Journal of Occupational Health
Online ISSN : 1348-9585
Print ISSN : 1341-9145
ISSN-L : 1341-9145
Volume 38, Issue 1
Displaying 1-9 of 9 articles from this issue
  • Ryoichi INABA, Seyed Mohammad MIRBOD, Hirotoshi IWATA
    1996 Volume 38 Issue 1 Pages 1-5
    Published: 1996
    Released on J-STAGE: May 15, 2006
    JOURNAL FREE ACCESS
    Pathophysiology of Vibration-Induced White Finger and Safety Levels for HandTransmitted Vibration: Ryoichi INABA, et al. Department of Hygiene, Gifu University School of Medicine-This review addresses the pathogenic mechanism and vibration safety values of vibrationinduced white finger (VWF). Sympathetic hyperactivity alone has long been postulated to account for VWF, but damage to vasoregulatory structures and functions in the finger skin now also seems to be involved. The physiological complexity of the response to cold is so great and the interaction between various vasoregulatory mechanisms so intricate that only a multifactorial etiology and pathogenesis is likely for VWF. These factors will be discussed in detail. Regarding vibration safety values, the prevalence of VWF and vibration magnitude (hand-transmitted vibration levels (HTVLs)) in various groups of workers which reported in our previous studies were reviewed. The prevalence rates of VWF were compared to the prevalence rates of Raynaud''s phenomenon (RP) in a large group of males and females without vibration exposure. It was observed that in subjects exposed to HTVLs of between 1.1 and 2.5 m/s2, the prevalence of VWF was 0.0-4.8%. The prevalence of VWF in workers exposed to HTVLs of up to 5.1 m/s2 was 9.6% and significantly higher than the prevalence of RP in males in the general population (2.7%). A significant positive correlation between VWF and HTVLs values was obtained. By employing the results obtained on vibration magnitude and the prevalence of VWF, estimated vibration safety levels are discussed. (J Occup Health 1996; 38: 1-5)
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  • Isamu KABE, Kazuyuki OMAE, Hiroshi NAKASHIMA, Tetsuo NOMIYAMA, Takamot ...
    1996 Volume 38 Issue 1 Pages 6-12
    Published: 1996
    Released on J-STAGE: May 15, 2006
    JOURNAL FREE ACCESS
    In Vitro Solubility and In Vivo Toxicity of Indium Phosphide : Isamu KABE et al. Department of Preventive Medicine and Public Health, School of Medicine, Keio University—This study was designed to clarify the in vitro solubility and the in vivo basic toxicity of indium phosphide (InP). InP powder was clearly soluble in synthetic gastric fluid and quite insoluble in saline or synthetic lung fluid. Male ICR mice (SPF grade) were given InP at the doses of 0, 1, 000, 3, 000, and 5, 000 mg/kg, intraperitoneally (i. p.) or orally (p. o.). During a 2-week observation, no mice died. In i. p. treated mice, the serum indium concentration showed a dose-dependent increase, and indium mainly accumulated in the lungs and liver. Dose-dependent increases in lung and spleen weight were observed. Black granules of InP were deposited in the lymph nodes, spleen, lungs, and liver. Extramedullary granulopoiesis was observed. And eosinophilic exudates and mononuclear cells were seen in the pulmonary alveoli. Considering these findings, InP particles were presumably transferred to the spleen, liver, and lungs by way of lymphokinetics, causing reticuloendothelial responses. Hematological examination showed increased proportions of stab cells and monocytes in 5000 mg/kg i. p. dosed mice. The p. o. administered mice showed no clear relationship between the dose and biological effects. (J Occup Health 1996; 38: 6-12)
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  • Ikuko AIBA, Toshikatsu INDO, Gaku ICHIHARA, Yasuhiro TAKEUCHI
    1996 Volume 38 Issue 1 Pages 13-19
    Published: 1996
    Released on J-STAGE: May 15, 2006
    JOURNAL FREE ACCESS
    Change in Magnetic Resonance Imaging and Clinical Signs in a Case of Chronic Toluene Intoxication by Sniffing: Ikuko AIBA, et al. Department of Neurology, Nagoya University School of Medicine-A 22-year -old man with an 8-year history of toluene abuse was admitted for disturbance of consciousness due to acute thinner overdose on June 19, 1990. On admission, he had distal dominant muscle atrophy with areflexia. Computed tomography revealed cerebral atrophy predominantly in the frontal lobe. Magnetic resonance imaging (MRI) of the brain in Oct 1990 revealed the following abnormalities: (1) cerebral atrophy predominantly in the frontal lobe and atrophy of vermis cerebelli and corpus callosum; (2) loss of differentiation between gray and white matter; (3) high intensity of middle cerebellar peduncle, brain stem and internal capsule on T2-weighted images; and (4) low intensity in the ventrolateral part of the thalamus on T2-weighted images. Muscle weakness gradually resolved, but the patient started thinner sniffing again in Sept, 1991. Cerebellar ataxia appeared in July, 1992 and pyramidal sign developed in Mar, 1993. MRI in May, 1993 also revealed high intensity of white matter on T2weighted images. Low intensity on T2-weighted images spread to the caudate nucleus, globus pallidus, and the dorsolateral part of the thalamus. Diffuse cerebral atrophy was found, and atrophy of the cerebellar hemisphere became prominent. High intensity of middle cerebellar peduncle, brain stem and internal capsule on T2-weighted MR images preceded clinical signs (cerebellar ataxia, pyramidal sign). The neuropathology of toluene-induced encephalopathy and the possiblity of MRI as a marker to detect changes in the brain were discussed. (J Occup Health 1996; 38: 13-19)
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  • Takayuki KAGEYAMA, Hideki IMAI, Michinori KABUTO
    1996 Volume 38 Issue 1 Pages 20-24
    Published: 1996
    Released on J-STAGE: May 15, 2006
    JOURNAL FREE ACCESS
    A Standardization Method for Respiratory Sinus Arrhythmia at Supine Rest as an Index of Cardiac Parasympathetic Activity Using Breathing Frequency: Takayuki KAGEYAMA, et al. Urban Environment and Health Project, National Institute for Environmental Studies-Two spectral components of heart rate variability, respiratory sinus arrhythmia (RSA) and Mayer wave-related sinus arrhythmia (MWSA) provide noninvasive indices of cardiac vagal activity and systemic sympathetic activity with vagal modulation, respectively. But the basic problem that breathing frequency (BF) appears to modify RSA without any change in the tonic level of vagal activity remains, indicating the need for respiratory standardization. In the present study, RSA amplitude at supine rest was examined as a function of BF intentionally maintained constant (0.18-0.33 Hz) for 1 1 nonsmokers (5 males and 6 females aged 19-28) with consideration of time after meals, which may affect RSA. The amplitude calculated by autoregressive spectral analysis linearly decreased with the increase in BF on a log-log scale. This held in the case of RSA for nonpaced regular breathing with the mean BF corresponding to the center frequency of RSA. The amplitude during nonpaced regular breathing could therefore be statistically standardized to that at BF of, e.g., 0.25 Hz, which agreed well with that at the paced BF of 0.25 Hz (r=0.958). This suggests a simple, efficient method for the reliable assessment of vagal activity based on RSA amplitude and of sympathetic activity indicated by the ratio of MWSA amplitude to RSA amplitude. (J Occup Health 1996; 38: 20-24)
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  • Naoki KUNUGITA, Nan MEI, Satoshi NOMOTO, Toshiyuki NORIMURA
    1996 Volume 38 Issue 1 Pages 25-29
    Published: 1996
    Released on J-STAGE: May 15, 2006
    JOURNAL FREE ACCESS
    Measurement of the CD3-4+ Variant T Cell Frequency by Flow Cytometry after XIrradiation on Mice: Naoki KUNUGITA, et al. Department of Radiation Biology and Health, School of Medicine, University of Occupational and Environmental Health, Japan-Variant cell frequency of mice T-lymphocytes defective in the T-cell receptor (TCR) gene expression was measured by flow cytometry. Splenic T-lymphocytes were obtained from mice after irradiation and stained with fluorescein-labeled anti-L 3 T 4 (CD 4) and phycoerythrinlabeled anti-CD3-ε antibodies. They were analyzed with a flow cytometer to detect variant T cells lacking surface expression of TCR/CD 3 complexes which showed CD3-4+ T cells. Variant T cells could be observed 3 days after 3 Gy irradiation. Frequency of variant T cells increased to the maximum level of 94×10-4 between 15 and 21 days after 3 Gy irradiation on BALB/c mice and gradually decreased with a half-life of approximately 17 days. We examined the strain difference in radiosensitivity of splenic T-lymphocytes in BALB/c, C57BL/6, C3H/ He and B6C3F1 mouse strains by this assay method. We observed that BALB/c showed the most radiosensitivity. This assay method is quick and easy in comparison with other methods and is considered useful for the mutagenicity test. (J Occup Health 1996; 38: 25-29)
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  • Kazuo AOKI, Wenyuan ZHAO, Junichi MISUMI, Takato YASUI, Masanobu KUDO
    1996 Volume 38 Issue 1 Pages 30-35
    Published: 1996
    Released on J-STAGE: May 15, 2006
    JOURNAL FREE ACCESS
    Changes in 2, 5-Hexanedione Concentration in the Sciatic Nerve, Serum and Urine of Rats Induced by Combined Administration of 2, 5Hexanedione or Methyl Ethyl Ketone: Kazuo AOKI, et al. Department of Public Health and Hygiene, Oita Medical University-To clarify whether there is a difference in the toxicokinetic changes in 2, 5hexanedione (2, 5-HD) on coadministration with acetone or methyl ethyl ketone (MEK), 108 rats were treated subcutaneously with 2, 5-HD at a dose of 2.6 mmol/kg alone (HD group), with 2, 5-HD and acetone both at 2.6 mmol/kg (HD+AC group), or with 2, 5 -HD and MEK both at 2.6 mmol/kg (HD+MEK group). At 0.5, 1, 2, 4, 8, and 16 hours after injection, 2, 5-HD concentrations in serum, the sciatic nerve and urine (16 hours only) were determined and some toxicokinetic parameters were then estimated. The 2, 5-HD concentrations in serum and the sciatic nerve were significantly higher in both the coadministered groups at 16 hours, and the AUC (area under the serum or nerve concentration versus time curve) in serum and the sciatic nerve of both the coadministered groups increased significantly during 8 to 16 hours compared with the 2, 5-HD alone group. The differences in urinary 2, 5-HD concentrations among the three groups were at the marginal level for significance by ANOVA (p=0.053), but the values for the total amount of urinary 2, 5-HD within 16 hours were not significantly different (p=0.55) among the three groups. There were good correlations between 2, 5-HD concentrations in the sciatic nerve and those in serum in the three groups (r=0.91, r=0.91 and r=0.85 for HD, HD+AC and HD+MEK groups, respectively). The ratios of 2, 5-HD concentration in the sciatic nerve/2, 5-HD concentration in serum were not significantly different among the three groups (0.17, 0.19 and 0.20 for HD, HD+AC and HD+MEK groups, respectively). The estimated biological halflife t1/2 in the HD+AC group was prolonged significantly as was that in the HD+MEK group when compared with that in the HD alone group. The retarded elimination of 2, 5-HD from serum seemed not to be directly related to urinary excretion in the coadministered groups. The present study revealed that the coadministration of 2, 5-HD with acetone produced similar toxicokinetic changes in serum and in the sciatic nerve as that with MEK. It was suggested that the retardation of disappearance of 2, 5-HD from serum and the sciatic nerve on administration of a combination of 2, 5-HD with acetone was not related to urinary excretion but to the overloading of the metabolic capacity of 2, 5-HD in the liver. (J Occup Health 1996; 38: 30-35)
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  • Kazuyuki OMAE, Chizuru ISHIZUKA, Hiroshi NAKASHIMA, Haruhiko SAKURAI, ...
    1996 Volume 38 Issue 1 Pages 36-42
    Published: 1996
    Released on J-STAGE: May 15, 2006
    JOURNAL FREE ACCESS
    Acute and Subacute Inhalation Toxicity of Highly Purified Phosphine (PH3) in Male ICR Mice: Kazuyuki OMAE, et al. Department of Preventive Medicine and Public Health, School of Medicine, Keio University-The acute and subacute inhalation toxicity of highly purified phosphine (PH3, CAS No. 7803-51-2, 99.995%) in male ICR mice was investigated. LC50 for one-hour exposure was greater than 59.2 ppm and that for four-hour exposure was between 26.5 ppm and 33.4 ppm. Experiments involving acute exposure to 25 ppm PH3 for one, two, four or eight hours, and subacute exposure to 5 ppm PH3 for six hours/day, five days/week, for two or four weeks were conducted. All mice subjected to acute eight-hour exposure died but a histopathological examination failed to reveal the actual causes of death. In the nasal cavity, exposure-time related inflammatory changes were observed in the acute two-, four-, and eight-hour exposure groups, and in the subacute four-week exposure group. Other histopathological, hematological, and serum biochemical examinations did not reveal PH3-related changes. Further study is necessary to assess the actual effects of PH3 on the cause of death. (J Occup Health 1996; 38: 36-42)
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  • Megumi NAGANO, Yan HE, Hideyuki YAMAMOTO, Eishichi MIYAMOTO, Makoto FU ...
    1996 Volume 38 Issue 1 Pages 43-44
    Published: 1996
    Released on J-STAGE: May 15, 2006
    JOURNAL FREE ACCESS
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  • Toshio KOBAYASHI, Ichiyo MATSUZAKI, Akio NISHIMURA, Nobuaki MORITA, Ma ...
    1996 Volume 38 Issue 1 Pages 45-46
    Published: 1996
    Released on J-STAGE: May 15, 2006
    JOURNAL FREE ACCESS
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