Industrial Health
Online ISSN : 1880-8026
Print ISSN : 0019-8366
ISSN-L : 0019-8366
Volume 30 , Issue 2
Showing 1-4 articles out of 4 articles from the selected issue
  • Seyed Mohammad MIRBOD, Ryoichi INABA, Hideyo YOSHIDA, Chisato NAGATA, ...
    1992 Volume 30 Issue 2 Pages 65-76
    Published: 1992
    Released: April 17, 2008
    JOURNALS FREE ACCESS
    In order to study noise levels associated with electronic arcade games, noise measurements were made in 3 selected game centers and 192 samples were taken in each location. The background noise was recorded at a level of 61 dB(A) and 64 dB(C). When the electronic games were performed these levels of noise reached to 8890 dB(A). The 1/3 octave bands analyzing sound pressure levels showed that more intense noise levels arose in a frequency range between 0.5 and 2.0 kHz. The computed values for noise pollution levels (LNP) and L90 (fast response A-weighted sound level exceeded 90% of the measurement time) ranged from 93.3 to 96.6 and from 85.1 to 87.3 dB(A), respectively. Concerning our results and according to Melnic (1979), it was estimated that these levels of noise might cause 4-8 dB temporary threshold shift (TTS) at 4.0 kHz in an individual with less than one hour of exposure to such a level of noise.
    As for the employees of the 3 game centers, the 8-hr equivalent continuous sound levels (Leq, 8) were in the range of 80.387.5 dB(A), although their exposure time could not be exactly determind. It was suggested that:
    1) The maximum levels should be limited to a reasonable level, either by the manufacturers or by the game center owners;
    2) Education programs in industry should inform the employees about other factors outside the work that may affect their hearing; and
    3) For policy-making on hearing conservation, recreational warning and standards should be established.
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  • Hideaki IWAI, Motohiro KUROSAWA, Hisao MATSUI, Osamu WADA
    1992 Volume 30 Issue 2 Pages 77-84
    Published: 1992
    Released: April 17, 2008
    JOURNALS FREE ACCESS
    Tributyltin inhibited compound 48/80-induced histamine release from rat serosal mast cells in a dose-related manner. Triphenyltin and tripropyltin also showed a strong inhibitory effect on the histamine release and the degree of the inhibition was the same as that of tributyltin. The inhibitory effects of other organometals were much smaller than those of the organotins. Tributyltin and triphenyltin also showed a tendency to inhibit histamine release induced by concanavalin A + phosphatidylserine and calcium ionophore A 23187. The present results suggest that certain triorganotin compounds may have a specific inhibitory effect on histamine release by acting on the same process in each of the three stimulus responses.
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  • Kazuhisa TOMITA, Takehito TAKANO
    1992 Volume 30 Issue 2 Pages 85-95
    Published: 1992
    Released: April 17, 2008
    JOURNALS FREE ACCESS
    Flufenamic acid (FA) is a widely used non-steroidal anti-inflammatory drug. It is also known to be an uncoupling agent of oxidative phosphorylation in mitochondria. The interaction of FA and ethanol has been of concern in the occupational health field, since alcohol consumption is a common habit among members of the working population. Thus, we investigated the effects of FA on ethanol metabolism in the rat. In the first experiment, FA and ethanol were administered intragastrically to male Wistar rats. Ethanol and acetaldehyde were measured in blood samples collected from the tail vein by head-space gas chromatography. In the second experiment, the interaction of FA and ethanol was observed in the perfused rat liver. The following items were monitored in perfused livers from both fed and fastd rats : uptake rate of ethanol, production rate of acetaldehyde, level of reduced pyridine nucleotides, and oxygen consumption rate. In the first experiment, the rats with FA showed significantly higher concentrations of both ethanol and acetaldehyde in blood after ethanol intake than the rats without FA. In the perfused liver, FA suppressed ethanol uptake, and increased acetaldehyde concentration in the effluent. FA decreased the level of intracellular reduced pyridine nucleotides which had been elevated by ethanol. FA caused an increase in the oxygen consumption rate, which was not altered by the coexistence of ethanol. It was concluded that FA suppressed ethanol metabolism due to suppression of acetaldehyde oxidation in the liver, despite its uncoupling effect on oxidative phosphorylation in mitochondria.
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  • Ashwin B. PATEL, H. Venkatakrishna-BHATT
    1992 Volume 30 Issue 2 Pages 97-101
    Published: 1992
    Released: April 17, 2008
    JOURNALS FREE ACCESS
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