Abstract
In 1967 two cohorts of 343 men each were formed and matched with respect to age, district of birth, and similarity of work. One cohort comprised viscose rayon workers with at least five years' exposure to carbon disulphide during any period between 1942 and 1967, and the other cohort consisted of workers from a paper-mill with no such exposure. The concentrations of carbon disulphide and hydrogen sulphide in the workroom air had been measured regularly since 1950, and about 4000 measurements were available. In all probability the concentrations had been very high in the 1940s, between 20 and 40 ppm in the 1950s, and about 10 to 30 ppm from 1960 onwards. On examination in 1967 it was confirmed that all of the relevant coronary risk factors had been kept under control. The only exception to this was blood pressure which was slightly higher among the exposed workers, a finding that was interpreted as a result of exposure rather than an independent risk factor. A five-year follow-up showed that 14 men had died from coronary heart disease (CHD) in the exposed group, against three in the control group (P smaller than 0:007). Other causes of death were evenly distributed. In addition, 11 nonfatal first infarctions had occurred in the exposed group as compared with four in the control group. On re-examination in 1972, nearly 25% of the exposed men, against 13% of the controls, had a history of angina (typical, probable, and possible) as measured by the World Health Organization questionnaire (P smaller than 0:0002). The prevalence proportions of typical angina were 12% and 5% respectively (P smaller than 0:001). As opposed to this, only slight differences were apparent for coronary ECGs. The higher degrees of prevalance in the exposed group may well have been attributable to chance. As in 1967/68, the mean systolic and diastolic blood pressures were slightly higher in the exposed group (P smaller than 0:001 and P smaller than 0:01, respectively). The relative risk was 4-8 for fatal attacks, 3-7 for all infarctions, 2-8 for nonfatal infarctions, 2-2 for angina, and 1-4 for ECG findings indicative of CHD. This implies that with increasing severity and specificity of the manifestations the causal role of CS2 in developing CHD becomes more evident. Further, it is inferred that exposure to CS2 seems to worsen the prognosis of CHD in addition to increasing its incidence. Although the exposure data in this study may not be representative of the personal exposure of the workers, the conclusion is drawn that a great deal of justification exists for lowering the threshold limit value of 20 ppm recommended by the American Conference of Governmental Industrial Hygienists.