Carbon Disulfide: Frumkin's Response

The September 1998 issue of EHP contained two articles about the neurotoxicity of carbon disulfide. The "NIEHS News" article (1) reported on a collaborative study that involved scientists from the NIEHS (Nashville, TN). In this study, the neurotoxicity of carbon disulfide was detailed from the earliest molecular alterations to neurobehavioral findings to electrophysiologic and morphologic changes, and the utility of intramolecular cross-linking in hemoglobin as a biomarker was defined. I was pleased to read this report, and even more pleased to have participated in this study, but I was distressed to see the cover story in the same issue. "Multiple System Atrophy Following Chronic Carbon Disulfide Exposure" (2), in the "Grand Rounds in Environmental Medicine," is a case report of an individual who developed a degenerative nervous system disease, olivopontocerebellar atrophy, and who had been chronically exposed to carbon disulfide while working for 34 years in a viscose rayon plant in the United States. Frumkin (2) concluded, "While this association has not previously been reported , it is clinically and pathologically consistent with a range of movement disorders seen in the setting of occupational carbon disulfide exposure." Frumkin never saw this patient, nor was he consulted by the patient's physicians during the course of this disease; he only reviewed the medical records and diagnostic studies as an expert witness for the plaintiff in a case that failed to convince a Texas jury that a cause-and-effect relationship existed between carbon disul-fide exposure and this man's disease (3). I also reviewed this material and concluded that such a relationship was not even remotely plausible; indeed, I thought that there were excellent reasons to conclude that his disease bore no relationship to the exposure. Thus, the publication of this paper raises several concerns: Why did Frumkin feel authorized to publish this report, and were the editors informed about his relationship to this case? Was the paper reviewed by experts in neurotoxicol-ogy, clinical neurology, and neuropatholo-gy? Will readers conclude that carbon disulfide causes multisystem atrophy? How many more lawsuits will be filed alleging that since B followed A, A caused B, and how many more physicians will reach this vacuous conclusion? The individual described in this paper (2) had classical olivopontocerebellar atrophy, beginning with cerebellar ataxia and progressing over years to involve long tracks and cranial nerve nuclei in the pons. Neither the cerebellum nor the pontine nuclei are affected in carbon disulfide toxicity. …