Chapter 3 - Cardiovascular System

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Chapter3CardiovascularSystem
PartITheBody
Franais
INTRODUCTION
LotharHeinemannandGerdHeuchert
Cardiovasculardiseases(CVDs)areamongthemostcommoncausesofillnessanddeathintheworkingpopulation,particularlyin
industrializedcountries.Theyarealsoincreasingindevelopingcountries(Wielgosz1993).Intheindustrializedcountries,15to20%ofall
workingpeoplewillsufferfromacardiovasculardisordersometimeduringtheirworkinglivesandthefrequencyclimbssharplywithage.
Amongthosebetween45to64yearsofage,morethanathirdofthedeathsamongmenandmorethanaquarterofdeathsamongwomen
arecausedbythisgroupofdiseases(seetable3.1).Inrecentyears,CVDshavebecomethemostfrequentcauseofdeathamongpost
menopausalwomen.
Table3.1Mortalityfromcardiovasculardiseasesin1991and1990intheagegroups4554and5564forselectedcountries
Country
Men
Women
4554Years
5564Years
4554Years
Rate
Rate
Rate
Rate
Russia**
528
36
1,290
44
162
33
559
49
Poland**
480
38
1,193
45
134
31
430
42
Argentina* 317
40
847
44
131
33
339
39
Britain**
198
42
665
47
59
20
267
32
USA*
212
35
623
40
83
24
273
31
Germany** 181
29
597
38
55
18
213
30
Italy*
123
27
404
30
41
18
148
25
Mexico**
128
17
346
23
82
19
230
24
France**
102
17
311
22
30
12
94
18
Japan**
111
27
281
26
48
22
119
26
5564Years
*1990.**1991.Rate=Deathsper100,000inhabitants.%isfromallcausesofdeathintheagegroup.
Becauseoftheircomplexaetiology,onlyaverysmallproportionofthecasesofcardiovasculardiseasearerecognizedasoccupational.Many
countries,however,recognizethatoccupationalexposurescontributetoCVDs(sometimesreferredtoasworkrelateddiseases).Working
conditionsandjobdemandsplayanimportantroleinthemultifactorialprocessthatleadstothesediseases,butascertainingtheroleofthe
individualcausalcomponentsisverydifficult.Thecomponentsinteractinclose,shiftingrelationshipsandoftenthediseaseistriggeredbya
combinationoraccumulationofdifferentcausalfactors,includingthosethatareworkrelated.
Thereaderisreferredtothestandardcardiologytextsfordetailsoftheepidemiology,pathophysiology,diagnosisandtreatmentof
cardiovasculardiseases.Thischapterwillfocusonthoseaspectsofcardiovasculardiseasethatareparticularlyrelevantintheworkplaceand
arelikelytobeinfluencedbyfactorsinthejobandworkenvironment.
CARDIOVASCULARMORBIDITYANDMORTALITYINTHEWORKFORCE
GottfriedEnderleinandLotharHeinemann
Inthefollowingarticle,thetermcardiovasculardiseases(CVDs)referstoorganicandfunctionaldisordersoftheheartandcirculatory
system,includingtheresultantdamagetootherorgansystems,whichareclassifiedundernumbers390to459inthe9threvisionofthe
InternationalClassificationofDiseases(ICD)(WorldHealthOrganization(WHO)1975).Basedessentiallyoninternationalstatistics
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assembledbytheWHOanddatacollectedinGermany,thearticlediscussestheprevalenceofCVDs,newdiseaserates,andfrequencyof
deaths,morbidityanddisability.
DefinitionandPrevalenceintheWorkingAgePopulation
Coronaryarterydisease(ICD410414)resultinginischaemiaofthemyocardiumisprobablythemostsignificantCVDintheworking
population,particularlyinindustrializedcountries.Thisconditionresultsfromaconstrictioninthevascularsystemthatsuppliestheheart
muscle,aproblemcausedprimarilybyarteriosclerosis.Itaffects0.9to1.5%ofworkingagemenand0.5to1.0%ofwomen.
Inflammatorydiseases(ICD420423)mayinvolvetheendocardium,theheartvalves,thepericardiumand/ortheheartmuscle
(myocardium)itself.Theyarelesscommoninindustrializedcountries,wheretheirfrequencyiswellbelow0.01%oftheadultpopulation,
butareseenmorefrequentlyindevelopingcountries,perhapsreflectingthegreaterprevalenceofnutritionaldisordersandinfectious
diseases.
Heartrhythmdisorders(ICD427)arerelativelyrare,althoughmuchmediaattentionhasbeengiventorecentinstancesofdisabilityand
suddendeathamongprominentprofessionalathletes.Althoughtheycanhaveasignificantimpactontheabilitytowork,theyareoften
asymptomaticandtransitory.
Themyocardiopathies(ICD424)areconditionswhichinvolveenlargementorthickeningoftheheartmusculation,effectivelynarrowingthe
vesselsandweakeningtheheart.Theyhaveattractedmoreattentioninrecentyears,largelybecauseofimprovedmethodsofdiagnosis,
althoughtheirpathogenesisisoftenobscure.Theyhavebeenattributedtoinfections,metabolicdiseases,immunologicdisorders,
inflammatorydiseasesinvolvingthecapillariesand,ofparticularimportanceinthisvolume,totoxicexposuresintheworkplace.Theyare
dividedintothreetypes:
dilativethemostcommonform(5to15casesper100,000people),whichisassociatedwiththefunctionalweakeningoftheheart
hypertrophicthickeningandenlargementofthemyocardiumresultinginrelativeinsufficiencyofthecoronaryarteries
restrictiveararetypeinwhichmyocardialcontractionsarelimited.
Hypertension(ICD401405)(increasedsystolicand/ordiastolicbloodpressure)isthemostcommoncirculatorydisease,beingfoundamong
15to20%ofworkingpeopleinindustrializedcountries.Itisdiscussedingreaterdetailbelow.
Atheroscleroticchangesinthemajorbloodvessels(ICD440),oftenassociatedwithhypertension,causediseaseintheorganstheyserve.
Foremostamongtheseiscerebrovasculardisease(ICD430438),whichmayresultinastrokeduetoinfarctionand/orhaemorrhage.This
occursin0.3to1.0%ofworkingpeople,mostcommonlyamongthoseaged40andolder.
Atheroscleroticdiseases,includingcoronaryarterydisease,strokeandhypertension,byfarthemostcommoncardiovasculardiseasesinthe
workingpopulation,aremultifactorialinoriginandhavetheironsetearlyinlife.Theyareofimportanceintheworkplacebecause:
solargeaproportionoftheworkforcehasanasymptomaticorunrecognizedformofcardiovasculardisease
thedevelopmentofthatdiseasemaybeaggravatedoracutesymptomaticeventsprecipitatedbyworkingconditionsandjobdemands
theacuteonsetofasymptomaticphaseofthecardiovasculardiseaseisoftenattributedtothejoband/ortheworkplaceenvironment
mostindividualswithanestablishedcardiovasculardiseasearecapableofworkingproductively,albeit,sometimes,onlyaftereffective
rehabilitationandjobretraining
theworkplaceisauniquelypropitiousarenaforprimaryandsecondarypreventiveprogrammes.
Functionalcirculatorydisordersintheextremities(ICD443)includeRaynaud'sdisease,shorttermpallorofthefingers,andarerelatively
rare.Someoccupationalconditions,suchasfrostbite,longtermexposuretovinylchlorideandhandarmexposuretovibrationcaninduce
thesedisorders.
Varicositiesinthelegveins(ICD454),oftenimproperlydismissedasacosmeticproblem,arefrequentamongwomen,especiallyduring
pregnancy.Whileahereditarytendencytoweaknessoftheveinwallsmaybeafactor,theyareusuallyassociatedwithlongperiodsof
standinginonepositionwithoutmovement,duringwhichthestaticpressurewithintheveinsisincreased.Theresultantdiscomfortandleg
oedemaoftendictatechangeormodificationofthejob.
Annualincidencerates
AmongtheCVDs,hypertensionhasthehighestannualnewcaserateamongworkingpeopleaged35to64.Newcasesdevelopin
approximately1%ofthatpopulationeveryyear.Nextinfrequencyarecoronaryheartdisease(8to92newcasesofacuteheartattackper
10,000menperyear,and3to16newcasesper10,000womenperyear)andstroke(12to30casesper10,000menperyear,and6to30
casesper10,000womenperyear).AsdemonstratedbyglobaldatacollectedbytheWHOMonicaproject(WHOMONICA1994;WHO
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MONICA1988),thelowestnewincidenceratesforheartattackwerefoundamongmeninChinaandwomeninSpain,whilethehighest
rateswerefoundamongbothmenandwomeninScotland.Thesignificanceofthesedataisthatinthepopulationofworkingage,40to
60%ofheartattackvictimsand30to40%ofstrokevictimsdonotsurvivetheirinitialepisodes.
Mortality
Withintheprimaryworkingagesof15to64,only8to18%ofdeathsfromCVDsoccurpriortoage45.Mostoccurafterage45,withthe
annualrateincreasingwithage.Therates,whichhavebeenchanging,varyconsiderablyfromcountrytocountry(WHO1994b).
Table3.1showsthedeathratesformenandwomenaged45to54and55to64forsomecountires.Notethatthedeathratesformenare
consistentlyhigherthanthoseforwomenofcorrespondingages.Table3.2comparesthedeathratesforvariousCVDsamongpeopleaged
55to64infivecountries.
Table3.2Mortalityratesfromspecialcardiovasculardiagnosisgroupsintheyears1991and1990intheagegroup5564forselected
countries
Diagnosisgroup
(ICD9thRev.)
Russia(1991)
USA(1990)
Germany(1991)
France(1991)
Japan(1991)
393398
16.8
21.9
3.3
4.6
3.6
4.4
2.2
2.3
1.2
1.9
401405
22.2
18.5
23.0
14.6
16.9
9.7
9.4
4.4
4.0
1.6
410
160.2
48.9
216.4
79.9
245.2
61.3
100.7
20.5
45.9
13.7
411414
586.3
189.9
159.0
59.5
99.2
31.8
35.8
6.8
15.2
4.2
415429
60.9
24.0
140.4
64.7
112.8
49.2
73.2
27.0
98.7
40.9
430438
385.0
228.5
54.4
42.2
84.1
43.8
59.1
26.7
107.3
53.6
440
441448
{50.0
19.2}
4.4
18.4
2.1
6.7
11.8
15.5
3.8
4.2
1.5
23.4
0.3
3.8
0.3
3.8
0.1
2.6
Total390459
1,290
559
623
273
597
213
311
94
281
119
Deathsper100,000inhabitants;M=male;F=female.
WorkDisabilityandEarlyRetirement
Diagnosisrelatedstatisticsontimelostfromworkrepresentanimportantperspectiveontheimpactofmorbidityontheworking
population,eventhoughthediagnosticdesignationsareusuallylessprecisethanincasesofearlyretirementbecauseofdisability.Thecase
rates,usuallyexpressedincasesper10,000employees,provideanindexofthefrequencyofthediseasecategories,whiletheaverage
numberofdayslostpercaseindicatestherelativeseriousnessofparticulardiseases.Thus,accordingtostatisticson10millionworkersin
westernGermanycompiledbytheAllgemeinenOrtskrankenkasse,CVDsaccountedfor7.7%ofthetotaldisabilityin199192,althoughthe
numberofcasesforthatperiodwasonly4.6%ofthetotal(table3.3).Insomecountries,whereearlyretirementisprovidedwhenwork
abilityisreducedduetoillness,thepatternofdisabilitymirrorstheratesfordifferentcategoriesofCVD.
Table3.3Rateofcardiovasculardiseaseamongearlypensioners*duetoreducedabilitytowork(N=576,079)anddiagnosisrelated
workdisabilityinthewesternpartofGermany,199092
Diagnosisgroup
(ICD9thRev.)
Maincauseofillness
Accesstoearly
retirement;number
per100,000early
retirees
Averageannualworkdisability199092
Casesper100,000
employed
Duration(days)per
case
Men
Women
Men
Women
Men
Women
390392
Acuterheumaticfever
16
24
49
60
28.1
32.8
393398
Chronicrheumaticheart
disease
604
605
24
20
67.5
64.5
401405
Hypertension,highblood 4,158
pressurediseases
4,709
982
1,166
24.5
21.6
410414
Ischaemicheartdiseases 9,635
2,981
1,176
529
51.2
35.4
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410,412
Acuteandexisting
myocardialinfarction
2,293
621
276
73
85.8
68.4
414
Coronaryheartdisease
6,932
2,183
337
135
50.8
37.4
415417
Pulmonarycirculatory
diseases
248
124
23
26
58.5
44.8
420429
Othernonrheumatic
heartdiseases
3,434
1,947
645
544
36.3
25.7
420423
Inflammatoryheart
diseases
141
118
20
12
49.4
48.5
424
Heartvalvedisorders
108
119
22
18
45.6
38.5
425
Myocardiopathy
1,257
402
38
14
66.8
49.2
426
Stimulusperformance
disorder
86
55
12
39.6
45.0
427
Cardiacrhythmdisorder
734
470
291
274
29.3
21.8
428
Cardiacinsufficiency
981
722
82
61
62.4
42.5
430438
Cerebrovasculardiseases 4,415
2,592
172
120
75.6
58.9
440448
Diseasesofthearteries,
arteriolesandcapillaries
3,785
1,540
238
90
59.9
44.5
440
Arteriosclerosis
2,453
1,090
27
10
71.7
47.6
443
Raynaud'sdiseaseand
othervasculardiseases
107
53
63
25
50.6
33.5
444
Arterialembolismand
thrombosis
219
72
113
34
63.3
49.5
451456
Diseasesoftheveins
464
679
1,020
1,427
22.9
20.3
457
Noninfectiousdiseasesof 16
thelymphnodes
122
142
132
10.4
14.2
458
Hypotension
29
62
616
1,501
9.4
9.5
459
Othercirculatory
diseases
37
41
1,056
2,094
11.5
10.2
390459
Totalcardiovascular
diseases
26,843
15,426
6,143
7,761
29.6
18.9
*Earlypensioned:StatutorypensionsinsuranceforformerFederalRepublicofGermany,workdisabilityAOKWest.
THERISKFACTORCONCEPTINCARDIOVASCULARDISEASE
LotharHeinemann,GottfriedEnderleinandHeideStark
Riskfactorsaregenetic,physiological,behaviouralandsocioeconomiccharacteristicsofindividualsthatplacetheminacohortofthe
populationthatismorelikelytodevelopaparticularhealthproblemordiseasethantherestofthepopulation.Usuallyappliedto
multifactorialdiseasesforwhichthereisnosingleprecisecause,theyhavebeenparticularlyusefulinidentifyingcandidatesforprimary
preventivemeasuresandinassessingtheeffectivenessofthepreventionprogrammeincontrollingtheriskfactorsbeingtargeted.They
owetheirdevelopmenttolargescaleprospectivepopulationstudies,suchastheFraminghamstudyofcoronaryarterydiseaseandstroke
conductedinFramingham,Massachusetts,intheUnitedStates,otherepidemiologicalstudies,interventionstudiesandexperimental
research.
Itshouldbeemphasizedthatriskfactorsaremerelyexpressionsofprobabilitythatis,theyarenotabsolutenoraretheydiagnostic.Having
oneormoreriskfactorsforaparticulardiseasedoesnotnecessarilymeanthatanindividualwilldevelopthedisease,nordoesitmeanthat
anindividualwithoutanyriskfactorswillescapethedisease.Riskfactorsareindividualcharacteristicswhichaffectthatperson'schancesof
developingaparticulardiseaseorgroupofdiseaseswithinadefinedfuturetimeperiod.Categoriesofriskfactorsinclude:
somaticfactors,suchashighbloodpressure,lipidmetabolismdisorders,overweightanddiabetesmellitus
behaviouralfactors,suchassmoking,poornutrition,lackofphysicalmovement,typeApersonality,highalcoholconsumptionanddrug
abuse
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strains,includingexposuresintheoccupational,socialandprivatespheres.
Naturally,geneticanddispositionalfactorsalsoplayaroleinhighbloodpressure,diabetesmellitusandlipidmetabolismdisorders.Manyof
theriskfactorspromotethedevelopmentofarteriosclerosis,whichisasignificantpreconditionfortheonsetofcoronaryheartdisease.
Someriskfactorsmayputtheindividualatriskforthedevelopmentofmorethanonedisease;forexample,cigarettesmokingisassociated
withcoronaryarterydisease,strokeandlungcancer.Atthesametime,anindividualmayhavemultipleriskfactorsforaparticulardisease;
thesemaybeadditivebut,moreoften,thecombinationsofriskfactorsmaybemultiplicative.Somaticandlifestylefactorshavebeen
identifiedasthemainriskfactorsforcoronaryheartdiseaseandstroke.
Hypertension
Hypertension(increasedbloodpressure),adiseaseinitsownright,isoneofthemajorriskfactorsforcoronaryheartdisease(CHD)and
stroke.AsdefinedbytheWHO,bloodpressureisnormalwhenthediastolicisbelow90mmHgandthesystolicisbelow140mmHg.In
thresholdorborderlinehypertension,thediastolicrangesfrom90to94mmHgandthesystolicfrom140to159mmHg.Individualswith
diastolicpressuresequaltoorgreaterthan95mmHgandsystolicpressuresequaltoorgreaterthan160mmHgaredesignatedasbeing
hypertensive.Studieshaveshown,however,thatsuchsharpcriteriaarenotentirelycorrect.Someindividualshavea"labile"blood
pressurethepressurefluctuatesbetweennormalandhypertensivelevelsdependingonthecircumstancesofthemoment.Further,without
regardtothespecificcategories,thereisalinearprogressionofrelativeriskasthepressurerisesabovethenormallevel.
IntheUnitedStates,forexample,theincidencerateofCHDandstrokeamongmenaged55to61was1.61%peryearforthosewhoseblood
pressurewasnormalcomparedto4.6%peryearforthosewithhypertension(NationalHeart,LungandBloodInstitute1981).
Diastolicpressuresover94mmHgwerefoundin2to36%ofthepopulationaged35to64years,accordingtotheWHOMONICAstudy.In
manycountriesofCentral,NorthernandEasternEurope(e.g.,Russia,theCzechRepublic,Finland,Scotland,Romania,Franceandpartsof
Germany,aswellasMalta),hypertensionwasfoundinover30%ofthepopulationaged35to54,whileincountriesincludingSpain,
Denmark,Belgium,Luxembourg,CanadaandtheUnitedStates,thecorrespondingfigurewaslessthan20%(WHOMONICA1988).Therates
tendtoincreasewithage,andthereareracialdifferences.(IntheUnitedStates,atleast,hypertensionismorefrequentamongAfrican
AmericansthanintheWhitepopulation.)
Risksfordevelopinghypertension
Theimportantriskfactorsfordevelopinghypertensionareexcessbodyweight,highsaltintake,aseriesofothernutritionalfactors,high
alcoholconsumption,physicalinactivity,andpsychosocialfactors,includingstress(Levi1983).Furthermore,thereisacertaingenetic
componentwhoserelativesignificanceisnotyetfullyunderstood(WHO1985).Frequentfamilialhighbloodpressureshouldbeconsidered
adangerandspecialattentionpaidtocontrollinglifestylefactors.
Thereisevidencethatpsychosocialandpsychophysicalfactors,inconjunctionwiththejob,canhaveaninfluenceondeveloping
hypertension,especiallyforshorttermbloodpressureincreases.Increaseshavebeenfoundintheconcentrationofcertainhormones
(adrenalinandnoradrenalin)aswellascortisol(Levi1972),which,aloneandincombinationwithhighsaltconsumption,canleadto
increasedbloodpressure.Workstressalsoappearstoberelatedtohypertension.Adoseeffectrelationshipwithintensityofairtrafficwas
shown(Levi1972;WHO1985)incomparinggroupsofairtrafficcontrollerswithdifferenthighpsychicstrain.
Treatmentofhypertension
Hypertensioncanandshouldbetreated,evenintheabsenceofanysymptoms.Lifestylechangessuchasweightcontrol,reductionof
sodiumintakeandregularphysicalexercise,coupledwhennecessarywithantihypertensivemedications,regularlyevokereductionsin
bloodpressure,oftentonormallevels.Unfortunately,manyindividualsfoundtobehypertensivearenotreceivingadequatetreatment.
AccordingtotheWHOMONICAstudy(1988),lessthan20%ofhypertensivewomeninRussia,Malta,easternGermany,Scotland,Finland
andItalywerereceivingadequatetreatmentduringthemid1980s,whilethecomparablefigureformeninIreland,Germany,China,Russia,
Malta,Finland,Poland,FranceandItalywasunder15%.
Preventionofhypertension
Theessenceofpreventinghypertensionisidentifyingindividualswithbloodpressureelevationthroughperiodicscreeningormedical
examinationprogrammes,repeatedcheckstoverifytheextentanddurationoftheelevation,andtheinstitutionofanappropriate
treatmentregimenthatwillbemaintainedindefinitely.Thosewithafamilyhistoryofhypertensionshouldhavetheirpressureschecked
morefrequentlyandshouldbeguidedtoeliminationorcontrolofanyriskfactorstheymaypresent.Controlofalcoholabuse,physical
trainingandphysicalfitness,normalweightmaintenanceandeffortstoreducepsychologicalstressareallimportantelementsofprevention
programmes.Improvementinworkplaceconditions,suchasreducingnoiseandexcessheat,areotherpreventivemeasures.
Theworkplaceisauniquelyadvantageousarenaforprogrammesaimedatthedetection,monitoringandcontrolofhypertensioninthe
workforce.Convenienceandlowornocostmakethemattractivetotheparticipantsandthepositiveeffectsofpeerpressurefromco
workerstendtoenhancetheircomplianceandthesuccessoftheprogramme.
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Hyperlipidemia
Manylongterminternationalstudieshavedemonstratedaconvincingrelationshipbetweenabnormalitiesinlipidmetabolismandan
increasedriskofCHDandstroke.ThisisparticularlytrueforelevatedtotalcholesterolandLDL(lowdensitylipoproteins)and/orlowlevels
ofHDL(highdensitylipoproteins).Recentresearchprovidesfurtherevidencelinkingtheexcessriskwithdifferentlipoproteinfractions
(WHO1994a).
Thefrequencyofelevatedtotalcholesterollevels(>6.5mmol/l)wasshowntovaryconsiderablyinpopulationgroupsbytheworldwide
WHOMONICAstudiesinthemid1980s(WHOMONICA1988).Therateofhypercholesterolemiaforpopulationsofworkingage(35to64
yearsofage)rangedfrom1.3to46.5%formenand1.7to48.7%forwomen.Althoughtherangesweregenerallysimilar,themean
cholesterollevelsforthestudygroupsindifferentcountriesvariedsignificantly:inFinland,Scotland,EastGermany,theBeneluxcountries
andMalta,ameanofover6mmol/lwasfound,whilethemeanswerelowerineastAsiancountrieslikeChina(4.1mmol/l)andJapan(5.0
mmol/l).Inbothregions,themeanswerebelow6.5mmol/l(250mg/dl),theleveldesignatedasthethresholdofnormal;however,asnoted
aboveforbloodpressure,thereisaprogressiveincreaseofriskasthelevelrises,ratherthanasharpdemarcationbetweennormaland
abnormal.Indeed,someauthoritieshavepeggedatotalcholesterollevelof180mg/dlastheoptimallevelthatshouldnotbeexceeded.
Itshouldbenotedthatgenderisafactor,withwomenaveraginglowerlevelsofHDL.Thismaybeonereasonwhywomenofworkingage
havealowermortalityratefromCHD.
Exceptfortherelativelyfewindividualswithhereditaryhypercholesterolemia,cholesterollevelsgenerallyreflectthedietaryintakeoffoods
richincholesterolandsaturatedfats.Dietsbasedonfruit,plantproductsandfish,withreducedtotalfatintakeandsubstitutionofpoly
unsaturatedfats,aregenerallyassociatedwithlowcholesterollevels.Althoughtheirroleisnotyetentirelyclear,intakeofantioxidants
(vitaminE,carotene,seleniumandsoon)isalsothoughttoinfluencecholesterollevels.
FactorsassociatedwithhigherlevelsofHDLcholesterol,the"protective"formoflipoprotein,includerace(Black),gender(female),normal
weight,physicalexerciseandmoderatealcoholintake.
Socioeconomiclevelalsoappearstoplayarole,atleastinindustrializedcountries,asinWestGermany,wherehighercholesterollevels
werefoundinpopulationgroupsofbothmenandwomenwithlowereducationlevels(undertenyearsofschooling)comparedtothose
completing12yearsofeducation(Heinemann1993).
CigaretteSmoking
CigarettesmokingisamongthemostimportantriskfactorsforCVD.Theriskfromcigarettesmokingisdirectlyrelatedtothenumberof
cigarettesonesmokes,thelengthoftimeonehasbeensmoking,theageatwhichonebegantosmoke,theamountoneinhalesandthetar,
nicotineandcarbonmonoxidecontentoftheinspiredsmoke.Figure3.1illustratesthestrikingincreaseinCHDmortalityamongcigarette
smokerscomparedtononsmokers.Thisincreasedriskisdemonstratedamongbothmenandwomenandinallsocioeconomicclasses.
Figure3.1Relativemortalityriskfromcardiovasculardiseasesforsmokers(includingexsmokers)andsocialclassescomparedtonon
smoking,normalweight,skilledworkers(male)basedonoccupationalmedicalcareexaminationsinEastGermany,mortality198589,N
=2.7millionpersonyears
Therelativeriskofcigarettesmokingdeclinesaftertobaccouseisdiscontinued.Thisisprogressive;afterabouttenyearsofnonsmoking,
theriskisdownalmosttothelevelofthosewhoneversmoked.
Recentevidencehasdemonstratedthatthoseinhaling"secondhandsmoke"(i.e.,passiveinhalationofsmokefromcigarettessmokedby
others)arealsoatsignificantrisk(Wells1994;GlantzandParmley1995).
Ratesofcigarettesmokingvaryamongcountries,asdemonstratedbytheinternationalWHOMONICAstudy(1988).Thehighestratesfor
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menaged35to64werefoundinRussia,Poland,Scotland,Hungary,Italy,Malta,JapanandChina.Morewomensmokerswerefoundin
Scotland,Denmark,Ireland,theUnitedStates,HungaryandPoland(therecentPolishdataarelimitedtolargecities).
Socialstatusandoccupationallevelarefactorsinthelevelofsmokingamongworkers.Figure3.1,forexample,demonstratesthatthe
proportionsofsmokersamongmeninEastGermanyincreasedinthelowersocialclasses.Thereverseisfoundincountrieswithrelatively
lownumbersofsmokers,wherethereismoresmokingamongthoseathighersociallevels.InEastGermany,smokingisalsomorefrequent
amongshiftworkerswhencomparedwiththoseona"normal"workschedule.
UnbalancedNutrition,SaltConsumption
Inmostindustrializedcountriestraditionallowfatnutritionhasbeenreplacedbyhighcalorie,highfat,lowcarbohydrate,toosweetortoo
saltyeatinghabits.Thiscontributestothedevelopmentofoverweight,highbloodpressure,andhighcholesterollevelaselementsofhigh
cardiovascularrisk.Theheavyconsumptionofanimalfats,withtheirhighproportionofsaturatedfattyacids,leadstoanincreaseinLDL
cholesterolandincreasedrisk.Fatsderivedfromvegetablesaremuchlowerinthesesubstances(WHO1994a).Eatinghabitsarealso
stronglyassociatedwithbothsocioeconomiclevelandoccupation.
Overweight
Overweight(excessfatorobesityratherthanincreasedmusclemass)isacardiovascularriskfactoroflesserdirectsignificance.Thereis
evidencethatthemalepatternofexcessfatdistribution(abdominalobesity)isassociatedwithagreaterriskofcardiovascularand
metabolicproblemsthanthefemale(pelvic)typeoffatdistribution.
Overweightisassociatedwithhypertension,hypercholesterolemiaanddiabetesmellitus,and,toamuchgreaterextentinwomenthan
men,tendstoincreasewithage(HeuchertandEnderlein1994)(figure3.2).Itisalsoariskfactorformusculoskeletalproblemsand
osteoarthritis,andmakesphysicalexercisemoredifficult.Thefrequencyofsignificantoverweightvariesconsiderablyamongcountries.
RandompopulationsurveysconductedbytheWHOMONICAprojectfounditinmorethan20%offemalesaged35to64intheCzech
Republic,EastGermany,Finland,France,Hungary,Poland,Russia,SpainandYugoslavia,andinbothsexesinLithuania,MaltaandRomania.
InChina,Japan,NewZealandandSweden,fewerthan10%ofbothmenandwomeninthisagegroupweresignificantlyoverweight.
Figure3.2Prevalenceofhypertensionbyage,sexandsixlevelsofrealtivebodyweightaccordingtothebodymassindex(BMI)in
occupationalmedicalcareexaminationsineastGermany(normalBMIvaluesareunderlined).
Commoncausesofoverweightincludefamilialfactors(thesemayinpartbegeneticbutmoreoftenreflectcommondietaryhabits),
overeating,highfatandhighcarbohydratedietsandlackofphysicalexercise.Overweighttendstobemorecommonamongthelower
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socioeconomicstrata,particularlyamongwomen,where,amongotherfactors,financialconstraintslimittheavailabilityofamorebalanced
diet.PopulationstudiesinGermanydemonstratedthattheproportionofsignificantoverweightamongthosewithlowereducationlevelsis
3to5timesgreaterthanthatamongpeoplewithmoreeducation,andthatsomeoccupations,notablyfoodpreparation,agricultureandto
someextentshiftwork,haveahighpercentageofoverweightpeople(figure3.3)(Heinemann1993).
Figure3.3Relativeriskfromoverweightbylengthofeducation(yearsofschooling)inGermany(population2564years)
PhysicalInactivity
Thecloseassociationofhypertension,overweightanddiabetesmellituswithlackofexerciseatworkand/oroffthejobhasmadephysical
inactivityasignificantriskfactorforCHDandstroke(Briazgounov1988;WHO1994a).Anumberofstudieshavedemonstratedthat,holding
allotherriskfactorsconstant,therewasalowermortalityrateamongpersonsengagingregularlyinhighintensityexercisesthanamong
thosewithasedentarylifestyle.
Theamountofexerciseisreadilymeasuredbynotingitsdurationandeithertheamountofphysicalworkaccomplishedortheextentofthe
exerciseinducedincreaseinheartrateandthetimerequiredforthatratetoreturntoitsrestinglevel.Thelatterisalsousefulasan
indicatorofthelevelofcardiovascularfitness:withregularphysicaltraining,therewillbelessofanincreaseinheartrateandamorerapid
returntotherestingrateforagivenintensityofexercise.
Workplacephysicalfitnessprogrammeshavebeenshowntobeeffectiveinenhancingcardiovascularfitness.Participantsinthesetendalso
togiveupcigarettesmokingandtopaygreaterattentiontoproperdiets,thussignificantlyreducingtheirriskofCHDandstroke.
Alcohol
Highalcoholconsumption,especiallythedrinkingofhighproofspirits,hasbeenassociatedwithagreaterriskofhypertension,strokeand
myocardiopathy,whilemoderatealcoholuse,particularlyofwine,hasbeenfoundtoreducetheriskofCHD(WHO1994a).Thishasbeen
associatedwiththelowerCHDmortalityamongtheuppersocialstratainindustrializedcountries,whogenerallypreferwineto"hard"
liquors.Itshouldalsobenotedthatwhiletheiralcoholintakemaybesimilartothatofwinedrinkers,beerdrinkerstendtoaccumulate
excessweight,which,asnotedabove,mayincreasetheirrisk.
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SocioeconomicFactors
AstrongcorrelationbetweensocioeconomicstatusandtheriskofCVDhasbeendemonstratedbyanalysesofthedeathregistermortality
studiesinBritain,Scandinavia,WesternEurope,theUnitedStatesandJapan.Forexample,ineasternGermany,thecardiovasculardeath
rateisconsiderablylowerfortheuppersocialclassesthanforthelowerclasses(seefigure3.1)(MarmotandTheorell1991).InEnglandand
Wales,wheregeneralmortalityratesaredeclining,therelativegapbetweentheupperandlowerclassesiswidening.
Socioeconomicstatusistypicallydefinedbysuchindicatorsasoccupation,occupationalqualificationsandposition,levelofeducationand,
insomeinstances,incomelevel.Thesearereadilytranslatedintostandardofliving,nutritionalpatterns,freetimeactivities,familysizeand
accesstomedicalcare.Asnotedabove,behaviouralriskfactors(suchassmokinganddiet)andthesomaticriskfactors(suchasoverweight,
hypertensionandhyperlipidemia)varyconsiderablyamongsocialclassesandoccupationalgroups(Mielck1994;Helmert,Sheaand
MaschewskySchneider1995).
OccupationalPsychosocialFactorsandStress
Occupationalstress
Psychosocialfactorsattheworkplaceprimarilyrefertothecombinedeffectofworkingenvironment,workcontent,workdemandsand
technologicalorganizationalconditions,andalsotopersonalfactorslikecapability,psychologicalsensitivity,andfinallyalsotohealth
indicators(KarasekandTheorell1990;Siegrist1995).
Theroleofacutestressonpeoplewhoalreadysufferfromcardiovasculardiseaseisuncontested.Stressleadstoepisodesofangina
pectoris,rhythmdisordersandheartfailure;itcanalsoprecipitateastrokeand/oraheartattack.Inthiscontextstressisgenerally
understoodtomeanacutephysicalstress.Butevidencehasbeenmountingthatacutepsychosocialstresscanalsohavetheseeffects.
Studiesfromthe1950sshowedthatpeoplewhoworktwojobsatatime,orwhoworkovertimeforlongperiods,havearelativelyhigher
riskofheartattack,evenatayoungage.Otherstudiesshowedthatinthesamejob,thepersonwiththegreaterworkandtimepressure
andfrequentproblemsonthejobisatsignificantlygreaterrisk(Mielck1994).
Inthelast15years,jobstressresearchsuggestsacausalrelationshipbetweenworkstressandtheincidenceofcardiovasculardisease.This
istrueforcardiovascularmortalityaswellasfrequencyofcoronarydiseaseandhypertension(Schnall,LandsbergisandBaker1994).
Karasek'sjobstrainmodeldefinedtwofactorsthatcouldleadtoanincreasedincidenceofcardiovasculardisease:
extentofjobdemands
extentofdecisionmakinglatitude.
LaterJohnsonaddedasathirdfactortheextentofsocialsupport(Kristensen1995)whichisdiscussedmorefullyelsewhereinthis
Encyclopaedia.ThechapterPsychosocialandOrganizationalFactorsincludesdiscussionsonindividualfactors,suchasTypeApersonality,as
wellassocialsupportandothermechanismsforovercomingtheeffectsofstress.
Theeffectsoffactors,whetherindividualorsituational,thatleadtoincreasedriskofcardiovasculardiseasecanbereducedby"coping
mechanisms",thatis,byrecognizingtheproblemandovercomingitbyattemptingtomakethebestofthesituation.
Untilnow,measuresaimedattheindividualhavepredominatedinthepreventionofthenegativehealtheffectsofworkstress.Increasingly,
improvementsinorganizingtheworkandexpandingemployeedecisionmakinglatitudehavebeenused(e.g.,actionresearchandcollective
bargaining;inGermany,occupationalqualityandhealthcircles)toachieveanimprovementinproductivityaswellastohumanizethework
bydecreasingthestressload(Landsbergisetal.1993).
NightandShiftWork
Numerouspublicationsintheinternationalliteraturecoverthehealthrisksposedbynightandshiftwork.Itisgenerallyacceptedthatshift
workisoneriskfactorwhich,togetherwithotherrelevant(includingindirect)workrelateddemandsandexpectationfactors,leadsto
adverseeffects.
Inthelastdecaderesearchonshiftworkhasincreasinglydealtwiththelongtermeffectsofnightandshiftworkonthefrequencyof
cardiovasculardisease,especiallyischaemicheartdiseaseandmyocardialinfarction,aswellascardiovascularriskfactors.Theresultsof
epidemiologicalstudies,especiallyfromScandinavia,permitahigherriskofischemicheartdiseaseandmyocardialinfarctiontobe
presumedforshiftworkers(Alfredsson,KarasekandTheorell1982;Alfredsson,SpetzandTheorell1985;Knutssonetal.1986;Tchsen
1993).InDenmarkitwasevenestimatedthat7%ofcardiovasculardiseaseinmenaswellaswomencanbetracedtoshiftwork(Olsenand
Kristensen1991).
Thehypothesisthatnightandshiftworkershaveahigherrisk(estimatedrelativeriskapproximately1.4)forcardiovasculardiseaseis
supportedbyotherstudiesthatconsidercardiovascularriskfactorslikehypertensionorfattyacidlevelsforshiftworkersascomparedto
dayworkers.Variousstudieshaveshownthatnightandshiftworkmayinduceincreasedbloodpressureandhypertensionaswellas
increasedtriglycerideand/orserumcholesterol(aswellasnormalrangefluctuationsforHDLcholesterolinincreasedtotalcholesterol).
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Thesechanges,togetherwithotherriskfactors(likeheavycigarettesmokingandoverweightamongshiftworkers),cancauseincreased
morbidityandmortalityduetoatheroscleroticdisease(DeBackeretal.1984;DeBackeretal.1987;Hrenstametal.1987;Knutsson1989;
Lavieetal.1989;Lennerns,kerstedtandHambraeus1994;OrthGomer1983;Romonetal.1992).
Inall,thequestionofpossiblecausallinksbetweenshiftworkandatherosclerosiscannotbedefinitivelyansweredatpresent,asthe
pathomechanismisnotsufficientlyclear.Possiblemechanismsdiscussedintheliteratureincludechangesinnutritionandsmokinghabits,
poorsleepquality,increasesinlipidlevel,chronicstressfromsocialandpsychologicaldemandsanddisruptedcircadianrhythms.Knutsson
(1989)hasproposedaninterestingpathogenesisforthelongtermeffectsofshiftworkonchronicmorbidity.
Theeffectsofvariousassociatedattributesonriskestimationhavehardlybeenstudied,sinceintheoccupationalfieldotherstressinducing
workingconditions(noise,chemicalhazardousmaterials,psychosocialstress,monotonyandsoon)areconnectedwithshiftwork.Fromthe
observationthatunhealthynutritionalandsmokinghabitsareoftenconnectedwithshiftwork,itisoftenconcludedthatanincreasedriskof
cardiovasculardiseaseamongshiftworkersismoretheindirectresultofunhealthybehaviour(smoking,poornutritionandsoon)than
directlytheresultofnightorshiftwork(Rutenfranz,KnauthandAngersbach1981).Furthermore,theobvioushypothesisofwhethershift
workpromotesthisconductorwhetherthedifferencecomesprimarilyfromthechoiceofworkplaceandoccupationmustbetested.But
regardlessoftheunansweredquestions,specialattentionmustbepaidincardiovascularpreventionprogrammestonightandshiftworkers
asariskgroup.
Summary
Insummary,riskfactorsrepresentabroadvarietyofgenetic,somatic,physiological,behaviouralandpsychosocialcharacteristicswhichcan
beassessedindividuallyforindividualsandforgroupsofindividuals.Intheaggregate,theyreflecttheprobabilitythatCVD,ormore
preciselyinthecontextofthisarticle,CHDorstrokewilldevelop.Inadditiontoelucidatingthecausesandpathogenesisofmultifactorial
diseases,theirchiefimportanceisthattheydelineateindividualswhoshouldbetargetsforriskfactoreliminationorcontrol,anexercise
admirablysuitedtotheworkplace,whilerepeatedriskassessmentsovertimedemonstratethesuccessofthatpreventiveeffort.
REHABILITATIONANDPREVENTIONPROGRAMMES
LotharHeinemannandGottfriedEnderlein
MostindividualswithrecognizedCVDareabletoworkeffectivelyandproductivelyinmostofthejobsfoundinthemodernworkplace.Just
afewdecadesago,individualssurvivinganacutemyocardialinfarctionwerecossetedandpamperedforweeksandmonthswithclose
supervisionandenforcedinactivity.Laboratoryconfirmationofthediagnosiswasenoughtojustifylabellingtheindividualas"permanently
andtotallydisabled".Newdiagnostictechnologythatprovidesmoreaccurateevaluationofcardiacstatusandthefavourableexperiencesof
thosewhocouldnotorwouldnotacceptsuchalabel,soondemonstratedthatanearlyreturntoworkandanoptimallevelofactivitywas
notonlypossiblebutdesirable(Edwards,McCallumandTaylor1988;Theorelletal.1991;Theorell1993).Today,patientscommence
supervisedphysicalactivityassoonastheacuteeffectsoftheinfarctionsubside,areoftenoutofthehospitalinafewdaysinsteadofthe
mandatory6to8weeksofyore,andareoftenbackonthejobwithinafewweeks.Whendesirableandfeasible,surgicalproceduressuchas
angioplasty,bypassoperationsandevencardiactransplantationcanimprovethecoronarybloodflow,whilearegimenfeaturingdiet,
exerciseandcontroloftheriskfactorsforCHDcanminimize(orevenreverse)theprogressionofcoronaryatherosclerosis.
Oncetheacute,oftenlifethreateningphasesoftheCVDhavebeenovercome,passivemovementfollowedbyactiveexerciseshouldbe
initiatedearlyduringthestayinthehospitalorclinic.Withheartattacks,thisphaseiscompletedwhentheindividualcanclimbstairs
withoutgreatdifficulty.Atthesametime,theindividualisschooledinariskpreventionregimenthatincludesproperdiet,cardiovascular
conditioningexercises,adequaterestandrelaxation,andstressmanagement.Duringthesephasesofrehabilitation,supportfromfamily
members,friendsandcoworkerscanbeparticularlyhelpful(BrusisandWeberFalkensammer1986).Theprogrammecanbecarriedoutin
rehabilitationfacilitiesorinambulatory"heartgroups"underthesupervisionofatrainedphysician(HalhubarandTraencker1986).The
focusoncontrollinglifestyleandbehaviouralriskfactorsandcontrollingstresshasbeenshowntoresultinameasurablereductioninthe
riskofreinfarctionandothercardiovascularproblems.
Throughouttheprogrammetheattendingphysicianshouldmaintaincontactwiththeemployer(andparticularlywiththecompanydoctor,
ifthereisone)todiscusstheprospectsforrecoveryandtheprobabledurationoftheperiodofdisability,andtoexplorethefeasibilityof
anyspecialarrangementsthatmaybeneededtopermitanearlyreturntothejob.Theworker'sknowledgethatthejobiswaitingandthat
heorsheisexpectedtobeabletoreturntoitisapotentmotivatingfactorfortheenhancementofrecovery.Experiencehasamply
demonstratedthatthesuccessoftherehabilitationeffortdiminishesastheabsencefromworklengthens.
Ininstanceswheredesirableadjustmentsinthejoband/ortheworkplacearenotpossibleorfeasible,retrainingandappropriatejob
placementcanobviateunnecessaryinvalidism.Speciallyprotectedworkshopsareoftenhelpfulinreintegratingintotheworkplacepeople
whohavebeenabsentfromthejobforlongperiodswhilereceivingtreatmentfortheseriouseffectsofstroke,congestiveheartfailureor
disablinganginapectoris.
Followingthereturntowork,continuedsurveillancebyboththeattendingphysicianandtheoccupationalphysicianiseminentlydesirable.
Periodicmedicalevaluations,atintervalsthatarefrequentinitiallybutlengthenasrecoveryisassured,arehelpfulinassessingtheworker's
cardiovascularstatus,adjustingmedicationsandotherelementsinthemaintenanceregimenandmonitoringtheadherencetothelifestyle
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andbehaviouralrecommendations.Satisfactoryfindingsintheseexaminationsmayallowthegradualeasingofanyworklimitationsor
restrictionsuntiltheworkerisfullyintegratedintotheworkplace.
WorkplaceHealthPromotionandPreventionProgrammes
Thepreventionofoccupationaldiseasesandinjuriesisaprimeresponsibilityoftheorganization'soccupationalhealthandsafety
programme.Thisincludesprimaryprevention(i.e.,theidentificationandeliminationorcontrolofpotentialhazardsandstrainsbychanging
theworkenvironmentorthejob).Itissupplementedbysecondarypreventionmeasureswhichprotecttheworkersfromtheeffectsof
existinghazardsandstrainsthatcannotbeeliminated(i.e.,personalprotectiveequipmentandperiodicmedicalsurveillanceexaminations).
Workplacehealthpromotionandprevention(HPP)programmesgobeyondthesegoals.Theyplacetheiremphasisonhealthconscious
behaviourasitrelatestolifestyle,behaviouralriskfactors,eliminatingorcopingwithstressandsoon.Theyareofgreatsignificance,
particularlyinpreventingCVD.ThegoalsofHPP,asformulatedbytheWHOCommitteeonEnvironmentalandHealthMonitoringin
OccupationalHealth,extendbeyondthemereabsenceofdiseaseandinjurytoincludewellbeingandfunctionalcapacity(WHO1973).
ThedesignandoperationofHPPprogrammesarediscussedinmoredetailelsewhereinthechapter.Inmostcountries,theyhavea
particularfocusonthepreventionofCVDs.Forexample,inGermany,the"Haveaheartforyourheart"programmesupplementstheheart
healthcirclesorganizedbythehealthinsurancecompanies(MurzaandLaaser1990,1992),whilethe"TakeHeart"movementinBritainand
Australiahassimilargoals(Glasgowetal.1995).
Thatsuchprogrammesareeffectivewasverifiedinthe1980sbytheWHOCollaborativeTrialinPreventionofHeartDisease,whichwas
carriedoutin40pairsoffactoriesinfourEuropeancountriesandinvolvedapproximately61,000menaged40to59.Thepreventive
measureslargelycomprisedhealtheducationactivities,carriedoutprimarilybytheorganization'semployeehealthservice,focusedon
cholesterolloweringdiets,givingupcigarettesmoking,weightcontrol,increasedphysicalactivityandcontrollinghypertension.A
randomizedscreeningof10%oftheeligibleworkersinthefactoriesdesignatedascontrolsdemonstratedthatduringthe4to7yearsofthe
study,overallriskofCVDscouldbereducedby11.1%(19.4%amongthoseinitiallyathighrisk).Inthestudyfactories,mortalityfromCHDs
fellby7.4%,whileoverallmortalityfellby2.7%.ThebestresultswereachievedinBelgium,wheretheinterventionwascarriedout
continuouslyduringtheentirestudyperiod,whilethepoorestresultswereseeninBritain,wherethepreventionactivitiesweresharply
curtailedpriortothelastfollowupexamination.Thisdisparityemphasizestherelationshipofsuccesstothedurationofthehealth
educationeffort;ittakestimetoinculcatethedesiredlifestylechanges.Theintensityoftheeducationaleffortwasalsoafactor:inItaly,
wheresixfulltimehealtheducatorswereinvolved,a28%reductioninoverallriskfactorprofilewasachieved,whereasinBritain,where
onlytwofulltimeeducatorsservedthreetimesthenumberofworkers,ariskfactorreductionofonly4%wasachieved.
WhilethetimerequiredtodetectreductionsinCHDmortalityandmorbidityisaformidablelimitingfactorinepidemiologicalstudiesaimed
atevaluatingtheresultsofcompanyhealthprogrammes(Mannebach1989),reductionsinriskfactorshavebeendemonstrated(Janssen
1991;Gomeletal.1993;Glasgowetal.1995).Temporarydecreasesinthenumberoflostworkdaysandadeclineinhospitalizationrates
havebeenreported(Harris1994).ThereseemstobegeneralagreementthatHPPactivitiesinthecommunityandparticularlyinthe
workplacehavesignificantlycontributedtothereductionincardiovascularmortalityintheUnitedStatesandotherwesternindustrialized
countries.
Conclusion
CVDsloomlargeintheworkplace,notsomuchbecausethecardiovascularsystemisparticularlyvulnerabletoenvironmentalandjob
hazards,butbecausetheyaresocommoninthepopulationofworkingage.Theworkplaceoffersasingularlyadvantageousarenaforthe
detectionofunrecognized,asymptomaticCVDs,forthecircumventionofworkplacefactorsthatmightaccelerateoraggravatethemandfor
theidentificationoffactorsthatincreasetheriskofCVDsandthemountingofprogrammestoeliminateorcontrolthem.WhenCVDsdo
occur,promptattentiontocontrolofjobrelatedcircumstancesthatmayprolongorincreasetheirseveritycanminimizetheextentand
durationofdisability,whileearly,professionallysupervisedrehabilitationeffortswillfacilitatetherestorationofworkingcapacityand
reducetheriskofrecurrences.
PHYSICAL,CHEMICALANDBIOLOGICALHAZARDS
Theintactcardiovascularsystemisremarkablyresistanttotheharmfuleffectsofphysical,chemicalandbiologicalhazardsencounteredon
thejoborintheworkplace.Withaveryfewexceptions,suchhazardsarerarelyadirectcauseofCVDs.Ontheotherhand,oncethe
integrityofthecardiovascularsystemiscompromisedandthismaybeentirelysilentandunrecognizedexposuretothesehazardsmay
contributetotheongoingdevelopmentofadiseaseprocessorprecipitatesymptomsreflectingfunctionalimpairment.Thisdictatesearly
identificationofworkerswithincipientCVDandmodificationoftheirjobsand/ortheworkenvironmenttoreducetheriskofharmful
effects.Thefollowingsegmentswillincludebriefdiscussionsofsomeofthemorecommonlyencounteredoccupationalhazardsthatmay
affectthecardiovascularsystem.EachofthehazardspresentedbelowisdiscussedmorefullyelsewhereintheEncyclopaedia.
PHYSICALFACTORS
HeideStarkandGerdHeuchert
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Noise
Hearinglossduetoworkplacenoisehasbeenrecognizedasanoccupationaldiseaseformanyyears.Cardiovasculardiseasesareatthe
centreofthediscussiononpossiblechronicextraauraleffectsofnoise.Epidemiologicalstudieshavebeendonewithintheworkplacenoise
field(withhighlevelnoiseindicators)aswellasinthesurroundingnoisefield(withlowlevelnoiseindicators).Thebeststudiestodate
weredoneontherelationshipbetweenexposuretonoiseandhighbloodpressure.Innumerousnewsurveystudies,noiseresearchershave
assessedtheavailableresearchresultsandsummarizedthecurrentstateofknowledge(Kristensen1994;SchwarzeandThompson1993;
vanDijk1990).
Studiesshowthatthenoiseriskfactorfordiseasesofthecardiovascularsystemislesssignificantthanbehaviouralriskfactorslikesmoking,
poornutritionorphysicalinactivity(AroandHasan1987;Jegadenetal.1986;KornhuberandLisson1981).
Theresultsofepidemiologicalstudiesdonotpermitanyfinalanswerontheadversecardiovascularhealtheffectsofchronicworkplaceor
environmentalnoiseexposure.Theexperimentalknowledgeonhormonalstresseffectsandchangesinperipheralvasoconstriction,onthe
onehand,andtheobservation,ontheother,thatahighworkplacenoiselevel(>85dBA)promotesthedevelopmentofhypertension,allow
ustoincludenoiseasannonspecificstressstimulusinamultifactoredriskmodelforcardiovasculardiseases,warrantinghighbiological
plausibility.
Theopinionisadvancedinmodernstressresearchthatalthoughincreasesinbloodpressureduringworkareconnectedtonoiseexposure,
thebloodpressurelevelpersedependsonacomplexsetofpersonalityandenvironmentalfactors(Theorelletal.1987).Personalityand
environmentalfactorsplayanintimateroleindeterminingthetotalstressloadattheworkplace.
Forthisreasonitappearsallthemoreurgenttostudytheeffectofmultipleburdensattheworkplaceandtoclarifythecrosseffects,mostly
unknownuptonow,betweencombinedinfluencingexogenousfactorsanddiverseendogenousriskcharacteristics.
Experimentalstudies
Itistodaygenerallyacceptedthatnoiseexposureisapsychophysicalstressor.Numerousexperimentalstudiesonanimalsandhuman
subjectspermitextendingthehypothesisonthepathomechanismofnoisetothedevelopmentofcardiovasculardiseases.Thereisa
relativelyuniformpicturewithrespecttoacuteperipheralreactionstonoisestimuli.Noisestimuliclearlycauseperipheralvasoconstriction,
measurableasadecreaseinfingerpulseamplitudeandskintemperatureandanincreaseinsystolicanddiastolicbloodpressure.Almostall
studiesconfirmanincreaseinheartrate(Carter1988;FisherandTucker1991;Michalak,IsingandRebentisch1990;MillarandSteels1990;
SchwarzeandThompson1993;Thompson1993).Thedegreeofthesereactionsismodifiedbysuchfactorsasthetypeofnoiseoccurrence,
age,sex,stateofhealth,nervousstateandpersonalcharacteristics(HarrisonandKelly1989;Parrotetal.1992;Petiotetal.1988).
Awealthofresearchdealswiththeeffectsofnoiseonmetabolismandhormonelevels.Exposuretoloudnoisealmostalwaysresultsfairly
quicklyinchangessuchasinbloodcortisone,cyclicaladenosinmonophosphate(CAMP),cholesterolandcertainlipoproteinfractions,
glucose,proteinfractions,hormones(e.g.,ACTH,prolactin),adrenalinandnoradrenalin.Increasedcatecholaminelevelscanbefoundinthe
urine.Allofthisclearlyshowsthatnoisestimulibelowthenoisedeafnesslevelcanleadtohyperactivityofthehypophysealadrenalcortex
system(IsingandKruppa1993;Rebentisch,LangeAsschenfeldandIsing1994).
Chronicexposuretoloudnoisehasbeenshowntoresultinareductionofmagnesiumcontentinserum,erythrocytesandinothertissues,
suchasthemyocardium(Alturaetal.1992),butstudyresultsarecontradictory(Altura1993;SchwarzeandThompson1993).
Theeffectofworkplacenoiseonbloodpressureisequivocal.Aseriesofepidemiologicalstudies,whichweremostlydesignedascross
sectionalstudies,indicatethatemployeeswithlongtermexposuretoloudnoiseshowhighersystolicand/ordiastolicbloodpressurevalues
thanthosewhoworkunderlessnoisyconditions.Counterpoised,however,arestudiesthatfoundverylittleornostatisticalassociation
betweenlongtermnoiseexposureandincreasedbloodpressureorhypertension(SchwarzeandThompson1993;Thompson1993;vanDijk
1990).Studiesthatenlisthearinglossasasurrogatefornoiseshowvariedresults.Inanycase,hearinglossisnotasuitablebiological
indicatorfornoiseexposure(Kristensen1989;vanDijk1990).Theindicationsaremountingthatnoiseandtheriskfactorsincreasedblood
pressure,increasedserumcholesterollevel(Pillsburg1986),andsmoking(Baronetal.1987)haveasynergisticeffectonthedevelopmentof
noiseinducedhearingloss.Differentiatingbetweenhearinglossfromnoiseandhearinglossfromotherfactorsisdifficult.Inthestudies
(Talbottetal.1990;vanDijk,VeerbeckanddeVries1987),noconnectionwasfoundbetweennoiseexposureandhighbloodpressure,
whereashearinglossandhighbloodpressurehaveapositivecorrelationaftercorrectionfortheusualriskfactors,especiallyageandbody
weight.Therelativerisksforhighbloodpressurerangebetween1and3.1incomparisonsofexposuretoloudandlessloudnoise.Studies
withqualitativelysuperiormethodologyreportalowerrelationship.Differencesamongthebloodpressuregroupmeansarerelatively
narrow,withvaluesbetween0and10mmHg.
AlargeepidemiologicalstudyofwomentextileworkersinChina(Zhao,LiuandZhang1991)playsakeyroleinnoiseeffectresearch.Zhao
ascertainedadoseeffectrelationshipbetweennoiselevelsandbloodpressureamongwomenindustrialworkerswhoweresubjectto
variousnoiseexposuresovermanyyears.Usinganadditivelogisticalmodelthefactors"indicatedcookingsaltuse","familyhistoryofhigh
bloodpressure"and"noiselevel"(p<0.05)significantlycorrelatedwiththeprobabilityofhighbloodpressure.Theauthorsjudgedthatno
confoundingwaspresentduetooverweight.Thenoiselevelfactorneverthelessconstitutedhalftheriskofhypertensionofthefirsttwo
namedfactors.Anincreaseinthenoiselevelfrom70to100dBAraisedtheriskforhighbloodpressurebyafactorof2.5.Thequantification
oftheriskofhypertensionbyusinghighernoiseexposurelevelswaspossibleinthisstudyonlybecausetheofferedhearingprotectionwas
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notworn.Thisstudylookedatnonsmokingwomenaged358years,soaccordingtov.Eiff'sresults(1993),thenoiserelatedriskof
hypertensionamongmencouldbesignificantlyhigher.
Hearingprotectionisprescribedinwesternindustrializedcountriesfornoiselevelsover8590dBA.Manystudiescarriedoutinthese
countriesdemonstratednoclearriskatsuchnoiselevels,soitcanbeconcludedfromGierkeandHarris(1990)thatlimitingthenoiselevel
tothesetlimitspreventsmostextraauraleffects.
HeavyPhysicalWork
Theeffectsof"lackofmovement"asariskfactorforcardiovasculardiseaseandofphysicalactivityaspromotinghealthwereelucidatedin
suchclassicpublicationsasthosebyMorris,Paffenbargerandtheircoworkersinthe1950sand1960s,andinnumerousepidemiological
studies(BerlinandColditz1990;Powelletal.1987).Inpreviousstudies,nodirectcauseandeffectrelationshipcouldbeshownbetween
lackofmovementandtherateofcardiovasculardiseaseormortality.Epidemiologicalstudies,however,pointtothepositive,protective
effectsofphysicalactivityonreducingvariouschronicdiseases,includingcoronaryheartdisease,highbloodpressure,noninsulin
dependentdiabetesmellitus,osteoporosisandcoloncancer,aswellasanxietyanddepression.Theconnectionbetweenphysicalinactivity
andtheriskofcoronaryheartdiseasehasbeenobservedinnumerouscountriesandpopulationgroups.Therelativeriskforcoronaryheart
diseaseamonginactivepeoplecomparedtoactivepeoplevariesbetween1.5and3.0;withthestudiesusingqualitativelyhigher
methodologyshowinghigherrelationship.Thisincreasedriskiscomparabletothatfoundforhypercholesterolemia,hypertensionand
smoking(BerlinandColditz1990;CentersforDiseaseControlandPrevention1993;Kristensen1994;Powelletal.1987).
Regular,leisuretimephysicalactivityappearstoreducetheriskofcoronaryheartdiseasethroughvariousphysiologicalandmetabolic
mechanisms.Experimentalstudieshaveshownthatwithregularmotiontraining,theknownriskfactorsandotherhealthrelatedfactorsare
positivelyinfluenced.Itresults,forexample,inanincreaseintheHDLcholesterollevel,andadecreaseintheserumtriglycerideleveland
bloodpressure(Bouchard,ShepardandStephens1994;Pateetal.1995).
Aseriesofepidemiologicalstudies,spurredonbythestudiesofMorrisetal.oncoronaryriskamongLondonbusdriversandconductors
(Morris,HeadyandRaffle1956;Morrisetal.1966),andthestudyofPaffenbargeretal.(1970)amongAmericanharbourworkers,lookedat
therelationshipbetweenthedifficultylevelofphysicalworkandtheincidenceofcardiovasculardiseases.Basedonearlierstudiesfromthe
1950sand1960stheprevailingideawasthatphysicalactivityatworkcouldhaveacertainprotectiveeffectontheheart.Thehighest
relativeriskforcardiovasculardiseaseswasfoundinpeoplewithphysicallyinactivejobs(e.g.,sittingjobs)ascomparedtopeoplewhodo
heavyphysicalwork.Butnewerstudieshavefoundnodifferenceinthefrequencyofcoronarydiseasebetweenactiveandinactive
occupationalgroupsorhaveevenfoundahigherprevalenceandincidenceofcardiovascularriskfactorsandcardiovasculardiseasesamong
heavylabourers(Ilmarinen1989;Kanneletal.1986;Kristensen1994;Suurnkkietal.1987).Severalreasonscanbegivenforthe
contradictionbetweenthehealthpromotingeffectoffreetimephysicalactivitiesoncardiovascularmorbidityandthelackofthiseffect
withheavyphysicallabour:
Primaryandsecondaryselectionprocesses(healthyworkereffect)canleadtoseriousdistortionsinoccupationalmedical
epidemiologicalstudies.
Therelationshipfoundbetweenphysicalworkandtheonsetofcardiovasculardiseasescanbeinfluencedbyanumberofconfounding
variables(likesocialstatus,education,behaviouralriskfactors).
Assessingthephysicalload,oftensolelyonthebasisofjobdescriptions,mustbeseenasaninadequatemethod.
Socialandtechnologicaldevelopmentsincethe1970shasmeantthatonlyafewjobswith"dynamicphysicalactivity"remain.Physical
activityinthemodernworkplaceoftenmeansheavyliftingorcarryingandahighproportionofstaticmusclework.Soitisnotsurprising
thatphysicalactivityinoccupationsofthistypelacksanessentialcriterionforcoronaryprotectiveeffect:asufficientintensity,durationand
frequencytooptimizethephysicalloadonbigmusclegroups.Thephysicalworkis,ingeneral,intensive,buthaslessofaworkouteffecton
thecardiovascularsystem.Thecombinationofheavy,physicallydemandingworkandhighfreetimephysicalactivitycouldestablishthe
mostfavourablesituationwithrespecttothecardiovascularriskfactorprofileandtheonsetofCHD(Saltin1992).
Theresultsofstudiestodatearealsonotconsistentonthequestionofwhetherheavyphysicalworkisrelatedtotheonsetofarterial
hypertension.
Physicallydemandingworkisrelatedtochangesinbloodpressure.Indynamicworkthatutilizesbigmusclemasses,bloodsupplyand
demandareinbalance.Indynamicworkthatrequiresthesmallerandmiddlemusclemasses,theheartmayputoutmorebloodthanis
neededforthetotalphysicalworkandtheresultcanbeconsiderablyincreasedsystolicanddiastolicbloodpressure(Frauendorfetal.
1986).
Evenwithcombinedphysicalmentalstrainorphysicalstrainundertheeffectsofnoise,asubstantialincreaseinbloodpressureandheart
rateareseeninacertainpercentage(approximately30%)ofpeople(Frauendorf,KobrynandGelbrich1992;Frauendorfetal.1995).
Nostudiesarepresentlyavailableonthechroniceffectsofthisincreasedcirculatoryactivityinlocalmusclework,withorwithoutnoiseor
mentalstrain.
Intworecentlypublishedindependentstudies,byAmericanandGermanresearchers(Mittlemanetal.1993;Willichetal.1993),the
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questionwaspursuedastowhetherheavyphysicalworkcanbeatriggerforanacutemyocardialinfarction.Inthestudies,of1,228and
1,194peoplewithacutemyocardialinfarctionrespectively,thephysicalstrainonehourbeforetheinfarctionwascomparedwiththe
situation25hoursbefore.Thefollowingrelativeriskswerecalculatedfortheonsetofamyocardialinfarctionwithinonehourofheavy
physicalstrainincomparisonwithlightactivityorrest:5.9(CI95%:4.67.7)intheAmericanand2.1(CI95%:1.63.1)intheGermanstudy.
Theriskwashighestforpeoplenotinshape.Animportantlimitingobservationis,however,thattheheavyphysicalstrainoccurredonehour
beforetheinfarctioninonly4.4and7.1%oftheinfarctionpatientsrespectively.
Thesestudiesinvolvequestionsofthesignificanceofphysicalstrainorastressinducedincreasedoutputofcatecholaminesonthecoronary
bloodsupply,ontriggeringcoronaryspasms,oranimmediatelyharmfuleffectofcatecholaminesonthebetaadrenergicreceptorsofthe
heartmusclemembraneasacauseoftheinfarctionmanifestationoracutecardiacdeath.Itcanbeassumedthatsuchresultswillnotensue
withahealthycoronaryvesselsystemandintactmyocardium(FritzeandMller1995).
Theobservationsmakeclearthatstatementsonpossiblecausalrelationshipsbetweenheavyphysicallabourandeffectsoncardiovascular
morbidityarenoteasytosubstantiate.Theproblemwiththistypeofinvestigationclearlyliesinthedifficultyinmeasuringandassessing
"hardwork"andinexcludingpreselections(healthyworkereffect).Prospectivecohortstudiesareneededonthechroniceffectsofselected
formsofphysicalworkandalsoontheeffectsofcombinedphysicalmentalornoisestressonselectedfunctionalareasofthecardiovascular
system.
Itisparadoxicalthattheresultofreducingheavydynamicmuscleworkuntilnowgreetedasasignificantimprovementinthelevelofstrain
inthemodernworkplacepossiblyresultsinanew,significanthealthprobleminmodernindustrialsociety.Fromtheoccupationalmedicine
perspective,onemightconcludethatstaticphysicalstrainonthemuscleskeletonsystemwithlackofmovement,presentsamuchgreater
healthriskthanpreviouslyassumed,accordingtotheresultsofstudiestodate.
Wheremonotonousimproperstrainscannotbeavoided,counterbalancingwithfreetimesportsactivitiesofcomparabledurationshouldbe
encouraged(e.g.,swimming,bicycling,walkingandtennis).
HeatandCold
Exposuretoextremeheatorcoldisthoughttoinfluencecardiovascularmorbidity(Kristensen1989;Kristensen1994).Theacuteeffectsof
highoutsidetemperaturesorcoldonthecirculatorysystemarewelldocumented.Anincreaseinmortalityasaresultofcardiovascular
diseases,mostlyheartattacksandstrokes,wasobservedatlowtemperatures(under+10C)inthewinterincountriesatnorthernlatitudes
(Curwen1991;Douglas,AllanandRawles1991;Kristensen1994;Kunst,LoomanandMackenbach1993).Pan,LiandTsai(1995)foundan
impressiveUshapedrelationshipbetweenoutsidetemperatureandmortalityratesforcoronaryheartdiseaseandstrokesinTaiwan,a
subtropicalcountry,withasimilarlyfallinggradientbetween+10Cand+29Candasharpincreasethereafteratover+32C.The
temperatureatwhichthelowestcardiovascularmortalitywasobservedishigherinTaiwanthanincountrieswithcolderclimates.Kunst,
LoomanandMackenbachfoundintheNetherlandsaVshapedrelationshipbetweentotalmortalityandoutsidetemperature,withthe
lowestmortalityat17C.Mostcoldrelateddeathsoccurredinpeoplewithcardiovasculardiseases,andmostheatrelateddeathswere
associatedwithrespiratorytractillnesses.StudiesfromtheUnitedStates(RogotandPadgett1976)andothercountries(Wyndhamand
Fellingham1978)showasimilarUshapedrelationship,withthelowestheartattackandstrokemortalityatoutsidetemperaturesaround25
to27C.
Itisnotyetclearhowtheseresultsshouldbeinterpreted.Someauthorshaveconcludedthatacausalrelationshippossiblyexistsbetween
temperaturestressandthepathogenesisofcardiovasculardiseases(CurwenandDevis1988;Curwen1991;Douglas,AllanandRawles1991;
Khaw1995;Kunst,LoomanandMackenbach1993;RogotandPadgett1976;WyndhamandFellingham1978).Thishypothesiswas
supportedbyKhawinthefollowingobservations:
Temperatureprovedtobethestrongest,acute(daytoday)predictorforcardiovascularmortalityundertheparameterswhichwere
handleddifferently,suchasseasonalenvironmentalchangesandfactorslikeairpollution,sunlightexposure,incidenceoffluandnutrition.
Thisspeaksagainsttheassumptionthattemperatureactsonlyasasubstitutevariableforotherdetrimentalenvironmentalconditions.
Theconsistencyoftheconnectioninvariouscountriesandpopulationgroups,overtimeandindifferentagegroups,isfurthermore
convincing.
Datafromclinicalandlaboratoryresearchsuggestsvariousbiologicallyplausiblepathomechanisms,includingeffectsofchanging
temperatureonhaemostasis,bloodviscosity,lipidlevels,thesympatheticnervoussystemandvasoconstriction(ClarkandEdholm1985;
Gordon,HydeandTrost1988;Keatingeetal.1986;Lloyd1991;Neildetal.1994;StoutandGrawford1991;Woodhouse,Khawand
Plummer1993b;Woodhouseetal.1994).
Exposuretocoldincreasesbloodpressure,bloodviscosityandheartrate(Kunst,LoomanandMackenbach1993;Tanaka,Konnoand
Hashimoto1989;Kawaharaetal.1989).StudiesbyStoutandGrawford(1991)andWoodhouseandcoworkers(1993;1994)showthat
fibrinogens,bloodclottingfactorVIIcandlipidswerehigheramongolderpeopleinthewinter.
Anincreaseinbloodviscosityandserumcholesterolwasfoundwithexposuretohightemperatures(ClarkandEdholm1985;Gordon,Hyde
andTrost1988;Keatingeetal.1986).AccordingtoWoodhouse,KhawandPlummer(1993a),thereisastronginversecorrelationbetween
bloodpressureandtemperature.
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Stillunclearisthedecisivequestionofwhetherlongtermexposuretocoldorheatresultsinlastingincreasedriskofcardiovasculardisease,
orwhetherexposuretoheatorcoldincreasestheriskforanacutemanifestationofcardiovasculardiseases(e.g.,aheartattack,astroke)in
connectionwiththeactualexposure(the"triggeringeffect").Kristensen(1989)concludesthatthehypothesisofanacuteriskincreasefor
complicationsfromcardiovasculardiseaseinpeoplewithunderlyingorganicdiseaseisconfirmed,whereasthehypothesisofachronic
effectofheatorcoldcanneitherbeconfirmednorrejected.
Thereislittle,ifany,epidemiologicalevidencetosupportthehypothesisthattheriskofcardiovasculardiseaseishigherinpopulationswith
anoccupational,longtermexposuretohightemperature(DukesDobos1981).Tworecentcrosssectionstudiesfocusedonmetalworkersin
Brazil(Kloetzeletal.1973)andaglassfactoryinCanada(WojtczakJaroszowaandJarosz1986).Bothstudiesfoundasignificantlyincreased
prevalenceofhypertensionamongthosesubjecttohightemperatures,whichincreasedwiththedurationofthehotwork.Presumed
influencesofageornutritioncouldbeexcluded.Lebedeva,AlimovaandEfendiev(1991)studiedmortalityamongworkersinametallurgical
companyandfoundhighmortalityriskamongpeopleexposedtoheatoverthelegallimits.Thefigureswerestatisticallysignificantforblood
diseases,highbloodpressure,ischemicheartdiseaseandrespiratorytractdiseases.Karnaukhetal.(1990)reportanincreasedincidenceof
ischemicheartdisease,highbloodpressureandhaemorrhoidsamongworkersinhotcastingjobs.Thedesignofthisstudyisnotknown.
Wildetal.(1995)assessedthemortalityratesbetween1977and1987inacohortstudyofFrenchpotashminers.Themortalityfrom
ischemicheartdiseasewashigherforundergroundminersthanforabovegroundworkers(relativerisk=1.6).Amongpeoplewhowere
separatedfromthecompanyforhealthreasons,theischemicheartdiseasemortalitywasfivetimeshigherintheexposedgroupas
comparedtotheabovegroundworkers.AcohortmortalitystudyintheUnitedStatesshoweda10%lowercardiovascularmortalityfor
heatexposedworkersascomparedtothenonexposedcontrolgroup.Inanycase,amongthoseworkerswhowereinheatexposedjobs
lessthansixmonths,thecardiovascularmortalitywasrelativelyhigh(Redmond,GustinandKamon1975;Redmondetal.1979).
ComparableresultswerecitedbyMoulinetal.(1993)inacohortstudyofFrenchsteelworkers.Theseresultswereattributedtoapossible
healthyworkereffectamongtheheatexposedworkers.
Therearenoknownepidemiologicalstudiesofworkersexposedtocold(e.g.,cooler,slaughterhouseorfisheryworkers).Itshouldbe
mentionedthatcoldstressisnotonlyafunctionoftemperature.Theeffectsdescribedintheliteratureappeartobeinfluencedbya
combinationoffactorslikemuscleactivity,dress,dampness,draftsandpossiblypoorlivingconditions.Workplaceswithexposuretocold
shouldpayspecialattentiontoappropriatedressandavoidingdrafts(Kristensen1994).
Vibration
Handarmvibrationstress
Itislongknownandwelldocumentedthatvibrationstransmittedtothehandsbyvibratingtoolscancauseperipheralvasculardisordersin
additiontodamagetothemuscleandskeletalsystem,andperipheralnervefunctiondisordersinthehandarmarea(Dupuisetal.1993;
Pelmear,TaylorandWasserman1992).The"whitefingerdisease",firstdescribedbyRaynaud,appearswithhigherprevalencyratesamong
exposedpopulations,andisrecognizedasanoccupationaldiseaseinmanycountries.
Raynaud'sphenomenonismarkedbyanattackwithvasospasticreducedfusionofallorsomefingers,withtheexceptionofthethumbs,
accompaniedbysensibilitydisordersintheaffectedfingers,feelingsofcold,pallorandparaesthesia.Aftertheexposureends,circulation
resumes,accompaniedbyapainfulhyperaemia.
Itisassumedthatendogenousfactors(e.g.,inthesenseofaprimaryRaynaud'sphenomenon)aswellasexogenousexposurescanbeheld
responsiblefortheoccurrenceofavibrationrelatedvasospasticsyndrome(VVS).Theriskisclearlygreaterwithvibrationsfrommachines
withhigherfrequencies(20toover800Hz)thanwithmachinesthatproducelowfrequencyvibrations.Theamountofstaticstrain(gripping
andpressingstrength)appearstobeacontributingfactor.Therelativesignificanceofcold,noiseandotherphysicalandpsychological
stressors,andheavynicotineconsumptionisstillunclearinthedevelopmentoftheRaynaud'sphenomenon.
TheRaynaud'sphenomenonispathogeneticallybasedonavasomotordisorder.Despitealargenumberofstudiesonfunctional,non
invasive(thermography,plethysmography,capillaroscopy,coldtest)andinvasiveexaminations(biopsy,arteriography),thepathophysiology
ofthevibrationrelatedRaynaud'sphenomenonisnotyetclear.Whetherthevibrationdirectlycausesdamagetothevascularmusculature
(a"localfault"),orwhetheritisavasoconstrictionasaresultofsympathetichyperactivity,orwhetherboththesefactorsarenecessary,isat
presentstillunclear(Gemne1994;Gemne1992).
Theworkrelatedhypothenarhammersyndrome(HHS)shouldbedistinguishedinthedifferentialdiagnosisfromvibrationcaused
Raynaud'sphenomenon.Pathogeneticallythisisachronictraumaticdamagetothearteryulnaris(intimalesionwithsubsequent
thrombosization)intheareaofthesuperficialcourseabovetheunciformbone(oshamatum).HHSiscausedbylongtermmechanical
effectsintheformofexternalpressureorblows,orbysuddenstrainintheformofmechanicalpartialbodyvibrations(oftencombinedwith
persistentpressureandtheeffectsofimpacts).Forthisreason,HHScanoccurasacomplicationorinconnectionwithaVVS(Kajietal.
1993;MarshallandBilderling1984).
Inadditiontotheearlyand,forexposureagainsthandarmvibration,specificperipheralvasculareffects,ofparticularscientificinterestare
thesocallednonspecificchronicchangesofautonomousregulationsoftheorgansystemsforexample,ofthecardiovascularsystem,
perhapsprovokedbyvibration(GemneandTaylor1983).Thefewexperimentalandepidemiologicalstudiesofpossiblechroniceffectsof
handarmvibrationgivenoclearresultsconfirmingthehypothesisofpossiblevibrationrelatedendocrineandcardiovascularfunction
disordersofthemetabolicprocesses,cardiacfunctionsorbloodpressure(Frkkil,PyykkandHeinonen1990;Virokannas1990)otherthan
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thattheactivityoftheadrenergicsystemisincreasedfromexposuretovibration(Bovenzi1990;Olsen1990).Thisappliestovibrationalone
orincombinationwithotherstrainfactorslikenoiseorcold.
Wholebodyvibrationstress
Ifwholebodymechanicalvibrationshaveaneffectonthecardiovascularsystem,thenaseriesofparameterssuchasheartrate,blood
pressure,cardiacoutput,electrocardiogram,plethysmogramandcertainmetabolicparametersmustshowcorrespondingreactions.
Conclusionsonthisaremadedifficultforthemethodologicalreasonthatthesecirculationquantificationsdonotreactspecificallyto
vibrations,butcanalsobeinfluencedbyothersimultaneousfactors.Increasesinheartrateareapparentonlyunderveryheavyvibration
loads;theinfluenceonbloodpressurevaluesshowsnosystematicresultsandelectrocardiographic(ECG)changesarenotsignificantly
differentiable.
Peripheralcirculatorydisordersresultingfromvasoconstrictionhavebeenlessresearchedandappearweakerandofshorterdurationthan
thosefromhandarmvibrations,whicharemarkedbyaneffectonthegraspingstrengthofthefingers(DupuisandZerlett1986).
Inmoststudiestheacuteeffectsofwholebodyvibrationsonthecardiovascularsystemofvehicledriverswerefoundtoberelativelyweak
andtemporary(DupiusandChrist1966;Griffin1990).
Wikstrm,KjellbergandLandstrm(1994),inacomprehensiveoverview,citedeightepidemiologicalstudiesfrom1976to1984that
examinedtheconnectionbetweenwholebodyvibrationsandcardiovasculardiseasesanddisorders.Onlytwoofthesestudiesfounda
higherprevalenceofsuchillnessesinthegroupexposedtovibrations,butnonewherethiswasinterpretedastheeffectofwholebody
vibrations.
Theviewiswidelyacceptedthatchangesofphysiologicalfunctionsthroughwholebodyvibrationshaveonlyaverylimitedeffectonthe
cardiovascularsystem.Causesaswellasmechanismsofthereactionofthecardiovascularsystemtowholebodyvibrationsarenotyet
sufficientlyknown.Atpresentthereisnobasistoassumethatwholebodyvibrationspersecontributetotheriskofdiseasesofthe
cardiovascularsystem.Butattentionshouldbepaidtothefactthatthisfactorveryofteniscombinedwithexposuretonoise,inactivity
(sittingwork)andshiftwork.
IonizingRadiation,ElectromagneticFields,RadioandMicrowaves,UltraandInfrasound
Manycasestudiesandafewepidemiologicalstudieshavedrawnattentiontothepossibilitythationizingradiation,introducedtotreat
cancerorotherdiseases,maypromotethedevelopmentofarteriosclerosisandtherebyincreasetheriskforcoronaryheartdiseaseandalso
othercardiovasculardiseases(Kristensen1989;Kristensen1994).Studiesontheincidenceofcardiovasculardiseasesinoccupationalgroups
exposedtoionizingradiationarenotavailable.
Kristensen(1989)reportsonthreeepidemiologicalstudiesfromtheearly1980sontheconnectionbetweencardiovasculardiseasesand
exposuretoelectromagneticfields.Theresultsarecontradictory.Inthe1980sand1990sthepossibleeffectsofelectricalandmagnetic
fieldsonhumanhealthhaveattractedincreasingattentionfrompeopleinoccupationalandenvironmentalmedicine.Partiallycontradictory
epidemiologicalstudiesthatlookedforcorrelationsbetweenoccupationaland/orenvironmentalexposuretoweak,lowfrequencyelectrical
andmagneticfields,ontheonehand,andtheonsetofhealthdisordersontheother,arousedconsiderableattention.Intheforegroundof
thenumerousexperimentalandfewepidemiologicalstudiesstandpossiblelongtermeffectssuchascarcinogenicity,teratogenicity,effects
ontheimmuneorhormonesystems,onreproduction(withspecialattentiontomiscarriagesanddefects),aswellasto"hypersensitivityto
electricity"andneuropsychologicalbehaviouralreactions.Possiblecardiovascularriskisnotbeingdiscussedatpresent(Gamberale1990;
Knave1994).
Certainimmediateeffectsoflowfrequencymagneticfieldsontheorganismthathavebeenscientificallydocumentedthroughinvitroand
invivoexaminationsoflowtohighfieldstrengthsshouldbementionedinthisconnection(UNEP/WHO/IRPA1984;UNEP/WHO/IRPA1987).
Inthemagneticfield,suchasinthebloodstreamorduringheartcontraction,chargedcarriersleadtoinductionofelectricalfieldsand
currents.Thustheelectricalvoltagethatiscreatedinastrongstaticmagneticfieldovertheaortaneartheheartduringcoronaryactivitycan
amountto30mVataflowthicknessof2Tesla(T),andinductionvaluesover0.1TweredetectedintheECG.Buteffectsontheblood
pressure,forexample,werenotfound.Magneticfieldsthatchangewithtime(intermittentmagneticfields)induceelectricaleddyfieldsin
biologicalobjectsthatcanforexamplearousenerveandmusclecellsinthebody.Nocertaineffectappearswithelectricalfieldsorinduced
currentsunder1mA/m2.Visual(inducedwithmagnetophosphene)andnervouseffectsarereportedat10to100mA/m2.Extrasystolicand
heartchamberfibrillationsappearatover1A/m2.Accordingtocurrentlyavailabledata,nodirecthealththreatistobeexpectedforshort
termwholebodyexposureupto2T(UNEP/WHO/IRPA1987).However,thedangerthresholdforindirecteffects(e.g.,fromthemagnetic
fieldforceactiononferromagneticmaterials)lieslowerthanthatfordirecteffects.Precautionarymeasuresarethusrequiredforpersons
withferromagneticimplants(unipolarpacemakers,magnetizableaneurysmclips,haemoclips,artificialheartvalveparts,otherelectrical
implants,andalsometalfragments).Thedangerthresholdforferromagneticimplantsbeginsat50to100mT.Theriskisthatinjuriesor
bleedingcanresultfrommigrationorpivotalmotions,andthatfunctionalcapacities(e.g.,ofheartvalves,pacemakersandsoon)canbe
affected.Infacilitiesinresearchandindustrywithstrongmagneticfields,someauthorsadvisemedicalsurveillanceexaminationsforpeople
withcardiovasculardiseases,includinghighbloodpressure,injobswherethemagneticfieldexceeds2T(Bernhardt1986;Bernhardt1988).
Wholebodyexposureof5Tcanleadtomagnetoelectrodynamicandhydrodynamiceffectsonthecirculatorysystem,anditshouldbe
assumedthatshorttermwholebodyexposureof5Tcauseshealthhazards,especiallyforpeoplewithcardiovasculardiseases,including
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highbloodpressure(Bernhardt1988;UNEP/WHO/IRPA1987).
Studiesthatexaminethevariouseffectsofradioandmicrowaveshavefoundnodetrimentaleffectstohealth.Thepossibilityof
cardiovasculareffectsfromultrasound(frequencyrangebetween16kHzand1GHz)andinfrasound(frequencyrange>20kHz)are
discussedintheliterature,buttheempiricalevidenceisveryslight(Kristensen1994).
CHEMICALHAZARDOUSMATERIALS
UlrikeTittelbachandWolframDietmarSchneider
Despitenumerousstudies,theroleofchemicalfactorsincausingcardiovasculardiseasesisstilldisputed,butprobablyissmall.The
calculationoftheaetiologicalroleofchemicaloccupationalfactorsforcardiovasculardiseasesfortheDanishpopulationresultedinavalue
under1%(Kristensen1994).Forafewmaterialssuchascarbondisulphideandorganicnitrogencompounds,theeffectonthe
cardiovascularsystemisgenerallyrecognized(Kristensen1994).Leadseemstoaffectbloodpressureandcerebrovascularmorbidity.Carbon
monoxide(WeirandFabiano1982)undoubtedlyhasacuteeffects,especiallyinprovokinganginapectorisinpreexistingischaemia,but
probablydoesnotincreasetheriskoftheunderlyingarteriosclerosis,aswaslongsuspected.Othermaterialslikecadmium,cobalt,arsenic,
antimony,beryllium,organicphosphatesandsolventsareunderdiscussion,butnotsufficientlydocumentedasyet.Kristensen(1989,1994)
givesacriticaloverview.Aselectionofrelevantactivitiesandindustrialbranchescanbefoundintable3.4.
Table3.4Selectionofactivitiesandindustrialbranchesthatmaybeassociatedwithcardiovascularhazards
Hazardousmaterial
Occupationalbranchaffected/use
Carbondisulphide(CS2)
Rayonandsyntheticfibrefabrication,
rubber,matches,explosivesandcellulose
industries
Usedassolventinmanufactureof
pharmaceuticals,cosmeticsand
insecticides
Organicnitrocompounds
Explosivesandmunitionsmanufacture,
pharmaceuticalsindustry
Carbonmonoxide(CO)
Employeesinlargeindustrialcombustion
facilities(blastfurnaces,cokeovens)
Manufactureandutilizationofgas
mixturescontainingCO(producergas
facilities)
Repairofgaspipelines
Castingworkers,firefighters,auto
mechanics(inbadlyventilatedspaces)
Exposurestoaccidents(gasesfrom
explosions,firesintunnelbuildingor
undergroundwork)
Lead
Smeltingofleadoreandsecondaryraw
materialscontaininglead
Metalindustry(productionofvarious
alloys),cuttingandweldingmetals
containingleadormaterialscoatedwith
coveringscontaininglead
Batteryfactories
Ceramicsandporcelainindustries
(productionofleadedglazes)
Productionofleadedglass
Paintindustry,applicationandremovalof
leadedpaints
Hydrocarbons,halogenated
hydrocarbons
Solvents(paints,lacquer)
Adhesives(shoe,rubberindustries)
Cleaninganddegreasingagents
Basicmaterialsforchemicalsyntheses
Refrigerants
Medicine(narcotics)
Methylchlorideexposureinactivities
usingsolvents
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Theexposureandeffectdataofimportantstudiesforcarbondisulphide(CS2),carbonmonoxide(CO)andnitroglycerinearegiveninthe
chemicalsectionoftheEncyclopaedia.Thislistingmakesclearthatproblemsofinclusion,combinedexposures,varyingconsiderationof
compoundingfactors,changingtargetsizesandassessmentstrategiesplayaconsiderableroleinthefindings,sothatuncertaintiesremain
intheconclusionsoftheseepidemiologicalstudies.
Insuchsituationsclearpathogeneticconceptionsandknowledgecansupportthesuspectedconnectionsandtherebycontributetoderiving
andsubstantiatingtheconsequences,includingpreventivemeasures.Theeffectsofcarbondisulphideareknownonlipidsandcarbohydrate
metabolism,onthyroidfunctioning(triggeringhypothyroidism)andoncoagulationmetabolism(promotingthrombocyteaggregation,
inhibitingplasminogenandplasminactivity).Changesinbloodpressuresuchashypertensionaremostlytraceabletovascularbased
changesinthekidney,adirectcausallinktohighbloodpressureduetocarbondisulphidehasnotyetbeenexcludedforcertain,andadirect
(reversible)toxiceffectissuspectedonthemyocardiumoraninterferencewiththecatecholaminemetabolism.Asuccessful15year
interventionstudy(NurminenandHernberg1985)documentsthereversibilityoftheeffectontheheart:areductioninexposurewas
followedalmostimmediatelybyadecreaseincardiovascularmortality.Inadditiontotheclearlydirectcardiotoxiceffects,arteriosclerotic
changesinthebrain,eye,kidneyandcoronaryvasculaturethatcanbeconsideredthebasisofencephalopathies,aneurysmsintheretina
area,nephropathiesandchronicischaemicheartdiseasehavebeenprovenamongthosewhoareexposedtoCS2.Ethnicandnutritionally
relatedcomponentsinterfereinthepathomechanism;thiswasmadeclearinthecomparativestudiesofFinnishandJapaneseviscousrayon
workers.InJapan,vascularchangesintheareaoftheretinawerefound,whereasinFinlandthecardiovasculareffectsdominated.
Aneurysmaticchangesintheretinalvasculaturewereobservedatcarbondisulphideconcentrationsunder3ppm(Fajen,Albrightand
Leffingwell1981).Reducingtheexposureto10ppmclearlyreducedcardiovascularmortality.Thisdoesnotdefinitivelyclarifywhether
cardiotoxiceffectsaredefinitelyexcludedatdosesunder10ppm.
Theacutetoxiceffectsoforganicnitratesinvolvewideningofthevasa,accompaniedbydroppingbloodpressure,increasedheartrate,
spottyerythema(flush),orthostaticdizzinessandheadaches.Sincethehalflifeoftheorganicnitrateisshort,theailmentssoonsubside.
Normally,serioushealthconsiderationsarenottobeexpectedwithacuteintoxication.Thesocalledwithdrawalsyndromeappearswhen
exposureisinterruptedforemployeeswithlongtermexposuretoorganicnitrate,withalatencyperiodof36to72hours.Thisincludes
ailmentsrangingfromanginapectorisuptoacutemyocardialinfarctionandcasesofsuddendeath.Intheinvestigateddeaths,oftenno
coronaryscleroticchangesweredocumented.Thecauseisthereforesuspectedtobe"reboundvasospasm".Whenthevasawideningeffect
ofthenitrateisremoved,anautoregulativeincreaseinresistanceoccursinthevasa,includingthecoronaryarteriae,whichproducesthe
abovementionedresults.Incertainepidemiologicalstudies,suspectedassociationsbetweenexposuredurationandintensityoforganic
nitrateandischaemicheartdiseaseareconsidereduncertain,andpathogeneticplausibilityforthemislacking.
Concerninglead,metallicleadindustform,thesaltsofdivalentleadandorganicleadcompoundsaretoxicologicallyimportant.Leadattacks
thecontractilemechanismofthevasamusclecellsandcausesvascularspasms,whichareconsideredcausesforaseriesofsymptomsof
leadintoxication.Amongtheseistemporaryhypertensionthatappearswithleadcolic.Lastinghighbloodpressurefromchroniclead
intoxicationcanbeexplainedbyvasospasmsaswellaskidneychanges.Inepidemiologicalstudiesanassociationhasbeenobservedwith
longerexposuretimesbetweenleadexposureandincreasedbloodpressure,aswellasanincreasedincidenceofcerebrovasculardiseases,
whereastherewaslittleevidenceofincreasedcardiovasculardiseases.
Epidemiologicaldataandpathogeneticinvestigationstodatehaveproducednoclearresultsonthecardiovasculartoxicityofothermetals
likecadmium,cobaltandarsenic.However,thehypothesisthathalogenatedhydrocarbonactsasamyocardialirritantisconsideredcertain.
Thetriggeringmechanismofoccasionallylifethreateningarrhythmiafromthesematerialspresumablycomesfrommyocardialsensitivityto
epinephrine,whichworksasanaturalcarrierfortheautonomicnervoussystem.Stillbeingdiscussediswhetheradirectcardiaceffectexists
suchasreducedcontractility,suppressionofimpulseformationcentres,impulsetransmission,orrefleximpairmentresultingfromirrigation
intheupperairwayregion.Thesensitizingpotentialofhydrocarbonsapparentlydependsonthedegreeofhalogenationandonthetypeof
thehalogencontained,whereaschlorinesubstitutedhydrocarbonsaresupposedtohaveastrongersensitizingeffectthanfluoride
compounds.Themaximummyocardialeffectforhydrocarbonscontainingchlorineoccursataroundfourchlorineatomspermolecule.Short
chainnonsubstitutedhydrocarbonshaveahighertoxicitythanoneswithlongerchains.Littleisknownaboutthearrhythmiatriggering
dosageoftheindividualsubstances,asthereportsonhumanspredominantlyarecasedescriptionswithexposuretohighconcentrations
(accidentalexposureand"sniffing").AccordingtoReinhardtetal.(1971),benzene,heptane,chloroformandtrichlorethyleneareespecially
sensitizing,whereascarbontetrachlorideandhalothanehavelessarrhythmogeniceffect.
Thetoxiceffectsofcarbonmonoxideresultfromtissuehypoxaemia,whichresultsfromtheincreasedformationofCOHb(COhas200
timesgreateraffinitytohaemoglobinthandoesoxygen)andtheresultingreducedreleaseofoxygentothetissues.Inadditiontothe
nerves,theheartisoneoftheorgansthatreactespeciallycriticallytosuchhypoxaemia.Theresultingacuteheartailmentshavebeen
repeatedlyexaminedanddescribedaccordingtoexposuretime,breathingfrequency,ageandpreviousillnesses.Whereasamonghealthy
subjects,cardiovasculareffectsfirstappearatCOHbconcentrationsof35to40%,anginapectorisailmentscouldbeexperimentally
producedinpatientswithischaemicheartdiseasealreadyatCOHbconcentrationsbetween2and5%duringphysicalexposure(Kleinman
etal.1989;Hinderliteretal.1989).Deadlyinfarctionswereobservedamongthosewithpreviousafflictionsat20%COHb(AtkinsandBaker
1985).
TheeffectsoflongtermexposurewithlowCOconcentrationsarestillsubjecttocontroversy.Whereasexperimentalstudiesonanimals
possiblyshowedanatherogeniceffectbywayofhypoxiaofthevasawallsorbydirectCOeffectonthevasawall(increasedvascular
permeability),theflowcharacteristicsoftheblood(strengthenedthrombocyteaggregation),orlipidmetabolism,thecorrespondingproof
forhumansislacking.Theincreasedcardiovascularmortalityamongtunnelworkers(SMR1.35,95%CI1.091.68)canmorelikelybe
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explainedbyacuteexposurethanfromchronicCOeffects(Sternetal.1988).TheroleofCOinthecardiovasculareffectsofcigarette
smokingisalsonotclear.
BIOLOGICALHAZARDS
ReginaJckel,UlrikeTittelbachandWolframDietmarSchneider
"Abiologicalhazardousmaterialcanbedefinedasabiologicalmaterialcapableofselfreplicationthatcancauseharmfuleffectsinother
organisms,especiallyhumans"(AmericanIndustrialHygieneAssociation1986).
Bacteria,viruses,fungiandprotozoaareamongthebiologicalhazardousmaterialsthatcanharmthecardiovascularsystemthroughcontact
thatisintentional(introductionoftechnologyrelatedbiologicalmaterials)orunintentional(nontechnologyrelatedcontaminationofwork
materials).Endotoxinsandmycotoxinsmayplayaroleinadditiontotheinfectiouspotentialofthemicroorganism.Theycanthemselvesbe
acauseorcontributingfactorinadevelopingdisease.
Thecardiovascularsystemcaneitherreactasacomplicationofaninfectionwithalocalizedorganparticipationvasculitis(inflammationof
thebloodvessels),endocarditis(inflammationoftheendocardium,primarilyfrombacteria,butalsofromfungusandprotozoa;acuteform
canfollowsepticoccurrence;subacuteformwithgeneralizationofaninfection),myocarditis(heartmuscleinflammation,causedby
bacteria,virusesandprotozoa),pericarditis(pericardiuminflammation,usuallyaccompaniesmyocarditis),orpancarditis(simultaneous
appearanceofendocarditis,myocarditisandpericarditis)orbedrawnasawholeintoasystemicgeneralillness(sepsis,septicortoxic
shock).
Theparticipationoftheheartcanappeareitherduringoraftertheactualinfection.Aspathomechanismsthedirectgermcolonizationor
toxicorallergicprocessesshouldbeconsidered.Inadditiontotypeandvirulenceofthepathogen,theefficiencyoftheimmunesystem
playsaroleinhowtheheartreactstoaninfection.Germinfectedwoundscaninduceamyoorendocarditiswith,forexample,
streptococciandstaphylococci.Thiscanaffectvirtuallyalloccupationalgroupsafteraworkplaceaccident.
Ninetypercentofalltracedendocarditiscasescanbeattributedtostreptoorstaphylococci,butonlyasmallportionofthesetoaccident
relatedinfections.
Table3.5givesanoverviewofpossibleoccupationrelatedinfectiousdiseasesthataffectthecardiovascularsystem.
Table3.5Overviewofpossibleoccupationrelatedinfectiousdiseasesthataffectthecardiovascularsystem
Disease
Effectonheart
Occurrence/frequencyofeffectsonheartincaseofdisease Occupationalriskgroups
AIDS/HIV
Myocarditis,
42%(Blancetal.1990);opportunisticinfectionsbutalsoby
theHIVvirusitselfaslymphocyticmyocarditis(Beschorner
etal.1990)
Personnelinhealthand
welfareservices
Endocarditis,
Pericarditis
Aspergillosis
Endocarditis
Rare;amongthosewithsuppressedimmunesystem
Farmers
Brucellosis
Endocarditis,
Rare(Gro,JahnandSchlmerich1970;SchulzandStobbe
1981)
Workersinmeatpackingand
animalhusbandry,farmers,
veterinarians
Myocarditis
Chagas'disease
Myocarditis
Varyingdata:20%inArgentina(AchaandSzyfres1980);
69%inChile(Arribadaetal.1990);67%(Higuchietal.
1990);chronicChagas'diseasealwayswithmyocarditis
(Gross,JahnandSchlmerich1970)
BusinesstravellerstoCentral
andSouthAmerica
Coxsackiessvirus
Myocarditis,
5%to15%withCoxsackieBvirus(ReindellandRoskamm
1977)
Personnelinhealthand
welfareservices,sewer
workers
Extremelyrare,especiallyamongthosewithsuppressed
immunesystem
Personnelwhoworkwith
children(especiallysmall
children),indialysisand
transplantdepartments
Endocarditis
Withlocalizeddiphtheria10to20%,morecommonwith
progressiveD.(Gross,JahnandSchlmerich1970),
especiallywithtoxicdevelopment
Personnelwhoworkwith
childrenandinhealthservices
Myocarditis
Rare(Riecker1988)
Forestryworkers
Pericarditis
Cytomegaly
Myocarditis,
Pericarditis
Diphtheria
Echinococcosis
Myocarditis,
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EpsteinBarrvirus
infections
Myocarditis,
Rare;especiallyamongthosewithdefectiveimmune
system
Healthandwelfarepersonnel
Erysipeloid
Endocarditis
Varyingdatafromrare(Gross,JahnandSchlmerich1970;
Riecker1988)to30%(Azofraetal.1991)
Workersinmeatpacking,fish
processing,fishers,
veterinarians
Filariasia
Myocarditis
Rare(Riecker1988)
Businesstravellersinendemic
areas
Typhusamongother
rickettsiosis(exclud
ingQfever)
Myocarditis,
Datavaries,throughdirectpathogen,toxicorresistance
reductionduringfeverresolution
areas
Earlysummer
Myocarditis
meningoencephalitis
Rare(Sundermann1987)
Forestryworkers,gardeners
Yellowfever
Rare;withseriouscases
areas
Pericarditis
Vasculitisofsmall
vasa
Toxicdamagetovasa
(Gross,Jahnand
Schlmerich1970),
Myocarditis
Haemorrhagicfever
(Ebola,Marburg,
Lassa,Dengue,etc.)
Myocarditisand
Noinformationavailable
endocardialbleedings
throughgeneral
haemorrhage,
cardiovascularfailure
Healthserviceemployeesin
affectedareasandinspecial
laboratories,andworkersin
animalhusbandry
Influenza
Myocarditis,
Datavaryingfromraretooften(SchulzandStobbe1981)
Healthserviceemployees
Haemorrhages
Hepatitis
Myocarditis(Gross,
WillensandZeldis
1981;Schulzand
Stobbe1981)
Rare(SchulzandStobbe1981)
Healthandwelfare
employees,sewageand
wastewaterworkers
Legionellosis
Pericarditis,
Ifoccurs,probablyrare(Gross,WillensandZeldis1981)
Maintenancepersonnelinair
conditioning,humidifiers,
whirlpools,nursingstaff
Businesstravellerstoendemic
areas
Myocarditis,
Endocarditis
Leishmaniasis
Myocarditis(Reindell
andRoskamm1977)
Withvisceralleishmaniasis
Leptospirosis(icteric
form)
Myocarditis
Toxicordirectpathogeninfection(SchulzandStobbe1981) Sewageandwastewater
workers,slaughterhouse
workers
Listerellosis
Endocarditis
Veryrare(cutaneouslisteriosispredominantas
occupationaldisease)
Farmers,veterinarians,meat
processingworkers
Lymedisease
Instage2:
8%(Mrowietz1991)or13%(Shadicketal.1994)
Forestryworkers
Myocarditis
Pancarditis
Instage3:
Chroniccarditis
Malaria
Myocarditis
Relativelyfrequentwithmalariatropica(Sundermann
1987);directinfectionofcapillaries
areas
Measles
Myocarditis,
Rare
Personnelinhealthservice
andwhoworkwithchildren
Pericarditis
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Footandmouth
disease
Myocarditis
Veryrare
Farmers,animalhusbandry
workers,(especiallywith
clovenhoofedanimals)
Mumps
Myocarditis
Rareunder0.20.4%(Hofmann1993)
Personnelinhealthservice
Mycoplasma
Myocarditis,
Rare
pneumonia
infections
Pericarditis
Healthserviceandwelfare
employees
Rare(KaufmannandPotter1986;SchulzandStobbe1981)
Ornamentalbirdandpoultry
raisers,petshopworkers,
veterinarians
Ornithosis/Psittacosis Myocarditis,
Endocarditis
Paratyphus
Interstitial
myocarditis
Especiallyamongolderandverysickastoxicdamage
Developmentaidworkersin
tropicsandsubtropics
Poliomyelitis
Myocarditis
Commoninseriouscasesinthefirstandsecondweeks
Qfever
Myocarditis,
Pericarditis
Possibletoage20afteracutedisease(Behymerand
Riemann1989);datafromrare(SchulzandStobbe1981;
Sundermann1987)to7.2%(Conollyetal.1990);more
frequent(68%)amongchronicQfeverwithweakimmune
systemorpreexistingheartdisease(Brouquietal.1993)
Animalhusbandryworkers,
veterinarians,farmers,
possiblyalsoslaughterhouse
anddairyworkers
Myocarditis,
Rare
Healthserviceandchildcare
employees
Businesstravellersandhealth
serviceworkersintropicsand
subtropics
Endocarditis,
Rubella
Pericarditis
Relapsingfever
Myocarditis
Noinformationavailable
Scarletfeverand
otherstreptococcal
infections
Myocarditis,
Endocarditis
In1to2.5%rheumaticfeverascomplication(Dkert1981), Personnelinhealthservice
then30to80%carditis(Sundermann1987);43to91%(al andwhoworkwithchildren
Eissa1991)
Sleepingsickness
Myocarditis
Rare
BusinesstravellerstoAfrica
between20Southernand
Northernparallels
Toxoplasmosis
Myocarditis
Rare,especiallyamongthosewithweakimmunesystems
Peoplewithoccupational
contactwithanimals
Tuberculosis
Myocarditis,
Pericarditis
Myocarditisespeciallyinconjunctionwithmiliary
tuberculosis,pericarditiswithhightuberculosisprevalence
to25%,otherwise7%(Sundermann1987)
Typhusabdominalis
Myocarditis
Toxic;8%(Bavdekaretal.1991)
Developmentaidworkers,
personnelinmicrobiological
laboratories(especiallystool
labs)
Chickenpox,Herpes
zoster
Myocarditis
Rare
Employeesinhealthservice
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