Document r6Q63QO1YJy2q64bom1nmDQDa

Industrial Hygiene Digest i a i. o June 1976 690/76 Effect of Methemoglobinemia on Carbon Tetrachloride Hepatotoxicity. D. Pankow and W. Ponsold. Toxi col. & Applied Pharmacol. 3: 143-150, April 1976. 16 refs. Injection of 0.8 mmol of NaNO^/kg ip after administration of 5.2 mmol of CCl^/kg po significantly enhanced the rise of glutamic pyruvic transaminase and leucine aminopeptidase activities in the plasma of rats over that observed after administration of CCl^ alone. Enzyme activity was not increased by nitrite administra tion alone, which produced a methemoglobin concentration of about 40%. The potentiation of the CCI4 effect was dependent on the presence of the adrenal glands. CCI4 depresses and retards the formation of methemo globin after nitrite administration. Similar combined effects of CCl^ and other methemoglobin-producing compounds as aniline, nitrobenzene, m-dinitrobenzene, phenylhydrazine, and hydroxylamine hydrochlo ride are described. --Author's abst. 691/76 Two Cases of Angiosarcoma of the Liver in Exposure to Vinyl Chloride . M. Zorica, et al. Arhiv Hig. RadaToks. 26(4): 275-281, 1975. 3 refs. (Yugoslav) Two cases of angiosarcoma of the liver in exposure to vinyl chloride are described. Both cases relate to the factory for the production and processing of PVC which started operating in 1949. The first case concerns a worker born in 1914 who worked on the polymerization of vinyl chloride for about 18 years (from 1953 to 1969) , and spent the last four years in the PVC processing works. The disease became clinically manifest in April 1973 and terminated with a lethal issue the same year in August. The other case was a worker born in 1931 who worked in vinyl chloride production for about 23 years (from 1950 to 1972), five i of which he spent in the hydrogen chloride works. The symptoms appeared in August 1972. The patient died in July 1973. In both cases the tumour was microscopically verified. It is assumed that the two de scribed cases of angiosarcoma are occupationally conditioned and that they occurred as a result of exposure to vinyl chloride. --Author's Summary in English 692/76 Immunological Mechanisms in the Pathogenesis of Vinyl Chloride Disease . A.M. Ward, et al, British I Med. J. 1: 936-938. April 17, 1976. 23 refs. Vinyl chloride (VC) disease is a multisystem disorder incorporating Raynaud's phenomenon, acro-osteoly- sis, thrombocytopenia, portal fibrosis, and hepatic and pulmonary dysfunction. Immunological and immuno chemical investigations showed the presence of circulating immune complexes in 19 out of 28 patients with the disease and in a further two out of 30 workers exposed to VC. The immunological data were reviewed in relation to the clinical picture of the disease and to the available evidence on the metabolism of VC. The results suggest that VC disease is an immune complex disorder and that the immune response is initiated by the adsorption of VC or a metabolite on to tissue or plasma protein. --Author's Summary 693/76 Exposure to Trichloroethylene Monitored by Analysis of Metabolites in Blood and Urine . O. Vesterberg and I. Astrand. J. Occup. Med. 18: 224-226, April 1976, 13 refs. When neurologic effects of excessive exposure to TRI are to be prevented, analysis of TCE in blood or measurement of the excretion rate of TCE in urine seem to give valuable information. However, concerning TCE in blood the proportion thereof present as TCE glucuronide seems to be variable, rendering the use of TCE in blood as an index of the uptake somewhat uncertain. Large differences in TCE in blood occur even at similar exposure levels. As an index of exposure, TCA in urine seems to give more helpful infor mation provided the results are evaluated judiciously. -~Cond. from text 694/76 Effects of 1,1,1-Trichloroethane Administered by Different Routes and in Different Solvents on Barbitu rate Hypnosis and Metabolism in Mice. H.C. Shah and H. Lai. J. Toxicol. & Environ. Health 1: 807-816, May 1976. 25 refs. A 24-hr inhalation of 1,1,1-trichloroethane (methylchloroform), 3,000 ppm, reduced pentobarbital hypno sis and increased hexobarbital oxidation by the 9,000 x g liver supernatant fraction in male mice. On the other hand, an ip injection of methylchloroform, 1 ml/kg, increased the duration of pentobarbital hypno sis and reduced hexobarbital metabolism by the liver microsomal enzymes. The potentiating effect of methylchloroform on pentobarbital hypnosis was diminished when it was diluted with olive oil, but was markedly enhanced when diluted with dimethylsulfoxide (DMSO) before injection. Three local applications i of methylchloroform (1:1 dilution with DMSO) had an effect similar to that of inhalation on pentobarbital hypnosis. --Author's abst. 16 CUSAROSS 02617