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656. Further studies on chronic benzene poisoning
THE CHEMICAL ENVIRONMENT
505
THE CHEMICAL ENVIRONMENT 656. Further studies on chronic benzene poisoning Thiele, H. (1964). Chronic benzene intoxication. Pracov. L~k. 16, 7. The production of leucopenia in experimental animals by exposure to benzene (CrHr) vapour at low concentrations of 16-65 ppm has been discussed before (Cited in F.C.T. 1964, 2, 67). It has been established that women, especially pregnant women, are more susceptible than men, and that a variety of physical and emotional circumstances can affect the toxicity of CrHr. The present author has described the picture of chronic CrH6 poisoning. Women over 40 yr old appear to be particularly susceptible, and in severely affected cases 97 Yo had hypoplasia of the bone marrow, as opposed to only 43 ~o in men. CrH6 poisoning is seen as being a composite of inhibited blood formation (radiomimetic effect); a facultative megaloblastic picture; vitamin C deficiency without scurvy; and capillary damage with extensive bleeding. Experimental CrH6 poisoning was induced in animals as a basis for testing various remedies. Folic acid and ascorbic acid prevented the development of megaloblastie anaemia, and cysteine prevented hypoplasia of the bone marrow. The two remedies given together however, cancelled each other out. 65~ Toxicology of a manganese sandwich compound Arkhipova, O. G. (1964). Mechanism of action of the new antiknock compound manganese cyclopentadienyltricarbonyl on the organism. Fed. Proc. (Transl. Suppl.) 23, T51. Common manganese (Mn) compounds exert a toxic effect on the central nervous system but this first report on the toxicology of a "sandwich compound" is welcomed with interest. It has been suggested that manganese cyclopentadienyltricarbonyl (CsHsMn(CO)3, I) be used instead of lead tetraethyl as an antiknock compound since it is less volatile, cannot penetrate the skin and is less toxic. However, an earlier investigation by the author (no reference given) showed that I is a cumulative toxin. The LD~0 for rats was found to be 80 mg/kg and for mice 150 mg/kg. The route of administration is however not given. Inhalation of 0.02--0-04 mg I/1 killed 50 ~o of rats. On the basis of inhalation studies on rabbits, guinea-pigs and rats, the USSR Ministry of Health has accepted a maximum permissible concentration of 0.0001 mg I/1. One manifestation of toxicity reported was a variable effect on the threshold excitability of the neuromuscular junction which was reduced when the dose was acute or subacute, but increased when the administration was chronic (but in the table of results no units are quoted). I was also found to cause disturbances in the blood, including an increase in the red and white cell counts and a reduction of osmotic resistance of red cells. Furthermore, the blood of animals killed by I was reported to be "raspberry-colored" (presumably an indication of intravascular haemolysis). Lethal doses of I also produced a marked fall in blood pressure, haemorrhages and hyperaemia of internal organs. A single dose of 100 mg I/kg dose (given to unspecified species) caused a 58 ~o increase in urine output but after inhalation of I for 2 months the urine output and its protein content were unaffected, although the acidity of the urine was reduced. Hyaline casts, renal epithelial cells and leucocytes were found in the urine sediments. The fate of I in the body is not known but it is assumed that inorganic Mn and carbon monoxide would be formed. This is substantiated by the similarity of the toxic effects of I on the nervous system with those of Mn. After the inhalation of small doses of I an increase in the blood earboxyhaemoglobin was detected by a biochemical method but not by spectroscopy. It was found that the inhalation of oxygen revived animals dying from poisoning by I and this is recommended as a method of treatment.
505
THE CHEMICAL ENVIRONMENT 656. Further studies on chronic benzene poisoning Thiele, H. (1964). Chronic benzene intoxication. Pracov. L~k. 16, 7. The production of leucopenia in experimental animals by exposure to benzene (CrHr) vapour at low concentrations of 16-65 ppm has been discussed before (Cited in F.C.T. 1964, 2, 67). It has been established that women, especially pregnant women, are more susceptible than men, and that a variety of physical and emotional circumstances can affect the toxicity of CrHr. The present author has described the picture of chronic CrH6 poisoning. Women over 40 yr old appear to be particularly susceptible, and in severely affected cases 97 Yo had hypoplasia of the bone marrow, as opposed to only 43 ~o in men. CrH6 poisoning is seen as being a composite of inhibited blood formation (radiomimetic effect); a facultative megaloblastic picture; vitamin C deficiency without scurvy; and capillary damage with extensive bleeding. Experimental CrH6 poisoning was induced in animals as a basis for testing various remedies. Folic acid and ascorbic acid prevented the development of megaloblastie anaemia, and cysteine prevented hypoplasia of the bone marrow. The two remedies given together however, cancelled each other out. 65~ Toxicology of a manganese sandwich compound Arkhipova, O. G. (1964). Mechanism of action of the new antiknock compound manganese cyclopentadienyltricarbonyl on the organism. Fed. Proc. (Transl. Suppl.) 23, T51. Common manganese (Mn) compounds exert a toxic effect on the central nervous system but this first report on the toxicology of a "sandwich compound" is welcomed with interest. It has been suggested that manganese cyclopentadienyltricarbonyl (CsHsMn(CO)3, I) be used instead of lead tetraethyl as an antiknock compound since it is less volatile, cannot penetrate the skin and is less toxic. However, an earlier investigation by the author (no reference given) showed that I is a cumulative toxin. The LD~0 for rats was found to be 80 mg/kg and for mice 150 mg/kg. The route of administration is however not given. Inhalation of 0.02--0-04 mg I/1 killed 50 ~o of rats. On the basis of inhalation studies on rabbits, guinea-pigs and rats, the USSR Ministry of Health has accepted a maximum permissible concentration of 0.0001 mg I/1. One manifestation of toxicity reported was a variable effect on the threshold excitability of the neuromuscular junction which was reduced when the dose was acute or subacute, but increased when the administration was chronic (but in the table of results no units are quoted). I was also found to cause disturbances in the blood, including an increase in the red and white cell counts and a reduction of osmotic resistance of red cells. Furthermore, the blood of animals killed by I was reported to be "raspberry-colored" (presumably an indication of intravascular haemolysis). Lethal doses of I also produced a marked fall in blood pressure, haemorrhages and hyperaemia of internal organs. A single dose of 100 mg I/kg dose (given to unspecified species) caused a 58 ~o increase in urine output but after inhalation of I for 2 months the urine output and its protein content were unaffected, although the acidity of the urine was reduced. Hyaline casts, renal epithelial cells and leucocytes were found in the urine sediments. The fate of I in the body is not known but it is assumed that inorganic Mn and carbon monoxide would be formed. This is substantiated by the similarity of the toxic effects of I on the nervous system with those of Mn. After the inhalation of small doses of I an increase in the blood earboxyhaemoglobin was detected by a biochemical method but not by spectroscopy. It was found that the inhalation of oxygen revived animals dying from poisoning by I and this is recommended as a method of treatment.