Document V3E95re31o62Bn8Eq2Jb6GMqj

C.wL'd T.t; ,.. ,-i . AAh;:.'..'. Ofc/AbAi'A rsi/.i-ii i>: ia s.'.:.t;: JCXIIT Ao/./dO b?y:ific;?!b::s re addx fiv fa a;::; t:.. v- C\ i'..'-i. i-.V i j Gi. 1%' ga'.aa b a:.. ce:':.i 1 x i-JiJ e;: i-coii ITP. AITV :i kiti o? ,, o lActAMA ... .'.aaa A Ah Li biAA.l ;.dc-j .'...iCAo ;::d ' c`:' ' a - ' ; rn- :j:o Gon-V-. 'A' A::- - r ' -- bbb/.'b/'O- j [;i) C/.FP/ DJATVT;'.'; '0/ Dr P. S. Dine (Consul bant) 2&ln&5UJZ&L Biochrmiio 'll_nsv'-?ctt; boat of carbon disnlfi.de (CD-) absorption occurs thr;.".~h the lungs after inhalation tut done car. be absorbed through the skin. VO-u-O^ are absorbed fron the air within 15 .minutes but the "`ate falls 'rapidly to during longer exposure. 5-13b is eliminated unchanged through the .lungs and 0.1-C. gl in the urine, St--95^ is metabolised. Blood becomes saturated quickly b..t there is slew diffusion to the tissues which way tuxe some weeks to achieve satu t.A.n in mimic (DUsir.g et al., 1903; Patty, 1958). CS9 acta as universal enzyme inhibitor and cc-llular poison by interference with oxidative phosphorylation and with fat rc-tabolis:.',. This produces r,yperchole;;tcrolacMia arid hyperldpaenia (5.1 1961) with eventual incrcasos in free placna cholesterol, phospholipids, neuv -! fat and p-lipcprooein (Arb^osio et al,,, 1957$ Patemi et al., 1953) and decroa;1 .ui lipolytic activity of vessel walls (Simon, 1961). CS,, in tissues binds to D-ec. taining compounds to form dithiocarbairates etc., some of which decompose to H,,S wir'.' subseouent oxidation to sulphate. Thus urinary excretion of sulphate is increased (Giovine, 1957). Guinea pigs show similar increases in dithiocarbamic acids after G3, inhalation (5oucek and Jiadlo, 1956). Rabbit liver detoxicates CS,, with concb .-itant sigu3 of changes in capillary permeabilifcy (llichalova ct al., 1959). Other evidence of hepatic damage appears ns increased urinary loss of Zn and tig with decreased alkaline phosphatase activity. This may be the result of chelation by dithiocarbamate- and thiasolidone, the reaction products of GS? with free mlncunid groups. Similar chelation ox' Cu may causa specific CDS' lesiens (SAoel et al., i960). Tho Issue of this rtocuinent coco rot constitute o.-itinl publication. It should not bo rovlswod, abalrcrtod or a'jQiod 'vlthaut tho nr.rcamont of the V'c-ld Hen*tli Crg.-nization. Authors aiono ere responsible for vl-swa expressed In elgned ftrtlc.'js. Ce document norntitue p~\z unc publication II no colt fcl-. I'obj'it d.iucun compte re^du ou rAe'itnA ni d'et. is citation ar.ns Cautorisation do rOrgaiiicstion ! --ndiala de la SanttW Lcs opinions oxprin.A-eo dar > lea articles signes n'ongag^nt que lours cuirird. ASI 00004234 Animal non Jo LB LCD P a f c fence Cat i.'jn Irhal a fcicn IaVO -ttj.vn 35 0 .0 p; ..1 (iO min .) 4 > '-3 p: m i.30 mi; s L'-'Ix; *, 15 i'9 u tg and. 4 J x - Acr, te no i. son.- a-'-; in z 1 s vjrcdu \ tin : nd d- . from if Exposure V. 0 'ni ; t : ':t . - J. * - ir; m. \ :-.L 1.. . .. .> ,, .'T u_ y ;ir;r a . 0 n:u;:o'i, in blood :T, ' M`.\ < v: " '.It;:. / ... c *'0 r ;m J - <3 11 w 1 (.0 (j.: ^ M 'M. ..or ' ; , j _ . . / '! rr''). j -t iuior:, r 0. -- ..J t f -- a resuir'.t or- j Hvra :.MM 0 mental c V f urd Mi MM 1..;: ", ' lens of ;.o. rci or :r: **; n C' vomiting a'1 'I occur nr ! .5 A ox;':rum r in 1 -) t r. scat!ere n ori hr- ' . .rtc \\ 1 O'., 3 rM 1 .ring cousen vc-J.t t ^ , 1' ,\m r. * ^ri . 1953)- " '.IfO: in; . from, d: ' n.' dug CO < 1 ' * oV..:' '. -.oil 0 'Ml ; /s * " ; ;..../ onlv nan 1 j .a .* ,1 * l or' 'Mr- m-M- rL- (a 0- S. (. C It d. 'y.. M r M'. r.'# _ y, im :?. 1::sir>ns cf r.o r:'cal J. o:'0 a can at au OO'vj; r (rutnsolj l`X'4). T. Value is 20 up r.i (Pat M 19 ; iM 19 :>7). :'r.. L Shortrip.TD ate Inton.iitter-i exposure over 12 months produced gloTivornlonsphrosis (Isler, 1954)* Babhjt. Inhalnlion ov.r 5 months produced excitement, crumps, tachycardia, weight loss and hepatic fatty aecoaer_.fion 0.3 well as cortical cell destruction in the ers with gliosis (Ransleiii; 1931). Exposure i'or 23 weaks produced interstitial nephritis mid adrenocortical hyperplasia (Cohen et al., 1959). IPi: Chronic exposure caused ganglion cell damage especially in the cerebellar area, vascular endothelial proliferation road peripheral axon dr.myelire Mon (liners and Levey, 1940). Intro vac some evidence of anaemia on chronic expo cure (Binet and Bourlic-re, 1944). irunkey. Chronic exposure produced neuronal lesions in the basal ganglia and prominent atherosclerotic vascular changes (Bricger, 1961), Hui;niT__gbse_ra-ations Chronic industrial exposure has produced diverse effects on the CHS, GI tract, renal tract and blood vessels. Damage in the CHS predominates and results from primary lesions of the nerve cells as well as induced atherosclerosis. Encephalo pathy, presenile cerebral atherosclerosis with loss of memory, insomnia, iriitauility and visual disturbances have occurred. A progressive Parkinsonian syndrome with perm-rent damage and mental disability due to striate or striato- ASI 00004235