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-10- the evening until the following morning. It was found that present exposure to passive smoking was more influentiaJl than past exposure; that active smoking had a fairly marked effect on the develop- ment of squamous cell carcinoma or small cell carcinoma; and that in these his- tologic types, current (up to the present time) exposure to passive smoking had a marked effect. On the other hand, there was virtually no effect of active smoking on the development of adenocarcinoma,but there was suspicion of the effect of past or present exposure to smoking in this type of tumor. The effect of passive smoking should be considered qualitatively and quan- titatively. In assessing the qualitative effect of passive smoking, the followingg items should be considered; The amount of carcinogenic material in secondary smoke is greater tran in the primary smoke1); when ten cigarettes are smoked in 1 hour, the level of CORb in the blood of the non-smoker rises to about the same concen- tration as that following the active smoking of one cigarette2);. the amount of urinary nicotine of a non-smoker increases in parallel to the number of active smokers generating smoke, demonstrating a dose response effect3);benzpyrene in the urine of a non-smoker exposed to smoke becomes detectable, and this amount de- creases when the non-smoker avoids exposure to smoke4) ; upon exposure to smoking for 6 hours, the amount of mutagens in the urine of a non-smoker increases marked- lys)s and that mice and dogs exposed to smoke develop lung tumors6). These results suggest the possibility of lung carcinogenesis through passive smoking. Quantitative assessment of passive smoking has been presented in the follow- ing findings: The increase in incidence of lung cancer in non-smoking wives of heavy cigarette smokers over that in non-smoking wives of non-smokers was x2.08 in Japan (Hirayama)7), x3.4 in Greece (Trichopoulos)9), x3.1t in the United States (Correa)'0), x1.94, also in the United States (Miller)11), x12.78 in Kanagawa Prefecture (IInoue)22) and x1.5-2.1 in Hiroshima and Nagasaki (Akiba)231. When the findings by Garfinkel (U.S.) 8) and Koo (Hong Kong)17) are excluded, mortality of non-smoking wives from lung cancer seems to increase about two-fold. Increase in the risk of passive smoking in the family is especially marked in non-smoking women under 50 years of age, while habitual smokers are subject to both active and passive staoking12) . Akiba23) found that of vomen who are not exposed to either Active or passive amokiflg, M develop either adenocarcinoma or large cell carcinomaf that the incidence of these tumors decreases to 64% in passive stnokers and to 42% in active smokers; and that in the latter cases there is a proportional increase in squamous cell carcinoma and small cell carcinoma 23?• These are similar to our findings. In these reports, however, there are no consistent results concerning signi- ficance or dose response, and there is no unified interpretation at this time.

Some of the explanations for the inconsistencies are the following: (1) Differences in the living environment, (2) lack of definite information on passive smoking before marriage, (3) differences between wornen who work outside and those who are self-employed, (4) duration of periods when husband and wife are together, (5) smoking habit of the husband and conditions in the home, (7) mealtime habits, (8) incidence of cancer in the family and (9) age when the cancer developed. The 6,13) paucity of information on these matters has been pointed out . The present study was a survey of the Nara region where most women who were the subjeets of the investigation were self-employed. Information was gathered regarding the his- tologic type of tumor, time of exposure to smoking, and incidence of cancer in the family, and although the number of cases was small, a certain degree of control was exercised. Correa10) studied the relation of lung cancer to past exposure to passive smoking, and concluded that the effect of smoking by the mother could be seen in male lung cancer patients but not in1women lung cancer cases. Extrinsic and intrinsic factors may interact in carcinogenesis. The leading extrinsic factor in lung cancer is presumably cigarette smoking, while genetic cancer may be an intrinsic factor. we investigated the history of relatives three times removed from the principal, and found that with adenocarcinoma there was a strong indication of association of familial incidence of cancer, while with squamous cell carcinomz and small cell carcinoma, association of familial incidence was seen but not to a sigr.ificant degree in comparison with controls. The associa- tion, however, was observed in 4 out of 5 cases of small~ cell carcinoma while in squamous cell carcinoma there was more variaaility_ There is need for further study in larger numbers of cases. In another investigation of familial factor, the risk of development of lung cancer when there has been a family incidence was 8-fold over cases without any familial occurrence of lung cancer in Kawasaki City, and 5.9-fold in Tokyo18). Aoki1'9) also pointed out that the risk of cancer of many organs was 2-3 times higher in families which had cases of cancer than in families without such history. Tokuhata2t) , in a survey of 2701cases of lung cancer, assessed the risk when familial incidence and active smoking were combined, and found: the following: Compared with individuals without either factor, the risk for the non-snroker with familial history was 3.96-fold; for the smoker without familial history it was. 5.45--fold; and for the smoker with familial history it was 13.64-fold. He stated that when corrected for smoking habit, the risk for those with familial history was increased 2.5-fold, approximately the same •level of risk as that of smoking, and claimed that the two factors are synergistic. Zn our present study, the findings indicated that compared with controls,

-12- passive smoking, current or paet, increased the risk for lung cancer .+her+ familial history was present. when the data were sorted according to histologic type of lung cancer, risk was increased for aquamous cell carcinoma and small cell carcinoma when active or passive smoking was combined with familial history, while with adeno- carcinoma the influence of familial history was considerable, and the effect of passive smoking in the past was suspected. Since the number of cases was small and the amount of passive smoking could not be determined so that dose response could not be demonstrated, no definite con- clusion could be drawn fron+ the present study, but there was a suggestion that for women in the Nara region, passive amoking is associated with development of lung cancer in women. The effect of passive smoking which has continued to the present time was especially marked, particularly notable in squamous cell carci- noma and small cell carcinoYna. With adenocareinanap the effect of passive smoking: in the past was suspected. Along with passive smoking, the association of some intrinsic factor (gene- tic tendency) to varying degrees in the different histologic types of lung cancer in women, especially in adenocarcinoma, was apparent.

-13- REFEREI3CES c 1) Stock, S.L.: Risks the passive smoker runs. Lancet 2: 1082, 1980. 2) Asano, M.: Passive smoking -- Relation to the body environme.nt. Igaku no Ayumi 103: 479-499, 1977. 3) Hatsukura, S. et al.: Effects of environmental tobacco smoke on urinary cotinine excretion in nonsmokers. Evidence for passive smoking. N EnSi J Ned 311: 828-832, 1984. '4) Maly, E.: A simple test for exposure to polycyclic hydrocarbons. bull EnvirOn Contam Toxicol 6: 4,22-425, 1971. 5) Bos, R.P., et al.: Excretion of mutagens in human urine after passive smoking. Cancer Letters 19: 85-90,. 1983. 6) Sasanami, T.: Passive smoking and lung cancer. Shindan to Jiryo 72: 1734-1736, 1984. 7) 13irayama, T.: Non-smoking wives of heavy smokers have a higher risk of lung cancer; a study from Japan. Brit lted J 282: 183-185,, 1981. 8) Garfinkel, L.: Time trends in lung cancer mortality among non-smokers an6a note on passive smoking. JNCI 66: 1061-1066,, 1981. 9)'Trichopoulos, D. et al.: Lung cancer and passive smoking. Inc J Cancer 27: 1-4, 1981. 10) Correa, P. et al.: Passive smoking and lung cancer. Lancet 2: 595-597, 1983. 11) Miller, G.H.: Cancer, passive smoking and nonemployed and employed wives. West J Med 140: 632-635, 1984. 12) Sandler, D.P.,et al.: Passive smoking in adulthood and cancer risk. Am J Epid'emiol 121': 37-48, 1985. 13) Shimasato, Y.: Lung cancer: Ita histological development, differentiation, and prognostic factors. Nippon B oishi 72: 29-57, 1983. 14) Kreyberg, L.: Aetiology of lung cancer: A morphological, epidemiological and ex;rerimental analysis. Oslo Qniversitets forlaget 17-26, 1969. 15) ginds, li.iT., et a1.: Diffezences in lung cancer risk from smoking among Japanese, Chinese and Hawaiian women in Hawaii.Int 3 Cancer 27; 297-302. 1981. 16) Kennedy, A.: Relationship between cigarette smoking and histological type of lung cancer in women. Thorax 28: 204-208, 1973. 17) Roo, L.C., et al!.: Is passive smoking an added risk factor for lung cancer in Chinese women? J Exp Clin Cancer Res 3: 277-283, 1984.

-14- REFERENCES (con't) 18) Hiraysma, T.: Lung cancer and smoking, Series on internal medicine -- lung cancer of ali types. 0. Kitamoto, ad., Nankodo Pubi., Tokyo, 11974, pp. 26-48. 19) Aoki, K., at al.: Rost factors in cancer. Gan to Kagaku Ryoho 9: 766-773, 1982. 20) Lynch, H.t., et al.: Cancer family syndrome. Lynch, H.T. (ed), Cancer Genetics, C.C.Thomas, Springfield, 111, 1976, p. 355-388. 21) Tokuhata, G.K.: Cancer of the Lung; Rost and environmental inter- action. Lyneh, H.T. (ed), Cancer Genetics, C.C. Thomas, Springfield, 111, 1',976, p. 213-232. 22) Inoue, R. tt al.: Controlled study of lung cancer cases in Miura City, Kanagava Prefecture. Haigan 26, 763-767, 1986. 23) Akiba, S., et a1.s Passive smoking and lung cancer among Japanese vomen. Cancer Res 46: 4804-4807, 1986. ((Received for publ:ication: 5/20/87)