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FB 2 2 1982
NEUROLOGICAL CHANGES IN VINYL CHLORIDE EXPOSED VORXERS
V. trttldVA*. V. (AUll), O. 6ROKBA&*. V. KIUIIOVA', v. saIkqva\ j. vtToveevAi, u ttAi*
l) 0*prmnt ot Neurology, Medical Faculty of Hyjiane, Charles University, Prague a] Outpatient Clinic of Occupational Health, District Centra of National Health,
MllaOt, Czechoslovakia
Vinyl chloride (VC] toxicity for the human organism Is net still fully dear. Tbs occupational exposure to VC is linked with the development of liver hemangioaarcomaa, or with other malignant processes of varying locality. Some authors diagnose changes in terms of scleroderma, universally are described roentgesologieally detected lesions of tntarphalangeal 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 detectable 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 ot peripheral vasomotor disorder*
Neurological manifestations are described only sporadically. Splrtas and colleagues (Id] 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 paresthesias (prtnckllng, formication). Langeuer-Lewowlckt (U) 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 headache^ end sleep disorders, but also trigeminal neuralgia.
Bacause of a lack of more detailed neurological studies among the VC-axposed parsons, we conducted field investigations among the occupationally ex posed workers in a plant where there woe six years before put into operation a workshop with a considerable VC hazard. * %
For Distribution by CMA SPECIAL PROGRAMS DIVISION
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ills), as* ; tlm* o loos with roup* e> i tbs t*otaa fr* and some ^tsgary ot hiro they .aing aod coaxprw :tvtly tow
\ A mcr* Q and NS itica was S parsons
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19.6 4.4 W 2Jl 0.0 u 0.0 00.0
5 o! BX* The rus hes and
Tibi* 2. Overview ol subjective complaints m wOTksn occupationally exposed to Ttajrl chloride, rslatlos to the level ol exposure
Complaints
Hcadaeba Sleep dimedera GIT disorders Vsrti** Psychic distuxbatioa Oyintiuiia Palpitations Total number of examinees
Total
number
%
44 1S.7 14 S.S
20 6.9 S 1.0 IS 4.S 9 3.1 14 4.S 293 106.0
Xforeaxpated number %
* If 7
11 1 4 7
S 109
17.4 M
10.1
1.S
S4
4.4 4.4
100.0
Lw exposed
somber
/a
ST 14.7 4.9
9 4.9 1 04 7 3.4 2 ^ 1.1 9 4.9 1S4 100.0
gastrointestinal disorders, and furthermore, of dysesthesia of extremities. There ws 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 heads* ehes was double the incidence In the group with a shorter time of exposed for more then 4 years. Sleep disorders, gastrointestinal eomplamts, vertigo and psychic disturbances were also more frequent In those with a longer time of ex*
Table 3. Overview ol subjective complaints Is worker* occupationally exposed to vinyl chloride, relation to the length of exposure
Complaints
Hesdacha Sleep disorders GIT disorders Vertigo Psychic distwbstioa Dysesthesia Palpitations ToiaI nsyber of txmiflttt
Total
number
"o
46 15.7 14 5.5 20 6.9
3 1.0 IS 4.5 9 3.1 14 4.S 29S 100.0
Exposure longer than 4 yeus ta
24 23.8 s 7.9 9 5.9 3 3.0 8 7.9 s 7.9 4 4.0 101 100.0
Exposure shorter
than 4 years
number
fQ
22 11.0 a 4.2 u 5.7 6 6.0 5 2.6 X 6.5
10 5.2 192 160.0
posed workers Is characterized is Table 4. The group of more exposed workers showed 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 aost'frvquent was the lesion of peripheral neurons, either motor or sensory, or both of them (15.&H: : 8.7 %). Diagnosed were impairments of muscle tonus or trophldty, reduction or loss of tendon and bone reflexes, abnormal sensitivity. Compared to controls.
If exposed
axpsuti ____ s_
}4J S* 1M.0
matology icrohypo* sesthesta.
diagnosed in vc-expoaed workers were predominantly episodic, En 5 cases com* blned with the diffusa abnormity. Three EEG recordings revealed only diffuse abnormities. Relatively frequent wea also the presence of sleep waves (in 46.5 % of cases). Is 16 % of workers the sleep activity manifestations were of
jartson to .a iMteas, logy. O -- so etatral up of VC*
i level of i lesions: :1L4 %]. .6% and jrrelatlon .TS of ex5 %) and erebellar
1 control rdlng* in the EEG ooraldu
Graph 2: Objectively dlegsoeed changes in VC-expotsd workers la relation to the level of exposure. X-axis ebjecOvely diagnosed changes: A-D see Graph 1. Blank column -- lower exposure levels, hatched column -- higher exposure level*. Y-axis -- % of the
total number of exposed subjects. higher degree of seventy (2c to 3, according to Roth (13)). Significant dif ferences were observed also In the photosUoulatlon 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 N5 and EOD (8, 7, 8, 9) questionnaire surveys ware used to improve analysis ot subjective complaints and to complement
Graph 3: Objectively diagnosed chsngee (a VC-xposed workers in rsiidem to the length of exposure. X-exlt -- objectively dltgBosed changes: A-D see Graph 1. Bleak column -- exposure shorter than 4 yeere, hetched, column -- exposure longer
then 4 years. Y-exls --* H ot the total number ot exposed subjects.
* ^"11*"" i'
traits as syudra* so-celled estiva of
chloride.
#
70.4 23.4
6
0.0
100.0
! by eaasnolence Sequent .hermore, :1c persa.cles chat :y. In ;h from the
changes mplaints, iring the action of terebellar lrtas and (15) and previous . benzene incidence zsoe. We ;ai cases isriphertl cure date
and to our own experience these changes are frequently associated with Ray naud's syndrome and may presumably, lead to even more severe coosequencies la terms of stenosis or occlusion, as described by Lange (1Z). Peripheral nerve lesions diagnosed In our group of VC-exposed examinees could be than explain ed by a direct neurotoxic action of VC, or as a consequence of hypoxia ac companying mere severe 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 CNS. Slight functional changes manifest themsel ves In fi8 recordings by waves typical for various stages of sleep, a* con firmed in a relatively high per cent (4&S%) of cases In our group of exami nees as well as in some of the examined subjects exposed to other organic solvents (19, 21, 22). Detection ot episodic or diffuse EG 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 15.8 % of workers. This frequency is in agree ment with the cited literature data as well as with our previous experience. This leads uj to a conclusion that even VC, particularly at higher erposure con centrations, can produce neurotic changes in the above described brain structures.
VC-induced pathophysiological changes ere believed by soma authors to manifest themselves by the central neurovegetattve dysregulation, as a result of changed hypothalamus functions (2). This localization, presumed by these autWors on the basis of their experimental studies, seems to be in agreement with our findings of EEG episodic abnormalities.
We also believe that even FS reaction changes, recorded in our group of exposed workers, may be of importance In the-early diagnosis of VC-induced damage. Comparable FS reaction changes were also described by Rouskovi (14) in persons exposed to other toxic agents.
CONCLUSIONS
1) Exposure to VC may lead, besides to other changes described la 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 is the periphery may further develop, leading consequently to
239
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APOOO17026
ir art the geavascular dla* urovagatatlve lesions esuslanisms. > tli assumed i*). It occurs 22) -and may :al structures i be ascribed )ns aecompestent changes
accentuated >rksrs at risk essary to en> rkers. Ot the both for prtostlmulatlon,
nally exposed ad of N5 and aulation, ware Jectt. Average rs. surovegatatlve cellar and/or al seurovegs* co depend on
isaatiy tpisojoeed showed episodic EEG o changes in
.part on the - system and natal symptousquanee ot
!t lyatemstie on the as*
tory. Supple*
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Stfblov*, V,, Leubt, V,' Cfcuscbel, O, JCellerovi. V, Pafko-
<, VH Vftovcofd, J^Sleh,
Linage Beerelogtqae ches las iajets xpos4s an
chlermre de vlnyle
tl a ltd 4tudI4 d*uat mielirt complexe I'lmage neurologique chan 253 su]ts ex* petit au chlorure de vlayta. Das treublea subjeetlfs eat 4ti ar.slyi4e an plan dttaUll 4 raid# dee anqultae XOD at NS. II a 4tl ml* ea tvfdeaee an eftet nturotoxiqu* slgnlfieatif preduit par chlorure de vinyls qui dlpaad de la qualit4 er da la quaatui de rexposuion subia.
Let troubles subject!!* reneoatrde la plus sourest; maux de t*ta*vyrap:Oms v*getatlts *t dytesthdtte. Lm donates objectives timoignent pour one affection dti systime vestlbuloc4r*beiieus et pour ctile de aeurone pirlpbirique at de riaaerratloa p4riph4rlque vigltative. La symptdmitologle p4rlph4rtque peut rlsulter de t'ettet toxlque direct prodult par chlorure da vlayle aussi blan qua du atcenlsme d*hypexie eyaat lieu lors da* cbangemtnts vasometsure plripblrtquaa.
0*s donals Issue* da t'ECG tdaoigoaot uaa actlvltl de sommeil ches 48,3 H de sujets dlraoatraat un aflat narcotlque du chlorure de viayle. L'aetlvlil dplsodlque |chaz 154 tt) associde partola a I'anomalfe de dlftssioa pourralt I'axpllquer par use attaints des structures mldtobasales, mimi Me aux changsnsnu du cortex.
Las sujets exposes a llnfluioee du cblorura de viayle oe se aoumatteae, Jusqu'4 ee jour, aux axamaas systdaauquea au plaa nturologlqua. U ast alcassalre da poursulvre, daax ca cat, un* prophylaxis aaurologtque itudiaat i'lmaga eUalque, 1m doania* issuas da l'EEG ou mime da l'CMG. II asx utile d'employer las aoqultts EOO et N5.
2GSAMMCNTASSUMO
S t ? blov4, V,, LambC v,, ChumchaL 0, Kellerovi. V., Palko 4, V,, Vltoveovi, V,, 2lab, L: Weurolofisehe* Slid bi dan dam VlarleUo* rid axposiartea Arbaitaadae
Man beobaebtate kompltxarwatsa das naurologische Blld bsl 2SJ Arbeltandan, die Vlnyicblorld axpotuert waren. Subjektlve Scbwitrlgkaitaa analytiartt man aingahendar mlt Hlife dsr EOO- und N S-Fragsbogeit. Dabei bat sea aloe signlllkaate neurotoxisebe Elowlrkuag von Vlnyicblorld nachgewtasan, die van dsr Inttasltlt usd Dautr dar Exporttlou abhlnglg lit.
O'le hluflgstea subjaktirso Sebwlerigktitea wares Kopfsehmerzea vagataUye Symp* tome und Dysesthiti*. Oar objakttva Bafund taugt von dar Affektioa dea Vestibularx*r*ballryst#ma, ftrntr von dar Affsktloo da* parlpbares Nsuroa* und dar partpheran vagitatlvin InnarveCon. Ola pertpbare Symptomatology kana man erkllran so* wabi eia dlrakt* Eiawlrkung yea Vlnyichlarld, *1* auch dan hypexlsebea Maebaalsmus bal perfpbtren vasoootorlsehtn Vertsderungea.
In dem EEG-Balund statlte men bal 44.5 H Title dar Gtsamtbelt die Scblefakavlttt fast, die die aarkousehe Einwtrkuag von Vlnyicblorld dokumtntlart. Die apisedische AktiTttit (bet 15,5 %} mancnmii in Varbiadung alt Diffusionsabnormitlt kcante man dureb Af>ktIoa von mediobasalta Strukturea, gefebenanXair durca Konexvertnderuagas arkllrea.
Die Vlsyleblorld exponlertca Arbeltsadta wardaa bisher systematised vom oaurologischan Stsadpuakt nlcht bsobachttc. Ole Vtrfasser hsltea die gertalte naurologische
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