著者

佐野 晴洋 山下 節義 川西 正祐 井口 弘 吉永 侃夫 小城 勝相 塚本 幾代 藤田 博美 岡本 浩子 加藤 伸勝 宮本 宣博 浮田 義一郎 山根 秀夫 森 律 池田 栄三 乾 修然 藤岡 惇 阿部 醇吉

出版者

日本衛生学会

雑誌

日本衛生学雑誌 (ISSN:00215082)

巻号頁・発行日

vol.37, no.2, pp.566-579, 1982-06-30 (Released:2009-02-17)

参考文献数

32

被引用文献数

1 3

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An epidemiological survey and clinical investigations were carried out on 162 retired workers from manganese mines and ore grinders, who were the residents of the Tamba district of Kyoto Prefecture. Most of the workers had been employed in small industrial factories with less than five employees under very poor working conditions. Fifty-five percent of them had worked in the mines and factories for longer than 11 years. Forty-six percent had been retired for 11-20 years, whereas 27% for longer than 21 years. A group of 124 people living in the same region but who had not been exposed to manganese served as the control group.The incidence of subjective symptoms associated with chronic manganese poisoning such as emotional instability, psychomotor irritability and neurologic abnormalities was apparently high in the experimental group and it increased with the period of exposure to manganese dust. Twenty-eight percent of the workers reported the subjective symptoms while they were employed, but 45% of them reported as late as six years after they retired.Of the retired workers, five (3.1%) had parkinsonism, three (1.9%) showed symptoms of hemiparkinsonism, and fifteen (9.3%) showed neurological symptoms including maskedlike, gait unbalance, slurred speech and imparied fine movements. Forty-five percent of these patients recognized these abnormalities for more than five years after they had left the contaminated workings. It is noteworthy that 39% of the retired workers were diagnosed as having pneumoconiosis.Some of the problems encountered in diagnosing manganese poisoning after exposure has been terminated is also discussed here.

著者

三浦 創 佐野 晴洋

出版者

社団法人 日本産業衛生学会

雑誌

産業医学 (ISSN:00471879)

巻号頁・発行日

vol.14, no.4, pp.279-285, 1972 (Released:2011-03-04)

参考文献数

30

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Lead poisoning is associated with characteristic urinary increases of δ-aminolevulinic acid and coproporphyrinogen III, elevated erythrocyte protoporphyrin concentration and partial block of δ- aminolevulinic acid dehydratase.In human lead poisoning a very small amount of increase of porphobilinogen and uroporphyrinogen III is reported, while in rabbits porphobilinogen increases but uroporphyrinogen III does not as in the human cases. The small amount of porphobilinogen or uroporphyrinogen III in the human urine may be explained by δ-aminolevulinic acid dehydratase inhibition, but the increase in coproporphyrinogen III is as yet inexplainable.An alternative pathway of coproporphyrinogen III formation from δ-aminolevulinic acid or porphobilinogen has and suggested in lead poisoning. We proposed that an intermediate, 2-amino-methyl-3-methyl-4-carboxyethyl-pyrrole, may be formed in vivo by enzymic condensation of δ-aminolevulinic acid and 1-amino-butane-2-one (β-ketobutylamine) or by prior decarboxylation of acetic acid sidechain of porphobilinogen. To test this hypothesis we made an experiment, the results of which are as follows.The pyrrole compounds were isolated from the urine or the incubation mixture with δ-aminolevulinic acid and tissue homogenates (bone marrow, liver and kidneys) of lead poisoned rabbits by using the column chromatography on Dowex 2. All the pyrrole compounds were further converted to porphyrins by chemical condensation technique, resulting in the formation of the mixture of uroporphyrin isomers, though no coproporphyrin was detected.The results indicate that the pyrrole compounds in lead poisoning are identical with authentic porphobilinogen and the prior decarboxylation of porphobilinogen appears unlikely. It is suggested that the increase of coproporphyrinogen III in lead poisoning may be caused by over-production of δ-aminolevulinic acid. The increased amount ofthe precursor seems to overcome the partial blocking of δ-aminolevulirlic acid dehydratase and thenormal rate of porphyrin synthesis may be formed.