Tobacco Documents Online

Abiwx% JpCRNAL or E11DEwiouoGY VoC.125.,No..1Cp,.rkot i 188: by Tbe Johns Hopkins Unrvenaty Scliool of Ny`iene and Public H.altR Rruued in U:SA.. w no" *-,.e PASSIVE SMOKING AND LUNG CANCER IN SWEDISH WOMEN GORAN PERSI9AGEN;' ZDENEK HRUBEC;' Ar+D CHRISTER SVENSSON" P.rsha9en, G. (National Institute of EnvkvwnentaI Medieina, P.O. dos $0208, S•10401 Stockhoim, Sw.d.n), L Mnrb.c, and C. Svensson. Passive snwkkfp and Nrnq eane.r in Swedish women. Am J Epka+eaol 1887;125:17-34. Th. e.lation between passive amokMp and king eanw was asamin.d by nnsans of a case-control study in a cohort of 27,409 nonsmokin8 Swadish women id.ntifwid from questionnaires maNed in 1861 and 1863. A total of T7 cases of prwnary carcinoma of the bronchus or Mrny were found in a follow-up of the eohort fircotqh 1980. A new questionnairs in, 1564 provieied WormaUon on snakin0 by Study svbj.cts and tAeir spouses as rrNl as on potential confounding factors. TM study reveal.d a relative risk of 3.3, constituting s statisticapy si0nificant increase (p c 0.05) for sqwmous c.M and smap cell ¢arainomas in woiren married to amokfrs and a positive dose-r.sponso nlation. No consistsnt eff.ct could be seen for ot>1.r histoloqic types, indkaMp that passive amohin0 Is r+siabd primarNy to those forms of king canctr which show the highest rnlative risks in smoicsrs. Aistolo0y; krnq neoplasms; smokinp; tobacco amoke poMution In recent years there has been a growing interest in the health effects of environ- mental tobacco smoke. Biologic monitoring has demonstrated that exposure to tobacco smoke constituents may be appreciable amongpassive smokers (1-4). Several stud- ies show that children with parents who smoke have an increased risk of bronchitis and pneumonia, and some data also indi- ate changes of pulmonary function in adlilts and children exposed to environ- mental tobacco smoke (5). A few epidemiologic studies have been Published on passive smoking and lung can- R.Deived for publieuion iaanary 22, 1g66, and in 4aa! 'form May 6, 1986. 'Department of Epidemioiogy, National Institute Of Eavironmental Medieine, P.O. Box 60208. S•10401 Stackholm, Sweden. (Reprint requests to Dr. GBran Pr+6asen:) e P+esent addteu: Radiation Epidemiology Brancb. National Cancer Institute. Betlxsda.,MD. Thi+ study was supported by a grant from the s0+duh,C.neer Society. T6e autbon are grateful to Kristina Pannone. N'a- t+owl Itutituu of Environmental Medicine, Lara Johnron. National Central Bureau of Statistics, and BirDaa Penhasen for help in data collection. cer (6-17). Some of these show increased risks for nonsmokers married to smokers, but the results are not fully consistent. Most of the studies were not specifically designed to investigate effects of passive smoking, and there are various potential sources of random and systematic errors which make it difficult to interpret the findings. One aim of the present investiga- tion was to try to minimize such errors, especially with regard to the validity of the information on exposure and effects. MATERIALB AND 1[ETHODS Study subjects This investigation is designed as a case- control study within a cohort of nonsmok- mg women. There are two sources for the cohort. Most of the subjects are taken from a sample of about 55,000 men and women aged 15-65 years in the 1960 National Cen- sus of Sweden for whom tobacco smoking was investigated by a questionnaire mailed in 1963. Detailed descriptions of the sam- pling strategy and the questionnaire are 17 N'OT1CE This materlel may De protected' by copyrlgit lilw (Title 17 U.S: Ccda1

18 PERSHAGEPI ET AL given elsewhere (18). The response rate among the women was 95.4 per cent. A total of 17,679 (66.8 per cent) of the women stated that they had never smoked any form of tobacco„ and these are included in the present study. The second source of subjects ia the "old" Swedish twin register which contains about 11,000 same-sex twin pairs born between 1886 and 1925 (19). The twins were iden- tified from birth certificates, and a ques- tionnaire was mailed to them in 1961, pri- marily to determine zygosity and tobacco smoking status. The response rate among the eligible femal'e twin pairs was 85.1 per cent. In all, 9,730 women (80.6 per cent) had never smoked, and they make up the rest of the study cohort. Cancer morbidity and mortality of the 27,409 women in the study cohort were determined through 1980 in the Swedish Cancer Register and the National Register on Causes of Death, respectively. The qual- ity of the information in these registers is high for most cancer diagnoses (20). A total of 92 cases of tracheal, bronchial, lung, or pleural cancer were identified (Interna- tional Classification of Diseases (Z'CD)4 Sev- enth Revision, codes 162-163) (21). These subjects constitute the case series. Two control groups, each containing two controls per case, were also selected from the study cohort. Control group 1 consisted of subjects who were matched to their re- spective case on year of birth (tl year). Control group 2' included subjects who were matched on year of birth as well as on vitaL status at end of follow-up. The subjects in both control groups were selected at ran- dom from subjects who fulfilled the match- ing criteria, with the exception that no woman could be used as a control for her twin sister. The entire study group con- sisted of 460 subjects: 58 cases and 232 controls from the 1963 smoking sample, as well as 34 cases and 136 controls from the twin regiater. - . Exposure irsformation There were two sources of exposure ui~ formation. First, as described above, data in the 1961 and'1963 questionnaires were used to define the cohort from which the cases and controls originated. The second source was a questionnaire mailed in 1984 to each study subject or, if she was dead, to the next-of-kin (excluding the husband), in order to validate the data on smoking as well as to assess the exposure to environ- mental' tobacco smoke from husbands and parents. If a woman had been married more than once, smoking was investigated only for the man with whom she had cohabited the longest. Questions on occupational and residential history were also included. If the questionnaire answers were incomplete, ad- ditional information was obtained by tele- phone interview. The methodology using next-of-kin to obtain data has been shown to provide exposure information of high quality (22-24). The residential history information from the 1984 questionnaire included data on addresses (parishes) and types of houses in which the study subjects had lived. A parish was classified as urban if 90 per cent or more of the population lived in built-up areas according to the 1970 National Cen- sus. One-famii'y houses made of material other than wood and with basements were classified as dwellings presenting a greater risk of radon exposure. Indoor radon mea- surements show that the average concen- trations in such houses are higher than in other common types of dwellings in Sweden (25). Statistical methods Several methods have been used in the statistical analysis. The matching was re- tained in some analyses, and mazimum likelihood estimates of relative risks (ap- proximated with odds ratios) and exact confidence intervals were computed ac- cording to the method of Miettinen (26). In other analyses, the matching was dissolved, and the relative risks and confidence inter- vals were estimated' as suggested by Mantel and Haenszel (27) and Cornfield (28), re- spectively: The method proposed by Mantel (29) was used to test linear trends in these N analyses. Besides the conventional' strati- Q ~ (,~? ~ G? L4 (A

PASSIVE SMOKING AND LUNG CANCER IN' SWEDEN 19 fied analyses, a conditional logistic regres- sion analysis (30) was carried out in an attempt to control residual confounding in the risk estimates and to study interactions. RESULTS A careful review of the medical records of the 92 lung cancer cases showed that in nine cases the primary site was not the bronchus or lung (there were no primary tracheal or pleural carcinomas), and in six cases the primaryy site was uncertain. Car- cinoma of the breast, which occurred in five cases, was the most common cause of sec- ondary carcinomas. For 64 of the 77 pri- mary carcinomas of the bronchus or lung, the diagnoses were based on histologic evi. dence, and for 12 diagnosis was based' on cytology. In one case, an autopsy was per- formed, but there was no histologic ezami- nation. The distribution of histologic types among the primary bronchial and lung car- cinomas is shown in table 1. The classifi- cation is based on~ the information in the medical records„panicularly the pathology reports. Adenocarcinoma is the most com- mon group, constituting 57.1 per cent of the totaL Squamous cell and small cell car- cinomas constitute 31.2 per cent. The av- erage ages at diagnosis and at death for the whole group of carcinomas are 69.0 and 69.6 years, respectively. In the following analy- sis, the squamous cell, and small cell carci- nomas are grouped together because these types have generally shown the highest rel~ ative risks among smokers (31). Table 2 shows the distribution of selected variables among the cases and the control groups. As a result of the matching criteria, the age distribution and vital status are similar for the cases and~ control group 2. In control group 1, there is a shift toward older ages, and more subjects were alive at the end of follow-up than in the two other groups. Questionnaires were returned for 90.2- 9V per cent of the study subjects in the different groups. Among the proxy respon- dents, 68.4 per cent were children of the study subjects, 21.3 per cent were brothers or sisters, and 10.3 per cent were other relatives. There were no differences in the type of proxy respondents between the case and controlgroups. All of the returned questionnaires con- tained information on smoking by the study subject and„with the exception of one sub- ject in each control group, on whether she had been married and whether her husban& had smoked. For the other questionnaire items, e.g., smoking habits of parents, em- ployment, and residential history, the in- ternal nonresponse rates ranged' from 9.6- 32.6 per cent. The percentages in table 2 are based on the number of respondents to each item, Eight (1.8'per cent) of the 436 women for whom questionnaire information could be TAsLE 1 obtained in 1984 had smoked daily during Xiaro,pathoror• of pri,nary bronchial and ru.s at least two years. Four of these had ca.cinomos ond mran oges at diojnosirand at denth stopped before answering the 1961 or the in n cohort o(TJ,109 nonsmokinj Surduh uomen 1963 questionnaire and one had started , Aye /y..n/, Diymosi. No. % Dwno" D..o ' Squamous cell carcinoma 12 15.6 68.5 70.1 Small cell carci- noma 12 15.6 65-6 65.8 Adenocarcinoma 44 57.1 69.7 70.2 l++re cell carci- noma 5 6.5 67.9 68.0 Other primary earcinomas 4 5.2 74.4 74.8 ToW 77, 100.0 69.0 69.6 after that. Two women smoked 1-7 ciga- rettes per day, and one was a pipe smoker. These eight women were excluded in the subsequent analyses. There were no pro- nounced differences between the groups with regard to the percentage of women who were married or the percentage who were married to smokers. For the remainder of the questionnaire items, no consistent differences were seen between the groups, with the possible ex- ception of a tendency toward a larger per- ~

20 PERSHAGEti ET AL. TABLE 2 Distribution of selected 1•ariabka among cases of lung concrr and two control groups matched for year of birth, from a cohort of nonsmoking women No. ri Cases Control group l Control group 2 Ca.n Control group E Control group 2 Total 92 184 184 100 100 100 Localization of primary tumor Bronchus or litng 77, 83:7 Other site or uncertain 15 16.3 Age at death or at end of follow-up (years) 40-69 44 38 93 47.8 20~7 50.5 70-79 40 90 73 43.5 48.9 39.7, 80-91 8 56 18 8.7 30.4 9.8 Vital sutus at end of follow-up Alive 5 121 10 5.4 65.8' 5.4 Dead 87 63 174 94.6 34.2 94.6 Total questionnaire eespondenta 83 178 175 90.2 96. 7, 95.1 Smoked daily+ 2 3 3 (2:4)' (1.") ( L-'): Marriedt 70 143 151 (84.31 (80.3) 18U1', Married to smoker+ 37 76 77 (44.6) (42.9) (44.3)' At lcasrone parent smoker+ 12 30 21 (21.1) (21.4) (1'5:9). Employed outside home+ 33 73 52 (44.0) (48.3) (34.7) Lived in urban area+ 39 78 82 (60.9) 161.4)t 162:61 Lived in dwelling presenting a greater risk of radon exposure+ 11 13' 9 (17.21 (10.8)I (7.0) ' Numbers in parentheses correspond to percentages of total number of questionnaire respondents to each item. • Minimum duntion of two vears. j Exposures occurring after the death of their respective case have been excluded for controls alive at the end of follow-up. centage of cases than of controls who lived Aduces a relatlve zis]f~ pf' 3.3~fo~ s~uamou , in dwellings presenting a greater risk of ill aiid'small ce~ csrcinomas (95 per cen ~ radon exposure. A detailed analysis of the nfldence interval _(CI~_,~.}-1-~4) asso ` occupations held by the cases and controls jiated with marriage to a smoker. Within did not reveal any differences between the this group, the relative risks were increased groups. The great majority of the occupa- for both histologic types. The relative risks tions were in the service sector and typical for the other histologic types and for the for women of the age group under study, entire group are 0.8 (95 per cent CI - 0.4- e.g., housemaid, cook, seamstress, cleaner, 1.5) and 1.2 (95 per cent CI = 0.7-2.1), and nurse. respectively. In the following analyses, the 15 cases Table 4 gives a dose-response analysis with primary sites other than the bronchus with regard to smoking by the husband. or lung have been excluded. Table 3 gives, The matching was dissolved in this analysis a p~tti.+e , in a matched analysis, the relative risks for as well as in table S ~ primary carcinoma of the bronchus or lung M~Ohd iyf'tbe eeLttivexsk forsqwmous celC g in women married to amokers. Never mar- "' but ried women and women married to non- '~J9r The re1= '~'tbe „e,,,~ist~lo, ~c t~pes , smokers constitute the reference category. risk in the.highest exposure group,- The results are consistent for both contro i.e.'~vomen with husbeAda who smoke~ ..,. ... . `~. groupa• #oolin= the oontrol groups Proz ~~iore than 15 e>Ear~ttes~er day or one pac a~ . .._ . ~ ~ C+,7 ~ N w ~ ~

PASSfVE SMOKING ANT LUNG CANCER IN SWEDEN 21 TABLE 3 Relatire risks (RR) and 955, confidencrintertxilb (Cl) for primary carcinoma o/ the bronchus or Gnw in nonsmoking uomen married to smokers with two controleroups in a matched analvsis' e ic t Hi t lo No. of Control group It Control group 2= Both control poupa yp s o g eases RR Cl RR Cl RR Cl Squamous cell or small cell carcinoma 20 3.8 1.1-16.9 3.4 0.8-20.1 3.3 1.1-11.4 Other types 4.7 0.7 0:3-Is6 0.8 0.4-1.7 0.8 0.4-1.5 Total 67 1.2 0;6-2.2 1.1 0.6-2.1 1.2 0.7-2.1 ' hever married women and women manied' to nonsmokers constitute reference category. Maximum likelihood estimates of relative risks and exact confidence intervals 126). i ylatched to cases on year of birth, j Matched to cases on year of birth as well as on vital sutus at end of follow,up. TABLE 4 Refatiue risks (RR) land 95Sitonfidence interuaLs1C1/ for primory carcinoma of the bronchus or lung in nonsmoking women in relation to estimated exposure to tobacco smoke from the husband' Never mamed m d t yo,,,, ezaosure to tobacco High e:posare to tobwcco Histolopc t~ye or ma e o a nonsmoker 101110ke of liyaband* amake of husbandS Chi. squax No. of paes RR No. of cases RR CI No., of eues RR Cl for taend{ Squamous cell'or small cell carcinoma 7 1.0 10 1.8 0:6-5.3 3 6.4 1.1-34.7 3:901 Other types 27 1.0 16 0.8 0.4-1.6 4 2.4 0.6-8.7 0.03' Total 34 1.01 26 1.0 0.6-1.8 7 3.2 1.0-9.5 1.45 ' Agr-standardized~relative risk estimates (27) and approximate confidence intervals (28). * Husband smoking up to 15 cigarettes per day or one pack (50 g) of pipe tobacco per week or any atnount during less than 30 years of marriage: t Husband smoking more than 15 cigarettes per day or one pack of pipe tobacco per week during 30 years of marriage or more. I Test for linear trend,4291: #fppe'lobaCco per week during 30 years of? SAarriage or aQore, is 3.2 ,595 per cent CI ~ 4=85)~or"` > ~ - a~e 5s shows the influc~e of entei smoking on the risk of primary carcinoma of the bronchus or lung, controlling for smoking by the husband. There is no con- sistent evidence of an effect, and the 95 per cent confidence intervals for the relative risks in women with at least one smoking par+ent encompass 1.0 for both histologic groups. These results must be interpreted with caution in view of the lack of infor- mation on parental smoking habits for 24 per cent of the questionnaire respondents. The results of the conditional logistic regression analysis, which included cases and matched controls with information on all variables, were consistent with the re- sults of the stratified analyses. There was no important confounding of the associa- tion between smoking by the husband and squamous cell and small cell carcinomas by occupation, by living in houses with a greater risk of radon exposure, or by living in urban areas. None of the relative risks associated with these factors deviated sig- nificantly from 1.0 upon statistical testing. For all histologic types taken together, the relative risks and 95 per cent confidence intervals associated with marriage to a smoker and with living in a house present- ing a greater risk of radon exposure were 1.2 (95 per cent CI se 0.6-2.6) and 1.4 (95 i

22 PERSHAGEN' ET AL. TABLE 5 Relative risks IRR/:and 95% confidence interuoLs (CI) for primary carcinoma of the bronchus or lung in nonsmoking uemen in relation to smoking habits of parents• Hi.tolopc Both parents nonsmokers At least one smaking parent type No. of eam FLR No.,of cues PR CI Sqwmow cell or small cell carcinoma 0 .0 6 .9 .5-6.2 (kher types 28 1.0 3 0.5 0.1-1.9 Total 38 1.0 9 LO 0.4-2.3 ' Mantel-Haensul estimates of relative risks (27) standardized for age and smoking of husband with approximate confidence intervals (28): per cent CI - 0.4-5.4), respectively. For women who had been married to a smoker and who had lived in a house presenting a greater risk of radon exposure the relative risk was 2.5 (95 per cent CI = 0.8-8.5), suggesting a positive interaction between the two variables. DiscussloN The results of our study indicate that exposure to environmental tobacco smoke is related to an increased risk of those histologic types of lung cancer which show the highest relative risks in smokers. This is in general agreement with the findings of Trichopoulos et al. (7), Garfinkel et al. (15), and Koo et al. (16), although these authors looked at somewhat different car- cinoma types and/or used other definitions of exposure. It would be of interest to see an analysis of the risks for different histo- logic types in the other published studies on passive smoking and lung cancer, eape- cially those with an appreciable number of cases, as well as in subsequent studies on this topic. Combining the published epidemiologic studies provides a weighted average relative risk of lung cancer of 1.5 associated with marriage to a smoker (5). The results of the present study are consistent with this esti- mate. A 50 per cent increase in risk does not seem unreasonable in view of exposure estimates among passive smokers (5, 32) and the excess risks of between 100 and 900 per cent for smokers in the lowest exposure category, as a rule 1-9 cigarettes per day, in the major cohorts studied (18, 33-39). It should be noted that relative risks for squamous cel'l and small eell, car- cinomas would be expected to be even higher, i.e., if the case group is not "diluted" with adenocarcinomas or other types with weaker association to smoking. Several sources of random and sys- tematic errors have to be considered in the interpretation of the findings. In contrast to eariier studies on passive smoking and lung cancer, the present study has a "double check" on the smoking status of all study subjects. Data were obtained from the 1961 and 1963 questionnaires that were used to define the cohort as well as from the 1984 questionnaire. Our results indicate that misclassification of nonsmokers was a mi- nor problem and that failure to take this problem into account would not severely bias the association between passive smok- ing and lung cancer. This is supported' by the findings of other Swedish studies, which show a high quality of questionnaire information on smoking, both when the data were obtained from the subjects them- selves and when data were obtained from next-of-kin (22, 23). Using smoking by the husband as the only measure of exposure to environmental tobacco smoke will result in misclassifica- tions in the exposure assessment. To the extent that such misclassifications are un- related to the disease in question, this would tend to reduce any true association between passive smoking and lung cancer. The similar percentages of exposed persons among the cases, excluding sq+lamous cell and small cell carcinomas, and the two control groups suggest that errors in the reporting did not affect the cases and con- trols dif@erently.. This knds further support to the association with smoking of the hus- bands, which was noted for squamous cell and small cell carcinomas only. Obviously, N 0 N w

PASSIVE SMOKING AND LISNG CANCER 1.14 SWEDEN 23' it is unlikely that the next-of-kin respon- dents were aware of the histologic subtypess diagnosed for the cases. pur results show that poor quality of the diagnosis may be a problem in studies of hing cancer in female nonsmokers. Second- sn pulmonary carcinomas or carcinomas with unknown primary sites appeared in about one-sixth of the cases reported in the cancer and/or cause of death registers. This is in close agreement with the findings of Garfinkel (8), which were based on death certificate diagnoses in the United States. If secondary tumors are not excluded from the case series, the relative risks associated with any factor that causes primarily lung carcinomas are likely to be underestimatedl As noted previously, the analysis may be further strengthened by separating differ- ent histologic types. Besides the quality of the exposure and diagnostic information, the validity of our study is also affected by the control of confounding factors. The association be- tween passive smoking and lung cancer of the squamous cell and small cell types was not confounded' by occupation, urbaniza- tion, or living in houses with a greater risk of radon exposure nor were any of these factors associated with a clear increase in risk when passive smoking was controlled. These findings should be interpreted with some caution in view of the internal non- response on the questionnaire for items other than smoking of the study subjecta and their spouses. It is,lio.rever, improba- ble that uncontrolled confounding by the factors under study explains relative risks of the magnitude observed, as well as the Positive dose-response relations. No infor- mation was obtained on intake of food items that may affect the lung cancer risk. Analysis of all the lung cancer cases sug- gested a positive interaction between mar- riage to a smoker and living in dwellings Presenting a greater risk of radon exposure, Le., one-family houses made of material other than wood and with a basement. In- creased risks of lung cancer associated with living in such houses have been observed previously (40-42); but our study also pro- vides data on exposure to environmental tobacco smoke. Our findings are consistent with an interaction between tobacco smoke and radon daughters similar to the one observed in uranium miners (43) and in smokers living in dwellings with a greater risk of radon exposure (41). It is also of interest to note that the radon daughter concentration has been shown to increase considerably as a result of attachment to aerosol particles in rooms filled! with to- bacco smoke (44). In conclusion, our results indicate that exposure to environmental tobacco smoke is related primarily to those forms of lung cancer which show the highest relative risks in smokers. The results are internally consistent and in general agreement with other studies. Our findings are of scientific interest and have public health implica- tions, although it is obvious that lung can- cer in passive smokers is a rare phenome- non. The accumulating evidence in children and adults shows that serious health effects can probably result from heavy exposure to environmental tobacco smoke. This should encourage further research, including both exposure assessments and etiologic studies. Rarcacr+czs 1. Feyer.bend C, Higgenbottam T. Rwael MAH! Nicotine concentrations in urine and saliva of smokers and non-smokers. Br Med J 1982; 28&i:1A42-4. 2. Juvis MJ, Russel,MAH.,Feyerabend C. Abeorp• tion of nicotine and carbon monoxide from passive smoking under natural1 oo»ditions of exposure. Thorax 1983:38:829-33. 3. Greenberg RA. Haley NJ. Etsel R, et al. Me.sur- ing the ezposure of infants to tobacco smoke. N Enj! J Med 188010:1075-8:. 4. Matwkun S, Taminato T. Kitano N; et al. Effects of environmental tobacco smoke on urinary eotin- ine excretion in non-smokers. N Fsu] J Med 1984:311:828-32. 5. Pershagen G. Review of epidemiology in relation to passive smoking. Arch To>vcol iSuppll 1986; 9:63- 73. 6. Hirayama T. Non-smoking wives of heavy smok- en have a higher risk of lung cancec a study from Japan. Br Med J 1981;282:183-5. 7: Trrchopoulos D. Kalandidi A, Sparros 1., et al. Lung cancer and passive smoking. lnt J Cancer 1981:27:1-14. 8 Garfinkel'L. Time trends in lung cancer mortality

t 24 PERSHAGEN ET AL among non-smokers and a note on passive smok- ing. JNC1 1981:66:1061-6. 9. Chan WC, Fung SC. Lung cancer in non-smokers in Hong Kong:. In: Grundmann, E. ed. Cancer campaign. VoL6 Stuttgart: Gustav Fischer Verlag, 1982:199-202. 10. Correa P, Pickle LW, Fontham E, at al. Passive smoking andlun; cancer. Lancet 1983:2:595-7: 11. Trichopouloa D, Kalandidi A. Sparros L. Lung cancer and passive amoking: conclusion of Greek study. Lancet 1983:2e677-8., 12. Gillis CR. Hole DJ, Hawthorne WM, et al. The effect of environmental tobacco smoke in two urban communities in the west of Scotland. Eur J Respir Dia 1984;651Yuppl 133):121-6. 13. Kabst GC. Wynder EL Lung cancer in non- smokers. Cancer 198+h53:1214-21. 14. Koo LC, Ho JHC, Saw D. Is passive smoking an added risk factor for lung cancer in Chinese wromen'.' J Ezp Clin Cancer Res 1984:3:2/7.-83: 15. Garfinkel L, Atxrbach 0, Joubert L. Involuntary smoking and lung cancer. a casetontrol study. JNCI 1985;75:463=9. 16. Koo LC, Ho JHC, Lee N: An analysis of some risk factors for lung caneer in Hong Kon;. Int J Cancer 1985;35:149-55: , 17. Wu AH, Henderson BE. Pike MC, etal. Smoking and other risk factors for lung cancer in women. JNCI 1985; 74:747-51. 18. Cederlof R. Friberg L, Hrubet 2, at aL The nl.- tionship of smoking and some social covariables to mortality and cancer morbidity:, Stockholm: Department of Environmental Hygiene, Karolin- ska Institute. 1'975: 19. Cederlof R. The twin method in epidemiological studies on chronic disease. Stockholm: Depart- ment of Env'tronmental Hygiene, Karolinska I'n- stitute. and Department of Sociology, University of Stockholm,,1966. 20: Mattson B. Cancer registration in Sweden: studies on completeness and validity of incidence and mortality registers., Stockholm:: Department of Oncology and Cancer Epidemioloty, Karolinska Institute, 1984. 21. International Classification of Diseases, Seventh Revision. Geneva: World Health Organization. 1957. 22. Pershagen G, A:elson 0. A validrtion of question- naiee information on oecupational' exposure and: smoking. Sund J Work Environ Health 1982; 8:24-8: 23. Damber L Lung cancer in males: an epidemiolog- inl study in northern Sweden with special regard' to smoking and occupation. Umei. Sweden: De- partment of Oncology, Umei University. 1983. 24. Pershagen G. Lung cancer mortality among men living near an arsenic-emitting amelter. Am J Epidemio11985;122:684-94. 25. Falk R Study of a method to estimate the expo- sure to radon daughters in d'wellings. In: Pilot .wdies and theoretical eonsider.tions on the pos- sibility to study the relation between radon daugh- ter exposure in dwellings and lung cancer. (In Swadishl: Stockholm: National Institute of Envi- ronmental Medicine. 1982. 26. Miettinen 0. Estimation of relative risk from in- dividually matched:series. Biometrics 1970;26:75- 86. 27: Mantel N: Haensul W. Statistical aspects of the analysis of data from retrospective studies of dis- ease. J N C I 1959:22:719-48. 28. Cornfield~ J. A sutistical problem arising from retrospecuve studies. In: Proceedings of the third Berkeley symposium on mathematical statistics and ptobability. Berkeley; CA: University of Cal- ifornia Ptess, 1956: 29. Mantel' N. Chi-square tests with one degree of fneedom:,estensions of the Manul-Hrenstel pro- cedure. Am Statistical Assoc J 1963:58:690-700. 30. Breslow N; Day N. Statistical methods in cancer research-the analysis of case-control studies. Lyon: IARC Scientific Publications. 1980. 31. Kreyberg L Histological lung cancer tvpes•: a mor- phologicaliandbioloRiaal correlation: Acta Prthol' Microbiol Scand 1962:Suppll 157:1-92. 32. Vutuc C. Lung cancer risk and passive smoking: quantitative aspects. Zbl Bakt Hyg I Abt Orig B 198337 7:90:5. 33. Hammond EC, Horn D. Smoking and death rates-report on forty-four months of follow-up of 187,783 men. II. Death rates by cause. JAMA 1958:166:1294-1308. 34'. Hammond EC. Smoking in relation to the death rates of one million men and women. Nat] Cancer Inst Monogr1966:19:127-204. 35. Best EWR. A Canadian study of smoking and health. Ottawa:, Department of Nliuonal Health and Welfare, 1966. 36. Kahn HA. The Dorn study of smoking and mor- tality among US veterans:, report on eight and one-half years of obscrvation. Nat1 Cancer Inst Monogr 1966;19:1-125. 37. Weir JM, Dunn JE. Smoking and mortality: a prospective study. Cancer 1970--25:105-12. 38. Hirayama T. Prospective studies on cancer epi- demiology based on census population in Japan. In: Cancer epidemiology and environmental fac- tors. Vol 3. Amsterdam: : Excerpts Medica. 1975:26-35. 39. Doll R. Peto R. Cigarette smoking and bronchial carcinoma: dose and time relationships among regular smokers and lifelong non-smokers. J Epi- demiol Community Health 198+1:32:303-13. 40. A:elson, 0, Edling C, Kling H. Lung cancer and residency-a aae-referent study on the possible impact of exposure to radon and its daughters in dwellings. Scand J Work Environ Health 1979; 5:10-15. 41. Edling C. Kling H, Arulson 0. Radon in homes- a possible cause of lung cancer. Scand J Work Environ Health 1984:10:25-34. 42. Pershasen G, Damber L, Falk R. E:posure to radon in dwellings and lung cancer-a pilot study. in: Proceedings of the Third International Con- ferenceon Indoor Air Quality and Climate. Vol 2. Stockholm: Swedish Council for Building Re- aearch. 1964:73-8. 43. Archer VE, Wagoner JK- Landin FE. Uranium mining and cigarette smoking effects on man. J' Oecup Med 1973:15:204-1 L 44., Bergman H, Edling C, A:elson 0. Indoor radon daughter concentrations and passive smoking. In: Proceedings of the Third International Confer- ence on indoor Air Quality and Climate. Vol 2 Stockholm: Swedish Council for Building Re- search 1984:79-84.