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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

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Subchronic exposure to CS2 at 225 ppm caused cardio-depressive effects and hypertension in rats, which were manifested before the appearance of histologic lesions in the brain, heart, lung, liver and kidneys (Morvai et al., 2005). Effects as distubances of lipid metabolism and accumulation in the coronary arteries, metabolic and structural changes in the myocardium and the aorta, and myocardial lesions were reported by the following authors Antov et al. (1985), Chandra et al. (1972), Wronska-Nofer et al. (1980), and Lewis et al. (1999). Such effects were observed at low levels. For instance exposure to 16 ppm and higher lead to cardiotoxicity, as revealed by distention of the lumen, attenuation of myocardial vessels, irregular thickening of the aorta wall, as well as several biochemical changes. The authors suggest a direct action of the substance on the heart muscle and the aorta (Antov et al., 1985). However due to limitations (Klimisch 4) it is not well possible to judge the quality of these studies.

Tarkowski & Sobczak, (1971) indicated that acute and chronic exposure of rats to 803 and 578 ppm, respectively, resulted in similar metabolic disturbances in the brain mitochondria. Short-term exposure of rats to relatively high levels of carbon disulfide (2000 mg/m3) caused altered catecholamine levels in the brain and adrenals, and increases in dopamine and its metabolites (Caroldi et al., 1984). Similarly, in the investigation of McKenna et al. (1977) inhalation of CS2 for several hours produced decreases of brain, adrenal and cardiac norepinephrine, as well as adrenal epinephrine concentrations. CS2 exposure at 476 ppm lead to a marked reduction in cytochrome P-450 and cytochrome c-reductase after 2-3 days, that returned to normal levels by the 23rd d of treatment. Exposure resulted also in increased lipid peroxidation in the liver (Järvisalo et al., 1977). Inhalation exposure of female Wistar rats to 200 ppm of CS2 for 8 h/d for 7 days caused no fatty infiltration of the liver (Freundt et al., 1974). Again, due to limitations (Klimisch 4) it is not well possible to judge the quality of these studies.


Oral administration of carbon disulfide resulted in transient decreases in blood pressure, ECG changes (Hoffmann & Klapperstuck, 1990), and liver drug-metabolizing system disturbances (Masuda et al., 1986). Klapperstuck et al. (1991) postulate that subacute oral exposure has a direct cardiotoxic effect, that might be mediated by the disruption of the energy supply in the heart. Oral treatment with 1 ml/kg of CS2 resulted in fat accumulation in the liver, and increases of liver transaminases in the serum (Freundt et al., 1974).

However due to limitations (Klimisch 4) it is not well possible to judge the quality of most of these studies.