Differential diagnosis between organic and inorganic mercury poisoning in human cases--the pathologic point of view.
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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. (+info)
Benchmark concentrations for methylmercury obtained from the Seychelles Child Development Study.
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Methylmercury is a neurotoxin at high exposures, and the developing fetus is particularly susceptible. Because exposure to methylmercury is primarily through fish, concern has been expressed that the consumption of fish by pregnant women could adversely affect their fetuses. The reference dose for methylmercury established by the U.S. Environmental Protection Agency was based on a benchmark analysis of data from a poisoning episode in Iraq in which mothers consumed seed grain treated with methylmercury during pregnancy. However, exposures in this study were short term and at much higher levels than those that result from fish consumption. In contrast, the Agency for Toxic Substances and Disease Registry (ATSDR) based its proposed minimal risk level on a no-observed-adverse-effect level (NOAEL) derived from neurologic testing of children in the Seychelles Islands, where fish is an important dietary staple. Because no adverse effects from mercury were seen in the Seychelles study, the ATSDR considered the mean exposure in the study to be a NOAEL. However, a mean exposure may not be a good indicator of a no-effect exposure level. To provide an alternative basis for deriving an appropriate human exposure level from the Seychelles study, we conducted a benchmark analysis on these data. Our analysis included responses from batteries of neurologic tests applied to children at 6, 19, 29, and 66 months of age. We also analyzed developmental milestones (age first walked and first talked). We explored a number of dose-response models, sets of covariates to include in the models, and definitions of background response. Our analysis also involved modeling responses expressed as both continuous and quantal data. The most reliable analyses were considered to be represented by 144 calculated lower statistical bounds on the benchmark dose (BMDLs; the lower statistical bound on maternal mercury hair level corresponding to an increase of 0.1 in the probability of an adverse response) derived from the modeling of continuous responses. The average value of the BMDL in these 144 analyses was 25 ppm mercury in maternal hair, with a range of 19 to 30 ppm. (+info)
Mercury intoxication presenting with tics.
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A 5 year old Chinese boy presented with recurrent oral ulceration followed by motor and vocal tics. The Chinese herbal spray he used for his mouth ulcers was found to have a high mercury content. His blood mercury concentration was raised. Isolated tics as the sole presentation of mercury intoxication has not previously been reported. (+info)
Methylmercury poisoning in common marmosets--a study of selective vulnerability within the cerebral cortex.
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Neuropathological lesions found in chronic human Minamata disease tend to be localized in the calcarine cortex of occipital lobes, the pre- and postcentral lobuli, and the temporal gyri. The mechanism for the selective vulnerability is still not clear, though several hypotheses have been proposed. One hypothesis is vascular and postulates that the lesions are the result of ischemia secondary to compression of sulcal arteries from methylmercury-induced cerebral edema. To test this hypothesis, we studied common marmosets because the cerebrum of marmosets has 2 distinct deep sulci, the calcarine and Sylvian fissures. MRI analysis, mercury assays of tissue specimens, histologic and histochemical studies of the brain are reported and discussed. Brains sacrificed early after exposure to methylmercury showed high contents of methylmercury and edema of the cerebral white matter. These results may explain the selective cortical degeneration along the deep cerebral fissures or sulci. (+info)
Reappraisal of the historic 1959 cat experiment in Minamata by the Chisso Factory.
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Autopsy specimens from the historic cat experiment were recently discovered in a storage area at the Kumamoto University School of Medicine. The specimens were from an experiment prompted by physicians in the Chisso Minamata Plant following the announcement made by the Study Group for Minamata disease. On July 14, 1959 the Group announced that the disease was most likely caused by a kind of organic mercury. In order to prove or disprove that industrial waste from the Chisso Factory was the culprit in Minamata disease, a total of ten cats were fed food mixed with industrial waste produced in the acetaldehyde-producing plant. One of the ten cats, No. 717, was subsequently autopsied but the autopsy findings have never been published or recorded in the literature despite their historic significance. The rediscovered specimens were studied pathologically and biochemically, and were analyzed chemically with currently available techniques. Characteristic lesions of methylmercury poisoning were observed in the central nervous system, and the mercury levels in the cerebrum, cerebellum, liver and kidney were found to be markedly elevated in this animal. (+info)
Logistic model analysis of neurological findings in Minamata disease and the predicting index.
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OBJECTIVE: To establish a statistical diagnostic method to identify patients with Minamata disease (MD) considering factors of aging and sex, we analyzed the neurological findings in MD patients, inhabitants in a methylmercury polluted (MP) area, and inhabitants in a non-MP area. MATERIALS AND METHODS: We compared the neurological findings in MD patients and inhabitants aged more than 40 years in the non-MP area. Based on the different frequencies of the neurological signs in the two groups, we devised the following formula to calculate the predicting index for MD: predicting index = 1/(1+e(-x)) x 100 (The value of x was calculated using the regression coefficients of each neurological finding obtained from logistic analysis. The index 100 indicated MD, and 0, non-MD). RESULTS: Using this method, we found that 100% of male and 98% of female patients with MD (95 cases) gave predicting indices higher than 95. Five percent of the aged inhabitants in the MP area (598 inhabitants) and 0.2% of those in the non-MP area (558 inhabitants) gave predicting indices of 50 or higher. CONCLUSION: Our statistical diagnostic method for MD was useful in distinguishing MD patients from healthy elders based on their neurological findings. (+info)
Clinical investigation of the lesions responsible for sensory disturbance in Minamata disease.
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To clarify the lesions responsible for sensory disturbance in Minamata disease (MD), we clinically investigated the characteristics of sensory disturbance. In all patients with the classical type MD, two-point discrimination was severely disturbed, but the involvement of superficial sensation was relatively mild. On short-latency somatosensory evoked potential study, the component corresponding to N20 was completely absent with normal N9, N11, and N13 components. Although 14 of 38 chronic MD patients demonstrated intact superficial sensation, 10 of these 14 showed mild to moderate disturbance in two-point discrimination. The two-point discrimination in chronic MD patients was significantly high irrespective of the disturbance of superficial sensation. These findings suggest that the sensory disturbance of MD patients may mainly be caused by a lesion in the sensory cortex rather than in the peripheral nerves. However, other foci could be also responsible for the sensory impairment, since 9 of 38 chronic MD patients showed intact two-point discrimination. (+info)
Health and neuropsychological functioning of dentists exposed to mercury.
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OBJECTIVES: A cross sectional survey of dentists in the west of Scotland and unmatched controls was conducted to find the effect of chronic exposure to mercury on health and cognitive functioning. METHODS: 180 dentists were asked to complete a questionnaire that included items on handling of amalgam, symptoms experienced, possible influences on psychomotor function, and the 12 item general health questionnaire. Dentists were asked to complete a dental chart of their own mouths and to give samples of urine, hair, and nails for mercury analysis. Environmental measurements of mercury in dentists' surgeries were made and participants undertook a package of computerised psychomotor tests. 180 control subjects underwent a similar procedure, completing a questionnaire, having their amalgam surfaces counted, giving urine, hair, and nail samples and undergoing the psychomotor test package. RESULTS: Dentists had, on average, urinary mercury concentrations over four times that of control subjects, but all but one dentist had urinary mercury below the Health and Safety Executive health guidance value. Dentists were significantly more likely than control subjects to have had disorders of the kidney and memory disturbance. These symptoms were not significantly associated with urinary mercury concentration. Differences were found between the psychomotor performance of dentists and controls after adjusting for age and sex, but there was no significant association between changes in psychomotor response and mercury concentrations in urine, hair, or nails. CONCLUSIONS: Several differences in health and cognitive functioning between dentists and controls were found. These differences could not be directly attributed to their exposure to mercury. However, as similar health effects are known to be associated with mercury exposure, it would be appropriate to consider a system of health surveillance of dental staff with particular emphasis on symptoms associated with mercury toxicity where there is evidence of high levels of exposure to environmental mercury. (+info)