Document n90jJBL44V72E263oqMnE0xxR

pox Eradication. ;o. 493, Geneva, smallpox eradi* and global car- SME/75.21, Ge-L: Towards the 19 May 1980. World Heaitii and JOURNAL OF HYGIENE, EPIDEMIOLOGY, MICROBIOLOGY AND IMMUNOLOGY 23, tMl, No. 3, 233--2 JAN 21 ',982 /r/SJr, - St*. f? CHEMICALS 2 py/ RESEARCH NEUROLOGICAL CHANGES IN VINYL CHLORIDEEXPOSED "WORKERS V. STlBlOVA', V. LAMBLl, 0. CHUMCAL*. V. K EILE RO V A1, V. FASKOVA1, f. VlTOVCOVA', L. 2 L A B ' l] Department of Neurology. Medical Faculty of Hygiene. Charles University, Prague 3) Outpatient Clinic of Occupational Health. District Centre of National health! , Mfilnlk, Czechoslovakia . Vinyl chloride (VC) toxicity for the human organism Is not stlU fully clear. The occupational exposure to VC is linked with the development of liver hemangiosarcomas, or with other malignant processes of varying locality. Some authors diagnose changes in terms of scleroderma, universally are described roentgenologicaily detected lesions of Interphalangeal joints and zonal osteoly* sis. They are described in association with Raynaud's syndrome (12, 10, 1, 4, 5 and others). Lange with his colleagues (12) describes angiologically detect able constriction of digital arteries, stenosis or partial occlusion of phalangeal blood vessels. Described are also various types of dysesthesia In fingers, parti cularly cold and numbness sensations. Also Byczkowska (3) reports frequent occurrence of finger paresthesia, whitening of fingers, but also of palms and soles, and other symptoms of peripheral vasomotor disorders. Neurological manifestations are described only sporadically. Spirtas and colleagues (15) emphasize particularly the narcotic action of VC at higher peak exposure concentrations. This manifests itself by vertigo, nausea and hea dache pains. Mentioned are also hand parestheslae (prlnckllng, formication). Langauer-Lewowicka (11) analyzes also the clinical symptoms In her group of 200 examinees who showed most frequently signs of cerebellar symptomato logy. She -recorded frequent occurrence of headaches and sleep disorders, but also trigeminal neuralgia. Because of a lack of more detailed neurological studies among the VC-ex posed persons, we conducted field investigations among the occupationally ex posed workers in a plant where there was six years before put into operation a workshop with a considerable VC hazard. * *- For Distribution by CMA SPECIAL PROGRAMS DIVISION 233 S > 5 Ke T, 5S & -**3 * &>* MATERIAL AND METHODS Tbe group of examinees consisted of 233 workers (263 males and 30 females), age 18--53 years, mean age 32.6 years. Of these 76 % were below 40. The average time of exposure was 2.5 years (range from 2 months to 6 years). After consultations with plant physician and plant toxicologist the group was divided into two subgroups ac cording to the level of exposure. The subgroup of high-risk workers, in which tbe ten tatively established maximum allowable concentration of 10 mg.m~3 had been fre quently and sometimes highly exceeded, involved polymerization worker^, and some maintenance workers (a total of 109 persons). The subgroup of lower-risk category of workers included those engaged in drying and bagging operations, but even here they were sometimes exposed to high peak exposure concentrations during cleaning and sampling operations, aod those from the other plant workshops -- combustion, compres sors, cracking, chlorination, regeneration -- where the exposure risk was relatively low (a total of 164 persons). AU the workers were examined neurologically, some of them repeatedly. A more detailed analysis of subjective complaints was performed on the basis of EOD and N5 questionnaire surveys. Electroencephalographlc examination with photostimulation was made in 232 persons (255 recordings). The group of controls consisted of 4S persons without exposure to toxic substances. RESULTS An overview of subjective complaints is presented in Table 1. Headaches occur frequently, but they are less frequent than in the control group. The in cidence of gastrointestinal disorders and other neurovegetative disorders (palpi tations, retrosternal pressure sensations) are significantly higher than in con trols. Psychic disturbances were observed only in those exposed. Table 1. Overview of subjective complaints in workers occupationally exposed to vi nyl chloride, in a comparison with controls Complaint* Headache Sleep disorders GlT disorders Vertigo Psvchie dirturbadas Dviesthesia Palpitation* Total number of examinee* VC -- exposed number % 46 15.7 16 5.5 20 6.9 3 1.0 13 4.5 9 3.1 14 4.8 293 100.0 Controls number 9 2 1 1 0 1 0 46_ 19.6 4.4 2.2 2.2 0.0 2.2 0.0 100.0 Significant differences were observed between the two subgroups of ex posed workers divided according to the level of exposure (Table 2). The sub group of more exposed workers showed a higher incidence-of headaches and 234 Table 2. Overvje Complai Headache Sleep disorders GIT disorders Vertigo Psychic disturbs!) Dysesthesia Palpitations Total number of e gastrotntestina. was observed ^ In persons wit: ches was doub: more than 4 y psychic disturb Table 2. Overv: Complai Headache Steep disorders GIT disorders Vertigo Psychic disturbat: Dysesthesia Palpitation* Total number of t posed workers showed a sign cent of more s Graph 1 p syndromes det< lesion of peripi : 8.7 %). Diagn or loss of tend VVC 000003235 ;e time of ions with i the ten* been freand some .tegory of here they .mng and compresuvely low \ A more D and N5 ation was 5 persons jadaches . The in- s (palpi- `n con- ed to vi- Q tO 19.6 4 .4 0.0 ** 0.0 00.0 s of exIhe subhes and Table 2. Overview of subjective complaints in workers occupationally exposed to vtnyl chloride, relation to the level of exposure Complaints Headache Sleep disorder* GIT disorders Psychic disturbation Dysesthesia Palpitations Total number of examinees Total number | % 46 15.7 16 0.0 20 6.9 3 1.0 13 4.5 9 3.1 14 4.8 293 100.0 More exposed number | % ' 19 7 11 2 6 7 5 109 17.4 6.4 10.1 l.a 5.5 6.4 4.6 100.0 Less exposed number | % 27 14.7 9 4.9 9 4.9 1 O.S 7 3.8 2 -*r 1.1 9 4.9 184 100.0 g-astrointestinal disorders, and furthermore, of dysesthesia of extremities. There was observed also a certain correlation with the length of exposure (Table 3). In persons with the exposure time longer than 4 years, the incidence of heada ches was double the Incidence in the group with a shorter time of exposed for more than 4 years. Sleep disorders, gastrointestinal complaints, vertigo and psychic disturbances were also more frequent in those with a longer time of ex- Table 3. Overview of subjective complaints in workers occupationally exposed to vinyl chloride, relation to the length of exposure Complaints Headache Sleep disorder* GIT disorders Vertigo Psychic disturbation Dvsesthesia Palpitations Total number of examinees Toijl number O' o Exposure longer than 4 year* number ; % 46 15.7 24 23.8 16 5.5 8 7.9 20 6.9 9 8.9 3 1.0 3 3.0 13 4.5 8 7.9 9 3.1 8 7.9 14 4.8 4 4.0 293 100.0 101 100.0 ! Exposure shorter than 4 years number j % 11.0 8 4.2 11 5.7 0 0.0 5 2.6 1 O.S 10 5.2 192 100.0 posed workers is characterized in Table 4. The group of more exposed workers showed a significantly lower per cent of normal findings and a higher per cent of more severe findings than the group of less exposed workers. Graph 1 presents incidence of the most frequent, objectively diagnosed syndromes detected in exposed and control groups. The most'frequent was the lesion of peripheral neurons, either motor or sensory, or both of them (16.8 % : :8.7/b). Diagnosed were impairments of muscle tonus or trophlcity, reduction or loss of tendon and bone reflexes, abnormal sensitivity. Compared to controls. 235 VVC 000003236 `... 1Z00000 DAA > f- m sodxa -- amnios 5-X 'ajnsodxa jo -Z3AU3s(qO qd?JD ui 03 pasn ajBM jouippa aqi ; ptrp pjaq spjaw jo % 0* ui Aiuo -0 ajaM saouajaj aajSap jaqSjq p 31 ajnsodxa J3mo[ ixb-x `ajnsodxa ;o -Z3A3atqo tjdsjo * 9K san;mjouqv *sjaAas jsaai sApmip ajaM siojjuoa am ui painajap samuuouqp 0S3 am `dnoj? itthuco am txi u*m jaqSiq s\ sjs>(jom pasodxa jo dnoaS am ci sguipjossj 033 TBmjouqs jo :uap Jad am *g ajqpx UI pajeduioo ajp sjsj{JOa\ jojuioo pasodxa-nou *18 pue pasodxa jo suojjauunBxa 033 30 sijnsaj am suosjad assy; ui (o/,, c-q : q/0 ] jaq8jq osip si amojpuAs jpnaqajaooinqjjsaA am jo Aouanbaj^ (o/0 ims : % q-zx ) siuauuiadn:] jpnsPja3 pn? [% 9TT % 9*ZZV suojsej uojnau I'ajaqduad Apuanbajj ajom aAaq ajnsod -xa 30 siaaA $ uam ajom mw* asom ' qdsjo aas `ajnsodxa jo qiSuai am nojimajjoo a 30 suouepipuj uicuap osia sjb ajaqj, '(XiaAjjoadsaj *o/0 fz: q/0 ^*9 pire %9Y:%0T) luanbaj; ajom osja si amojpuAs JBtnqjjsaA pup jpuaqaiao (% fi'II: % 9'SZ) uaijo sp 93IM1 upqi ajom pajoajja ajp saa^JOM pasodxa aaom tsuojsa} uojnau ipjaqdijad 30 aauappui am 01 si aouajaujp pa^jpui y -ajnsodxa 30 I3A3I am 0; uoijpisj ui smoiduiAs pasouSpip ^laAjjaalqo smoijs z qdpjQ saauitncxa 30 c/D -- stxb-a 'pasodxa* PA 3 dnojS -- urnnioo paqoiaq `sjojjuoa jo dnojS umnioa jpiBig XSoiojBmojdmXs jejjaao asjadsjp 0 'iSojojsmojdmAS iBpimBjAdejjxa -- y `ASoiojetaoidiEAS jeinqjisaA -- a 'iSoioiatuoidmAs JBnaqajao -- p \{SoioiujojdmAS aAiijaSaAO.inau iBJaqdprad -- g *snoisa| uojnan iBjaqdtjad -- v :ss3ueqa pasouScip AfaAtaaatqa -- rtxs-x `Sjojjaoo 03 uostisdmop b ui SJa^iDM pasodxa-^A U! saSuaqp pasouSsip AiaAuaafqo qdaJC (sbspd yo %s*9^ lay *saniuuouqp o aqj qj|M painq -DA pasouptp msamsasAp mpvi pajppossp `sjtaSun jo SuiuajiqM jo sisojptqjadAqojpp `Anuam -odAqojop Anpojjioads sjapjosrp aAnPia8aA0jnau ipjaqduad 30 iSojojpmojdmAs api Apnanbaaj ajom osjp paMops sjb^jom pasodxa 30 dnojS am 0*001 E"E 5*fE S~9 t8I SIX 0*001 0*6 o*sv 0*9t 601 01 OS 0*001 o*s 0*3E o*:s 6Z 91 5TI 91 saaonsaxa jo xaqoran pno^ saxuvrp jsajRrvj^ 3811*43 xq^rx pnuot^ % j xaqnrnn pasodxa % xaqnraa pasodxa uej^ 0/o nqvno 1 *380043 JO XxUA3S ajnsodxa ]o |dA8i aqj 01 nop?iaj err apjjomo Iaota 01 pasodxa Anpuopednppo sj8^jom ai saSusqa pasouSijp AiSAiiaatqo jo AiiiaAas > siq^I m ti ... : iv;; -Sv-v" Ay ' f' .'5-9-'*yJ^,i"T !>> ....o * '*--*'$!> :T,!*-*"- iV*'`.V^t-iep'r'vr. iitii 1*1 fcnTiY n*' i II ' ly exposed exposed O' 62.5 54.2 3.5 100.0 noatology acrchyposesthesia. diagnosed in VC-exposed workers were predominantly episodic, in 5 cases com bined with the diffuse abnormity. Three EEG recordings revealed oniy diffuse abnormities. Relatively frequent was also the presence of sleep waves {in 46.5 % of cases). In 16 % of workers the sleep activity manifestations were of in!?tSVI.ji. V -prison to n lesions, logy. 0 -- se central up of VC- level of i lesions: : 11.8 %]. .5 /o and jrrelatioQ rs of ex5 *rt) and erebellar i control rdings in the EZG normities Graph 2: Objectively diagnosed changes in VC-exposed workers in relation to the level of exposure. X-axis abjectively diagnosed changes: A-D see Graph 1. Blank column -- lower exposure levels, hatched column -- higher exposure levels. Y-axis -- % of the total number of exposed subjects. a higher degree of severity [2c to 3, according to Roth (13)). Significant dif ferences were observed also in the photostimulation reaction that was normal oniy in 40 /b of cases. The most frequent was extension of photic driving to wards beta and theta waves (in 43.4 H of cases). The additionally conducted N5 and EOD (5, 7, 8, 9) questionnaire surveys were used to improve analysis of subjective complaints and to complement ls|S5S 3 'i.t.^a-T, Graph 3: Objectively diagnosed changes in VC-exposed workers in relation to the length of exposure. X-axis -- objectively diagnosed changes: A-D see Graph 1. Blank column -- exposure shorter than 4 years, hatched column -- exposure longer than 4 years. Y-axis -- % of the total number of exposed subjects. '*r 237 A, WC 000003238 r Hr#42h*H' v -- .1 J*J #. . .j-'v'"} 'Tuca 1 5H VV,| .--5 - - ..5. s?a Jfc'V-TJ I anamnestic data. The questionnaire N5 examines superficial personal traits as well as certain clinical symptomatology, particularly neurovegetative syndro me, neurasthenic, depressive and anxiety-phobic symptoms, and the so-called toxic syndrome. Data provided by this type of questionnaire were suggestive of Table 5. Severity of ESG changes in workers occupationally exposed to vinyl chloride, in a comparison to controls _^ EEC Normal Suspect Abnormal Total slight medium total Exposed number i 148 [ 48 30 ! 61 36 1 232 O 0' 63.8 20.7 12.9 2.6 15.3 100.0 Controls number % 57 70.4 19 23.4 5 6.2 0 0.0 s 6.2 81 100.0 a higher frequency of sleep disorders (36%) than originally revealed by .ana mnestic data, highly frequent (S /o level of significance) was also somnolence (76%), which had not been also indicated in personal histories. More frequent were also feelings of bad performance, fear of loosing life or health. Furthermore, the frequency of hyperhidrosis was also very high (73 /o). The Eyseneck perso nality questionnaire examines neuroticism. It reveals subjective tendencies that are evaluated by the examinee and confronted with the objective reality. In the examined group there were not detected any significant deviations from the norm; increased neuroticism could not be demonstrated. DISCUSSION Clinical examination of VC-exposed workers revealed significant changes predominantly in neurologic symptomatology. Some of the subjective complaints, such as headaches, vertigo, sleep disorders or increased sleepiness during the day, es revealed by questionnaire N5, are suggestive of the narcotic action of VC, similarly as the occurrence of the cerebellar and/or vestibulocerebellar symptomatology. These changes have been, already described by Spirtas and colleagues (16), Langauer-Lewowicka (11), but also by Schwartzovd (15) and others. This characteristic symptomatology was also described in our previous studies concerned with the occupational exposure to trichloroethylene, benzene and other organic solvents (17, 18, 20). Here we also observed a high incidence of dysesthesia alter exposures to some solvents, particularly to benzene. We ascribed it either to peripheral vasomotor changes, or -- at least in some cases -- to initial phases of polyneuropathy. In case of VC the presence of peripheral vasomotor changes Is evidently very significant: accordin^_to literature data 238 4. and to our owr nauds syndrom in terms of ste: lesions diagnos ed by a direct companying me The narcot changes in the irreversible ch: ves in EEG re firmed in a re: nees as well ; solvents (19, 21 more serious z cortical brain diffuse abnorm ment with the This leads us t centrations, cz structures. VC-Lnduce manifest them, of changed tr> authors on th*. with our findir We also t exposed work? damage. Come In persons ext 1) Expose terature, also these neurolo: of exposure. 2) Some tion of VC, su locerebellar s 3) Amon^ tion Is, no do-, bination with motor change Vvc 00000 3^39 ..aits es * syndroso-called restive of ; chloride, Oo' 70.4 ZZ.i 6.2 0.0 6.2 100.0 1 by anamnolence frequent thermore, rk perso:cies that a the r.uin the changes mpiaints, uring the action of zerebeilar irias and (15) and previous benzene incidence :zene. We :me cases zeripheral .rare data and to our own experience these changes are frequently associated, with Ray naud's syndrome and may presumably, lead to even more severe consequencies in terms of stenosis or occlusion, as described by Lange (12). Peripheral nerve lesions diagnosed in our group of VC-exposed examinees oould be then explain ed by a direct neurotoxic action of VC, or as a consequence of hypoxia ac companying more severe vasomotor changes Ln the periphery. The narcotic action of VC can be either transitory, Inducing only reversible changes in the brain function, or persistent, causing more permanent, sometime irreversible changes In the CNS. Slight functional changes manifest themsel ves in EEC recordings by waves typical for various stages of sleep, as con firmed in a relatively high per cent (46.5 /o] of cases in our group*^f exami nees as well as in some of the examined subjects exposed to other organic solvents (19, 21, 22). Detection of episodic or diffuse EEG abnormalities is rather more serious and may be indicative of chronic changes in mediobasal and/or cortical brain structures. In our group of examinees, the joint episodic and diffuse abnormality occurred in 15.6 % of workers. This frequency is in agree ment with the cited literature data as well as with our previous experience. This leads us to a conclusion that even VC, particularly at higher exposure con centrations, can produce neurotic changes in the above described brain structures. VC-induced pathophysiological changes are believed by some authors to manifest themselves by the central neurovegetative dysregulation, as a result of changed hypothalamus functions (2). This localization, presumed by these authors on the basis of their experimental studies, seems to be in agreement with our findings of EEG episodic abnormalities. We also believe that even r S reaction changes, recorded in our group of exposed workers, may be of importance in the-early diagnosis of VC-induced damage. Comparable ?S reaction changes were also described by RouskovA (14) in persons exposed to other toxic agents. CONCLUSIONS lj Exposure to VC may lead, besides to other changes described in the li terature, also to lesions of the nervous system. The onset and development of these neurologic changes depend on the VC exposure level and on the length of exposure. 2) Some of the neurologic manifestations are caused by the narcotic ac tion of VC, such as certain subjective complaints and cerebellar and/or vestibu locerebellar syndrome. These symptoms can be transitory or persistent. 3) Among the -important manifestations that are characteristic for VC ac tion is, no doubt, the peripheral vasomotor symptomatology, sometimes in com bination with the Raynaud's syndrome described in the literature. These vaso motor changes Ln the periphery may further develop, leading consequently to =>??*r**T i-V'.'-'-^'t'-TV--- iAr: - -ar^*-; SS*~ was-ge 'tti_____ j- & m *?.-__r*4 JSSsy r^5; 3i,.-. '1 .i-l - -r. _;. ../- . -''. -- -i l i :$ St 1 . 'v .-..r .', > St- v '-.. more severe lesions of peripheral blood vessels. Equally important are the ge neral neurovegetative manifestations (gastrointestinal and cardiovascular dis orders, hyperhldrosls, etc.) that might result from the central neurovegetative dysregulatlon. Important are also symptoms of peripheral neuron lesions caus ed by a direct neurotoxic action of VC or by hypoxia-related mechanisms. 4) Episodic abnormality in EEG recordings seems to agree with the assumed involvement of hypothalamic structures (Basalajev and colleagues). It occurs even at exposure to the other types of organic solvents (15, 19, 21. J2] and may be indicative of a more diffuse affliction of mediobasal and cortical structures of the brain. Less severe manifestations of EEG sleep activity can be ascribed to the nacrotlc action of VC, more pronounced sleep manifestations accompa nied with abnormal EEG changes may be suggestive .of more persistent changes in the CNS. 5] Neurological changes have not been so far sufficiently accentuated in the professional literature and, therefore, the monitoring of workers at risk is not conducted systematically and by suitable methods. It is necessary to en sure a neurological prevention in these occupationally exposed workers. Of the supplementary methods of examination there are recommendable, both for pre vention and research purposes, to use EEG examination with photostimulation, questionnaires N5 and EOD, and electromyographic examination. SUMMARY Neurological examinations were conducted in 233 workers occupationally exposed to vinyl chloride. Subjective complaints were evaluated on the background of N5 and EOD questionnare survey analysis. EEG examinations, including photostimulation, were performed In 232 persons. The control group comprised 46 nonexposed subjects. Average time of exposure was 2.3 years, the longest time of exposure was 6 years. Among the most frequent subjective complaints were headache, neurovegetative disorders and dysesthesiae, among objective findings dominated cerebellar and/or vestibulocerebellar syndrome, lesions of peripheral neurons and peripheral neurovegetatlve symptomatology. Subjective and objective symptoms were found to depend on the exposure level and the time of exposure. EEG examinations confirmed in 15.5 % of cases abnormities, predominantly episo dic, sometlnmes combined with the diffuse abnormality. 46.5 H of the exposed showed presence of sleep activity as a consequence of VC narcotic action. The episodic EEG activity could be ascribed to lesions of mediobasal structures, or even to changes tn brain cortex. Our data have confirmed that vinyl elorlde has a considerable impact on the human nervous system. Most frequent are lesions of vestibulocerebellar system and viglllty disorders due to VC narcotic action. Frequent occurrence of peripheral sympto matology can be explained by a direct neurotoxic action of VC, or as a consequence of hypoxia caused by peripheral vasomotor changes. As a rule, regular check-ups of VC-exposed workers do not include systematic neurological examinations. The systematic neurologic prevention, based on the as sessment of clinical. EEG and/or EMG examinations, should become obligatory. Supple mentary use of N5 and EOD questionnaire surveys^ Is highly.advisable. 240 < S19 b 1 o v v 4, V.. Vito chlorure de Tin 11 a *t* St posts au chlcr l'aide des an ficatlf prodult l'expositlon sue Las troubl gfttatlfs et dys ttme vestibule ptriphtrique % xique direct p ayant lieu lor? Des donne sujets d&mont jehez 15,5 aneinte des s Les sujets jour, aux exar dans ce cas, sues de l'EEC St?b1o vi, V.. VI t rid exponierte Man beot Vinylchlorid : mil Hilfe her Einwirkung Exposition ab Die haul; tome und Dy zerebellarsys: ren vegetattv wohl als dire hei peripbere In dem EE fest, die die Aktlvitat (be durch Alfekt gen erkl&ren. Dle Vinv gischen Stan VVC 000003241 nt are the geovascular disiurovegetative lesions caushanisms. 2 the assumed -S), It occurs 22} and may cal structures n be ascribed cns accompastent changes accentuated :rkers at risk essary to en>rkers. Of the both for pretostimuiation. :naiiy exposed ` of N5. and ition. were ejects. Average rs. aurovegetatlve oellar and/or al neurovegsto depend on inactly episoposed showed episodic EEC :o changes in tpact on the - system 2nd here! symptoinsequence of ia systematic 1 on the as* jtory. Supple- RESUME Stfblovfi, V., Lambl, V., Cbumchi 1, 0., Kellerovfi. V.. PaSkov4, V., Vltovcovi, J., 2 1 a b, L.: L'image necrologtqoe chez les sujets exposes an c&lorore de vinyls I! a 4t6 fitudifi d'une manure complexe l'image neurologique chez 293 sujets ex poses eu chlorure de vinyle. Des troubles subjectifs ont fitfi analyses au plan dfitailifi A l'alde des anqufites EOD et N5. II a fitfi mis en fivldence un effet neurotoxlque slgnificatif produit par chlorure de vinyle qul dfipesd de la quaUtfi et de la quantitfi de 1'exposltion suble. Les troubles subjectlfs rencontrfis le plus souvant: maux de tfite^ymptOmes vfi* gfitetlfs et dysesthfisie. Les donsfies objectives tfimoigsent pour une affection du systfime vestlbulocfirfibelieux et pour celle du neurone pfirlpbfinque et de I'innervation pfirlphfirlque vfigfitatlve. Le symptfimaiologie pfiriphfirique peut rfisulter de 1'effet toxique direct produit par chlorure de vinyle aussi bien que du mficanisme d'hypoxie ayant lieu lors des changements vasomoteurs pfiripbfirrques. Des donnfis issues de I'EEG tfimoignant une activitfi de sommeil chez 46,5 % de sujets dfimontrent un effet narcotique du chlorure de vinyle. L'activitfi fipisodique [chez 15,5%] associfie parfols 4 renomalie de diffusion pourrait s'expliquer par une attelnte des structures mfidiobasales, mfime lifie aux changements du cortex. Les sujets exposfis fi 1'mfluence du chlorure de vinyle se se soumettent, jusqu'4. ce jour, aux examens systfimatlques au plan neurologique. 11 est nficessaire de poursuivre, dans ce css, une prophylaxie neurologique fitudiant l'image cilnique, les donnfies is* sues de 1'EEG ou mfime de' 1`EMG. 11 est utile d'emptoyer les anqufites EOD et N5. 2USAMMENFASSUNC S15* b 1 o v 4, V., Lambl. V.. Chumchal. 0.. X e 11 e r o v 4. V.. P a S k o vfi, V., V 11 o v c o v 4, V., 2 1 2 b, L.: Neurologiscbes Bild bei den dem Vinylchlorid exponierten Arbaltenden Man beabachtete kompiexerweise das neurologische Bild bet 2S3 Aroeuenden, die Vlnylchlorld expomert wareo. Subjektive Schwierlgketten aaalysierte man etngeheader mit Hilfe der EOD- und N 5-Fragebogen. Dabel hat man eine signifikante ceurotoxische Einwirkung von Vlnylchlorld nachgewsesen, die von der Intensitfit und Dauer der Exposition abhfingig 1st. D'le bfiufigsten subjektiven Schwierlgkeiten waren Kopfschmerzen vegetative Symptome und Dysesthfisie. Der objektive Befund zeugt von der Affektion des Vestibular* zerebellarsystems, ferner von der Alfektion des peripheren Neurons und der penphe* ren vegetativen Innervation. Die periphere Symptomatologie kann man erklfiren so* wohl als dlrekte Einwirkung von Vlnylchlorld, als auch den hypoxlschen Mechanlsmus bei peripheren vasomotonschen Verfinderungen. In dem EEG-Befund stellte man bei 46.5 /o Tiele der Gesamtheit die Schlafaktlvitfit fest, die die narkotische Einwirkung von Vlnylchlorld dokumentlert. Die episodische Aktivttfit [bei 15,5%) m&nchmal in Verbtndung mit Dlffusions&bnormitfit kdnnte man durch Affktlon von mediobasalen Strukturen, gegebenenfalf durch Kortexverfinderun* gen erklfiren. Die Vlnylchlorld exponierten Arbeltenden werden btsher systematised vom neurolo* gtschen Standpunkt nicht beobachtet. Die Verfasser balten die gezielte neurologische v -5- 241 WC 000003242 5~,r."'VL tSm '-Mi. " v. '5 W*: t,ytl --. W.*J"V * sr&i* Sy.'-r' ; Wv-.' -V > -> *.. c>r* i2fc si' *3#; t-#M** W *ji,T. Vorbeugung id Verbindung mit Beobachtung des klinischen Slides, des EEC- eventuell auch des EMG-Befundes far notwendig. Sehr geeignet ist die Anwendung der EOD- und N 5-Fragebogen. RESUMEN S t f b 1 o v 4, V., Lamb I, V., Chumchal, 0., KeUerovd. V., P a S k o v a, V., V J t o v c o v 1, 7., 2 I a b, L.: El cuadro nenroldgico en trabajadnrcs expuestos al viniIelora.ro Se ha examiaado globalmente el cuadro neuroldgico ea 293 trabajedoces expuestos ai viniicloruro. Las dificultades subjehvos se las aoalizd detalladamente mediante los cuestionarios 00 y N 5. Se mostrb el resultado neurotCxico marcado del vinilcloruro, el que dependia de la altura y duracidn de la expostcidn. Las dificultades subjetlvas mis frecuentes eran los dolores de la cabeza. los sintomas vegetativos asl que la disestesia. 1 bailazgo oofetivo muesrra la afecracidn del siscema vestibuiocerebelar, as! que !a de la neurona vegetative perifSrica y de a inervacidn vegetattva perlferica. La sintomatologla perifSrica la puede explicar tanto por el efecto tdxico directo del viniicloruro, como por el mecanlsmo hipoxico con los cambios vasomoidricos perifdricos. Se hallfi en hallazgos electroencefalograflcos una actividad del suefio en el 46.5 p. c. del coniunto, lo que prueoa el resultado narc6::co del viniicloruro. La actividad epizbdica (en el 15,5 p. c.), a veces en la eombtnacid:. con la anormidad difusa podrSa se explicar por afectacifin de las estructuras mediobasales. eventuaimente por cambios de la epidermis. Los trabajadores expuestos al viniicloruro no son aun exam:nados neuroldgscamenie de manera sistematica. Hace falta que se haya realizado neuroldgica prevention encamir.ada incluso el cuadro cllnico, el haliazgc electroencefalogrAfico. evenrualtnente el eiectroraiogrdfico. Se recomienda usar los cuestionarios EID y N 5. REFERENCES 1. Angulescn, F., Oloio, m,, Dobrooesca, E.: Med. InL 4, 1269, pp. 473--480. -- 2. Basaiajev, A. V.. Vazin. A. .V., Kocetkor, A, G.: Gig- truda 2, 1972, pp. 24--27. -- 3. Byczkowska, Z., et al.: Pol. tyg. lekar. 29, 1374, 25, pp- 1461--1464. -- 4. Diomaa, B. D.t Warren, A., Whiteboose, W. M-: Arch. Environ. Kith. 22, 1971, 1, pp. 61--73. -- 5. Dodson. V. N., Bertram, D., Dinmaa, B. D., Whitehouse, W. M.: Arch. Environ. HIth. 22. 1971. 1. pp. 53--91. -- 6. Engelsmass, F.: Cs. psycbol. 3, 1960, pp. 322-- 337. -- 7. Engelsmann, F., DrdkovA, S.: Cs. psychol. 4, 1S64, pp. 340--348. -- 8. Engelsmans. F., Drdkovi, S.: Activ. nerv. sup. 2, 1959. pp. 108--118. -- 9. Eysenck, H. J., Eysenck, S. G. B.: Manual of the Eysenck Personality Inventory. Univ. of London Press, London 24. 1S64. -- 10. Harris, D. K., Adams. W. G. M.: Brir. Med. J. 16, 1S67, pp. 712--714. -- 11. Langauer-Le- wowleka, H., Kurzbauer, H., Byczkowska, Z., Wocka-Marek, T.: Activ. nerv. sup. 21, 1374, 4, pp. 290. -- 12. Lange, C. E., Jube, S., Slein, G., Veltman, C.: I at. Arch. Arbeitsaed'. 32, 1974. pp. 1--32. -- 13. Roth, B.: Narkolepsie a hypersomnie z hlediska fysiologie spdnku. Praha, SZdN, 1957. -- 14. Rooskovd, V.: Int. Arch. ArDeitsmed. 34, 1375. pp. 253 --29S. -- 15. SchwartzovA, SL: Neurologickg a EEG nAlezy u chronicktfch prilmyslovych otrav nfikterymi organickyml rozpauStfidly. FIzeftsk? lfik. sb. Suppl. 25, 1370, pp. 5--88. -- 16. Spirtas. 242 R.. Me Michael, A. 1 M-: Am. led. Hyg. pp. 779---769. -- 1 ]6k. VII, 195S, 5. Stfblov*. V.: Acta L 12, I960, pp. 269--2 Cs. neuroi. 26, 1SS3 Received Novec VVC 000003243  eventuell EOD- und PaSkoadores ax is expuesmediante 1 viouclo;ades subas as! que ulocerebeitiva pen* ca directo Sricos pe- m ei 46,5 actividad :sa podrla : cambios 'jroidgicarevencidn tualmeate London Harris, D. ed. J. 16. gaaer-Leizkowska. . sup. 21, E., Jube. Arch. Ar12. Roth, hiediska 1257. -- smed. 34. t20T&, JL: chronic* /ml arga14k. sb. . Spirtas, R., Me Michael, A_ L-, Gamble, J., Van Ert, M.: Am. Ind. Hyg. Ass. J. 36, 1975, 10, pp. 779--7S9. -- 17. Stfblov*, V.: Prac. 14k. VII, 1955, 5, pp. 260--263. -- 16. Stfblovi, V.: Acta Unlv. Carol. Med. Suppl. 12, 1950, pp. 269--274. -- 19. Stfblovfi, V.: Cs. neurol. 26, 1963, p. 399. -- 20. Stfblo- v4, V.: Dlagnoza a preveoce v prumyslove neurologll. Praha, SZdN, 1963. -- 21. Stfblav*. V.: Int. Arch. Occup. Environ. HIth. 38, 1977, pp. 263--262. -- 22. St?blov4, V., Halaaovi, V.: Prac. 16k. 25, 1973, pp. 90-- see Received November 10,1380 V. St?blov6, Dept. Neurology, Medical Faculty of Hygiene, Charles University, Srobirova^SO, 100 42 Praha 10, Czechoslovakia Vs#?**' tsstswr-- v- `-fJg&I ~jggV~y wm - 4r mk-. ri * 2, 243 WC 000003244 SCrV tiss&ii `r ^SrttvcA.V^r ^'yyF.*- "a? JOeCSl'^-S*r ?&&> ,j>iv>; 7n'4"*-; - *.3*V'*:-.*--*r-**.*,. '.at. -