two-shift or three-shift system), working hours a day, and working days a week, physical effort, subjective sleep quality and subjective mental state. It was found that the rotating shift workers, namely, two- and three-shift workers, exhibited higher risks of sleep disturbance than with the fixed day-shift workers did (OR 1.37; 95% CI 1.07to 1.74; and OR 2.19; 95% CI 1.52 to 3.15, respectively). The risk was particularly high among two- or three-shift workers who worked more than 8 hours a day or more than 5 days a week and among three-shift workers who reported both light and heavy physical effort at work. Moreover, the two- and three-shift workers (rotating shift workers) suffered from poorer sleep quality than the fixed night shift workers did (OR 1.84; 95% CI 1.01 to 3.32; and OR 2.94; 95% CI 1.53 to 5.64, respectively). Consequently, rotating shift work (two- and three-shift work) is a risk factor for sleep disturbance, and the fixed work rhythm may contribute to the quality of sleep.