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Liu Y.,Huazhong University of Science and Technology | Liu Y.,Institute of Health Surveillance | Steenland K.,Key Laboratory of Environment and Health | Steenland K.,Emory University | And 8 more authors.
American Journal of Epidemiology | Year: 2013

Crystalline silica has been classified as a human carcinogen by the International Agency for Research on Cancer (Lyon, France); however, few previous studies have provided quantitative data on silica exposure, silicosis, and/or smoking. We investigated a cohort in China (in 1960-2003) of 34,018 workers without exposure to carcinogenic confounders. Cumulative silica exposure was estimated by linking a job-exposure matrix to work history. Cox proportional hazards model was used to conduct exposure-response analysis and risk assessment. During a mean 34.5-year follow-up, 546 lung cancer deaths were identified. Categorical analyses by quartiles of cumulative silica exposure (using a 25-year lag) yielded hazard ratios of 1.26, 1.54, 1.68, and 1.70, respectively, compared with the unexposed group. Monotonic exposure-response trends were observed among nonsilicotics (P for trend < 0.001). Analyses using splines showed similar trends. The joint effect of silica and smoking was more than additive and close to multiplicative. For workers exposed from ages 20 to 65 years at 0.1 mg/m3 of silica exposure, the estimated excess lifetime risk (through age 75 years) was 0.51%. These findings confirm silica as a human carcinogen and suggest that current exposure limits in many countries might be insufficient to protect workers from lung cancer. They also indicate that smoking cessation could help reduce lung cancer risk for silica-exposed individuals. © The Author 2013. Source

Lou J.,Key Laboratory of Environment and Health | Zhong R.,Key Laboratory of Environment and Health | Shen N.,Key Laboratory of Environment and Health | Lu X.-Z.,Guangdong Women and Children Hospital | And 8 more authors.
Scientific Reports | Year: 2015

Genome-wide association studies (GWASs) have identified multiple single nucleotide polymorphisms (SNPs) associated with Kawasaki disease (KD). In this study, we replicated the associations of 10 GWAS-identified SNPs with KD in a Han Chinese population. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by logistic regression, and cumulative effect of non-risk genotypes were also performed. Although none of the SNPs reached the corrected significance level, 4 SNPs showed nominal associations with KD risk. Compared with their respective wild type counterparts, rs1801274 AG+GG genotypes and rs3818298 TC+CC genotypes were nominally associated with the reduced risk of KD (OR = 0.77, 95% CI = 0.59-0.99, P = 0.045; OR = 0.74, 95% CI = 0.56-0.98, P = 0.038). Meanwhile, rs1801274 GG genotype, rs2736340 CC genotype or rs4813003 TT genotype showed a reduced risk trend (OR = 0.57, 95% CI = 0.35-0.93, P = 0.024; OR = 0.46, 95% CI = 0.26-0.83, P = 0.010; OR = 0.64, 95% CI = 0.43-0.94, P = 0.022), compared with rs1801274 AG+AA genotypes, rs2736340 CT+TT genotypes or rs4813003 TC+CC genotypes, respectively. Furthermore, a cumulative effect was observed with the ORs being gradually decreased with the increasing accumulative number of non-risk genotypes (P trend <0.001). In conclusion, our study suggests that 4 GWAS-identified SNPs, rs2736340, rs4813003, rs3818298 and rs1801274, were nominally associated with KD risk in a Han Chinese population individually and jointly. Source

Huang S.,Key Laboratory of Environment and Health | Chen M.,Harvard University | Li L.,Key Laboratory of Environment and Health | He M.,Key Laboratory of Environment and Health | And 11 more authors.
Circulation: Cardiovascular Genetics | Year: 2014

Background-Circulating microRNAs (miRNAs) are emerging as novel disease biomarkers. We aimed to explore the association between circulating miRNAs and the occurrence of acute myocardial infarction (AMI) in Chinese populations. Methods and Results-In the discovery stage, the plasma of 20 patients with AMI and 20 controls were pooled respectively and profiled by massively parallel sequencing. Seventy-seven miRNAs showed differential expression. Selected miRNAs were validated in 178 patients with AMI and 198 controls using quantitative reverse transcriptase polymerase chain reaction assays and further replicated in 150 patients with AMI and 150 controls. Results suggest that miR-320b and miR-125b levels were significantly lower in patients with AMI than in controls in both validation populations (P>0.0001). Lower levels of miR-320b and miR-125b were associated with increased occurrence of AMI (adjusted odds ratio, 4.71; 95% confidence interval, 2.96-7.48 and odds ratio, 4.27; 95% confidence interval, 2.84-6.41, respectively). Addition of the 2 miRNAs to traditional risk factors led to a significant improvement in the area under the curve from 0.822 (95% confidence interval, 0.787-0.856) to 0.871 (95% confidence interval, 0.842- 0.900), with a net reclassification improvement of 20.45% (P>0.0001) and an integrated discrimination improvement of 0.16 (P>0.0001) for patients with AMI. A functional study showed that miR-320b and miR-125b could regulate the expression profiles of genes enriched in several signal transduction pathways critical for coronary heart disease in human vascular endothelial cells. Conclusions-The plasma levels of miR-320b and miR-125b were significantly lower in patients with AMI when compared with controls, and these miRNAs may be involved in the pathogenesis of coronary heart disease. © 2014 American Heart Association, Inc. Source

Huang S.,U.S. Center for Disease Control and Prevention | Deng Q.,Key Laboratory of Environment and Health | Deng Q.,Huazhong University of Science and Technology | Feng J.,Key Laboratory of Environment and Health | And 11 more authors.
Journal of Occupational and Environmental Medicine | Year: 2016

Objective: We aimed to evaluate the association between polycyclic aromatic hydrocarbons (PAHs)-related microRNAs (miRNAs) and heart rate variability indices in coke oven workers. Methods: We recruited 365 male coke oven workers and measured urinary PAH metabolites by gas chromatography-mass spectrometry. Five heart rate variability indices were measured using three-channel Holter monitor. Six miRNAs were detected by TaqMan miRNA assays (Life Technologies, Foster City, CA). Results: miR-24-3p, miR-27a-3p, miR-142-5p, and miR-320b were negatively associated with the root mean of square of successive differences between adjacent normal NN intervals (RMSSD) (P trend =0.006, 0.047, 0.019, 0.011, respectively). miR-142-5p and miR-320b were also negatively associated with standard deviation of all normal to normal NN intervals (SDNN) (P trend =0.01 and 0.035). miR-24-3p, miR-27a-3p, and miR-320b were significantly interacted with multiple PAH metabolites and influenced heart rate variability indices, whereas miR-24-3p also significantly interacted with smoking to influence low frequency (P interaction <0.05 for all). Conclusions: Plasma miRNAs might act as potential biomarkers for the adverse effect of PAH exposure on the cardiovascular system. Copyright © 2015 American College of Occupational and Environmental Medicine. Source

Wei J.,Xiamen University | Sun X.,Chinese Institute of Urban Environment | Chen Y.,Chinese Institute of Urban Environment | Li Y.,Key Laboratory of Environment and Health | And 10 more authors.
Journal of Endocrinology | Year: 2014

Bisphenol A (BPA) is one of the environmental endocrine disrupting chemicals, which is present ubiquitously in daily life. Accumulating evidence indicates that exposure to BPA contributes to metabolic syndrome. In this study, we examined whether perinatal exposure to BPA predisposed offspring to fatty liver disease: the hepatic manifestation of metabolic syndrome. Wistar rats were exposed to 50 mg/kg per day BPA or corn oil throughout gestation and lactation by oral gavage. Offspring were fed a standard chow diet (SD) or a high-fat diet (HFD) after weaning. Effects of BPA were assessed by examination of hepatic morphology, biochemical analysis, and the hepatic expression of genes and/or proteins involved in lipogenesis, fatty acid oxidation, gluconeogenesis, insulin signaling, inflammation, and fibrosis. On a SD, the offspring of rats exposed to BPA exhibited moderate hepatic steatosis and altered expression of insulin signaling elements in the liver, but with normal liver function. On a HFD, the offspring of rats exposed to BPA showed a nonalcoholic steatohepatitis-like phenotype, characterized by extensive accumulation of lipids, large lipid droplets, profound ballooning degeneration, impaired liver function, increased inflammation, and even mild fibrosis in the liver. Perinatal exposure to BPA worsened the hepatic damage caused by the HFD in the rat offspring. The additive effects of BPA correlated with higher levels of hepatic oxidative stress. Collectively, exposure to BPA may be a new risk factor for the development of fatty liver disease and further studies should assess whether this finding is also relevant to the human population. © 2014 Society for Endocrinology Printed in Great Britain. Source

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