Passive Smoking During and After Pregnancy
Thestudypopulationcomprised183womenconsecutivelyenrolledat20–24weeksof pregnancyatthetwoantenatalcareunitsandultrasoundbiometricmeasurementsoffoetal
bi-parietaldiameterBPD,abdominalcircumferenceACandfemurlengthFLwere performed.Also,serumcotinineconcentrationwasdeterminedat20–24weeksofgesta-
tion by gas chromatography with mass spectrometry detector GCMS to assess ETS exposureduringthepreviouseveningandthemorningofthesamedaybloodcollection
at1,200–1,300h.ETSexposurepassivesmokingwasassumedtooccurwhenthelevel ofserumcotininerangedfrom2to10ngml.Theauthorsdemonstratedthatastatistically
signiicantnegativeassociationwaspresentbetweentheBPDandserumcotinineconcen- tration.Asimilarassociationwasidentiiedforsubjectswithserumcotinineconcentra-
tionsbelow10ngmlcorrespondingtopassivesmokingp=0.06.Aftercontrollingfor pregnancyduration,maternalpre-pregnancyweightandinfant’sgender,wefoundthat
serumcotininelevelsat20–24weeksofgestationwasinverselyassociatedwithinfant birthweightp=0.004.Forthesubjectswithserumcotininelevelsbelow10ngml,a
borderlineassociationp=0.09withinfantbirthweightwasfound.Itwasconcludedthat maternalexposuretotobaccosmokeinearlypregnancy,asmeasuredbyserumcotinine
concentrationsat20–24weeksofgestation,adverselyaffectsfoetalBPD [75]
. InchildrenwithlowbirthweightfollowingETSexposure,thevasodilatorresponse
followingforearmcuffocclusionandreleasewasstillreducedatage9–11yearscompared withthatinnormalbirthweightchildrenborntonon-smokingmothers.Thephysiological
vasodilatorresponseistriggeredbyNOreleasefromendothelialcells [76]
.Amongother things,thisharmfuleffecthasitsoriginsintheprenatalperiodandisrelatedtothesmok-
ingbehaviourofthemother-to-beduringpregnancy;itmanifestsitselfasearlyastheirst decadeoflifeasapreludetolateratherogenicchanges.Evidently,inthedevelopmental
phasescharacterisedbyrapidgrowthsuchasthefoetalperiod,theendothelialcellsalso undergoadversechangeswhichlimitphysiologicalfunction
[77] .
Urinarycotininelevelsweredeterminedin199ETS-exposedchildrenbetweentheages of4monthsand4yearswithobstructivebronchitis.Comparedwithhealthychildrenofthe
sameage,urinarycotininelevelswerefoundtobe5.7µgl,insteadof4.4µgl.Theriskof developingbronchitiswasincreasedinlinewiththeextentofpassivesmokingandtherise
inurinarycotinine.Thisriskwasincreasedthreefoldataurinarycotinineconcentrationof 20 µgl
[78] . Similar results have been reported in 69 children
[79] . The incidence of
Nicotinengml Cotininengml
Activesmokingwomenn=36 19.2
4.9 6.3
4.0 Newbornsofactivesmokingwomen
2.4 0.9
2.8 0.8
Passivesmokingwomen
a
n=23 3.2
0,8 0.9
0.3
b
Newbornsofpassivesmokingwomen 0.28
0.05 0.6
0.15 Non-smokingwomenn=35
1.2 0.4
0.3 0.06
Newbornsofnon-smokingwomen 0.4
0.09 0.26
0.04
Table 9.4
Hairconcentrationsmean±SEMofnicotineandcotinineinwomenandtheirnewborn infants
[56]
a
Deinedasregularandsteadygestationalexposuretootherperson’scigarettesmoke,eitherat homeorintheworkplace
b
p0.01whencomparedtonewbornsofactivesmokingwomenandnewbornsofnon-smokers
spastic bronchitis increased by 14 where maternal tobacco consumption was 4 ciga- rettesday,andby49at14cigarettesday
[80] .
ETS-inducedhypoxiacauseschronicpulmonaryhypoventilationinchildrenattherisk ofSIDS
[81] .Inresponsetohypoxia,adeclineinmitochondrialcytochromeoxidasehas
been observed in conjunction with reduced succinate oxidase and palmitoyl carnitine capacityduringcirculatorycollapse.Thebrownmitochondriaofadiposetissuewereacti-
vatedinresponsetoincreasedbloodlow,causingthetissueapparentlytotakeonabrown discolouration
[82] .Thehypoxiahypothesisisthusamorelikelystartingpointforfoetal
andpostpartumharmfuleffects,aheadofnicotineanditsmetabolites. Althoughsofardemonstratedonlyinanimalexperimentsrats,exposureofpregnant
animalstosmokecausesthedevelopmentofhypoplasticlungswithfewerorlargersacculi andareducedlungsurfaceareaforgasexchange.Transposedtothesituationinhumans,
thiswouldmeanthatthepulmonarychangeshavetheirorigininuteroandarethusconsis- tentwithreducedrespiratorycapacityatbirth
[52] .
Overall,ETSexposureisharmfulforpaediatricdevelopment,startingwiththesmok- ingbehaviourofthemotherandtoalesserextent,ofthefatherbeforebirth,butofboth
parents after birth. Exposure of children to ETS in rooms where smokers are actively smokingshouldbeviewedassimilarlyharmful.
Maternalsmokingduringandafterpregnancyexertssubstantialharmfuleffectsonthe healthoftheneonateorinfant
[83] :smokingcessationshouldthereforebeencouragedin
themothereitherbeforeshebecomespregnantorduringtheearlyweeksofpregnancy.