title: Electrophysiological investigation of central, peripheral and autonomic nerve function in workers with long-term low-level exposure to carbon disulphide in the viscose industry.
abstract: OBJECTIVE
  Neurotoxicity of carbon disulphide (CS2) is well known. The air concentration at the workplace at which such adverse effects can first be observed is the subject of controversial discussion.
  
  
  METHODS
  In a cross-sectional study on CS2-exposed workers peripheral motor and sensory nerve conduction studies, somatosensory evoked potentials, thermotesting and investigation of forced respiration sinus arrythmia have been carried out. The data from 222 workers exposed to CS2 in the viscose industry were evaluated and compared with data from 191 employees from the same factory with similar physical and psychological stress factors but without detectable occupational contact to neurotoxic substances. Median exposure to CS2 was below the currently valid occupational-medical threshold limit value (MAK-value) of 10 ppm. Multiple linear or multiple logistic regression analysis was used to check for statistical differences.
  
  
  RESULTS
  Binary evaluation (comparison of exposed persons versus controls after multiple linear regression) revealed a slightly lower value in the exposed group for the motor nerve conduction velocity (MNCV, -0.76 m/s, median 48 m/s), but a long way from pathological thresholds. No dose-response relationship could be found within the exposed group for any evaluation criteria of CS2-exposure. Somatosensory evoked potentials, thermotesting and analysis of heart rate variability yielded no indication of a neurotoxic effect of CS2.
  
  
  CONCLUSIONS
  Isolated decrease of MNCV in binary evaluation is, with regard to the known mechanism of CS2-neurotoxicity and the lack of a dose-response relationship, obviously not due to toxic effects. We interpret our results as showing that an adverse effect of carbon disulphide at the exposure ranges found was not detectable in the exposed group.
authors.affiliation: Department of Neurology, University of Erlangen-Nuremberg, Germany.
authors.forename: F
authors.initials: F
authors.lastname: Reinhardt
authors.forename: H
authors.initials: H
authors.lastname: Drexler
authors.forename: A
authors.initials: A
authors.lastname: Bickel
authors.forename: D
authors.initials: D
authors.lastname: Claus
authors.forename: K
authors.initials: K
authors.lastname: Ulm
authors.forename: J
authors.initials: J
authors.lastname: Angerer
authors.forename: G
authors.initials: G
authors.lastname: Lehnert
authors.forename: B
authors.initials: B
authors.lastname: Neundörfer
mesh_terms: D000328:Adult; D000395:Air Pollutants, Occupational / Q000009:adverse effects*; D001341:Autonomic Nervous System / Q000187:drug effects* / Q000503:physiopathology; D001833:Body Temperature Regulation / Q000187:drug effects / Q000502:physiology; D002246:Carbon Disulfide / Q000009:adverse effects*; D002482:Cellulose; D002490:Central Nervous System / Q000187:drug effects* / Q000503:physiopathology; D004305:Dose-Response Relationship, Drug; D005073:Evoked Potentials, Somatosensory / Q000187:drug effects / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology; D009422:Nervous System Diseases / Q000139:chemically induced* / Q000503:physiopathology; D009431:Neural Conduction / Q000187:drug effects / Q000502:physiology; D009460:Neurologic Examination / Q000187:drug effects; D010525:Peripheral Nerves / Q000187:drug effects* / Q000503:physiopathology; D012016:Reference Values; D011984:Sensory Receptor Cells / Q000187:drug effects / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects* / Q000502:physiology
chemical_list: D000395:Air Pollutants, Occupational; D002482:Cellulose; C012024:rayon, purified; D002246:Carbon Disulfide