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41 (PPL:L-L A B S T R A C-T 4b1endVe_.T_ ~,.. c~amoog nartsmolrers tum; not Y tmdastuod. To fiuthcr eval- trata thc: relatinn. between:n passive expotatre and lung cancer in nonsmakingwomen; we oonductcda population-based, casc-control stuay._' ". ~-°thods- Case patients (n '= 618), identified through the IvFis- souri,t`uncer Regstty for the;pcriod 1986'thmugh 1991;"indudet! 432 life- tima noa4molocrs:and 186 exsmok-. erswhohad stoppedatleast 15 yeats before diagnosis or who hadsraoked' fbr°less than I pacIcyear...Control subjects (n ~= 1402) were seltcted' 6om driver's license and Medicare filtx Iiesullx No increased risk.of'. lung cancer was associated with childhood passive smokz ; exposute. Adulthood analyses showed! an in- cceased lung cancer risk for lifetitne nonvnolaers with exposure of moree than 40'padt-years from all liouse' hold tnembers (oddsratio [CDR] = i.3; 95% oottfdeacc intereal [QJ = 1.0, 1.8)orfnomspousesonly(OR ~ 1.3; 95% Q, = 1:0,11'E): When the time- weighted'producx of paclt:-years and avetage hours exposed per day was considered, a 30% emcess risk was shown at the highest quartfle of pc poaute A mong li6etime nonsmokers. Conclresiorctr Ours and other r+e •- cxat studics strggesT a small but con- sistent inatased risk of lung cancer fronr passive stookit[g. Cot[rprehen- siere actions to limit smoking in public plaees: and! worksites are well-ad~ vised. (Am J Public, Health. 1992;82:1525-1530) Passive Smoking and Lung Cancer in Nonsmoking Women Ross C' Bn7svnsorS Phl), tLfichael'C R AlaHanjq IArPH,' F.,dwmd T. Hock, B$, and:Trntodry S' Loy,1lLD IrrbnducYion Although rnost lung cancer occurs in smokets, approximately 9'Xc' to 13% of lungcaneercases in US women develop in lifetime nonsmokers.t-5 The causes of lung canr er in nonsmokers have not been widely studied, but probably comprise a diverse set of factors including genetics, occupationall factors, radon exposure, die4 and a history of'nonmalignant, lung disease. In addition to these risk factors, the etiologic role of passive smoke exposure has received increasing scrutitty over, the past decade. Numerous studiess-m have suggested an elevation in lung,cancer risk for nonsmoking females who live with a smoker, , with a summary excess risk of approximately 30%:2°•22 However, sev- eral l recent studiest-23-27 have shown no increased lung cancer risk due to spousal smoking. Limited evidence7•26 also suggests that exposure to passive smoke in child- hoodimay increase riskof lungcancer. For example, a,recent casecontrol study from New York found that hottsehold exposure to tobacco:smoke during childhood of 25 or more smoker-years' duration was as- sociated with i a doubling , of lung cancer risk.?6 Most previous: studies of' passive smoking and' lung cat[cers although sug- gestive of a positive effect, have had sev- eral deficiencies. These deficiencies in- clude sample sizes insufficient to singly demonstrate significant elevations in risk, limited dataion passive,smoke exposure in both childhood and adulthood. and lack of histologic review of cases to verify lung, cancer diagnosis and'to allow analyses by cell I type . To more fully evaluate the relation- ship between lung cancer andl passive smoke exposure in childhood and adult- hood, we conducted' a large case-control study of lung cancer among nonsmoking women. Met+llodS Case Group Case patients were identified through the Missouri'1 Cancer Registry, which is maintained by the Missouri IIDepartment of Health. The Registry began collecting data on incident cancer cases from pubhe and private hospitals in 1972, and hospital'l reporting was mandated by law in 1984. Registry reporting procedures have beenn discussed I in more detail elsewhere.ffi Too ensure complete reporting of lung cancer cases in women,for the current study, we had Registry staff complete special case ascertainment visits to participating,hos- pitals. The case series included White Ivfissouri women, aged30 ito 8Io years, who were diagnosed with primary lung cancer between January 1986 and June 1991. Se- lection was limited to Whites because of small numbers of' other racial/ethnic Ross C. Brownson is with the Division of Chronic Disease Prevention , and Health Pro- motion, Missouri Department of Health, Co- lumbia, Mo. MichaeliC. R. Mavanjais with rthe Epidemiology, and Biostatistics Program, Na- tionaltarrcerlnstitute, Rockville, Md. Edward T. Iilock,is with Information ivtanagement Ser- vices, Rockville„ Md. Timothy S. l.oy is with the Pathology Departmenti University of Mis- souri School of Medicine, Columbia~ Mo. Requests for reprints should be sent to Ross C. Brownson, PhD, Division of Chronic Disease Prevention,and Health Promotion, Missouri Department of Health, 201' Business Loop 70 West. Columbia, Iu11765203'. This paperwas submitted to the Journal February 19, 1992, and accepted Iwith revisions August 12. 1992. November 199'ti., Vol. 82, No. ll American Journal of Public Health 1525

Browoso.a et alL groups. Thecase groupinduded both lifee time nonsmokers and' ex-smokers who had stopped smoking at least~ 15 years be- fore diagnosis:orwho had!smoked for less than 1 pack-year. From the 3475 cases of, lung cancer in women reported for the study period; 650 eligible patients were identified. Physicians i denied' interview permission for 24 (4%) of these patients andanadditional 8 women i(1%)',refused too be interviewed. The final , case group 1 in- duded 432(70%) li.fetitne nonsmokers and 1 1'86 :(3096) ex -smokers. Of the 618 case : interviews, 216 were conduded'with 1 pa- tients themselves and 402 were conducted with surrogates because the patient was, too t1lto be interviewed or had died. Of the surrogate interviews,1Q5 (2696) wcreeon- ductad with the patient's spfluse and 29'f' (7496) were omnduded Iwith lattotlier rela- tive (e.g., offspring or stbling).. FI'cstolcgic Cvnfimtat;ion o}'Cases. Tissue slides were reviewed for his- tologic verification for468 (76%) of the 618 cases. Slides for these cases were exam- ined'simultaneously by three pathologists (T:L, E:I., and ].M.) using a multiheaded microscope without knowledge of the re- fening' pathologi.st°s diagtosis. In surgical specimens, consensus diagnoses were ob- tained with the criteria outlined in the World Health Organization classification scheme.29 When only cytologic material was available, consensus was obtained with standard cytologic criteriai30 Corttsol Crotrp. A population-based sample of con- trol subjects was asctrtained by two meth- ods. For women younger than 65 years, a sample of state drnrer's license files was provided by the Missouri Department of Revenue: For women aged 65 to 84 years, .)ontnol subjects were generated from the Health Care Finance Administration's roster of Medicare recipients.» On the ba, sis ofiagedistnbution of lung cancer cases previously reported to the Registry, the final aontnol I group was matched by age group to case patients at an i approxamate 2.2 to 1! ratio. All controli subjrets were interviewed I directly. Of the 1862 poten• tially eligible control'subjects, 335 (18%)) refused the initial screening interview and 125 (7%) of those screened and found el- ig»ble refused the full interview. The final control group numbered 1402:. Questionnaire Design, and Ad,minisbnttion Telephone interviews were con- ducted by trained interviewers. The first phase of~ the interview consisted of a screening questionnaire to verify the age, race, and smoking status of'case patients and control subjects. For subjects who were screened and found eligible and 4vho agreed to the full interview, the study questionnaire consisted ofsections onires- idential history, passive smoke,exposure; personal healthtiistory, family health~his- tory, reproductive history, occupational exposure, and dietary factors. Questions regarding passive smoking focused onexposure in both ciu7dhood (17 years and younger) and adulthoodl (18 years and older). For each, time poriod, respondents were questioned about the source of exposure (e.g:, a parent orr spomsc): After an individual source was determined, a series of detailed questions were asked on the type of tobacco used, duration of exposure, intensity of expo: sure, and average number of' hours per day exposed. These questions were par- tially modeled after those developed I by Wynder et al.32 In additionto quantitative estimates of exposure, respondents were asked to estimate a perceived level of ex- posure during childhood and adulthood i ("During most of youradult years, wouldd you say that your average exposure to smoke at home was hght; moderate, or heavy4"). Analyses Odds ratios (ORs) and 95%~ confi- dence intervals.(CIs) were cakailated with multiple logistic regression73 The linear- iry of trends in risk according toJevel.ofo passive smoke exposure was: evaluated with Mantelis one-tailed test.}' We ini- tially examined numerous:potential con- founding factors. These included'age, ac- tive smoking (for ex-smokers), history of previous lung diseases, dietary beta caro- tene,,and dietary fat. Of these variables, only age, active , smoking, and previous lung, disease appeared to confound pas- sive smoking findings; therefore, the re- sults presented are adjusted!for these fac- tors: Histologic type-specific analyses were conducted for cases for which con- sensus diagnoses were determined. These analyses were undertaken because earlier studiess•19A 'have shownvariations in risk by cell type, and biological mechanisms have been proposed'that might,aocount for: these variations.m-3s Rem& Sociodemographic and smoking-re- lated characteristics of case patients and control subjects have been presented in detail eLsewhere?6 In brief, the average ages of case patients and!control subjects were 71.5' years and! 693 years, respec- tively. The tiwo groups were also cornpa- rable on level of education i and income. Among ex-smokers, the median; interval since cessation was 24 years, and average smoking intensity was 16.4 cigarettes perr day. There was little evidence of increased lung cancer risk associated with passive smoke exposure in childhood (Table 1'). This lack of association was apparent forr both the dichotomous variables (never vs ever exposed) and quantitative measures such as pack-years.llte only suggestion of elevated risk was noted!for less quan- titative exposure variables (not'shown in table). Among lifetime nonsmokers, an in- creased risk of lung cancer was shown ifor thosereportittg moderate (OR = 1.7; 95% CI' = 1.1, 2S) and heavy (OR = 2.4; 95% CI = 1.3, 4:7) exposure to passive:smoke, in childhood. Risk estimates for most childhood exposure variables weree slightly higher (approximately 20% to, 30%) when analyses induded lonly di'rect interviews, although none achieved statis- ticalisigtificartee. An elevated risk of lung cancer was identified i for lifetime nonsmokers at the highest quartile of passive smoke expo- sure in adulthood (Table 2). At an expo- sure levellof more than 40 pack-years,,life- time nonsmokers showed a 30% increase in tiskwhet;herthe soureeof exposure was all household members or spouses only. Similarly, when the product of'pack-years and average number of tiours exposed per day was considered, lung cancer risk for lifetime nonsmokers was elevated for the highest exposure quarrtile whether the source was all household members (OR = 1.3; 95% CI = 1.0, 1.8) or spouses only (l7R' = 1.3; 95!'l0 ~ Cl = 1.0, 1.7): Among lifetime nonsmokers, a positive in- ereasing trend in~r,sk was noted'for pack- years (P = .06)1 Passive smoking-related risk estimates for adulthood exposures were , slightly lower for all I subjFcts (i.e., both ex-smokers and lifetime nonsmok- ers) than for lifetime nonsmokers alone, although the same general, elevations in risk were noted. When analyses were lim• ited to direct interviews, no clear pattern of increase or decrease in risk estimates was apparent. Regarding less quantitative exposure variables, elevated risk was shown for all subjects (O'I2' = 1.7; 95% CI = 11.1, 2.6) and for lifetime nonsmok- 1526 American Journal of Public Health TJo++ember 1992, WVol. 82, No. llt

r Diwussion~, -MABLIE•1.-,Aq~NM4jOddsfiatloo..y01~'~~nd !5%0oNMlanoa YNwwdr(CQ ~q~i[UMNotNhlp,b~lwa«f P..rlw-Sttwk! E~Onw ~~ :. = exdut4gl>NMood rtd ltmp Car>m.'in ANotmt% iYs.otrU ti9a~o~It~9Y1 _ •.JqJ $ttbjectS° A1fa0me Monarnokets. ;.8cta qe of Eivosune No. Pase s No. Corwds OR 959L t:1 ~,i;N& tases No. Conttols OR ^a5l6 Cl N'hoteehdd membsra f4erer 430 •Ever' 165 '-DWMM peck'Years 0 - 430 >0='15 . 42 :>a5=25 3i1' ZQS~K , r~ r~ .. ~~ 34.~.. r 426 928 1.0, 3M 472 Q8 0.7,1.1 • 108 928 1.0 129 Q7 OS,;f.D 1na 0.6 Q4,0.9 ` 117 Q7 OA.d.~ ''yQ21. . .+G:,1021 Q4 ; . D.3,,.' A.5 ': ~ ~--0.3,a . osAA ioR.c..hw-yot tx.~aaA~w~i..ess..no.ra.a~++okkb{e+r+ofeUS ..- -lva.rthfm.,ara+dopsand.eF«,dors.rf,~haa alopqsastl.a~tlSp.ers bek~n. :rs (OR:= 1.8; 95% Q= 1.1, 29),who eported heavy exposure to passive u>mke. In general„tticne was noele+vated lung anaer risk associated with passive smoke xpttsura in the workplace (not shown in able)1 Only lifetime nottsmokers showed slight iitcte,a,se in risk at thehighest quar- ile of workplace exposure (OR = 1.2; 59bQ=0:9,1.7). Among the 468 lung cancers tharwere eci<ied histologicaliy, the predonunartt cell /pesware adenocarainoma (62.4%), other/ iboed rtlltypes (?5.291;), squarnous cell car- atoma (5.8°.b), bnonchioalvemlarcatcinoma l.P%), and small cell carcinoma (2:5%')- he r'her/miaced cell type rategory con- stec -iainly of large cell lung cancers,. tough these lacked sufficienu pathoiogic videnoc for precise dassifkation. Table 3 resents results of oell'type-speaific analy- x'for adulthood eposunes. Elevated riskk as shown for other/muoed cell types at iore than 40 pack-years of exposure )R = 1.6; 95%CI'= 1.0, 2S)..4lthough it as based on small numbers, a risk estimate ' 1:7wasobsetved forsmallioell rarcutoma the higltest level of exposure. We also examined risk among omen who had been exposed to,passive ooke in both childhood and adulthood, c1u'Idhoodbut not in adulthood, and in, (ulthoad but not in chil(ihood. There was ) evidence of'interaction between expo- re duting,the two periods. 20 ' 91 0~6 ~~ t A 21: t3P ::'(:7 .,"12' PaSSivV smuloM and ILAMg Gneer 802 364 1.0 0.8 ' 0.8;1.1 .a1D 74 ':0.9 'KA.S,'~A': fi.a~ occupational eacposttres) that may'intaact with passive smoke exposure to increase risk above tharobsetved in women. Pres- enoe orabsence of, a smoking spouse is a relatively tattde measure of passive smoke . expostue, with a! potential ! for wide vari- ability in ~aetual exposure. It was noted in one survey, for example, that, 47% of' women married to smokers neponted'zero hours of' passive smoke exposure at home:r It has also been shown that con- sidering spousal exposure albne may un- derestimate total household passive smoke exposure.38 ' Another factor, tltau may account for the differences in ilung cancer risk due to : spousal smoking, be- tween our study and earlier studies may be . time trends in smoking patterns. Tlie de- clining prevalence of smoking among, men39 has probably resulted,in decreasing , years and perhaps levels of exposure to passive smoke in the home among non- smoking women whose husbands smoke. Contrary to the findingsof two earlier case-control'studies,7.26 our data showed no evidenee of excess 3ung cancer tisk due to passive smoke exposure in childhood. The risk of:lung cancer due to childhood passive smoking may have some analogy to risk among ex-smokers. After 10 years of abstinence, the lung cancxr risk for ex- smokers declines to 30% to 50% of the risk for continuing,smokers.'0 Similarly, lung' cancer: risk due to passive smoke expo- sure in childhood may decline by adult- hood, especially in the absence of adult- Our study suggats thaU exposure to high levels of environmental tobacco smoke in adulthood increases the risk of lung cxnoer in ttot>smokets. Exposure of~ more than 40 pack-years' duration in- creased the risk of lung cancer among!non- srttokers by appnoxdmately 30%. This re- lationship was consistently demonstrated I among, , lifetimenortsmokers whether the exposure variable was pack-years or the time-weighted product of pack-years and average numberof hours exposed per day. Ourfmdings are similar to thoseoffianother large study of lung,cancer in nonsmoking womenm that identified'an ~OR of apptox- imately 13 due to exposure togreaterthan 40 pack-years of spousal smoking. In earlier studies, the most com- monly reported index of passivcsmoking' exposure has been the presence or ab- sedee pfa smoking spouse. In our data set, no elevated risk was noted i for this vari- able. Since our study was limited to womenipart of the difference between,our findings and those of'earlier studies may be due toidifferencxs in the effects of1pas- sive smoke exposure by gender. The Na- tional Research Council's summary of' 13 studies21 found overall relative risks of lung cancer in nonsmokers due to spotual smoking of ~ 1.32 for women and'.1 L62 for men, (although the estimate for men was based on few cases). It is possible that men are exposed to other factors (e.g., 1A Q7 -.rs ~ 1.0,,.: 3w3~' ~ 802 ~~ 1.0 . 27 1041 0.7 0st.1.1 wernber~ 1992, Vol. 82, No. 17 American Joumal of'Publie Health 1527

Br;vw'moo et aL °;75U1BIE 2~,A~OtfdrRag0s (Of)'=ratld i57G' GD/MIdw10OIrMln/ali (CQ for.'IM RN.tlowHUp bNwesn iPietsiws Smoke Etq)orAre "~dtal~yAidraltlqod.rdlLurtqCaroxlnM/omen,'Mlnoutt,~<198a fhrwrwll "Ip91 ':- - /Rl Swbjecl5°' UJpgtimg'Nmns moPoets sotsee aExposure ' No. Caes No. COaOls OR 95% C1 No. Cam No. Control s ofB'' 9596 a l M trousehold membets Never 221 527 1.0 170 470 1.0 : Ever- 394 873 1.0 0.8,112 261 696 1.1 018. J.3 ;:-Corstle1eek-'YearS ~ 2211 527 1.0 170 470 1 A 15~c 88 234 0.9 0.8,,si2 56 181: .0.9 0i6„ 12 .ts dp IYs ,: ~,~ 261 '0J8 D.6,:1A • ' 62' 19~9 = 0B 0~8,12 ` 146 264 13 1A"I~ 107 12 1A 18 ~"Yaert x hourslday° ~ rt, . . r : •, , ~ ~ ~ _ ~ 527 -- 1.0 170., , ~-470 > v::4A pr 261 63 . 206 0 9 - Q6, 32% ~1 :i»89~ .f~ 24G D8 ~ _-061.7 ~/ 58..': 189 .09 06 y2~ ;y•~::238 24~ ~ . .=~3 ,.1D,y8i ~ ` - . ., _ ~. tleaef fc+ . , _ VL287 QTr_ 650 .1-0 ~, 213 56g ]A_ k7~28 ~" 750 0•9 . 0,8,' 1.1 218 596 :1.0 0 6,12b 650 1.0 166, 0.7'r ", 05,qJ0 7"- ~; 213 -32 ` : 568 • ~,128 ' • Qi~; - :-0•7 ,<, 05,1.1;t: 81 -t~f_258 : 07- " ..05;0_9`~,.: 54 .. .200•.,. W•- . .05.'1.0._, .v-150 266 12 0•9.1.5 110 -. '216 13 1.0.1.7 L~.,~.. ; "'f'287 650 ;aA 213 -'568 A _0 1-:64 201 ~+y«OT. ~:OS09 °. 41 161- _`Q7 0.5,1.0 M ~r: : tr c g ~- 237 Q7F. 'S0 175 -_ 0-5.:1.0 - 52 163 ° .;1) 8 _ 0 5;11 ; ~ 175 ` ~ . rtti'-: 126 . 2411, .7h;, ;'0.9.7Z ' 94 . 193< <^i ;. 'i_LYTN--• "4P-r"-L.,..yRl, Y `~% 4L/0V _O~tA~M~n1111~1~ t.{it/1711RJ.10i.w1M1..61~1~~''AmL1.S~~1Yq11.P~.Yq~.~~Y.a/~11YqIIM.Op.l1~~1 ~r(~(r• ' ''~E1EM prodtstct Id.I pdf~pssarKtaMSepe ouaber o(tptsa.~osod penday b p~seFAfrtoks i~l~s'lrortr ~,TABLE 3-~d Qdd: Rd10s`(OF1yc.nd 95% C01MfdalCa kdetYals ~ 1Gr tte siteliitlOndYp di.tYYSen PseaNre Srm0lpri E]postx e' . ~~~rg AddCwod rrdLtny"Cancer tn Wm~m, 6y FMsldqylcT~pr,lMsaoutl,199611rouph 1991 SAde nocarcino ttita Ot' hedtAbaa d SquemaisC6M .'"dtnaOiGeit -•q~ ~Vlll{.O{l1 ~B.~.Fi'.Rl..LrmQJM~tJ11 u•95AN~=:.R/.lQ1~a:.:~:.. ,.OW.qSA. .:IRl- V!1 ,;':AIAVI ' IRl.lIasQ'J .:1/fl 95% Cl;';. '.lV /RJllX11NId .1A1L.O1D . . . .. .. . tJe+~er.. •-. _ 100 1.0 37' 1.0 " ' 10, 1.0 _ 3 1.0, :r:_Ever V 192 1.1 0.8, lS - 80 12 0.8.118 ..16' 0.7 0.3. T7 9 12' 0.3; 4:5 .. D.-row Pod(-Y-7s w.,.0. 100 1A,: 37 1.0 10 tA 3 1.0' 49 :. -1.1 0;8:J.6 17 1•0 0.5,1•7' 4 0•7 02, 22 1 015, Q0.418 >15 40 48 O•9' O&J_4 18 018 05 1.6 ' 5 0•7 -02,20 2 018' 0.1;418 >40' 61 12' 0;8:1.7 31 1S' 0•9.2i61 ' 2' 0:3' : 0•1,1.4, 5 -22' 0:5,97 SpDuse ortY • Plever ,• 131 <, 1.0 48 1.0 14 1.0 4 1.0 Ever - 16'I , - ,,1.0 018,1.3 > 69 1.1 0.7,1.7 12 , 0.6 0:3,1.3' .8' 12 0:3J4.1' Ogarete pack-yem 0-., 131 1.0 48 1.0' 14 1.0 4 '>0-15 36 _1.0 0.7;1•6 10 0.7' •0.4,1.5' 3 0•7 0J2,24 1 0.7 0:1„6J6' >15-40 41- =0.8 0.5,1.1 16 0.8 0.4;1.4' 6 0.8 0:3j2'1 3 12 0:3:'SJ6: >4!D - 62 . 1.1 0.8,1'.5' 34 1.6 ! 1.0, 2'S 2 0.2 0.1,1.1 4 1.7 0;4; 7.01 A~ad wnape. Jio ay ot prswlo,n Lrg pseesa, and adWe ramolft hood exposure. In addition, there may be }ow' re6abt7ity for quantitative measures (intensity and duration) of passive smoke exposure ini childhood,a1•4P which makes assassment'of lung cancer risk due to pas- sive smoke exposure in childhood partic- ularly difficult. Reliability and validity of measures of childhood!exposure may'be especially problematic when a large per- centage of'surrogate interviews are con- ducted (as in our study): Partially because of these limitations, few studies of child- 1528 American Journal of'.Public 1Health November 1992, Vo6. 8Z No. 11

I Pauire Smoldng and l.uog Canoer 17 hood' passive smoking and lung cancer .iave been conducted, and further re- search in this area is needed. Our analyses by histologic typc showed the largest increase in risk for :)tlier/moted cell' types and, although the xtimate was based on very small inumbers, ~or small cell'cartinoma. Ptevious studies tre inconsistent and often lacking in sample ;ize when evaluating risk by cell type. 3arfinkel let al.ta found an elevated risk for quamous cell carraitoma and' for ot}ierJ nured cell types. Others5-ta have observed atget elevations for squamous andd small xlt carcinoma than for adtrtocarartoma. n contrast, Wu et at.n and gontham et J..m found larger increases for adettotxnei- oma ~. An:additional diffiiatlty in evatuating meviotrs studies of passive smoking and ing cancer by histologic type is that few tudies have conducted systematic pathol- ly reviews to venfy cell type- cr sttdy has s everal major sttengths. heseiitclude! the large sample size-one of x largest series of noasmokinglttng cancer ases to date. In addition, we had irelatiwely igh resportse rates from both case:patients nd control sttbjects. Firtally, we cottditated pathology review of cases: The main: of our study is te possability of recall bias for, passive noke exposure vatiables. The less qttan- tative measures of passive exposure .e., light, moderate, or heavy exposure) sulted lin larger risk estimates than more iantitative estimates such as pack-years. ecause there is no way to confum pre- ous passive smoke exposure, it is diffi- tlt to determine the best index for esti- atiitg exposure. However, we found that ng cancer risk due to adulthood passive aoke exposure was elevated at the high- t qt le of exposure whether, we ttsed more quantitative (e.g., pack-years) or >s quantitative (e:g:, heavy exposure) riable: Another possible source of bias in our idy is the large nttmber of surrogate in- cviews for cases. Earlier studies;38'-4B Wever, have shown relatively close reement on most passive smoke expoe re variables as reported by subjects and atses. Vlle found fairly minor alterations risk estimates when anahyses were re- icted to directly interviewed cases. In dition, we compared soci©demographic araeteristics of direct, and surrogate ;e-graoup interviews and found close ;eement: for most variables. As one ght expect, the exceptionwas age; there s a rtendency toward,more younger case ients in ~direct interviews. In stunntary, our study andlothers conducted duringthe past decade suggest a stnall'but consistent elevation in the risk of' lung cancer in nonsmokers due to pas- sive smoking. Tlie pnoliferation of federal, state, and local regulations that restrict smoking in public places and work sites" is well founded. 0 AclnaWedgment§ This study was aopported in part by National Canoer, Institute contracts NO1-CP7=1D9fi-01 and NO11GY7-1096402 T)ttauthorsgratefully acknowledge the assistance of numerous indiwiduaLs and orptti- zations who tnade this study posvble: Sartdi Esatirte, Patsy Henderson, Joan Huber, and other staff of Survey Reseatrlt Assoedates,,Inc,. for valuable helpin all phases of the study; Dr. Jian Chattg, C3dene Anderson, Debbie Pimtey.y andileanie Sharkbargerofrthe Missouri!C..anoer. Registry, Missouri Department:of Health, for assistance in data eolltctiott and patient tradt- iitg;lDr. Ellis Inl of the University of'Mis- souri School of Medicine and,Dr. Je&ey Mey- ers of the Mayo Clinic for their assistance in rcviewittg'pathotogy slides; Dts. William Blot and Jay Lubin of the National Cancer Institute for helpful comments on the manuscript; and the Missouri Department of Revenue and the Health Care Finance AdministUation for their help in seiertiitg,population-based oonttols: References 1. Kabat GC, Wynder EL Lung cancer in nonsmokers. Cancer. 1984;53:1294-1P21. 2. Pathak DR, SametJM;,Humbk CG, Sk'iEr per BJ- Determinants'ofilung cancer tusk in cigarette smokers in New Mexieo. J Natl Cancer Inrt. 1986;76:597-604. 3. Higgins IT, Wynder EL Reducuon,in risk ofliutg cancer among ex-smokers with par- tiaul9r reference to histologia type. Cancer. 1988;62097-24011 4! Schoenberg J13, Wilcox HB, Mason TJ, Bill J, Stemhagen A. 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