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03' THE \EW E-NGL.~ND)OLRNAL OF %IEDICI~sE LUNG CANCER AND EXPOSURE TO TOBACCO SMOKE IN' THE HOUSEHOLD DwIGHT T. JLA."'ERICH'. D D.S.. \'I.P'H.. W. DOUGLAS THOMPSOV. PH.D., Luts R. VARELA. M.D. PH D.' PETER GREENLV.ALD.. M.D.. DR.P.H..SHERRY CHOROST., \I.S,. CAT!HYTL'CC1. B~Si. ~ILHa>t~t.~D B. ZA?fAN. \I,.D:. %IYRO\ R. MEL.04ED- \IID.,, MAUREEN KIELY. R. Nl. AND MARTIV' F. M:CI\`EALLY- M.D., Abstract Background2 The relation between passive smoking and lung cancer is of great public health impor- tance. Some previous studies have suggested that expo- sure to envlronmental' tobacco smoke in the household can cause kJrng cancer. but others have found no effect. Smoking by the spouse has been, the most commonly used measure of this exposure. Methods. In order to determine whetheriung cancer is associated wtth, exposure to tobacco smoke wlthtn the household. we conducted a population-based case-con- trol study of1191 patients with histologically confirmed pri- mary lung cancer who had never smoked and an equal number of persons without lung cancer who had never smokedl Ufetime residential hlstones including informa- tion ion exposure to envtronmental tobacco smoke were compiled and analyzed. Exposure was measured in terms of -smoker-years." determined by multiplying the number of' years in each residence by the number of smokers in the household. Results. Household exposure to 25 or more smoker- years during childhood and adolescence doubled the risk of lung cancer (odds ratio, 2.07: 95 percenC contiden¢e interval, 1.16 to 3.68), Approximately 15 percent of' the control'subjects who had never smoked reported this level of exposure. Household exposure of less than 25 smoker- years dunng childhood and adolescence did not increase the nsk of lung cancer. Exposure to a spouse's smoking, which constituted less than one third of total household exposure on average,, was not associated'wtth , an in- crease in risk. Conc/usions. The possibility of recall I bias and other methodologic problems may influence the results of case-,l control studies of environmental tobacco smoke. fyonettw Iess, our findings regarding exposure during earfy life sug- gest that approximately 17 percent of lung t:ancers'ar4)ong nonsmokers can be attributed to high tevets of ezposure to cigarette smoke during childhood and adolescence. (N Engl J IMed 1990; 323:632-6.). T HE 1972 Surgeon General's report dealt with the health consequences of passive smoking or envi- ronmental tobacco smoke for the first time." In 1'986 the entire report was devoted to the issuc: it concluded that "invollJntar.- smoking is a cause of disease includ- ing lung cancer in healthy non-smokers.-` More than a d'ozen epidemiologic studies have assessed the rela- tion between passive smoking and lung cancer.''' The findings have ranged from, no detectable increase in risk"' to a moderate (about twofold), statistically sig- nificant increase.'" Most studies have found only small elevations in risk, which are frequently not sta- tistically significant.s °'' In a meta-analvsis of all' the a.'ailablt studies in 19861, Wald et al. found a slightly increased risk of lung cancer associated with environ- mental tobacco smoke.i° We undertook the currenr study in an attempt to clarif}• further the role of passi've smoking in causing lung cancer. In this report we discuss exposure to t'o> bacco smoke in the household as a possible cause of lung cancer among nonsmokers. MrrrtoDs We conducted'a population-based. individually matched case- control studv in New York State from, 1982 to 1985. The cases were drawn from seven Sundard' Stetropolitan Statisticali Areas From the Ikp.nnscnt,.ofEpdemotoly and Public He.1tL..Yak Universtty. SchoolloLMedtctnr. Nkw Ha.en,,Conn. tD.T.J.I: th umventry of!Soudsrrn Maine. Ponland tW D1.t: thr Populaoon.CouncJof Meztcu. !Ylesieo Ciq. tL V RR t: the Nanonsl Cancer Institute. w'ashtnpon..D-C. IP G,t:afte Ne_Yort State Department of Health. Slb.ny.IS.C ..C T.t: tM Slo.n•Kenrnng Memorul Insatute..Piew York iM B.Z...M:R.M.1: andAlb.nrMedtcal CotkI Albany. V.Y. tM K.. .M:F M.t. At7Creurtpnnt npucus to Ur Janench at~the Dep.rt- ment of Ep+OtmtotoFv and Public Health. Yak. UntrerstryScNool!of Mediane. 60CoIleEe St iLEPH t05lj New Haven. CT 063'10.. Supponedtn pan try pamu tP01 CA.+21qCsid ROI CA.)2(lddt tronsthc National Insututrs of'Hea/th. • Drcrased: (BulTalo. Rochester. Svracuse., l'tica-Rome. .%Jbanv-Schenecnd.- Trov, Binghamton. and'greater New 1'orkN excluding the five bor- oughs of New York Cih l. Thts geographic area compnses 23 coun- ties. with approximately 125 diagnostic or treatment factltties. and a population base of nearly I0mdlion,people .a special satemiorthe rapid~ascertainment of cases of lung cancer was established in these 125 facilities so that patients couldbe identified and enrolled as soon after diagnosis as posstble.,Alllnew cases of lung canccr Atagnosed clinicallv„ histologscalli;, or both) were rrgularlv tdenufied' at the participating hospitals. The New York State Cancer Registrv was checked routinely to idenufv anv cases that might have been mused by the hospftallbased reporting system. Information on smoking was initially obtainedTrom the patients' medical records. .-Ul the case patients reported as haang never smoked' or as former smokers or whose smoking historv was un- known were contacted'bv telephone. and thetramoking status was confirmed. To be includedu a'case" in the studv, a patient had to, reside in the 23-county area- be between 20 and~ 80 vean of age., never have smoked more than 100 cigarettes Inonsmokcni or have smoked at some time but not have smoked more than 100 cigarettes in the 10:vears before diagnosis (former smoken). and' have been given a dia;nosisof pnmarv llsng cancer between Julv It 1982: and December 31. 1984. that was confirmed on reexamtnatton of: the pathological'spectmens and clinical records. Slides or blocks of tis- sue were available for all but five of the case patients All matenals were reviewedbv investigators who were blinded with respect to the patient's initial diagnosis. smoking historv: and other ruk facton: N Interviews were conducted with 76 percent of'. the eligtble panenu O or their cJosest available relauves or fnends tsurrogatesl. Control subjects were individually matched'to the patients and ~ were selected'bv screening the files of the New York State Depart- r. ment of Motor Vehicles. This source of controls was considered appropnate since it was population-based and provided most of th v`e informadon nece»arv to perform the matching A list of potentiaJ )sA control subjects for each case patient was selected on the baais of ~ age (within five vean), sex„and'counrvaf resid'ence. Potential con- ~ trol subjects were contacted bv telephone. The first cGgsblesubject who was found to match the case pauent,.in terms ofl smoking huto- 04 ry(nonsmokenor former smokerl and who agreed to pantctpate wu ~ enrolled in the studv. An additeonal matching vanable constdered a V,t the time of data collection was the type of interview - i e.. direct interview with thrpatient or control subject versus interview wtth a surrogate respondtrtu When a surrogate case patient had to be intcrviewedl.we afsointervtewed a surrogate for htsor her matched'

% ~I ;:3 \o 1'0 LC`G CA`CER'AND HOLSEHOLD:TOBACCID SMOKE -J.A~~£RICH ET kL convol: e%en when the control subject was available and willing to be intcnaewed. Further information on the methods used in the studs is a.atlable elhewhere 's Data were collected for 439 casc--controi pairs. Of these. 242 pairs ,.ere former smokers and 197 pairs had never smoked' Separatnng the rostdual effects of direct smoktn¢ from those of passta smok'tng imon¢ former smokers in.ol%es more complex analvuc and tnter- precanonal issues than does anxxamination of'theetRcts of.passrve smokin¢ m those ~.ho hasc nc.ersmoked. This report is therefore limited to persons %•ho ne.ersmoked Six of the 197 pairs who had nerer smoked were mismatched m terms of the type of interview direct ~s. surrogate and hace therefore been excluded. Tfius, the anal.scs reported here were based on 191 matched ease-control' pa rs. A total of t:9'patrs were tnter.uwed direcdv. and surrogates %.ere mtentewed for 62. All inl'ormauon was collected dunng a face-to-faceinterview with use oli a precoded questionnaire. Casepatienta and'eontrol subjects wcre tntentewed tn exactlv the same fashion;,and except for items concerning the clinical aspects of the current medical condition. both groups answcred ehe same questions. Ihformnon about smoking in the household was collected sepa- ratel, for each residence in which the subject had lived 1'or one vear or more. up toa mactmum of'. 12 residences. The number of "smok- er-.ears" Of exposure was calculated by multiplying the number of' ,cars the subjecnli.ed in each residence by the number of smokers including the spousel in that residence. The produets for all rest- dences were summed. Smokine by the spouse was also recorded separately from that by other household members in a subsequent section of the question- naire. The information conststed~of the number of years the spouse had smoked while lig ing with the cue patient orcontrol subject and thcnumber of cigarettes smoked per day. Smoker-vears of exposure from the spouse s smoking were calculated in the same manner as for the entire houseNolti. Pack-vean of exposure from the spouse were calculated by multiph ing the number of paeks smoked per day bv the number of cean that the spouse smoked while living wsth,the subject. If the subjeerhad been marned to more than one smok'er, then the numbers of smokcr-.ean and pack-vean of exposure for all spouses were summed. The questionnaire allo included secdons on exposure to environ- mental tobacco smoke in the workpiace and' in social settings out- side the home. The format for these questiom differed from, that used'to collect data on exposure in the household. The summary results of this anahsis are presented here; detailed findings are asatlable elsewhere.'s Statistical techniques appropriate for the analysis of individually matched easrcontroi studies were used.°'D For clanry of presenu- tian, percentages were eabulited for case patients and control sub- jccts separatelv; rather than for matched pairs. However. odds ra- tios were computed on the basis of the matehed, pairs. The conditionallogisuc-regrnsion motietwas used in themultivanau analvses." Comparisons of the effects of exposures that occurred d'uring different periods of the subjects' lives were based on evalua- tion of differences in the magnitude of appropriate logiseic-regres- sion coelficienu. For statistical testing of these di6erenca. we used the vanance-covariance nutru from the logutic-regression analyses, Rrstn.-ts Smoking by spouses contributed a large propor- tion of lifetime exposure to environmental tobacco smoke but was not the chief source of exposure. Table 1' shows the amount of exposure to environmental tobacco smoke (expressed in smoker-years) during, childhood and adolescence, during adulthood, and' from the spouse for the 191 control subjects who had! never smoked. There were only small differences be- tween men an&women. The spouse contributed about 30 percent of the lifetime smoker-years of exposure;, the correlation coefficients for exposure from the spouse and lifetime exposure were 0.37for men and Table 1' Distnbutton of Srnoker,Years of Exposure to Environ- mental Tobacco in the Household.' C.ncae. o. Exrosu:u Meu wort. . L feume smoker-years. 46 mean _SD Smoter-yean dunnt chikDiood:and adokxence* 6_ y3.7 1',I I 7_ e2 9 Mesn : 5D 15 4 :210 6 16 1 e 16 2 f snc~ent of Idenme e.posure Corre/auon.w-nh,llfenme eaposue 33. I 092 30 ~6 0'61 Smoter~yesn frcxn spouse Mean _5D 13.0_170 16'I'-16.7 fkrcem..of lifetime eaposna :S 0 30:7 Correlaswn .rtn.hfenme esposuvt 0 37 0.51 Smoker-ye.rs.dunnt adulthood Irom sources other oun spouse Mean-SD IlIa310 '-05_=99' Percent of.lifenmeexqosure. 38 9. 3! 9Cortetation with lifenme exposuwc 091 0!3 •erM an 43 m.L rre t46./enWe cawoN wwr.c:s.ho nd nner u+waa mae tfr.n 100 citrefu. lnfanrno. ee smoeer-y.an.of eapo.uR Inan tlr rpeiuen.ICr.r5.mn4.rtl Ie0trmW eavd rrE7RV Smetersan .•aereNCU/a.G trr nwlupyip Cr iweiear of jun.dr rwr.n iwWu./sdnce Ey, ee numear d'.rtoeasuiee nworn/d 1lsar der 21.ys1 d op:. 0.51 for women, Exposure during childhood and ado- lescence (<21 years of age) contributed a similar per- centage of the lifetime smoker-years but correlated more closely with lifetime exposure (correlation coeffi- cient, 0.92 for men and 0.61 for women). The average lifetime exposure was 46.6 smoker-years for men and 52:7 smoker-yean for women. During adultliood,, household exposure from sources other than the spouse was somewhat greater than from the spouse. Table 2 shows the odds ratios for developing lung cancer in relation to the degree of exposure to tobacco smoke in the household for the 19'I nonsmoking case- control pairs. The data are stratified by levels of expo- sure ('measured'in smoker-years)'and by the periods of life when the exposure occurredl Exposures during childhood and adolescence were defined as exposures that occurred when the subjects were less than 21 years of age. Exposures during adulthood include all household exposures from 21 years of age to the time of diagnosis. Although the odds ratios for the higher exposure categories are somewhat higher than those for the lower categories, no clear dose-response rela- tion is evident, and most of the 95 percent confidence intervals include 1.0. For exposures in childhood and adolescence, the highest level of exposure is,assrxiated with the greatest elevation in t~al~`in~ 95 percent confidence interval excludes the null'value (odds ratio, 2.07; 95 percent confidence interval, 1.16 to 3.68). For the 129 case-control pairs who were interviewed di- rectly, the odds ratio for persons with 25 or more smoker-yean of exposure in childhood'and adoles- cence was 2.31 (95 percent confidence interval, 1.16 to 4.61)1 With smoker-years during childhood and adoles- cence and smoker-yean during adtilthood' treated as continuous variables and included simultaneously in a logistic model, each increment of five smoker-years of exposure during childhood and adolescence was found to increase the risk of lung cancer by 6.5 percent (95 percent confidence interval„0:1 to 13.2). On the other hand, each additional five smoker-yean of exposure

634 THE NEw'EvGL{.N p,JOI;RyAL OF MEDICINE Sept 6: 1990, Tatilb 2. Re4atron of Smoker-Ysars of Exposun to Envtrt3nmenty Tobacco Smolie to the Rask of Lung Cancer among Persons Who Never Smoked More trtan 100 CiQarettes.• .o or Cmtt AwwY1wP.m,m Co.r.ouS ODn: K.no,9!% Q) ro A1 ChJdtioad ~ ud,adokuence•. 0 37 :9!) 6!t)J6) 1-.:a 62't4Z91 9aU921 1.09 ~0.61-1 73)~ >2S 32 t27 :) 29'115 21 2~~071I 16-3691 >dulqrood 0 +A t230P ?9(20.) I-:• 37.t19..1+dt2Sli 0 64 40 34-I 211 25-19 +6 2s u 5011.62), 0at(04s-I,.s) ~0_ '4 36t1A.91 32t16R1. 1 00 t0.32-1-931 ;P 7 5 :il n1. 71 . 22 u l s) I I f ~0 36-2 :0) Lttenrne 0 32 (16 {1 33 (17 3) 1_;. :0110.31L7id41D 0 73 (0:36-1 67) :S-s9 3S(I{3) a6(24 1) 0 10 10 143-1 301 yt)-'a +A 23 01 40 120 91 1 19 (0 63-1:27) 33 (I1 3). 21 .111 0) I $0 10 i3-3 90) a 100 27 (I4 1) :4 (12:6) 1 13 (0.56-2.231i •L..G - 191 'e.ce.a c~ p.vr Cl Oevor• re.Mroo anr~N' 0ri rtrm w Man !a r pvfor. rim ft rapovr.fpsitl.t ta caepd .4 r PRris .A M rspr/e .0. w.ola7~+t ~ e.oir.dtitly. p.vs" ee M L.q4 d 100., •lsssmr2ly..>te[r& during adulthood'were estimated to have virtually no effect on risk (95 percentconftd'ence intervali - 3.3 to +2.8'percent). The difference in the magnitude of the effect between exposure during childhood and adoles- cence and exposure during adulthood did not achieve statistical significance (P = 0.12). On the basis of the distribution of exposure ltvels during childhood and adolescence among the control subjects and the magnitude of the effect of early exposure, we estimate that approximately„ 17 percent: of all Iung :uncers in nonsmokers cin be-attributed to`°ex~oiure-to pas- sive smoke iaAhe household during childhood and adolescence. On the basis of the odds ratios for the 129 case-control pairs who' were interviewed di» rectly, approximately 19 percent of lung cancer in nonsmokers appears to be attributable to exposure to environmental cigarette smoke in childhood and adolescence. Since smoking by the spouse has been the most commonly reported measure of exposure to environ- mental tobacco smoke in previous studies, we exam- ined exposure from the spouse separately, although exposure to environmental tobacco smoke from the spouse is also included in the results shown in Table 2. The odds ratios for exposure frequently differed ac- cording to the type of interview, especially for the data on exposure to a spouse's smoking. Table 3 there- fore shows the results of the analyses of exposure to environmental tobacco smoke from the spouse separately for subjects interviewed' directly and those for whom surrogates were interviewed. The odds ratio for the development of lung cancer for those who ever had a spouse who smoked, as compared with those who did not, was 0.93 (95 percent confidence interval, 0:55 to 1.57) for those interviewed directly. In terms of smoker-years of exposure to the spouse's smoke. the results show little effect, with am od'ds ratio of 1.07 for 25 or more smoker-years of exposure (95 percent confidence intervall 0.59 to 1.97)., Estimates ~ based on pack-years of exposure from the spouse were similar to those based on smoker-yean. For both measures, there was little evidence of a trend accord, ing to amount of exposure among those who were exposed. All analyses were repeated for only the case-control' pairs for whom we had complete and internally consis- tent data for all residences and marriages. rlnv pair was dropped from these analyses if data were incom, plete or missing for either the case patient or the con- trol subject, leaving t'13 pairs of nonsmoken. Our purpose was to ensure that our conclusions were not dependent on the particular methods we adopted to handle inconsistencies or missing,items in the data set. The findings were similar to those for the entire group of 191 pairs. The odds ratio for exposure to 25 or more smokgr-year3 in 'childhood and adolescence was 2.59 (95'pescent i:onfi~ence'iiitervii:''G.22 to 5.49). Exposure in the workplace was mevured' by record- ing the number of smokers who worked with each study subject during his or her lifetime and the amount of time the subjects spent working with these smokers. These exposures were compared fbr case patients and control subjecrs. Estimating the odds ratio as a continuous variable for an equivalent differential of 150 person-years of exposure gave an odds ratio of 0.91 (95 percent confidence interval, 0.80 to 1.04), indicating no evidence of an adverse effect of environmental tobacco smoke in the work- place. Our assessment of smoking in social settings used' an untested, semiquantitative index in which the case patient or control subject used a score of 0 through 12 to indicate his or her regular exposure to tobacco smoke in social settings during each decade of life. Cumulative lifetime reported scores ranged from nearly 0 to more than 70. The odds ratio for an increase of 20 in the cumulative score was 0.59 (95 percent confidence interval; 0:43 to 0.81). Our analysis of exposure in social settittgs, with use of this index showed a statistically signifiunt inverse as- sociation between environmental tobacco smoke and lung cancer. IDtS1GVSilON We found a statistically significant adverse effect of relatively high lewel;t of exposure to environmental to- bacco smoke during the early decades of life (up to the age of 21). For those who were exposed to 25 or more smoker-years during their first two decades of life, the risk of lung cancer doubled. This amount of exposure is equivalent to livmg with more than ooe smoker throughout childbood and addesceace - a high but not uncommon level of exposure. An expoeare of this level was reported for approximately 15 percent of tbe txntrol group. By contrast, we found no adverse affect of exposure to envitvnatentil tobacco smoke during adulthood, induding exposure tn s spom- who

\ o l 3': 3 \" o i J~ LLNG C.-k:\CER AND HOISEHOLD TOSACCO S~tOtlE - JANER1CH ET ~L 635 Table 3. Relation of Spouse's Smoking to the Risk of Lung Can- cer among Persons Who Never Smoked AAore ttnan t0©C9a. retfes, According to Type ot Intervlew:• r.rror I.ro~n. ordi ww i91 % Cl,. ENer' Aad a spouserlso smoked No - Yes 0 93'(0 iSS- 1 57) Smoker-years of expos.urc from spouse 0 - 1-.4s. o'e.f0;41I-I.SO) a25 1 07 (0,59-1 97) Pack-ean of exposure from spouse 0 - 1-24'. 0 71 (0iJ7-1 35) '-3-i9' 098 (0:47-2:03) a50~ c.10(0:47-2 36) ,t.111ta.,t 044 (0 19- 1 02) 0 3310 tl-I 0]s 033f0IC-09S) 0 16 (0 0+-012) 0 68 10 t A-2. 60) 0 20'l0 03- 1.22) • Swd on I 29 crss-<onerol pun inom ered di~Nj, oiC J9ptys fer +nons sv+otief eee 'nrerva.edrMte of Te 191 pw:.ert eacludeC Decwe for onememEer ol tlrepurtlsere.r zuin1 intvm.epn atau,.r/iktfstr th suepn,ludt spou.e .AO snnted: Dra on unater- -en of.e.puwrt .enr e•u11a1e fot 129 cutKeneol p.v+.iss Cuan innnK+. sne36 pun -A Surrol.¢ ~nuF.t.s Dui onpnck-re.n of t.pn.un wea+Y4Ek for 122'peus..1N Oirecm -err,ea ud 71 pun .rdf smretre ~ner.r+s CI OonoescanlSOence~n,erv&J Odds nuos ere sno.n for .. ptnan atlr dreaposurt spaih.d:u.comp.reA.-eh a person -tll0 no ttpoture. iua syouse fw smok'.0 smoked. Although, problems of recall and other poten- tial biases may have inHuenced'the results, our data suggest tharexposure in early life may be a limited but important contributor to the risk of lung cancer in nonsmokers. A previous study with a small number of subjects found littlE evidence of an elevated risk of lung cancer among nonsmokers whose parents had' smoked." Children of parents who smoke have been shown to be especially susceptible to respiratory prob- lems that occur soon after exposure to environmental tobacco smoke.' This type of susceptibility might initiate changes that eventually lead to lung cancer when the exposed children become adults, but we know of no specific mechanism that would explain our findings. We found no adverse effects of exposure to tobacco smoke in the workplace, although we did' not have enough information about the level of exposure in the workplace to assess the precision of our measure- ments. The apparent, protective effect of exposure in social settings is difficult to explain. During the course of this study, regulations in New York began to restrict smoking in the workplace and' in social set- tings such as restaurants. We did not anticipate this devdopment and cannot estimate how' much the awareness of these new restrictions might have af- fected the responses of the study subjects or their surrogates. Evidence is clearly mounting that tobacco smoke inhaled passively by nonsmokers is potentially car- cinogenic. In a recent study, Maclure et al.11 found elevated levels of carcinogens in the blood of passive smokers. Levels of hemoglobin ad'ducts of 4-aminobi- phenyl and adducts of 3-aminobiphenyl were signih- cantly elevated' in subjects with confirmed exposure. The validity of this finding was supported by addi- tional evidence that showed a sharp decline in the Itvels of adducts among smokers who qu)t.21 At present, information on past exposure to envi- ronmental tobacco smoke can be obtained onlv bv interview. The availablt• biologic markers, such as co- tinine, cannot be used to confirm exposure that oc- curred years or decades earlier. The use of interviews to obtain a lifetime history of exposure to passive smoking requires that the questionnaire be structured and the interview techniques be standardized so that all subjects are interviewed in the same wav. We took steps to ensure such standardization. Two recent re- ports may lead to improved ways to measure lifetime exposure to environmental tobacco smoke by means of interviews.2"s In one of these studies, which at- tempted to evaluate the reliability of interview data by repeat interviews, information on exposure during childhood was found to be very reliable." It was necessary to use surrogate respondents for about one third of the interviews, usuallv because the patients were too ill to be interviewed~ To minimize potential bias„surrogates were also interviewed for the matched control subjects, and separate estimates were calculated for respondents interviewe& directly and surrogate respondents. We used equal care in all types of interviews and in all' subject areas covered in the interviews; however, the data we obtained in inter- views with surrogates still differed somewhat from those obtained in direct interviews. Inaccurate report- ing of exposure tends to bias odds ratios toward the null value unltss a svstematic bias is present. Data from surrogate respondents are likely to introduce random error because of the surrogate's lack of de- tailed knowledge of the subject's exposure. On the other hand, it is possible that the surrogates for pa- tients with lung cancer might tend to underreport the exposure contributed by their own smoking to a great- er extent than surrogates for controll subjects. Such a difference could mask an actual increase in risk or reverse the direction of the association. The findings shown in Table 3 indicate that the use of data from surrogates may have led to an underestimatiomof the effect of exposure from the spouse. Although our re- sults for exposure due to smoking by the spouse differ from those of earlier studies,'" our findings regarding other types of household exposure support the conclu- sion that exposure to environmental tobacco smoke can cause lung cancer. Akiba et al'.,' Dalager et al.,' and Garfinkela have reported elevations in risk of 30 percent, 50 per- cent, and 1I0 percent, respectively, associated with ex- posure to a spouse's smoking; none of these increases were statistically significant. With the exception of Chan et al." and Koo et al.'' in Hong Kong, these and most other investigators have reported'point estimates that suggest an increased' risk for those exposedL The duration of exposure, as measured by the number of years the spouse smoked while living with the sub- ject, did not have a statistically significant effect in our data. Two studies that used the same measure

3 636 THE NEW ENGLAND JOURlVAL OF MEDICINE Sept. 6. 1990 of exposure also failed to exclude the null value.a•9 Garfinkel et al.,' using a difTerent measure for duration of exposure (husband's smoking in the last 5 and 25 years), found one significant association among the large number examined. Exposure due to smoking by the spouse. expressed in terms of pack-years while the spouse was living with the subject,, was found not to be significantly associated with lung can- cer. Using a comparable measure of ezposure, Tricho- poulos et al.' reported relatively large increases in risk (greater than twofold). erhaps our data_ do not. show that smoking bc the sus ' "' ch~~`ns •bv itself because smoking .b~ t.e..~s ,•~ s~mA,,sadup on~y, a~~~(~of the subjects lifeume,*exposure to' en°vironmenial'`tobaccd1 smoke: I n is also` possibte that physical circumstances and`~difkrences in study areas. the size of residences, ventilation, and other important physical aspects of the living conditions, as weil' as social habits that affect exposure within the familv, will need to be measured and anahzed before the differences in findings among the studies can be reconciled. The evidence we report lends further support to the obsq,,e~that~ass~yae~stnoktng may incieasrthe l~o su sec~n un~canceY;C4art~d tt suggests that it r... . . - .v ma~be~ a~rticu ar ~* tmportant to protect children and adoles,,ents frorn thts`enviconmenEal°haiard. W'e are indebted to Andreas Nicolaou for his auistance with the computer programming used' in our analyses. RLF7RLNCLS I!. Departirent of Hea1tE. Educaoatt. and Welfarc. The health coroequenees of satofune a reputof die Surjeon General: 1972. Wasfitnpon. D C.: Gov- envorntPrinttng Ofhee. 19i2:121-33. tDHEW pubi+catwn oo. lHSM172- 7116:1' 2. Depvmttent of Health and Hanue Serwes. The health conaequences of involuntary snwkin{: a nrpm of ttrc Surteoe Gemal. WastunBtott. D.C.: Governmcet Pnonttll OfRce. 1966. (Pubtierooa m. DHHS (CDC) E7. A396. ) 3. Garfinkel L Tieoe eteda in lung cacer reoTdiry .monB noenmolias and a note oo paatve smoting. I NWC aecer tst 1961: 66:1061-6. 4. Hinyam. T. Cancer ntortaliry tn noaunoksn1 .omee ~tf+ srtrok,nj nus. lan+d~ ti.sed cn a l.rge-acale cohiort endy u+ l.p.n. Ptsr Med 196a: I J 6t14 90 S. Ttxtqpoub. D. Kal.ndidi A. Spsaioe L. Lung casxtt sod passive smoliin{ conclusion of Grcek sttrdy laneet. l9fl3. 2:677.{0. 6. Cortu P. Pictik LW. Fontham E. 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