Interest in the biological effects of maganetic fields is increasing with the widespread use of magnetism in such devices as synchrotrons, funsion reactors, magnetically levitated trains, and medical equipments. However, the biological effects of magnetism have not yet been well explained. In this paper, the whole-body exposure to large magnetic field is distinguished from the local exposure to small magnets. Similary, in considering biological effects, systemic and local responses are distinguished. Systemic biological effects were noted after long-term whole-body exposures, but it was difficult to verify the existence of biological effects after short-term exposures even at high doses. The effects of magnetism on animals appear to be weak; it initially acts as a stimulant, and later as a depressant. These findings may have medical applications, and in any case, they certainly indicate the need for continuing hygienic studies.

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Using T & T Olfactometer which had been developed and standardized for clinical use in Japan recently, measurements of olfactory thresholds of odor detection and of odor recognition were carried out on 33 subjects (26 males and 7 females), who had worked in a chromate producing factory. The subjects had left the factory before 7 years or more. Five kinds of test odors were used; beta-phenyl ethyl alcohol, methyl cyclopentenolone, iso-valeric acid, gamma-undecalactone, and scatol. The degree olfalfaction loss was expressed with the number of powes of 10 in series of multiple concentrations by 10 of each test odor with reference to the concentration of the detection threshold of young normal people. Seventeen of 33 subjects (51.4%) had a perforation of the nasal septum. Middle and high grade decrease of odor recognition faculty were found in 18 (54.5%) including 2 anosmia, one of whom complained also the disorder of taste. Any specific patern of olfactogram chracterizing them were not found, namely, chromates impair olfactory sense for all kinds of odors, which means the impairment of olfactory epithelium itself. The degree of olfaction loss was related to the duration of employment in the chromate producing facory. The existence of septal perforation had no direct relation to the degree of olfaction loss.

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The concentration of organic solvents in plastic bags is decreased with time elapsed. It was supposed to permeate in plastic films. Therefore, we assumed that this phenomenon will be approxiamately regulated by the first order reaction (C=C₀e^-kt). We got the permeation coefficient (K) by experiments and used in to correct organic solvent concentrations in the plastic bags. In the present experiment, we used Tedlar bags, toluene and ethyl methyl ketone (MEK) as organic solvents and determined the values by gas chromatography. Initial organic solvents concentration and that after t hr standing being taken as C₀ and C. k Values are obtained by the formula C=C₀e^-kt. Mean values of k about toluene and MEK were found: k^^-=6.00×10^-3 and k^^-=4.86×10^-3. The results by this correction were as follows: Retention of toluene concentration in 24 hr standing bags showed to increase from 81% to 93%, or, in the case of 96 hr standing bags, it was shown to increase from 56% to 100%. Retention of MEK concentration in 24 hr standing bags showed to increase from 86% to 97%, or, in the case of 96 hr standing bags, it was shown to increase from 68% to 109%.

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Effects of noise exposure on aural reflex (AR) were investigated. The threshold of AR (ART) was measured in two groups exposed to occupational noise (Group A and B) by the electro-acoustic impedance bridge (Madsen, ZO-72). White noise (WN), and pure tones of 1 and 4 kHz were selected as activating stimuli for AR, and ARTs for these stimuli (ART_WN, ART_1k, ART_4k) were determined respectively. The results were compared with the ARTs in the normal group (Group C) reported by the authors previously. Group A consisted of 31 male workers exposed mainly to steady noise, and Group B included 65 male workers exposed maily to impulsive noise. Group C consisted of 50 males and 50 females, who had normal hearing acuity without any history of occupational noise exposure (Fig. 12). Mean age was 37.2 years in Group A, 49.9 in Group B. Mean period of noise exposure was 13.3 years in Group A, 26.1 in Group B. In both groups, the hearing loss was observed in the higher frequency region at 4 and/or 8 kHz, while normal hearing acuity was reserved at 1 kHz (Fig. 3 and 4). Because of no significant difference between Group A and B in each of the mean ARTs (Table 3), Groups A and B were summarized as the exposed group to noise. ARTs for three different stimuli (ART_WN, ART_1k, ART_4k) in the exposed group showed significant differences compared to those in the non-exposed group (Group C); i.e. mean ART_WN was 92.0 dB SPL in the exposed group and 83.8 in Group C, mean ART_1k was 93.8 dB SPL in the exposed group and 96.2 in the non-exposed, mean ART_4k was 102.1 dB SPL in the former and 97.5 in the latter group (Table 5). There was a significant negative correlation between the hearing level at 4 kHz (HL_4k) and the value of [ART_4k-HL_4k] (Fig. 14). The difference between ART_1k and ART_WN, [ART_1k-ART_WN], was significantly reduced in the exposed group; i.e. 1.9 dB in the exposed group and 12.4 in Group C (Table 6). For the purpose of our study, the exposed group was re-classified into another two groups according to their HLs at 4 and 8 kHz; i.e. Group D (HL_(4k+8k)/2<25 dB) and Group E (HL_(4k+8k)/2>__=25 dB). The mean values of ARTs and HLs in Groups D, E and C, which are summarized in Table 7, show two interesting points. First, the significant elevation of ART_WN is observed not only in Group E but also in Group D with normal hearing acuity. Second. the lowering of ART_1k is observed in Group E only. These results indicate that the elevation o ART_WN probably depends upon the exposure history to occupational noise but not upon the hearing loss, and that lowering of ART_1k may be caused by the hearing loss of the subjects in the higher frequency region. These estimations may be supported by the fact that [ART_1k-ART_WN] was 3.7 dB in group D and 0.6 dB in Group E (Table 8). Since damages of outher hair cells (OHC) in the Corti's organ do not always lead to hearing loss, it is conceivable that the reduction of [ART_1k-ART_WN] is the results of the widening of the critical band width for AR due largely to the damage of OHC caused by the occupational noise exposure. Under this conception, the value of [ART_1k-ART_WN] may be used as a sensitive and objectibe indicator for detecting and evaluating the early stages of noise-induced hearing impairment and individual susceptibility to noise.

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