It is likely that in the near future industrial physicians will have to deal with more and more cases of extremely slight intoxication without appropriate diagnostic means. Therefore, newer methods must be developed to detect the latent damages which have been overlooked by the conventional methods of examination. It was reported by several papers that the mice chronically exposed to CS₂ died at higher death rate than the untreated mice when they were exposed secondarily to CS₂ of higher concentrations. In these cases any signs of intoxication prior to the secondary exposure could not be found. This fact implies that the latent CS₂ poisoning in mice could be detected by the secondary loading of CS₂. To clarify the nature of the inapparent abnormality in these mice and to find some clues for establishing a new method to detect the latent CS₂ intoxication in man, experiments were performed with the following results. (1) Mice exposed to 300 ppm CS₂, eight hours a day, for 30 days did not show any signs of chronic CS₂ poisoning, judged from the usual toxicological criteria such as growth rate, leucocyte count, hemoglobin concentration and histopathological findings of the lung, kidney, spleen, bone marrow and the brain. The respiratory rates of the exposed group, however, decreased much more rapidly than those of the control group, when the both groups were exposed secondarily to 3000 ppm CS₂. (2) The above findings were ascertained more clearly when intraperitoneal injection, instead of inhalation, of CS₂ was adopted as the route of administration. In this case, the respiratory rates of the exposed group decreased remarkably, and more than half of them died of respiratory paralysis, while those of the control group remained normal. (3) Moreover, intraperitoneal injections of some central nervous system depressants were tested on the assumption that these drugs, with their remarkable respiratory depressant action, could manifest the same effect as the administration of CS₂. As anticipated, one of them, thiopental sodium, depressed definitely the respiratory rates of the exposed group and no depressions were found in the control group. (4) The latent CS₂ intoxication in mice as detected with the above mentioned methods was found to be established by a 19-day exposure to 300 ppm CS₂ and recovered by discontinuation of the exposure for 100 days. From these results, as well as from references, it was discussed and estimated that the inapparent abnormality in the latently CS₂ poisoned mice was located at the respiratory center. This work suggests the possibility of finding some practical methods to detect the latent CS₂ intoxication in man.

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In spite of many efforts in studies on the toxicity of organic phosphates, which have been well known as agricultural insecticides, no attempts have been made to obtain an understanding of the effects which the organic phosphite might have on man and domestic animals. Organic phosphites are about to be used as antioxidants and stabilizers of resin or transparency promoters of alkyd resin paints. Investigations on the effects of organic phosphites upon living bodies should be made before their industrial use. For this reason we have attempted to make experimental studies of the toxicity of organic phosphites in vitro or in vivo. Organic phosphites we used were tridecyl-, phenyldidecyl-, diphenyldecyl-, and triphenyl-phos-phite. We have studied the peroral LD₅₀, the rate of organ weight, and the inhibitory action of cholinesterase activity in the red blood cells and the plasma, and still more, have attempted to elucidate whether the triphenyl phosphite has the same toxic effects as triphenyl phosphate. The results obtained were: 1. Peroral LD₅₀ in mice of tridecyl-, phenyldidecyl-, diphenyldecyl-, and triphenyl-phosphite were 13.9, 13.1, 16.0 and 3.1 grams per kilogram body weight respectively. According to the classification of Hodge et al., the former three compounds are harmless and the latter, triphenyl phosphite, is slightly toxic. 2. The rate of the organ weight to the body weight at the 8 th day following the single peroral administration in mice was higher in the heart, spleen, kidney and testis as compared respectively with those of normal mice. Lung weight of mice treated subcutaneously with triphenyl phosphite increased more than that of mice treated perorally. 3. Subcutaneous LD₅₀ in mice of triphenyl phosphite and triphenyl phosphate were 0.47 and 1.05 gram per kilogram body weight respectively. The toxicity expressed by LD₅₀ of triphenyl phosphite was approximately three times higher as compared with that of triphenyl phosphate. 4. When triphenyl phosphite was administered subcutaneously to rabbits in a dose of 30 mg/kg a day for consecutive 20 days, slight anemia appeared and inhibitions of the activity of cholinesterase of the blood cells and the plasma occured. 5. Triphebnyl phosphite or triphenyl phosphate showed an extreme inhibition of the cholinesterase activity in the blood plasma from 12 to 24 hours after the injection and recovered after 2 or 3 days, but no remarkable inhibitory action was found in the cholinesterase activity of the red blood cells in the case of single subcutaneous injections in rabbits. 6. When triphenyl pshophite or triphenyl phosphate were added to human blood cell suspension and plasma in vitro, the cholinesterase activity was more inhibited in the plasma than in the red blood cells.

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This study was taken up for the purpose of clearing up the state of the central nervous system affected with lead. I Methods Nine chronically lead-poisoned patients of the age ranging from 18 to 30 years and seven normal clerical employees of the age ranging from 23 to 29 years were chosen at lead smelting works and the examinations were performed as follows: (1) Blood specific gravity, (2) Hemoglobin, (3) Microhematocrit, (4) Basophillic stippled cells, (5) Lead in the whole blood, (6) 24 hours' excretion of urine, (7) Coproporphyrin, (8) Lead in the urine (9) Bluish line along the gums, (10) Subjective symptoms, and (11) EEG and their frequency analysis. II Results 1. The results of the examinations which were statistically significant between the lead poisoned group and the control group are as follows: Microhematocrit, hemoglobin, basophillic stippled cells, lead in the whole blood and in the urine, coproporphyrin, and bluish line along the gums. 2. As to the results of EEG and their frequency analysis of the lead poisoned group, increases of 4∼6 c/s and decreases of 8∼12 c/s and 12∼16 s/c were recognised. The amplitude of EEG of the lead poisoned group was lower than that of the control group. 3. As regards the relation between these examinations and the distribution of EEG frequencies; 1) Increases of 4∼6 c/s and decreases of 12∼16 c/s in the Ht 39.0∼43.3% group were recognised in comparison with the Ht 43.7∼47.4% group. 2) Increases of 4∼6 c/s and decreases of 12∼16 c/s and 16∼20 c/s were recognised in the group of which the lead concentration in the whole blood showed the poisoning level. 3) Increases of 4∼6 c/s and decreases of 12∼16 c/s in the coproporphyrin positive group were recognised. 4) Increases of 4∼6 c/s and decreases of 8∼12 c/s, 12∼16 c/s and 16∼20 c/s were recognised in the group of which the lead concentration in the unine showed the poisoning level. These changes of EEG were statistically significant, and from the relation between those results of examinations and the distribution of EEG frequencies, chronic diffuse changes of the central nervous system in the chronically lead-poisoned group have been briefly discussed.

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