Document 44BaDJkMRRBqpby4MJqkqbRER

rrr Industrial Hygiene Digest Dcccrotxf, 1962 Vn Indc i \ i hydrolysis And precipitation aft the alto of injection with subsequent development of peritonitis. 115f The citrate* and edctatc complexes are absorbed from the Injection site and show a general pattern of decreasing toxicity from the lower to higher lanthanons. Cross and histopathologic 4* cal examination of bone marrow (sternal), liver, kidney, spleen, adrenals, sex organs, lungs, myocardium, and mesenteric lymph nodes indicate that lesions, when found, were similar t for all rare earth*. There appears to be a predilection for liver and kidney. Citrates pro* i duce an acute passive congestion of lungs and liver within 4 hours after injection, which is of a transitory nature. Renal changes are found later but not consistently* In general, the ! citrates^ were more toxic than the edetate complexes. Authors' summary 1(46 The Determination of Thallium io Urine. M. B. Jacobs. Am. Ind. Hyg. Assn, J. 23, 411-414 (Sept.-Oct. 1962). A variation of the triphenylmefthane dye method for the determination of thallium has been modified to be suitable for analysis of urine samples in a small laboratory. Thallium is oxidised to the thallic state by bromine water, and is reacted with methyl violet for the colorimetric measurement. A maximum of 200 micrograms thallium per liter was found in the urine of 21 exposed individuals. Urine of unevposed persons showed virtually no thallium. *"* Author's abst. list 1147 A Modification of the McCord and Zcmp Method for the Determination of Lead in Urine. A. frank.- Am. Ind. Hyg. Assn. J. 23, 424-430 (Sept.-Oct. 1962). In the determination of the total lead content of urine by the dtthisone method a large part of the analysis time is spent in ashing. McCord and Zemp deicribed s method using 'wet ashing", which shortened the ashing time to JO minutes. The author, by using a modi fication of the above method, found that no loss of lead occurred as compared with a deter mination carried out with a longer ashing time. This method may be used for the analysts of urine from persons suffering from lead poisoning even after treatment with EDTA or penicii* (amine. - - Author's abst. -* 1152 1146 Toxic Properties of PUlkylnitrosamlnes and Some Related Compounds. D. F. Heath and P. N. Magee. Brit. J. ind. M.d, 19, 276-2,2 (Oct. 1962). This paper is mainly a review, but It also includes observations which have not base published elsewhere. Same dialkynltrossmines are valuable chemical intermediates or sol vents, and their uae as insecticides has been suggested. In the present paper their toxic action is reviewed. Most'resuiis refer to rats. Their main acute effect is hepatic centrilo* * bular necrosis, though lung lesions may appear. The compound* also indue* tumors in Uver, lung, and kidney. One, dimethylnitrosamine, has been shown to cause kidney tumors after a single dose. The necrotic and carcinogenic doses of the compounds are closely related. Analogous formamides are much less toxic (the LDSO's in rats by intraperitoneal injection of dimethyl* and diethyi-formatnides are 3,800 mg./kg. and 1,740 mg. /kg. and they do not cause ccntrilobular necrosis or tumors. Nitroaamines are oxidited in vivo and by liver pre : parations in vitro. Their toxic action is due to the release of powerful alkylating agent* in i the Uver. Thuy also inhibit protein synthesis and alkylate liver protein and ribonucleic acid. In all cases the effective agent appears to be a metabolite. The possible hazard to man in i the uses of these compounds is emphasised. 1153 1149 A Study of Acrylonitrile Poisoning in Relation to Mcthaemoglobin-CN Complex Formation. i U, Magos. Brit, J. |nd. Med. V*. 263-2*6 (Oct. 1962). 1 Observations are recorded on mcthacmoglobin-CN complex formation in rats poi soned with acrylonitrile, potassium cyanide, and acetone cyanohydrin. In methaemoglobin- t CN formation, the methaemoglobin level was increased by sodium nitrite. The results show that the rate of methacmoglobin-CN formation in rats kilted by acrylonitrile is lower than t in animals surviving potassium cyanide or acetone cyanohydrin poisoning, and much lower i than tn animals killed by potassium cyanide. These findings Indicate that the toxicity of acry i lonitrile cunnot be solely due to the liberation of cyanide. i t I \