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Description of key information

See discussion below

Key value for chemical safety assessment

Additional information

The studies provide information on the neurophysiological, histopathological, neurochemical, and behavioural effects associated with subacute, subchronic and/or chronic CS2 exposure. The studies have usually been done in rats. In summary it was demonstrated that CS2 exposure at high concentrations resulted in:

* Nerve conduction velocity alterations - Subacute, subchronic and chronic exposure of rats to CS2 at 285 and 507 ppm produced reduced conduction velocity in the sciatic and tibial nerve, which was fully or partly reversible, depending on the concentration and exposure time (Knobloch et al., 1979). Exposure of rats to 500 or 800 ppm CS2 for 13 weeks decreased the ventral caudal tail nerve conduction velocity (Herr et al., 1988). Nerve conduction dysfunction in the auditory brainstem responses was detected by Hirata et al. (1992), who exposed female rats to 800 ppm CS2 by inhalation 6 h a day, 5 days a week, for 15 weeks. Gagnaire et al. (1986) demonstrated that exposure of rats to 500 ppm of CS2 via inhalation, 5 days a week for 25 weeks, results in reduced peripheral nerve conduction velocity (sensory & motor tail nerve).

Changes in behaviour - Two weeks of exposure to CS2 at 250 ppm, exhibited effects on behaviour, with an inhibition of avoidance response to shocks (Goldberg et al. 1964). Marked gait abnormalities were seen in rats exposed to 396 ppm of CS2 for 12 weeks (Sun et al., 2009), or treated orally with 300 mg/kg bw for 12 weeks (Sills et al., 2006a&b).

* Hearing and visual damage - Irreversible severe reductions in visual acuity with degeneration of retinal ganglion cells (Merigan et al. 1988), axonal swelling of the optical nerve (Eskin et al. 1988), as well as loss of hearing (Rebert & Becker, 1986), after exposure of monkeys to 256 ppm for 6 h/d, 5 d/w, 5 -13 w.

* Neuromuscular dysfunction - Symptoms of motor impairment (Frantik, 1970- 770 ppm for 8 w), manifested in the hind-limbs (Colombi et al., 1981- rats, 700 ppm, 5 h/d, 5d/w for 12 w; Moser et al., 1998 -rats, 500 ppm, for 13 w) or decreased neuromuscular integrity (Clerici & Fecher, 1991 -rats, 500 ppm, 5 -12 w).europathology - Neuron axonal swelling in the peripheral as well as in the central nervous system (Sills et al., 1988; Valentine et al., 1998; Valentine et al., 1997, Towes et al., 1998, Sills et al., 2000), usually accompanied by neurofilamentous accumulation, due to covalent cross-linking (Valentine et al., 1998; Valentine et al., 1997; Song et al., 200a & b) and myelin thinning (Sills et al., 1998). Axonal swelling was usually detected at concentrations of 500 ppm and above, while the neurofilamentous cross-linking was seen at 50 ppm, although significant only at 13 weeks (Valentine et al., 1997 & 1998), and axonal swelling was not detected at this level.

The recently carried out EOGRTS (see section 7.8.1) did not show changes in neurobehaviour or neurodevelopmental toxicity up to and including 120 mg/kg bw/day.

Justification for classification or non-classification

The results of the studies concerned with the neurotoxicity and related effects of carbon disulfide in experimental animals (see also section 7.5.2 and 7.9.4) combined with the effects of the compound on the nervous system that have been observed in humans, may point to the need for classification for specific target organ toxicity (STOT) repeated exposure (RE). However, in animals significant neurotoxicity was generally seen at high doses (viz. >100 mg/kg bw) or at high concentrations (viz. > 200 mg/m3 (63.5 ppm)). It would therefore maximally justify for Category 2 (inhalation exposure).