To find the residual effects of long term exposure to mercury vapour, neurobehavioural tests were given to ex-mercury miners about 18 years after the end of mercury exposure. Seventy six male exmercury miners who had been exposed to high concentrations of mercury vapour (over 1.0 mg/m3) and with a history of mercury intoxication were compared with controls matched for age (within 3 years), sex, and education. Although the extent of the workers' symptoms caused by mercury poisoning, termed erethismus merculialis, decreased considerably after the end of exposure, matched paired comparison showed that performances of motor coordination, simple reaction time, and short term memory had deteriorated significantly in the exposed group. Multiple linear regression analysis of exposure variables with neurological examination measures showed positive correlations between poorer neurological performance and variables related to mercury exposure. Thus the duration of exposure correlated with poorer performance of hand-eye coordination, tapping, and a colour card reading test. Job categories classified by exposure to mercury also had a significant negative correlation with these performances. The period of years after the end of exposure hada significant correlation with better performance of reaction time and digit span. On the other hand, the history of intoxication itself had no significant correla- (1) disturbances of the motor system, such as fine tremor of the extremities and poor psychomotor performance,2" (2) deterioration of intellectual capacity, such as memory disturbances and poor verbal intelligence,5-'0 (3) alterations of the emotional state such as depressive mood, irritability, and listlessness,' and (4) peripheral neurotoxicity, such as polyneuropathy with prolonged motor and sensory nerve conduction. '1-4 There are, however, only a limited number of reports on neurobehavioural effects after the end of exposure. Albers et al recently examined 247 ex-workers who had been exposed to mercury vapour for 20 to 35 years previously to identify potential exposure related neurological abnormalities."5 They found that subjects with a history of peak urinary mercury concentrations above 0-6 mg/l showed significantly decreased strength, decreased coordination, increased tremor, decreased sensation, and increased prevalence of Babinski and snout reflexes when compared with the subjects with lower exposure. In our study we have surveyed symptoms and neurobehavioural performances of ex-mercury miners about 18 years after the end of exposure to mercury to find if there were any adverse residual effects of long term exposure to mercury vapour. Methods STUDY POPULATIONSThe subjects were ex-miners of a mercury mine in Hokkaido, Japan, which started mining in 1939

Summary The brains of two autopsy cases from long term mercury mine workers were studied histopathologically, histochemically and by electron microscopy and neutron activating analysis Histopathologically, any specific changes were not observed. The mercury in the brains showed a high concentration; high in the cerebral cortex and the substantia nigra, low in the spinal cord and in the cauda equina. By histo‐chemical analysis, small granules of mercury were seen scattered in the cytoplasm of nerve cells, in particular in the Purkinje cells. Electron microscopy revealed electron dense granules in the cytoplasm of Purkinje cells which were assumed to correspond to mercury granules. Jt was concluded that the nervous tissue in the case of chronic inorganic mercury poisoning keeps high concentration of mercury over a long period whereas morphophysiological normally is well retained.

Differences in pathology were found between acute and chronic exposure to methylmercury, mercury vapor, and inorganic mercury. Characteristic pathologic changes produced by organic mercury in the brain have previously been described in patients with Minamata disease. The brains of patients who presented with acute onset of symptoms and died within 2-mo showed loss of neurons with reactive proliferation of glial cells, microcavitation, vascular congestion, petechial hemorrhage, and edema in the cerebral cortices, predominantly in the calcarine, pre- and postcentral, and transverse temporal cortices and in the cerebellar cortex. The neuropathologic changes in the patients with acute onset of symptoms who survived for a long period (>10 yr) were also included neuronal loss with reactive proliferation of glial cells in similar anatomic locations. The neuropathologic changes in patients with inorganic mercury poisoning are quite different. Autopsies performed on 3 individuals with fatal cases of acute inorganic mercury poisoning who were exposed to mercury vapor for about 2 wk revealed diffuse organized pneumonia, renal cortical necrosis, disseminated intravascular coagulopathy, and infarctions in the brain and kidneys. In 2 other patients who worked in mercury mines for about 10 yr and who suffered from chronic inorganic poisoning, no specific lesions were demonstrated in the brain. However, the assay and the histochemistry of mercury revealed that inorganic mercury was present in the brain in all 3 groups irrespective of the brain lesions and the duration of clinical signs.

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