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Overexposure to carbon disulfide (CS2) 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 CS2 exposure and oxidative stress markers, in order to clarify the oxidative mechanisms involved in CS2-induced atherosclerosis.A total of 89 workers from a viscose rayon plant were recruited for this study, and 111 workers not exposed to CS2 served as controls. Cholesterol, triglyceride, malondialdehyde (MDA), superoxide dismutase (SOD), catalase, GSH peroxidase, as well as total antioxidants were analyzed.The workers exposed to CS2 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 CS2 exposure of over 60 ppm-years. Dyslipoproteinemia was borderline significantly associated with CS2 exposure and MDA level.These results indicate that CS2 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.