years after exposure. In all of the studies reported here, doses are inferred on the basis of clinical effects. No dose reconstruction appears to have been performed.

A case series at one of the nearby hospitals reported that 17 of 18 patients admitted soon after the attack had an average reduction of plasma cholinesterase activity of 94 percent (Suzuki et al., 1997). In a larger case series, medical records were collected for 264 people who sought treatment, and health examinations were performed on 155 residents 3 weeks postexposure (Morita et al., 1995). This case series found that severely symptomatic patients examined at 3 weeks continued to exhibit decreased activity of plasma cholinesterase and RBC AChE; reduced serum triglyceride, serum potassium, and chloride; and elevated serum creatinine kinase, leukocytes, and ketones in urine. Blood cholinesterase levels returned to normal within 3 months. Most patients recovered by 6 months. Yet two of the nine severely poisoned patients displayed epileptiform abnormalities (although details of these abnormalities and their timing were not given) (Morita et al., 1995).

In a later follow-up examination by the same research team, four of six severely poisoned patients were reported to display visual field defects, hypoxia, low-grade fever, and what were described as “epileptic electroencephalographic changes” up to 2 years postexposure (Sekijima et al., 1997). At 7 months postexposure, one patient also developed sensory polyneuropathy and reduced sensory nerve conduction velocity. The minimal clinical information reported on this single case is not consistent with classic OPIDN, which manifests primarily as a motor deficit, or a mixed motor–sensory deficit, but never as an isolated sensory deficit (Lotti, 2000). With the exception of this poorly documented case of delayed sensory neuropathy, there appear to be no other cases of delayed neurotoxicity resembling OPIDN among the numerous cases of documented accidental or experimental exposure to sarin. Nevertheless, on the basis of animal studies (see earlier), researchers assert that OPIDN is possible in individuals who are rescued from otherwise lethal doses of sarin or in those exposed to lower levels for prolonged periods (Brown and Brix, 1998; Spencer et al., 2000).

The Matsumoto incident also triggered the first population-based study of the long-term effects of a single exposure to sarin. Nakajima and colleagues (1998, 1999) surveyed all residents (n = 2,052) living within a defined geographic area surrounding the sarin release site (1,050 meters from north to south; 850 meters from east to west).10 They mailed questionnaires at various times until 3 years after the incident. At the outset of the study (3 weeks postexposure), about 27 percent of the cohort (n = 471) was classified as “victims” based on their reports of either receiving a diagnosis or reporting symptoms of acute cholinergic syndrome. They were compared with so-called “nonvictim” controls (n = 669) who lived in the same geographic area as the victims but did not report having acute cholinergic symptoms or diagnosis.

10  

It was estimated, from police reports, that 12 liters of sarin may have been released (Nakajima et al., 1998); however, the exact amount of sarin and its purity are unknown.



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