- 著者
- 三角 順一 小山 和作 三浦 創
- 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.25, no.1, pp.3-9, 1983-01-20 (Released:2008-04-14)
- 参考文献数
- 11
- 被引用文献数
- 4 6
An occupational disease in tobacco cultivating farmers has been reported in Florida, North Carolina, and India. This disease is termed "Green-tobacco sickness" with characterized symptomsdizziness, nausea, and generalized weakness. The symptoms develop after the exposure to wet and raw tobacco leaves, and are probably caused by absorption of nicotine through the skin from the leaves. No case of this disease has been reported in Japan until now. In the present study, two cases of the disease were detected in the southern part of Kumamoto Prefecture. These cases, who were tobacco harvesters, have exhibited the "green symptoms" after cropping wet tobacco leaves every year since 7-8 years ago. One was a man aged 55, the other a 42-year-old woman. They were non-smokers and non-drinkers. These cases were diagnosed as the Green-tobacco sickness by the following reasons: 1) They showed the characteristic symptoms of the disease after cropping tobacco leaves in rainy days. 2) Those symptoms have repeatedly observed since 7-8 years ago under the same circumstances; i.e., they handled wet and raw tobacco leaves without rain coats, and were exposed to dew on tobacco leaves. They had no evidence to handle any other toxic substances at that time. 3) The symptoms usually disappeared on the next morning. 4) Food poisoning was neglected. 5) Efforts to avoid the contact with wet tobacco leaves made them free from the disease. An additional experiment using animals revealed that minimum toxic dose of nicotine through the skin was less than 21 mg/kg of body weight in the rat. Furthermore, analysis of the literatures on the Green-tobacco sickness permitted the suggestion that the toxic dose of nicotine through the skin in humans might be less than 1.96 mg/kg of body weight.
1 0 0 0 OA 鉛中毒におけるPorphobilinogenについて
- 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
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.