To obtain a vibration-dose limit for Japanese workers exposed to hand-arm vibration, the prevalences of vibration-induced white finger (VWF) and numbness of the hand were studied in 5 different groups of workers exposed to 'segmental vibration. In addition, the prevalence of primary Raynaud's phenomenon (PRP) in the general population without occupational vibration exposure was computed. The vibration levels in the exposed groups (except chain saw operators) ranged from 124.1-129.2 dB (reference value, 10-6 m/s2). The prevalence of VWF in these groups was 2.2-4.8%. This value was not statistically significant (p > 0.05) when compared to the prevalence of PRP in the general Japanese population (2.7-2.9% in our study and 0.5-4.6% in other surveys in JaPan36, 54-58). Although the prevalence of numbness of the hands fluctuated among the groups, no significant differences could be demonstrated. Our results were then compared to those of previous reports by literature study [319 papers on hand-arm vibration syndrome (HAVS) and 25 reports on PRP]. At a glance the Japanese population showed a lower prevalence for PRP compared to other countries, which suggested that exposure to cold and biological abilities should also be considered to assess vibration syndrome. A comparison of the vibration characteristics of different tools and the occurrence of VWF in the hands of workers in the literature with those of our data suggested that a daily hand-arm vibration exposure at a level lower than 2.5 m/s2 (128 dB, reference value 10-6 m/s2) could possibly decrease the risk of VWF among workers exposed to segmental vibration.
Effects of exposure to O3 on EEG activity, sleep-wakefulness and heart rate were examined using conscious rats which had been chronically implanted with electrodes for EEG, EMG and ECG recordings. Exposure to 0.5 ppm O3 for 6 hrs and 1.0 ppm O3 for 3 hrs suppressed amounts of wakefulness (W) and paradoxical sleep (PS) at the expense of an increase in slow-wave sleep (SWS), and lowered the amplitude of fast EEG waves and heart rate (HR). The lowered EEG amplitude and the suppressed PS recovered more rapidly during the post-exposure period than did the lowered HR. The ip administration of atropine sulfate blocked the suppressed W, the increased SWS and the lowered HR, while the lowered EEG amplitude and the suppressed PS were not blocked. These observations suggest that the O3-induced bradycardia results from enhanced activity of cardiac para-sympathetic nerves and that the O3-induced changes in W and SWS result secondarily from some circulatory factor including the bradycardia.
A method for determining atmospheric diborane in concentrations higher than 1/10 of TLV, i.e., 0.01 ppm, has been developed using the adsorption sampling method. Silica gel impregnated with potassium permanganate, synthetic resin activated carbon im-pregnated with or without mercury(II) chloride and activated carbon impregnated with chromate salt showed adsorption capacities larger than 18l of 3 ppm diborane test gas when the test gas was drawn at 300 ml /min. Complete desorption of the adsorbed diborane was possible only from silica gel impregnated with potassium permanganate into a hydroxylamine hydrochloride solution. As methods for determining the desorbed boron, both the chromo-tropic acid-HPLC method and ICP-AES were applied. The former was more sensitive, but the latter was less influenced by coexistent substances. The most sensitive and reproducible procedure for diborane determination was as follows : diborane is collected with silica gel impregnated with potassium permanganate (0.05% (w/w)) and desorbed into hydroxylamine hydrochloride solution (400 μg/ml) followed by the determination of boron by the chromo-tropic acid-HPLC method. When diborane in 3l of 0.1 ppm test gas was collected, the desorption efficiency was 105.3% with an RSD of 13.5%. The limit of quantitation of this method was 0.0026 ppm in 3l air. Much lower concentrations can be determined by sampling larger amounts of air.
The two-probe microdialysis (TPMD) method, in which two probes were applied simultaneously to the rat head, was developed to directly investigate the effects of chemicals on the brain. The first and the second probes were implanted into the right striatum and the left ventricle, respectively. Chemicals were dissolved in the perfusion fluid and given into the brain by diffusion through the ventricle probe. Monoamine metabolites were recovered through the striatum probe to investigate changes in neurotransmitter substances. Both intraperitoneal and intraventricular administration of haloperidol (a dopamine receptor blo-cker) increased 3, 4-dihyrdoxyphenylacetic acid (DOPAC) and homovanillic acid (HVA, dopamine metabolites) concentrations in the striatum. On the other hand, apomorphine (a dopamine receptor stimulant), which was given both intraperitoneally and intraventricularly, decreased striatal DOPAC and HVA concentrations. 5-Hydroxyindoleacetic acid (5HIAA, a serotonin metabolite) concentration was not affected by these drugs. Regarding changes in monoamine neurotransmitters, systemic and intraventricular administration produced similar effects. These findings indicate that the drugs were effectively incorporated into the brain by the TPMD method and the drug effect was observed in the opposite brain hemisphere. In the same procedure as used in the administration of haloperidol and apomorphine, methyl bromide was given into the rat brain. DOPAC and HVA in the striatum were increased by methyl bromide given by the TPMD method. These changes were the same as observed in the homogenate of rat brain exposed to methyl bromide. 5 HIAA was reduced by intraventricular administration by the TPMD method, and this change in 5HIAA was not observed in the exposure experiments. We could detect the direct effects of methyl bromide on the brain by the TPMD method.