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Smoking, passive smoking and histological types in lung cancer in ong Kong Chinese women t+oT ~~.C~ H ThiS r.telerial rr?7 be protected tY cc7ino T.H. Lam'', I.T.M. Kung2. C.M. Wong', W.K. Lam', J.W.L. Kleevens', D. Saw•°, C. lfiWaiUg 17~ U.S. Ct:ea S. Seneviratnes,, S.Y. Lam2, K.K. Los & W.C. Chan• Deportrrunts of'Corremunity? Medicine, =Pothology,''Medtcute. Universiiyof Hong Kong; • Quern Ei:abeth Hospito/ ond tKowloon Hospital, Hong Kong. Swsary in a case control study in Hong Kong. 445 cases of Chinese female lung ancer patients alll confirmed pathologially were compared with 445 Chincye female healthy neigbbourhood~conuols matched for age The predominant histologial type was adenocaronoma (¢7.2'L.). The relative risk (RR) in ever- smokers stnokers was 3.91 (P<0.001. 95% C1 -2:86; 5.0g): The RRs were statisucally significantly raised for all major cell types with significant trends between RR and amount of tobacco smoked daily. Among never smoking women RR for passtve smoking due. to a smoking husband was 1.65 (P<0 01 95•h Cl - 1 16, 2.35) .n broketi do.rn` by csll t ,"gxufieant.trWd`l~ ~~~') .r.a '.the ~ husbncd Wheti: R~ + ~ the numbeis~Yere..substantial-,oa) anma~RR~212.~P<b.01: 9S•%.C1~~.3X 3.39) witti`i gaibant tmtd between RR 4taoue~ tmoli~d'~a7y by the Eushaad: 73e results tatgarst that passive S~smoking is a risk factor for lung artcer„ particularly adenocarcdnotoa in Hong Kong Chinese women who never s•moked. In Hong Kong, lung cancer is the major cause of death in both malts and females. In 1985; there were 2,223 deaths attributed to malignant neoplasms of the trachea, bronchus and lung (1CD 9th Revision Code 162) which accounted for 29:5%% of deaths due to all1 forms of cancer; 1,457 in males, (31.7°ie) and 766 (26:0%.) in females (Director of Medical & Health Services of Hong Kong, 1986). On a world scale, male lung cancer death rates are nott particularly high in Hong Kong.. However, the female rates are among the highest in the world with an age-standardized incidence rate of 23,4per 100,000:in 1974-1977 (Waterhouse et nl., 1982), resulting in an unusually low male to female ratio. The most common cell type in males is squamous cell carcinoma (33.3%) and in females, adenocarcinoma (49.6%) (Kung et al:, 1984). A case control study in 1976-1977 confirmed the relationship between lung cancer and smoking in males. but in females about half the lung cancer patients were found to be non-smokers, of whom two thirds were suffering from adenocarcinoma (Chan rt a!„ 1979). Further studies on passive smoking and other risk factors have been carried out in Hong Kong but they failed' to throw much light on the causes of lung cancer in never smoking females (Chan & Fung. 1',982; Lam et ol:, 1983; Koo et al:, 1984;. Koo et al:. 1985): The present study aimed to answer the following questions: 1. Is smoking a major risk factor for lung cancer in Hong Kong Chinese women and if so, what is the relationship between smoking and' the histological types of lung cancer' 2. Is passive smoking due to a smoking husband a risk factor for lung cancer in Hong Kong Chinese women who have never smoked themselves and if so, what is the relationship between passive smoking and histological type? Materiak and metlsod.s A standardized structured questionnaire was designed for interviewing both cases and controls. The questions on Correspondrncr: T.H. Lam. Department of Community Medione, Universit,v of Hong Kong: li Shu~ Fan Building, 5 Satsooo Road, Hong Kong:. Received 17 March 1987: and in revised form, 17June 19g7, smoking habit were modified from those of the Questionnaire on Respiratory, Symptoms of the Medical Research Council (1966). The subject was asked whether she smoked, or had ever smoked as much as one cigarette a day (or one cigar a week or one ounce of tobacco a month), for one year. If the reply was negative, we checked again by asking a further question on whether she had ever smoked any amount of any type of tobacco at all in her whole life up to the time of the interview. Because of very few positive responses to this additional qtxstion, we were drttisfied that under-reporting of the smoking habit was not a major problem. As elsewhere, an ever-smoker was defined as one who had ever smoked as much as one cigarette a day or equivalent for as long as a year. If a subject had ever smoked, questions on the type of tobacco and amount usually smoked per, day, age when smoking started regularly and for e>c-smokers only, age when smoking was given up permanently, were asked: A never-smoker was defined as one who had never smoked as much as one cigarette a day or equivalent for the duration of one year. The smoking history of the subject's husband was ascertairted' in similar way if the subject was marned. The same definitions of ever- and never-smoker were used for the husband. A women was considered exposed to her, husband'ss tobacco smoke if she had lived together with her smokingg husband in the same household for at kast one year continuously. If the husband was an ever-smoker, information on the type of tobacco and' amount usually smoked per day' by the husband and the duration of exposure was obtained. The questionnaire also contained sections on demographic and other variables. ]t was tested, amended and finalised before use in the study. Eight government or government- assisted hospitals in which most of the lung cancer patients were treated in Hong Kong granted us permission for interviewing of patients. During the interviewing phase of the study, we intended to include all lung cancer patients of the eight hospitals whose diagnosis was based on strong chnico-radiological criuria and with histologicali and/or cytological confirmation. Patients admitted to these hospitals who were suspected by the hospital clinicians to have lung cancer or who had already been given a confirmed diagnosis of lung cancer were interviewed as soon as possible after their admission. before thei>•r physical condition deteriorated. Only patients with their diagnosis confirmed by a pathologist's report(s) t

1 1W 6?4 T H LANtrra! 1 were included as cases. Patients with a provisional diagnosiss were considered onl'y as suspected cases and they were followed up after being tnterviewed! Only those who subsequently had a pathology report confirming the diagnosis of lung cancer were includ'ed'. Those without such canfirmauon were not included in the present study. The pathology report was required to state unambtguousl}~' that the patient was suffering from litng cancer before it was accepted. Information on cell' type if' available. was noted. Cases without information on cell type or unclassified because ofl undifferentiated tumours were grouped under 'others and unclassified'. The few patients with rare tumours such as carcinoid were excluded. Because these hospitals were visited frequently by the interviwers so that all eligible patients would be interviewed other than the few patients who declined to co-operate or were too ~ ill. we believed than we had missed only very few eligible patients. For each ~ case. a healthy female control matched for age (± 5 years) living in the same neighbourhood of the case was interviewed. The procedure of control selection was that when a patient was interviewed and included as a pathologically confirmed case. the age and address of the case was noted. The interviewer then went to the address of the case and statted to~visit the nearest neighbourhood addresses until she found a woman who appeared healthy and was within 5 years of age of the case. A few questions om present state of health~ were asked to check that the subject was indeed healthy and if so, the same questionnaire was completed. Thus the controlS were matcbed for sex, age and place of residence. Interviewing took place between 1983 and 1986, and involved experient~ female intetvi•ewers. The fanguage used was mainly Cantonese. Each interview took about 30min to complete. Cooperation of interviewees was good and non- response was rare ( - 1%): The present paper presents the findings on the smoking history of the subjects themsttves and for the never-smokers, the history of passive smoking due to a smoking husbandi Four hundred and forty-five cases and 445 controls were included. Relative risks (RR)' and 95% confidence intervals (CI) (Woolf's logit limits) were calculated for each level of risk factor. Fishcr's exact test (two-sided) was used to check whether the RR was significantly different from unity. x' test for linear trend was performed to t:est whether, tthere was a trend between RR and the levels of exposure (Breslow & Day. 1980). Subjects with missing data were excluded from the analysis. We carried out separate analysis on cigarette only or on all forms of tobacco, by including single (never-married) women or by excluding them, by amount smoked daily, by duration of exposure or by total amount of exposure (amount smoked daily multiplied by duration). Because of the similar results and space limitation, only the results on all' forms of tobacco,, with single women included and by amount smoked daily are reported in the present paper. Results Thirty four, percent ofi the cases were confirmed pnmanly by bronchial or lung biopsy, 12% by lung resection. 8%by, lymph node biopsy. 9% by pleural' biops. 17°i°, by sputum cytalog., 12% by' pleural fluid cytology. 6% bv bronchial aspirate. brushing, etc.., 0!2%o by autopsy and 2'i% by other methods. The distribution of the cases by cell type and by smoking history is,shown in Table I. The distnbution of' cell types differed somewhat according to the basis ofi diagnosis. Resection and pleural bropsy yield'ed' 70% adenocarcinoma while other methods resulted in 30-35% adenocarcinoma. Bronchial and lung biops} resulted in -30% while other methods resulted in about 10% squamous cell carcinoma. A comparison of cases and' controls by age and place of residence confirmed that they were similar in, the two matching variables. The mean age of the cases was 65:6 years (s.d. 11.2 years) and that of the controls was 65.3 years (s.d. 10:9 years): Comparison by other demographic variables showed that the cases and controls were comparable in place of binh, duration of stay in, Hong Kong, kvel of education, mantal' status. and husband's occupation. Thus, by matching the controls with the cases by age and residence, a high degree of' comparability was achieved with regard to many other demographic vanables. Table II shows the Relative Risks (RR) by history of ever- smoking and cell types. Among the cases for alli cell types combined. 54.5°/% were ever-smokers and 45.5% were never- smokers whereas among the controls, the corresponding percentages were 23.9% and 76.1 °id. The overall RR , f~r - ,` ever-smoking was 3.81_.T3x RRs were Iu tach of; tDe 4,_ ce3Y types, being famnoris (RR~~ F3 00);•-: foliow~i-v~ ,; oat~ cell carSt~f~imat (RR~$:30), luge ca31'catcinotna (1RR=6".93) and ° n =1.87). ib1e: tI showsV the` RR by' amount of~,tobacco :smoked dat~y~by` t3x 3~t~jects~ Significant tretids were found for all cell types combined and for each of the 4 cell types. Table IV shows the RR for passive smoking due to a smoking husband and cell' types_ Single (never marned)) women were treated as non-exposed to husband's smoking. The RR was 1.65 for all cell types combined. For individual cell types, the numbers were too small to be statistically significanr except for adenocarcinoma, with a RR of' 2.12. Table V shows the RR for passive smolung b~ amount smoked daily by the husband. Signifwant trcnds~were found for all cell types combined and for ad'enocardno"tn~`'only. No significant RR or trend was found for other cell types and the details are not reported here. Because similar results were obtained when single women were excluded. these are also not reported. It should be noted' that the proportions of single (never-married)' women in the cases and controls was 6.8%% and 5.2% respectively. N 11 'T.Ne 1 Distribution of eel] type by smoking habit oficases and comparison with Kung et.al't ((984) series 7~ 1 Squmnout crll carcLcoma Smull cell cmcinoenn %. rt % Present Series Never smoker 28' 304 9 Ip.6. Ever smoker 63 68,5 42 82.4 Missing dau I I.I, - - Total 92 1000 51~ 100.0 (7..of4M.cases). ('.017) (ttl5) Senes of Kung rr al (1984) 77 43 ( : of 341',crses) /22~.6t tl~''6), Large eell' Others and Adrnocaccn°orno carcinoma wclactffied Total U1 n~ %% n %~ n. % n %.~. " 131 62 4 9 450 25 347 202 45 4 79' 376 I I 55 0 47 65.3 242 544 I 02 210 100!0 ?0 1000 72 100.0'~ 445 10010 (47.2): (4.51 (16.2) (a000) 169 34 18 ?41 (496) (100)' (53) 110001 ~ ' A W V I

T.blt 11 Hrstorn of' ever smoktng (all I forms or' tobacco) in 4" cases a-nd 443 controls by cell types Smoking htstorr, of sublmrs Cell npe Casr. A'o Yes Control No Yes Relti n ue ruk (B 95 io Cn P Squamoou cell carcinoma 28 63 72 20 8 10 <0001 (4.16, 15.77) Small cell'caninoma 9 42 36 14 12.00' <0,00i (4 65: 341918) Adenocarcinoma 1311 79 158 51 1197 <0;011 (1 23 . 2.85) Large cell carcinoma 9 11 17 3 6.93 <0;05 (1(53;,31.38) Others and unclassified 25 47 54 18 5.64 <0;00! (2.71. 111.60). All cell types 202 242 337 106 3.81 <0:001 (2.86,5.08) Nores: For each cell type. the cases were compared with thein matcbed controls. One case and 2 controls with tnissing data on smoking were excluded. T.bk 1111 Amount smoked daih (a11 forms of tobacco) in cases and controls by cell types All'cell rvyes Squamoutcrll carcinoma Amount senoked dailnb't srb)erts Case Relative risk' Control (d 9S`: CI) P Case Relativt ruk Control (d 93'6 CIY P Nil 202 337 1 28 72 I 1-10 101 63 2.67 23 111 5.38 (1'.87: 3.93) <0!001 (2.32. 12,46) <0!001,. 11-20 90 28 5.36 28 6 12.00 f~~¢y~?~i;as2> (3.39. 8' 48) <0!001 (4.49. 32,10) <0!001 21 + 39 9 7,23 10 1 25.71 (3.43:15:.24) <0001 (3.14; , 210,30) <0!001 Totall 432 437 89 90 Test for trend z==89.5. P<0.001! x2 - 41.9G P<0.00)1 Small 'cell rarcinorna Adrnocarcinoma Amount,smoked' daih br sybjects Case Rtlarive ruk, Control (d, 95%. Cl), P Case Relarive ruk, Cantrol (d 95% C!)', P Nil 9 36 1 131 158 1 1-10 16 10' 6.4 36 29 1.50 (2.18. 18.77) <0.001. (0.87. 2.57) >0.05 11-20 14 4 14:01 27 14 2.33 (3:70, 52.92), <0.001 (1.17, 4.62) <0.05 21+ 11 0 - 9 5 2.17 <0:001 (0.71, 6.64): >0.05 Total 50 50 203 206 Tesi for trend Z' '- 32.61, P<0.100 1 xYa8.04, P<0.01 Large pell'carcinonta Othtrs and 1llcla.tsifKd Amount smoked Relarive risk R[latt vr risk daih bs subjects Cau Conrrol' (a 95% CI) P Case Control (4 9S'G Cl) P N Nill 9 17 1 25 54 1 07~~ 1-10 6 3 3.78 20 10 4.32 lV (0:76, 1819), > 0.05 (1.77, 10;57) <0 01 11-20: 4 0 - 17 4 9.18 <0.05 (280 30!11) <0 001' v't 211+ 1 0 _ 8 . 3 5.76 . ~ > 0;05 (1.41, 23.57) <005' Total 20 20 70 71' Test for trend x7- 8.17. P<0.01 x"=19:86. P<0.001 hores. Sub1ecu with missing data on amount smok'ed datly were excluded ~

I the relau~e nsks fon adenocarmnoma found' in other Hong Kong studies 1.59' (Chan ei al.', 1979). 1.80 (Lam ei al.', II983)j , 1.88 (Koo rr al:. 1985): and 2 1 (Lam., 1985). The stgnificant' trend observed for adenocareinoma provides further evidence that smoking is also a nsk factor for this cell type. The association between histological! types and smoking was reviewed recently by an IARC Working Group (11985) which concluded that all the three principal types of lung cancen. rir. squamous cell, small cell and adenocarcinoma, were probably caused by smoking, although the relative risk was least extreme for adenocarcinoma. The results of the present study have therefore supported the IARC conclusion. It should~ be noted& however, that the proportion of never- smokers was 62.4°, in adenocarcinoma, as compared with 26.1'% in squamous and small cell carcinomac and~ that some of the adenocarcinomas among smokers may well not have been caused by smoking. The causes of the high rates of lung cancer. particularl'y, adenocarcinoma in never smoking women in Hong Kong remained unoertain, and prompted the presenu study: Furthermore, this problem had become more urgent since Kung er a1. (1984) showed that there appeared'to have been aniinerease in the relative frequency of adenocarcinoma in both sexes in the comparison of their senes of lung cancer cases in 1973-1982 with an earlier series in 1960-1972: Since the publication of the results on passive smoking by Hirayama (1981) and Trichopoulos er al. (1981)4 passive smoking was postulated as a risk factor for lung cancer in never smoking women in Hong Kong and elsewhere. In Hong Kong. Chan and Fung (1982) reanalysed the case control study data of Chan er al. (1979) an& found that among non-smoking women there were more passive smokers in controls (661139) than cases (3484), The 84 cases included 34 adenocarcinomas and other cell types. In a case control study by Koo ei ni. (1994) on 200~female lung cancer patients and' 200 healthy district controls, 69 adeno- carcinomas and 19 cases not confirmed pathologically' were included. The RR in never smoked wives with smoking husbands was 1.48 (P=0.16) and is close to that in the present study (1.65). The RRs for passive smoking in never smoking females by cell types were: squamous cell' 1.75, small cell 1.10. adenocarcinoma 1.11 and large cell'. 1.44 (Koo er al', 1985), However, in a study by Lam (1985) on 163 female lung cancer cases and 185 ortbopaedic controls, the author focussed the analysis for passive smoking on 60 adenocarcinoma cases and 144 controls, both cases and controls being non-smokers. For peripheral tumour, he found an increased RR of 2:64 (P<0.05) for passive smoking due to a smoking husband. For central tumours,, the RR was 1.61, but was not signifrcant. The RR for adenocarcinoma, central and peripheral ttanour combined was 2.01 (95%. Ct -1.09„ 3.72; P<0.05; our calculauon): Passive smoking in other cell types was not teported! In the present study the overall RR for passive smoking due to a smoking husband was 1.65 (P<0.01) in all cell types combined. When broken down by cell types, a statistically significant RR was found only in adeno- carcinoma but not in the other cell types, although this may have reflected chiefly the smallness of the numbers involved. The value of RR of 2.12 was very close to that of 2.01 rrponed~ by Lam (1985). The 95% CI for the present study (1.32, 3.39) was narrower than that in Lam's study (1.09; 3.72); however, because the number of subjects was smaller in the latter study: Analysis by oentnl', or peripheraL positions of the tumour was not possible in t.be present study because of lack of information, It is probable than the true relative risk is nearer to the lower end (1.30): than to the upper en& (3.36) of the confidence interval, because it is difficult to believe that passive exposure is morr hazardous than active exposure, an& for adenocarcinomas the relative risk (companng all smokers with all! never-smokers, including passively exposed' neverrsmokers) for active smoktng was only 1.87. The significant trends observed between RR and amount smoked daily by husband for, all cell typescombined and for adenocaranoma provides suppon the view that the relationship is likely to be causal Recently;, Blot and Fraumeni' (19861: revtewed! the epidemiological an& other evidence on passive smoking and lung cancer and concluded that. the existing evidence is highly, suggestive that long-term exposure to environmental tobacco smoke increases the risk of lung cancer. Summarising the available data, they estimated that the excess risk was -30%. The excess risk rose with increasing exposure, reaching -70%% among heavily, exposed non- smokers. Wald ei a/. (1986) also calculated a relative risk of 1.35 for, lung cancer among non-smokers living with smokers by pooling the results of 10! case control studies and three prospective studies and concluded that brrathing other people's tobacco smoke is a cause of lung cancer. Compared to the 13 studies included by Wald er a1: (1986) the present study included the largest series of never smoking lung cancer cases (199 cases), Results of the present study would add more evidence on passive smoking as a risk factor and they would contribute towards part of the explanation for the high incidence of lung cancer in txver, smoking women in Hong Kong. With regard ~ to the possibility, of bias through the misclass- ification of current and ex-smokers as lifelong non-smokers, Wald et a/:,(1986) stated that the extent of misclassification bias was influenced by the proportions of men and women in the population who had smoked' at some time and the greater the proportions (of women in particular). the greater the bias. By choosing the high proportions of 50'i% of smokers in women and ~ 70% in men and a low observed relative risk of 1.35, they concluded that the misclassification bias was unlikely to account for all the association between lung cancer and passive smoking: In Hong Kong, the proportion of smokers in men was 32:8°i, and in women 4:1 °/. (Hong Kong Census and Statistics Department, 1985): These figures. particularly in women. were much lower than the figures used by Wald ef a1. (1986). Also, the observed' RR was higher in the present study. Thus the extent of influence by misclassification bias woul& be much less and~ could not account for the relatively high RR in the present study. Furthermore, a comparison for adenocarcinoma on the RR due to active smoking (1.87), and thar due to passive smoking (2.12) seemed to suggest that the risk for passive smoking was quite similar to that for active smoking for this particular cell type. This was not the case for all other cell types in which active smoking posed much higher nsks than passive smoking. The apparently greatcr risk of adenoa carcinorna than of~ other cell types from passive smoking conflicts with findings in other studies an& this may be a feature of small numbers. However, Peto and Doll'(1986) in their recent editoriali on passive smoking stated that the observed risk need not necessarily be the same in all countries as type of tobacco, past changes in smoking habits, and the extrnt of passive exposure both at home and elsewhere may all differ substantially between differcnt countries. In places like Hong Kong where people lived in more over-crowded conditions with poor ventilation, passive exposure msy be heavier resulting in a higher RR. Moreover, Wynder and Goodman (1983) noted that the predominann cell type of lung cancer in non-smokers is adenocarcinoma and postulated that passive inhalation may primarily increase the risk for adenocarcinoma because side- stream smoke, which contains many gaesous components, can reach the deeper parts of the lung more readily than can mainstream smoke with more particulates. Together with the findings by Lam (1985) on peripheral adenocarcinoma. ourr results do offer some support for Wynder an& Goodman's postulate that passive smoking may be a nsk factor particularly for adenocarcinoma. At the very least, reviews

A 676 T', H LAM e, al~ Table IV Passive smoking due to a smoking husband (all forms of tobacco) in 199 never smoktng cases and 335 never smoking controls by cell types Case Control t atrvr risk. Crll rvtx No Yes No Yes (d 95°4 Cl) P Squamous eell'earsanoma 15 12 37 35 0.85 > 0.05 (0;35, 2:06) i Small cell carcinoma 2 6 18 18 3.00 >0A5 (0.53. 16.90), Adenocaninoma 53 78 92 64' 2.12 <0.01 (1.32. 3.39), Large cell'earcinoma 2 7 8 9 3.11 >0.05 (0.50. 19.54)'. Others and~ unclassificd 12 12 28 26 1.08 >0:05 (0.41. 2.82)', Allcellitypes 84 115 193 152 1.65 <0.01 (I.16; 2.35). Notes- For each cell type. the cases were compart:d'with their matched controls on passive smoking for ever smokers and never-smokers. Results on ever-smokers were not included here. One case and 2 controls with missing data on smoking and 3 cases and 2 controls with missing data on hustiand's smoking were excluded. Table V Passive smoking due to a smoking husband (all forms of tobaoco) in never smoking tasess (all cell types and adenocartanoma),and never smoking controls by amount of tobacco smoked daily by husband AA cefl types Adrnocarcuwma Amounr tmoktd daily b,v lovband' Cau Connol Relatirr .nsk (d 95% CI) P Rr/atire ruk Case Control' (d 95%i Cl); P „ Nil 84 183' 1 53 92 1 I-ID 22 22 2'.18' 17 12 2:46 (1.14, 4 115) ) <0.05 (1.D9, 5.54) <0.05 11-20 56 66 1_85 37 28 2:29 (1.19; 2.87) <0.01 (1.26. 4.16) <0.01 21+ 20 21 2.07 15 9 2:89 (1.07, 4.03) <0.05 (1.18, 7.07): <0.05 Total 182 292 122' 141 Test for trend: x'- 10.17;P<0:OIi x'-I1.07,P<0.001 Norer. Sub)ecta witb missing data on amount smoked daily by husband were excluded!, Discmaioo The present study was a caw control study on lung cancer in Hong Kong Chinese women with a larger number of subjects included than i.n the two previous local case control' studies (Chan rr al., 1979; Koo et al:, 1984). All our eaYes were pathologically confirmed, unlike these two previous studies which included cases tbnfirtne& only by ctinico- radiological criteria. The primary advantage of its relatively large-siu (the largest such series yet reported) and the improvement over previous Hong Kong studies by including only pathologically confirmed cases enabled txlculations of' histologic-specific risk estirnates. The controls used were healrhy women from the same neighbourhood matched for age. Comparability between cases and controls with rcgar& to basic decrnographic variables was good; suggesting that thesc demographic variables may not have a major confounding effect on the results reportedl As shown in Table I, the distribution of cell type in the cases in the present study was comparable to the large pathological study of Kung et al: (1984) which included surgical material such as bronchial biopsy, trans-bronchial biopsy, needle biopsy and resection specimens.. Biopsy of lymph nodes alone were not included. Cases without histo- Smoking kutoa of kusbandi r R logical examination of the primary tumour of the lungs. or which were diagnosed by, cytology alone were excluded. Despite the difference in the basis of diagnosis between the present study and that of Kung er al: (1984), the similarity in the results suggests that the cell type distribution observed in the present study should be close to the true disttabution, For smoking by the subject herself, the present study confirmed' the increased risk of lung cancer found in previous studies in Hong Kong, but indicated' a slightly higher relative risk (3:81) than in the study of Chan er al. (1979) (3.48) or of Koo et al:, (198'S) (2.77), The significant trend observed suggesas that tbe association is likely to be causali, With regard to cell types, statistically significant RRs were found for all cell types, including adenocarrinoma. in previous studies in Hong Kong, the RRs for adeno- cardnoma were greater than unity but did not rtzch a statistically significant kvel', perhaps due to the smaller number of subjects studied (Chan er al., 1979. Lam et al. 1983; Koo rr al., 1985), This led to the hypothesa that smoking was not a risk faetor, for adenocarcinoma in Hong Kong Chinese women. The results of the present study suggest that smoking is significantly associated with adeno- carcinoma, although to a lesser degree than with squamousor small cell carcinoma. The RR of L87 cAmpared wclllwithi 1

W 678 T H LAN9 rt al 01 passive smoking and~ lung cancer can no longer suggest that the results in Hong Kong fail to support the existence of a real relationship. In conclusion. however, we note that 2s?°o (53"210) of our patients with adenocarcinoma were neither smokers themselves nor passive smokers due to smoking husbands. Although smoking an& passive smoking may account partly for the high incidence of adenocarnnoma, exposure to other factors should be further ezamined'to elucidate the aetiology of lung cancer, particularly the high incidenee of adeno- carcinoma in this population. We are most grateful to the International Development Research Centre and' University of Hong Kong for their very generous Refereeces BLOT. W:1. & FRAUMENI. J.F (1986); Passive smoking and lung cancer. JNorl'Cancer Inst.. 77, 993. BRESL!OR'. N.E & DAY:, N.E 119801 The ana(vsir of cast control srudtm International Agency for Research anCancer. Lyon. CHAN. wC.. COLBOURNE. M:J.. FL'NG S.C & HO. H.C. (1979); Bronchtal.cancer in Hong Kong 197fr77. Br. J. Cancer. 39, 182. CHA'.. w C & FL'T:G. S.C. (198.1. Lung cancer in non-smokers in Hong Kong In. Cancer campaign. Vol. 6. Cancer epidemiology. Grundmann: E. led) p. 199: Fischer Verlag: Stuttgart and New York. DIRECTOR OF MEDICAL AND HEALTiH'. SERVICES OF HONG KONG 0986). 1985-1986 Departmental Report: Government Pnnter: Hong Kong. HIRAYAMA, T fL981). Non-smoking wives of heavy smokers have a higher risk of lung cancer: A study from Japan. Br. Med. J.. 7E2; 183. HONG KONG CENSUS & STATISTICS DEPARTMENT (1985). Special Topics~ Report Ill. Social' Data Collected by the General Housetiold! Surve). GovernmenrPnnter: Hong Kong. IARC WORKING GROUP (1985): IARC Monographs on rha Evaltiatron of tAe Carcorogcnrc Risks of Chemica/s to Htanaru: Tobacco Smoktng. VoL 38. Internauonal Agency for Research'~on Cancer:L.on. KOO. L C.. HO. I H.C & SAW. D(1984). Is passive smoking an added risk factor for lung cancer tn~ Chinese women? J. Exp: CGn. Cancer Res.. 3, 3. KOO. L.C.. HO. 1.H.C. k LEE. N (1985), An analysis of some risk facton for htng cancer in Hong Kong. Inr:,J: Cancer. 35, 149. support in providing the research grants to this project and!to Dr D W' Hbn,for his conttnuous support and advice We w•tsh,to thank the medical supenntendents of Grantham Hospital. Kowloon Hospital. Kwong Wah Hospital. biam Long Hbspttal. Ruttonlee Sanatonum and'Untted Christian Hospital for their permission to interview the patients and the staff involved. paruculaoh the pathologists for thetrco-operauon;,to Mrs 1 Cheang, Mrs J. Wong. Miss S.C. Wong, Miss Connie Wu. Miss C W Yip and Miss Rita Lo for interviewing and other research asststanex: to Miss Agnes Chow and Mrs T. Lam fbr their secretanal assistance and to all the interviewees for their. co-opcration and, partidpation. Finally. we are indebted to Dr M.J. Colbourne for his comments on the technical reporv submitted to LD:R.C. We arr: parttcularly grateful to Mr Richard Peto and Sir Rictiard! Doll for reading and commenttng on the reporuand for their encouragement. KUNG. LT.M'.. SO.,K.F t LAM. T.H. (;1984). Lung cancer in Hong Kong Chinese. Mortality and histological types. 1973-1982. Br J. Canctr,,50, 381. LAM. W K. (1985). A clinicat and epidemtologicd sn,Qc of carcinoma of lung in Hong Kong. M:D. Thesis. University of Hong Kong: Hong Kong: LAM. WK.. 50. S Y k YU. D Y.C (1983). Clinical features of bronchogenic carcinoma in Hong Kong: Revtew of' 480: patients. Canrer. 52, 369. MEDICAL RESEARCH COUNCIL'S COMMITTEE ON RESEARCH INTO CHRONIC BRONCHTTIS (1966). Questionnaire on Respiratory Symptoms. UK. PETO; 1I A DOLL. R. (:1986). Passive smoking. Br. J: Cancer. Sl, 381. (editortal ) i TRICHOPOULOS. D.. KALANDIDI. A.. SPARROS. L. a MACMAHON. B(1981), Lung cancrr.and passive smoking. Inr: J. Cancer.27.I. WALD. N.J.. NANCHAHAL., K.., THOMPSON. S.G. 3 CLCKLiE. H S. (1986). Does breathing other people's tobacco smoke cause litng eancer? Br. Med. J.. 293. 1217. WATERHOUSE. 1.. MLiIR- C. SHANMUGARATNAM. K k POWELL. 1: (eds) (1982): Cancer Incidence in Five Continents. Vol. IV. IARC Scientific Publications No. 42. Internauonal Agency for Research on Cancer: Lyon, VVYNDER. E L & GOODMAN: M.T (1983): Smoking and Ibng cancer: Some unresolved rssues. Epidinuof. Rev.. S. 177