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ETS - Environmental Tobacco Smoke Report from a workshop on s effects and exposure levels March 15-17, 1983, Geneva, Switzerland Editors: R. Rylander,, Y. Peterson M.-C. Snella European Journalof Respdrat®ry Disemses Supplement N'u.133, Vol. 65, 1984 MUNKSGAARDLCDPENHAGEIti

Contents PREFAEf ....................................... S IN'I'RODUCIION' ................................ 7 Rq.o Rylou+. 1. EXPOSUR.E LEVELS .............................. 9 1.1. Environmentai, tobscco smoke mcasureaunts: tetro:pect and Procpea . N.d.i+ V. F'mr 12 In-micg+tioru on che effect of regulating unoking on IeveU of indoor roUution utd oc the perception of hctilch and comfort of office .orkera Tf+.1.• D. .tar>5.q ..r F.Lc N. Srrr-,q 1.3. Analytieal chcmicsl methoda for the detection of environmental tobaeeo tmoke constituent, . ., . . . . . . . . . . . . . . . . . . . . . . . . . . . R.d.- A. Jmkm s.d Mi<6w1 R. Gw*>:m 1.4. CArbon awnovde as an indcs of environmental'i robac,o smoke espo- ture ..................................... jksasffle At: iisaade 1.5. D;in+•~ion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . it:p7o.^.tura: Alr.T:-j Jarru oid Cornr.iYt J: Lrttb , i~~-- "._7 '. ~; i:^~r`::1=`:I'S LN H U N ~ 11N:i . . . . . . . . . . . . . . . . . . . . ~ i. }iz'tf-l;vcs ot scicecd tobacco smoke uposure nurkers ., .... ... Cc+r _1 J L,rLb hfcu.;remcnt usd cstunation of smoke dosagc to non-smokcrs faom,envi- ronmcntil tob'acro smokc . . . . . . . . . . . . . . . . . . . . . . . . . . MorTV J. fo,,u d .tif:tb.d A. H. R..ll 23. Vrlidit7 of quesootusaire data on smoking and other eaposures, vith speci.l rtfcrnncc to env-ronmentaJ tobracco tmoke . . . . . . . • . • • • • • • GarM Pnsbel.n 2.4 Duc•.u•.iar. . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . Ripportcun Ro3+- .-4, Jmtrw .ua Ta..adar D. Jr.+s:xt 9 17 33 47. 61 63 Fj 68 76 E1

1. FFFEC'I5 IN HUVJW5 .............................. 953.1. Doca eaviroonmeatal tobaeco smoke aflcct lung function? ........ 95, dj1r+r A.& 32 Fc.iroameatal oobaccco smoke and puimon.rT Eunction tadn; .... 88 .4,.e6+V M. Gr-rto- 3.3. The e$ects of ca.ironmentalitobacco smoke espo.urt and gtas sto.a on daily peak floa rates in asthmatie and non- asthmatic fatniliea ..... 90, M:rdwl D. L.i+sYrr 3.4. Acute eEfects of enviroamennl tobacco smoke . . . . . . . . . • . . . . 98 Etm.rt& ri.drr 3.5.. Respiratory symptoma in the children of smokers: an overview ...... Paniu:E' G. Ho(t aud Knm J. Trnnrr 3.6. The cfTea, of environmental tobacco smoke in two urban commur.itics in the wcst oi Scotdand . . . . . . . . . . . . . . . . . . . . . . . . . . . . Cl&-r<t R. Gillir; Darwd i -, ir. Virror .lf. Hasaborni ane Prin 6o)ii 3.7. Eavironmcntal tobacco smoke usd' lung cancer . . . . . . . . . . . . . RVo Rylosdrr 3.9. Discuaion . . . . . . . . . . . . . . . . . . . . . . . Rapporteuts: G+rm. Pmberw ai.d Anrbp.j M. Caurlr+se 109 127 134 4. WORK GRCU'P RESULTS . . . . . . . . . . . ... . . . . . . . . . . . . . . 13' . 4.1. Expos ure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131, Churman and rapponcur: .NdwR W. Firrr CZ Effects on health . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140 Chairman : Mitbar! .i, Ff. R.uirll Rappc rteur: .4ficb..! D. Lberuz 5. WORKSH'OP PERSPECTIVES . . . . . . . . . . . . . R.rsnar RJAordr+ 6. GENERAL REFERENCES ON STUDIES OF ENVIRONMENTAL TOSACCOSMOKE ............................... 143

Preface a The Second Workshop on Environmental Tobuxo Smoke .ith particular reference to effects ande:poaure levels was held inGeneva, Svitarland. March 15•1J, 1983. The workshop was organined' by Ragnar Rylander M. D. University of Gothcnburg. S.eden, and University of Gtneva, S.ritsca- land, together with Yvonne Peterson and A!arie-Claire Snells, rucarch assistants and Isabelle Gourdon. It was supported by a grant from the Tobacco Institute, Waahir.gton D. C., to the University of Geneva_ The symbol l for the 'uorkshop was desrgned by Anane Catry:, The participants in the VCorkshop arc Lsted' belw. Dom:n~~ ~:. .1v:.du. .... • r::,:r.e I :ual::: :i.:er,ee1, ii:c 1' 0 Itoa 30, Sitort Ilills, Ncw )cncv 0'U'd - USA B~orn Dake Depatsmenr of Clinical! Phiniology Sahlgrcn's ijospital 413 45 Gothenburg - SVCEDEN' Anthony Ai. Cosentino St. Jt.r-,'s I Insr•rtal and'.Mcd:cal (=.ntcr -450 StarsvamSrrccr San Franc:sc.-), Calrsorn:a 9s"',1" - USA Melvin W. First Department of Environmental Health Sciences Harvard University 665 Huntington Avenue So.ron, Mauachusuts 02115 - USA Csarles R. Gillis Greuer Glasgow Health Board West of Scotland Cancer Surveillance Unit RuchiP. Hospital Glascov, G20 9NB - SCOTLAND Roger Gutllerm Centre d'Etudes ct de Recherehes Techniques sou-marines D.CA.N. 83800 Tuulbn Naval - FRANCE Patrick G. Holt C!+n:ral Immunolqi- I:czcarch lintr Pnncess Musarcr Child'rcn's Meorcal Rcsearch Foundation c/o Pnneess `{argaret Hospitallfor Chi;d.ron G P 0 Box 184 D Perth, Western .luatra',ik - AL'$TRILLtA Horst Fluckauf Freie Unrvrntrac Berlrn Unrv.,nrtitsklnnk,:m Stegliu \Icc:' FJinik und Yoltklrn:kum Hrndcoburgdamm 30 1(RlU Berlin a5 - WFST GERNGV,I' ~ lV N 0~ t...

Ma,r= J. jtr„is Iastirutc of Ps- ::aiatrv Addicvcn Reseireh Unir I C I Dersaurit Hil f London SE5 BAF - E:tiGLA/`D RoIIer A- Jenkana Bio/Orginic Analnia Section Analyttic Cheasisay , Di.ision Oc: '.tidgc National Laboratory PObo:X Oak Ridge. Tennessee 37820 - USA Michael D. Let+o.ii: Division of Respiratory Sciences The Universii7, of Arizona Fiealth Sciences Center 2 College of Medicine Tuoon, Arisona 84'24 - USA Cotneliua J. Lynch Franklin Inatirute PmGe7 Analysir Center 1320 Fen.ick Lsne Silvei Spring, Maryiand 20910 - USA Goran Penhagcn National Insrucutc of Envtronmenral `Icdi- csne Box G0'.08 104 0` Stockholm - Svc'EDE` Michael: A. H. Russcll !. ,a~~i . ~ i'-. . ..... 1(D1 L)cnuurk Hill London SE5 BriF - ENGLAND Theodor D. Srcrding, Simon friscr U,•nrversrn Deparsmenr nf Compurang Science: '_91!- j`-- Burnabt•: Britrsh Colombia - CA'NAD.1' V5:1 lSu Annctv Weber Deparvnenr of Hygiene and Work Phirsio- lo® ETH-Zentsurn 8092' Zarich, - SVCTf'ZERLAND Andicss Z,obcr Inatiture for Oecupational and Social Medc- eine and Polielihic for Oetupational Diu- usea University of Erlangen-N'tlrnbcrg Sehillerstr. 25/29. 8520 Erlangen - WEST GEP-MA.`JY ORGANtZLNG COMNTTTLL Ragnar Rvlander Department of Environmental Hvgiene University of Gothenburg P O Box 33031 400' 33 Gothenburg - SWEDEN Yb:, n:... L•nt+cntrv ot Gothcnburg P'O Boc 33031 400 33 Gotnenburg - SWEDEN Marre•Clatre Snc11a Environmental \ledicinc Unit Institute for Social and Prevcnrtve Nkdicinc Quar Charlcs-Px~,e =- Iaff C,c-icva - ~A['1TZERL•1ND

3.6. The effect of environmental tobacco smoke in two urban communities in the west of Scotland CItAltyLt R. (in.Lti, DAVID J. Hoi.L, VlCTOR M. HAiVTNORNt AND PLTLR BoTLZ txrROatXTtoN The question of whether environmental tobaceo smoke (ET$) can damage health has not yet been clurly anwered. It is known that a lighted cigarette emits more aidettzum smoke than mainstream and that the smoke ava:lable for involuntary inhalation contains aubtt.ntial amounu of carbon monozide, ur, ttieotine, benra(a)pyrene and other earci- nogens, and oiides of nmogen (1). Studies from Japan (2) and Greece (3) hsvc suggested that non-smoking wives of heavyy amokers have a t+.o-fold incresscd risk of' lung canccs when :orr- xrtd with non-smoking vivea of non-smokers. In eontrzxt, analysis of data from the prospective study of the Amc- rican Cancer Society .olunteen (4) has sug- gested that very little, if any, incrraed risk of lung cancer esisw when non-smoking women married to smoking husbands and non- amokers married to non-smoking huabandaarc compared. The ptrscnt trudy has been carried out in a defined population group in an area of high incidence (5) of lung cancer with t preciselyy defined population usse.. It reports lung cancer data on both males acid females.. NATLRiAIi AND 1IlTMOtK The study comprnes 16,171 apparently healthy individuals aged between 43 and 64, resident in Renfrew and Paisley, two urban arsaa in the West of Scotland. They took pan in a multi- phaaic screening survey for eardiotsspirstory disease between 1972 and 1976: This repre- sentec: a re.sponse rate of 80 % of those ran- domiy sampled from the resident population. Lktailr ot this survey, have been descr,:xd by, VMH (6)~ Information on each rapondent't smoking habits and their experience of symp- toms of respirstory and cardiovascular disease vest colleete& using a self-completed ques- tionnaire, earefully checked ar the time of attendance ac the screening unit. The diagnosis of cancer in each individual has been checked in the West of Scotland Cancer Registry and follow up for mortality ar ied out by record7inkage (7) with data from the Regi.tnr General for Scotland. Follov up is complete until 31 December 1982. As members of the same household attended the ureening unit, it was possible to identify smoking and non•smoking p:rtners of smokers and non-smokers. 'Ihese were allocated tu categories defined so as to reprtsent an increasing measure of tobacco exposure. NOTICE This moterial' may ba ptntetteQ by copyright Mw (T1Ub 17 U:S. Coje).

122 . . Ia ' TA®1! E 1L N.nir• ..e pno..ur uJ.r:.:..ir I) ~..). Ns.W.• .f a.1n.1..4 .k+mdfq ++..wa - 16; ,t 77 Na.1.r a:clni per.ns#rju x+aaJ - d, T?d (n-s..brr sa6l.!) Ci"or7, M.lc N K Fsault N' K Coatsol, 517 12.7 323 12.9 ET5 esQo.ure 310 7:6 1394 34.3 Smoking 1395 34.3 310 7.6 Smoking + ET5 ciposurc 1645 45.4 1834 45.2 . Toa1 4067 100 4061 100 TABLE 2Ar n..4ctL.J pv.n.fa..1«t~ rrp...r/ r.rpr.r.) +1'7-- k 1 °114'r1. Arw ne .j.B .:eb. .ai jn.p rif.io Respir.tory symptom Control4 ETS ezpoaurc Smoking Smoking T @75 ssposurc Iafeetad spit 3.3 4:2 11.1 12.5 Petaiatent spit 10.1 14.5 • 33.9 39.6 Drpoon 7.4 11.90 14.0 13.4 H7Pessectetion 7.2 11.90 20.6 21.6 llumber of indiriduaL 517 7 310 1395 1845 ' P valtx < 0.05 for eompatison of control and ETS espasurs group TABLE 3. Ar Tpn.r'tJ rrn=n). Arr nv .f dF .iitlb ..rl lnwp.. F..rIn Smoking Rnpirntor7 ET5 + ET5 symptom Controls exposure Smoking exposure Infcaed spit 21 2.B 10.0 9.1 Penutcnt spit 6.3 7.2 239 23.1 Dyspnoea 9.7 14.7 •• 16.2 18.3 H7Pcrsccsctton 3.9 4.8 17.u 1711 Numbcr of tndinduaG S23 1304 310 1834 ••R value < 0.01 (or compsnsomoi control and E'S exposure group 9;

t 123 1. Convol-an indi.idual who dou not smoke and who lives at the sarne sd'dresi as anochcr individual who does not smoke. 2 ETS e:poscd-an individua7 who does not smoke but who lives at the same addren aa anotbr.r in6' -idual who does amoke. 3. Smoker-an indi+.idual who is a smoker or who has given up smoking up to five years ago but who li.ea at the same address as an iudi.nduat who does not ttnolte. 4. $moker and ETS atpoacd-an individua, who ls or who haa been a gtssoker up to five Ya.n ago aad who lis at the same addrea at an iadividual who aLo timokes. All individuals in thcae categories were aged 45-64 at the time of the vsrvey. Es-tmokers who had given up smoking for five years or more have been escluded from this analysis. The number of males and females in each of the categories defined above is shown in Table 1. 97:6 % of the pairings were male/female partnerships. The prevalence of self•rcported respiratory symptoms (6) found at the survey is ahowmfor each eategory fon males itr Table 2 and for femalu in Table 3. For each measure, infccted spit, persistent spit, dyapnoca and hrpenccrt- tion an increasing do.e response reJationahip was evident in maict. Tuc prevalence of these four symptoms vaa slightly higher in the exposed to ET5 than in the controls. This ohaervation was conailtent in both rnales and fcrnales. The pnevalence of cudiovaactiil.r symptoms found at the time of the survey ia shown in Table 4. In femslea angina and ECG abnorm.- lities (6) were slightly more common in the group espoaed' to ETS than ib the eontrols, although the rnagnitude of the diffcreaces was anall. The reverse trend vu aFw.n for malea. Male mortality for the different categories is abown in Table S. A dose-responsc relation- ship vaa found for lung caneu rising from a rate of 4 per 10,000 for the control poup to 13 per 10,000 for the group ettpo.ed to ETS to 22 per 10,000 for the smoking group and 24 per 101000 for tsu smoking group also etpo.cd to ETS. The ratea for other smoking related cancers and for smoking rel.tcd'diseYaa (8) did not shoo^w a difference betwcen the control and groups exposed to ETS except for the rate for myocardial inf.rction (ICD410) which was TABi E 4. Aj+ dioali•lsnd p....4wn .~,.rdiwarr.ln gwnr.., 1rj t.+.j.7. Pn nor .J.t/ rirb.. wcb jnwP Cardiovaacular .aymptom Controla E I5 acpt»urc Smoking Smoking t ETS exposure Adi/t!! Angina 6.6 6.4 9.6 12.3 Mapr ECG abnormaliry 1.4 1.3 20 Z.2 Fr..k, Angina 4.2 ' 5.3 5.4 6.1 Mapi ECG abnormaGrv 014 0.6 0.6 0:5

124 TABLE S. .4smidvp a..i.>liwJ'w.ri'rJ nrr p.. /'O;00d'Ij s..4.98 ..nevJ Al.ir G+»c of death Coeaob BT3 t~awue Sasokint signown + E!S s9owc AJ' esu.a 91 90 156 156 Lang a 4(2) 13(4) 22(30) 23(4) Odser CA 12(6), i(2) 3"), 22(41) w (410), 31(16) 43(14) 60(84) 46(64) ¢ID (411-4) 4(2) 0(0) t1(1S) 14(23) CVD 1U(S) 3(1) 12(17) 16(29) Othen 31(16) 23(7) 27(38) 3S(64) Satoking nt]ated 7S(39) 77(24) 140(19S) 1'4(247) Non•unokiug Rlatedl 1'6(8) 13(4) 17('27), 22(40)' Total number of durhs 47 28 21'8 287 Figutn in parentficsu ue the numbers of dcarha TABLE 6. Ass.Jqd r-lerdiJ.d .wr.Gij ntar pn 10,000 Jt7 f.akrnj rsaj.7 Fiw+G+ Gatue of deaths Controle ETS c:poaune Smoking Smoking + ETS cupoaure All eausew 40 SB 87 77 Lung Ca Other Ca MI (410) IHa (41164) CVD C4hen Smoking rclatcd Non-smoking related Total numbcr, of dcaths 4(2) 19(10) 4(2) 0(0) 2(1) 12(6) 1SO) 23(12) 21 4(6) 24(33) 12(117'), 1(2) 4(S) 1 1'3(18)1 30(42): 27(37): 81 7(2) 26(8) 19(6) 3(r) 7(2) 26(8) SS(17) 36(11) 27 6(11). 22(40) 21(39) 2(4) 9(16) 17(31) S2(96) 24(K) 141 Figures in p.rcathcsia arc the numben of dcaths TABLE 7: Pnrr*ujw nw1iq 1S w.wr errnrtd p- 1ej ETS Smoking + ETS Controls uposuee Smoking exposure .%taln Fernalta 0' 0 41.8 57;3 0 0 46.5 53.4 N C N Li CJ1 ~ N ~ CJi 1 11

i I slightly higher in the group exposed to E75 than in the controls. Female mortality is shovn in Table 6. All causes mortality is highcr, in the group exposed to ETS than in the controls. This was not the case for lung cancer although mortality from myocardial infarction,vas higher in the group exposed to ETS when compared with the con. trols. Division cf all diatascs into those considered smoking and non-smoking related (8) pro- duced a higher ratc in the group exposed to ETS when compared with controls. On account of the apparcntlr unusual relr- tionaliip between lung cancer risk and tobacco consumption in the West of Scotland (9) the amount smoked by individuals in the defined categories is shown in Table 7. In the smoking group also exposed to ETS 57.3 % of tnales and 53.4 % of females smoked more than 15 ciga• rettes per day. This compares with 41.8 % of tnalts and 46.5 % of females in the smoking group. DriClJatrON Insuf£ocicnt time has elapsed since the comple- tion of the recruitment phase of this study (1976) for sufficient numbers, either a inci- dent eues of cancer or of other discases, to allow firm conclusions to be based on the results. The results have been expressed as annual age standardised rates per 10,000, aa the total number of incident cases and the number of deaths is small in the control'and ETS e:apo- sure groups (Tables 5, 6). The results relate to only 8,128 of the 16,171 individuals who attended the multi•phasic screening unic(50 %). Sornr of this discrepancy can be accounted for by those living alone, those living with a oartner, ourwith the age ranSe, and those living with a partner who has not attendcd. Thosc who have been es- 12S smokcn for five years or more .+cre also excluded from the analysis As t}ierc is rtilll doubt whether these groups account for the total discrcpancy; givcn an initial response rate of E0 %, the authors require to continue their investigation of this apparsnt dtscrepancy. Thit study has unique featuru which allow even preliminary, results to be of interest. These an: 1. The atudy has been carried out in an area with the highest national i»cidence rate of lung cancer rceatd'ed (S). 2- It is a prospective cohort study eirtied out in a gcognphically, defined population whose mertsbern are homogeneous by social class and ethnic group. 3. Other rt:porn (2, 3. 4) concentrate on females. ntis study includes both sexes. 4. No questions concerning exposure to ETS .erc asked, thus avoiding the bias inherent in self-reported asaenments of partnership doaage. Glven the strength of the epldcmlologieal association bsrveen cigarette ~asokin= and lung cancer, It is this d3sease rather than ischaemic heart disease that would be firtt to appear in excess in the cohort if a doae response relationship existed, especially as the respon- dents were all apparently healthy at the time of aereenirtg. tn a~p, tLe.en.a of lung canar,oavrrirsg iti etlti~ne- tet~s;nere fosuid inoie fretltaenc!'y in thbie°e:poaed to E'I7(4/31A) tga:i' iet the oon- teoh !2/517) (Table 5)j No dose-responae rela- tionship was apparent in females for lung cancer deaths though an effect .u present when all' smoking related (8) deaths including deaths from myocardial infarction were taken into account (Table 6):. These findings may be supported to an extent by the dose-response relstionship thsn exist• for self-reported rupiratory symptoms