Coronary Heart Disease Cardiovascular Disease
CAEPAand1.23ScientiicCommitteeonTobaccoandHealth,SCOTH [90]
.Platelet aggregation induced by tobacco smoke products has been proposed as the mechanism
responsibleforthisnon-lineardose–responseanomaly [90]
. ThepurposeofstudiesbyPitsavosetal.performedinGreecewastoinvestigatethe
associationbetweenpassivesmokingandtheriskofacutecoronarysyndromesACS amongnon-smokers
[91] .Intotal,848patientswiththeirsteventofACSand1,078car-
diovasculardisease-freematchedcontrolscompletedadetailedquestionnaireregarding
1.5 1.0
P = 0.006 for linear trend
1.23 95 CI,
1.13−1.34 1.29
95 CI, 1.21−1.42
1.00
0.5
Level of Exposure to cigarettes [cpd] Relative Risk
1
−
19 20
1.00 P = 0.01 for
linear trend 1.18
95 CI, 0.98
−
1.42 1.31
95 CI, 1.11
−
1.55 1.29
95 CI, 1.16
−
1.43
1.5 1.0
0.5
Duration of Exposure to Smoking [years]
1
−
9 10
−
19 20
Fig. 9.5
Relativeriskof coronaryheartdisease
associatedwithpassive smokingamongnon-smokers
[84] .Numberofcigarettes
smokedaboveandduration ofexposurebelow.95CI
95conidenceinterval Studiesincludedinthemeta-analysis
Number Relativerisk95CI
p-value Allstudies
18 1.251.17–1.32
0.001 Peer-reviewedstudies
15 1.251.17–1.33
0.001 StudiesusingdeathfromAMIorCHD
asanoutcomemeasure 14
1.241.17–1.32 0.001
Studiescontrollingforimportantrisk factorsforCHD
10 1.261.16–1.38
0.001
Table 9.5
Relativeriskofcoronaryheartdiseaseassociatedwithpassivesmokingamongnon- smokers
[84]
their exposure to environmental smoke. Two hundred and ninety-seven 35 of the patientsand25924ofthecontrolsweredeinedasnon-smokersandpassivesmokers,
respectively.Aftercontrollingforseveralpotentialconfounders,theresultsshowedthat non-smokersexposedtocigarettesmokeincreasedtheriskofACSby51OR,1.51;
95CI,1.21–2.99comparedwithnon-smokersnotexposedtosmoke.Itwasestimated that34coronaryeventsper134subjectswouldoccurasaresultofpassivesmokingduring
their lifetime. Consequently, this study supported the hypothesis that passive smoking increasestheriskofdevelopingACS
[91] .
A British study examined the associations between a biomarker of overall passive exposuretotobaccosmokeserumcotinineconcentration,andriskofCHDandstrokeby
theuseofaprospectivepopulation-basedstudydesigntheBritishregionalheartstudy [92]
.Intotal,4,729menin18towns,whoprovidedbaselinebloodsamplesforcotinine assayandadetailedsmokinghistoryin1978–1980,itwasshownthat2,105menwhosaid
theydidnotsmokeandwhohadcotinineconcentrations14.1ngmlweredividedinto fourequal-sizedgroupsonthebasisofcotinineconcentrations.Relativehazards95CIs
forCHDinthesecond0.8–1.4ngml,third1.5–2.7ngml,andfourth2.8–14.0ngml quarters of cotinine concentration compared with the irst ³0.7 ngml were 1.45
1.01–2.08, 1.49 1.03–2.14, and 1.57 1.08–2.28, respectively, after adjustment for establishedriskfactorsforCHD.Hazardratiosforcotinine0.8–14.0nu³0.7ngmlwere
particularlyincreasedduringtheirst3.73,1.32–10.58andsecond5-yearfollow-upperi- ods1.95,1.09–3.48comparedwithlaterperiods.Therewasnoconsistentassociation
betweencotinineconcentrationandriskofstroke.Inconclusion,thisstudyindicatedthat thestudiesbasedonreportsofsmokinginapartneraloneseemtounderestimatetherisks
ofexposuretopassivesmoking.Furtherprospectivestudiesrelatingbiomarkersofpassive smokingtotheriskofCHDareneeded
[92] .
However,allETS-studiesclearlyshowthatETSrepresentsasmallerriskthanactive smokingintermsofthedevelopmentofCHD.Theindingsfromacancerprevention
studyindicatethattheriskofCHDforsmokersis1.7timeshigherthanfornon-smokers, andforwomenthefactoris1.6
[93] .Relatedlifestylevariablesinpassivesmokersmust
betakenintoaccountinaconsistentmanneriftheconclusionsreachedaretobeusable [94,95]
.Variousstudiessuggestthatpassivesmokersdifferfromnon-smokersintermsof dietlessfruitandvegetables,morefatandmeat
[96–99] .ETScausesincreasesinCO
andCO-Hb,whereasheartrateandbloodpressureriseonlyminimally [37]
.