Document qm56qRMVkbmddbqNKDk7Z1aD5

ABSTRACTS FROM CURRENT LITERATURE 421 Permissible Tolerance of Hydrogen Sulfide in the Atmosphere. L. F. Glebova, Gigiena i Sanit., 1950, no. 4, p. 19. Experiments with children kept in nurseries associated with viscose plants showed typical symptoms of sulfide intoxication caused by the toxic materials carried over by the mothers' clothing. The symptoms were evident, although determinations of CS2 gave negative results and H2S concentrations in the air under the clothes were 0.028 to 0.05 mg./M.3 or lower. Apparently the effect is caused by cumulative action of small amounts of H2S. The solution was to transfer the nursing mothers to another department. Adaptation of Chem. Abst. Toxicity of Vapors of Organic Compounds of Mercury (Ethyl Mercuric Phosphate and Chloride) in Acute and Chronic Intoxications. I. M. Trakhtenberg, Gigiena i Sanit. 1950, no. 6, pp. 13-17. Acute and chronic toxicities of ethyl mercuric phosphate (I) and ethyl mercuric chloride (II), aqueous solutions of which are being widely used in Soviet agriculture under the names of NIUIF-1 and Granozan, respectively, were determined on white mice by the vapor technique. Acute poisoning is characterized by respiratory symptoms, and of nervous ones to a lesser extent; in chronic cases, attack on the central nervous system prevails. The vapors of I and II are more toxic than metallic Hg, and the results indicate that for safe human working conditions even traces (0.00001 mg./l.) should not be tolerated. Exposures to 0.01-0.03 mg./l. caused death in mice within the experimental period of three to five hours. Chem Abst The Toxicity of Methyl Iodide: Preliminary Survey. Monamy Buckf.ll, Brit. J. Indust. Med. 7:122-124 (July) 1950. This preliminary report has been prepared because of increasing interest in methyl iodide (CHal). CHal is used as a methylating agent in petrography, as an intermediate in the chemical industry and has been proposed for use in fire extinguishers. Toxicity studies with rats and mice revealed that by subcutaneous administration it is 10 times as toxic as carbon tetrachloride (CCU) and about as toxic as methyl bromide. It produces a vestibular burn if closely applied to human skin, and therefore any clothing contaminated with CH3I should be removed immedi ately. There is often a considerable time lag between contact and eruption of lesion. Arnold A. Lear, Boston. Phosphine Poisoning. Meinhardt Lowenthal, Schweiz. Ztschr. Path. u. Bakt. 12:313, 1949. A case of PH3 poisoning is described. The clinical, pathologic and toxicologic aspects of the case are compared with results obtained from animal experiments with varying concentrations of PH3. Pronounced blood and lymph stasis, accompanied by brain and liver lesions of a special nature occurred as a result of subacute intoxication. Subchronic poisoning produced degenerative changes of the ganglion cells, indicating that gaseous PH3 must be considered a central nervous system poison. The lesions of the brain and the liver appear to be due to a chemical reaction between the PHs and the red cells, damage to the vascular wall resulting in spastic and paralytic conditions, and osmotic disturbance of permeability. JoHN p Crispeix [Chem. Abst>]. Vascular Disturbances of the Central Nervous System in Carbon Disulfide Poisoning. Enrico C. Vigliani and Carlo L. Cazzullo, Med. lavoro 41:49 (Feb.) 1950. Vigliani and Cazzullo say that polyneuritis, psychosis and extrapyramidal syndromes were the only disturbances due to the chronic occupational CS2 poisoning previously reported in the literature. The authors report on chronic diffuse encephalopathy which occurred in 16 men working in the viscose industry, where they were exposed for a period of 15 or more years to a toxic concentration of CS2 ranging bewteen 0.10 and d.00 mg./L. in the atmosphere. The predominant symptoms were asthenia, paresthesia, progressive impairment of gait and mental deterioration similar to that observed in pseudobulbar paralysis, and either moderate or acute hemiplegia. Arterial hypertension was a frequent complication. Clinical symptoms of arterio- 1 1, !>' \