わが国の悪性新生物死亡について, 全部位および部位別に, 性別・年齢5歳階級別のコホート分析を行い, その動向を検討した。
資料は, 人口動態統計を用い, 各種演算は東京大学大型計算機センターHITAC 8800/8700システムによった。作図は, X-Yプロッターを使用した。
1881年∼1965年までの5年毎の出生群を対象に, 横軸に年齢, 縦軸に人口10万対死亡率をとって, 経年的に変化をみると, 全部位では, 高年層と若年層で, 後から生まれたコホートの死亡率上昇が認められた。ただし, 女子では, 40・50歳代で, 死亡率低下がみられた。
部位別にみると, コホート現象を示さぬもの (肝臓・男, 乳房・女) とコホート現象を示すものに大別された。
さらに, コホート現象は4つの型に分類された。分類1は, 男女の胃の悪性新生物死亡にみられ, 後から出生したコホート程, 同一年齢における死亡率が減少していく型である。
型2は, 型1の変型ともいえるもので, 一時期死亡率が上昇し, その後は型1と同様の減少を示す。2相性であることが特徴で, 女子の肝臓の悪性新生物死亡に認められた。
型3は, 男女の肺の悪性新生物, 男女の膵臓の悪性新生物に代表されるもので, 出生の遅いコホートほど, 死亡率の高まる現象を示している。これは, 型1とは逆の動きであり, 管理上, 重要な動向である。しかし, 若いコホートでは, 死亡率増加速度は減少しているので, 近い将来, ある一定の死亡率へ収束するものと思われる。
型4は, 男女の白血病に認められた現象である。従来, 加齢とは余り関りのない死亡パターンであったものが, 全体的に死亡率が増加し, 年齢階級別死亡率曲線が, 高齢で高くなる方向に直線化, 即ち非特異化の方向への死亡構造の変化を示した。

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The study covered 40 Itai-itai disease patients and 61 suspected patients who were considered to be heavily damaged by cadmium. The reference group was comprised of 27 inhabitants in a nonpolluted area.
Blood specimens were collected, and the erythrocyte counts, hemoglobin and hematocrit values were measured. Blood and urine were also examined biochemically. Erythrocyte counts, hematocrit and hemoglobin values decreased significantly in the Cd-exposed groups. The mean M.C.H., M.C.V. and M.C.H.C. were higher in the Cd-exposed groups than in the reference group.
Significant correlation coefficients in the Cd-exposed groups were observed between the erythrocyte counts and abnormal blood or urine, e.g. Cd, RBP, β₂-microglobulin and lysozyme in the urine and creatinine, BUN, total protein, uric acid, alkaline phosphatase, TRP%, LDH and iron in the plasma.
The correlation coefficients between the erythrocyte counts and the levels of creatinine and BUN in plasma were -0.61 and -0.50, respectively.
We concluded that anemia in patients with or suspected of having Itai-itai disease is not hypochromic nor microcytic. Renal damage caused by cadmium exposure may be one of the factors that cause the anemia.

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Phosvel is an organophosphorus pesticide that produces a delayed neurotoxic effect in hens. Residues of Phosvel have been reported to be present in adipose tissue of birds up to 21∼28 days following a single oral dose of 250mg/kg. We here describe accumulation of the pesticide in the fatty tissue of hens given a single, daily administrations of small doses.
Hens (22 months old) were given a single oral dose of 5, 10 or 20mg/kg b.w. of Phosvel daily, and were killed 24 hours after test periods of 7, 14, 21 or 28 days. Three birds that developed signs of paralysis died 3 days before the final dose (28 days).
The concentraion of Phosvel in the fat of hens given 5mg/kg and 10mg/kg increased during the first 21 days, but fell slightly by the termination of the experiment at day 28. Phosvel storage in the fat of birds given 20mg/kg was relatively stable up to 14 days of administration, but increased sharply thereafter. At day 25, the Phosvel concentration in the fat reached a maximum. The level of Phosvel in the fat was proportional to the amount of the daily dose. Three birds given 10mg/kg showed signs of ataxia after the 19th∼26th dose and paralysis after the 20th∼28th dose. Six hens given 20mg/kg showed signs of ataxia after the 17th∼20th dose and paralysis after the 21st∼26th dose.
The results clearly show that Phosvel accumulated in the adipose tissue of hens after continuous exposure and that delayed neurotoxicity in hens was produced following the daily oral administration of 10∼20mg/kg.

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Adsorption of HgCl₂ and CH₃HgCl in aqueous solutions by the hair was measured at 20°C and 30 °C. The concentration of adsorbed Hg was higher at 30°C than 20°C; both isotherms adapted well to Freundrich equation.
An increased mercury concentration on the hair was clear even in extremely dilute mercury solutions.
Desorption of HgCl₂ adsorbed by the hair was poor when hair was washed with HCl solutions. But the CH₃HgCl on the hair was eluted very well with 1N HCl solution. A washing with 1mM of L-cysteine did not elute the mercury on the hair much.
Thus, desorption of only the outer-adsorbed mercury on head hair is considered impossible. Measurement of methylmercury is recomended as a sign of internal organic mercury absorption.

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Audiometrically normal, male students (ages 18 to 22, 6-12 persons) were exposed to intermittent and steady-state noise (480 minutes, pink noise), after which the Temporary Threshold Shift (TTS) and urinary 17 OHCS levels were measured.
The rise-decay time of an exposed noise (trapezoidal noise, cf, Fig. 1) was ca 500ms and the duration was 6.5 seconds. Peak levels of the intermittent noises were 80dB (A) and 90dB (A).
Experimental Conditions
Exposure 1: Control
Exposure 2: Peak level 90dB (A); duty cycle 2 minutes.
Exposure 3: Peak level 90dB (A); duty cycle 1 minute.
Exposure 4: Peak level 90dB (A); duty cycle 24 seconds.
Exposure 5: Peak level 90dB (A); duty cycle 12 seconds.
Exposure 6: Peak level 80dB (A); duty cycle 2 minutes.
Exposure 7: Peak level 80dB (A); duty cycle 1 minute.
Exposure 8: Peak level 80dB (A); duty cycle 24 seconds.
Exposure 9: Peak level 80dB (A); duty cycle 12 seconds.
Exposure 10: Steady state noise; sound level 90dB (A).
Exposure 11: Steady state noise; sound level 80dB (A).
Results
(1) TTS growth
The coefficients of regression of TTS growth by exposures 1, 2, 3, 6, 7 and 8 were not significant. The coefficient of regression of TTS growth induced by exposures 4, 5, 9, 10 and 11 were significant.
The TTS₂ of noise exposure for 480 minutes, calculated according to regression equations, were determined by the on fraction rule. This gave a TTS for exposures 4 and 5 (on fraction 25%, 50%) that equaled 29% and 40% respectively of the TTS of exposure 10.
(2) Urinary 17 OHCS levels
There was a significant difference between the 8 hours-urinary 17 OHCS levels induced by exposures 6 and 7 and that induced by the control. No significant difference appeared between the urinary 17 OHCS levels induced by other noise exposures (exposures 8, 9 and 11) and that induced by the control.
The coefficient of regression between the 8-hour-urinary 17 OHCS levels to the logarithm of the on fraction was significant.

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The amounts of daily arsenic intake from food have been reported by the joint FAO/WHO Expert Commitee on Food Additives, by Schroeder and Balassa, and by Nakao. Published values vary widely from 0.073mg per capita per day to 2.0mg per capita per day, mainly because no accurate methods for the determination of arsenic in various foods have been established.
I previously reported an accurate and highly sensitive method for the determination of arsenic in biological material that uses combined solvent extraction and carbon furnace atomic absorption spectrometry. I here report the accurate amounts of arsenic contained in various fuods. The amount of arsenic in the average Japanese diet was calculated based on the analyzed data from this study, and the per capita intake of foods was compiled by food groups. The daily intake of arsenic was determined to be approximately 0.126mg per capita per day in a diet of 1, 399g per day. This value compared fairly with Nakao's reported value of 0.073mg to 0.173mg per capita per day. The principal source of arsenic in the Japanese diet is fish, 72%; followed by seaweed, 10%; and rice, 10%.

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Untrained healthy male volunteers were studied to observe the effects of muscular exercise (bicycle ergometer, 920kpm/min for 15min and 30min) on the levels of carbonic anhydrase B (CA-B) and C (CA-C) isozymes and 2, 3-diphosphoglycerate (2, 3-DPG) in the blood. Significant decreases in the levels of CA-B and total esterase activity were observed after 15min and 30min of exercise, but the level of CA-C did not vary much. The level of 2, 3-DPG increased after 30min of exercise. Positive correlations were observed between the levels of CA-B and total esterase activity after each exercise (r=0.675, 0.619). The decrease in total esterase activity is caused by the decrease in CA-B. The mean value of 2, 3-DPG after exercise increased to 19.3per cent after 30min of exercise. This indicates that the magnitude of increase in 2, 3-DPG was sufficient to shift the oxygen dissociation curve to the right. A negative correlation was found between the levels of CA-B and 2, 3-DPG after 30min of exercise (r=-0, 618), but no significant correlation was found after 15min of exercise. The blood lactate-pyruvate ratio increased above the pre-exercise values after 15min, but not after 30min of exercise. After 30min of exercise the increase in lactate concentration and the change in 2, 3-DPG showed good correlation (r=0.667). These observations suggest that the decrease in CA-B plays a part in the combination of 2, 3-DPG and deoxyhemoglobin under hypoxic conditions, and that enhancement of oxygen delivery through an increase in 2, 3-DPG is important for adequate homeostatic adjustment to prolonged exercise.

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Testicular injury is known to be provoked by a single dose of cadmium administered to rats or mice. We have studied the effects of environmental temperatures on cadmium-induced testicular injury. Macroscopic experiments were performed twice. In the first experiment, 18, 4-week-old male rats of the Sprague-Dawley strain were acclimatized to environmental temperatures of 8°, 22°or 32°C for 10 weeks; then they were given a single subcutaneous dose of cadmium chloride at levels of 0, 3, 6 or 12mg/kg. In the second experiment, 37, 4-week-old male rats were acclimatized to 8°, 22°or 38°C for 4 weeks, after which they were given a single injection of 0, 3, 6, 12 or 24mg/kg cadmium chloride. The degree of cadmium-induced testicular and epididymal hemorrhage was related to the environmental temperature: the higher the environmental temperature, the more severe the cadmium-induced testicular injury.

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