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Carbon disulfide exposure and neurotoxic sequelae among viscose rayon workers
Author(s) -
Aaserud Olaf,
Hommeren Ole Jörgen,
Tvedt Björn,
Nakstad Per,
Mowé Gunnar,
Efskind Jon,
Russell David,
Jörgensen Eva B.,
NybergHansen Rolf,
Rootwelt Kjell,
Gjerstad Leif
Publication year - 1990
Publication title -
american journal of industrial medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.7
H-Index - 104
eISSN - 1097-0274
pISSN - 0271-3586
DOI - 10.1002/ajim.4700180104
Subject(s) - medicine , viscose , encephalopathy , subclinical infection , anesthesia , carbon disulfide , transcranial doppler , electroencephalography , cerebral atrophy , atrophy , psychiatry , chemistry , materials science , organic chemistry , composite material
In Norway's only viscose rayon plant, carbon disulfide (CS 2 ) concentrations in ambient air usually were between 30 and 50 mg/m 3 during the first 23 years of production. From 1970/1971 until the factory was closed in 1982, corresponding values were 10–25 mg/m 3 . Through all of these years, high peak exposures of CS 2 and H 2 S occurred. In 1986, 16 of the 24 men still at work in 1982 and with at least 10 years' experience in the spinning room agreed to participate in this study. Clinical neurological examination demonstrated abnormalities in 15; neuropsychological tests showed impairments of probable organic origin in 14. Thirteen had cerebral atrophy demonstrated by cerebral computed tomography (CT). Electromyography (EMG) was abnormal in six, neurography in 11. Regional cerebral blood flow measurements indicated flow asymmetries in eight, whereas Doppler investigation of the extracranial carotid and vertebral arteries, electroencephalography (EEG), and evoked response investigations were mostly normal. Based on these results and the exposure data, a diagnosis of CS 2 ‐induced encephalopathy was reached in eight workers; another six had an encephalopathy in which CS 2 exposure was regarded as a partial cause. Correspondingly, seven had a neuropathy probably caused by CS 2 exposure alone; in three others, CS 2 was found to be the partial cause of a neuropathy. This indicates that long‐term, relatively moderate exposure to CS 2 in association with high peak exposures to CS 2 and H 2 S involves a substantial risk of developing neurotoxic disease.