Bronchial Carcinoma Respiratory Tract
of lung cancer [164–170]
. No differences in GST polymorphism have been discovered betweenactivesmokersandpassivesmokers
[171] .NAT2slowacetylatorsevidentlydis-
playreducedmetabolismofcarcinogenicarylamines.Inaddition,asigniicantassociation hasbeendemonstratedbetweenGSTM1allele0:GSTM1-0andlungcancerOR,1.41;
CI,1.23–1.61 [172]
.SmokerswiththeGSTM1nullgenotypehaveconsiderablyhigher PAH–DNAadductlevelsthansmokerswiththeGSTM1+genotype
[170] .Combinationof
GSTM1-0togetherwithtwoallelicvariantsofcytochromeP4501A1m2m2andValVal furtherincreasestheriskoflungcancerseeTable
5.3 in
Chap.5 .CombinationofGSTM1-0
andNAT2slowacetylationisassociatedwitha7.8-foldincreaseCI:1.4–78.7intherisk ofbronchialcarcinoma
[172] .Thenon-smokerisatgreaterriskasaslowacetylator,whereas
thesmokerisatagreaterriskasarapidacetylator,asafunctionofpack-yearsofsmoking [168,173]
.Otherauthorshavedisputedthisassociation.NAT1polymorphismisreportedto beimportantforthedevelopmentoflungcancer
[174] .p53mutationsareclearlyincreased
in smokers compared with ex-smokers and non-smokers OR, 9.08; CI, 2.06–39.98, whereasK-rasmutationsdisplayednodifferencesbetweenthevariousgroupsdeinedin
termsofsmokerstatus [175]
. EarlystudiesonETSexposureinwomenfocusedoncountriesinAsiaandtheFarEast:
increasedcancerriskswerereportedforETS-exposedwomenwhoalsoinhaledcarcino- gensfromcookingoilsathightemperatures
[176–178] .Asanadditionalfactor,theseETS-
exposed women may also themselves have been smokers in the past. Epidemiological studiesfromtheUSAandotherindustrialisedcountrieshaveshownaslightbutdetectable
riskincreaseforbronchialcarcinomainpassivesmokers:inNewZealand,forexample, relativerisksof1.3CI:1.1–1.5havebeenreportedforbothmenandwomenexposedto
passivesmokingathome,andof2.2CI:1.4–3.0forbothmenandwomenexposedto passivesmokingintheworkplace
[179,180] .Inafurtherstudy,theriskoflungcancer
morethandoubledforwomenwhoreported40ormoresmoke-yearsofhouseholdexpo- sureduringadulthoodOR,2.4;CI,1.1–5.3,or22ormore-smoke-yearsofexposuredur-
ingchildhoodoradolescenceOR,2.4;CI,1.1–5.4 [181]
.Recentresearchhasconirmed thatnever-smokingwomenexposedtoETSfromspousesareatincreasedriskoflung
cancercomparedwithunexposednever-smokingwomenOR,1.29;CI,1.17–1.43 [161]
. ThepossibleassociationbetweenETSexposureduringchildhoodandthedevelopment
ofbronchialcarcinomainlateryearshasbeeninvestigatedinamulticentrecase-control studyFig.
9.8 .Whiletheassociationwasrejectedonthebasisoftheresults
[182] ,weak
evidenceemergedforapositivecorrelationemergedbetweentheriskoflungcancerand exposuretoworkplaceandspousalETS
[182] .
OtherstudieshavereportedlowerlungcancerrisklevelsforpassivesmokersOR,1.3; CI, 0.8–1.8
[183–185] . The risk of lung cancer was increased where ETS exposure
occurredatayoungage:theriskwashighestforchildrenexposedbelowtheageof7years OR,3.46;CI,1.80–6.65,butwasalsosigniicantforchildrenagedbetween7and14
years OR, 3.08; CI, 1.62–5.57 and for adolescents aged between 15 and 22 years OR,3.10;CI,1.52–6.31
[186] .Similarly,highriskrateshavebeenrecordedinwomen
whosehusbandssmokedparticularlystrongRussiancigarettesknownas“papirosy”OR, 2.12; CI, 1.32–3.40
[187] . The data recorded in ETS-exposed children were not con-
irmedinanotherstudy [182]
orthelungcancerriskwasincreasedonlyforwomenexposed
toETSintheworkplaceOR,1.5;CI,0.8–3.0 [188]
.Inacomparisonof3,138ETS- exposednon-smokingwomenwith1,747smokingwomen,deathfrombronchialcarci-
nomawasrecordedin0.2ofnon-exposednon-smokingwomen,0.9oftheETS-exposed non-smokingwomenand8.0ofthewomenwhosmoked,indicatingthatETS-exposed
womenhada4.5-foldhigherriskoflungcancerthannon-exposednon-smokers [189]
. NotallstudieseverconductedtoassesstheriskoflungcancerwithETSexposurecan
beaccepted [190]
.Whileanevaluationofnumerousstudiesindicatesthattheexcessrisk oflungcanceris24
[190] ,itisrecommendedthatallthedatashouldbere-analysedwith
Odds Ratio 95 CI
0.1 1
S D1
D2 D3
GB F
P2 P1
ES I1
I2 I3
10
0.60 0.55
0.45 0.95
0.62 0.60
0.33–1.08 0.19–1.59
0.25–0.82 0.38–2.35
0.27–1.40 0.17–2.12
0.94 0.82
1.08 0.77
1.09 2.09
0.78 0.51–1.75 0.51–1.33
0.42–2.81 0.31–1.92
0.53–2.26 0.71–6.11
0.64–0.96
Odds Ratio 95 CI
S D1
D2 D3
GB F
P2 P1
ES I1
I2 I3
0.1 1
2.29 2.01
1.35 2.04
2.03
0.73 1.39
1.14 1.12
1.10 0.72
1.22 0.88
0.65–8.07 0.71–5.67
0.43–4.28 0.71–5.80
0.76–5.38
0.32–1.66 0.30–6.48
0.35–3.56 0.46–2.66
0.38–1.36 0.66–2.23
0.40–1.95
0.88–1.47
10
Fig. 9.8
RiskofbronchialcarcinomaoddsratioORassociatedwithpassivesmoking,basedon studiesinvariouscountries
[170] .Upperpanel:ETSexposureduringchildhood;heterogeneity
testbetweencentres:c
2
=10.45,df=11,p=0.49.Lowerpanel:Exposuretoworkplaceorspousal ETS;heterogeneity:c
2
=6.76,df=11,p=0.82.Ovoverall
caution.SimilarriskincreaseshavebeenreportedforETS-exposedwomen24and men34
[191] .Accordingtoanothermeta-analysisofETSexposureandlungcancer
basedon14publishedstudies,theincreaseinlungcancerriskis39fornon-smoking womenwhosehusbandssmoke25cigarettesday,and91whereETSexposureoccurs
predominantlyintheworkplace [192]
. InETS-exposednon-smokers,additionalradonexposureisreportedtobeparticularly
dangerousintermsofthedevelopmentoflungcancermaximalORincreasefrom1.08 [0.8–1.5]to1.44[1.0–2.1]
[193] .