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Passive smoking and cardiorespiratory health in a general population in the west of Scotland R'est ofScotland Cancer Surveillance Unit, Ruchill Hospital, Glasgow G20 9NB David J Hole,.usc, statistsnian Charles R Gillis,.%tD, director Department of Epidemiology;,School of Publlc Health, hnivenity, of Michigan{ Ann Ar1>or, Michigan,,United States Carol!Chopra, research stwient' Vfctor St Ha~thorne, .aD, professor Correst+ondence and I requests for reprlnts ro:Ur Hole B, .N.d J~,19M294~.a23J David J Hole, Charles R Gillis, Carol' Chopra, Victor M Hawthorne Abstract Objective-To assess the risk of eardiorespiratory symptoms and' mortality in non-smokers who were passively exposed to environmental smoke. Desigr-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. Setring-Renfrew and Paisley„adjacent burghs in urban west Scotland. Subjecu-15399 Men and women (80%0 of aff those aged 45-64 resident in Renfrew or Paisley), comprised 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 outcome measure-Cardiorespiratory signs and symptoms and mortality: Resulrs-Each of the cardiorespiratory symptoms examined produced relative risks > 1•0!(though none were significant) for passive smokers compared with controls. Adjusted forced expiratory volume in one second was significantly lower in passive smokers than controls. All cause mortality was higher in passive smokers than controls (rate ratio 1•2T(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)) and'mortality from lung cancer (rate ratio2-41 (045 to 12•83))~and ischaemie hearf disease (tate ratio 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 death. Conclusion-Exposure to environmental tobacco smoke cannot be regarded as a safe involuntary habit. Introduction Though evidence has accumulated about the risk to health of involuntary, or, passive„exposure to environ- mental tobacco smoke, further informationis require& from cohort studies to confirm these observations.. Deleterious effects on the respiratory system of infants and children have beeni observed" as have chronic effects on lung function in adults," but these findings have beenrriticise&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 passicely exposed compared with non-expose& controls." Three studies have reported increase& (though notsignificant) risks of'ischaemic heart disease in non-smokers with partners who smoke.-"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 analvsis„and failure to measure other poten- tialhimportant variables.'o This report is based on the Renfrew-Paislev survey,,, which was carried'out in an area with a high incidence of'lung,cancer; it overcomes many of these criticisms. The survey prospecuvelystudied a general popul9uon 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'directlyfrom cohabiteesand did not relyy on self reporting. Data on prevalences of symptoms of respiratory and tardiovasculardisease, forced expiratory volume in one second, mortality, and incidence of cancer are all available for this population. The findings reported here update an earlier report; it adds 567 further deaths to the previous findings'' and extends the range of'baseline measurements to include forced expiratory volume in one second. Confounding variables such as socialiclass, blood pressure, choles- terol concentration, body mass index, and social class have been allowed for in calculating relative risks for passive smokers. Subjects and methods This general population cohort comprises all men and women aged';45-64 years resident in the towns of Renfrew and Paisley in the west of Scotland~betw•een 1972'and~1976."Eligibility was establishedby a door to door census of all' households in the two towns. Everyone who met the age and residency criteria w•ass invited to attend one of 1'2 temporary centres for a multiphasie cardiorespiratory screening examination." Between 1972 and 1976, 15399 ' 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 screening. Respira- tory symptoms were assessed' with the /titedical Research Council's bronchitis questionnaire. By identi- fying participants from the same household iv was possible to study varying exposures to tobacco smoke in a subsample of 3960 men and 4037 women and to calculate relative risks for a range of cardiorespiratorv variables including mortality. Fourgroups, in which the index case was aged 45-64 at the time of the survey, were defined based on the index case and on the cohabirees ever or never having smoked. (1) 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 at the same address as a subjecnwl, had: (3) Single smoking: the index case was a smoker or ex-smoker and fived 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 smokerr or ex-smoker who lived at the same address as a svbject who was also a smoker or ex-smoker. If the index cases were ex-smokers thev, uere classified as single smokers ordouble smokers depend- ing on whether the cohabitees had never smoked! or BMJ votU.ME 299 12 AUGUST 1989 423

ever smoked~ If the cohabitees were ex-smokers the index cases were classified as passive smokers if they had never smoke& or as double smokers if they had ever smoked. Thus the controls represeml a group whose passive exposure was as low aspossible within the constraints of the study design. Results for thetwo active smoking groups have been'i.ncluded to give some indication of dose-response and provide a perspective for am differences found between the control and passive smoking groups. A cohabitee was defined as a respondent sharing the same household environmenn and examined at the same time in the survey as the index case. Some households contained cohabitees of the same 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 usedas the measure of passive exposure for eligible index cases. Mortality data was obtained from the National Health Service central register and the General Register TABLE t-Composition of groups exposed to ngarette ssnok'e riot%3ofinen l:o(?.o)of~omen (tndtx cases (Indtxcases) ToIlI Contro6sineith'er m~dexcasrnor cohabueceversmoked426,106. 489!12- 1) ' 917 (6) i 1295i321). Ptsswrsmokmgonltcohabneresrrsmked 143 Ssnglesmoktngon4-ndex.nsersrrsmokrd1420359, 331 1 2• 1538 1751 Doublesmokmg lwthsndexcaseandcoliabuteeever,smoked' 18694741922~ 476). 3791 Total 3960~ 100 4037,100, 7997 TABLE n-Sona! cfass of mcn in g.oups exposed to tiga retu smoke. Figures in parentheses are peruntages Exposuregroup Socul class Control5 Passist smokmg Single smoking Double amokmg 2a. 4 13 53 6t (4!3~ 78 (42n~~ II 85{199~~ 3: ,152 225;15.g' 235'12i6, ^1 non-manual 6314 T 23 (95 ~ 197 , 13-9 204. 109: tllmanwal 15736.7 96?9S 538,37~9 771(413~ I1' 10(187? 59(243 315(22.2) 438i23-4 V 17. 1401 11 (451 68 (4-8) 122 16`51 losufficrenrinformation 3(07) 4(1-6? 16 (111) 21 (11) Toul 4281001' 2431999 . 1420000' 1869;100'. Office for Scotlandl 1'ncidence oflcancer, uasobtained through the cancer registm- system and used to veri6 that the classification on the death certificate was the same as that received by the registry. Data presented are complete to the end of December 1985, an a% erage follow up of 115 veara. Prevalences forrespiratorn and cardiocascular sNmp- toms were standardised for age and sex usingthe age and sex distribution of the whole cohorras standard Similarl%', mortalitv was standardised for age and''sex using life tables to estimate survival at 11 years of follow up;" Mean forced expiratorv volumes in one second for the four exposure groups were adjusted for age, height, and sex by determining the best fit set of parallel regression models for forced expiraton' volume in one second as a linear function of age and height for men and women separatelS in each group. The mean adjusted forced expiratorv volume in one second for each group v.'asthen calculatedSor the average age and height of men and women separately, and a weighted average (corresponding to the proportion of men and women) was computed. Probability values were obtainedfrom the analysis of variance. Estimates of relative riskand 95% eonfidence inter- vals for passive smokers compared with controls were adjusted for age, sex, social class, diasaolic blood pressure, serum cholesteroll concentration and bodp mass index (weight (kg)/(height (m))'x 100i using the logistic regression model'" for cardiorespiratory symp- toms and' Cox's proportional ha2ards model for mortality.'° Levels of significance were derived from the partial likelihood funcuon." The biomedical data processing programs (BMDP) package was usedl to compute estimates of risk and7evels of probabilit%~." A supplementary questionnaire in two of the 12 centres in which tha survey was carried our asked subjects the extent to which they were exposed to cigarette smoke from any other person in the house- hold, irrespective of whether these people were eligible for or attended the surve}•„ and also in their work envirorunent. Resitlts groups is shown in table 1. Passive smokers comprised TABLE ]ll -Sirsoking kabit ofcohab'itees in passive smoking and doab(t srnoking groups. Figures are per.entages i numbers I ]ridex asr No of cigareves Men R omen smoked perday by cohabner Passnrsmokusg group Double smoking group Pissive smok,ing group Double smokinggroup 1 - 1 4 3 1 ( 3 ( 7 6 ' 30~0(561) 15 1 (196' 11~4 (219 3 1 5 461 t1 12) 52~7(985) 41~8(541 56 2i,1060` 15-24 420(102i. 45'9(858~ 306t399 371013~ z25 41 (90~ 68(1271 110,142.1 191h367i Ex-smoker 22-6(S5), 173(323) 431(558i 32 4 623' TABLE rv-Age and sex standurdised rates af respiratorv and cardiotwscular svmp,toms related [oe:posvre to rigarette smokr Nvmberr cases withsymptoms are given in parentheses indrx Eaposuregroup Controls (nc917) Pus-mok'ing (n=1538i Single smokzng (0.=17517 Double smok'tng (nc3791i Respvato, smpio- l nftcu rdspuwm 23;22) 1 33 (44; 105(189. 105 (396 Prrvstem spumm 78(7,2) 1 99122J 260,541 267()019 D, spror 1011(95 122 197; gll 69 134,2.29 17, 6 327 166 (618 163 (681 H ,pr rarcrcntom Grdmvascvlar symptoms~ Angvsa 5~3U6 46.1431: ( 47~~ 74 ,. 7r7!165 9)i334 Ma(on abnorrruhnfaun on rlersrocirdiogram 1~0 (8~ 11 ()3 1,4 ~ 31 15 (49 Mcan fbrccd'ezpsramm.rHt in one second ((I) Unudiusted 292 22d 212 209 Adlusmd 231 2Z3 212 2-07 424 BMJ c'oLuME 299 12 AUGt'S:r 1989

TABLE v- Ageandsez.adju.ucd morrality. per 10.000peryear bycaugoryof exposure rocigaretsesrnnke. Ftgures in parenr)vses are acrual numbers of'deatlu Conwls Passive smoksng Susgic smoktng Double smoksng AUcauser 8'~.31 (99): 97'4(164) 160~0a420r IS5`6(734)~, Lungcancer 1~6~.(2)~. 5.0 (7) 23'2~(54)~. 21 4 4 (93)i Ischaemehnndtsease 27'3,30l~ a7~7. (54) 61 0 1 17 1) ~. 607,260)~ Allcnusesofdeathrelated~to~smokmg 60~:g'17.1)', 72'2~(104) 130~4'i3621~ 129:9;592)' TABLE vi-Age adjsuted prrrxilence of respiratorv and cardurenscular sryrrrpumu and age standardr'sed' mortalsryper 10 000 per year for women in control and pasnve smoking groups: Figures in parentheses are numbas of actual cases . Passive smokers, Controls (n=489)'. Low exposure (n=754). High e:posure. (n=541) Respiratorc . s,vm ptoms: tnfectedspunun Arrz,aJn~e 2-11u0) 2~4U8) 3V1 P'r Peresstenv sputum 6~4 ( 31) . 5`8'i 45°) 8~6 , 46) D)spnoea 12.7 (60). 11:¢ t84) 16 2 k88) H j-persecreGoo 4! 1(19) . 3-8 (29) 5-7(30) Cudiovascularayrnptorns; Angina 3-6(17) 41 (32) 5B(31) Maioraboormalitvfoundonelearocardiagrarn 0-4' (2). 1-1 l8) 0'5 (2) All causes Manatw 58-3(32). 64'6(70) 87 864) Lungcancen 34(16 b5(2) 57 (3) IscAaermc heart Aisnse 6 8 (3). 14'204) 28-0 16) AOausoofdothrdatrdhosmoktng 34.9'(17). 35:4i39) 47'3k30) 6•1°k (243/3960) of men and 32•1%a (1295l4037) of women.,Of the cohabitees, 91•6%ri (7325),were of the opposite sex. The composition'of the groups by social class is shown in table II. The extent of passive exposure experienced by' passive smokers in relation to subjects in the double smoking group is shown in table 111. In all, 46- 1% (112) men and 41-8% (541) women in the passive smoking group lived im households where the cohabitee was smoking 15 or more cigarettes a day. This compared with 52'7'% (985) men'and 56•2°io (]080)'women in the double smoking group. Ex-smokers were more common in households in which the index case had never smoked. The prevalence of signs and symptoms for the four exposure groups' is shown in table IV'. For each of the founrespiratory measures (infected sputumt persistent sputum, dyspnoea, andbyperseeretion) the rates in the control group were lower than those in the passive smoking group and considerably lower than in the single and double smoking groups. The rates for angina and major abnormalities found on electro- cardiography were similar in the control and passive smoking groups and lower than in the active smoking groups. Mean forced expiratory volumes in' one second adjusted for sex, age, and height were significantly higher (p<0-01) in controls than in those passively exposed' to cigarette smoke and were significantly higher than among active smokers. Mortalityadjusted for~ageand'sex in the four groups is presented in table V. Total mortality was higher among passive smokers than controls. This was reflected in the categorynCall'causesof death related to smokingg and was highesti for ischaemie heart disease. Lung, cancer mortality was higher among passive smokers than controls, but the number of deaths involved was small. The supplementary questionnaire on' exposure 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%I (2144), of controls compared with' 69% (27/39) of passive smokers. Ofl womeny 21% (13/62) of controls lived in households with a regular smoker compared' with 63% (1125/197) af passive smokers. Women reported that most of their passive exposure was at home rather than at work,,which suggested that they were the appropriate group in which to examine whether there was a dose-response relation. A high exposure passive smoking group was therefore defined'' as women whose cohabitee 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 low 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 angina but not for major abnormalities detected bv'electrocardiography:. The ad/usted forced'' expiratory, volume at one second''was significantly'lowcr in passive smokers with high exposure compared with those with low exposure (mean 1'•831 u1 •891;p<0•05). No significant difference was found between passive smokers with low exposure and controls (1 • 89l''v 1• 881). Age adjusted mortality was increased for the passive smokers with high exposure compared with low' and with controls for all cause mortality, alU cause mortality related to smoking, ischaemic heart disease, anddtrng cancer. Table VII shows the adjusted relative risks for passive and active smokers compared with controls. For each variable the relative risk associated! with passive smoking was > 1•0. The confidence interval included 1•0 except for ischaemic heart disease, for which the estimate of' risk was significantly different from unity (p=0-008). Table VIII shows the relative risks for double smokers compared1with single smokers after additional' adjustment for quantity smoked. Dyspnoea was signi- TAsLE v1i-Relativerisksassociated wuk passirx.smakingadjasred fnorage; sez;.andsacialclassandforcardunxascularvanables, diastolic blood pressure; smrmcholesterol concentration, and body mass iitdex. •V (passive srnakers compared: 95% Confideoce (uti(e smokers compare~ wuhcantrols) snterval pYalue w,rlrcontrolsl Resptra..cnrn' s.cm p toms: lnfected spurum P 1 34 ' erslst[nt spwtLLm Dyspnoca Hvpersecretwn 1 19 1 09 1 21 Cardio.' asculu symptoms : . Anguw 1' I II Ma)mr abnornulitiesfound on mhctrocardiogram. 1'27 MorrtaLrv: Z~causes eausa.of death ~rclatod ,o smokng 1 27 1'30 Itchacmic.bran dnnse 2.'01 Lung cancer 241 0~76to 2~'36 03 3~ 4.53. 085ro 1'67 0:3~ 4~~.49. 0~82to 1'45 05~ 1~60 0~8'~.1 to 1 '82 0:3 3 77 0 7.3to. 1~70~~ 0`6~ 1~89~. 0~48to 3`35 0:6~ 1-5.1 0~95rto 1~70~~ 0:10. 2~07~ 0~9to IB5~ 0!IS 2~33'. 1-2~1 ro 3"35 0-008~~ - 0~45~to12~83 0 3 10'64'. BSi) VOLUME 299 12 AUGUST 1989 425

TABLE vHI-Relanr nski in~doubte mwknt campared uhtbnnRle smokers, adJusted fo+aRe;.srx„omnwn,. smoked;.; and'socml'class and lor catdwvascular uarwbles, diastolrc blood pressunc, snvmcJtolrurrolconcrntrancm;,andb'rwii.nmas tndn Rdat,er mk 95"p CnnfidEnen rniereal q, \'afuc Renpvmnn scmpinmsInfecsed spuium 0 vb 0~79toJ~l6, 0~16c~ Permnem spwum I`06. 0~92~toa4.l 0~45 ITspnoco I .2.c. I~0SmJ~49'~ 0-02 H+-persecrcunn I' 03 0~87to1 -20: ~ 0: ~75 Card-ascular -piems fI 7 0~95 1 ~44 0~ ~15 Arsguu Atalor abnormxliwa:found ondcctrocud,opnm I' I I .to 0~68~0 to d~ 79'~ 1 065 MonaGn All ouses: I r0 1 0~,87 ta l ~ 18I 0: ~9~ AIl causm:of doth nl3ied to sm,ukmg 099 0~~84to1 ~16~~ 0~9. lschaemioheari dtse" 0.69. 07]InJ~I1 0~3'. Lung cancer l:13 0^79,oi1~63: 0~55 ficanthy more common among double smokers (p= 0-02), and' though none of the other variables was significant„six had risks > 1 •0. Discussion Whether inhaling other people's tobacco smoke is a risk factor for lung caneerand 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 contains 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 smokers will probably be of a similar magnitude to those found in active smokers of up to three cigarettes daih ; consequendy, onlv very large studies will have sufficient power to detect such risks. A meta-analysis is currently the onlv K•ay to establish precise estimates of risk,and it is essential thatall studies are included. This paper updates a previous publication" with mortality now extended to an average follow up time of 11 - 5 vears and'the control and passive smoking groups redefined to exclude those who smoked only pipes or cigars and those who smoked cigarettes inegularly: The original qyestionnaire in its coded form' did' not distinguish pipe and cigar smokers and those who smoked~ fewer than five cigarettes a day from non, smokers. Written information on the questionnaires allowed this to be clarified, and these additional data were added~to the computer files. The sample size in thi's study does not provide sufficient statistical power to detecu risks of' the magnitude expected. Thus the lack of significance should not be the sole criterion of whether a genuine effect may be present. Several'findings should be borne in mind when interpreting these results. Firstly; for each of the 10 measures examined, from respiratory, symptoms to causes of mortality, the relative risk was consistently larger than;unity.LLThis remained so after adjusting for interveningrisk factors such as age, sex, social class, blood pressure, cholesterol concentration, and body mass index. Secondly, the one measure for which sufficient statistical powerwasavailable-thatis, forced expiratory volume in one second-gave a significant result. Thirdly, when a group of passive smokers with high exposure was defined there was an increase in the dose-response relation for nine of the 10 variables. Fourthly, imcomparison with the relative risks found for the two active smoking groups, each increased' risk was biologically plausible, with the possible exceptioniof that for ischaemic heart, disease. Thefindings for'respiratorysymptoms are similar to those of othen studies: a decreased forced expiiatory volume in one second in passive smokers has been found previouslv,'°'and the risks for lpng cancer are consistent with, those in the overview bv lt: ald er Q7.' Few data relate passive smoking to cardiovascular disease, but alrelati4•e risk as higti as 2-2 for mortalns, from ischaernic heart disease in passive smokers hass been quoted.' Our risk of 2`0 seems large in com- parison with that found' for active smokers, and the possibility that chance has inflated this risk cannot be excluded, but as the lower 95p/u confidence lunit, for the relative risk isgreaterthanone it would appear that chance alone is not responsible for the excess. VI'heminvestigating risks close to unitv it is impor tant to consider, the effect of potential biases. Biases may operate at the time data are collected', Between 197Z and 1976;,however, passive smoking was not an issue. Subjects reported their own smoking'habits and no self reporting of passive exposure was undertaken. It was not untiL 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 environmentalidose 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% of controls said that there was a current smoker in the household, compared with' 63% of passive smokers.. Greater exposure to tobacco smoke at work supported the idea that passive smokers were more likelr'than controls to be in contact with environmental tobacco smoke outside the home. This was measured by'Wald and Ritchie,t' who showed that non-smoking husbands of smoking wives had higher urinary cotinine concentra- tions than non~smoking husbands of non-smokingg wives. Our definition, of categories of exposure is comparable with tharof other studies and would seem to identify groups with different mean Ievels of passive exposure. The high level of heavy smoking in our cohort=' might also indicate that this difEerence is greater than that found in other studies.. The problem of smokers deliberately classifying themselt•es as non-smokers" is a far less serious bias in cohort studies than in case-control studies„beeause at the interview stage there is no indication which subjects will'' subsequently die. The likelihood of differential misclassification rates-that is, higher in the passive smoking than in the control group-is debatable as this implies than someone in the double smoking group is more likely to pretend to be a non-smoker than someone in the single smoking group, Vfhen the cohabitee is a smoker the reverse may be more likely to be true. It has beenisuggested that non-smokers who marry' smokers mav be different from non-smokers who marry non-smokers." A higher proportion of' passive smokers were ini social classes I'II manual, IN', and V, but no differences were found for other possible risk factors such as occupation„ raised blood pressure,, cholesterol concentration, or body mass index. In any case the final analysis, which estimated!the relative risks, adjusted for each of these factors. The effect of passive smoking on those who already smoke is far, harder to isolate. The dose reeeive&bv' active smokers from smoking ranges' widelv," " and adding a small extra component due to passive ex- posure may not lead to much of a: difference in mean doses for double smokers compared with, single smokers. Hence, the increased risk for double smokers relative to single smokers mae• be substantialh, lesss than that for passive smokers relative to controls. Thus the statistical power of a single studv is an important consideration and in the absence of other published data on this aspect it is difficult to interpret our results 426 BMJ VOLUME 299 12 AusUsT 1989

for the effects of passive smoking on smokers. There- 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 provi'd'e an estimate of'dose-resportse. Our results are based on a general population cohort study carried'out in an area with a high level of diseases related to smoking. A consistent increase in risk was observed in passive smokers for each of the 10 variables measured covering respitatory'symptoms, forced ex- piratory volume in one seconds cardiovascular symp- toms, and subsequent mortality, including lung cancer and ischaemic heart disease. A dose-response relation was seen, and the risks were biologically plausiblt in relation to the size of'the risks found for the active smokers. These three factorstaken together increase our concern that exposure to other people's tobacco smoke cannot be regarded as a safe involuntary practice. Department of Medicine and Protein Reference Unit, Royal Hallamshire Hospital, Sheffield SlO 2JF A Kapur, BMEDSCt, mrdical' srudenr G Wild, Bst, seniar scientisr A Milford-Ward, FRCP.ATH, dirertor ofprotein rejerence unit' D R Triger, FxCP;,readn rn meduvne Correspondence to: Dr Trigen. B..s1edJ 1989;:99.a2.7, -31 I Colk>-, JRT, Holland!R'W, CorkluB.RT. tngueoceof puvve smakng and parental phlegmon.pneumonua and bronchuus mn early,childhood. Lma<rr. 1974;11,1031-1. 2Vt'esss~ST- Tager IB, Spesur FE, Rosrseo B. Persrsnens rhrea-as relatson to resptnton dlbesa, ci6arear smoksng. and ksrl of pulmoaary f...... populauon vmpk m childran. AtnRm Rnpv Du 1978;18'679-52:. 3\t'hate JR. Froeb H F. Small wiwa5s, dysfuuutson in nm-smokets chroo'oBy. e:pased to tobacco smokr..\ E,yl J.ifod 198U:302:720-3. 4'Kawffmann F,.Tnster JF, OriollW: AdulE pussve smokersin the bomc emironment: arnk (acsor for.elirosuc airfb. Issrtiusson.. Aw. J Epsdenoef 1983:117:269-80. 5Lrlxw-tsz MD: f nfluessce of passive.smoksng on pulmonvy,functson: a survey , Prrr.Nrd 1984,13-6{5-55. 6Raid N J. \anchalzl i K; Thompson SG, Cuck,c H S.. Doa brcatLmg othar people's tobaceo smoke causr Ismg..cancer? Br Med J 1986a93:12 t7; 22:. 7Garland C. Barren-Comxr E. Swre: L. n al. Effects of'passsve smokrng ooochaemsc heart dtlnsc.monaWn.af non-smoken:. a prospecuse ussd). A.J.Epdesmol 1985 321 ~. M5JS0! 8 H-y.- T.P.- arnow,g anr.t„ttetofrp,dem,aog>.rd. Je=p,C/U .Nrd1985,10.:67~93, 9 Svendxn KH, Kullrr LH, Mamm MJ, (kkrneJK. Effnuof passrvr smokm{ -thz muJr~plr nsk fanoemservrnuon usai AI. JEpdn+w'1987:126.. 783-95 10 US. tkparsmena o6 Hcahh and. HumanServ,cn Rnpvaory e/lnu nJ, usmo/- nvu~ rspcm rpsdm„aioav.sndv, Reponoton.wc,6op, 1-3 hfav198J~Brthrsda:Mirelandtiauosul Insnm+nofHeafth. 198311 GNnCR. Huk.D/. Haahome VM. 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Brunnemann KD: Adams J D, er. ot. Ibdbor poil'uuon by ,ob.cco smokr: modcl stud,n on the upsakee by nonsmokrrs. In. Brrslund B, ed- Adcn. en: .~udne, posrme nMtug, Dunscsdmrs ewdwwss.g rptdr.relop" Vol 2. Staektudm. SWCdssh Councd for BuddsnRnnrch, ,198a313-8. (Proreeduspof the 3rd tnsernatsonal conference on sndbor aur qualat, and ' cLmate,suppLD17i 21! N%ald N, RiscEse C- Valddaswn of uudses on lung cmr tn non-sawken srwrsxd tm smokers. La- 198a:t:1067. 22G'iW, CR; HokDl. Hawehorx VM. C.eareste.,moksng and mak lung cancer tn, an area of wen.hfgh snctdentt. 11. Reporr of a general populatwn cnhon . ssudT tn tlie VI'ess of Smeland-. J Eputnn,d Cewonuesn HtsLA 1988:42:"8: 23. Lee. PN. ~Lsclasstbcatwo u a fxtar m passtve smokusg nik.. Lmet. 1986:si .867. 2a Burch ~PRJ . Passve sowiwy in sdulthood and oncmr . risk. Ai. J Epde.wf . 1986;12336&9. 25 Q>Id NJ, Boeeham J., BailryA. RucEu C, Haddo. 1F..Kmyss G:.Unnary coumme as a marker,af breathmg.aGer.peopk's tob+ttos®oke. Laxrt 1984j:~130-'1:. (AcuDied ?t .kuy/989) Carbohydrate deficient transferrin: a marker for alcohol abuse A Kapur, G Wild, A Milford-Ward, D R Triger Abstract Objective-To assess the value of serum carbohydrate deficient transferrin as detected by isoelectric focusing on agarose as an indicator of alcohol abuse. Design-Coded analysis of serum samples taken from patients with carefully defined alcohol intake both with and'without liver disease. Comparison of carbohydrate deficient tfansferrin with standard laboratory tests for alcohol abuse. Serring-A teaching hospital unit with an interest in general medicine and liver disease. Patients-22 "Self confessed" alcoholics admitting to a daily alcohol intake of at least 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 confirmed by biopsy attending outpatient clinics and claiming to be drinking less than 50 g alcohol daily; 47 patients with non-alcoholic liver disorders confirmed by biopsy; and'38 patients with disorders other than of the liver and no evidence of excessive alcohol consumption. Intera,entima-Serial studies performed on the 15 patients undergoing alcohol withdrawal in hospitalL Main outcome measure-Determination of relative value of' techniques for detecting alcohol'l abuse. Resulrs Carbohydrate deficient transferrim was detected in 19 of the 22 (86%) self confessed alcohol abusers„none of the 47'patients with non-alcoholic liver disease, and one of the 38 (3%6) 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 conventionalmarkers for alcohol abuse. Conclusion-As the technique is fairly simple, sensitive, and'inexpensive we suggest that it may be valuable in detecting alcohol abuse. Introduction The medical and social' consequences of alcohol, abuse are major problems throughout the world. Although'many people readily acknowledge the extent of'.their alcohol Iconsumption, others attemptto conceali it, and we lack reliable obj"ve means of identifying surreptitious alcohol consumption. Currently available laboratory markers have considerable limitations, being insensitive, non-specific, or dependenton, liver damage. The mean corpuscular volume rises in patients w'ith'thyroid disease, folic acid deficiency, and liver disease,' whereas serum y-glutamyltransferase activity is affected by drugs that, induce microsomal enzymes as well as rising in all forms of obstructive liver damage-= Serum aspartate aminotransferase activity is more commonly raised in alcoholics than alanine aminotransferase acui.'ity is, and whereas a ratio ofaspartate to alanine aminotransferase activitvof greater than 2:1 is strongly suggestive of alcoholic liver disew' ttus is,of little value in subjects in whom the B:MJ VOLL'.ME.J991Z AliGL'ST 1989 427