To evaluate risk factors for coronary heart disease and factors which can influence the course of acute myocardial infarction in workers exposed to CS2 we performed a cross-sectional study of 247 workers in the viscose industry. The control group of 222 men from the same plant was comparable for age, social status and physical work. The CS2 exposure determined by personal air sampling ranged from < 0.2 ppm to 65.7 ppm (median: 4.0 ppm) and the duration of exposure ranged from 4 to 220 (median: 66) months. Using a multiple linear regression model we found neither higher blood pressure at rest or after exercise, nor hyperlipoproteinaemia in a higher degree, nor lower high-density lipoprotein (HDL) or lower apolipoprotein A-I levels, nor higher blood glucose values, nor indicators of direct cardiotoxic effects or signs of disturbances in blood coagulation in the exposed group in comparison to controls. Regarding the influence of chronic exposure on the investigated parameters, we found an inverse correlation of the cumulative exposure (mean CS2 exposure in the department multiplied by the duration of work in this department) with the HDL concentration. The HDL levels correlated with the duration but not with the intensity of exposure. In the same way the apolipoprotein A-I levels showed a negative association with the duration of exposure in the exposed group as well as in the control group. The HDL concentrations showed the same trend for the controls. It therefore seems that this finding is more likely due to confounding factors than to the CS2 exposure. As all subjects (exposed and controls) have done shift work, in some cases for a long time, this kind of work could be responsible for the negative relationship between the duration of employment as a shift worker and the apolipoprotein A-I and HDL levels. At the current air-borne levels no significant differences were found between the exposed persons and the controls in the distribution frequency for blood pressure values, lipoproteins, blood glucose, blood coagulation and indicators of direct cardiotoxic effects.