Document mbdXjexxM1JvwQ0XmXm20pLMQ

DOW CHEMICAL U.S.A. August 22, 1977 MIDLAND, MICHIGAN 48640 ERRATUM July 12, 1977 report titled "Resolution of Dose-Response Toxicity Data for Chemicals Requiring Metabolic Activation: Example Vinyl Chloride" by P. J. Gehring, P. G. Watanabe and C. N. Park, Page 8, 2nd. paragraph, line 3 should read (95% confidence limits are from .03-8.7 ppm). Enclosed is the correct version. P. G. Watanabe, Ph.D. Toxicology Research Laboratory Health & Environmental Research The Dow Chemical Company Midland, Michigan 48640 Enc. alw 870073 AN OPERATING UNIT OF THE DOW CHEMICAL COMPANY Using the foregoing equation, a projection below the levels of exposure producing an experimentally discernible response has been made (dashed line). Assuming no threshold for the induction of angiosarcoma in rats exposed to VC, the exposure concentration producing one angiosarcoma in 10,000 rats can be calculated. The probit percent representing an incidence of 0.01% is 1.28. Substitution of this value into the equation (4) yields: Log v = 1.8827 v = 76.33 yg VC metabolized/4 hours Using equation 3, the concentration of exposure to VC needed to give this value for v is 11.66 pg/S, or 4.6 ppm (approximate 95% confidence limits obtained by substituting the upper and lower 95% confidence limits for v in equation 3 and solving for S are 0.03-8.7 ppm). Hence, exposure of rats to 4.6 ppm VC for 4 hours daily, 5 days/week for 1 year can be expected to produce one angiosarcoma per 10,000 rats if the dose-response curve remains valid at exposures less than those producing a discernible experimental response. 870074 AIk3?om , Olh-ifo 4L4t :a a <s / February 22, 1982 Mr L Husband Mgr Industrial Relations Goodyear - Niagara Falls, N Y Dear Laurel: Would you please pass the attached on to Dr Kim for his information. The purpose is to alert him of the potential for neurologic effects from vinyl chloride exposure. I would doubt that employees at your plant would experience these findings since the levels of possible exposure at the Niagara Falls plant are -far below the exposure levels described in this article. >/ J C A Johnson, M.D. jap Att 870074.1 Eradiee'.ioa. (S3, Geneva, itlpoi eradl- global carE/75-21. GeTcwerds the My iaaa rid Health v. Sill'. OVA'-, v. UKU'. 0. CHOMCA*.V. K Et-l't J* 0 V A v. paSkova'. virovcovA'. t, ila*' M Department ol Neurology, Medical Faculty o* Hygime. Claries University. Prague J] Outpatient Clinic ol Occupational Health, District Centre of National Health, MilnOc. Czechoslovakia ig Vinyl chloride (VC] toxicity lor the human organism Is not still folly 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 roentgenologically detected lesions of tnterphalangaal 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 anglologlcally detect able constriction ol digital arteries, stenosis or partial occlusion of phalangeal blood vessels. Described ere 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. Splrtas and colleagues (16) 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 paresthesiae (prlnekllng, 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. i 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 T a workshop with a considerable VC hazard. , :: "W ;4h For Distribution by CMA SPECIAL PROGRAMS DIVISION 233 Ref. No. .' - -: : Data ____________ 1 870074.2 bt:i >w i jI4 " ,: r 53 5*; 0^1 /'i- i MATERIAL AND METHODS The croup of examinees consisted (263 males and 30 females). ag 18--58 yean, mean age 32.3 years. Of these 76 % were below 40. The average time of exposure was 2.3 years (range from 2 months to S yean). After consultations with plant physician nd plant toxicologist the group was dll3> uiiu"twu suligiRHfpy >C^ | ||eelessnir~> Ca^iarairTT.pJ.f-faiT>.. 1.1 I .... ...........Wisrum- L f MM^j-wifiwy^e^i^pnsrtni-^n-ftnerfirhmu iwherrr^h~~r-x~v"***ilifcl**'****'',*"~tT~*"** 4m*gti1^nWperaonsV All the workers were examined neurologically. some of them repeatedly. A more detailed analysis of subjective complaints was performed on tbe basis of EOO and N5 questionnaire surveys. Electroencephalographlc examination with photostimulation was made in 232 persons (255 recordings). The group of controls consisted of 46 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 m the control group. The In* cidence of gastrointestinal disorders and other neurovegetatlve 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 t comparison with controls Complaints Hnriarhft Slcco disorders GlT disorders Vertigo Psvchic dixtuxbatinn Dvsesthesia Palpitation* Total number of fjaminecK VC -- exposed number ) % 46 15.7 16 S.5 20 6.9 3 1.0 13 4.5 9 3.1 14 4.8 293 100.0 Controls number | Q 9 19.6 2 4.4 1 2^ 1 2J 0 0.0 1 2.2 0 0.0 44 _ 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. Overviev j Complain Headache Sleep disorder* C1T disorders Vertigo Psychic disturhatio: Dysesthesia Palpitations Total number of ex. gastrointestinal was observed el: In persons with ches was double more than 4 yet psychic disrurba. Table 3. Overne* Compilin'. Headaehe Sleep disorders GIT disorder* Vertigo Psychic disturhstioi Dysesthesia Palpitations Total nmnbcr of ex. posed workers ii showed a slgnif cent of more se\ Graph 1 prt syndromes detec lesion of periphs : 3.7 %}. Diagno: or loss of tender WTf, 870074.3 Sl. age Ime of s with 2% tenso frei some ;ary of re they ig end impressty low V more and N3 an was Persons laches lie In spi re vl- .6 .4 2 .0 ** 'o .0 o ex- e sub- :s ar.d Table 2. Overview of subjective complaint* In workers occupationally exposed to vlnyl chloride, relation to the level of exposure Complaints Headache Sleep disorders GIT disorder! Vertigo Fivchic discurbatioa Dysesthesia Palpitations Total number of examinees Total number | % 46 15.7 16 +5 to 6.9 3 1.0 13 4.3 9 3.1 14 4.8 193 100.0 More exposed number | % ' 19 7 11 t 6 1 5 109 17.* 6.4 10.1 1.8 5.5 6.4 4.6 100.0 Leu ecpoeed Dumber O/O' z~ 14.7 9 4.9 9 4.9 1 0.5 7 3.8 2 1.1 9 4.9 18* 100.0 gastrointestinal 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 oi subjective complaints in workers occupationally exposed to vinyl chloride, relation to the length of exposure Complaints Headache Sleep disorders GIT disorders Vertigo Psvcbie distuxbation Dvscstheaia Palpitations Total number of examinees Total number * O' /O 46 15.7 16 3*0 :o 6.9 3 1.0 13 4.5 9 3.1 14 4.8 93 100.0 Exposure longer than 4 yean number 0/ 'O 24 Z3.8 8 7.9 9 8.9 3 3.0 8 7.9 8 7.9 4 4.0 101 100.0 Exposure shorter than 4 year* Dumber O' fO 11.0 a 4.2 li 5.7 0 0.0 5 .6 i 0.5 10 5Z 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 par 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'frequeot was the lesion of peripheral neurons, either motor or sensory, or both of them (16-S % : :8.7%). Diagnosed were Impairments of muscle tonus or trophlclty, reduction or loss of tendon and bone reflexes, abnormal sensitivity. Compared to controls, - 235 870074.4 rS? fl.vn 5 X*?-* **W; filOJ ytii gSgjpiwl*. i-5,^4- i 'Ss: i tVss m*3-eH"j*i ^5 3*\.-* s* 3!S ; i\J V. Table 4. Severity or ob|ectlvety diagnosed changes In workers occupationally exposed to vinyl cblorlda la relation to the level o( exposure - Seventy of change* Normal Light change* Manifest change* Total number of examinee* Total number | 0,o 165 57.0 ns 3S.0 16 5.0 293 100.0 More exposed number | % 50 46.0 49 45.0 10 9.0 109 100.0 Lena exposed number | % 115 6" 184 62-5 54.2 3.3 100.0 the group of exposed workers showed also more frequently the symptomatology of peripheral neurovegetatlve disorders (12%: 4-4%), specifically acrohypothermy, acrohyperhidrosis or whitening of fingers, associated with dysesthesia. 201 y V. 10- / / A / PP / )/ ' / SC ' n_R"in_ D E F Ga Graph 1: Objectively diagnosed changes in VC-exposed workers in a comparison to controls. X-axis -- objectively diagnosed changes: A -- peripheral neuron lesions. B -- peripheral neurovegetadve symptomatology, C -- cerebellar symptomatology, D -- vestibular symptomatology, F -- extrapyramidal symptomatology. G -- disperse central symptomatology. Blank column -- group of controls, hatched column -- group of VC- exposed. Y-axis -- % of examinees Graph 2 shows objectively diagnosed symptoms In relation to the level of exposure. A marked difference is in the incidence of peripheral neuron lesions: more exposed workers are affected more than twice as often (25.6 % : XU %]. Celebellar and vestibular syndrome Is also more frequent (10 %: 7.8 % and 6.4 % : 3.3 %, respectively). There are also certain Indications of a correlation with the length of exposure, see Graph 3: those with more than 4 years of ex posure have more frequently peripheral neuron lesions -f22.8 %: 13.6 %] and cerebellar Impairments (13.9 %: 5.7 %]. Frequency of the vestibulocerebellar '.syndrome Is also higher (S % : 0.S %) in these persons. The results of ZZC examinations of exposed and 81 nan-exposed control workers are compared in Table 5. The per cent of abnormal ESG recordings In the group of exposed workers Is higher than in the cornel group: the EEG abnormities detected in the controls were always least severe. Abnormities 236 diagnosed In VC-e bined with the d: abnormities. Rela 46.5 % of cases). L Graph 2: Objective: of exposure. X-axis lower exposure lev a higher degree ferences were ot qnly In 40 % of wards beta and tf. The addition, were used to let Graph 3: Objective of exposure. X-e; column -- expos-. than 4 y 870074.5 exposed .-poied 63.5 34-3 3J 100,0 natology crohypoestbesta. diagnosed In VC-exposed workers were predominantly episodic, in 5 cases com bined with the dllluse abnormity. Three EEG recordings revealed only 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 ^Hbn to ^Tesioas, ogy. D -- se central 4p ol vc- level of leslo'ns: : LLS %]. 5 % and rrelatlon rs of ex, S] and erebellar : control rdlngs In the ZZG lormltles Graph Z: Objectively diagnosed changes in VC-exposed workers in relation to the level ol exposure. X-axis abjectlvely diagnosed changes: A-D see Graph i. Blank column -- lower exposure levels, hatched column -- higher exposure levels. Y-axls -- ol 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 phoiostimulatlon reaction that was normal only in 40 % of cases. The most frequent was extension of photic driving to wards beta and theta waves [in 43.4 % of cases). The additionally conducted NS and EOD (6, 7, 8, 9J questionnaire surveys were used to improve analysis of subjective complaints and to complement of exposure. X-axls -- objectively diagnosed changes: A-D see Graph 1. column -- exposure shorter than 4 years, hatched column -- exposure than 4 years. Y-axls -- % of the total number of exposed subjects. length Blank longer J * 3 " 1 I A\ P d ... .'5 td: -(- $ anamnestic data. The questionnaire NS examines superficial personal traits as well as certain clinical symptomatology, particularly neurovegetatlve syndro me, neurasthenic, depressive and anxiety-phobic symptoms, and the so-called toxic syndrome. Da`ta provided by this type ol questionnaire were suggestive o Table 5. Seventy ot EEC changes in workers occupationally exposed to vinyl chloride. In a comparison to controls _ EEC changes Normal Suspect Abnormal Total slight medium total Exposed oamber | o 148 63.8 48 20.7 30 12.9 6 2.6 36 15.5 232 100.0 Controls atimber | % 5T 70.4 19 23.4 5 6.2 0 0.0 5 6^ 81 100.0 a higher frequency of sleep disorders (36 Vo] than originally revealed by ana mnestic data, highly frequent (5 % level of significance] was also somnolence (76 %], which bad not been also Indicated in personal histories. More frequent were also feelings of had performance, fear of loosing life or health. Furthermore, the frequency ol hyperhidrosls was also very high (73 %). The Eyseneck perso nality questionnaire examines neurotlcism. 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 neurotlcism 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, as 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 Splrtas and colleagues [16], Langauer-Lewowlcka (11], but.also by Schwamovd (15) end 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 after 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 and to our own naud's syndrome In terms ol stent lesions diagnoset ed by a direct i companylag mor The narcotic changes In the b Irreversible char ves in EEG recc firmed In a rela nees as well as solvents (19, 21, more serious an conical brain s diffuse abnormal ment with the c This leads us to centrations, can structures. VC-lnduced manifest themse of changed hyp authors on the with our finding We also be. exposed worker damage. Compa: in persons expo 1] Exposuri teramxe. also u these nsurologi of exposure. 2] Some o tion of VC. me locerebelW;- sy 3] Among tion Is, no uju; binadon w,:: motor changes 870074.7 W as yndrocalled tlve or Olorfde. o )-4 IA 0.0 6j: o.o by ananolence requent ertnore, persoies that :he #the changes r.plaints, ring the ictlon of erebellar rtas and ;15) and previous benzene ncldence :ene. We me cases eripheral ure data and to our own experience these changes are frequently associated with Ray naud's syndrome and may presumably lead to even more severe coosequencles 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 sevtere vasomotor changes In 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 CMS. Slight functional changes manifest themsel ves in EEG recordings by waves typical for various stages of sleep, as con firmed in a relatively high per cent (46.5%) of cases in our group"^ 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 ratber more serious and may be indicative of chronic changes In mediobasal and/or cortical brain structures. In our group of examinees, tbe 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. V'C-lnduced pathophysiological changes are believed by some authors to manifest themselves by tbe central neurovegetative dysregulaBon, 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 ebnonnallties. We also believe that even r S reaction changes, recorded in nor group of exposed workers, may be of Importance in the-early diagnosis of VC-lnduced damage. Comparable ?S reaction changes were also described by Rouskovd (14) in persons exposed to other toxic agents. CONCLUSIONS 1) Exposure to VC may lead, besides to other changes described In the li terature, also to lesions ol the nervous system. The onset and development of these neurologic changes depend on the VC exposure level end on the length of exposure. 2) Some of the neurologic manifestations ore-caused by the narcotic ac tion ol 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. Ihese vaso motor changes in the periphery may further develop, leading consequently to 'rZ.i ] TfXn !i -IT-;" . .. -"Ttr- . ,>>r more severe lesions of peripheral blood vessels. Equally Important are the general neurovegetatlve manifestations (gastrointestinal and cardiovascular dis orders, hyperhldrosls, etc.) that might result from the central neurovegetatlve 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, Zl^Z] 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 nacrotic 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 photostimulatlon, questionnaires N5 and EOD, and electromyographic examination. 332*iNttX-r Neurological examinations were conducted in 233 workers occupationally exposed to vinyl chloride. Subjective complaints were evaluated on the background of NS and 00 quesuoanare survey analysis. EEG examinations, including photostimulatlon. were performed In 232 persons. The control group comprised 46 nonexposed subjects. Avenge time of exposure was 2.5 years, the longest time of exposure was 6 years. Among the most fcequeut <sub(active,^ompiainu were heertecde-. uidicvegetttWe dtsocdars-and dweestheeiae. among atofecttoe^indtags dominated uawilei1 ^end/or viiihiiliwrrhillag^oyodnome. Tyvna--ifyiwnpOtT-il vvernm -end pinphnif 'HfTfigttatt---ayispenmetoiogy. SubJecdv^ettd-^vefctwe syjiHmKiia .waee fwind-xo-oaynd--on EEG examinations confirmed in L5.5 % of cases abnormities, predominantly episo dic, sometlnmes combined with the diffuse abnormality. 46.5 S of the exposed showed presence of sleep ectlvity as a consequence of VC narcotic action. The episodic EEG activity could be ascribed to lesions of mediobasal structures, or even to changes in brain cortex. Our data have confirmed that 'MMyfci,lTlryile -hes .a^flnnsldarnfrl, Iiiijii'i hi illi Ti111 ii hiii wni ejitein Most frequent are lealrneunfnreesthuln--eainHei i iti'iii uni vigttwyXISoedTMdue ie'WOverconrtecTum. rii;(r>1~r*1-*T,,Tf~- mextgY-g*n-h*-*aplaln*d-hM-adlreoX,Munorlr Jdian oUQ-OI>a teiXiOnfKlueaCB of eeueed.by^>eiTpberii'^efr'moioenchDges. 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 obligator/. Supple mentary use of NS and EOD questionnaire surveys is highly .advisable. 240 st y biov vi, V, V It 0 chlorure de vie tl a 4t4 6t posts au chlcr t 1`alde des ac. flcatif produit Texposltloa sut Les trouSl g Status at dvs time vestibule pirlphirlque v xique direct p ayant lieu lore Des donnt sujets dimont: tchex 15,5 "4 1 arteinte des s Les sujets jour, aux txar dans ce cas, sues de 1*1EC stybio vi, V, VI t rid exponierte Man beoc Vlaylchlond mu Kllle der Elnwlrkuag Exposition ab Die bfiuf: tome und Dv xerebellarsys' ren vegetan*. wohl als dire bel perlphere In dem EE lest, die die Akavuat (be durch Affelr gen erkl&ren Die Vln\ gischen Stan -~r^r }1 i.""aiL 870074.9  , 4.-V--i- ire the geiscular disbvegetatlve siotis causilsms. le assumed . It occurs :) and may structures ie ascribed ; accompant changes ccenmaied ers at risk lary to eners. Of the :h for pretimulatlon. illy exposed N5 and *n, were average rovegetattve :llar and/or neurovegedepend on antly episosed showed pisodlc ~~C changes in ict on the system and ;ral symptosequence ot systemauc on the asory. Supple- * ' is.- '' -s'n*-'1 VT^-c^r RESUME S t ? b 1 o v 4. V., LambL, V., Chumche!, 0., Kellerovl, PaIko- v 4, V., V 11 o v c o v 4, J., 2 1 a b, L.: L'lmage ncaroLogiqae chei les tujeti xpo4x an chlornre da vinyl* 11 a tit 4tudl4 d'une manitre cocnplexe t'lmage neurologique chei 2S3 su)ets ex poses au cblcrure de vinyle. Des troubles aubjectlts ont tit analysts au plan d4taill4 4 1'alde des anquetes EOD et NS. II a 4tt mis en 4vtdence un etfet neuratoxique slgrufleatlf produit par cMorure de vinyle qul dtpend de la qoalltt et de la quanm4 de rexposttion suble. Las troubles subjectlfs rencoatrts le plus souvast: meux de ttta*^yraptOtnes vtgttatlts et dysesth4sie. Les donates objectives ttmolgnent pour une aflecrlon du sysI4me vestlbuloctrtbelleux et pour celle du neurone ptrtpbtrtquc et de rinnervanon ptrtphtrtque vtgttative. La symptOraatologte p4nph4rtque peut rtsulter de 1'eflet toxique direct produit par chlorure de vinyle aussi bien que du ratcanlsme d'bypoxie ayant lieu lors des changements vasomoteurs ptriphtnques. Des donnts Issues de l'EEG ttmoignant une actlvut de sommeil-Chez 46,5% de sujets dtmontrent un etfet nercotlque du chlorure de vinyle. L'actlvltt tpisodlque [chex 15.5%) associte parlols 6 l'anotnalle de dltfuslon pourreit s'expllquer par une attelnte des structures mtdlobesales. mime lit* aux changements du cortex. Les suiets exposts 4 l'ln'luence du chlorure de vinyle ne se soumetteot. jusqu'i ce Jour, aux examens systtmaaques au plan neurologique. 11 est ntcessaire de poursulvre, dans ce ces. une prophylaxie neurologique ttudlant I'image cllmque, les donates is sues de l'EEG ou tntme de l'EMG. II est utile d'employer les anquttes EOD et NS. ZUSAMMENFASSUNG S t ? b 1 o v 4, V., LambL V.. ChumchaL 0.. K e 11 e r o v 4. V,, Palkov 4, V., V 11 o v c o v 4. V,, 2 1 a b, L.: Naorologisches Bild bei den dem Vlnylchlorid exponierten Arbeitenden Man beobachtete korapiexerweise das neurologiscbe Blld bel 2S3 Arbeitenden, die Vlnylchlorid expomert weren. Suojektlve Schwierlgkelten analysierte man elngehender ml: Hllfe der EOD- und N 5-Frageoogen. Oabcl bat man eine slgnifikante neurotoxtsche Elnwirkung von Vlnylchlorid nachgewtesen, die von der Intensitit und Oauer der Exposition abhfingtg 1st. Die htuflgsten subjektlven Schwiertgkeiten waren Kopfschmerxen vegetative Symptome und Dysesthasle. Der objektlve Befund xeugt von der Affekxton des Vestibularzerebellarsystems, terner von der Aftektion des peripheren Neurons und der peripheren vegetaOven Innervation. Die penphere Symptomatologle kann men erkldren sowobl els dlrekte Elnwirkung von Vlnylchlorid, als auch den Lypoxlschen Mechanlsmns bel peripheren vesomotonschen Verinderungan. In dem EEG-Befucd stetlte man bel 46.5% Tlele der Gesamtheit die Schiataktlvltat test, die die narkotische Elnwirkung von Vloytchlorld dokumentiert. Die eplsodlsche Aktlvltlt (bel 15,5 %) manchmal in Verbtndung mlt DlfJustonsabnormitar kOante man dumb Af>ktion von mediobasalen Strulcturen, gegebeaenfeir durch Kortexveranderungen erkliren. Die Vlnylchlorid exponierten Arbeitenden werden bisher systematlsch vom neurologlscben Standpunkt nlcht beobachtet. Die Veriasser halted die gezielie neurologische - ' >ir *=zn V , -- . LIST'S. - .mj B*r - - 870074.10 Varbeugung in Verbinbung mit Beobachtung des klimseben BUdes. des EEC* eventuell auch des EMG-Befundes far notwendig. Sehr geeignet ist die Anwendung der EOD- und R~ Me Michael. A. I*. M.: Am. led. Hvg. , N 5-Fragebogen. pp. 77S--749. -- 17. 16k. VII, 19S5, S. ; Srfblovi, Vl Acta Un: RESUMEN 12, 1350, pp. 269--274. Cs. neuroL 2S. 1SS3. p 'I S t 7 b 1 o v 6, V.. L a a b 1, V,, Cbutnchal, 0-, K e 11 e r o v 4. V.. P a S k o * Received Noverob< v a. V,, V 11 o v e o v a, v,, 2 1 a b, L.: El cuadro neoroldgicn an trabaladores et- puestot el vinilclarttro Se ha examinado globalmente el cuadro neurolbglco en 2S3 trabeladores expues- I tos a! vinilcloruro. Las dificultades subjer.vos se las anallzd detalladamenie medlante Ios cuestionanos EOD y N 5. Se raosrri el resultado neurotdxtco marcado del vinilclo ruro, el que dependia de la altura y duracldn de la exposlcidn. Las dificultades subjetlvas mis frecuentes eran los dolores de la cabeza. Ios simonies vegetauvos asI que la disestesia. El hallazgo objetlvo muestrs la afectaclOn del sistema vestlbulocerebe! lar, as! que la de la neurona vegetative perlf4rlca y de a inervacidn vegetative penferica. La sintomatologla perlferica la puede explicar tanto por el efecto tdxico dlrecto del vinilcloruro. como por el mecanismo hipOxico con los catnbios vasomotOricos penfericos. Se baud en hallazgos electroencefalagriflcos una actlvidad del suefio en el 48.5 ;i p. c. del conjunto. lo qua pnieba el resultado narcdtlco del vinilcloruro. La actlvidad epizddlco [en el 15,5 p. c.), a veces en la combined^:. con la anormidad dlfusa podrla i se explicar por afecxacidn de las estructuras medlobasales, 'eventualmente por cambios de la epidermis. Los trabajadores expuestos a! vinilcloruro no son eun examinado* neurolOgica- mente de manera slstemauca. Hace falta que se have reallxado neuroldgica prevencidn encaminada tnciuso el cuadro cllnico. el ballezgo electroencefalogrillco, eventualmeme el eiectromlogrdfico. Se recomitnda user los cuestlonarios EID y S S. REFERENCES 1. Angnlescn, F., Otoio, m., Oobronescu, Personality Inventory. Unlv. of London E.: Med. Int. 4, 1969, pp. 473--430. -- 2. Press, London 24, 1934. -- 10. Harris. D. Sasalajev. A. V., Vazio, A. N,, Kocetkov, K-. Adams, W. G. M.: Brit. Med. J. 16. A. G..- Gig. truda 2, 1972, pp. 24-- 27. -- 3. 1967, pp. 712--714. -- 11. Ungauer-UByczkawskn, Z., at aL; Pol. tyg. tekar. 29, wowlcka. fL. Knrxbauer, H., Bycxkawska, i 1974, 26. pp. 1461--1464. -- 4. Dloman. B. Z,, Wocka-Marek. T.: Actlv. nerv. sup. 21. D., Warren. JL, Wfcitehonsa, W. M.: Arch. 1974, 4, pp. 290. -- 12. Lange. C. EL, Jena, Environ. Hltb. 22. 1971. 1. pp. 61--73. -- S Stein, G-, Veitman, Cl lnt. Arch. Ar5. Dodson, V. N-, Bertram, D-. QLnman, B. beitsmedl 32, 1974, pp. 1--32. -- 13. Roth. Whitebons*. W. M-: Arch. Environ. B.: Narkolepsie a hypersomme z hlediske Hltb. 22. 1371, 1. pp. S3--91. -- 6. Eagels- fyslologia spdnku. Preha, SZdN, 1967. -- mann. F.: Cs. psycbol. 3, I960, pp. 322-- 14. RonskoTa, Vl Int. Arch. Aroeitsmed. 34, 337. -- 7. Engalsmann, F.. Drdkova, S.: Cs. 1S7S. pp. 243--293. -- 15. Schwartxovl. K.: psycbol. 4, 1364, pp. 340--346, -- 6. Engelx- N`eurologick6 a EEG nilery u chronic* mann, F,, Drdkavi, S.; Acttv. nerv. sup. 2. fcfeh prOmyslovVch otrav nfikterymi orga1939. pp. 103--118. -- 9. Eysenck, H. J,, mckfml rczpouii&dly, Plzeflsky 14k. sh. Eysenck, S. G. B.: Manual of the Eysenck Suppl. 26. 1570, pp. 5--83. -- 13. Spirt**. 242 \ r-'-rtt* 870074.11  r~ -.-j.^-7 v "SS*- *' r;- .; - 4 :-"'*- ^ -7.T1'' *tj- .--.rvi.V5*""-''. ' iv >- -J.il.'- --- -^Vvi- ''"-V . 'f: -x1-> V-t V ;--~*- ----------7I~- 4-11>min 1 --^- - ti_ ---." .?y ^- _ _ C -- * i^rr v, - -* :>; -^"irivuTr: jell ) und SVom ei- rpuesdiante ailclos subsi que erebe* penirecto as pe- -1 46.5 lvidad podria imbios Idgiea* eacibn are .ondon Tis. D. I- 16. ocr-Le* ovfska, up. 21. - Jnhe, :b. Ar. Rotb. edlska 157. -- sd. 34. vi, K.: bcntnc- 1 arga li- sb. ipirtax. R., Me Michael, A, L, Gamble, f.. Van Ert. M.: Am, Ind. Hyg. Ass. J. 36, 1975, 10. pp. 779--789. -- 17. St?blav6, V.: ?rac. 16k. VII, 1S55, 5. pp, 260--263. -- IS. Stjblori, V.; Acta Umv. Carol. Med. SuppL 12, 1950. pp. 2SS--274. -- 19. Stfblova, V.: Cs. neuroL 26, 1963, p. 399. -- 20. Stfblo- vi, V.; Dlagno?a a prevenee v prumyslove neu.-ologll. Praba, SZdN, 1968. -- 21. StfbIot4, v.: lot. Arcb. Occup. Environ. Hltb. 36, 1977, pp. 263 --282. -- 22, Sljblovi, VHolanovi, Vj Prae. 16k. 2S,- 1973. pp. 90-- 96f Received November 10, 1980 V. Sryblova, Dept. Neurology, Medical Faculty of Hygiene, Charles University. SrobArova^SO, 100 42 Praba 10, Chechoslovakia *TiSaf^cisfsTec*H-oeCr'TCir._i W** 'V'C*- * ; j! * ^j*frL.-.i,`,,'7. t jtt2ssS* s~ -v\. * .T.-r-- 2Visvir rC^r?V'Vr. K tiiJC* *a*.'^. '^TTe- 243 -'-'i -r 'rfriW - 870074.12