Occupational exposure to low concentrations of carbon disulfide as a risk factor for hypercholesterolaemia.

Objective: The objective of this study was to investigate the effect of occupational exposure to carbon disulfide (CS2) concentrations below threshold limit value (TLV)-time-weighted average (TWA) (31 mg/m3) on total cholesterol, blood pressure and the prevalence of coronary heart disease (CHD).
Methods: A cross-sectional study involving 141 viscose rayon workers (64 men), and 141 age- and gender-matched controls without occupational contact with noxious chemicals, was carried out. The probability for CHD was determined by means of the WHO questionnaire and was 12-lead electrocardiography-coded using Minnesota criteria. Blood pressure was measured by the standardized method of the WHO and blood was examined for total cholesterol. A cumulative exposure index (CS2 index) was calculated for each worker by multiplying the number of years held in a particular job, by the CS2 concentrations in that job-environment. According to the CS2 index, the exposed workers were distributed into two groups: group 1 (CS2 index < 100) and group 2 (CS2 index > or = 100).
Results: Depending on the job and specific work place the CS2 concentrations were between 1 and 30 mg/m3. Cholesterol levels were significantly higher in the exposed group (4.9 +/- 0.7) compared with the controls (4.6 +/- 0.7). Adjustment for age, smoking, body-mass index (BMI) and gender showed the significant effect of the CS2 index on the total cholesterol (P < 0.001). The prevalence of hypercholesterolaemia was significantly higher in the exposed group (42.6%), compared with the controls (26.2%); odds ratio (OR) (adjusted for potential confounders) was 2.56, 95% CI 1.47-4.46. Logistic regression showed a significantly increased risk for elevated cholesterol in group 2 (OR 5.52; 95% CI 2.81-10.83). No significant effect of CS2 index on blood pressure and CHD prevalence was found.
Conclusions: The results of our study show that occupational exposure to CS2 concentrations below 31 mg/m3 and a CS2 index > 100 may increase total cholesterol. Our results imply that even the CS2 concentrations below TLV-TWA may produce morbid changes, and suggest the mechanism of the effect of CS2, leading to lipid metabolism disturbances and acceleration of atherosclerosis.