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Objeasives. The causes of lung.. cancer among nonsmokers are not clearly understood. To fwther eval- uate the reladon between passive smoke exposure and' lung cancer in nonstnolang women{•ve con ducted a population-based, case-control study. iNethods. Case patients (n~= 618)„identified'throughtheivfis- souri Cancer Reeistry for the period 1986 througli 1991, incltided 4321ife- time nonsmokers and 186 ex-smok- ers who had stopped at least 15 years before diagnosis or who had smoked for less than 1 pack-year. Control subjects (n = 1402) were selected from driver's licerue an& Medicare files. Results. \'o increased risk of lung cancer was associated with childhood passive smoke exposure. .ldulthood analyses showe&an in- creased lung cancer risk for lifetime nonsrrtokers with exposure of' more than 40 pack-years from all house- bold members (odds ratio [OR] =1.3; 95"'o confidence interval [Qa] = 1.0, , 1'.8) or from spouses only (OR = 1.3; 95% CI = 1.0, 1.7)i When the tima. weighted product of pack-years and ' average hours exposed per day was considered, a 309o excess risk was shown at the hishest quartt7c of ex- posure among li#etime nonsmokers. Conckuiors. Ours and other re- `. cent studies suggest a small but con- sistent increased risk of lung cancer from passive srvoking. Comprehen- sin+e actions to limit srnoking in public places and worksites are well-ad- vised. (Am J Public Health: 1992;8`~~:1525-1530) Passive Smoking and, Lung Canc6 in Nonsmoking Women Ross C Brownson, PsD, M+chael C. R AJavanja, DrPH, Edw'ard T. Hocl; BS, and T'unothy S. Loy, MD Inirodtactfon Although most lung cancer occurs in smokers, approximately 9% to~ 13% of lung cancercases in US women develop in lifetime nonsmokersJ'-s The causes of litng cancer in nonsmokers have not been widely sttidied{ but probably cornprise a diverse set of factors including genetics, occupational factors, radon exposure, diet, and a history of nonmalignant lung disease. In addition to these risk factors, the etiologic role of passive smoke exposure has received increasing scrutiny over the past decade. Numerous studies`-=0 have suggested an elevation in lung cancer risk for nonsmoking females who live with a smoker, with a summary excess risk of appro.ximately 30%.-t-= However, sev- eral recent stUdiest=1-=' have shown no increased~ lung cancer risk due to spousal smoking. Limited evidenceT=6 also suggestss that exposure to passive smoke in child- hood may increase risk of lung cancer. For example, a recent case-control study from New York found thathousehold exposure to tobacco smoke during childhood of 25 or more smoker-years' duration was as- sociated with a doubling of lung cancer tisk.=a Most previous studies of passive smoking and' lung cancer, 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 data on 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 ceu type. To more fully evaluate the rclation- ship between lung cancer and passive smoke exposure in childhood and adult- hood, we conductedia l§rge case-controli study of lung cancer among nonsmoking women. Methodr Case Group Case patients were identified throughh the Missouri Cancer Registry, which is maintained by the Missouri Department of Health. The Registry began collecting data on incident cancer cases from public and private hospitals in 1972, and'hospital reporting was mandated by law in 1984. Registry reporting procedures have been discussed in more detail elsewhere.s To ensure complete reporting of lung cancer cases in women for the current study;,we had Registry staff complete special' case ascettainment visits to participating hos- pitals. The case series included White Missouri women, aged 30 to 84 years, who were diagnosed with primary lung cancer between January 1986 and June 19911. Se- lection was limited to Whites because of small numbers of other racial/ethnic Ross C. Browason is with the Division of Chronic Disease Prevention and Health Pro- motion, Missouri Department of Health, Co- lumbia, hfo, Michael C. R, Alavanja is with the Epiderniology and Biostatistics Prograrn, Na- tional Cancer Institute„Rockville, Md': Edward T. Hock is with Information Management Ser- vices, Rockville, Md. Tunothy S. L.oy is with the Pathology Department, University of Mis- souri School,of' Medicine, Co4umbia„ Mo. Requests for reprints should be sent to Ross C. Elrowrtsan, PhD„ Division of Chronic Disease Prevention and Health Promotion, Missouri Department of Health, 201 Business Loop 70 West,,CoEumbia„M© 65203. This paper was submitted'to the Journal February 19, 1992, and accepted with revisions August 12, 1992. November 199"_ Vo1182; No. Il American Joumal of Publi¢ Health 15Z5

Y. siv»nson et at. groups. The case group included both life- time nonsmokers and ex-smokers who had stopped smoking av least 15 years be- fore diagnosis or who had smoked for less than 1 pack-yean From the 3475 cases of lung cancer in women reported for the study period, 650 eligible patients were identified. Physicians denied interview permission for 24 (4%) of these patients and an additional 8 women (1%) refused to be interviewed. The final case group in- cluded 432 (70%) lifetime nonsmokers and 186 (30%) ex-smokers. Of the 618 case interviews, 216 were conducted with pa- tienu themselves and 402 were conducted with surrogates because the patient was too ill to be interviewed or had died. Of the surrogate interviews, 105 (26%) were con- ducted with, the patient's spouse and 297 (74%)',were conducted with another rela- tive (e.g., offspring or sibling). Histologic Con ftrmation of Cases T'usue slides were reviewed for his- tolbgicverification for 468 (76%) ofthe 618 cases. Slides for these cases were exam- ined'simultaneously by three pathologists (T.L, E.I., and J.lvf.) using a multihead'ed microscope without knowledge of'the re- ferring pathologist''s diagnosis. In surgical specimens„consensus diagnoses were ob- tained with the criteria outlined in the World Health: classification scheme.=9 When only cytologic material was available, consensus was obtained' with standard cytologic criteria.30 Control Group A population-based sample of con- trol isubjeets was ascenained by two meth- ods. For women younger than 65 years, a sample of state driver's license files was provided by the Missouri Department of R'evenue. For women aged ~65 to 84 years, control subjccts were generated from the Health Care Finance Administration's rosier of Medicare recipients.st On the ba- sis of age distribution of lung cancer cases previously reported to the Registry, the final control group was matched by age group to case patients at~ an, approximate 2.2 to 1 ratio. Allicontrol'subjecu were interviewed directly. Of the 1862 poten- tialty elieTble control subjects, 335 (18%) refused the initial screening interview and: 125 (7%) ~o£ those screened and found el- igtble refused the full interview. The finali control group numbered' 1402. Questionnaire De.sign and Adrnuv'stration. Telephone interviews were con- ducted by trained interviewers. The first 152A Amr.ire, . Tnn.+net n! P,d.Ge LL-lih phase of the interview consisted of a screening questionnaire to verify, the age, race, and smoking status of, case patients and controll subjects. For subjects who were screened and Sound eligible and who agreed to the fuU interview, the study questionnaire consisted of'sections on res- idential history, passive smoke exposure, personal health history, family health his- tory,, reproductive history, occupational exposure, and dietary factors. Questions regarding passive smokingg focused on exposure in both childhood (17 years and younger) and adulthood (18 years and older). For each time period, respondents were questioned about the source of exposure (e.g., a parent or spouse). After an individual source was determined{ a series of'detaBed'1 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 by Wynder etial?2 In addition to quantitative estimates of exposure, respondents were asked to estimate a perceived level of ex- posure during childhood and adulthood ("During most of your adultyears, would you sav' that your average exposure to smoke at home was light, moderate, or heavy?"). Analyses Odds ratios (ORs) i and! 95% confi- dence intervals (CIs);were calculated with multiple logistic regression33 The li.near- ity of trends in risk according to level of passive smoke exposure was evaluated with, Mantel's one-tailed test.s" We ini- tiaUy 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•t41= have shown variations in risk by cell type, and biological mechanisms have been proposed that might account for these variations.mx Results Sociodemographic and smoking-re- lated characteristics of' case patients and control subjects have been presented~ in detail elsewhere.36 In brief, the average ages of case patients and control subjects were 71.5 years and 69.9 years, respec- tively. The two groups were also eompa- rable on level of education and income. Among ex-smokers, the median interval since cessation was 24 years, and average smoking intensity was 16:4' cigarettes per day. There was little evidence of increased lung cancer risk associated with passive smoke exposure in ctiildhood (Table 1). This lack of association was apparent for both the dichotomous variables (never vs ever exposed)!and quantitative measures such as pack-years. The only suggestion of elevated risk was noted for less quan. titative exposure variables (not shown in table). Among lifetime nonsmokers, an in, creased risk of7ung cancer was shown~for those reporting moderate (OR = 1.7; 95% Q= 1.1, 2.5) and heavy (OR = 2.4; 95% Q= 1.3, 4.7) exposure to passive smoke in, childhood. Risk estimates for most childhood exposure variables were slightly higher (approximately 20% to 30%) when analyses included only direct interviews, although none achieved statis- tical significance. An elevated :isk of lung cancer was identified for lifetime nonsmokers at' the highest quartile of passive smoke expo- sure in adulthood (Table 2): At an expo- sure level of more than 40 pack-years, life- time nonsmokers showed a 30% increase in risk whether the source of exposure was aUihousehold members or spouses only.. Similarly, when the product of pack-years and average number of hours exposed per day was considered, lung cancer risk for lifetime nonsmokers was elevated for the highest exposure quartile whether the source was all household members (OR = 1.3; 95% CI = 1.0,1.8) or spousess only (OR = 1.3; 95% CI = 1.0, 1.7). Among lifetime nonsmokers, a positive in- creasing trend!in risk was noted for pack- years (P = .06). Passive smoking-related risk estimates for adulthoo& exposures were slig}itly lower for alll subjects (i.e., both ex-smokers and' lifetime nonsmok- ers) than for lifetime nonsmokers alone, although the same general i elevations in tiskwere noted. When analyses were lim- ited to direct interviews, no clear pattern of increase or decrease in risk estimates was apparent. Regarding less quantitative z exposure variables, elevated risk was r shown for all subjects (OR = 1.7; 95% Q= 1.1, 2.6) and for lifetime nonsmok- 1001 V..1 R'1Nn 11

TABLE 1-Adfusted Odds Ratios (OR)' and 95% Confidence Intmais (Cl) for the Raiatlonahip between Passtve Smoke Exposure durtrV ChiJdhood and Lung Cancer In Women, Missoutl, 1986 through 1991 Source of Fxposure No. Cases All SubjecLs° No. Contrds OR 95% CI' 928 129 119 117 Lifetirne Nonsmokers No. Cases No. CorRrols OR 95% Cl 357. 74; 357 12 17 21 802 1.0 0.4.1.1 1041 0:7, 91 0.6 0.4,1.0 87 0.7. 0.4,1.2 8T7, 1.0 289 O 7 . -,: 0.5, 0.9 877 1.0 70 oS` 97 . '. , 0.5 74: 0.8 •hdjusted for age; hatory of pre,iars 4un dsease, and acrive arafdrg (ad subjocs orM. °trxhudes fife6me rwxamokers and ex•snokars who had stopQed ai least 15 yeers before dragwsis or, who had smksd'for lass than t paclc-yeat. ers(QR = 1.8; 957o CI = 1i.1, 2:9)~who reported heavy exposure to passive smoke. In general~ there was no elevated litng cancer risk associated with passive smoke exposure in the workplace (not shown in table). Only lifetime nonsmokers showed a slight increase in risk at the highest quar- tile of workplace exposure (OR = 1.2; 95% Cl = 0.9, 1.7). Among the 4681ung cancers that were verified histological}y, the predominant cell types were adenocarcinoma (62.4%), other/ rniiced cell itypes (25.2%), squamous celDcar- cinoma (5.8%), bronchioalveolar carcinoma (4.19'0); and small cell carcinoma (2:5%).. The other/mnred' cell type category con- sisted mainly of large cell lung cancers, though, these lacked sufficient pathologic evidence for precise classification. Table 3 presents results of cell type-specific analy- ses for adulthood'exposures. Elevated risk was shown for other/mpted cell types at more than 40 pack-years of exposure (OR = 1495% CIi = 1.0, 23). Although it was based on small numbers, a risk estimate of 1.7 was observed forsmall cell rarcinoma at the highest level of'exposure. We also examined risk among women who had been exposed~to passive smoke in both childhood and adulthood~ in childhood but not in adulthood, and in adulthood but not in childhood.Therewas no evidence of interaction between expo- sure during the two periods. Discussion Our study suggests that exposure to high levels of environmental tobacco smoke in adulthood increases the risk of lung cancer in nonsmokers. Exposure of more than 40 pack-years' duration in- creased the risk of lung cancer among non- smokers by approximately 30%. This re- lationship was consistently demonstrated among lifetime nonsmokers whether the exposure variable was pack-years or the time-weighted product of pack-years and average number of hours exposed per day. Our findings are sirrtilar to those of another large study of lung cancer in nonsmoking women2O that identifiedan OR of approx- imately 1.3 due to exposure to greater~ than 40 pack-years of spousal smoking. In earlier studies, the most com- monly reported index of passive smoking exposure has been the presence or ab- sence of asmoking spouse. In ourdata set, no elevated risk was noted for this vari- able. Since our study was limite& to womeni part of the dufference between our findings and those of eariier, studies may be due to differences in the effects of pas- sive smoke exposure by gender. The Na- tional Research Council's summary of13 studies'-l found overall relative risks of lung cancer in nonsmokers due to spousalI smoking of 1.32 for women and 1.62 for men (although the estimate for men was based on few eases): It is possible that men are exposed to other factors (e.g., occupational exposures) that may interact with passive smoke exposure to increase risk above thanobserved in women. Pres- ence or absence of a smoking spouse is a relatively crude measure of passive smoke exposure, with a potential for wide vara- abt7ity in actual exposure. It was noted in one survey, for example, that 47% of women martiedto smokers reported zero hours of passive smoke exposure at home?T It has also been shown that con- sidering spousal exposure alone may un- derestimate total household passive smoke exposure.38 Another factor that may account for the differences in lung cancer risk due to spousal smoking be- tween our study and earlier studies may be time trends in smoking patterns. The 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 findings of two earlier case-control studies,7=6 our data showed no evidence of excess lung cancer risk due to passive smoke exposure in childhoodi The risk of lung cancer due to childhood passive smoking may have some analogy to risk among ex-smokets. After 10 years of abstinence, the lung cancer risk for ex- smokers declines to 309'o to 50~ic of the risk for continuing smokers!0 S{milarly, lung cancer risk due to passive smoke expo- sure in childhood may decline by adult- hood, especially in the absence of' adult- Nbvember 1992, Vol. 82, No. 11 American Journalof Public Health 1527

Sro"nson ct al. TABLE 2-Ad/usted Odds Ratlos (Qq' and 95% Cortftdencr Interva4s (CQ for tfx Rd4tSonshlp between Passive Smoke EXPosure during Adufthaod and Lung Cancer in Women, Mlssouri, 1986 through 11491i All Sutje=° Lifetime Nor>srnokers Soarce of Exposure No. Cases No. Consrol$ OR 95% Cli No: Cases No. Controls OR 95% CI Ap 1 housetlold members , ; : Never : 221 . ; . : . . 527 - 1 i0 170 . 470. 1.0 ' Ever 394: 873 1.0 0.8.1.2 . 261' 696 1.1 0.8.1.3 C5a'ette Pad('Ye= 221 .,: 527 . 1.0 170 470 . 1.0: ' : >0-15 : 88 . 234 0.9 0.6.12 56 181 03 ' . .0.6. 12 >15-40, 91 261 . 0:8 0.6. 1.0 62 ., 199 0.9 " `- 0.6, 1,2 . >40 . : ': :146 264 1.3 1.0,1.6 . ' 107 . 217 , 1.3.. .. 1.0. 1.8 CSaretts pack-yeets x harsjday` '. 0 221.. ` 527 1.0 170 '. 470 1.0 ;; : . >0-50 ° 90 . 261 . 0.8 0,6 1.1 . '.. ; 63 206 0.9 : " 0.6:1.2 .. , >50-175 :, 89 246 0.8 0A 1.1 58 189 0.9 .. 0.6,1.2' > 175 . 124 238 1.2 0 9,1.6 92 192 1.3 1! 0, 1.8 SpexsE onty hlever 287 650 1.0 213 568 1.0 Ever 328 750 0:9 0.8.1.1 218 598 1Z 0.8.1.2 C'garer.e pacc-years . 0 287 650 1.0 213 .. -568 ' >0-15 58. . 166 . 0.7 0.5,1.0 32 128 0.7 0S, 1.1 > 15-a0 81 258 0.7 0.5~ 09 54 200 0,7 0.5.1.0 >4(! 150 265 1.2 0!9;1.5 110 216 1.3 1.0, 1.7 Gigarette pacSc"ats x hoursjdaY` 0 287 650 1.0 213' 588 1.0 >650 64 201 0.7 0.5.0.9 41 161 0.7 0.5, 1i0 >50=175 81 237 0i7 0.5. 1l0 52' 183 0.8 0A 1.1 > 175 126 241 1.1 : 09. 1.5 94 183' 1.3 1.0, 1.7 `Adus:e0lor age, hstoy of pre.+ious Irg dzoase, arxl ac8ve amok.q (aA su*cs orly). 'Srcl.xxes Etaime norurrokers and ex•anokers who had saopped at tea.q 15 yeers beiore diapnost or wf» had smokad icr tess Vwn 7 pack year. 'The product of tota, pack-years and averaQe nurtber of:hours e~osed Per daylo passtva arnoke in ttie hame. TASLE 3-Acqusted Odds Ratlos (OR)~ and 95% Cenfldence Irrter+rala (Ct) for the Retatlotnhlp between Pssstve Smoke Exposure during Adutthood and'Lung Cancer In Women, by HislofoglcType, AtlssaxG 1996 Cfuough 1991 .,_ Aderlo carcib orr>a Other!lvfaed :: Sqytarrou.s Cell Small Cell l Source of E.Vosura : No. Cases OR 95% Cy : . No. Cases OR 95% CI No, Cases OR 95% Cl: No. t'•ases,:.OR " . 95% C1 : All househald members . -., Never . 100 = 1.0 " . 37 1.0 10 .; 1.0 _ 3 1! 0. . _ Ever . 192 .. 1.1 0.8,1 S ::: 80 .:: 12. 0.811.81 . 16. ' . 0.7 03,1.7 . 9. , 1.2 ,. 0.3, 4.5 CgareUe pacc-yeass . . 0 - 100 -. 1.0 , 37 1.0 10 "~;' 1.0 : 3- : 1.0 . ` >0-15 49'_ . 1.1 0.8.1X _ 17 : . 1.0 05,1.7 . 4 0.7 0.2,2.2 "; ' : 1< 0.5 0.0,4.8. > 15-40 48 ' 0.9 0.6.].4" 78 ` . 0.8 '0.5,1.6 , 5. ;. 0.7 0220 ; 2 08 " .0.1,a.6 >40 61' .. . 12 0.8,1.7 31 ".: 1.5 0.9,2.8 2..; 0.3 0.1,1.4 .' 5. ::_. 22 : 05.9.7 ,. Spouse o.* . . :..:Ne,*w : 131.•. 1.0 48 1.0 .: 14 , 1.0 : 4 1.0.: ` Ever :.; 161 1.0 0.8,1.3 69 : 1.1 0:7,:1.7. 12_: 0.6 03.,1.3 8' 1.2. 0.3,4.1 C+gareGe pacc-years 0' 13T`. •" 1.0 48 1.0 .. .. 14, 1.0 4". ` 1.0 . ,. >0-15 36: 1.0 0.7,t.fi i 10 ". • 0.7 0.4,15 : 3 0.7 02,24 1 0.7 0.1,6.6:. - > 15-40 41 ' 0.8 0.5, 1.1 16 0.8 0.4,,1.4 6' 0.8 0.3„21 3 12. 0.3, 5.6 > 40 62 .,'. 1.1 0.8,1.5 34 1.6 1.0, 25 2. 02 0!1,1.1 : 4 ...1.7 ' 0:4„7:0 •~,quqed f« aqe• h®o«y of pfsvioua lns dmease. and aGHe amdcn¢ hood exposure. In addition, there may be low reliability for, quantitati4e measures (intensity and duration) of!passivesmoke exposure in childhood,"t•'= which makes assessment of lung cancer risk due to pas- sive smoke exposure in childhood panic- ulaily di8icult. Reliabiliry and validity of'measures of childhood exposure may be especially problematic when a large per- centaee of sun-o¢ate interviews are con- ducted (as in our study). Partially because of these limitations, few studies of ehild- 1c^a

Passive Smutd'ng and Lung Cancer hood passive smoking and lung cancer have been conducted; and further re- search in this area is needed. Our analyses by histologic type showed the largest increase in risk for other/mixed cell types and, although the estimate was based on very small numbers,, for small cellicarcinoma. Previous studies are inconsistent and'often lacking in sample size when evaluating risk by cell type. Garfinkel et al.to found an elevated risk for squamous celli carcinoma and for other/ tnixed cell types. Otherss•ts have observed larger elevations for squamous and small cell carcinoma than for adenocarcinoma. In contrast, Wul ec al.tt and Fontham et al.m found larger increases for adenocarci- noma. An additional difficulty in evaluating previous studies of passive smoking and lung cancer by histologic type is that few studies have conducted systematic pathol- ogy reviews to verify cell type. Our study has several major strengths. These include the large sample size-one of the largest seties of nonsmoking lung cancer cases to date. In addition, we had relatively hieh response rates from both case patients and control subjects. Finally, we conducted a pathology review of cases. The main limitation of our study is the possibility of recall bias for passive smoke exposure variables. The lbss quan- titative measures of passive exposure (i.e., light, moderate, or heavy exposure)i resulted in larger risk estimates than more quantitative estimates such as pack-years. Because there is no way to confirm pre- vious passive smoke exposure, it is diffi- cult to determine the best index for esti- mating exposure. However, we found thatt lung cancer risk due to adulthood passive smoke exposure was elevated at the high- est quartile of exposure whether we used a more quantitative (e.g., pack-years) or less quantitative (e.g., heavy exposure) variable. • Anotherposstblesource of bias in our study is the large number of surrogate in- terviews for cases. Earlier studies,M•jJ however, have showm relatively close agreement on most passive smoke expo- sure variables as reported by subjects and spouses. We found fairty minor alterations in risk estimates when analyses were re- stricted to directly interviewed cases. In addition, we compared sociodemograpliic characteristics of direct and surrogate case-group interviews and found close agreement for most variables. As one mightexpect, the exception was age;,there was a tendency toward more younger case patients in direct interviews. In summary, our study and others. ; conducted during the past decade suggest ~ a small but consistent elevation in the risk ~ of lung cancer imnonsmokers due to pas- I, stve smoking.'Ihte proliferation of federal, state, and local regulations that restrict. ,+ smoking in public places and work sites" ~ is weuifounded. 0 F Acknowledgments This study was supported in part by National Cancer Institute contracts NO1-CP7-1096-01 and NOt-CP7-1096-U2. The authors gratefulty acknowledge the assistance of numerous individuals and organi- zations who made this study posstble: Sandi Ezrine, Patsy Hendersoni Joan Huber, and othenstaS of Survey Research Associates, Inc, for valuable help in all phases of the study; Dr. Jian Chang, Carlene Anderson, Debbie Pinney, and Jeanie Shanebarger of the Missouri Cancer Registry,, Missouri Departrnent of Health, for assistance in data collection and patient track- ing; Dr. Ellis Ingram.of the University of Mis- souri School of Medicine and Dn Jeffrey.~tey- ers of the Mayo Clinic for their assistance in, reviewing pathology slides;, Drs. William Blot and Jay Lubin of the National Cancer Institute for helpful comments on the manuseript;,and the Missouri Department of Revenue and the Htalth Care Finance Administration for thei'r help in sclecting population+based'controls. References 1. Kabat GC, Wynder EL. Lung cancer in nonsmokers. Cancer. 1984;53:1214-1221t. 2. Pathak DR, Samet JM, Humble CG, Skip- per BJ. Determinants of lung cancer risk in cigarene smokers in New Mexico. J Narl' Cancer Inst. 1966;76:597-604. 3: Higgins IT, Wynder EL Reduction in risk of hing cancer among ex-smokers with par, ticuJar reference to histologic type. Cancer.. 1988;62:2397-2401. 4. Schoenberg JB, Wilcox HBi Mason TJ, Bill J, Stemhagen A. Variation in smoking- related lung cancer risk among New Jersey women. Am J EpidemioL 1989;130:688- 695. S. Dalager NA, Pickle LW, Mason TJ, et al:. The relation of passive smoking to lung cancer. Cancer Res. 1'986;46:4804--t807. 6. Gartinkel L. Tune trends in lung eancer mortality among nonsmokers and a note on passive smoking. JNad Cancer Inst 1981; 66:1061-1066. 7: Cotrea P, Piekle LW, Fontham E, Lin Y, Haenszel W. Passive smoking and lung cancer. Lancer. 1983;2:595-597: 8. Trichopoulos D, Kalandidi A, Sparros L Lung cancer and passive smoking: conclu- sion of Greek study. Lancer. 1983;2:677- 678. 9. Hiuayama T. Cancer mor[aliry in nonsmok- ing women with smoking husbands based on a large-scale cohort study in Japan. Prrv Med'1984;13:680-690. 10. Garftnkel L, Auerbach 0, Joubert L. In- voluntary smoking and lung cancer: a case- contro6 study.JNarl Cancerl'rcrt. 1985;75: 463-469. llt Wu AH, Henderson BE, Pt7ce MC, Yu MC. Smoking and other risk factors for lung cancer in women. J Narl Cancer /nsr. 1985;7047-751. 12: Akiba S, Kato H„Blot WJ. Passive smok- ing and lung cancer among Japanese women. Cancer Res. 1986;s6::SOt-s507. 13, Brownson RC, Reif TS, Keefe TJ, Fergu- son SW, PritzJ JA. Risk factors for adeno- earcinoma of the lung. Am J Eprdemiob 1987;1250-34: 14. Gao YT, Blot WJ, Zheng W; et al. Lung cancer among Chinese women, Inr J Can- cer. 1987;40:604-609. 15. Hole DJ; Gtllis CR; Chopra C, Hawthorne V.M. Passive smoking and cardiorespiratory health ~in a general population in the west of Scotland. Br,S1ed J, 1989;299:423--427; 16. Humble CG, Samct JMi Pathak DR. Mar- riage to a smoker and lung cancer risk.Am J Public XealtA. 1987;77:598-b02: 17. Lam TH, Kung ITM, Wong CM, et al. Smokirtg,,passive smoking, and histological types in lung cancer in Hong Kong Chinese women. BrJ Cancer. 1987;56:673-678. 18. Pershagen G, Zdenek H„Svensson,C. Pas- sive smoking and lung cancer in Swedish women.Am J EprdemioL 1987;125;17-24: 19: Kalandidi A, Katsouyanni K, Voropoulou N, et a1. Passive smoking and diet in the etioVogy of lung cancer among non,smok- ers. Cancer Causes{ontroL' 1990;1:15-21. 20. Fontham ETH, Correa P, Wu-Williams A, et al. Lung cancer in nonsmoking women: a multi-center case-control study. Cancer Epidemiol Biomarkrn Prev. 1991;1:35-43. 21. National Researeh Council, Board on En- vironmental Studies and Toxicology; Com- tninee on Passive Smoking. Emi,orvnental' Tobacco Smoke: t}easuring E_-posures and Assessing Health E/fects. Washing- ' ton, DC: National Academy Press;,1986:. 22. National Institute for Occupational Safety and Health. Ein.irortrnental Tobacco Smoke in the ii!orLplace,• Llueg Cancer and'OMer Ffealfh EJfectr: Cincinnati, Ohio: National Institute for Occupational Safety and Health; 1991. DHNIS publication NIOSH 91-108. Current Intelligence Bulletin 54. 23. Chan WC, Fung SC. Lung cancer in non- smokers in Hong Kong. In: Grundmann E, Clemmesen J; Muir CS, ads. CancerCam- paigr; VoL 6: Geographical Parhology in Cancer Epidemiology. New York, NY: Gustav Fischer Verlag; 1982:199-20? 24. Buffler PA, Pickle LW, Mason TJ, Contant C. The causes of lung cancer in Texas. In: Mizet! M, Correa P, eds. Lung Cancer.. Causes and Pnrvenrion New York, NY: Verlag-Chemie International, Inc; 1984. 254 Lee PN, Chamberlain J, Alderson MR. Re- lationship of passive smoking to risk of lung cancer and' other smoking-associated d'ts- eases: Br J Cancer. 1986:54:97-105. 26, Janerich DT„Thompson WD; Varela LR, et al. Lung cancer and exposure to tobacco smoke in the household. N Engf J Med 199(y,323:632-636. 27. Wu-Wil6ams AH, Dai XD, Bloc WJ, et al. Lung cancer among women in northeast China. BrJ Cancer. 1990;6?'982-987: 28. Brownson RC, Davis JR, Chang JC, DiLorenzo TM, Keefe TJ;,Bagby JR Jr, A study of the accuracy of cancer risk factor information reported to a central registry compared with that obtained by interview. Am J EpidemioL 1939;129:616-624! November 1992„Vol. 82, No. 11i American Journal of Public Health 1529

Btv.vnscn ~ eC 21. 29. World Health Organization. The World Health Organization histologic typing of lung tumors, 2nd ed. Am I Clin PathoL 1982;77:123-136. 30. Koss LG. Dlvgnastic Cytolosy and its li'is• topathodogic Bases. 3rd ed. Philadelphia, Pa: JB LiPpincott Co; 1979. 31. HanenJ, Medicare's common denomina- tar the covered population. HeaWr Care Finance Rev. 1980;2:53-64. 32. VWynder EL, Goodman MT,13offnann K Lung cancer etiology- challenges of the fu- ture. Carc>ttogene.nr 1985;8:39-61. 33. Breslow NE, Day NE. Starfsrical Methods in CancesResearch. Volume 1-73uAna1- ys'rs of Case•Conrrol Studies. Ly,on,. France: International Agency, of' Research on Cancer, 19801 LkRC publiration 32. 34. Mantel N. Chiisquare tesu with one degree of freedom, extensions of the Mantel'. Haenszel procedure. Am StarAssoc J. 1963;58:690-i00. 35. Wynder EL, Goodman MT. Smoking and lung cancer: some unresolved issues. Epi- duniol Rev. 1983;5:177-207: 36. AJavanja MCR, Brownson RC, Boice JD,. Jr, Hock ET. 1.'onmalignant lung disease and lung cancer in nonsmoking women. Am I EpidemioL'In press. 37. Friedman GD, Petitti DB, Bawoll RD. Prevalenee and correlates of passive smok- ing. Am JPublic Flea/th 1983;73:401-A05. 38. Cummings KM, Markello SJ, Mahoney MC, Marshall JR :yfeasurement of lifetime exposure to passive smoke. Am I Epide- mioL 1989;]30:122-132: 39. Fiore MC, Novotny TE, Pierce JP, Hatzi- andreu EJ, Patel KM,,Davis RM. Trends in cigarette smoking in the United States: the changing influence of gender and race. .IAMA 1989;261:49-55. 40. US Depcof Health and Human Services. Jhe Health Benefits of SrnoAting Cessa- tio,a, Roclvil)r, Mdt Centers for Disease Control; 1990. DHHS publication CDC 90-8416. 41. Pron GE, Bturh JD, Howe GR,,Miller AB. The reliabiliy of passive smoking histories reported in a cast-control study of lung t:an- cer. eSm.7 EpidnnioL 1988;127:257-273. 42. Coultas DB, Peake GT, Samet 1M. Ques- tionnaire assessment'of lifetime and recent exposwe to environmental tobacco smoke. Am J EpidernioL ]989;130:338-3d7: 43. Lerchen ML, Samtt JM: An assessment of the validity of questionnaire responses pro- vided by a surviving spouse. An+ J Epide- mioL'1986;]23:481`489. 44. Rlgotti NA, Pashos CL. No-smokingdaws in the United States: an analysis of'state and city actions to limit smoking in public places and workplaces. JAMA. 1991;266: 31b2-3167.

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