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C Xintaras

Publications and source records attributed to C Xintaras.

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Effects on the peripheral nervous system of workers' exposure to carbon disulfide.

An evaluation of the effects of occupational exposure to carbon disulfide was performed in a sample of 156 male viscose rayon workers. A composite group of 233 workers drawn from two other artificial fiber plants located on the same premises as the rayon plant was used for comparison. Effects of CS2 on the peripheral nervous system (PNS) were evaluated in ulnar and peroneal nerves using measurements of maximum motor nerve conduction velocity (MCV) and distal latency; and sensory conduction velocity (SCV) in the sural nerve. Self-reported symptoms related to PNS disorders were also obtained from each study participant. Industrial hygiene records showed the rayon workers to have had CS2 exposures that generally had not exceeded 20 ppm. The overall mean number of years of CS2 exposure was 12.1 years (+/- 6.9 S.D.). The viscose rayon workers were divided prior to the study into three groups according to historical mean CS2 levels calculated for job titles, and area and personal CS2 samples were obtained during the conduct of the study to characterize each job. For these three groups the median CS2 levels were measured to be 1.0, 4.1 and 7.6 ppm. The comparison group's median CS2 level approximated 0.2 ppm. Results showed CS2-exposed workers to have small but statistically significant (p less than .05) reductions in sural SCV and peroneal MCV. Other neurophysiological measures consisting of distal latency, residual latency, and muscle or nerve action potential amplitudes showed no significant differences between study groups. A reduction in the ratio of amplitudes of muscle action potentials obtained from peroneal nerve stimulation was significant (p less than .05). Reductions in the peroneal nerve MCV were found to be related, in a dose response sense, to workers' cumulative exposure to CS2. No increase attributable to CS2 was found in the prevalence of symptoms related to PNS disorders. The results from this study generally agree with similar findings from Finland, Sweden and Italy, but at CS2 exposure levels lower than those previously reported for occupational exposure.

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Clinical epidemiology of occupational neurotoxic disease.

Occupational exposures to neurotoxic chemicals have produced large outbreaks of illness in chemical and pesticide workers worldwide. Outbreaks of occupational neurologic disease in the United States have included (1) the Kepone episode in Hopewell, Virginia, in which 76 workers at a pesticide plant producing the chlorinated hydrocarbon insecticide, Kepone, developed a previously unrecognized syndrome of nervousness, tremor, ataxia, weight loss, opsoclonus, pleuritic and joint pain, and oligospermia; (2) an outbreak of 104 cases of autonomic neuropathy in polyurethane foam workers in Marblehead, Massachusetts, manifest principally by urinary bladder dysfunction, which followed exposure to a new catalyst, dimethylaminopropionitrile (DMAPN); and (3) an outbreak of acute mixed motor and sensory neuropathy in 48 plastic fabric workers in Columbus, Ohio, exposed to the solvent methyl butyl ketone (MBK). These outbreaks underscore the vulnerability of chemical workers to neurotoxins. In addition, occurrence of these large, easily detectable epidemics suggests that many more smaller clusters and single cases of neurologic disease of undetermined origin, particularly in younger adults, may be caused by exposure to occupational or to other toxic chemicals. Detection of the etiology of chemically induced neurologic illness requires a high index of suspicion and careful ascertainment of occupational history.

Adult