title: Blood oxidative stress in Taiwan workers exposed to carbon disulfide.
abstract: BACKGROUND
  Overexposure to carbon disulfide (CS(2) ) has been associated with an increase in coronary heart disease, but the mechanisms mediating this effect remain unclear. We aimed to examine the relationship between CS(2) exposure and oxidative stress markers, in order to clarify the oxidative mechanisms involved in CS(2) -induced atherosclerosis.
  
  
  METHODS
  A total of 89 workers from a viscose rayon plant were recruited for this study, and 111 workers not exposed to CS(2) served as controls. Cholesterol, triglyceride, malondialdehyde (MDA), superoxide dismutase (SOD), catalase, GSH peroxidase, as well as total antioxidants were analyzed.
  
  
  RESULTS
  The workers exposed to CS(2) had significantly higher MDA levels and lower SOD levels than the controls. The average MDA levels were 776 ± 268.2 (240-1,220) in the high exposure (≥10 ppm; n = 38), 751.6 ± 274 (170-1,320) in the low exposure (<10 ppm; n = 51), and 550.4 ± 199 (115-1,050) mM in the control group (n = 111). The average SOD levels were 36.5 ± 38.8 (0-223.5), 39.3 ± 38.8 (0-160), and 58.8 ± 60.8 (5.25, 400) U/ml in the high exposure-, low exposure-, and control group, respectively. MDA level increased significantly at a cumulative CS(2) exposure of over 60 ppm-years. Dyslipoproteinemia was borderline significantly associated with CS(2) exposure and MDA level.
  
  
  CONCLUSIONS
  These results indicate that CS(2) exposure can induce oxidative stress as well as reduce the levels of antioxidative enzymes, and that a cumulative exposure level of 60 ppm-years may be a threshold value for the oxidative and the antioxidant response. Am. J. Ind. Med. 54:637-645, 2011. © 2011 Wiley-Liss, Inc.
authors.affiliation: Chang Gung Medical College, Tao Yuan, Taiwan, Republic of China. luo5485@ms29.hinet.net
authors.forename: Jiin-Chyuan John
authors.initials: JC
authors.lastname: Luo
authors.forename: Tung-Sheng
authors.initials: TS
authors.lastname: Shih
authors.forename: Cheng-Ping
authors.initials: CP
authors.lastname: Chang
authors.forename: Chin-Chang
authors.initials: CC
authors.lastname: Huang
mesh_terms: D000328:Adult; D000395:Air Pollutants, Occupational / Q000633:toxicity*; D000975:Antioxidants / Q000032:analysis; D050197:Atherosclerosis / Q000097:blood / Q000139:chemically induced* / Q000201:enzymology; D015415:Biomarkers / Q000097:blood; D002246:Carbon Disulfide / Q000633:toxicity*; D002374:Catalase / Q000097:blood; D002482:Cellulose; D002784:Cholesterol / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D005979:Glutathione Peroxidase / Q000097:blood; D006801:Humans; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D009784:Occupational Diseases / Q000097:blood / Q000139:chemically induced* / Q000201:enzymology; D016273:Occupational Exposure / Q000009:adverse effects*; D018384:Oxidative Stress; D013482:Superoxide Dismutase / Q000097:blood; D013624:Taiwan; D013784:Textiles; D014280:Triglycerides / Q000097:blood
chemical_list: D000395:Air Pollutants, Occupational; D000975:Antioxidants; D015415:Biomarkers; D014280:Triglycerides; D008315:Malondialdehyde; D002482:Cellulose; D002784:Cholesterol; C012024:rayon, purified; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D002246:Carbon Disulfide