Nippon Eiseigaku Zasshi (Japanese Journal of Hygiene)
Online ISSN : 1882-6482
Print ISSN : 0021-5082
ISSN-L : 0021-5082
Volume 29, Issue 3
Displaying 1-5 of 5 articles from this issue
  • Sumie Yamanaka, Kiichi Ueda, Tamao Yoshida
    1974Volume 29Issue 3 Pages 359-364
    Published: August 28, 1974
    Released on J-STAGE: April 03, 2009
    JOURNAL FREE ACCESS
    The formation of methylmercury compounds from inorganic mercury in vivo was investigated in rats and fish.
    1. Chemical methylation of mercuric chloride mercurochrome with methylocbalamine, a vitamin B12 analog, was confirmed in vitro experiments.
    2. In rats exposed to inorganic mercury, methylmercury formation was not accelerated by the injection of methylcobalamine.
    3. A small quantity of methyl mercury compound was formed in rats administered inorganic mercury without methylcobalamine.
    The methylmercury content was particularly increased in the kidneys.
    4. In homogenates of whole fish, 203Hg-labeled methylmercury compound was found 10, 21 and 101 days after the injection of labeled mercuric chloride.
    5. No difference in degree of methylation was noted among various spesies of fish: catfish, carp and trout.
    Therefore the high level of methyl mercury in tuna and catfish in non-polluted water, as reported in the 2nd report, appeared to be unrelated to the high activity of biological methylation in vivo.
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  • Yasushi Kodama, Eizaburo Kunitake, Koichi Nobutomo, Michiko Urabe, Nob ...
    1974Volume 29Issue 3 Pages 365-378
    Published: August 28, 1974
    Released on J-STAGE: April 03, 2009
    JOURNAL FREE ACCESS
    In view of the changes in exposure of the Japanese to atmospheric lead in recent decades, it seems important to reconsider the normal lead level in the blood of the Japanese in relation to the environ mental concentration of lead. The lead levels in the blood of 361 people were determined by the dithizone method, and atmospheric lead was measured either by the atomic-absorption method for samples collected by a high volume air sampler or by the impinger and dithizone method for workers in printing offices.
    1. In Fukuoka City, the effect of atmospheric lead from gasoline engine emission on the blood lead level was studied in 45 people (m: 21, f: 24) living for over three years beside a congested intersection and in 55 people (m: 28, f: 27) living in a residential area away from the intersection. The atmospheric lead levels were 5.65-1.33μg/m3 along the roadside, and less than 1.0μg/m3 in the residential section. The arithmetic mean lead levels in the blood of men and women near the intersection were 14.9μg/100g and 10.0μg/100g and in the residential section 12.1μg/100g and 10.6μg/100g, respectively. The difference of the geometric mean lead levels in both groups was not significant.
    2. In Ishigaki Island of Okinawa, the atmospheric lead concentration was less than 1.0μg/m3, and the average concentration of lead in the blood was 18.8 and 14.4μg/100g in 28 men and 28 women.
    3. At 3 printing offices, the average concentration of atmospheric lead was less than 1.5μg/m3, but a relatively high lead level of 30μg/m3 was detected near the melting bath. Lead concentrations in the blood of 155 workers (m: 141, f: 11) were determined, and the highest mean blood lead level in 3 printing offices was 15.9μg/100g in 122 workers in “C” printing office.
    4. In a basement parking area where about 1, 500 cars park in a day, the atmospheric lead levels of the working room were less than 2.0μg/m3 and the mean lead levels in the blood were 19.9μg/100g in 10 men and 15.8μg/100g in 5 women in the fee collector's room, 16.6μg/100g in 7 men's driver, 9.7μg/100g in 9 men and 14.1μg/100g in 3 women in the main office.
    5. In a room where workers were soldering radio parts, 0.30-5.81μg/m3 of lead was detected, the average concentration of lead at 10 places being 2.1μg/m3. The mean blood lead level of 8 women who were soldering radio parts was 15.7μg/100g and that of the control group was 15.4μg/100g.
    6. The lead levels in daily foods collected by 10 families in Fukuoka City ranged from 39.6 to 182.4μg/day.
    7. The average blood lead levels and 95% fiducial limits obtained from the basis of the theoretical log-normal distribution curve were 12.4μg/100g and 40.9μg/100g in 249 men, 11.1μg/100g and 28.8μg/100g in 112 women, 12.0μg/100g and 36.1μg/100g in a total of 361 people respectively.
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  • Kazuro Sho
    1974Volume 29Issue 3 Pages 379-387
    Published: August 28, 1974
    Released on J-STAGE: April 03, 2009
    JOURNAL FREE ACCESS
    Urinary increase of δ-aminolevulinic acid and coproporphyrin as well as basophilic stippled cells in the peripheral blood are the characteristic signs of lead poisoning. The biochemical lesion of porphyrin biosynthesis in lead poisoning is the partial inhibition of δ-aminolevulinic acid dehydratase, but whether or not δ-aminolevulinic acid synthetase is induced (stimulated) or not by lead is still unknown. This paper reports that δ-aminolevulinic synthetase activity in bone marrow in lead poisoned rats was 6.8 times higher than that of normal rats. Activity was found to increase within three or four days after lead administration and in parallel with the urinary increase of δ-aminolevulinic acid.
    The levels of urinary δ-aminolevulinic acid and coproporphyrin in lead poisoned rats decreased markedly following the administration of mitomycin c. This phenomenon were also observed in the case of hepatic porphyria caused by diethyl-1, 4-dihydro-2, 4, 6-trimethylpyridine-3, 5-dicarboxylate poisoned rats when treated with mitomycin c.
    These results strongly suggest that δ-aminolevulinic acid synthetase activity is induced either directly or indirectly by lead. Excessive δ-aminolevulinic acid thus formed seems to overcome the partial blocking of δ-aminolevulinic acid dehydratase resulting in the increased formation of coproporphyrin in lead poisoning.
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  • Takao Watanabe
    1974Volume 29Issue 3 Pages 388-398
    Published: August 28, 1974
    Released on J-STAGE: April 03, 2009
    JOURNAL FREE ACCESS
    Comparative studies on serum calcium and magnesium levels were carried out among the male and female inhabitants (aged 40 and over) of two inland agricultural districts (farm villages H and U) and one urban district (city S) in the Tohoku area of Japan, districts where the rates of mortality from cerebrovascular diseases were significantly different.
    (1) Serum calcium levels in males and females in the two villages were lower than those in city S. No significant difference was observed in magnesium levels among the three districts; the male values tended to be lower than the female values.
    (2) Comparison between summer and winter levels of calcium and magnesium in the serum as measured in village U revealed that the calcium level was higher in winter while the reverse was true in the case of the magnesium level.
    (3) Health conditions, as judged by stature, body weight, skinfold thickness and specific gravity of blood, were worse in the agricultural districts than in the urban district.
    (4) Blood pressure levels, both systolic and diastolic, were equal in the three districts. No seasonal variation was observed.
    These observations, together with the results of a nutritional survey, suggest that the low calcium level in the serum, due to insufficient dietary intake of the mineral is closely related to the higher incidence of cerebrovascular diseases in the farm villages of Tohoku.
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  • Naoki Sagawara
    1974Volume 29Issue 3 Pages 399-402
    Published: August 28, 1974
    Released on J-STAGE: April 03, 2009
    JOURNAL FREE ACCESS
    To determine the calcium binding activity of duodenal mucosa, renal cortex and medulla, drinking water containing cadmium (300ppm) was administered to rats (Wistar strain, _??_) for 30 days.
    In the experimental group, the calcium binding activity of the duodenal mucosa (16, 000g supernatant) was decreased to about 1/5 (t-test, p<0.05) that of the control group.
    In the renal cortex supernatant, this activity was decreased to about 1/2 (t-test, p<0.01) that of the control group. But this activity of renal medulla protein did not differ from that in the control group.
    The loss of this protein's activity may contribute to the calcium deficiency in cadmium poisoning.
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