Methylmercury toxicity in spontaneously hypertensive rats (SHR).
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Biomedical subjects
Publications and source records attributed to H Tamashiro.
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Seventy-two strains of Hg-resistant bacteria (Pseudomonas) were isolated on agar plates containing 40 micrograms/ml of HgCl2 from Minamata Bay sediment, which was heavily polluted with mercury (45.8 micrograms/g). The minimal inhibitory concentrations (MICs) of mercurial compounds were determined for the Hg-resistant pseudomonads and 65 strains (Pseudomonas sp., Bacillus sp., Vibrio sp., and Corynebacterium sp.) isolated from Sendai Bay sediment (1 microgram/g of mercury) as control. The MICs to HgCl2, CH3HgCl, C2H5HgCl, C3H7HgCl, and C6H5HgOCOCH3 for the Hg-resistant pseudomonads from Minamata Bay were significantly higher than those of strains from Sendai Bay. The volatilization from liquid culture containing 20 micrograms/ml of HgCl2 was observed in all of the Hg-resistant pseudomonads from Minamata Bay (70 strains). The mean loss of mercury from liquid culture was 60.4 +/- 17.3%. Further study is warranted to determine what role the Hg-resistant bacteria, particularly the Pseudomonas species, play in the mercury cycle in Minamata Bay.
This study was designed to investigate the effect of different doses of ethanol on the morbidity, mortality, and distribution of mercury in the tissues of groups of rats treated orally once daily with methyl mercury chloride (MMC: 5 mg/kg . d) for 10 consecutive days. Ethanol potentiated the toxicity of methyl mercury in terms of neurological manifestations (hindleg crossings and abnormal gait) and mortality. The magnitude of effect depended on the concentration of ethanol administered. The concentration of mercury in the kidney and brain also increased with the dose of ethanol given. These findings indicate that epidemiologic studies designed to evaluate methyl mercury toxicity must take into account the multiple environmental burdens that can affect the population cumulatively and simultaneously.
This study examines mortality patterns by cause of death to investigate the effect of exposure to methylmercury in a small area of Minamata City (Kumamoto Prefecture, Japan), which has the highest concentration of patients with Minamata disease. Standardised mortality ratios (SMRs) are computed by cause of death for the study area, using the age specific rates of the entire city as a standard. The SMRs for liver cancer and chronic liver disease in the study area are significantly higher than unity and are consistent with the mortality patterns of registered Minamata disease patients. While an excess mortality is observed for cerebral haemorrhage, mortality from cerebral infarction and other cerebrovascular diseases is considerably lower in the study area. The multiple risk factors of liver related diseases and a possible explanation for the cerebrovascular mortality patterns are discussed to suggest further investigation.
Analysis of mortality of 439 deaths that occurred among 1483 patients with Minamata disease (MD) in Kumamoto Prefecture, Japan was performed from the end of 1981. Causes of death and survival rates were studied by means of the standardized mortality ratio (SMR) and life-table technique. Of the 439 deaths (29.6%) in MD cases, the first death occurred in 1954. There was a first peak incidence in 1956 when MD was initially reported, however, the majority of deaths occurred after 1972 when a second and much larger peak was evident. In 1970 an important milestone occurred when the Public Nuisance Relief Law (an anti-pollution law) was enacted. Among its provisions, this law required and enabled verification of MD among people suspected of having been exposed. In contrast to the early cases, later cases of MD were older and their mean age-at-death was not different from that of the general population. The mortality rate for all causes of death was significantly higher in both sexes compared to the general population. Significantly lower survival rates were noted for older patients. The cause-specific mortality rates also showed significantly increased SMRs for liver diseases and nephritis-nephrosis-nephrotic syndrome in male patients, and for nephritis-nephrosis-nephrotic syndrome and other diseases in females. On the other hand, the SMR for senility without mention of psychosis was significantly lower than expected in both sexes.
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The causes of death in Minamata disease were analyzed and compared with those of control subjects. Of the 1422 Minamata disease patients in the Kumamoto Prefecture, 378 had died by the end of 1980. Of these 378, the first death occurred in 1954 with a peak incidence in 1956 when Minamata disease was officially reported for the first time. The number of deaths increased rapidly after 1972 with a second peak in 1976. The male:female ratio was 1.8:1 and the mean age-at-death was 67.2 years (SD = +/- 18.65). The mean age-at-death was younger in the cases of the initial outbreak than in those recently. There were, on the average, 2.8 causes of death per person. Of these cases, 157 (41.5%) had Minamata disease indicated on the death certificate, though 64 (16.9%) had Minamata disease coded as the underlying cause. Minamata disease and the noninflammatory diseases of the central nervous system (CNS) were the main underlying causes of death between 1954 and 1969, while, in the multiple cause data, pneumonia and non-ischemic heart disease were the most prevalent. Cerebrovascular diseases (18.0%) were the main underlying causes of death followed by malignant neoplasms (14.7%), cardiovascular diseases (14.1%) and Minamata disease (14.1%) in 1970 or later, while cardiovascular diseases (18.6%), Minamata disease (14.5%), cerebrovascular diseases (10.4%) and malignant neoplasms (7.1%) were the major multiple causes of death. As compared with the control, the proportions of deaths due to noninflammatory diseases of CNS and pneumonia were higher in the initial outbreak. Although the difference in the causes of death was less apparent recently, malignant neoplasms and hypertensive diseases tended to be lower. These results suggest that there is a need for a long-term follow-up of Minamata disease patients. The data also show the potential value of multiple causes of death coding in analyses of mortality.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
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The effects on life expectancy from elevated methylmercury (MeHg) exposure were studied in five coastal towns of southern Japan. Hair concentrations of MeHg in the study area were 3 to 6 times higher than the surrounding areas. From 1969-1972 to 1978-1982 life expectancy increased in the study area, with no appreciable difference between that area and the two control areas. When four major causes of death were deleted analytically in both study and control areas, malignant neoplasms contributed the most in recent years to potential gains in life expectancy for both sexes. For the duration of their working ages, however, accidents were the leading contributor for males, followed by malignant neoplasms, heart disease, and cerebrovascular disease. The relative contribution of these causes of death to gain in life expectancy in the study area population is discussed in the context of elevated MeHg exposure.