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Passive smoking and cardiorespiratory health in a general population in the west of Scotland r DaKid J Hole, Charles R Giliis, Carol Chopra, Victor M Hawthorne Abstract Objecrive-To assess the risk of cardiorespiratory symptoms and mortality in non-smokers who wene passively exposed to env'uotunental smoke. Desige-Prospective study of cohort from general population first screened between 1972 and'1976 and followed up for an average of 11 •5 years, with linkage of data from participants in the same household. SettirtQ-Renfrew and Paisley, adjacent burghs in urban west Scotland. Sybjeetr-15399 Men and women (80'/% of all those aged 45-64 resident in Renfrew or Paisley) eomprised the original cohort; 7997 attended for multiphasic screening with a cohabitee. Passive smoking and control groups were defined on the basis of a lifelong non-smoking index case and whether the cohabitee had ever smoked or never smoked. Main orrtcmrte nteasure-Car+diorespiratory signs and symptoms and mortality. Results-Each of the eardiorespiratory symptoms examined produced relative risks >1-0 (though none were signi6cant) for passive smokers compared with eontrols. Adjusted foreed exptratory volume in ooe second was sigaificastly lower in passive smokers than controls. All cause mortality was higher in ' passive smokers than controls (rate ratio 1~27 (95% confidence interval 0•95 to 1•70)); as were all causes .of death related to smoking (rate ratio 1•30 (0'•91 to 1-85)) aad'mottality from lung cancer (rate ratio 2•41 (0•45 to 12-83)) and ischaemic heart disease (rate iatio 2•01 (1-21 to 3•35)). When passive smokers were divided into high and low exposure groups on the basis of the amount smoked by their cohabitees those highly exposed had higher rates of symptoms and deatb, Goncitrsion-Exposurs to environmental tobacco smoke cannot be regarded as a safe involttntary. •-1'tabit. West of Scotland Cancer Inuoduetion Surveillance Unit, Ruchill Though evidence hu accumulated about the risk to Hospitall Glasgow health of involuntary, or passive, exposure to environ- 4',20 9NB David J Hole, ktsc,. at4dsnnas Chi r1ts R t?itlis, Mn, atirxtar 1.*epammew of tpidemioloxy, School of Public fi2altti'„Univeaitr of Michigaa, .Ynn Arbor, Michigan, United States Cara4 Chopra, remarch uwier+i Victor M Hawthorne, stn, proJessor Correspondence and requests for reprintsto: Mr Hole. , . mental tobacco smoke, further information is requirrd' from cohort studies m confirm these observations. Deleteriotu effects on the respiratory system of infants and children have been observed" as have chronic effects on lung function in adults,' " but these findings have been criticised on methodological grounds.'' An overview of 10 case-control and three cohort studies estimated a relative risk of 1!•35' for lung cancer in people passively exposed compared with non-exposed controls.' Three studies have reported increased (though not significant) risks of ischaemic heart disease in non-smokers with partners who smoke.' I* Problems in interpreting these findings include lack of an objective measure of dose or exposure, failure to adjust for confounding variables, inappropriate methods of statistical analysis, and failure to measure other poten- tiaUy important variables." This report is based on the Renfrew-Paisley survey,, e,Mdl m+a++:.2a.7 which was carried out in an area with a high incidence BMJ VOLUME 299 12 AL•GUST 1989 of lung cancer; it overt.vmes manyof these criticisms. The survey prospectively studied a general population aged 45-64 years, and the collected data allowed participants from the same household to be identified. The measure of exposure to environmental tobacco was obtained directly from cohabiiees and did not rely on self reporting. Data on prevalences of symptoms of respiratory and'ardiovaxvlar disease, forced eYpitatory volume in one second, mortality, and incidence of cancer are all availabie for this population. The findings reported here update an earlier rrport; it adds 567 further deaths to the previous findings" and extends the range of baseline measurements to include forced expiratory volume in one second. Confoundingg variables such as social class, blood'pressure,,choles- terol concentntion„body mass index, and socia[class have been allowed for in calculating relative risks for passive smokers. Subjects and methods This general population cohort comprises all l men and women aged 45-64 years resident i in the towns of Renfrew and Paisley in the west of Scotland between 1972 a»d 1976." Eligibility wu established by a door to door census of all households in the two towns. Everyone who met the age and residency criteria was ir111ted to attend one of 12 temporary centres for a multiphasiccardiorespiratory screening examination." Between 1972 and 1976, 15 399 residents (an 80% response) completed a standardised self administered questionnaire that included questions on smoking behaviour and was checked by experienced inter- viewers when subjects attended for scmning. Respira- tory symptoms were assessed with the Medical i Research Council's bronchi tis q uestionnaire. By identi- fying participants from the same household it was possible tostudy var}•ing,exposures to tobacco smoke in a subsample of 3960 men and 4037 women and to calculate relative risks for a range of cardiorespiratory variables including mortality. Fourgroups, in which the iadex case was aged 45-6i. at the time of the survey, were defined based on the index case and on the cohabitees ever or never having smoked. (l ) Control: the index case had never smoked and lived at the same address as another subject who had' never smoked. No one else in the household who attended for screening was a smoker or ex-smoker. (2) Passive smoking: the index case had never smoked and lived atittte same address as a subject wt: had. (3) Single smoking: the index case was a smoker or ex-smoker and lived at the same address as a subject who had never smoked. No one else in the household' who attended for screening was a smoker or ex- smoker. (4) Double smoking: the index case was a smoker or ex -stnoker who lived at the same address as a subject who was also a smoker orex-smoker. If the index cases were ex-smokers they were classified as single smokers or double smokers depend- ing on whether the cohabitecs had never smoked or 423

. ever smoked. If the cohabitees were ex-smokers the index cases were classified as passive smokers if'the% had' never smoked' or as double smokers if they'had ever smoked. Thus the controls represent a group whose passive exposure was as low as possible within the constraints of the study design, ResuRs for the two active smoking groups have been included to give some indication of dose-responsc and provide a perspective for any differences found between the control and passive smoking groups.. A eohabiteetc•as defined as a respondent sharing the same household environment and e2:amined' at~ the same time in the surves as the index case. Some households contained'cohabitees ofthrsame sex. Some of the subjects who were examined were above or below the age range eligible for inclusion in the study. These subjects were not analysed as index cases but information on their smoking behaviour as cohabitees was used as the measure of passive exposure for eligible index cases. Mortalit}• data .ras obtained from the National Health Service et:ntnl register and the General Register TMls ]-Cansycsinoe af rroaeps Ispa.rd so awa+rnta.aii No(!wIdmml:m(%)of.osen (mdo: ou> (mdc. o.n; 7ou1 (:mt:ols (nnther uudca ax nm,rob+tluee r.er mwk'ed: L•n.rvvcnolungI onlp,rnhabum.aer,rnkcd' 428 (10-g~) 213. (61; 419M 1) 1295(32-1) 917 is36 SurElcamwkmg.: onliL udi>.nw ner.moked 1420(35,9:; 331 (62` 175.1 13oubktmakmg(borAmdez:n.eandcvlubneceMeranoked1869iA7-2.) 1922,47-6) 3'91 7ou!. 3960 (100, 4037 (100) 7997 TAa]S 11-Sona1 zltiss of.or JX rarrpt tzposed so eifaaru a.o4e. Fyrca a pnrxs6efu erc pe.n.Wcs Fsposu'e group sooalcLss canuols. Pumc vnwkmt Sm81r WnokSng Dwbk wror+oa I I3 (SJ;. 13. (k3) 61 (4,3,~ 78. (4L2+ II 65(199!'. 3`(1.5-2) 225(15•8~ . 235T12•61 llleon-manual 63:14-7). 23' (9-S, 197(13-9:, 204 (IO•9, ' + Itlmamoal /V 157(367;. /10(18..7). 96(395) 39(24;3) 538(37•9) 315(222) 771 (41i 438R3'4). V 17(1•0) II (4-5) 68 (1g) 122(6•S) ~ Inv,ff~iiinformulon~. 3~ (0L7): 4(lb; 16 (1•1) 21 . (1-1), Toul 428 n00-V 243 (99^9;, 1420(100): 1669(I0o) Office for Scotland. Incidence of cancer was obtained tlxrougli the cancer registry system and used to verify t31at the classification on the death i certificata was the same as that received by the registry. Dau presented are crtlmpltte to the end of December 1985, en average follow up of 1'1'5 years. Prevalencesforrespil•atory and cardiorascularsynrtp• toms were standardised for age and sex using the age and sex distribution of the whole cohort as standard.. Sirrularly; mortality was standardised'for age and sex using life tables to estimate survival at 11 years of, follow ,up." Mean forced expiratory volumes in one second'for the four exposure groups were adjusled for age, height, and sex by determining the best, fit set of parallel regression models for forced expu•atory volume in one second as a li.near function~of age and height for men and women separately in each group. The mean adjusted forced expiratory volume in one sccond4or each group was then calculated for the average age and height of', men and'women separately, and a weighted average (carresponding to the proportion of men and women) was computed. Probability values were obtained from the analvsis of variance.. Estimates of relative risk and 95% con6den(x inter- vals for passive smokers compared with controls were adjusted for age, sex, sociall class, diastolic blood pressure, serum cholesterol concentration and body mass index (weight (kg)/(height (tn)}x1U0)iusing the logistic regression model" for ardiorespiratore symp• totas and Cox's proportional hazards model for morlality." Levels of significance were derived from the partial likelihood function." The biomedical data processing programs (BMDP) package was used to compute estimates of risk and levels ofprobability.° A supplementary' questionnaire in~ two of the 12 centres in which tbe etirveti• was carried out, asked subjects the extent to which they were exposed to cigarette smoke from any other person in the house- holds iirespectiveof whether these people 9cere eligible for or attended the surve.•,, and also in their work environment.. Results 7~'hc number ofinen and women in the four exposure groups is shown in table 1. Passive smokers comprisod TAaLt il1-Sww44np 6abn of coAabvetr rn parnvc swrokinp and deublr uwokmrrwps. Fr(rvcs asr yntnuCtrs (wrenbrn ) lnda nu N6dciErsrner Mrn, t omen Sooked pa d.l.. (y mhabnr: Pmve >mokly pcup Double wookaua group Pnu.e anY.ma group 13oubk makut group 1•14 ~, 31•3 (76)', - 3)" (561)'. 15-1!(196). 11.4 . (IIl9) s15~ ~ 46-~1012)I 32•7(98S). 41•t(541): 56~2{I0t0) 15-24 42-0(102)'~ 4Si(a58)'. • 30-a(399). 37,1(J13) i25~ 4-I (10)~, 6-a(127). U-0(142). 19~1,(367) 6mWokn 22! (SS)', 17•3(323). 13L](S38). 324 (6239 Taat.E ]v-Atc ad sa 6ttndardurd rates eJYSrybatdyad rediocvrtvJar rvr~p/orru n1msd to rryansr to cymrar neoAi: A'wlba: of l V r.ca mid rympowu ae jeeen nr pmaaAerrs Em-u,r group Cmvu14 luv.e®okaog f.aBk-W~ Duubk.no6m8 (n-917) (n-1b38) (n-1751): (6-3791) W ' ~ ~ 1Y/ 1 aeq>.r.ron' ~pam+` tbleaied spunun. ' 2-3(72) 3•3. (44) 10~-5(189)~~ 103. (396)~. Iggh Perusrrnu tpurum. 7-t.(72) 9-9(122) 29-0(5+1)i 28.70079;~. 1753CDoCa 101(95i 122097) 13-4(229i~. )6`6 (61a)~. Hlymeereom 53(49) 6-9I (81) 17t(327)~ 18.3'~ (6f1)~. CGrd/ov..cvb 1rmpama* . tkn8uo+ 44(43) 7~7 065i, 9~1 (331)~. ALqr.boarvubev .faud'ouekrtrarndiap.m , 1-0 (a) 11 (13) 1-4 (D1Y P5~. (49)~. M® (orced eipr.wry ews . me acmd (I); Ua.dw'<ad 2-32 2~21 2-12~ 2-09~ Ndrysud, 2-31 2-23~ . 2-12~ 2-07~ 424 BMJ vol.untf 299 12 AUCUrr 1989

T.atE v--.Area.d sa adJ,m.d .ea.bo-ye* ro0a7 ys3.o. by carpry rf ewa.rs aP qOanm ,woie. Fqccr in yosietrtierrs arr ucnuJ os.bes of dcrAr r....r Pad.c amkam Smdf~ mmkw Dwbh~ mookw s Allcouo Rlr 1(99) ~1 fl-4(tf4) t60e~.(42o) 1554(73q Lunjaem 1-6 R)! 5-0 (9) 21-2 (54) 7114 (") 4mrma t,en.~r 37:3 (D0; ~~, 47n (54) 61-0.(171)6U7(260) 1Woneeofdelial.udemookwS 60.i(?1)', ?2-S(tON) 1!W(367) 129-9(b92) TJtaLE vl-A/r .dpc>ud jreLYls.K of /tSavC7oryy and OoRllOYt0/(0 lJ1.p- 0d Sje -d@Jtaidmortnl+y,paJ0000 prr ysm for uowem m camw' mid p¢mar >..otua pwrpi. Fwva n pmenrhem mr .raben aJ.cauJ cmo P.mK umokm csI (2.409) Ln.ecIpmm (.-75s)~ Hghergaa,c (s-5t1). Amp-Rory vympm>=: lu&ctedipa= Pa +.+nci 2-1(t0)~ 2-1(10)~. 31(1T) Paainmt .pnt® ir(l1), S-a(45)~. a<(46) Dlspom U •7(60)1 1t~2(a4)~. 162(p) 17yp- 4'1(19) , 1.3(29) ~. S-7 (30) CAedmw.wl.rrya~mmc: . Anpr 3s (r+) ~ 4-1(32) ~. sa(st) Ataprabnms.tiry(4md'mdleovoedn~ 0+ (2)~ 1-1 (i)~. 0-5 (s) Aamus r..m* S8~3(32) M-6(70)~. 1nd (Sq LunFcanecr l-I~~ (1t~ 2i. Rl. 57 (3~ 1xL.wic6artd- 6•6 (3) N~3fl4i. 20•0 ( I6) AO au`a of dea>h eelamd m~uI 3`4-9 (t7) 352(39) ~. 47•3(30) 6• 1% (24313960) of inen and 32• 1%(1295/4037) of women. Of the cohabitees, 91-6% (7325),were of the opposite sez The composition of the groups by social class is shown in table 11. The extent of passive exposure experienced byy passive smokers in relation to subjects in the double anoking 8roup is shown intable Ilt: ln all, 46• 1% (112) men and 41-8% (541) women in the passive smoking group lived in households where the cohabitee was smoking 15 or more cigarettes a day. This compared with 52 - 7% (985) men and 56-2%: (] 080) women in the double smoking group: Fs-smokets were more commnn in households in which the indez case had never smoked. The plevalence of signs and' symptoms for the four exposure groups is shown in table IV. Foa each of'the four respintorymeasures (infected sputum, persistent sputum, dyspnoea; and livpersecretion) the rates in the control I group were lower thaa those in the passive smoking group and considerably lower than in the single and double smoking groups. The rates for angina and major abnormalities falnd on elecmo- tardiography were smmaar in the comaol: and passive smoking groups and lower than in the aMive smoking groups. Mean forced ezpiratory volumes in tloe .second' adjusted for sa, age, and height were cgaificaatlyI higher (p<0-01), in controls than in those pasvvelyy exposed to cigarette smoke and were significaady higher than among .ctive smokers. Mortality adjlutedfor ageand>a in the four groups is presented in table V. Total morulirv was higher among passive smokers than mmrmis. This was reflected m the category of all tauses of death related to smoking and was highest for ischaemic heart disease. Lung tsncer mtatalrry was higher amoog passive smokers than conunls, but the number of deaths involved was imall. The suppktnentary questionnaire on espostlrL to cigarette smoke at home and work allowed a check to, be made of the smoking habits of other household members who were not part of the survey : A regular smoker living in the same household was reported by 5% (2/44) of controls compared with 69% (27l39), of passive smokers.,Of women, 21% (13/62) of controls lived ~ in households with a regular smoker n1lmp.red with 63% (125/197) of passive smokers. Women repotted'that most of their passive espoaae was at home rather than at work,.vhich suggested that they were the appropriate group in whicb to tr.,,,ine whether there .vas a dose-mpoasr re.latiom. A high I exposure passive smoking group was therefore defined' as women whose cohabitec was smoking 15 or more cigarettes daily, and the remaining female passive smokers were defined as a low exposure group:,Table VI presents the age standardised rates for respiratory and cardiovascular symptoms and mortality for the control and the loa-and high exposure passive smoking groups. For each of the four respiratory symptoms the highly exposed' passive smokers had rates that were higher than those in passive smokers whose exposure was low and those in the controls. There were no consistent differences between the low passive exposure group and the controls. A similar pattern was found for artgina buM not for maj(a abnntmaluies detected by electrocardiography. The adjusted forced expiratory volume at one second was significantly lower in pssivo smokers with high exposure comuared with those with low exposure (mran 1.-831 c 1-891; p<0•05): Nosigni5canr diffettace was found between passive smokers with low exposure aad controls (1 •891 v I-881). Age adjusted mortalitywas increased for the passive smoke:s with high expostue compared with low and with controls for all cause mortality, al1 cause mortaliiy, related to smoking, ischaemic heart disease, and lung,cancer. Table VIl shows the adjusted relative risks for passive and active smokers compared witb controls. For each variable tbe relative risk associated with passive tmoking was >I •Q The mnfideace interval included 1•0 except for ischaemic bearx disease, for svhieh~the estimate of risk was signi6cantly diSenmt, fro® unity (p=0-008): Table VM shows the relative risks fas double mokers compared with single smokeis afteradditional adjustment for quantity smoked. Dyspnoen was signi- TAai[ Iv-RrJaa<er risks aaacimed>xv4 peaior a.e1a3.djsaI se, .rz, .wd.oeid elm a.d for cmdiomadoamia6la, baaoi+r iJaodDrwx, ~e~o. c6o(me.mf co.unaanoa, md 6o~.aa ade nd.m.crek (pmiveaokvscomyred 95KGm5doa.uL cvaec4) oiv.al 1 Rd.ove ru! wodcvs oomt+orad yv.>e .,mmo.d.) 2V Rnpvavnrvsypspooa: . In(srodqutuv, 1 14 0.7610 2-36 0-1 4-53 Ptruurn,qr¢um. Dym- 1.19 1.0 41 1-67 tr92 m ,i.a5 0-3 Qi 4-49 1.0 H.pencie®. 1 -21 0.9110 hJ2 0-3 T77 [ardwva.oYr qalms:: Ang- t•IJ F7l~e 1~,70 O6 1.0 ' Mawr atamrmaYO tuud.m dicvoa.io~m. 1,.77. 040 b 3-33 1-31 MonaYn : AIJ CumRs trn 0-95 tc 170 d••W - 2-07 AL tauae d Aeaub ,dneEto aakry 1-)0 liliw 1'35 0 15 : 2-33 t.dum,r 6en dser 2.01 1-2110 1-D5 0-001. r27 \[ Lutq mca 241 045 m 12•03. 0-3 I0b4 425 Bdu1J voLamE 299 12 AUGUSr 1989

TaeLt vtn -Rtlanos riiks se doub'lrawo4asaowparedmuli riej)t awoken, adpaled Jor atc, trx, awamtr a~toked; atd suial clax aud Jot emdioasuswbr oanabin, d+aualu blaod precmr, ir.um cio7eurrol tonceearanan,:and body naass tedrx 95% c,mrtaetiv Aebo.e nnk . etm•al I p v.lm Re~pvnmc n-mpartr .. 1h(csed tpuaum: 0'% 0.79'to. l • 16. 0-165. Pcrsmc+mn spunun 1.06 ~ 0•92~to1~21 0,45~ nKao- 1 ts I.ostol•.v 002 HrPerseesr•uom l •02 0-i7.to~l40~ 0^75. cmdo.•.wuLff .n=atom:: Anoo+ ata,mabmotmaLues foum oo ekarocirdwp3m : t't7 1.11 0•qstoa•44 0-68 10 1-79 oas o-65 asor,at,t ; Au ~ Au =,es ol docam raaed m =wt,ag t-0a o-w o•s7tot•la 0•s.to1•l6 e•s 0.9 lre~r eon msa+e 099 072toI- 11 0-3 t,noa aocQ 1,13 0A.to1i3. 0-~5 ficantly, more common among dbuble smokers (p= 0•02), and' though none of the other variables was si.gnifianti six had risks > 1•0. Discussion Whether inhaling other people's tobacco smoke is a risk faaorior lung cancerand other diseases related to smoking is now under serious scientific consideration. Studies of the concentrations of cotinine in the urine and saliva of passive smokers suggest that the dose received may be equivalent to smoking up to three cigarettes a day." Though sidestream smoke containss different proportions of chemical constituents than does mainstream smoke and the same dose received passively might not translate directly to the same risk as in active smokers, the risks expected for passive smokerswill probably be of a similar magnitude to those found in active smokers of up to three cigarettes daih•;, consequently, onh• very Lvge studies w•ill have sufficient power to detect such risks. A meta-analysis is currently the only way to establish precise esti,mates of risk, and it is essential that all studies are included. This paper updates a previous publiation" with mortality now extended to an average follow up time of 11 •5 years and the control and passive smoking groups redefined to exclude those who smoked onl.• pipes or cigars and those who smoked cigarettes irregularly. The original: questionnaire in its coded form did'not distinguish pipe and cigar smokers an& those whoo smoked~ fewer than five cigarettes a day from non- smokers. Written information on ~ tlie questionnaires allowed this to be clarified, and these additional data were added to the computer files. The sample size in this study does not provide sufficient statistical power to detecr risks of the magnitude expected. Thus the lack of significance should not be the sole criterion of whether a genuine effect may be present. Sel eral findings should be borae in mind when interpreting thesc results. Firstly, for each o[ the 10 measures czamined, from respintory syrnptoms to causes of mortality, the relative risk was consistently luger than unity. This tzmained so after adjusting for intervening risk factors such as age, sez,, social class, blood pressure, cholesterol contxntration,, and body mass index. Secondly, the one measure for which sufficient statistial power was available -that is, , ioreed expiratory volume in one seoond~-6ave a significant~ resultL Thirdly; when a group of passive smokers with high exposure was defined there was an . iacrease in the dose-response relation for nine of the 10' •-variables. Fourthly, in - comparison with the relative risks found for the two active smoking groups, eaeh increased risk was biologically ~ plausible, with the possible exception of that fonischaemic heart~disease. The findings for respiratory symproms are similar too those of other studies: a decreased ~ forced expiratory, vvolume in one second in passive smokers has been found ptxviousl%,' and the risks for.lpng cancer are consistent with those in the ovetvicu by Wald rt at," Few data relate passive smoking to cardiovascular disease, but a relative risk as high as 2-2 for motulityy from ischaemic heart disease in passive smokers has been quoted.' Our risk of 2-0 seems large in com- parison with that found for active smokers, and the possibility that~ehance has inflated this risk eannot be excluded, but as the lower 95% confidence limit~ for tbe relitive risk is greater than one it would appear that ichance aiooe is notrtesponsible for the acess. When investigating,risks close to unity it is impor- tant to,oonsider the effect of potential biases. Biases may operate ar the time data are collected. Between 1972 and 1976, however, passive smoking was not an issue. Subjects reported their own smoking habits and no self reporting of passive exposure was undertaken. Iv was not tmtil 1983 that subjects within the same household were linked, and this was carried out without any reference to the measures of outcome examined subsequently. There is no direct measure available to prove that the passive smokers received a higher environmeatal dose of tobacco smoke than the controls, but in the supplementary questionnaire that covered the smoking habits of household members irrespective of whether they attended the original survey only 5°ro of controls said that there was a curtent smoker in the household, compared with 63% of passive smokers. Greater etposureto tobacco smoke at work supponed the idea that passive smokers were more likely than controls to be in contact with environmental tobacco smoke outside the home. This was measured by Wald and Ritchie; ' who showed that non-smoking husbands of smoking wives had higher urinary cotinine concentra- tions than non-smoking husbands of non-smoking wives. Our definition of categories of exposure is comparable with that of other studies and would to identify groups with different mean levels of passive exposure. The high level of heavy smoking in. our cohort" might also indicate that this difference is grnter than that found in otherstudics. The problem of smokers deliberately . classifving themselves as non-smokers" is a far less serious bias in cohort studies than in case-control studies, because at the inten•iea• stage there is no indication which subjects will subsequently dic. The likelihood of: misclassification ntes-that is, higher imthe passive smoking than in the control group-i's debatable as this implies tli.at; someone in the doublt smoking group is more likely to pretend to be a non-smoker than someone in the single smoking group: When the cohabitec is a smoker the reverse may be more likely to be true. It has been suggested that non-smokers who marryy smokers may be different from ~ non-smokers who marry non-sntokers.' A higher proportion of passive smokers were in social classes III manual, IV, and'1 V, but no differences were found for other possible risk factors such as occupation, raised blood prrssure,) sholesterol concentration, or body mass index. In any ~ casc the fmal ~analysis, which atimated' the relative h+ risks, adjusted for each of these factors. C The effect of passive smoking on those who alheady &I smoke is far harder, to isolate. The dose received by active smokers from smoking ranges widel~•,"'' and ~*~ adding a small extra component due to passive ex- ~I t posure may oot ~ lead to much of a difference in ~ mean ~A doses for double smokers compared with single ~ j smokers. Hence, the inereased risk for double smokers= relative to single smokers may be substantiallc, less _ ~ than that fonpassive smokers relatit•e to controls. Thus GO the statistial' power of a single stud% is an important 1z consideration and! in ~ tlie absence of other published data on this aspect it is difficult to interprxt our results 426 ' BMJ vOLUM£ 299 12 AUCUST 1999

\ Deputment of Medicine and P.ot?ia 8eference Uniti RoJal S3allamhire Hospitatl, Shzf5eld81ll 2JF A Kapur, arAtostl, wdical midenr G W ild, asc, serlior rcirnlm A Milford- W ard , FRCPATtt; direclor ojprotenR.eJerence umir D R Tnger, rRc?,,naderiw wediaine Correspondence to: Dr Tnger.. B.Ma[J J9W;IMa27-31 for the effects of passive smoking on smokers. Therr fore the main emphasis of this paper is an estimation of the risks of passive smoking in lifelong non-smokers; data are presented for the active smoking groups to provhfe an estimate of dose-response. Our results are based on a general'populat3oD cohort study carried out in an ar!o with a high level of disena related to smoking. A consistent increase in tisk was observed in pRssive smokers for each of the f 0 variables measurcd coverittg respiratory symptoms, , foroed' e=- piratOry'volume in ooe eecond, cardiovascular symp tom5, and subsequent mortalJty, including lung cancer and tschaemtc beart dssease. A dose-response relation was seen, and the risks were b;okJgically plausible in relation to the sia of the risks found for the active smokers. These three factors taken together increase our concern that exposure to other people's tobacco .imoke cannot be tegarded as a safe mvt3luIItaly pACtICG• I Cdk7 JRT. tidYtlVV'. GmYiRT..LEiea dP~ matiq ad p.,an.l /Akrn,oe ppeumar rd lYmrWm r rr1, dJdsoad. L.ra 1974y:1031a.. 2tomc 574 Ta{a la, Spna FE, arec 6. Feris~ !.Ys:-e r.loa. o rsspunmr, dluen, e,prene trtag. aedk+d d pJ.aary 1~ a a . poqdi- sunpk m clWdn:a. Aw Rer Rnpv !h+ 197t:11:M952, 3 wlnc JR. Fab HF. SnaY .,+'.ri dv¢~ a nm-..oMam cYmoly. apoxd ro,eE.cso -ok<..k Eq/ Y Md 1 WUJOI:72P3. 4 K.u(f~ , F', Tmer lF, 4adt<. Aduli.paaa< aa.aYen mt6r bnKl annemmea[: a nat. haer fr elumr a,n6o. Iwuuan. A. JEPrr~d 1993.117:269-80. S LebmaMD. dJlv~dpra.c:okuRmpdmon.rytvncvm:asvey. P.er.Md196/13:645-55. {9 .Id: N3, l:anch.W K. TUep.m SG. CycLJrHS. Du. Ms[Woe etecpeopk-r wE.cto mwta a.rt Wy osce? B. 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Repsm ma6ei .d Yie .bin.: J-f .J W Ryd Sa~o1 S'.rrry re11m3f: H17.220. 17 Cs DR. Prod 4kd,rnal. ar.W Imf2:7lN.7x. uDRrn. tol, an+a )da. E"dms L.. d a~w.ebr.t/r La~lt 1A~~ 5ramr.lY.Jl_ e 19tS; Lr A.p1n- uv.avry d Citlorlr Pes, 19tS:. 19 . Maoukun S, Taoe.e T. IGn- N, a d. Enarn d o.uaaomdaoM.no m,N<. ao vmvr _ s.nam r. sa-Ulnltas. N'EYI1Md t1N:r11a2432.. 20 Hdimus D: ane.m.r KD. Adw ID,.J. ladev PoOnues.bf alrso . ®oke: radd aird,e a.lle epuka b..ee-. In: Ih0uod a, tl.: f.i.. ~. w~a tro~r ..rk.l..P-rlr, .d'f-W q'/rbp'- Vd 2. SwriYde:S.eds6 Gund tr tk,iN.y Rssreh. NN:113.1,. (Peaceed,op d 1h. 04 re..om.l mak,ma ~.Oaer rr W+1+7 rd • dunuc,.upplDl9.) 21 Vald N,,RnAm C.. VJitlm da.de as Y.r mow doa,mnot~s .aned b wa~es. La NM;t:10i7: . 22 GJW CR. Hok D). HssLora VM. Cprme .mtat a.d a.k A.,e a.~ ~e ao aie d.enh*h mcdeea- 13. t4pa, d a~e+enl popW.- mhen . vud,e tbr im d Sm,iud. J Elr.+d C.~.~n Hrw 19Y;<2:w. 23Lee PN. Alnrid6ouoe. r.6cr r Pm,re. s>~ rot../,.~ra 19f6w:867: 24 nu~A PRJ. tf Wa . mmaL~q a tlYUmd -d ov'.k. A. JErYr 19%323:lY•9. 25. , '.Id Nl, lrelr® J I 31.itrf A. Rari. C, Haddo. lE. Ragsc G. lJrwr m~m,rr a erka d bstEp. nc- pmptr'. e6aaearoYc Lo 19Na130•1. (AaaMd II M..11N) ~ Carbohydrate deficient transferrin: a marker for alcohol abuse A Kaptu, G Wild, A Milford-Ward, D R Triger Abstract Objective-To assess the value of serum earbohydrate deficient transferria as detected byy isoelectric focusing on agarose as an indicator of alcohollabuse. Design-Coded analysis of serum samples taken from patients with carefully defined alcohol intake both with and without liver disease. Comparison of carbohydrate de6cient transferrin with standard laboratory tests for alcohol abuse. Setriig-A teaching hospital unit with an iatetest in general medicine and liver disease. Patientr-22 "Self confessed" alcoholics admitting to a daily alcohol intake of at kast 80 g for a minimum of three weeks; 15 of the 22' self confessed alcoholics admitted'to hospital for alcohol withdrawal; 68 patients with alcoholic liver disease confumed by biopsy attending outpatient clinics and claiming to be drinking Ikss than SO g alcohol daiiy; 47 patients with eon-alcobolic liver disorders confirmed by biopsy; and 38 patients with disorders other than of the liver and no evidence of excessive alcohol consumption. Intenxntibn-Seriat studies performed on the 1S patients undergoing alcohol withdrawal in hospital. Main outcome m.earure-Determinatioa of relative value of techniques for detecting alcohol abuse. Resulu-Carbobydrate deficient transferrin was detected in 19 of tbe 22(86°/.) self confessed alcohol abusers, none of the 47 patients with non-alcoholic BMJ vot.u/.te. 299 12 AuGt,ST 1989 liver disease, and one of the 38 (3%) controls. Withdrawal of alcohol led to the disappearance of carbohydrate deficient transferrin at a variable rate, though in some subjects it remained detectable for up to 15 days. Carbohydrate deficient transferrin was considerably superior to the currently available conventional markers for alcohol abuse. Conclusion-As the technique is fairly simple, sensitive, and inexpensive we suggest that it may be valuable in detecting akohof abuse. Introdtsctioa The medical and social consequences of alcohol abuse are major problems throughout the world. Although many: people rndily acknowledge the eztcnt of their alcohol consumption, others attempt to conceal it, and we lack reliable objective means of identifying surreptitious alcohol consumption. Currently available laboratory markers have considerable limitations, being insensitive, non-specific, or dependent on liver damage. The mean corpuscular volume rises in patients with thyroid disease, folic acid deficiency, and liver disease,' whereas serum yrglutamyltransferase activity is affected' by drugs that induce microsomal enzymes as well as rising in all forms of obstructive liver damage.' Serum aspartate aminotrsnsferase activity is more commonly raised in alcoholics than alanine aminottansferasc activity is, and whereas  ratio of aspartate to alaaine aminotransferase activity of greater than 2:1 is strongly suggestive of alcoholic liver disea~e this is of little value in subjccts in whom the 427