Evoked potentials (short-latency somatosensory, visual and brainstem auditory evoked potentials), event-related potential (P300), electrocardiographic R-R interval variability, peripheral nerve conduction velocity, distribution of nerve conduction velocities, postural balance, neurobehavioral test batteries, and questionnaires and psychiatric interview methods appear to be promising techniques for assessment of subclinical neuro-psychobehavioral effects in occupational, environmental and community health. In this paper, an overview of recent methodology and findings is provided. The available data indicate that these techniques are valid, reliable and standardized, and are easily applied in field studies.

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We compared the mortality rate of sumo wrestlers with that of the contemporaneous Japanease male population, and inferred the usefulness of an index for predicting longevity in sumo wrestlers. The standardized mortality ratios (SMR) for sumo wrestlers were very high in each period, and also high for ages from 35 to 74. Cox's proportional hazards model analysis revealed that the variables in “nyuumaku” entry year and BMI were statistically significant (p<0.05) factors in mortality. In the survival curves, the lower BMI group had good life expectancy compared with the higher BMI group. In conclusion, the higher rate of mortality in sumo wrestlers seems to be due to the markedly higher rate of mortality from 35 to 74 years old. In sumo wrestlers, also, this study provides evidence that the higher overweight groups have substantially higher risks for mortality.

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We performed correlation analysis on the relationship between changes in air pollution and the consultation rate for bronchial asthma in the Yokkaichi region, taking effects of various socioeconomic factors into consideration. The effects of changes in air pollution on the mortality rate due to bronchial asthma were also evaluated.
1. Evaluation of annual changes in the simple correlation coefficient between the consultation rate and the concentration of each pollutant showed no significant correlation with a decrease in the air pollutant concentration in the age group less than 10 years old. However, in the middle-advanced male and female groups aged 40 years and above, the influence of past air pollution still remained. In addition, the partial correlation coefficients between the consultation rate for bronchial asthma and the degree of pollution, socioeconomic factors, and the rate of heavy smokers were calculated. A significant correlation was observed between the consulation rate for the females in each age group and the rate of patients receiving public assistance.
2. The mortality rate due to bronchial asthma in the polluted area increased rapidly with a time lag of several years after the peak of air pollution but decreased gradually thereafter. Presently, the mortality rate in the polluted area is similar to that in the non-polluted (control) area.
3. The mean age of death due to bronchial asthma was elevated because of a decrease in the deaths of those aged less than 60 years. As a result, the difference in the mean age of death due to bronchial asthma between the polluted area and the control area disappeared.
With the recent remarkable alleviation of air pollution, the consultation rate and mortality rate due to bronchial asthma have decreased considerably. However, differences are still observed compared with the control area in some age levels so that continuation of monitoring of air pollution as well as consultation and mortality rates is considered necessary.

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We measured vibratory sense thresholds (VSTs) at 63Hz and 125Hz on the third fingertip of the right hand and on the third toe of the right foot of 74 male workers. The subjects were workers engaged in manufacturing ceramic color and transfer printing paper, whose blood lead (Pb-B) levels were 2-58μg/dl. They were divided into three groups according to the Pb-B levels, namely, below 9, 10-19, and 20μg/dl or more. For statistical analysis, simple and partial correlations, and Scheffé's multiple comparison between the least squares means were used. The VSTs on the fingertip as well as on the toe showed a significant correlation with age. The VSTs at 125Hz on the fingertip were also significantly correlated with alcohol consumption and cigarette smoking. Controlling for age, systolic blood pressure, alcohol consumption and smoking habit, a significant dose-effect relationship was observed between the VSTs at not only 63Hz but at 125Hz on the fingertip, and each of the corresponding Pb-B levels. A similar tendency was also observed at the two frequencies on the toe. The measurement of VSTs was considered to be an effective screening test for sensory nerve disorders caused by lead poisoning.

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Effects of undernutrition on development of cadmium (Cd) poisoning were investigated in mice over a long experimental period ranging from 29 days to 24 months. The study was designed to examine low in calcium, low in vitamin D and low in vitamin E diets, which were considered neither to induce lesions of Ca, vitamin D and vitamin E deficiency nor innutrition.
Twenty-nine-day-old female ICR strain mice were separated into 7 groups and different diets were given to each group. Group I a commercial diet (Intact), Group II a low in Ca and low in D diet, Group III a low in Ca, low in D and low in E diet, Group IV a low in Ca, low in D and 20ppm Cd diet, Group V a low in Ca, low in D and 40ppm Cd diet, Group VI a low in Ca, low in D, low in E and 20ppm Cd diet and Group VII a low in Ca, low in D, low in E and 40ppm Cd diet.
Using X-rays of the hind legs, the bone density was measured at the middle of the femur employing a densitometer; effects of the undernutrition and the cadmium-added diet on bone density were investigated referring to five indices: 1) peaks of the density of the middle of the bone cortex (h1, h2) (the maximum density of the bone cortex (h1+h2)/2 [hmax]), 2) the lowest density of the middle of the bone marrow (h3) (the minimum density of the bone marrow [hmin]), 3) the bone cortical width (d1+d2), 4) the bone marrow width (d) and 5) the cortical bone index (the ratio of cortical bone width to bone width. [CBI]).
The long-term effects of cadmium.
a) Comparisons among groups II, IV and V.
At 18 months it was found in group IV that hmax and d were small, while hmin, d1+d2 and CBI were not appreciably different compared with group II. In group V hmin, d1+d2 and CBI were small, and hmax and d were not appreciably different compared with group IV.
At 24 months it was found in group IV that hmin and d were small, whereas hmax, d1+d2 and CBI were not appreciably different compared with group II. In group V hmax and hmin were small, d was large, and d1+d2 and CBI showed no appreciably different compared with group IV.
b) Comparisons among groups III, VI and VII.
At 18 months it was found in group VI that hmax and hmin were small, d1+d2 and CBI were large, and d was not appreciably different compared with group III. In group VII hmax, hmin, d1+d2 and CBI were small, and d was large, compared with group IV.
At 24 months it was found in group VI that hmax, d1+d2, d and CBI were small, and that hmin was not appreciably different compared with group III. In group VII d was small, and hmax, hmin, d1+d2 and CBI were not appreciably different compared with group VI.
The Cd concentration exhibited essentially the same pattern as aging.
We concluded from these results that aging progressed quickest in the 40ppm Cd-administration
low-Ca, D, E diet.
The diets promoted the effects of Cd in the following order: low Ca, D, E diet>low Ca, D diet.
These results indicate that Cd promotes aging of bone.

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To clarify the effect of chronic cadmium exposure on muscles, 29-day-old female ICR strain mice were separated into 7 groups and various diets were given to each group. Group I a commercial diet (Intact), Group II a diet low in calcium and low in vitamin D, Group III a diet low in Ca, low in D and low in vitamin E, Group IV a low in Ca, low in D and 20ppm cadmium-added diet, Group V a low in Ca, low in D and 40ppm Cd diet, Group VI a low in Ca, low in D, low in E and 20ppm Cd diet and Group VII a low in Ca, low in D, low in E and 40ppm Cd diet. The levels of vitamin D and vitamin E were designed to be low in each diet but their amounts fulfilled the minimum nutritional requirements.
The experimental period was long, ranging from 29 days to 24 months. Using a microscope, two skeletal muscles, the soleus (red muscle) and the gastrocnemius (white muscle) of mice with chronic Cd effects were observed after staining with H. E. and analyzed after enzyme histochemical reaction to ATPase. Using ATPase stain, type I muscle fibers were distinguished from type II muscle fibers.
The long-term effects of cadmium.
1) Comparisons among groups II, IV and V.
After 18 months it was found in group IV that myopathic muscle damage (increased random variation of fiber size [Size] and widening of interstitial tissue [Widening]) were more prominent that in group II. In group V myopathic muscle damage (Size and Widening) and type II atrophy were more prominent that in group IV.
At 24 months it was found in group IV that myopathic muscle damage (Size, internal nuclie [IN] and Widening) and type I and type II atrophy were more prominent than in group II. In group V myopathic muscle damage (Size, IN and Widening) and type I and type II atrophy were more prominent than in group IV.
2) Comparisons among group III, VI and VII.
At 18 months it was found in group VI that myopathic muscle damage (Size, IN and Widening) and type I and type II atrophy were more prominent than in group III. In group VII myopathic muscle damage and fiber size showed no appreciable difference compared with group VI.
At 24 months it was found in group VI that myopathic muscle damage (Size, IN and Widening) and type I and type II atrophy were more prominent than in group III. In group VII myopathic muscle damage and muscle fiber size showed no appreciable difference compared with group VI.
Myopathic muscle damage (Size, IN and Widening) and type I and type II atrophy were found to be ptominent in all mice with Cd their diets. These findings were more promineent in the 40ppm Cd diet group than in the 20ppm Cd diet group. Similar findings were observed in 24-month-old mice and 18-month-old mice given Cd-added diets and the damage increased with age.
We concluded from these results that aging progressed quickest in the 40ppm-Cd administration low Ca, D, E diet.
The diets promoted the effects of Cd in the following order: low Ca, D, E diet>low Ca, D diet. Aging progressed quicker in the soleus muscle than in the gastrocnemius muscle.
These results indicate that Cd promotes aging of skeletal muscles.

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