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Passive smoking and cardiorespiratory health in a general population in the west of Scotland West of Scotland Cancer Surveillance Unit, Ruchill Hospital, Glasgow G20 9NB David J Holt, Msa, smtistician Charles R Gillis, ++D, director Department of Epidemiology, School of Public Health, University of Michigan,:Ann Arbor,.. Michigan, United States Carol Chopra, researchh studenr Vicctor MHawthorne, ntn;. ProfffsOr Correspondence and requests for reprints to: Mr Hole. B..Nrd) I1989~,29~I~t23~-7 David~ ) Hole, Charles R Gillis, Carol Chopra, Victor M Hawthorne Abstract Objective-To assess the risk of cardiorespiratory symptoms and mortality in non-smokers who were passively exposed to environmental smoke. Design-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. Serring-Renfrew and Paisley, adjacent burghs in urban west Scotland. Subjecrs-15399 Men and women (80%9 of all 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. Resufrs-Each ofthe 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•27 (95% confidence interval 0,95 to 1•70)), as were alfcauses of death related'to smoking (rate ratio 1•30 (0491 to 1.85))'and mortality from lung cancer (rate ratio 2•41 (0-45 to 12-83)) and isehaemic heart disease (rate 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 information is required from cohort studies to confirm these observations. Deleterious effects on the respiratveysystem of infants and ehildren 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 control's.' Three studies have reported increased (though not significant) risks of ischaemic heart disease in non-smokers with partners who smoke.P `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 otherpoten- tially importantvariables,'°' This report is based on the Renfrew-Paisleysurvey, which was carried out in an area with a high incjdence of lung cancer; it overcomes many of these criucisms. The survey prospectively studied a general populauon aged 45-64 years, and the colkcted' data allowed' participants from the same household to be identified.. The measure of exposure to envirotunentalitobacco was obtained directly from cohabitees and did not rely on self reporting. Data on prevalences of symptoms of respiratory and'cardiovascular disease, forced expiratoryy volitme in one second, mortality,, and~ incidence of cancer are all available for this populauon, The findings reported here update an earlier report; it adds 567' further deaths to the previous 5ndings" and extends the range of baseline measurements to include forced expiratory volume in one secondl Confounding variables such as social class, blood pressure, choles- terolieoncentrauon„body mass ind'ex„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 between 1972 and 1976."Eligibility was established by a door to door census of all household's in the two towns. Everyone who met the age and residency criteria was invited' to attend one of' 12 temporary centres for a multiphasic cardiorespiratory screening examinauon." 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 screening.. Respira- tory symptoms were assessed with the Medical Research Council's bronchius questionnaire. By identi- fying participants from the same household it 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 cardiorespiratory variables including mortality. Four groups, 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 cohabitees everor, 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 subject wl. 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-smoker who lived4t the same address as a subject who was also a smoker or ex-smoker. If the index cases were ex-smokers they were classified as single smokers or double smokers depend- ing on whether the cohabitees ha& never smoked or BMJ VOLUME 299 12 AUGUST 1989 423

0 ever smoked. If the cohabitees were ex-smokers the index cases were classified as passive smokers if they had never smoked on as double smokers if they had ever smoked. Thus the controls represent a group whose passive exposure was as low as possible w•ithin the constraints of the study design. Results for the two active smoking groups have been included to give some indication of dose-response and provide a perspective fon any differences found between the control and passive smoking groups. A cohabitee was defined as a respondent sharing the same household'environment and examined at the same time in the sun,ey 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 rthe 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. Mortality data was obtained from the National Health Service central register and the General Register r,tstE t-Cmnposilion of araaps exposed to eiaareru srnoke No(%)afsnen (index cases) No:(1.)ofnrumen (index cases) Toul.. Controls(neiQierindesnsrnorcobabineeeversmoked7i P.ssivesmok'ingronlccobabiteeeversmoked~ 428(10g~ 243(6'1) 489(121) 1295(3:1) 917 IS38 Ssnglesmoking!onlcmdesnseeversmol:ed)' 1420;35'-9) 33] f82, 1751 Double smoking'botli isdex pse and eolubiuee.ever smokedY'~ 1869 i4721 1922 (47-6) 3791 Tool, 3960 i 100) 4037 (100) 7997 TABLE tt-Saeiaf tlau of tness in groups exposed io cigaresv arnaEr, Figures ie yaremlesel an yerceluages E.pos- group Sociil~clus Controls ~ Passive~ smoking ~ SutgIe.. smokmg ~. Double vnok+ng. t 23~ (S`4)~ ] 3 (53, 61'. (4~3)~ 78 (AQIi Il 8S(19:9)~ 37.(I54n 225~(15-8, ~ 23'S(12~6~: ~ UIbon-manua] 63<14-7)~ 23~~ (9.5i. t97~i13-9;~ 204 t10~91~, /1limanurl 157(36~7)i %~~(39~5)~ 538(37-9)~ ~ 771i(41-3) ~ ~ IV ~ g0(18~.~7)~1 54(24;3)~ 315 (22~2): -4)', 43g (2l ~ v~ 17~ (4-0): 11 (4'5) 68 (4•8)~ 122 ~ (6'5)', Insuf6cicntinfammuion 3(0d)', 4(1-6) 16 (1-1): 2t(1-1). Office for Scotlandl Incidence of cancer was obtained' through the cancer registrv.system and used!to verifA that the clalssification on the death certificate was the same as that received by the registry. Data!presented are complete to the end of December 1985, an average follow up of 1i1F5 years,, Prevalences for respiratory and cardiovascular symp- t'oms were standardised for age and~ sex using the age and sex distribution of, the whole cohort as,standard. Similarly, mortality was standardised for age and sex using life tables to estimate survival at 1:l1 years of follbw up:" Mean forced expiratory volumes inione second for the four exposure groups were adjusted for age, height, , and sex by determining the best fit set of parallell regression models for forced.expiratory volume in one second as a linear function of age and height for men and' women separately in each group. The mean adjusted forced expiratory volume in one second'for each group was then calculated for the average age and height of men and women separately; and a weighted average (corresponding to the proportion of men and women), was computed.. Probabiliiy values were obtained from the analysis of variance. Estimates of relative risk and 95% confidence inter- vals for passive smokers compared with controls were adjusted for age, sex, social class, diastolic blood pressure, serum cholesterol concentration and bodyy mass index (weight (kg)I(height (m)y k 100) using the logistic regression model" for cardiorespiratory symp- tolns and Cox's proportional hazards model for mortality." 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 of probability:1e A supplementary questionnaire in two of the 12 centres in which the survey was carried out asked subjects the extent to which they were expose& to cigarette smoke from any other person in the house- hold, irrespective of:whether these people were eligible for or attende& the survey, and also in their work environment. Results The number of inen and women in the four exposure Tot,1 42s rtoo l! z~3r99-9) t42auoo; tsa9(loo> groups is shown in table I. Passive smokers comprised 'r6s1.E rrl-Snwtking habir oJcohablsea in passrw ssno+king and'daabk srnokirsg groups. Figures are yercenaages (monbers) Nocdciprettes smoked per dar: by cotiabbsee P.esrve smokiog group lndex ose Men a'omen Double mwkiog group Pun•esmoksng Qoup. Double smoksng.OWp 1-14 31-3 (76). >15 46.I()12). 15-24 42-0(102) a234+ (10). Ea-smoker 22-6. (55). 300(561). 151(1%) 11.4 (2l9)i 5D7.(985): 4U8(541) 562(1080)~45~9(8S8)30-8(399). 37 1013) 6-g(127)11'0(1421 1941(367) 173.(323). 43:d (558) 324 (623), rA]stetv-Agr and sex sraedardiied rorrs of.espirarory and cardievaxrlanrynepsottxs related ra erpvsseee so ciganru nnoke. T'sonben of index N rosa u,irA syrnpto.u are prssen m}>mnedseses' Respiratary symppams: Infected sputum ' Penistent sputum D)wpooea Hyperseaerwn CGrdiovaaeutr rysnprorns: A.&= Malor abtsasm.bnr found ao elensaord'aerw M® forced expiawry ree 1n osr second (I):~ Umdiusted Adlusted: 424 Eaposur: vuup . V Controls Pnsive srnokins Siogk tmwk'ing (y.917) (n-1538): (o-t751). Double ovrokmg (n- 3791) W Ca 2•3(22): 3-3. (41): 10~5(199). 103 (396) ~ 74(72)9 9.(122): 28-0(541): 28'7(1079') 10~1(95)y. 12 2(197). 13-4(229) 16-.6(61g, '- 53(48): 69. (81) V-6(327): ,89 1) 4~6(43)~. 4 7 (74)~ 7-7,065). 9~.1~ (334) CJ . 1-0i(8): 1'1 (13): 14 (31). ],5 (49) CJ 2i2~ 2-21 2~12~ 2•09 ~ 2-31 2~23' 2~12' 2,07~ BMJ vot.tmE 299 12 AUGUST 1989

t 7Aat.e v- Age asd sex ady4sad tnortaliry per 10 000 per yrar bY ca7egory of exposare so ciparztu smolie. Fqtaes ie parentheses are acnual rtrmeben of deaslsi Gontro)s r.s,u" sutsk Double msokio8 smokine smolun8 All ousa 83+1 (99) 97r((64): 160-0(420) 155,6(734). Lut4 nancer 1-6 (2) 5•0(7): 232 (54) 2'1-4 (93). Ischaemx hevt disnse All.wusaofOeatAuel.tedtosmoKinB 2713.(30) 60.8(71)) 477. (54) 72-2(104). 61-0(i171) 130-4(d61) 607.(260) 1199(592) TAat.e vt-A'Qe adjucted'pnnalence of respirarory and cardiocascvl6r ryrnptonu and aQe slandrsrdised nsorrality per 10000 Der yem far nrrtsee ue conAO! ardpasnoe s.w,kinp prwps. FiBsnes nt parentheses are srrnnbers of actual cascs !'asure smokcr, eootzols (0=489) I.o.aposure (n-754). [•tiahesposure (n-541) Respirnory.rymWoms:. ucum Icfecteds I'recaLwre 2~1(10) -4(18) 311(17) p Pemsrenn sput- 6-4 (31) . 5~ 9(45), 8'6 (46) Dyspran 127(60). 1112(84), 164{88) Hyyersecretioo 41(19) (19) . 33 (29) i 5-7(30) Carerowcvl>tr symwoms: Anyna 3r6 (77): 41 (32) i Y8(31) Ma$or.(marmalirylouodoodectmeardiop.m 0-4 (2): Il. (8)i 0.5 (2) Allnusez MwmEtiy 58-3(32) 646(70): 87,8~(54)~~ LusKc.ncer. 3-2 (1): 2r5(2): 5.7 (3). Ischaemicheandisnx 6•8 (3) 144(14)', 28-0(16)~. Allausesofdeath.rclaaedtosmokin8 34-9(17): 352(39)'. 47d~(30) ~, BMJ vOLUM1:299 6-1% (24313960) of men and 32-1% (1295/4037) of women. Of the cohabitecs, 91 •6% (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 II I. In all, 46• 1%(112) men and 41-8% (541)iwomemin the passive smoking group lived in households where the cohabitee was smoking 15 or more oigarettes a day. This compared wtith 52-7% (985) men and 56•2% (1080) 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 four respiratory measures (infected'sputum, persistent sputum,dyspnoea,and hypersecretion) the rates in the control i 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 expintory, 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. Mortality, adjusted for age and sex in the four groups is presented in table V. Total mortality was higher among passive smokers than controls. This was reflected in the category of'all causes of death related to smoking and was highesn for ischaemie heart disease. Lung cancer mortality was higher among passive smokers than controls, but the number of deaths involved was small! The supplementary, qquestionnaire on exposure to cigarette smoke at home andiwork aUowed 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% (27/39) of passive smokers. Of women, 21% (1:3162) of controls lived in households with a regular smoker compared with 63% (125/197) of passive smokers. Women reported that most of their passive exposure was at home rather than at work, which suggested'ahat 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 respintory and cardiovascular symptoms and mortality for the control and the low and'high exposure passive smoking groups. For each of'thetour 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 control9. A similar pattern was found for angina but not for major abnormalities detected by electroeardiography:. The ad)usted forced expiratory volume at one second was significantly lower in passive smokers with high exposure compared with those with low exposure (mean 1• 83 1 b 1•891; p<0•0S). No signifieant difference was found between passive smokers with low exposure and controls (1 F 891 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, all cause mortality related to smoking, ischaemie heart disease, and lung 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 compared with single smokers after additional adjustment for quantity smoked. Dyspnoea was signi- 7Aat.8 vf t-Relatisx risks aasoeiaud rs,irlr passive InsokieE odjsured fo. age, sex, and socias cbss asd /w cardiooascrlar omiobli.s, diassolit blood pressure, senon cAolessnol'rencenaatimr,:and body mau index Relative tisk (passWe snsokencomp.red wiuhcanuols) 95%CmBdenm usterval y VYue ~ Relativc risk (ectivt ssnoken~, compvtd : .itA aontrds) ~~ Respuatory syvsptoms: Infectedspunun Pcrsistent tpurum nyiFooe. Hypersecsetion 1''34. 1.19 1'09. 1 ~21 0-76so 2•36 0`85to 1.67 0~82to 1-45 o~~8tto Da2 0-3 0<3 05 o-a 4-53 449 1i60 177 e.ediorros,d,r symptoms: An ina , . 11 0' 73 to 1~70 0-6. P89. g Maior aboormalYties found on ckctsucudioerun 1 12 01.48 to 3•35: 0-6 1~-51 ~~ Morulisy; AL auses "27 0,95to 170 o-10, 2r07, All nusn o( Ae.rh related tosenokin8 1.30 0.9tto P85 0~15 b33 tsd.emic hert diseue 2-01 i. 121to3-35 0_008 2~-27 LunB cancer 2'41'~ 0•45.to 12'83 0-3 10-64. 12 AUGUST 1989 425

TAeLYvltt-Relative risks m doub7t swsoken tomyaredauuhsingle ssnokers, adJsssud forage, sts;.amount »nohed; and saia!'ctassand facasdiasxisn/lar vanables, d,asmlicb(ewd pxssure,, serum.m chollsrnol' coruensrunon,.and bodjmass indrs 95+% cnnhdence Rclarve riskl smenal. p Value Respsraior.•sanp+toms: , InfKted sputum ~ 0~96. 0~79to~1~~16 0* 65 Persistem spuoum 1 ia6 092to1-21 045 ~ 1'25 ~. 1,05 'to I ~-49. 0~02 penerreuon H. 1 0~87.to 1-20~. 0-75, Careio~.sculu s.,nptorns: ArsBvu 1~17~ 0~95.to 1-44 0~1S~ Major .bnosnuli tin found on elcarocardtogram 1~11' 0.68'.so1~79~. 065~ Monalih : AO nuses 1,0)1 0~,87.tn~.l~ 18 0.9 All our- ot dnth rehied to smok,ns 099 a'8<tolls 09 Isch'acntichean diseax 0`69. 0102~to 1~11~. 0~3 Lung canatr 1. 13. 0~~79to1-63 03 ficantly more common among double smokers (p= 0-02), and though none of the other variables was significant, six had risks > 1. •0. consistently larger than unity. This remained so afte Discussion Whether inhaling other people's tobacco smoke is a risk factor for lung cancer and other diseases related to smoking is now under serious scientific consideration. Studies of the concentrations of eotinine 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 tham does mainstream smoke and the same dose receivedi passively might not translate dicectly to the same risk as in active smokers, the risks expected for passive smokers will probably be ofa similar magnitude to those found in active smokers of up to three cigarettes daily; consequently, orily very large studies will have suf6cient, power to detect such risks. A meta-analysis is currently the only way to establish precise estimatesof risk, and ic 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 years and the control and passive smoking groups redefined to exclude those who smoked only pipes or cigars and those who smoked cigarettes irregularly. The original questionnaire in its coded folirt'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 this study does not provide sufficient statistical power to detect 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, frorri respiratoty ,fympto®s to csuses of morulity, t6e t+elative risk t>rL& . social class, blood pressure, cholesterol concentrationi and body, mass index. Secondly,,the one measure for which sufficient statistical powerwas available-t'hat is, 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, in comparison with the relative risks found for the two active smoking goups, each increased risk was biologically plausible, with the possible exception of that for ischaemic heart disease. The findings for respiratory symptoms are similar to those of other studies: a decreased forced expiratory volume in one second in passive smokers has been found previously,'°'and the risks for lung cancer are consistent' with those in the overview by Vfald'.et al.° Few data relate passive smoking to cardiovascular disease„but a relative risk as high as 2-2 for mortality 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 chance has inflated this risk cannot be exel'uded, but as the lower 95% confidence limit for the relative risk is greater than one it would appear that chance alone is not responsible for the excess. When investigating risks close to unity it is impor tant to consider the effect'of potential biases. Biases may operate at the time data are collected. Between 1972 and 1976„however, passive smoking was not an issue. Subjects reported theirown smoking habits and no self reporting of passive exposure was undenaken, 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 environmental 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 origjnal'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 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 seem to identify groups with different mean levels of passive exposure. The high level of heavy smoking in our cohon,' might also indicate that this difference is greater than that' found in other studies. The problem of smokers deliberately classifying themselves as non-smokers"'is a far less serious bias iit cohort studies than in case-control studies, because 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 that someone in the double smoking group is more likely to pretend to be a non-smoker than someone in the single smoking group. When'm the cohabitee is a smoker the reverse may, be more likely, to be true. It has been suggested that non-smokers who marry smokers may be different from non-smokers who marry non-smokers."'A higher proportion'of passive smokers were in social classes III manual, IV, and V, but no differences were found for other possible risk factors such as occupation, raised blood pressure, adjusting for intervening risk factors such as age, sex, , cholesterollconcentration, or body mass index. In any case the final' analysis, which estimated~ the relative ?Q risks, adjustedYor eachofthese factors. C The effect'of passive smoking on those who already ~ J smoke is far harder to isolate. The dose received by active smokers from smoking ranges widely,"" and'' ~ adding a small extra component due to ~ passive ex- W' posure may not lead to much of a difference in mean Go doses for double smokers compared with single N smokers. Hence, the increased risk for double smokers relative to single smokers may be substantially less N' ~) than thanfor passive smokers relative to controlf. Thus the statistical power of a single study is an important ~ n consideration and in the absence of other publishe ~l id data on this aspect it is difficult to interpret our results 426, BMJ VOLUME 299. 1:2~AUGUST. 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 prov[de an estimate of dose-response. 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 respintory'symptoms, forced ex- pintory volume in one second, cardiovascular symp- toms, and subsequent mortality, including lung cancer and ischaemic heart disease. A dose-response relation was seen, and the risks were biologically plausible in relation to the size of the risks found for the active smokers. These three factors taken 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 Refennce Unit, Royal Haltamshire Hospital, Sheffield SIO 2JF A Kapur, aMEDscI, rrudical soadenr G Wild, Bse, renior scienriu A Milford-Wud, FRCPATH', dlrectorofJlro[t7A reJerplEe ItAit D R Triger, rRCP, rrader ilf esedicine Correspondence to: Dr Triger. 8. M o d J.19 t9 299:127-31 I Colky JRT, HollmdWW, CorkhiB! RT. toBucncs d puai.esmnkine .nd parcnub phkpn on pncumotua .ud MonchuWS ih orly chddhaod. Loxa.. 1974y:1031:4. 2Weac ST. Tayer IB, Spnsr FE, Roaaa B. Prn'strm wheett-m rdaoon tuo rtspirarory J1Yrcas; cquenc sewkng. aed Irvd d puloaoary fuactm in a pu{wbtiaa umpk (h. ehildrcn. Ant Rer Rerpr Du 1978;13:61951: 3. Whae JR. Ftoeb HF. Small:av.o5'F.dy,fwtctwo (n mmanakkn chtoecaay. azpoud to tobacco smaks.. l.' Ea1I7,Ned1980:302:720-3. • Kauffmann.F„Tnsirr JF;:Orio1.5r. Aduh pauevr itook- inthe botor envwoment:. rsk faaor.for cdtoote aiAb. Wtiuuon. A+7Epdr.ed' 1983;117r269-80., 5Lebo.irs MD.: lnfluence of paasiie smok.aj oe:tiulaanvy funcuon: a wr.q. P.re.Nrd19'Mt13:615-53: 6. Wald NJ, Nanchalll K, Thomqon SG.:Cuckk HS..Don bnatliityotticrpeoplr'„o6ocro smok< auu luo`. caoccr? & Md J 1986;293:1217,22- 7Gatiud C, Barren-Cuancr,E. Suarcz L. n d: Eftea, of paurvr unokuq on. uchaemx 6'ran dumr nortWtnof noo->muken:: a pposyecuvr wady.. A.J EpdJ.,ol 1915;121:645-50. t Hvyrm. T. Pa,re.e ,moLiq: a on. urtn al.npdrmwlop:. TwYa J Ezy CS. M.d1985,10.281<93. 9. S•rndun KH, Kidkc L:H; Manin MJI Qckeor JK. Eftrrn ofpautrr vnokuy mtlie mulupk rnk ranor mrrmouon tnal- A. J Ep4ono1 19t7;126: 783-95. 10 US Dep.rtmcot of Holth and Human Semcn.. Rnyvaury rjJao nJ uodwory. a.oie cspxre:.rpde+uloge uadvt. Rrpert of atoork,Anp::1,3. Mny 1983 . Bettinda. Maqiand:. Natwnat Inwm~tn of Hda@h, 1993, 11 GilLs CR; Hok DJ. Hanhoror VM;,BqIr.P. T1w rfkctw d emt,onmrnu6 whaeeo ,nw1a m.neo urhaocommuaroia (a thr .ra of',Soodrd. Er J. 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Vol 2. S(ockhob: S.edusE.Cound, fer Bwld,ty Reawrch:, 19N:31t-t. (rhacadiop of thr 3nl teteroationd conf~ oen intoor r.quWryand' clunau, suppl D)7.p 21 Wa1d N;.RachrC..Validation. d'atodies on hue6 uesr r eoa-mukm: oannrd to smcten.. Lwwt 19Hi:1067. 22 GJ41< CR, Hok DI, Hoaliwne VM. Ciprtttr atwk~ry aod mde huK c.ecer to ao un of vrryy tii`A urcbdence. 11.: Report of a paerJpopuhtiea mhon uudy w the Wrse of Scul.nd. JEpdrnool Co.atrwyHaW 19t/;42:1+t. 23 tus PN.. Mud.aJows a a 6cwr m.paw•r ..okur riek. Lww 1986;ti:867: 24 Btvch PRJ. Pamirrt .nkutr la dtMnodrd oaorr rsk. A. J.EpMrt 1986;123:368•9: 25 Wa1d NJ, Botrh'.m Ji.Bailcy. A, Riuhie C, tladtla. JE, Rmtht G. Urmary cotimar n:a m.rtcr of brethnt otErpnPlc'. robnsc mobe.. Laara 1984a:2361. (Accqud~ 24 May~.19ir9) ~. 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 6ver disease. Comparison of carbohydrate deficient transferrin with standard laboratory tests for alcohol abuse. Setting-A teaching hospital unit with an interest in general medicine and Gver disease. Parienu-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' alcoholies admitted to hospital for alcohol withdrawal; 68 patients with alcoholic liver disease confirmed by biopsy attending outpatient clinics and claiming to be drinkiag less than 50 g alcohol daily; 47 patients with non-alcoholic liver disorders confrrmedby biopsy; and38 patients with disorders other than of the Gver and no evidence of excessive alcohol consumption. /nterverrtiort-Serial studies performed: on the 15 patients undergoing alcohol withdrawal in hospital. Main outcome raeasure-Detetmination of relative value of techniques for detecting alcohol abuse. Results-Carbohydrate deficient transferrin was detected in 19 of the 22 (86%) self confessed alcohol'' abusers, none of the 47 patients with non-aacoholic 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 valtrable 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 consumption, others attempt to conceal it, and we lack reliable objective means of identifying surreptitious alcohol consumption. Currcntly 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 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 activity, is, and whereas a ratio of aspat'tate to alanine aminotransferase activity of greater than 2: f is strongly suggestive of alcoholic liver diseW' this is of little value in subjects in whom~the 427' BMJ vor.uME 299 12 AUGUST 1989