Document ZBeDne2eXwxwrRk03b70eZMaO
FILE NAME: Chemical Abstracts (CHAB) DATE: 1966 DOC#: CHAB054 OCUMENT DESCRIPTION: Abstract Originally Published in 1964 by Rath
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was not indicative insofar as exposure to low concns. of PhNOt sirard (Univ. Paris). Nature 204(4956), 387-88(1964); cf. CA
was concerned. On the other hand, even with low concn. of 60, 2244d. DL-Thyroxine, 200 7 or 1 mg./kg., injected intra-
I'hNOj and I'hNHj in the breathed air, urinary I and II levels pcrito'ieally daily into mice, increased the toxicity of subsequent
were often too high. Dctn. of urinary I and II was therefore injections of DL-amphetamine sulfate and ephedrine hydro
suggested as a routine check in poisoning prophylaxis.
chloride, depending on dosage and duratioi. of hormonal treat
Jerzy Lange a ment.
BBJN
Semi-quantitative determination of urobilinogenuria as an Panmyelopathy from exposure to toluene; comments^ R.
early diagnostic test for liver Impairment due to poisoning. Hloschek. Zentr. Arbeitsmed. A'belit;sschulz 14(8), 189(1964)
Henryk Boinski, Irena Kodura, and Halina Bomska (Zaklady (Ger). Pure toluene contg. <0.03% benzene has no appreciable
Przemyslu Barwnikarskicgo Boruta, Zgierz, Poland). Med. hepatotoxic activity. Infectious etiology is suggested for a case
Pracy 14(2), 119-27(1963). In 136 workers exposed to amino_ of alleged poisoning. Concluding remarks. H. Gattner.
and nitro compds., urobilinogen (I) was detd. in the urine accord Ibid. 190. Polemic.
Andrew L. Reeves
ing to Watson, el al. ( CA 39, 2085). Abnormal values (over 1.5 Phosphorylated thiocholine and choline derivatives. I.
units/2 hrs.) were found in 22 cases, of which 80% was diagnosed General toxicology and pharmacology. Sten-Magnus Aquilo-
as toxic impairment of the liver. Detn. of I was suggested as a nius, Torsten Fredriksson, and Anders Sundwall (Res. Inst.
routine test in occupational exposures of the type referred to. Natl. Defence, Sundbyberg, Swed.). Toxicol. Appl. Pharmacol.
Jerzy Lange fc 6(3), 269-79(1964). Diethoxy, diisopropoxy, methylethoxy,
Methanol determination in expired air and in urine in acute and methylisopropoxy derivs. of (2-diinethylaminoethylthio)-
poisonings. K. Antczak and J. Piotrowski (Inst. Med. Pracy, phosphine oxide, phosphorylthiocholine, (2-dimethylamino-
Lodz, Poland). Med. Pracy 14(4), 321-33(1963). The air ex ethyl)phosphine oxide, and phosphorylcholine were screened for
pired during 5 min. is bubbled through 30 n:l. H20 , 1 ml. of this acute toxicity in the mouse and rabbit, and for in vitro inhibition
soln. is mixed with 0.2 ml. H2SO( (1:1) and 5 drops 2% KMnO<, of cholinesterase activity of human erythrocytes and plasma.
left 5 min., treated with 2 drops satd. NajbOj, 0.2 ml. 2% Twelve compds. prepd. according to Tamtnelin were used ( CA
chromotropic acid, and 4 ml. coned. H2SO<. *In the presence of 52, 13810g). Intraperitoneal L.D.Mvalues of the O analogs in
MeOH the mixt. turns purple and is assayed by colorimetry at mice ranged from 1000 to 1310 micromoles/kg.; the correspond
570 m;x. The sensitivity of the detn. is 1 y/ml., which is equiv. ing range for the S analog was 0.074-140 micromoles/kg. Anti
to 6 7/min. To det. MeOH in urine, a 50-ml. sample is acidified cholinesterase activities (human erythrocytes), expressed as the
with 5 ml. QN HjSO and distd. until 10 ml. is collected, 0.2 ml. neg. log of the inhibitory doseM(pIw) ranged from 4.6 to 4.7 for
of this distillate is dild. to make 1 ml., treated with 0.2 ml. the O analogs, and from 5.8 to 9.4 for the S analogs. A correla
HjSO( (1:1) and 5 drops 2% KMnCh, the further procedure being tion was evident between the plw and the pL.D.to (neg. log of
as above. EtOH interfered with the detn. to some extent, but its L.D.m expressed in moles/kg.) of the S analogs. Effects on
concn. has to be 1000 times higher to produce the color reaction blood press., heart rate, respiration, and neuromuscular and
of comparable intensity.
Jerzy Lange ganglionic transmission in the anesthetized cat were investigated
Effect of cadmium oxide and nickel salts upon the upper re- -- for 5 of the compds., viz. methylisopropoxy(2-dimethylamino-
spiratory tract. Barbara Pazolowa (Przychodnia Med. Przemy- ethylthio)phosphine oxide, methylisopropoxyphosphorylthio-
slowej, Poznan, Poland). Med. Pracy 14(5), 407-11(1963). choline, methylisopropoxy(2 - dimethylaminoethyljphosphine
Examn. of 78 workers of a Cd-Ni storage battery plant revealed oxide, methylisopropoxyphosphorylcholine, and diethoxy(2-di-
symptoms of poisoning wherever the CdO and Ni salts concns. in methylaminoethyl)phosphine oxide. The S analogs of this group
the air exceeded permissible limits (0.1 mg. Cd/m.' and 0.5 mg. gave essentially the same effects as did Sarin, though the effects
Ni/tn.*). The typical symptoms included irritation of nose and d, developed much more slowly than after Sarin. The O analogs
throat, edema of the palatal tonsil and posterior palatal arches, in this latter group evidenced pharmacol. effects attributable to
inflammatory changes in the larynx, and others. Jerzy Lange direct actions on cholinergic receptors. Substitution ofqhe S by
Histological pattern of endocrine glands in chronic furfural O thus reduced the potency of the compds. and also produced a
poisoning. Bronislaw Gicdosz (Akad. Med., Krakow, Poland). change in the mechanism of action.
Frank A. Smith
Med. Pracy 14(6), 455-8(1963). Rats were poisoned by breath-_ The acute oral toxicity of sodium chloride. Eidon M. Boyd
ing, 1-4 months, air contg. 0.132 mg. furfural ( I ) / l 30 mg. I and M. N. Shanas (Queen's Univ., Kingston, Can.). Arch.
being simultaneously added to the daily fodder. Distinct histol. Intern. Pharmacodyn 144(1/2), 86-96( 1963)(Eng). The median
changes were noted in the pituitary, thyroid, adrenal cortex, and lethal dose of NaCl given orally to young adult albino rats on an
ovaries.
Jerzy Lange empty stomach was 3.75 g./kg. body wt. The mean interval to
Metabolism of y-hexachlorocyclohexane. II. y-HCH de death was 8.6 hrs. The reaction in males was similar to that in
termination in urine by the method of Armstrong. Wladyslaw e females. The clin. syndrome included convulsive movements,
Rusiecki, Halina Bronisz, and Bozena Wysocka (Akad. Med., diarrhea, muscular rigidity, prostration, and death due to re
Warsaw). Med. Pracy 14(6), 459-65(1963); cf. CA 61, 6307f. spiratory failure. At autopsy, dehydration and vascular con
In quant, tests with urine 95.4% of y-HCH (I) added to the urine gestion were present in most organs except skeletal muscle,
was detd. by the method of A., el al. (CA 45, 7740/). In rats lungs, and skin. Congestion was esp. marked in the meninges
poisoned with I (125 mg./kg.) 0.33-0.55% of the intake was de and brain. Columnar epithelium lining the gastrointestinal tract
tected in urine. Urinary elimination of I was at the peak on the -- was lysed. Survivors had a brief convalescent anorexia, poly
5th-8th day of the expt. (up to 42 y/aniinal/day) and no I was uria, fever, and acidosis; appearance, wts., and water contents
detected in urine after 17-18 days.
Jerzy Lange of organs were essentially normal at autopsy 2 weeks after drug.
Acute Frenolon intoxications. Imre Lazar (Tanacs Koranyi The cause of death, therefore, was respiratory failure assoed.
Frigeyes Sandor Korliaz, Budapest, Hung.). Orv. Hetilap 105 with an acute encephalopathy, accompanied by a fulminating
(41), 1943-6( 1964)(Hung). Frenolon [W-(/3-hydroxyethyl)-Ar'- , gastroenteritis and dehydration and congestion of many organs,
[y-(3-chloro-10-phenothiazinyl)propyl] piperazine 3,4,5-trimeth- ' due to oral administration of a single lethal dose of NaCl. From
oxybenzoate difumaratc] produced in 22 cases a 2-phase acute in Biol. Abstr. 45(19), Abstr. No. 81607(1964).
TCCG
toxication, with tachycardia, dryness of the mouth, and dizziness, The form and changes in the form of asbestocis bodies [in the
in addn. to the tranquilizing effect. Then, independent of the lungs]. R. Rath. Beilr. Silikose-Forsch. No. 81, 3-10(1964)
intoxicating dose, dystonia of extrapyratnidal origin developed. (Ger). Old and new data are given on the so-called asbestosis
GGJH -- bodies occurring in the lungs in fatal asbestosis. Such pathol.
Fundamental parameters influencing the accumulation and bodies arise from the inhalation of fibers of the chrysotile (I) form
elimination of carbon monoxide by adult human beings. T. H. of asbestos. Since I has the form of a tube, the formation of as
Allen and R. W. Allard (Army Med. Res. & Nutr. Lab., Den bestosis bodies is interpreted in terms of the diffusion of dissolved
ver, Colo.). U.S. Dept. Com., Office Tech. Serv., AD 265,519, Si, Fe, and Mg out of the ends of the tubes of I (whose chem.
pp.(1961). The basis of a math, system for accumulation- compn. is interpreted in relation to reactions in the lung tissues).
elimination of CO by humans is described. The system can be 0 The breakdown of the bodies may result from a breakup of I
solved by algebraic methods, and is able to predict the level of fibers arising from a local narrowing of the tube diam. caused by
carboxyhemoglobin as a function of time from the initial level of diffusion of sol. materials. 15 references.
W. C. Tobie
carboxyhemoglobin, the concn. of inspired CO and O, expiratory Lung lesions observed one month after intratracheal injections
flow rate, total body hemoglobin, and total pressure of gas [in rats] of coesite containing 1.5 percent quartz. Heinrich
breathed. These findings suggest that future physiol, investiga Breiger and Paul Gross (Jefferson Med. Coll., Philadelphia,
tions, using CO as a tracer, should include the measurement of Pa.). Beilr. Silikose-Forsch. No. 81, 43-50( 1964)(Eng). The
further parameters than often included. Examples are given of title injections of coesite dust gave a marked, generally multi
the method of calcn., and this is used to illustrate the importance focal, cellular and stromal reaction. The coesite lesions con
of each parameter. Although scarcely any data are available tained much reticulin and collagen in contrast to lesions produced
on elimination of CO it is shown how the system may predict the by quartz dust alone. The effects of coesite (<0.5 /1) were thus
rate of elimination, esp. when using the newest method of treat- ^ much more fibrogenic than quartz dust alone (1-3 u). Produc
ing CO poisoning by means of artificial ventilation with pure O tion of alveolar thickening probably was related to the smaller
at a total ambient pressure of 2 atm. 31 references. From U.S. size of coesite particles rather than to its crystn. compn.
Govt. Res. Kept. 37(2), 52-3(1962).
TCTT
W. C. Tobie
Exaltation of toxicity of sympathomimetic amines by thyroxine. Mercury poisoning from an unsuspected source. M. Tamir,
Bernard N. Halpcrn, Carola Drudi-Baracco, and Denise Bes- B. Bornstein, M. Bchar, and M. Chwat (Beilinson Hosp.,