Document DvK0na16vEG6RgqEaDpa2YD4M
Kci>rit] from AMERICAN INDUSTRIAL J1YCIKNE ASSOCIATION JOURNAL Volume 30, Novcmbcr-Di-ccinber, 1969
Monitoring Exposures to Vinyl Chloride Vapor: Breath Analysis and Continuous Air Sampling
EDWARD D. BARETTA.* RICHARD D. STEWART, M.D.,* and JOHN E. MUTCHLERt
Department of Environmental Medicine, Marquette School of Medicine, Milwaukee, Wisconsin, and Environmental Health Section, Biochemical Research Laboratory, The Dow Chemical Company, Midland, Michigan
@ An environmental survey was conducted to determine the time-weighted average exposure (TWA) of a group of chemical plant workers to vinyl chloride (VC1)
vapor. This survey featured continuous multipoint air sampling and analysis using an infrared spectrophotometer. The inhalation exposure data were digitized and record ed on paper tape for subsequent computer analysis and derivation of daily TWA values for each worker. A breath sampling program was conducted concurrently with the environmental survey, and a series of breath decay curves relating postexposure breath concentration to vapor exposure were derived front the data. To validate the breath curves derived from on-the-job data, postexposurc breath curves were also constructed from breath data obtained following experimental human exposures to carefully controlled concentrations of VC1 vapor. The close agreement between postexposurc breath concentrations at the corresponding TWA's obtained by each of the methods suggests that cither continuous air monitoring or breath analysis is valid for estimating the worker's individual daily exposure to VCI, and provides further evidence that breath analysis is a useful industrial hygiene technique for evaluating vapor exposure.
Introduction
HTHK QUESTION THAT MAY ARISE following an environmental survey is
whether the chemical vapor concentrations measured arc truly representative of the ex posure being experienced by the workmen. Evaluation of the ranges of atmospheric con centrations and estimates of time-weighted average concentration (TWA) arc all too often based on a few spot samples obtained under conditions which are not representa tive ol all phases of a given operation. A more exact measurement of vapor exposure would have to he based on continuous moni toring of air in the workman's breathing zone during his entire work shift. Obviously this task is made difficult and often impossible
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by the large number and variety of tasks per formed by today's modern chemical plant worker.
Recent improvements in automatic moni toring and data processing equipment have provided a means for a more satisfactory so lution. Sequential samplers and automatic analyzers and recorders can now be used to continuously monitor several locations or operations to provide more valid data on which to base estimates of chemical exposure. Computers can be utilized to manage the large volume of data generated by continu ous monitoring.1
Meanwhile a technique lias been under de velopment which more precisely defines the level of individual exposure. The realization that the total body burden of a volatile chem ical is directly related to its concentration in expired air led to the development of tech niques for collecting and analyzing breath samples useful in estimating the more indi-
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Fkuirk 4. Glass pipet (50 ml) used for collect ing breath samples. One cap has a predrilled hole for gas sampling. Both caps have Saran liners which seal the pipet chamber.
times. After expelling the fourth breath he quickly caps the tube, trapping a portion of alveolar air. The iinjx>rtancc of writing the name, date, exact time of sampling, and the workshift most recently completed, on the label attached to each pipet, was stressed.
Aliquots were drawn from the pipets with a 1-ml Hamilton gas-tight syringe and ana lyzed in an Aerograph A-600B gas chromato graph using N- carrier gas and a hydrogen flame detector. Separations were made with a 6-fool, j4-inch I.D. stainless-steel column packed with Carbowax 20M alkaline on Chromosorb \V 60/80 mesh acid-washed.
Exposure Chamber Operation
Three experimental human exposures to VC1 were conducted at nominal vapor con centrations of 50, 250, and 500 ppm. The exposure chamber was a room measuring 41 feet by 6 feet wide by 7.5 feet high. The room had a continuous positive air supply and exhaust system capable of maintaining a slight negative pressure within the cham ber. Continuous distribution of the cham ber air was achieved by recirculating the air with a squirrel cage fan through a series of inlet and outlet ducts spanning the length of the chamber. The VC1 was metered into the duct carrying air exhausted by the squirrel cage fan and entered the room atmosphere via the recirculation system at a rate sufficient to maintain the desired atmospheric concen tration. The vapors were introduced from a pressurized storage cylinder through 6 feet of /i-inch I.D. stainless-steel tubing into a rotomeler prior to entering the circulating air duct. A heating tape wrapped around the stainless-steel tubing prevented condensation of the VOl and stabilized the flow of the sapor.
The concentration of YC1 in the chamber was constantly monitored with a Perkin-EI-
mer infrared spectrophotometer equipped with a 10-metcr path-length gas cell. A sam pling probe, consisting of 5/16-inch I.D. Sa ran tubing, was centrally located during the exposure to represent the breathing zone of all subjects within the chamber. The probe was moved about prior to each exposure to detect imbalance of vapor concentrations within the chamber so that necessary cor rections in the recirculating system could be made. Air samples collected periodically within the chamber throughout the exposure day were analyzed by gas chromatography for added assurance of analytical accuracy. Both the infrared spectrophotometer and the gas chromatograph were calibrated before each experiment and at intervals throughout the exposure day.
Each 7.5-hour exposure day included a 0.5-hour lunch period in an uncontaminated area outside the exposure chamber. The TWA concentration was calculated on the basis of 7.5 hours of exposure.
Clinical and Laboratory Procedures
Each subject had been under careful medi cal surveillance by the medical department for a number of years, and each was given a complete medical examination a few days prior to the VC1 exposures. Included were a complete urinalysis and 24-hour urine for urobilinogen, complete blood count with sed imentation rate, reticulocyte count, SCOT, SGPT, LDH, alkaline phosphatase, BUN, creatinine, and bilirubin.
Each subject received a repeat physical examination 1 hour before entering the ex posure chamber. This examination included measurement of temperature, blood pressure, and pulse rate, a neurological examination, and collection of blood and breath samples. A questionnaire noting the presence of any symptoms of illness (for example, headache, nausea, dry throat) completed the pre-ex posure medical evaluation.
After the subject entered the chamber, total expired breath samples were collected every hour by having him breathe out through a Saran tube leading to a Saran plastic col
lection bag located outside the chamber. Tidal volume and total expiratory capacity
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were measured in the morning and again late in the afternoon exposure periods.
Subjective and neurological responses were measured before the subject entered the chamber, 15 minutes after entrance, and at 1-hour intervals thereafter. Flannagan Co ordination and Crawford Manual Dexterity Tests were conducted at midmorning and again in the afternoon. Breath sampling be gan immediately after the subject left the exposure chamber. A 24-hour postexposure urine sample was collected and a blood sam ple was drawn the following morning for SGPT, LDH, alkaline phosphatase, BUN, creatinine, and bilirubin determinations.
Analysis of Breath Data
The decay curves for the breath vinyl chlo ride concentrations were constructed by step wise multiple regression using a digital com puter. An empirical relationship of the form Concentration = / (TWA, time) was select ed from a choice of several terms, each based on TWA and/or time. The resulting regres sion equation best represents the ordered re lationship between breath vinyl chloride con centration, time-weighted average exposures, and postexposure time.
Each breath decay curve has an associated standard error of regression which can be used to compute the confidence band for any chosen level of significance. The 95% con fidence band for the mean of a group of ob servations was chosen in this case to describe the statistical error associated with the breath data and the regression technique.
Tabi.e 1 Experimental Human Exposure to Vinyl Chloride
Chamber Concentration
(ppm) X S.D.
59 2 2M 8 493 7 491 5
Range (ppm)
65- 5.1 289-243 1 518-471 525-475
TWA* (ppm)
48 248 459 491*
Number of Subjects
6 4 4 7
Time-weighted average concentration based on 7.5 hours including a 0.5-hour lunch period in an uncontaininated area.
^Continuous exposure for 3.5 hours.
Table I shows the analyzed concentration to which the subjects were exposed. Calcu lations of the mean and standard deviation of exposure concentration are based on chart readings from the infrared spectrophotometer taken at 5-minute intervals over the two 3.5hour exposure periods. The TWA is based on the total 7.5 hours which included a 0.5hour lunch period in an uncontaminated area.
The final breatli decay curves intended for use as an index to VC1 exposures were ad justed to TWA concentrations of 50, 250,
Results
Exjrerimnital Breath Curves
A total of 13 men participated in the three experimental chamber exposures at nominal concentrations of 50, 250, and 500 ppm pro ducing a total of 160 valid breath data points. Five of the six subjects exposed to 50 ppm were re-exposed at 500 ppm 2 days later. There was no measurable residual vinyl chloride, detected on the breaths of the sub jects prior to the second exposure. Serial breath sampling was initiated immediately after the subjects left the exposure chamber anil continued up to 20 hours following the
exposures.
1'icuke 5. breath decay curves based on experi mental human exposures to 50, 250, ami 500 ppm of VOI (7.5-hour TWA).
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DAILY VARIATION IN EXPOSURE TO VCL VAPOR (8 hr TWA)
with confidence bands only slightly wider than those from controlled human experi ments. The close similarity between these curves and those constructed from controlled exposure data are further illustrated in Fig ure 8.
Human Responses
Figure 6. Variation in VC1 vapor exposure for three shifts.
and 500 ppm (Figure 5). A 100-ppm decay curve was interpolated from the available data using regression analysis. These curves are presented with the calculated 95% con fidence bands for the mean of a group of ob servations.
On-the-job Breath Curves
Ten workmen participated in the on-thejob breath sampling program, producing a total of 91 usable sets of data. Ten percent of the breath samples collected were discard ed because of pipet leakage or poor sampling techniques.
Absolute breath levels ranged from about 20 ppm in one sample taken less than 1 hour after an 8-hour T\VA of 250 ppm, to barely detectable levels (<0.05 ppm) in samples taken after exposures at TWA's below 50 ppm.
The extremely broad variation in the TWA's experienced by workmen during one of the periods in which breath sampling was being conducted is demonstrated for three shifts of men bearing the job classification "coagulator operator" (Figure 6). Minute, hourly, and daily fluctuations in the concen tration of a contaminant are most descriptive ly revealed by continuous monitoring. This method of sampling quickly points out the fallacy of judging TWA and peak exposure concentrations on the basis of spot sampling or periodic surveys of brief duration.
The remarkable correlation between breath concentration and corresponding TWA val ues made it possible to construct the series of breath decay curves shown in Figure 7.
From a subjective standpoint no significant untoward affects were noted at any of the exposure concentrations. The only complaints were those of two subjects who reported mild headache and some dryness of their eyes and nose during the 500-ppm exposure experi ments.
No odor was detected by anyone entering the exposure chamber at 50 ppm. At 250 ppm all four subjects entering the chamber initially reported that they could detect a very slight odor of the chemical. Five of the seven subjects entering the exposure cham ber at 500 ppm were able to detect the odor of VC1, but after 5 minutes of exposure those five were unable to detect it even with forced inspiration. Three of the four subjects re entering the chamber after lunch were able
Figure 7. Breath decay curves derived from breath data collected from workers following onthe-job exposures to VCI vapor (8-hour TWA).
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to detect a faint odor of VCl. One subject could detect a faint odor on deep inspiration for approximately 15 minutes after entering the exposure chamber.
The exposure had no noticeable effect on neurological responses, nor did it produce sig nificant changes in the results of mental, co ordination, or manual dexterity tests conduct ed during the exposure period. All clinical lalxrratory studies performed in the postexposure period were normal and not signifi cantly different front pre-exposure values.
Discussion
The object of the environmental health survey is to identify the atmospheric contam inant, determine, the exposure level, and re late this to the health hazard it presents. If one is to judge hazard by ambient concen tration measurements, then those measure ments must accurately describe the exposure on a continuing individual basis. A carefully conducted survey combining continuous anal ysis of the work room atmosphere with a comprehensive job study will provide data valid for estimating time-weighted average exposure.
On the other hand, breath decay curves constructed from breath data collected dur ing continuous plant monitoring arc in close agreement with those obtained from exposure chamher experiments with VCl. These curves should therefore be useful as a second meth od for assessing exposure to VCl vapor.
The choice of whether one or both meth ods should be used depends on prevailing circumstances and on the thoroughness de sired. For example, data useful in describ ing peak exposures are obtained from con tinuous monitoring. Concurrently, exposure trends and concentration gradients may help identify plant operational inefficiencies and equipment malfunctions by revealing specific sources of emission. Correcting these prob lems not only restores a healthful work en vironment but often results in bonus savings by reducing losses of raw material and prod uct.
Continuous monitoring, however, is ex
tremely costly both in time and in the equip ment required. The scope of data acquired is
Fioure 8. Comparison of breath decay curves derived from the on-the-job data and the experi mental human exposure data.
limited by the number of sampling probes, and these proues are not always capable of accurately measuring the individual's daily exposure experiences, especially should these involve unusual incidences such as chemical spills or oxjvsnves outside the monitored area.
Breath analysis has the advantage of in dividualizing each, worker's integrated daio exposure. Brea::', decay curves, as an index of exposure, oner a means of estimating the average dado iruo -.dual exposure on the hastof a few brearh. samples taken serially in tie jtostexposure period. Consequently luvnth. analysis can he used to diagnose as well aquantitate an exposure which has already occurred. 1: is a relatively inexpensive am! simple method which can bo put into o;'ela tion withorr: extensive and costly prelimmarpreparations.
However, .vs: exposure breath analysts do not prov ide in:.".'.nation on the daily dm 'na tions of exposme. ami the peak exposure con centrations are no: made evident by hteat:data. Fina'd.v. h:ra:h analysis is not apph. a-
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blc to all chemicals, and breath decay curves established for one chemical are not useful as an index of exposure to any other chem ical.
The decay curves presented here arc in tended to serve as an index of exposure to vinyl chloride vapor and are based on an exposure duration of 7.5 hours for the experi mental exposures, and 8 hours for the on-thejob study. The close agreement between the two sets of curves and the narrow confidence bands obtained in each ease demonstrate the usefulness and accuracy of both methods for estimating TWA exposures and indicate the importance of breath analysis and the need for expanding its use in evaluating ex posures to other widely used volatile organic chemicals.
References
1. Peterson, J. K., H. R. llovi.R, am) E. J. Sciineiukr: The Application of Computer Science to Industrial H>> gienr. Amcr. Ind. Hyg. Assoc. J. 27: 180*185 (March 1966).
2. Stfavart, K. D., II. H. Gay, D. S. Erlf.y, C. L. Hake, and A. W. Schaffer : Human Exposure to Tctrachiorocthylcne Vapor: Relationship of Expired Air and Blood Concentrations to Exposure and Toxicity. Arch. Environ. Health 2: 516-522 (May 1961).
3. Stf.wart} R. D., H. H. Gay, D. S. Erley, C. L. Hake. and J. E. 1*etekson: Observations on the Concentration of Trichloroethylene in Blood and Expired Air follow* ing Exposure of Humans. Atner. Ind. rlyg> Assoc. J.23: 167-170 (April 1962).
4. Stewart, R. 1)., and V. K. Rowt: Ouinie A* d'Etudes sur 1c 1,1,1-Trichloroethane. Arch. Maladies Profess. 28: 194*201 (1967).
5. Stewart, R. D., H. C. Dodo, E. 1). Baretta, and A. W. Schaffer: Human Exposure to Styrene Vapor. Arch. Environ. Health 16: No. 5 (May 1968).
6. Stewart. R. D., E. D. .Baretta, H. C. Dodo, and T. R. Torkelron: Experimental Human Exposure to Tetrachlorocthylenc. ASIA Arch. Environ. Health. (In print).
7. Stewart, R. Dm H. C. Dodo, E. D. Baretta, A. W. Schaffer, and J. E. Mutchlfa: Chronic Overexposure to Benzene Vapor. Presented at the Sixth Annual Meet ing of the Society of Toxicology, March 23-25, 1967, Atlanta, Georgia.
Received May 26, 1968
**(/I."NI**-o
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TOXICOLOGY
[voi. si] im
113966. I'AIJON, V. N. (Mod. Int., Novoslblrnk, USSR.) 0 / icKpclstfiohesklkh pncvmontyakh prt sllikozc. (Nonspecific pneumonia
jerumpanylni; silicosis. I GIG TR PROF ZADOT 13(2): SB-66. I(!S. --Observations ol 22 patients suffering from silicosis and non-
elite pneumonia revealed that the course and outcome of nonspecific ,'umonla In such cases Is highly dependent on the condition of the oronrhlal tree. In cases of chronic deforming bronchitis, the pneu monia Is protracted and results in the formation of large foci of fibrosis In the sltlrotlr lung. Chronic deforming bronchitis was chiefly ob served tn patients who had long ceased to have contact with mineral dust.--A. M. H.
113969. KMADZiriFVA, E. D. (Inst. Ind. Ilyg. Occup. Dts., Acad. Med. Set. USSR, Moscow, USSR.) Vllyanle kaprolaktama na prolzvodiiiT nuyu lunktslyu belykh krys. [Effect of caprolactam on the rjinuturtive function of white rats) 1 fclfa SAN1T 36(7): Zb-28. 169. JTtii;l. sum.]--The eltect of caprolactam was studied on the reproductive funi'iionx ot albino rats. A dynamic Inhalation poisoning of 107 albino lemaic rats after their Impregnation with caprolactam at different concentrations proved this substance to affect the conception, the multiplication, the fertility, the course of pregnancy, and the Intra uterine development of the fetus in experimental animals.--L. L.
113970. IZRAEL'SON, Z. I., [Editor.] Tokslkologlya novykh khimirhrskikh veshchestv, vnedryaemykh v rezlnovuyu 1 shlnnuyu promyshlcnnost' . [The toxicology of new chemicals being Introduced into the rubber and tire Industries. 1 236p. illus. M editsIn*: Moscow, T5CH.Tr. S2 kopcclu. From: REF ZH OTD VYP FARMAKOL KHIMK)TER SREDSTVA TOKSIKOL, 1969, No. 1.56.888.
113971. KULINSKAYA, I. L. (Dep. Ind. Hyg., Kharkov Inst. Postgrad Med., Kharkov, USSR.) Nekotorye izmenenlya mediatornogo obmena prt ostrom 1 khronlcheskont otravlcnlt scrouglerodom. [Some changes ol acetylcholine metabolism In acute and chronic poisoning
WnK7aTEgr3i7ulfidc. [ C1C SANTf ''54TI): 2fl^X 1959. f Engl,
sum. [--In chronic intoxication with CS2 at a concentration ol 10 mg/m* certatr. periodical changes were noted In the cholinergic system of the blood and the acetylcholine content norepinephrine. After chronic intoxication for a period of 11 1/2 mo. a fall of acetylcholine concen tration was noted In the cerebrum, the liver, the kidneys and the spleen. A certain tendency to decrease the acetylcholinesterase activity in the spleen was also noted. The norepinephrine content in the cerebrum and the heart and the epinephrine content in the adrenal glands --esented no significant changes. Norepinephrine was discovered
:he adrenal glands in some of the rabbits. After acute poisoning --rth CS2 (12, 500 mg/m*) for 2 hr. the acetylcholinesterase activity decreased in the blood and Increased In the cerebrum. The concen tration of acetylcholine in the spleen diminished. Acute CS2 poisoning brought about a pronounced fall of catacholamine content in the cere brum, the heart and the adrenal glands. More pronounced shifts of the cholinergic system developed in chronic Intoxication and In the sympathlco-adrenal system In acute poisoning. The acetylcholine system Is a sensitive test for detecting functional changes In the action of noxious Industrial factors of small Intensity.--C. M. M.
113972. BAR5EGYAN, G. B. (Dep. Ind. Hyg., Yerevan Med. Inst., Yerevan, USSR.) Predel' no dopustlmaya kontsentratslya 1, 3-dlkhlorbutcna-2 v vozdukhe prolzvodstveonykh pomeshehenll. [Maximum permissible concentrations of 1,3-dlchlorobutene-2 In the air of IndustrlaTpr'emises'7 ZB EKSpkUN MED 'g[8T: 66-72. 1865.-- Studies conducted on white mice, rats, rabbits and humans showed that the concentration of this compound is 0.01 mg/1 In a chronic experi ment. The recommended permissible concentration for working estab lishments is 0.001 mg/1. --S. T.
113973. DOSK3N, V. A. (Dep. Hyg. Child. Adolescents, I. M, Serhrnov 1st Moscow Med. Inst., Moscow, USSR.) O chuvstvltel nosti orgamzma pudrimtkov I yuiiushel k promyshlennym yadam. [Sensitivity nf ailiili'iiri nln and youths In Industrial poisons. J GIG SAN1T 36(9): 99-103. IfKifl. -Tin' uvulTulilu llii'ruiurn on ilin effect of Industrial toxic suimlunrn, on growing utkilesrenls and youths Is revlowed.--J. 8.
113976. ALEKPEROV, 1. I., V. G. KNABENGOF, and M. 1. VINOKUROVA. (E. M. Efendl-Zad Inst. Ind. Hyg., Occup. Dls., Baku, USSR.) Punktslonal' noc sostoyanle serdechno-sosudlstol slstemy u rabotayushchikh 8 uglcvodorodmnl neltl. [Functional state ot the cardiovascular system ol persons who work with petroleum hydrocar bons- r~ftlG TK PROF ikndi. 11(2): 69-50. 1969. --Clinical studies ol 50 petroleum Industry workers (20 lo 60 yr of age), who worked under conditions of direct contact with petroleum products, were contrasted with data on 20 Institutional workers of the same age distribution to / delect functional shifts In the cardiovascular system under the Influence of exposure to such products as styrene, divinyl, ethylbenzene, etc. ' CC changes were basically expressed in small dystrophic alterations
ihe myocardium resulting In a slightly Impaired myocardial con.settle function. Oscillographic study of the vascular tonus revealed a prevalence of cases with a reduced mean arterlnl pressure, a con dition typical for persons frequently exposed to hydrocarbons. The oscillographic Index, which reflects the affects of autonomic regulation,
was asymmetric. CaplUaroscopy revealed spastic-atonic functional reactions with Impaired resistance.--A. M. H.
113975. PENKOV1CH, A. A. (Inst. Ind. Hyg. Occup. Dls., Gor'ki, USSR.) K otsenke Izmenenll v malom kruge krovoobrashchcnlya u bol' nykh pylevyml zabolcvanlyaml leglkh. [Assessment of changes in pulmonary circulation In pneumoconiosis patients,) GIG TR PROF-- iABOL 13(h): 60-63. W69. --The character, frequency and ex pressivity of shifts caused by changes In pulmonary circulation In patients with occupational bronchitis and pneumoconiosis were evaluated on the basts of ECG, polycardiography and pulmonary rheography data. Morphological deviations and functional disturbances In the apparatus of external respiration are significant In the development of changes tn pulmonary circulation In pneumoconiosis patients. The use of these methods sometimes reveals even at early stages of pulmonary in sufficiency, n number of functional shifts tn pulmonary circulation, which can be regarded ns the result of an Increase of pulmonary arterial resistance. --J. S.
113976. VAZIN, A. N., and E. I. PLOKHOVA. (Inst. Ind. Hyg.,
Occup. Dls., Gorki, USSR.) Dlnamlka eoderzhanlya adrenalinopodobnykh veshchestv v krovl krollkov prt khronicheekom vozdeiatvii parov vinllkhlorlda. [Dynamic changes In epinephrine-like sub stances in rabbit blood following chronic exposure to vinyl chloride fumes.] " GlCTH-PKOirnSOI IT(6]:lrT7.IB6.-Ch?5gc~
action of vinyl chloride fumes causes profound functional changes In the anterior and, most particularly. In the posterior nuclei of the hypothalamus. This leads to hyperadrenallsm, resulting In a patho logical toxic angloneurosla.--R. B. C.
113977, VOL'FOVSKAYA, R. N., and L D. MAKULOVA. (Inst. Ind. Hyg. Occup. Die., Acad. Med. Set., USSR, Moscow, USSR.) K voprosu o techenll anglodlstanlcheskikh sostoyanll s artertal'not glpertonlel tcksicheakol etlologil. [Course of anglodygtonlc conditions with arterial hypertension of toxic etiology. | GIG TR pkOF ZABOL l2(ll): 12-15. ufais. 1968. [EngL sum.[--Observations were made lor as long as 6 -10 yr or mare on 69 motor car drivers up to the age of 40 (65 males and 4 females) with a long record of chronic CO poisoning (38 persons) and chronic poisoning with ethylated gasoline and CO (31 persons). Note was taken of the intensity of the angiodystonic syndrome, such as encephalia, vertigo, diencephalic crises and manifestations of coronary spasms. As well as Increasing organic symptoms which were apparent In 15 casen, 25 persons developed hypertensive disease within the observation period (mostly at the age of 40-45). Hypertensive disease ordinarily proceeded against the background of residual manifestation>i or remote consequences of tbs sustained poisoning, being distinguished by a specific evolution. Pro nounced vegetative symptoms, diencephalic crises, syncopes, short lapses of consciousness endocrine disturbances in assoclailon with an organic brain lesion or affection of the peripheral nervous system were noted. The toxic anglodystonlc syndrome as well as arterial hypertension furthered the development of hypertensive disease.
--L. M. L.
113978. SEDOV, A. V., and A. N. MAZDt. (Inst. Blophys., Min. Health USSR, Moscow, USSR.) K voprosu o normlrovanll vrednykh prlmesel vo vdykhaemykh gazovykh smesyakh. [Problem of standardi zation of noxious admixtures in inhaled gaseous mixtures.) dCnSOT? 33(2): 52-94. 1968.--Data on gaseous toxic substances (C02> CO, NHv) in exhaled air compiled from their maximum permissible con centrations in the air of Industrial establishments show that their maximum permissible concentrations do not depend on their concentra tions In air exhaled by humans.--L. K. R.
113979. VENGERSKAYA, Kh. Ya., and N. M. DEMIDENKO. (Tash kent Med. Inst., Tt-\. t, USSR.) Metod opredelenlyapentaktdartenab v vozdukhe pri sel'skckhozynltvennykh rnbotnkh. [Method for detcrmlntng pentachlorophenol In the sir during agricultural work!) C6J HANIT 33(2): 57-68. 196H,--Thla method consisted of using liquid mciltn (a O.S'JT, solution of sodium carbonate, 0.01 and 0.001 N aoiullima of sodium hydroxtdo, acetone and ethyl alcohol, as well a* silica gel) and certain fitters. The reaction was verified with various agents. The best effect was obtained with the reaction with plramldon (dimethylamlnoantlpyrlne). The sensitivity of the method Is 0.5 pg.
--L. K. 1
113980. MATYSYAK, V. G. O vliyanli parov benzlna na menstrual'nuyu 1 detorodnuyu funktsll 1 glnekologlcheskuyu zabolevaemost' rabotnits rezinovol promyshlennosti. [The effect of gasoline vapors on the menstrual and childbearing functions and the gynecological morbidity-
of female workers at a synthetic rubber factory. I TR AZERB hAul'ri15SLED fit'ST GIG TR PROV ZABOL T. 74-80. 1968. Translated
from REF ZH OTD VYP FARMAKOL KHMIOTER SREDSTVA TOKSI KOL, 1969, No. 11.54.1199.--Examinations were made of 3017 female workers [19-40 yrold] in the synthetic rubber Industry, whose length of service In the Industry wns 6-16 yr. There were disturbances of tbs menstrual cycle and menopausal disorders. A decrease la the aver*** Dumber cf pregnancies, and increase In tbs frequency of ^entmai abortions and premature births. In tbs number of infanta born d*n ms
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11 -- M^mritilinn Biochemistry Vol. 71, 1969
110573
animals, llie major difference lies in the larger maintenance rci/nircim-nts of the mouse due to its higher metabolic rate.
I'hilip Jacobson
110563j Levels of immunoglobulins - GMA) in normal children. Tabula, Kiharhiro (Kyoto Univ., Kyoto, Japan). .''Ihiiiika A;vn 1008. M'li), 379-Mi (line.). LcviK-of scrum miinunoglnbiiliin, were detd. by the antihoily agar pfalc method in
maternal and cord blood at the time of delivery and in groups of
normal infants and children up to age 17>. 7A was absent from cord blood, yM present only in traces, whereas the levels of yG
in cord blood were equal to or above those in maternal blood.
Minimum levels of yG were found at 3 and f> months, then rose slowly, not attaining the adult range until age 11. Levels of yM reached half the range found in adults by 3 months, but did not reach adult levels until 3 yrs. Levels of yA were less than half
the adult range up to age o, then rose rapidly. Jacob Sacks
110564k Polymorphism of transferrins of bovine, porcine, and
canine sera, as determined by means of acrylamide-gel disc
electrophoresis. Dorncr, Joseph L. (Univ. of Illinois, Urbana,
111.). 1968,66 pp. (Eng). Avail. Univ. Microfilms, Ann Arbor,
Mich., Order No. 09-10,687. From Diss. Abstr. B 1969, 29(12),
4727.
SX'DC
110565m Hemoglobin-Lepore Baltimore, a third type of a 4/3
crossover (4s0, pM). Ostertag, Wolfram; Smith, Ernest Wendell
(Sch. of Med., Johns Hopkins Univ., Baltimore, Md.). Eur. J.
Biockem. 1969, 10(2), 371-6 (Eng). A new Lepore-type Hb in a
person of Xegro descent has been identified. In this person a
minor Hb (Hb-Lepores.itimore) was detected. An abnormal
4d-chain was isolated and fingerprinted. This hybrid-type pro
tein presumably arose as a consequence of unequal crossing over
between the 4 and 0 genes, as was concluded for Hb-LeporeB<t<m
and Hb-LcporeHoiundi.- In the new Lepore-type Hb described
here the crossover could be placed between residues 4" and 0".
This type of crossover should occur with the highest frequency if
crossing over is equally frequent between any nucleotides and if
selection favors none of the crossover types.
RCBY
110566n Genetic and developmental regulation of hepatic
4-aminolevulinate dehydratase in mice. Doyle, Darrell J.;
Schimke, Robert T. (Sch. of Med., Stanford Univ., Stanford,
Calif,). J Biol. Chem. 1969, 244(20), 5449-59 (Eng). The
mechanism by which the levulinate locus (Li ) regulates the tissue
activity of 4-aminolevulinate dehydratase in mice has been examd.
The assayable hepatic enzyme activity in homozygous Lvb mouse
^strains, represented by C57B1/6, is between one-third and one-
half that of homozygous Li* strains. This difference in enzyme
activity is due to a difference in amt. of enzyme protein as demon
strated by immunochem. techniques with an antibody specific for
4-aminolevulinate dehydratase. Combined immunochem. and
isotopic techniques show that the levulinate locus regulates the
concn. of hepatic 4-aminolevulinate dehydratase by acting at the
level of enzyme synthesis. The rate of degradation of hepatic
enzyme is the same in both low and high activity strains; when
expressed as a half-life, this is equal to 5-6 days. The pattern of
4-aminolevulinate dehydratase development with age is similar
in livers of both low and high activity strains. The specific
activity of the enzyme is high in fetal liver, decreases during the
several days prior to birth, and increases to the adult level during
the first 3 weeks of postnatal life. The activity of 4-am:no-
levulinate dehydratase in fetal liver is also regulated by the
levulinate locus. The enzyme in fetal liver is approx, twice as
active catalytically as the enzyme in adult liver relative to its
function as an antigen. The fetal enzyme also appears to be
different in stability to heat and proteolytic inactivation. How
ever, fetal and adult enzymes are similar by other physiochem.
criteria, including electrophoretic mobility, sedimentation coeff.,
and A',, for the substrate.
RCJN
110567p Identification and genetic control of two new low*
density lipoprotein allotypes: phenogroups at the Lpq locus-
Albers, John J.; Dray, Sheldon (Med. Center, Univ. of Illinois,
Chicago,.111.). J. Immunol. 1969, 103(2), 155-62 (Eng). See
C.l 69: 104403z.
VXTJZ
110568q Modification by crude histones of gene activity for lactate dehydrogenase. Latner, A. L.; LongstafI, E. (Roy.
Victoria Infirmary, Newcastle upon Tyne, Engl.). Nature (London) 1969, 224(5214), 71-3 (Eng). Addn. of crude calf thymus histone to the mouse kidney organ culture increased the
proportion of the lactate dehydrogenase (LDH) isozymes which
moved more rapidly toward the anode during electrophoresis. If a crude rat liver histone fraction was added to the culture, the ncrease was in the direction of the slower moving LDH isozymes. ^ n the cultures exposed to the crude calf thymus histone, the
percent of LDH-1 and the H subunit contribution to the total LDH activity significantly increased, whereas the opposite was
found with the rat liver histone prepn.; LDH-5 and the M sub unit significantly increased. Enrichment of the medium with amino acids present in the calf thymus histone prepn. did not alter the isozyme pattern, indicating that the changes in LDH pattern were not caused by hydrolysis of the histone. Gene
masking by histones apparently is nonspecific, and the crude ext.
may contain factors, not necessarily histones, which affect gene
activity in a manner that e. not sjmcus specific.
BSJN
llOSOOr Changes in the activpv i f isolated vascular smooth
muscle in response to reduced osmnl.iiity. Jnii-sun. < >lof lUniv.
Gotcborg, Gotclxirg, Swell. 1. ,\thi I /
Snnul. 1969, 77(1),
191-200 (Eng). The ii';V.t- "f liy; i.n.hinty on the spon taneous activity of the Mimnth muscle in the isolated portal vciu
of the rat have been stu lied in solus, with varied ionic cotnpti. A
comparison between the stimulatory effects of lowered osuiolarity
and increased (K+]o (external K' count.) indicated that at
normal [K'|n-in the control state the excitation caused by hypo-
tonicity is not mediated only via changes in the [K+] j/|K*|o ratio.
The response to hypoosmolarity at a higher |k+)n is. however,
more readily explained by the change in |K')i,[K+]i> which
occurs in assocn. with the swelling ol the cells. This might be
attributed to the fact that the membrane potential of smooth
muscle is more dependent on the iransmeinbrane concn. gradient
for K+at higher levels of [K+|o. The stimulatory effects of hypo
osmolarity are markedly reduced at a low [N'a+lo but are not
considerably affected by comparable redns. in [K.+)o or (Cl-]*.
This indicates that the transmembrane Na+ gradient is involved in the mechanisms by which hypoosmolarity excites the spon
taneous activity of vascular smooth muscle. One possible
interpretation is that the swelling of the muscle cells in hypotonic
solns. causes an increase in the permeability of the cell membrane
to the relatively larger Na+.
RCVV
110570j Secretion of rat pancreas perfused with plasma from
rats fed soybean trypsin inhibitor. Khayambashi, H.; Lyman,
R. L. (Univ. of California, Berkeley, Calif ). Amer. J. Physiol.
1969,217(3), 646-51 (Eng). When plasma from rats fed soybean
trypsin inhibitor was perfused through an isolated, fasted rat
pancreas, amylase secretion was 2-3-fold greater than that of a
pancreas perfused with plasma from rats fed the same diet without
trypsin inhibitor. Addn. of atropine to the perfusate did not
inhibit the secretory response. The plasma factor was relatively
unstable upon storage at 4 (50% loss of activity in 4 days) and
appeared to be assoed. mainly with those plasma proteins of
10,000 mol. wt. or less. Thus, active soybean trypsin inhibitor enhanced the formation and (or) release of a humoral pancreozy
minlike substance that markedly stimulated external enzyme
secretion of the rat pancreas.
RCDH
110571k Effects of diet and catechol amines on bile acid
metabolism in dogs. Gans, Joseph H.; Cater, Marilyn R.
(Coll, of Med., Univ. of Vermont, Burlington, Vt.). Amer. J.
Physiol. 1969, 217(4), 1018-24 (Eng). Five adult male dogs
were surgically prepd. with polyvinyl tubing placed in the upper
duodenum. Each dog was given cholic-corfeoxyM'C acid and samples of gallbladder bile were withdrawn over a 10-day period.
The taurocholic acid pool was 1.09 g./lO kg. body wt- and half-
life was 3.2 days when dogs were given a dry dog food diet.
Epinephrine in oil, 0.8-1 mg./kg./day, increased plasma cho
lesterol concns., produced a 23.99r redn. in the taurocholic acid
pool size, and increased the rate of decline of specific radioactivity
of both taurocholic and taurodeoxycholic acids. The half-life of
taurocholic-,4C acid during epinephrine administration was 1.6
days. Norepinephrine in oil, 0.8-1.0 mg. free base/kg./day,
produced a modest decrease in the half-life of taurocholic-14C acid
without significant elevations in plasma cholesterol concns. A dietary supplement of l/t lb. beef plus 2-3 g. of cholesterol per day
resulted in increased plasma cholesterol concns., increases in the
taurocholic acid pool size, and a decrease in the half-life of
taurocholic-14C acid. Epinephrine administration further in
creased plasma cholesterol concns. in cholesterol-fed dogs, but
did not significantly alter bile acid metabolism.
RCDH
110572m Effect of osmolarity on canine renal vascular
resistance. Gazitua, Sergio; Scott, Jerry Benjamin; Chou,
Ching-Chung; Haddy, Francis J. (Michigan State Univ., East
Lansing, Mich.). Amer. J. Physiol. 1969, 217(4), 1216-23 (Eng). The effects of changes in renal blood osmolarity, pro
duced by close intraarterial infusion of solns. of dextrose, NaCI,
and urea, on renal resistance were systematically examd. in the dog. Infusion of a hyperosmotic soln. of dextrose for 3 min.
produced a fall in renal vascular resistance which was sustained
for the entire infusion period. On termination of the infusion,
resistance returned to the control level. Infusion of a soln. of hyperosmotic NaCI or urea, on the other hand, produced a fall in resistance which waned with time. Furthermore, oil stopping
the infusion, resistance transiently rose well above the control
level, particularly in the case of urea. Intraarterial infusion of
an isosinotic soln. of urea and of hyposmotie solns. of all three
substances produced large increases in resistance. Studies con cerning lymphatic vessel pressure and cell-free perfusion, as well
as the findings of others, are consistent with the hypothesis that
the changes in resistance result, to a large extent, from active
vasomotion, possibly due to osmotic changes in the water content
of the smooth muscle cells.
RCDH
110573n Metabolism of allyl compounds in the rat. Clapp,
J. J.; Kaye, C. M.; Young, Leslie (St. Thomas's Hosp. Med.
Sell., London, Engl.). Biochew. J. 1969, 114(1), 5P--1E (Eng).
A mcrcapturic acid was isolated from the urine of rats treated s.c.
SPI -12903
110574
Chemical Abstracts
1969
Pag* 152
% with CH:CUOAc or CIIjiCIIOII and identified as 3-hydroxy-
_ aA dose of 2IXX1 I.U. L-asparaginasc/kg. evoked hyper- '
propylmcrcapturic acid ((V-acctyl-.V+i-hydroxypropyO-L-cys- ^fjfccmia and glycosuria in most of the animals; this is equal to a
teine, I). There was no evidence for the presence of aliyhuer-' dose which induced hyperglycemia when given to patients. Ad
capturic acid (JV-acctyl-.Y-allyl-i.-cystcinc, II) in the urine of rabbits receiving 10,000 I.U. L-asparaginasc/kg. or more showed these animals. II, however, was detected in the urine of rats diabetogenic responses, but these effects were temporary (2-13 injected s.c. with C113: C1 i C1, .Y-allylglutatliionc, and .V-allyl-L- days) and were not assoed. with any histological changes in the
cysteine. Rats treated with ClliiCIlCl also excreted 1. Mer- pancreatic islets, except in 1 rabbit which showed islet hyaliniza-
capturic acids apparently nrisc by the reaction of allyl compds. or tion.
DDJX
their active derivs. with glutathione.
BQJN
110581 p Effect of Bidrin on the metabolism of dietary com
U0574p Metabolites of octoclothepine eliminated in human ponents by the bovine. Lowrey, R. S.; Bowman, Malcolm C.;
and rat urine. Qucisnerova, Milena; Svatek, Is.; Metysova, Knox, P\ E. (Coastal Plain Exp. Sta., Agr. Res. Scrv., Tifton, Jirina(Res. Inst. Pharin. Biochcin., Prague, Czech.). Biochem. Ga.). J. Dairy Sci. 1969, 52(9), 1460-3 (Eng). Six steers
J. 1969, 1 14(2), 359-42 (Eng). h'our metaiiolites and unchanged averaging 400 kg. in wt. were used in a switchback trial to study
octoclothepine were extd. with diehloroethanc from the urine of the effect of spiking corn silage with 15.7 ppm. (0.24 mg./kg.
humans Riven octoclothepine. These substances were isolated body wt.) of the pesticide Bidrin [3-(dimethoxyphosphinyloxy)-
and purified by column and thin-layer chromatOR. By ehro- IV, N-dimethyl-ctj-crotonamide) on blood cholinesterase, digest matORraphic, spectrophotonictric, and polarographic anal., ibility of dietary components, utilization of X', and rumen fermen
unchanRed octoclothepine and 3 of the metabolites were identified tation. Bidrin residues were not found cither ill the urine or in
(noroctoclothepine, noroctoclothepine .V-oxide, and octoelothc- the feces of animals ingesting Bidrin. Azodrin, a metabolite of
pine .V-oxide). The presence cf glueuronides in human urine Bidrin, was not present in the feces of treated animals but aver
was shown. The same metabolites and unchanRed octoclothepine aged 0.430 ppm. in the urine. Based on urine vol. this repre
were also found in rat urine by chromatoy.
RCh'G
sented 1.5% of the ingested Bidrin. Blood cholinesterase was
110575q Mechanism by which leucine and arginine stimulate depressed to 30% of pretreatment values by the end of the 42-day insulin release in vitro. Milner, R. D. G. (Univ. West Indies, exptl. period, whereas activity of steers fed untreated silage was
Kingston, Jamaica). Biochim. Biophys. Acta 1969, 192(1), unaffected. In the metabolism trial conducted during the last
154-6 (Eng). Basal insulin release in young rabbit pancreas 14 days of the 42-day period Bidrin had no effect on the digest
slices in vitro was higher in the presence of leucine (5m.it/) than ibility of dietary components (dry matter, crude protein, ether
of arginine (5m,t/) (in the absence of glucose). Glucagon (5 ext., crude fiber, N-free ext., and gross energy), the utilization
jig./ml.), theophylline (lmf!/), dibutyryl cyclic AMP (lm.il/), or of N, or rumen fermentation.
RCLD
L-arginine (5m.l/) stimulated insulin release in the presence of
110582q Effect of a second dose of cadmium salts on vascular
leucine but not in the presence of arginine. Arginine-stimulated permeability in the rat testis. Clegg, E. J.; Carr, Ian; N'iemi,
basal insulin release perhaps works by releasing glucagon from M. (Univ. Sheffield, Sheffield, Engl.). J. Endocrinol. 1969, 45
the a-cells. The mechanism of the leucine-induced stimulation (2), 265-8 (Eng). Two doses of CdCU were given to rats at
is different, probably via the adcnyl cyclase system. BSJN
intervals varying from 76 to 194 days. After the second dose the
110576r Cytochemical study of the distribution and content of blood vessels in the testis and initial segment of the epididymis
nudeoproteins and of some functional groups of proteins in iso showed increased permeability, as demonstrated by i.v. markers.
lated formations of the central nervous system following foreign In the testis, leaking vessels were usually found in areas where
protein injection. Tumanyan, E. L. (Erevan. Med. Inst., interstitial cells were abundant.
RCKV
Erevan, USSR). Biol. Zh. Arm. 1969, 22(5), 97-8 (Russ).
110583r Acid-base and electrolyte changes induced by acute
Cytoplasm of various parts of rabbit central nervous system isotonic saline infusion in the nephrectomized dog. Rosenbaum.
(including intervertebral ganglia, nuclei of the XII cranial nerve, Barry J.; Makoff, Dwight L.; Maxwell, Morton H.; Hogh-
and skin motor area of brain cortex) displayed higher ribonucleo- oughi, Michael (Cedars-Sinai Med. Res. Inst., Los Angeles.
protein content in animals treated with repeated i.v. injection of Calif.). J. Lab. Clin. Med. 1969, 74(3), 427-35 (Eng). The
normal horse serum. The peak effect was observed on the 4th mechanism and extent of "dilution acidosis" by acute infusions
day after the last injection. N > changes were seen in content of isotonic saline was studied in nephrectomized dogs. Infusions
and distribution of protein SH groups.
X. Jasinczuk
of 50, 75, and 100 ml./kg. of body wt. (BW) (Groups 1, 2, and 3)
110577s DNA synthesis in mouse embryonic fibroblast-like over a 30-min. period resulted in extracellular fluid expansions of
cells in vitro, stimulated by various factors. Vasil'ev, Vu. M.; 24.4 1.7%, 28.8 2.2%, and 33.9 5.5%, resp. pCCh was
Gel'fand, I. M.; Gershtein, V. I.; Fetisova, E. K. (Mosk. Gos. kept const. Body spaces were measured isotopically, and intra
Univ., Moscow, USSR). Dokl. Akad. Nauk SSSR 1969, 187(4), cellular H+ activity by 5,5-dimethyl-2,4-oxazolidinedione-14C.
913-15[Cytol) (Russ). Autoradiography was used to follow the The extracellular bicarbonate concn. decreased only --2.4 0.7
DNA synthesis in single-layer cultures of mouse embryo fibro- tneq./l. and --2.5 0.4 meq./l. in Groups 1 and 2 and --3.0
btast-Iike cells in lactalbumin hydrolyzate and ox serum media in 1.0in Group 3. The total amt. of extracellular bicarbonate in
the presence of thymidine-1// added at various periods of culture creased +0.6 0.2 meq./kg. of BW, +0.8 0.2 meq./kg. of
age. The index of 'H inclusion was increased by addn. of tes BW, and +1.5 0.4 meq./kg. of BW in each group, resp. Con
ticular or bacterial hyaluronidascs, RXase, and digitonin. The comitantly, the total amt. of extracellular fluid K increased +0.3
rise of *H intake was the result of stimulation of the entry of the 0.0 meq./kg. of BW, +0.5 0.1 meq./kg. of BW, and +0.4
cells into the S-phase of development.
G. M. Kosolapoff
0.1 meq./kg. of BW, resp., while there was no decrease in
110578t Effect of pregnancy and oral contraceptives on glu extracellular K concn. 11 was suggested that the extracellular bi
cose and insulin metabolism. Taskinen, Maria R. Duodecim carbonate and K concns. were defended by shifts of H+ into cells
1969, 85(11), 67(i-83 (F'innish). A review. The effect of both (or bicarbonate out of cells), in conjunction with a shift of K
pregnancy and oral contraceptives is diabetogenous, and they out of cells. Despite the presumed H+ (or bicarbonate) flux,
may cause deterioration of glucose tolerance in healthy women. there were no net changes of H+ activity. The conceptual
The organism tends to compensate this by enhanced insulin theory of extracellular "dilution acidosis" is valid but of limited
secretion, which leads to hyperinsulinism. 43 references.
magnitude and little clin. significance when expansion is relatively
I. G. Zewi
slow. Cellular buffering minimizes the extracellular acidosis,
110S79U Effect of pyridoxal 5'-phosphate on the strength of and the shift of K out of cells prevents hypokalemia. RCKY
skin in vitro. Harkness, Robert D. (Univ. Coll. London, Lon
110584s Effect of erythropoietin on bone marrow a-axnino-
don, Engl.). Experientia 1969, 25(10), 1048-9 (Eng). Treat levulinic acid synthetase and heme synthetase. Bottomley.
ment with lOm.V pyridoxal 5'-phosphate (I) in vitro reduced the Sylvia S.; Smithee, G. Ann (Veterans Admin. Hosp., Oklahoma
strength of rat tail skin progressively with time of incubation. City, Okla.). J. Lab. Clin. AUd. 1969 , 74(3), 445-52 (Eng)
The redn. was reversible, with strength returning when the skin An in vitro culture method has been adapted for rabbit bone
rings were placed in buffered saline. Pyridoxamine or pyri- marrow and has permitted measurement of the effect of erythro
doxinc at lOm.1/ had no comparable effect. The effect of I was poietin on A-aminolevultnic acid synthetase and heme synthetase
reduced in the presence of lysine. Prctrcatmcnt of the skin with activities in'marrow cells. In this system, erythropoietin en
NaBH,. followed by washing in saline buffer, largely inhibited hanced A-aminolevulinic acid synthetase activity. This effect
the effect of I. Pretreatment with XH;OH also inhibited the was detectable as early as 6 hrs. after contact with erythropoietin.
effect of I. Treatment with NH:OH after I prevented the re The max. enzyme activity observed was 200' ) greater in stim
covery of strength on subsequent transfer tc the saline buffer; ulated than in control cultures. Studies with inhibitors of pro
HjNN'Hi had a similar effect. The cfTect nf I skin strength is tein synthesis suggested that erythropoietin increased tlie syn
apparently brought about by rupture of a nethine linkages thesis of the enzyme. No stimulatory effect by erythropoietin
formed between ail aldehyde and an amino gr. ip.
BSJN
on heme synthetase activity was observed.
RCK5
11058On Diabetogenic effect of i.-aspc aginase. Khan,
11 OSSSt Action of adenosine triphosphate on the depressed
AmanuUah; Adnrlii, Mitsun; Hill, Joseph M icGUtshan (Wad- spontaneous electrical activity of the dog cerebral cortex. IF nr
ley Inst, of Mol. Med., Dallas, Tex.). J. Clin. Endoi rinol. Gian; Arriguni, Elena; Ferrara, A.; Maschcrpa, 1'. <1 ;
Alctub. 1969, 29(10), 1373-0 (Iingl. The effects of Escherichia Pharmacol., Univ. Pavia, Pavia, Italy). J. Phamt. i. to*iC
coti I.-asparaginase (.->(K)--.r>0,(XX) 1.1 la-., i.v. 1, which lias been 58(D), lllil-3 (Eng). The repeated suppression nf the venti1.-
used to induce umissiou of human acuo- O -.nohatic and myelog tion and the circulation of the brain in tnc do.' iinlii cs a high i i
enous leukemias.via depletion of an amino acid essential for some pression or a silence of cicc. activity of the cortical .and sub
neoplastic celts, on rabbit blood and urinary glucose levels were cortical centers. The recovery of respiratory and circulator..
SPI -12904
Ps*s X99
14--Toxicology Vol. 71, 1969
89628
l'V' ooisonmg and manic-dcprcssivc psychosis arc discussed and Before the exposure to I anil also in the control group of rabbits
s<riV:ni; similarities between them noted. It is suggested the II and Ha levels varied little and averaged 3.5 *ig.%. After
'a*. W may be a toxic delcnninant in this psychosis. The 20 days exposure the level of II and Ila rose to <'>.15 fig-%, after
test 'Javis and Amlelman, 1907) was used for the 40 days it reached G.0.fig.% and it remained const, thercater.
V
,'cV1 o' vrinriry A-atninolcvulinic acid (I) levels in patients and The biopotential of the posterior hypothalamus also changr-?. controls. Results showed an increasingly significant rise in 1 These effects of I arc the direct cause of hypertension. CPJR
ii-ve's between controls and untreated patients and patients
89622r ATP and lipid contents in the liver of mice after in
treated with LijCOs. Li may interfere with Hb synthesis in a halation of chlorinated hydrocarbons. Ogata, Masana; Tomc-
similar way to 7*6. 41 references.
S. M. Maxwell
kuni, Katsumaro; Watanabe, Shinsaku (Med. Sch., Okayama
S9616s Effects of DTPA [dietbylenetriaminepentaacetic Univ., Okayama, Japan).- Ind. Health (Ka-xasaki, Japcr.
acid; aerosol on lung contamination by lanthanum. Pasquier, 1968, 6(3), 116-9 (Eng). The hepatic ATP level decrease and
Christian, Yoisir., Dominique; Thicblemout, Pierre; Perrault, the onset of fatty liver as indicated by the increase in the amt. of
Oerard Bayard, Jean P. (Dir. Prot. Surete Radiol., C.E.N., the total lipids and triglycerides in the mice exposed to ? kinds of
'oitenay-aux-Roses, Fr.). Commis. Energ. At. (/>.], Rapp. chlorinated hydrocarbons are in the following order: CCL,
'969, CEA-R-373S, 19 pp. (Fr). Avail. CEA. By use of tetrachloroethyleue, and trichloroethylene. The total lipid and
HTPA aerosol in the treatment of pulmonary contamination by triglyceride contents increased proportionately to the fall in the
:,,a its effectiveness was detd. as a function of time. Provided ATP level before and after the exposure to 3 kinds of chlorinated
that it is administered at an early stage, in the 2 hrs. after expo hydrocarbons. It was suggested that there is some close rela
sure, >50% can be eliminated using lower therapeutic doses than tionship between the decreased hepatic ATP levels and the de
hos" '"escribed *`or other methods of administration. Its velopment of fatty liver in chlorinated hydrocarbon poisonings.
assocn. with some enzymes did not enhance the therapeutic
B. V. Shetty
effect of the chelator. The const, for the passage of the DTPA-
89623s Influence of subacute intoxication with manganous
La complex rrom the lung to the blood is ~0.016/mip., corre chloride and carbon tetrachloride on the lethal dose of digitoxin,
sponding to a period of 44 min. A significant nonchelatable lanatoside C, and strophanthoside in guinea pigs. Lence, P.;
fraction, persisting after prolonged action of the DTPA, of the Valentincic-Budihna, Metka (Med. Fac., Ljubljana, Yugo
order or 40-45% is observed.
DWJF
slavia). Jugoslav. Physiol. Pharmacol. Acta 1968, 4(2), 157-64
69617: Ferric cyanoferrate(II): an effective antidote in (Eng). In guinea pigs the toxicity of the title cardiotonic gluco-
thallium poisoning. Heydlauf, Horst (Inst^ Strahlenbiol., sides is modified in subacute intoxications with MnCli and CCL
Kemforschungszentrum, Karlsruhe, Ger.). EuK J. Pharmacol. (when evident morphological changes are restricted to the liver).
1969, 6(3), 340-4 (Eng). The influence of orally administered The following doses were used: 0.01 ml./kg. CC1 in 2% oil soln.
ferric cyanoferrate(II), (Prussian Blue, PB) on the distribution and 0.003 g./kg. MnCli in 3% aq. soln., i.m., twice a week, or 10
and excretion of *MT1 was studied in the rat. PB lowered the times successively; glucosides were administered 30-39 days
retention of "Tl by inhibition of its absorption and reabsorption after the last dose of CCL or MnCli- In intoxicated guinea pigs
from the intestinal tract. The toxicity of Tl,SO, was decreased the lethal dose of digitoxin did not differ significantly from that of
by PB. PB is suggested as an antidote in T1 poisoning.
controls. The lethal dose of lanatoside C was significantly
V. N. Gupta
smaller only in CCl, treated animals and the lethal dose of stro
89618u Cyclohexunide-induced ultrastructural changes in phanthoside was significantly smaller in both intoxicated groups.
the adrenal cortex of the rat. Dzsinich, Cs.; Szabo, D.; Okros,
G. Muacevic
I. (Inst. Exp. Med., Hung. Acad. Sci., Budapest, Hung.).
89624t Antidotes for phosgene-induced pulmonary edema.
Experientia 1969, 25(8), 836-6 (Eng). Wistar rats of both sexes Boyd, Eldon M. (Queen's Univ., Kingston, Ont.). J. Pharm.
weighing about 180 g. were used. Conspicuous changes in the Pharmacol. 1969, 21(8), 557 (Eng). Death rates from phosgene
ultrastructure of the zona fasciculata cells were observed follow were reduced in rabbits, cats, and rats if the animals were allowed
ing decapitation at 50 min. even after the lowest (5 mg.) dose. to inhale the phosgene through the nose rather than directly into
At low-power magnification, compact masses of irregular shape, the trachea.
David B. Sabine
medium d. and blurred outlines were seen to have accumulated
89625u Demethylphalloin. Puchinger, Herwig; Wieland,
between organelles. In expts. involving both cycloheximide and Theodor (Univ. Frankfurt, Frankfurt, Ger.). Justus Liebigs
ACTH treatment, the changes were similar, although the cells Ann. Chem. 1969, 725, 238-40 (Ger). Demethylphalloin-*// (I)
appeared swollen. Similar observations were made in some cells was obtained by redn. of the CO group of ketophalloidin with
of the zona reticularis, but not in the zona glomerulosa. The *H-labeled NaBH(. I had almost the same toxicity as phalloidin.
findings suggested a correlation between the substance seen to During storage I gave a degradation product whose uv spectrum
accumulate among organelles and the increased cholesterol indicated a sulfoxide structure.
BTJG
content of the adrenal cortex. The ultrastructural changes were
89626v Histochemical study of cytochrome oxidase and
the consequence of an impairment of the enzyme system.
succinic dehydrogenase activity in encephalon of rabbits poisoned
P. J. Parisek
by alcohol. Lo Menzo, G.; Chiara, A. (Univ. Catania, Catania,
896l9v Effect of acetone on the level of ketone bodies in the Italy). Med. Leg. Assicurdtioni 1968, 16(3-4), 163-72 (Eng).
blood and urine of experimental animals of different species. An increase in both cytochrome oxidase and succinic dehydro
Linyucheva, L. A.; Tiunov, L. A.; Kolosova, T. S. (USSR). genase was observed in the cells of the cerebellar cortex of rabbits
Farmakol. Toksikol. (Moscow) 1969, 32(4), 465-7 (Russ). Rats which had undergone either chronic or acute ale. poisoning, as
and mice exposed to 30 mg. MeiCO/1. and rabbits and guinea compared to the nonpoisoned control animals. No change was
pigs exposed to 72 mg./l. for 2 hrs. showed increased levels of evident in other encephalic regions. The increase of these en
MeCO, acetoocetic acid, and 0-hydroxybutyric acid in their zymes at cerebellar level agrees with the symptomatological
blood and urine immediately after inhalation and 24 hrs. later. data indicative of functional damage of the area during ale.
In all 4 species the 0-hydroxybutyric acid level increased to a poisoning.
Murrie W. Burgan
greater extent than did the other ketone bodies. The largest in
89627w Nicotine degradation in hamsters and rats and its
creases in the MeCO and acetoacetic acid levels in the blood both modification by foreign substances. II. Effect of carbon mon
immediately and 24 hrs. after acute inhalation occurred in rats oxide treatment of the animals on their nicotine metabolism.
and the smallest changes appeared in rabbits.
BJJR
Harke, Hans P.; Frahm, B.; Schultz, Ch.; Dontenwill, W.
89620p Nature of the acute action exerted on the organism (Inst. Wiss. Forschungstelle Verband, Cigarettenind., Ham
by monoethanolethylenediamine. Tikhonova, G. P.; Sidorov, burg, Ger.). Naturwissenschaften 1969, 56(8), 418 (Ger). Deg
K. K. (Inst. Med.-Biol. Probl., Moscow, USSR). Farmakol. radation of nicotine to cotinine in rat and hamster liver homog
Toksikol. (Moscow) 1969, 32(4), 473-5 (Russ). Monoethanol enates was not affected by prior exposure to CO.
GKJG
ethylenediamine (I) injected into the stomach of rats in a max.
89628x Toxic effects of calcium, titanium, and niobium
tolerable dose (2.5 g./kg. in 30% aq. soln.) disrupted the acid- borides in rats. Kasparov, A. A.; Zhilova, N. A. (USSR).
base balance in the blood after 3-5 hrs., increased the pH from Nov. Dannye Toksikol. Redk. Metal. Ikh Soedin. 1967, 152-60
7.18-7.35 (control) to 7.4-7.49, and increased the level of free (Russ). From Ref. Zh., Farmakol., Khimioter. Sredstva, Toksi
bases. One day after I injection the Ca level in the serum in kol. 1968, Abstr. No. 7.54.779. LD of CaB, (I), during i.p.
creased, the time of blood coagulation decreased, the blood pH administration to rats, was 1.045 mg./kg. Intoxication with I
dropped to 7.11-7.24, and the amt. of free bases was below nor is expressed by depression and disorder in movement coordina
mal. The level of globulins decreased and the content of albu tion. Chronic oral administration of I to rabbits (100 mg./kg./-
mins increased in the blood; the level of chlorides in the urine day for 4 months) caused leukocytosis, lymphocytosis, increase
decreased. I caused necrosis in the mucous membranes of diges in concn. of a-y-globulins and activity of aldolase, and decrease
tive system organs, probably through its alk. properties. BJJR
in albumin in blood. Prothrombin in blood at beginning de
8962lq Changes in adrenaline-like substances in rabbit creased and then increased to the end of expt. In lungs them
blood following chronic exposure to vinyl chloride fumes. Vazin, was polyemia of tissues and thickening of interalveolar septums.
. A. N.; Plokhova, E. 1. (Inst. Gig. Tr. Profzabol., Gorki, In intestines there was sclerosis of all vessels in submucosal
USSR). Gig. Tr. Prof. Zabol. 1969, 13(6), 40-7 (Russ). A layer, decreased glycogen in liver, and accumulation of acid
group of $ chinchilla rabbits was exposed for 4 hrs. daily, during mucopolysaccharides in the region of hepatic triad. Moderate
5 months, to the vapors of vinyl chloride (1) in air at 0.02- intensification of lung pattern was observed by x-ray studies in
I 0.03 mg./l. Samples of blood were taken from the ear veins and animals 0-9 months after single intratracheal administration to
analyzed for adrenaline (II) and adrenaline-like (Ua) substances. rats of Ti boride (II). Nb boride (III), and esp. of I (60 mg.).
SPI -12905
Pag* 179
14--Toxicology Vol. 70. 1969
113464
cnees in the fatty acid compn. of the brain between HCN-
treated and untreated rats.
N. Constantsas.
113452n Curative antagonization of liver damage caused by
phalloidin with silymarin as a model of antihepatotoxin therapy.
Vogel, Guenther; Tcminc, Inge (Biol. Inst. Madaus, Cologne, Ger.). Arzneim.~Forsch. 1060, 19(4), 613-15 (Gcr). Silymarin, the antihepatotoxic agent in the seeds of Silybvm marianum,
prevented the toxic effects of phalloidin in mice. Silymarin was
also effective in reversing the toxic effects of phalloidin in mice
intoxicated first with this compd. and then treated with sily marin. The antiphalloidin effect of silymarin depended on the
time interval between intoxication and treatment, and on the
degree of liver damage.
BQJG
U3453p Evidence for the bioactivation of slaframine. Aust,
Steven L). (Michigan State Univ., East Lansing, Mich.). Bio-
chem. Pharmacol. 1969, 18(4), 929-32 (Eng). Max. salivary activity in pentobarbital-anesthetized cats occurred ~1 hr.
after i.v. administration of slaframine (0.3 mg./kg.); the dura
tion of salivation was extremely long, usually lasting for 6 hrs.
after a single dose. In addn. to salivation, most of the exocrine
glands were specifically stimulated by slaframine. Upon ad ministration of slaframine to cows, sheep, and goats with pan
creatic cannulas there was also a substantial delay before an in crease in pancreatic flow was observed. In mice, a longer delay
occurred after i.v. injection of 2 mg./kg. than with i.p. adminis
tration at the same dose; this delay wafgdecreased by injection
directly into the portal vein. Delay of the effect of the drug at
4 mg./kg. was significantly extended by briefly isolating (with
clamps) the liver of rats; the effect was completely eliminated
by the permanent isolation of the liver. Common inducers of
liver drug-metabolizing enzymes consistently reduced the delay
in the induction of salivation in mice, while inhibitors of the en zymes consistently lengthened the delay. Thus, slaframine
seems to require activation by the liver before stimulating exo
crine glands. The enzymes involved in this activation are
probably those responsible for the metabolism of most xeno-
biotics.
BYJN
113454q Metabolism of phospholipids in the brain and liver
of rats during intoxication with organophosphorus compounds.
Dvorkin, V. Ya.; Tofilo, A. P. (Pavlov Inst. Physiol., Lenin
grad, USSR). Byull. Eksp. Biol. Med. 1969,67(3), 60-2 (Russ).
Organophosphorus compds. LG-63 (5 mg./kg.) and GA-81 (0.4
mg./kg.) administered i.m. to rats did not affect the level of
phospholipids in the brain and liver or the rate of restoration of
phospholipids in the brain. The metabolism of phospholipids
in the liver was increased 24.8% by organophosphorus compd.
LG-63 and 32.4% by GA-81. The increased intensity of phos
pholipid metabolism may be connected in some way to increased
activity of the hepatic cells during detoxication of the cholin
esterase inhibitors.
B JJR
I13455r Toxicity studies in mice treated with 1-0-D-arabino-
furanosylcytosine (ara-C). Leach, William B.; Laster, W.
Russell, Jr.; Mayo, Joseph G.; Griswold, Daniel P., Jr.;
Schabel, Frank M., Jr. (Med. Center, Univ. of Alabama, Birmingham, Ala.). Cancer Res. 1969, 29(3), 529-35 (Eng).
Optimum therapeutic dosage schedules of 1-0-D-arabinofurano-
sylcytosine (ara-C) administered i.p. in mice (15 mg./kg., every
3 hrs. for 24 hrs.) result in karyorrhectic damage to the crypt
epithelial cells of the intestinal mucosa. This damage is most severe at 4 hrs. (earliest observations made) after the end of the
24-hr. course, after which there is a rapid recovery to completion
in 72 hrs. The damage is thus transitory and resembles that of
hydroxyurea. This cycle of transitory intestinal damage fol lowed by recovery occurs after each therapeutic dosage schedule
of ara-C as long as the schedule is not repeated more often than
every 4th day. Progressive damage to the intestinal mucosa
accompanied by changes in the hematopoietic tissues occurs
only if this optimum therapeutic dose (15 mg./kg., every 3 hrs.)
is continued uninterrupted to the LDioo dose (360 mg./kg. in
72 hrs.) and beyond. Irreversible changes are seen in the in
testinal mucosa, and a progressive depopulation of the bone
marrow with ultimate aplasia ensues as the LDioo dose is reached
and surpassed.
RCTT
113456s Effect of butylated hydroxytoluene (BHT) on rat
liver cytochrome oxidase activity. Pascat, Gerard; Terroine,
Thcrese (Centre Rech. Nutr., C.N.R.S., Bellevue, Fr.). C. R.
Acad. Set., Paris, Ser. D 1969, 268(11), 1529-31 (Fr). The oral
administration of BHT (0.05% in the food, a concn. 50-fold
greater than that authorized for human food) for 8 weeks caused
a 13.4-22.4% decrease in hepatic cytochrome oxidase activity
in rats of both sexes. The addn. of BHT to rat liver homoge
nates at the level of 10 mg./g. liver caused a 12% decrease in
cytochrome oxidase activity. Thus, BHT appears to exert an
antioxidant effect on in vivo metabolism.
DFJF
U3457t Activity of guanine deaminase in rat kidney, liver,
and blood dining experimental uranyl nitrate intoxication.
Bastide, Janine; Bastide, Pierre (Fac. Mixte Med. Pharm.,
Clermont-Ferrand, Fr.). C. R. Soc. Biol. 1968, 162(5-0),
1169-71 (Fr). Guanine deaminase activity (I) was studied in
the liver, kidney, and blood of rats during exptl. intoxication
with uranyl nitrate (1 ml. i.p. of a soln. contg. 2 g./l. per 100
g. body wt.). As early as 24 hrs. later a progressive elevation of
I was noted in all organs, but there was a definite lowering of 1
in the kidney for the first 12 hrs. after the start of intoxication.
Dorothy J. Buchanan-Davidson 113458U Excretion of tetraethylgermanium in the rat. Ous-
trin, J.; Clavel, M. J.; Pitet, G. (Centre Rech. Toxictes,
C.N.R.S., Toulouse, Fr.). C. R. Soc. Biol. 1968, 162(5-6),
1226-9 (Fr); cf. G. Pitet (1967). Et(Ge (I), a very resistant
compd. in vitro, is degraded very easily in the rat. Although I has a vexy high b.p., it is eliminated in large amts, during respira
tion. The metabolites of I found in rat urine arc GeOj or the
gennanates. The metabolism of I is different from that of tetra
ethyllead (II) or tetraethyltin (III). N'o evidence was found
for the formation of tricthylgcrmanium, which explains the weak
toxicity of I compared to II and III.
Dorothy J. Buchanan-Davidson
113459v a-Hydroxybutyrate dehydrogenase activity of rat
kidney homogenate fractions after experimental uranyl nitrate
intoxication. Bastide, Janine; Bastide, Pierre (Fac. Mixte
Med. Pharm., Clermont-Ferrand, Fr.). C. R. Soc. Biol. 1968,
162(8-9), 1492-3 (Fr). Most of the a-hydroxybutyrate de
hydrogenase activity of the rat kidney is found in the super
natant after centrifugation at 24,000 g for 2 hrs. This activity
decreased with time during exptl. uranyl nitrate poisoning,
whereas the contents of protein, DNA, and RXA were relatively
low and underwent but little variation.
C. W. Ackerson
113460p Effect of ethyl bromide on the liver. Karimullina,
N. K.; Gizatullina, A. A. (Ufim. Nauch.-Issled. Inst. Gig.
Profzabol., Ufa, USSR). Farmakol. Toksikol. (Moscow) 1969,
32(2), 165-7 (Russ). EtBr fumes (2.4 mg./l.) inhaled by rats
and rabbits for 4 hrs. daily for 6 months disrupted the func
tional ability of the liver, decreased the hepatic glycogen and
fat levels, and prolonged hexenal sleep. Granular dystrophy
in the hepatic cells and a decreased RNA level in the cytoplasm
were detected.
BJJR
113461q Hemopoiesis in chronic heliotrine poisoning of
Wistar rats. Levin, G. S.; Novachenko, Z. I. (Uzb. Nauch.-
Issled. Inst. Gematol. Pereliv. Krovi, USSR). Farmakol.
Toksikol. (Moscow) 1969, 32(2), 170-1 (Russ). Heliotrine
administered s.c. at 3-10 mg./lOO g. once a week for 1-8 months
to Wistar rats caused hepatic lesions, hypochromic anemia,
severe reticulocytosis, normoblastosis, and leukopenia. Erythro
blastic sprout hyperplasia, an increased no. of mitoses, and an
increased no. of reticular and esp. plasmatic cells were observed.
The observed changes in the blood and bone marrow suggest
development of an autoimmune form of hemolytic anemia in
response to chronic heliotrine poisioning.
BJJR
113462r Benzene metabolism in the liver of experimental
animals and man. Tiunov, L. A.; Sokolova, T. I.; Bandman,
A. L. (USSR). Farmakol. Toksikol. (Moscow) 1969, 32(2),
185-8 (Russ). The rate of CH metabolism during 24 hrs. of
incubation was similar in liver homogenates from humans and
rats, more rapid in homogenates from guinea pigs, and slower
in rabbit liver homogenates. Species-specific differences seemed
to be involved in CH, conversion, since the activities of aryl-4-
hydroxylase and glucuronyltransferase increased while the
sulfonating system activity did not change in CH-treated rats.
In CHc-treated rabbits the sulfate adenyltransferase and aryl
sulfotransferase activities decreased during disruption of the
sulfonating system. The high rate of CH conversion in guinea
pigs may be connected with the relatively high liver catalase
activity.
BJJR
113463s Effect of the sodium salt of adenosine triphosphate
on experimental cyanide poisoning of rats (mechanism of the
antidotal action). Mosketi, K. V.; Ganzhara, P. S. (Odess.
Med. Inst., Odessa, USSR). Farmakol. Toksikol. (Moscow)
1969, 32(2), 214-15 (Russ). Na ATP (0.5 ml. of a 1% soln.)
given s.c. or i.m. to rats 1 hr. prior to administration of the min.
lethal dose of NaCN prolonged survival. When given s.c. im
mediately after lethal cyanide poisoning it substantially extended
the life span of 50% and prevented death in the other 50% of
the rats. The antidotic effect of ATP may result from its
ability to restore respiration by bypassing cyanide-sensitive
enzymes.
BKJR
1134641 Changes in the cardiac activity of rats chronically
exposed to vinyl chloride vapors. Vazin, A. N.; Plokhova,
E. I. (Gor'k. Nauch.-Issled. Inst. Gig. Tr. Prof. Zabol., Gonki,
USSR). Farmakol. Toksikol. (Moscow) 1969, 32(2), 220-2
(Russ). Chronic (5 months) exposure of rats to vinyl chloride
vapors at 0.03-0.04 mg./l. disrupted cardiac work rhythm, in
duced bradycardia and arrhythmia, and 'educed the relative
duration of I-II and T-II sound intervals. The relative dura
tion of the Q-T complex did not change significantly. Within
15 days after termination of poisoning, the rat cardiac activity
rhythm returned to normal, but the duration of the I-II and
T-II sound intervals remained below the initial level for another
15 days. The maximal permissible concn. of vinyl chloride
apparently is significantly less than the 0.03 mg./l. level pre
viously cstd.
BJJR
SPI -12906
41109
Chemical Abstracts Vol. 72, 1970
2t
14--TOXICOLOGY
T. R. TOEKEBLSON gk
41109x Toxicology of vinyl chloride. Schottek, Wolfgang
(Abt. Arbeitstoxikol., Holzweissig, Ger.). Chem. Tech. (Leip-
tit) 1969. 21(11), 708-11 (Ger). A review with 24 refs. The
toxicity of vinyl chloride in animals and humans, and the relation
of the chem. structure of the compd. to its toxicity were dis
cussed.
CCJG
41110r Microscopically contrasted heavy metal intoxication.
Silver sulflde process, a method for localized histochemical de
tection of heavy metals in tissues. Haider, Gerhard (Ger.).
Mihrokosmos 1909, 58(9), 272-5 (Ger). A review of work is pre
sented which illustrates the value of the combination of light mi
croscopy with histochem. techniques for the detection, localiza
tion, and identification of Hg, Pb, Bi, Fe, Zn, and Cu in cells and
tissues. Highlights of the silver sulfide histochem. procedure are
presented along with representative photomicrographs. 6 refs.
Nellie G. Dehnbostel
41111s Development of the hemodynamic, biochemical, and
morphologic changes in experimental endotoxin shock. Sten-
gert, Krzysztof (Z Zakl. Anestezjologii, AM, Lodz, Poland).
Postepy Hig. Med. Dosvi. 1909, 23(5), 601-59 (Pol). A review
is given of methods for detg. hemodynamic, biochem., and mor-
phol. changes, the course of changes in dogs, clin. evaluation and
patterns, and damage to tissues and organisms during exptl. endo
toxin shock. 146 refs.
Y. Pomeranz
41112t Saponins. Birk, Yehudith (Hebrew Univ., Re-
hovoth, Israel). Toxic Const. Plant Foodst. 1909, 169-210
(Eng). Edited by Liener, Irvin E. Acad. Press: New York,
N.Y. Dietary source, metabolism, and effects of various sapo
nins are given with methods for qual. and quant, analyses. 167
refs.
E. A. Hodgdon
41113u Chromatographic identification of psychotropic drugs.
Phillips, Geoffrey F.; Gardiner, Jane (Lab. Govt. Chem., Lon
don, Engl.). J. Pharm. Pharmacol. 1909 , 21(12), 793-807
(Eng). The thin-layer chromatog. of 3 classes of psychotropic
drugs, phenethylamines, tryptamines, and erganes, has been in
vestigated. Published methods are reviewed and Rf data, nor
malized by a graphical technique, are reported for extensions and
modifications of some of these systems. Optimum forensic sort
ing procedures are recommended.
RCHQ
41114v Estimation of lead in urine by atomic absorption
analysis. Taira, Yoshiko. Nippon Eiseikensa Gishikai Zasshi
1969, 18(5), 389-91 (Japan). The Pb,+ was extd. into iso-Bu-
COMe soln. from 30% NH,OH. The recovery rate was 99.9%.
The reproducibility of at. absorption measurement was 1.4%.
No interference from other ions was noticed.
T. L. Chang
41115w Determination of toxic substances and their me
tabolites in biological fluids by gas chromatography. I. Tri-
chloroethanol in urine. Sedivec, Vaclav; Flek, Jan (Ustav Hyg.
Prace, Prague, Czech.). Prac. Lek. 1969, 21(7), 301-5 (Czech).
See CA 70: 113446p.
VNJZ
41116x Aflatoxin Bi in the excretion of aflatoxin-poisoned rats. Chou, Ming-Wu; Tung, Ta-Cheng (Coll. Med., Nat. Taiwan Univ., Taipei, Taiwan). 7"ai-Wan I Hsueh Hui Tsa Chih
1969, 68(8), 389-91 (Eng). Aflatoxin Bi was detected in the rat urine and feces after i.p. injection of the toxin. Most of the
aflatoxin Bi was excreted in the first 24 hr. The percentage re covery was about 1.5%. A thin-layer chromatographic method
was a simple way for detg. the aflatoxin conen. of the excretions, and could provide useful information for detecting it in humans.
N. M. Wright 41117y Paper chromatography of Taxus baccata toxin. Bubien, Zenon (Wyzsza Szk. Roln., Wroclaw, Poland). Zesz. Nauk. Wyzsz. Szk. Roln. Wroclawiu, Wet. 1968, No. 23, 215-21 (Pol). The presence of toxin in T. baccata (English yew) needles,
in fodder, and in the alimentary tract content was detected by paper chromatog. The alkaloid was extd. from the biol. ma terial by Et,0, purified with active C, and chromatographed in
the form of aq. HC1 soln. The chromatograms were developed at 18* by the ascending technique, using as solvent either BuOH-
80% AcOH-anhyd. EtOH-H.O (50:7:2:15), or 75% aq. (NH,),SO. The Rf values were 0.95 and 0.75, resp. The toxin spots
were stained by the Draggendorf reagent.
Irena Kloczko
41118z Errors of converting a urine alcohol value into a blood
alcohol level. Kaye, Sidney; Cardona, Eduardo (Sch. Med.,
Univ. Puerto Rico, Rio Piedras. P.R.). A mer. J. Clin. Pathol.
1969, 52(5), 577-84 (Eng). Evidence is presented for the in
advisability of ealeg. blood EtOH levels on the basis of urine
EtOH content. EtOH content was detd. in the blood and urine
of 148 patients and the ratio of urine/blood was ealed. The
range of ratios was 0.21-2.60 with a mean ratio of 1.28. Blood
levels were ealed. from urine levels using a conversion factor of
1.28 and compared with measured values. Calcd. values ex
ceeded actual values by at least 0.02 g /nl in 21.5% of the cases
and were lower by the same amt. in 34.5% of the cases.
J. R. Macnab
41119a Ethylene glycol toxicity in the monkey. Roberts,
Jd Seibold, H. R. (Tulane Univ., Covington, La.). Appl, Pharmacol. 1969, 15(3), 624-31 (Eng). The
toxic effects of ethylene glycol in several macaque species are re ported. The compd. was administered in the drinking water at
concns. of 0.25-10%, and histol. studies were made after acute
and chronic administration. With the exception of a few animals
(which had Ca oxalate crystals in the brain), significant pathol.
alterations were limited to the kidneys. Animals receiving 15
ml/kg or more of ethylene glycol had Ca oxalate crystals within
proximal renal tubules and assoed. tubular degeneration. De
spite the absence of crystals in animals receiving <15 ml/kg, mild
glomerular damage was found, and azotemia occurred in some
animals, suggesting a toxic effect of ethylene glycol apart from its
conversion to oxalic acid.
RCZB
41120u A clinicopathologic study of the effects of riot control
agents on monkeys. TV. o-Chlorobenzylidene malononitrile
(CS) grenade. Striker, G. E.; Streett, C. S.; Ford, D. I-'.;
Herman, L. H.; Helland, D. R. (Edgewood Arsenal, Md.).
U.S. Clearinghouse Fed. Sci. Tech. Inform., AD 1967, AD-808-
732, 39 pp. (Eng). Avail. CFSTI. From U.S. Govt. Res. De
velop. Rep. 1969, 69(19), 123. A study was made of the order,
severity, and resolution of pathol. changes in monkeys exposed to
CS. Monkeys were exposed to CS (2700, 8500, 28,500, or
80,000 mg min/m1). The most prominent lesions seen after the
2 lower doses were mild pulmonary congestion, bronchorrhea,
emphysema, and atelectasis. These lesions cleared by 72 hr but
recurred at 1 week and 30 days. Oral and nasal discharges and
dyspnea appeared early after a level of 28,500. They were most
severe between 12 and 24 hr.and were resolved by 72 hr. Pneu
monia, emphysema, and atelectasis were present 1 week and 30
days after exposure. Significant lesions were seen radiographi
cally only in those monkeys exposed to a level of 80,000. These
lesions paralleled those seen on necropsy. At this level edema
appeared by 12 hr, peaked between 24 and 48 hr, and cleared by
1 week. Emphysema and bronchiolitis were present 1 week and
30 days after exposure.
TCVL
41121v Experimental study on gas embolism with particular
reference to the differentiation between embolic gas and gas
from putrefaction. Pierucci, Giovanni; Gherson, Gemma (Inst.
Med. Legale, Univ. Pavia, Pavia, Italy). Zacchia 1968, (3] 4(3),
347-73 (Ital). Embolism was induced by injecting air or He
i.v. into living (followed by instant death), and i.v. or intracardi-
ally into sacrificed, rabbits, and gas was aspirated from the heart
at intervals. Putrefaction gas was aspirated from the heart and
abdominal cavity of rabbits and human cadavers 1-13 days, and
15-236 days, after death, resp. In samples of air embolic gas,
Oj decreased and 1 hr after death was insignificant; COt was
present immediately; Ni levels were relatively stable, similar to
air, for 2 days, then decreased sharply. In He embolic gas,
Oj, N, and COi were present immediately. Results were essen
tially the same in rabbits injected before and after death. Av.
values for putrefaction gas contents in rabbit and cadaver heart
were, resp.: Oi 1.32 and 2.05%, Ni (usually <50%) 12.13 and
22.06%, COi 31.08 and 50.62%; CH appeared early and almost
constantly in the rabbit.
F. Farnam
41122w Early effects of carbon tetrachloride on the synthesis
of phospholipids in the rat liver and their possible pathogenetic
role in fatty liver induction. Halbreich, A.; Mager, J. (Hadassah Med. Sch., Hebrew Univ., Jerusalem, Israel). Biochim. Biophys. Acta 1969, 187(4), 584-7 (Eng). In rats, i.p. injections
of COI* in doses as low as 0.5 <il/100 g reduced the ability of liver microsomes to incorporate choline-1*C into total phospholipids and labeled L-leucine-l-"C into protein, discernible as early a10-15 min postinjection and lasting for 20 hr. Incorporation
patterns of choline were identical whether the radioactive choline was labeled in the Me groups or in the 1,2-carbon atoms. Tlic magnitude of choline inhibition was not altered by varying the
dose of labeled choline over a 1000-fold range, attesting to the independence of this phenomenon of the attendant variations in
the internal pool size of free choline. Ethionine (1 mg/g) and dimethylnitrosamine (10 mg/100 g) did not affect the incorpora
tion of choline into liver phospholipids, although they inhibited protein synthesis. CC1 enhanced the incorporation of cthanolamine-2-"C into liver microsomal phospholipids. The early onset.and the long persistence, as well as the specific nature, of the de
rangement of phospholipid synthesis by CCU suggest a possible role of this phenomenon in the pathogenesis in fatty liver.
BKJN
41123x In vitro inhibition of succinate and pyruvate oxidation by ethanolic extracts of grasses, legumes, and dystrophogenic
forages. Checke, Peter R.; Oldfield, James K. (Oregon State Univ., Corvallis, Oreg.). Can, J. Anim. Sci. 1960, 49(3), 41)2--1
(Eng). EtOH exts. of title plants inhibited in vitro oxidn. 1,1 both succinate and pyruvate by rat liver homogenates. Exts. of
2 dystrophogenie forages did not inhibit succinate oxidn. more than those of two nondystrophogeuic samples. The succinic
SPI -12907