Chronic peripheral neuropathy in workers with previous exposure to carbon disulphide.

Corsi, Gabriele; Maestrelli, Piero; Picotti, G. B.; Manzoni, S; Negrin, P

doi:10.1136/oem.40.2.209

Cited by 14 publications

(13 citation statements)

References 3 publications

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“…It should be kept in mind that the findings are slight at both neurological and neurophysiological investigations and that the mean age of the workers is relatively high. However, Seppäläinen and Tolonen [1974] found electrophysiological polyneuropathy in 48% of long-term CS 2 -exposed men, whereas Corsi et al [1983] found both clinical and electromyographic evidence of neuropathy in 36% of 33 rayon viscose workers 10 years after discontinuation of exposure.…”

Section: Discussionmentioning

confidence: 96%

Carbon disulfide exposure and neurotoxic sequelae among viscose rayon workers

Aaserud

Hommeren

Tvedt

et al. 1990

American J Industrial Med

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In Norway's only viscose rayon plant, carbon disulfide (CS2) concentrations in ambient air usually were between 30 and 50 mg/m3 during the first 23 years of production. From 1970/1971 until the factory was closed in 1982, corresponding values were 10-25 mg/m3. Through all of these years, high peak exposures of CS2 and H2S 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 CS2-induced encephalopathy was reached in eight workers; another six had an encephalopathy in which CS2 exposure was regarded as a partial cause. Correspondingly, seven had a neuropathy probably caused by CS2 exposure alone; in three others, CS2 was found to be the partial cause of a neuropathy. This indicates that long-term, relatively moderate exposure to CS2 in association with high peak exposures to CS2 and H2S involves a substantial risk of developing neurotoxic disease.

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Section: Discussionmentioning

confidence: 96%

Carbon disulfide exposure and neurotoxic sequelae among viscose rayon workers

Aaserud

Hommeren

Tvedt

et al. 1990

American J Industrial Med

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“…Some studies have reported an improvement in NCV after removal of occupational exposure to CS2 [17][18][19] . Huang et al 17 ) observed a tendency toward an improvement in NCV in 6 polyneuropathy patients with 3 years of followup.…”

Section: Discussionmentioning

confidence: 99%

Changes of median nerve conduction velocity in rayon manufacturing workers: A 6-year cohort study

Yoshioka¹,

Takebayashi²,

Nishiwaki³

et al. 2017

Journal of Occupational Health

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Objectives:We conducted a 6-year cohort study to evaluate the relationship between carbon disulfide (CS2) exposure and reductions in the motor and sensory nerve conduction velocity (MCV and SCV) of the median nerve. Methods : Study subjects at baseline included 432 exposed workers and 402 unexposed workers. Among the exposed workers, 145 workers terminated CS2 exposure during the followup period ( ex-exposed workers ) . MCV and SCV were measured at baseline and followed up. CS 2 personal exposure concentration was measured two times a year during a 6-year follow-up period and mean (range) CS2 exposure concentrations ( ppm ) were 5.96 (0.8-16.0) and 3.93 (0.6-9.9) in the exposed and ex-exposed workers, respectively. Results: Reductions in MCV during the follow-up period did not differ among the exposed, ex-exposed, and unexposed workers. Reduction in SCV (m/s) of the exposed workers (-4.47±3.94) was significantly larger than that of the unexposed (-3.38±3.97) and ex-exposed workers (-3.26±3.79). For SCV reduction, a partial multiple regression coefficient of (exexposed workers)/(unexposed workers) was significantly positive (+0.915, p < 0.01) after adjustment for confounding variables. Conclusions : This cohort study showed that 6-year CS 2 exposure around a mean level of 6 ppm did not affect MCV reduction but induced significant SCV reduction beyond the influence of aging. The effect of CS2 on SCV around a mean exposure level of 4 ppm may be reversible, since it disappeared in the ex-exposed workers after CS 2 exposure cessation for a mean period of 4.1

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“…In a reexamination of a group of patients with chronic carbon disulfide neuropathy, findings consistent with an irreversible axonal change were found (20). In delayed neuropathy of acute organophosphorous pesticide poisoning, electromyography reveals changes of denervation in nearly every case.…”

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confidence: 90%

Occupational toxic neuropathies--an update.

He¹

1985

Scand J Work Environ Health

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Occupational toxic neuropathies--an update.by He F This article in PubMed: www.ncbi.nlm.nih.gov/pubmed/2999969 REVIEWS Scand j work environ health II (1985) [321][322][323][324][325][326][327][328][329][330] Occupational toxic neuropathies -An update by Fengsheng He, MD1 HE F. Occupational toxic neuropathies -An update. Scand J Work Environ Health II (1985) 321-330. Peripheral neuropathy is the commonest neurol ogical syndrome produced by indu strial and agricultural chemicals. A number of chemicals have been recently found to be neurotoxins; in addition some known occupational neurotoxic hazards more often produ ce subtle alterat ions in the peripher al nervous system. Ther e have been problem s of both evaluating neuroto xic effects and identifying toxic causes. This article reviews and discusses th e current research and progress covering neurophysiological, neuropathological, biochemical , and epidemiologic approaches in clinical and experimental neurotoxicology, as related to the assessment and path ogenesis of occupa tion al toxic neuropathies.Key terms: assessment , clinical neur ophysiological testing, distal axonopathy, epidemiologic investigation, identi fication, neuropathological approach, pathogenesis, toxic causes.Alon g with the development of various chemical industries there has been a growing list of indu strial chemicals which can cause damage to the peripheral nervous system . On the other hand, occupational exposure to low levels of known neurotoxins more oft en causes subtle alterations of peripheral nervous function. This occurrence raises problems in occupational health practice and stimulates research concerning the early diagnosi s and prevention of occupational toxic neuropathies. In the meantime , modern technique s of neurophysiology, neuropathology, and biochemistry have been introduced and utilized to explore the mechani sms of some neurotoxic effects . All these methods lead to a substantial amount of progress in evaluat ing and understanding occupational toxic neuropathies, which have been reviewed in this article. PROGRESS IN ASSESSMENT AND IDENTIFICATIONThe diagnosis of chemically-induced neuropathies can be reasonably made in those subj ects who have a verified history of exposure to neurotoxins and characteristic clinical evidence of neuropathy with exclusion of other causative factors. But there are some asymptomatic individuals under neurotoxicologic risk who may be suspected of having subclinical peripheral neuropathies and, on the other hand, a number of symptomatic patients having the presumptive diagnosis of polyneuropathy without a known etiology. In these cases, the question of either the existence or the etiology of the peripheral neuropathies remain s to be settled. Detection of neurotoxic effects on the peripheral nervous system

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Chronic peripheral neuropathy in workers with previous exposure to carbon disulphide.

Cited by 14 publications

References 3 publications

Carbon disulfide exposure and neurotoxic sequelae among viscose rayon workers

Carbon disulfide exposure and neurotoxic sequelae among viscose rayon workers

Changes of median nerve conduction velocity in rayon manufacturing workers: A 6-year cohort study

Occupational toxic neuropathies--an update.

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