Carbon disulfide exposure induced lung function reduction partly through oxidative protein damage: A cross-sectional and longitudinal analysis.

[1]  T. Shi,et al.  Cross-sectional and longitudinal relationships between urinary 1-bromopropane metabolite and pulmonary function and underlying role of oxidative damage among urban adults in the Wuhan-Zhuhai cohort in China. , 2022, Environmental pollution.

[2]  Weihong Chen,et al.  Cross-sectional and longitudinal associations of acrolein exposure with pulmonary function alteration: Assessing the potential roles of oxidative DNA damage, inflammation, and pulmonary epithelium injury in a general adult population. , 2022, Environment international.

[3]  Weihong Chen,et al.  Acrylamide exposure increases cardiovascular risk of general adult population probably by inducing oxidative stress, inflammation, and TGF-β1: A prospective cohort study. , 2022, Environment international.

[4]  W. Guan,et al.  Gene expression of oxidative stress markers and lung function: A CARDIA lung study , 2021, Molecular genetics & genomic medicine.

[5]  Weihong Chen,et al.  Longitudinal relationships between polycyclic aromatic hydrocarbons exposure and heart rate variability: Exploring the role of transforming growth factor-β in a general Chinese population. , 2021, Journal of hazardous materials.

[6]  Yohan Han,et al.  CC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells during Klebsiella pneumoniae Infection , 2021, International journal of molecular sciences.

[7]  Y. Wan,et al.  Repeated measurements of 21 urinary metabolites of volatile organic compounds and their associations with three selected oxidative stress biomarkers in 0-7-year-old healthy children from south and central China. , 2021, Chemosphere.

[8]  Limin Cao,et al.  Acrylamide exposure and pulmonary function reduction in general population: The mediating effect of systemic inflammation. , 2021, The Science of the total environment.

[9]  Jianhua Tan,et al.  Exposure to volatile organic compounds may be associated with oxidative DNA damage-mediated childhood asthma. , 2021, Ecotoxicology and environmental safety.

[10]  Limin Cao,et al.  Associations of urinary carbon disulfide metabolite with oxidative stress, plasma glucose and risk of diabetes among urban adults in China. , 2020, Environmental pollution.

[11]  Limin Cao,et al.  Acrylamide Exposure and Oxidative DNA Damage, Lipid Peroxidation, and Fasting Plasma Glucose Alteration: Association and Mediation Analyses in Chinese Urban Adults , 2020, Diabetes Care.

[12]  Weihong Chen,et al.  Plasma CC16 mediates the associations between urinary metals and fractional exhaled nitric oxide: A cross-sectional study. , 2019, Environmental pollution.

[13]  D. Riggs,et al.  National secular trends in ambient air volatile organic compound levels and biomarkers of exposure in the United States. , 2019, Environmental research.

[14]  Yang Zhang,et al.  8-Hydroxy-2’-deoxyguanosine as a biomarker of oxidative stress in acute exacerbation of chronic obstructive pulmonary disease , 2019, Turkish journal of medical sciences.

[15]  D. Giustarini,et al.  Protein carbonylation in human bronchial epithelial cells exposed to cigarette smoke extract , 2019, Cell Biology and Toxicology.

[16]  Jing Yuan,et al.  Association of lung function with cardiovascular risk: a cohort study , 2018, Respiratory Research.

[17]  Lingxin Chen,et al.  Evaluation Selenocysteine Protective Effect in Carbon Disulfide Induced Hepatitis with a Mitochondrial Targeting Ratiometric Near-Infrared Fluorescent Probe. , 2018, Analytical chemistry.

[18]  Yun-Chul Hong,et al.  Association between phthalate exposure and lower lung function in an urban elderly population: A repeated-measures longitudinal study. , 2018, Environment international.

[19]  Jing Yuan,et al.  Urinary polycyclic aromatic hydrocarbon metabolites, Club cell secretory protein and lung function. , 2018, Environment international.

[20]  Daniel R. Schonhaut,et al.  Tau pathology and neurodegeneration contribute to cognitive impairment in Alzheimer’s disease , 2017, Brain : a journal of neurology.

[21]  J. Llorens,et al.  Continuous exposure to low‐frequency noise and carbon disulfide: Combined effects on hearing , 2017, Neurotoxicology.

[22]  Shuo Wang,et al.  Oxidative Stress Mediated Hippocampal Neuron Apoptosis Participated in Carbon Disulfide-Induced Rats Cognitive Dysfunction , 2016, Neurochemical Research.

[23]  P. C. Ford,et al.  Carbon disulfide. Just toxic or also bioregulatory and/or therapeutic? , 2017, Chemical Society reviews.

[24]  M. Dellarco,et al.  Assessment of Exposure to VOCs among Pregnant Women in the National Children’s Study , 2016, International journal of environmental research and public health.

[25]  M. Imboden,et al.  Relation between circulating CC16 concentrations, lung function, and development of chronic obstructive pulmonary disease across the lifespan: a prospective study. , 2015, The Lancet. Respiratory medicine.

[26]  J. Patel,et al.  Carbon Disulfide (CS2) Mechanisms in Formation of Atmospheric Carbon Dioxide (CO2) Formation from Unconventional Shale Gas Extraction and Processing Operations and Global Climate Change , 2015, Environmental health insights.

[27]  Tangchun Wu,et al.  The Wuhan-Zhuhai (WHZH) cohort study of environmental air particulate matter and the pathogenesis of cardiopulmonary diseases: study design, methods and baseline characteristics of the cohort , 2014, BMC Public Health.

[28]  W. Uter,et al.  Current and historical individual data about exposure of workers in the rayon industry to carbon disulfide and their validity in calculating the cumulative dose , 2014, International Archives of Occupational and Environmental Health.

[29]  Y. Yuan,et al.  Oxidative stress and DNA damage in utero and embryo implantation of mice exposed to carbon disulfide at peri-implantation , 2014, Human & experimental toxicology.

[30]  Alisa Rich,et al.  An exploratory study of air emissions associated with shale gas development and production in the Barnett Shale , 2014, Journal of the Air & Waste Management Association.

[31]  B. Blount,et al.  Simultaneous analysis of 28 urinary VOC metabolites using ultra high performance liquid chromatography coupled with electrospray ionization tandem mass spectrometry (UPLC-ESI/MSMS). , 2012, Analytica chimica acta.

[32]  T. Tsuji,et al.  DNA damage as a molecular link in the pathogenesis of COPD in smokers , 2012, European Respiratory Journal.

[33]  Chin‐Chang Huang,et al.  Blood oxidative stress in Taiwan workers exposed to carbon disulfide. , 2011, American journal of industrial medicine.

[34]  T. Treasure,et al.  Oxidative modification of albumin in the parenchymal lung tissue of current smokers with chronic obstructive pulmonary disease , 2010, Respiratory research.

[35]  S. London,et al.  Pesticide use and adult-onset asthma among male farmers in the Agricultural Health Study , 2009, European Respiratory Journal.

[36]  Hao-feng,et al.  Changes of lipid peroxidation in carbon disulfide-treated rat nerve tissues and serum. , 2009, Chemico-biological interactions.

[37]  L. Jönsson,et al.  Lung Function in Relation to 2-Thiothiazolidine-4-Carboxylic Acid and Genetic Effect Modification Among Rubber Workers in Sweden , 2008, Journal of occupational and environmental medicine.

[38]  Jing Yuan,et al.  Elevated serum polybrominated diphenyl ethers and thyroid-stimulating hormone associated with lymphocytic micronuclei in Chinese workers from an E-waste dismantling site. , 2008, Environmental science & technology.

[39]  A. von Eckardstein,et al.  Evidence for oxidative stress at elevated plasma thiol levels in chronic exposure to carbon disulfide (CS2) and coronary heart disease. , 2007, Nutrition, metabolism, and cardiovascular diseases : NMCD.

[40]  J. Hankinson,et al.  Standardisation of spirometry , 2005, European Respiratory Journal.

[41]  Y. Nishiwaki,et al.  A six year follow up study of the subclinical effects of carbon disulphide exposure on the cardiovascular system , 2004, Occupational and Environmental Medicine.

[42]  Mark B Pepys,et al.  C-reactive protein: a critical update. , 2003, The Journal of clinical investigation.

[43]  T. Shih,et al.  Accumulation of urinary 2-thiothiazolidine-4-carboxylic acid (TTCA) among workers occupationally exposed to carbon disulfide for 1 week. , 2003, The Science of the total environment.

[44]  J. Nofer,et al.  Increased oxidative stress in subjects exposed to carbon disulfide (CS2) – an occupational coronary risk factor , 2002, Archives of Toxicology.

[45]  D. De Bacquer,et al.  The cross‐sectional study of the health effects of occupational exposure to carbon disulfide in a Chinese viscose plant , 2001, Environmental toxicology.

[46]  E. Stadtman,et al.  Protein Oxidation in Aging and Age‐Related Diseases , 2001, Annals of the New York Academy of Sciences.

[47]  L. Jian,et al.  Antioxidative stress response in workers exposed to carbon disulfide , 2000, International archives of occupational and environmental health.

[48]  F. Pallardó,et al.  Contraction of human airways by oxidative stress protection by N-acetylcysteine. , 1999, Free radical biology & medicine.

[49]  H. Schünemann,et al.  Oxidative stress and lung function. , 1997, American journal of epidemiology.

[50]  S. Q. Que Hee,et al.  Urinary 2-Thiothiazolidine-4-Carboxylic Acid (TTCA) as the Major Urinary Marker of Carbon Disulfide Vapor Exposure in Rats , 1996, Toxicology and industrial health.

[51]  T. Stijnen,et al.  Oxidative epithelial damage produces hyperresponsiveness of human peripheral airways. , 1994, American journal of respiratory and critical care medicine.

[52]  S Greenland,et al.  Modeling and variable selection in epidemiologic analysis. , 1989, American journal of public health.

[53]  R. A. Neal,et al.  Oxidative metabolism of carbon disulfide by isolated rat hepatocytes and microsomes. , 1987, Biochemical pharmacology.

[54]  L. Delbressine,et al.  Identification and determination of 2-thiothiazolidine-4-carboxylic acid in urine of workers exposed to carbon disulfide , 1981, Archives of Toxicology.

[55]  P. Apostoli,et al.  [Validity of urinary 2-thiothiazolidine-4-carboxylic acid (TTCA) as biomarker of exposure to very low concentrations of carbon disulphide: preliminary results]. , 2008, Giornale italiano di medicina del lavoro ed ergonomia.

[56]  H. Lebel With Carbon Disulfide , 2005 .

[57]  D. Anthony,et al.  Pathogenetic studies of hexane and carbon disulfide neurotoxicity. , 1995, Critical reviews in toxicology.

[58]  K. Peltonen,et al.  Assessment of exposure to carbon disulfide in viscose production workers from urinary 2-thiothiazolidine-4-carboxylic acid determinations. , 1992, American journal of industrial medicine.