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1254 ZHOU rr nL EXPOSURE TO INDOOR AIR POLLUTANTS AND LUNG ADENOCARCINOMA AMONG FEMALES Table 1. Variables and codes in the case-control study on female lung adenocareinoma. Variables names Age Income Education BMI ETS exposure At working place in childhood from parent At home of husband's smoke Location of the kitchen Extent of eye irritation Extent of smoke in kitchen Cookin~ oil smoke Cooking times for fried food per week Luns TB Family history of cancer Family history of lung cancer Age of first menarche Length of menstrual cycle Number of live binhs Intake of vitamin C Intake of vitamin E Intake of Li-carutene Continuous Codes Monthly RMB yuan per person per family in 1987 Four categories based on 25%, 50%. 75% quartiles 0: None 1: Primary school 2: Junior school 3: Senior school and high Four categories based on 25r9n, 50%, 75% quartiles 0: No 1: Yes 0: No 1: Yes 0: No 1: Yes 0: Separate 1: In living room 2: In bed room 0: Never l: Occasional 2: Sometime 3; Frequent 0: None 1: Slight 2: Medium 3: Heavy 0: Slight 1: Medium and heavy 0: 0-1 time I: 2 or more 0: No I: Yes 0: No 1: Yes 0: No 1: Tes Two categories based on 50% quartile Two catezories based on 50% quartile 0:0-1 1:2 2:3 3:24 Two categories based on 50% quartile Two categories based on 50% quartile Two categories based on 50% quartile , -- - 2505655852 to diagnosis of lung cancer and noticeable deterioration of health. Diet data were converted into unit consumption of specific dietary constituents/ingredients using food tables compiled by the Institute of Nutrition. Chinese Academy of Preventive Medicine (5). Completed questionnaires and relevant medical records were checked for accuracy by a supervisor, coded (Table I) and stored in a computer. The Mantel-Haenszel method and multivariate logistic model analvsis were used to estimate the odds ratio (OR) and 95% CI tor different risk factors and test the statistical sienificance of their association with adenocarcinoma of the lung. Results All seventy-two cases with pulmonary adenocarcinoma and controls were inter,iewed. There was no difference in the distribution of age, marital status, body mass index (BMI) and educational level between cases and controls. The economic status (based on income) five years prior to interview in the cases was higher than that in the controls and the difference was statistically significant (Tables 11 and III). Ladoor air pollution. The most common source of indoor air pollution is cooking fumes. Exposure to cooking fumes was divided into categories of never. occasional, sometimes. and frequent. and according to the degree of eye irritation, and were compared between cases and controls. There was a statistically significant increase in the risk of pulmonary adenocarcinoma and increased exposure to cooking fumes. based on the level of eye irritation experienced. The odds ratio for different levels of eye irritation from exposure tu cooking fumes were 1.33, 7.33. and 1.67. respecti%ele

1256 ZHOU rt al: EXPOSURE TO INDOOR AIR POLLUTANTS AND LUNG AOENOCARCENOMA AMONG FEMALES Table V. Previous history of lung discases, family history of Table VIL Menstruation, reproduction and risk of lung adeno- lung cancer and risk of lung adenocarcinoma. carcinoma. Factors Case Control OR 95'm CI p-value TB No 57 62 1.00 Yes 15 10 1.63 0.63-4.29 0.27 Years of TB No 57 62 1.00 <_25 years 5 5 1.09 0.26-4.63 0.90 >25 years 10 5 2.18 0.63-7.85 0.17 Cancer family history No 64 64 1.00 Yes 8 8 1.00 0.32-3.16 1.00 Lung cancer family history No 65 71 1.00 Yes 7 1 7.65 0.90-169.84 0.03 Table VI. Cigarette smoking and risk of lung adenocarcinoma. Factors Case Control OR 95c1CI p-value Smoking No 52 49 1.00 Yes 20 23 0.82 0.38-].78 0.59 Ezposure to environmental tobacco smoke (ETS). Overall. no significant increase in risk was observed for exposure to ETS. Table IV showed that for workplace ETS exposure, the OR was 0.89 (95% CI, 0.25-3.16); for exposure to ETS during childhood, the OR was 0.89 (95% Cl, 0.43-1.84). Exposure to ETS from husband who smoke, the OR was 0.94 (959o C1.0.45-1.97). Famih ltistorv of cancer-. Family history of lung cancer among first-degree relatives was significantly associated with pulmonary adenocarcinoma, OR was 7.65 (95% CI. 0.90-. 169.84). However, no significant association existed between family history of cancer in first-degree relatives and risk of pulmonary adenocarcinoma (Table V). Previous leuig disease. No statistically significant association was observed between previous lung disease. i.e.. tuber- culosis. and risk of pulmonary adenocarcinoma. Historr of niensrruation and reproductio+r The number of live births was significantlv associated with risk of pulmonary adenocarcinoma. The OR was I.11. 1.i1. and 2.0, respectivel, in 2. 3. or 4 live births, compared tn 0 or 1 live Factors Case Control OR 959o CI p-value Age of first menstruation (years) ?16 38 30 1.00 <16 34 42 0.64 0.31-1.30 0.18 Menstruation cycle (days) ?30 61 62 1.00 <30 11 lo 1.12 040-3.10 0.81 Number of live births 0-1 3 5 1.00 2 8 12 1.11 0.16-8.23 3 11 14 1.31 0.20-9.04 ?4 50 41 2.03 0.39-11.54 0.46 p trend 0.12 Table VIII. Intake of vitamins C, E and B-carotene and risk of lung adenocarcinoma. Factors Case Control OR 95°k CI p-value Vitamin C Q1 36 24 1.00 Q2 15 26 0.38 0.16-0.94 0.02 V itamin E QI 8 27 1.00 Q2 33 23 2.15 0.90-5.19 0.06 B-carotene Q1 38 25 1.00 Q2 13 25 0.34 0.14-0.86 0.01 2505655854 births. No statistically significant association was observed between regularity of menstruation cycle and age of first menstruation and risk of pulmonary adenocarcinoma (Tables VII and IX). Nutrients. Univariate analysis showed that intake of 6- carotene and vitamin C from vegetables and fruits were protective factorst the level of protection had an OR of 0.34 (95% CI, 0.14-0.86) and 0.38 (95Tr CI- 0.16-0.94), respectively (Table VIII). Multmariatc logistic regression analrsrs. Only variables with p=0.I0 in the univariate analysis were considered in the logistic regression model. The following parameters were

ONCOLOGy REPORTS 7. 1253-I350. 2000 I8. Liu ZQ. Zhu ZG and Wang XS: Mutagenesis of smoke from cooking oils in the kitchen. 1 Environ Health 4: IO-13. 1991. 19. He XZ. Chen W. Liu Z. er af: An epidemiological study of lung cancer in Xuanwei County. China: current progress. case- control study on lung cancer and cooking fuel. Euviron Health Perspect 94: 9-13.1991. 20. Brownson RC. Reif 1S, et aF. Risk faetors for adcnocareinoma of the lung. Am J Epidemiol 125= 25-34. 1987. 21. Maurice L and Paul Se Differential exposure misclassifieation in case-control studies of environmental tobacco smoke and lung cancer. 1 Ciin Epidemiol 51: 37-54. 1998. 22. Wang TJ and Zhou BS: Meta-analysis of the potential relationship between exposure to environmental tobacco smoke and lung cancer in nonsmoking Chinese women. Lung Cancer 16:145-I50,1997. 23. Dockery DW and Trichopoulos D: Risk of lung cancer from environmenta] exposures to tobacco smoke. Cancer Causes Control 8: 333-345, 1997. 24. Tredaniel J. Boffetta P. Saracci R, et a7: Non-smoker lung cancer deaths attribute to exposure to spouse's environmental tobacco smoke. lnt J Epidemiol 26: 939-944, 1997. 25. Nybcrg F. Agrenius V. Svartengren K, er al: Environmental tobacco smoke and lung cancer in nonsmokers: does time since exposure play a role? Epidemiology 9: 301-308. 1998. 26. Wells AJ: Lung cancer from passive smoking at work. Am 1 Public Health 88: 1025-1029, 1998. 27. Hackshaw AK. Law MR and Wald NJ: The accumulated evidence on lung cancer and environmental tobacco smoke- Br Med I 315: 980-988. 1997. . 1259 28. Tokuhata GK and Lilienfeld AM: Familiar aggregation of lung cancer in humans. J Natl Cancer Inst 30: 289-312, 1963. 29. Wu AH. Fontham ET, Reynolds P, er al: Family history of cancer and risk of lung cancer among lifetime non-smoking women in the United States. Am J Epidemiol 143: 535-542, 1996. 30. Anderson KE. Woo C, Olson JE. et al: Association of family history of cervical, ovarian, and uterine cancer with histological categories of lung cancer: the Iowa Women's health Study. Cancer Epidemiol Biomarkers Prey 6: 401-405. 1997. 31. Liao ML. Wang JH, Wang HM, er af: A study of the association between squamous cell carcinoma and adenocarcinoma in the lung, and history of menstruation in Shanghai women, China. Lung Cancer 14 (Suppl. 1): S215-S221. 1996. 32. Bjelke E: Dietary vitamin A and human lung cancer. Int 1 Cancer 15: 561-565, 1975. 33. Doll R and Peto R: The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. ] Nad Cancer Inst 66: 1 193-1308. 1981. 34. Peto R. Doll R, Buckley 1D. et aJ: Can dietary 6-carotene materially reduce human cancer rates? Nature 290: 201-208. 1981- 35. Gilbert S Omcnn: Chcmoprevcntion of lung cancer: the rise and demise of B-caroeene. Annu Rev Public Health 19: 73-99, 1998.

F1e ONCOLOGY REPORTS 7: 1253-1259. 2000 ETS C, I'LnOO S Indoor air pollution and pulmonary adenocarcinoma among females: A case-control study in Shenyang, China BAO-SEN ZHOUI''-- TIAN-JUE WANG2, PENG GUAN2 and JOSEPH M. WUI 'Department of Biochemistry and Molecular Biology, New York Medical College. Valhalla, NY 10595, USA; =Department of Epidemiology, School of Public Health, China Medical University, 100011 Shenyang, China Received July 25, 2000; Accepted August 21, 2000 Abstract. Factors that affect the risk of lung adenocarcinoma among females were investigated in Shenyang, China, using a population-based case-control study design. A total of 72 new cases, ages 35-69. diagnosed with incident, primary pulmonary adenocarnoma, were collected between April 1991 and December 1995, and were 1:1 a_e-matched with healthy females randomly selected from the general population. A questionnaire covering demographics. diet/nutritional preferences and cooking habits, living conditions, family history of cancer, sources of indoor/outdoor/occupational pollution. exposure to ETS from spousal smoking, workplace exposure. and exposure during childhood. history of men;truation and pregnancy- was given to each subject in a structured in-person interview given by trained field workers. Univariale analysis was performed on the data collected. The results showed that cooking fumes, family history of lung cancer, economic status, and number of live births and intake of vitamin E were risk factors significantly associated with adenocarcinoma of the lung. In particular, exposure to different levels of cooking fumes, an indoor air pollutant, increased the odds ratio of lung adenocarcinoma by 1.33. 7.33 and L67, respectively (trend p=0.006). Another important risk factor was family history of lung cancer, which gave an OR of 7.65 (95 % Cl. 0.90-169.84). Intake of li-carotene from vegetables and fruit offered protection against lung adeno- carcinoma, giving an OR of 0.28 (95r9r- Cl. 0.12-0-69). These results were confirmed by multivariable logistic regression analysis. Introduction Lune cancer is a major cause of death among men and women. Compared to other forms of malignancy, lung carcinoma is Correspondence to: Dr Joseph M. Wu. Department of Biochemistry and Molecular Biolog.y, New York Medical College. Valhalla, NY 10595, USA E-mail: joseph_wu @nymc.edu i:ec wurds: pulmonary adenocarcinoma. indoor air pollution, cnvhonmental tohacco smoke. R-carotene, logistic regression model unique in that detection usually occurs at relatively late stage of disease development, which probably accounts for its rapid and aggressive metastasis, resulting in high mortality and poor rate of survival. In China, the incidence of lung cancer has been rising steadily for the past 3 decades and it has become the leading cause of cancer deaths in some cities of China (1). The earlier studies have shown that cigarette smoking is the primary risk factor responsible for squamous cell carcinoma and small cell carcinoma of the lung; however, its association with lung adenocarcinoma is weak and less certain (^_,3). Adeno- carcinoma of the lung accounts for 55% of major lung cancer histologic types among females in China (4). We investigated risk factors for pulmonary adenocarcinoma in Shenyang, China, using a case-control study design and focusing on its association among females with exposure to indoor air pollutants. Materials and methods Seventy-two cases of newly diagnosed primary lung cancer in females, ages 35-69, diagnosed according to International Classification of Diseases, ICD-9 were collected and identified in 18 major hospitals serving the city of Shenyang from April 1991 to December 1995. All cases in this study were diagnosed with lung adenocarcinoma, based on relevant medical records, chest X-ray and CT films, and pathology reports obtained after operation. Controls, matched 1:1 for age (±5 years), were randomly selected from the general population located in various urban areas of Shenyang. The number and age distribution of the controls were determined in advance based on the number and age distribution of existing primary• lung cancer cases reported to the Liaoning province anti-epidemic stations between 1988-1989. Two trained personnel inter- viewed all subjects in cases and controls using a standardized questionnaire, within two weeks of diagnosis. Items in the questionnaire were designed to collect information on: demo- graphic characteristics, exposure to environmental tobacco smoke (ETS), indoor and outdoor pollution, certain types of occupational exposure, history of previous diseases, family histories of disease and cancer, hormonal and menstruation cycle records. dietary habits and preferences and nutritional factors (amount and frequenc) of intake of food groups) approximately 5 vears prior to interciew. This time frame was chosen to approximate status of diet and nutrition prior

ONCOLOGY REPORTS 7: 125 3-1259. 2000 Table II. General characteristics of cases and controls. Case Control p-value Numbero- Mean arze (v-ears) Income Level of education None Primary Junior Senior or high 72 56.6 115.1 21 17 16 18 72 57.2 93.6 10 30 25 7 0.67 0.04 .002 p-value from I-test for continuous variables: i'- test for category variablcs. Table 111. Education, income and bod_v mass index and risk of lunc adenocarcinoma. Factors Case Control OR 95 % Cl p trend Education None 21 10 1.00 Yrimar_v 17 30 0.27 0.09-0.78 Junior 16 25 0.30 0.10-0.90 Senior or high 18 7 1.22 0.33-4.53 0.87 Income QI 10 18 1.00 Q2 12 18 1.20 0.36-3.98 Q3 18 16 2.03 0.65-6.44 Q4 32 20 2.86 1.01-8.39 0.01 BMI Q4 ]2 16 1.00 Q3 22 23 1?8 0.44-3.68 Q2 18 15 1.60 0.50-5.02 QI 20 IS 1.48 0.50-4.46 0.396 (trend-p=0.006). The risk of lung adenocarcinoma in relation to the extent of exposure to cooking fumes were 0.73, 2.71. and 13^_, respectively (trend. p-0.027) (Table IV). Comparing cooking practices that frequently or sometimes generate cooking fumes with those that generate little to no cooking fumes, the odds ratio for pulmonary adenocarcinoma was 4.53 (95r:.Cl. 2.09-9.94). After adjusting for confoundinge the same results were obtained in multivariate losistic regression analysis (Table IX). The other most common indoor air pollution comes from coal burning. Exposure to burning coal fumes was compared between cases and cnntrols. Since there was a hioh level of exposure to burning coal fumes in both groups, no significant difference was detected between cases and controls (OR=0.97. 95% CI. 0.6-3-1.481. 1255 Table IV. ETS exposure, conditions of housing/kitchen and risk of lung adenocarcinoma. Factors ETS at work place No Yes ETS in childhood from parent No Yes ETS in childhood exposure years No I D years 20 years FTS from husband's smoke No Yes ETS from husband's smoke - exposure years No 10 years 20 years Location of kitchen Separate, nearby In living room In bed room Eye irritation from smoke: Never infrequent Sometime Frequent Extent of smoke when cooking None Slight Medium Heavy Cooking oil fumes Sllght Medium and heavy Cooking: times of deep fried food per week O-1 2 and more Case Control OR 95%, CI p-value 7 6 1.00 61 59 0.89 0.25-3.16 0.84 29 27 1.00 43 45 0.89 0.43-1.84 0.73 29 27 1.00 12 13 0.86 0.30-2.45 31 32 0.90 0.41-1.97 0.94 p rrend 0.78 26 25 1.00 46 47 0.94 0.45-1.97 0.86 26 25 1.00 5 8 0.60 0.14-2.42 41 39 1.01 0.47-2.17 0.68 p trend 0.93 6 8 1.00 63 60 1.40 0.41-4.88 3 4 1.00 0.11-8.93 0.85 p trend 0.83 12 20 1.00 35 44 1.33 0.53-3.35 22 5 7.33 1.92-29.76 3 3 L67 0.22-12.93 0.003 p trend 0.006 19 25 1.00 15 27 0.73 0.28-1.90 35 17 2.71 1.09-6.80 3 3 1.32 0.18-9.50 0.0] p trend 0.027 30 55 1.00 42 17 4.53 2.09-9.94 0.0002 2505655853 5 -_ 67 64 1.66 0.45- 6.84 0.38

ONCOLOGY REPORTS 7: 1253-7259, 2000 71257 Table IX. Multivariable logistic regression analysis of risk factors for lung adenocarcinoma among females, Shenyang, China. Factors 6 OR S.E. (6) 95% CI p trend Income QI 1.00 Q'- 0.38359 1.467 0,58791 0.464-4.645 Q3 0.91874 2.506 0.57846 0.807-7.787 Q4 1.28374 3.610 0.54226 1.247-10.442 0.003 Eve irritation from smoke Never 1.00 SGsht 0.45539 1.577 0.47852 0.617-4.028 Medium 2 43827 1 1.453 0.66763 3.095-42.387 Heavy 1.22613 3.408 0.96408 0.515-22.549 0.002 History of lung cancer No 1.00 Yes 2.86406 17.533 1.21260 1.627-188.886 0.01 No. of live births 0-1 1.00 _ -0.02798 0-972 0.95426 0.116-4.906 3 0.33208 1.394 0.92375 0.227-8.522 >_4 0.84198 2.321 0.63947 V447-12-020 0.04 Table X. Results of multivariable logistic regression model for lung adenocarcinoma. Factors 14 OR S.E. (6) 95% CI p trend B-carotene 1.25996 0.284 0.45335 0.11-0.689 0.005449 Vitamin E 0.98993 2.691 0.43868 1.I90-6358 0.024031 found to be statistically significant risk factors for pulmonary adenocarcinoma: eye irritation from cooking fumes, OR=11.4 (95% CI, 3.09-42.39); family history of lung cancer, OR=17.53 (95% CI. 1.63-188.89): economic status, OR,= 3.61 (95% CI, 1.25-10.44); number of live births, ORa 2.3 2 (95% CI, 0.447-12.02): vitamin E, OR=2.69 (1.19-6.361. 6- carotene. OR=0.282 (95% Cl, 0.12-0.69), was a statistically sitvnificant protective factor for pulmonary adenocarcinoma (Tables IX and X1. Discussion Lung adenncarcinoma reportedly comprises 55% of major lung cancer histologic types amongg females in China (4)_ and may represent 70.8`7o and 59.4% of all lung carcinomas among non-smoking men and women in the US, respectively (6). Because of the continuing worldw'ide increase in the incidence of adenocarcinoma (7-8), delineation of risk factors contributing to this global trend is of significant scientific and public health interest. Results of the present study provide additional confirmation of the previously reported association between indoor air pollution from cooking fumes, family history of cancer among first-degree relatives, number of live births, and an increase in risk of lung adenocarcinoma. An additional risk factor revealed by the present study for this form of lung cancer, similar to that previously reported in Fuzhou, China (9). is high economic status (measured as income 5 years prior to interview). Indoor air pollution. Cooking fumes are a primary source of indoor air pollution in Northeast China. In this study, three indices - the level of eye irritation, the intensity of cooking fumes generated during cooking. and degree of exposure to cooking fumes - were used in our analysis; all showed that the risk of lung adenocarcinoma is statistically significantly increased, in a manner indicative of a dose-response relationship. Xu and coworkers reported that lung cancer among females in Shenyang was associated with cooking in living rooms (10). Similar results were reported in studies conducted in Shanghai, Nanjing and Taiwan (11-13). Moreover. in vitro and animal studies confirmed that volatiles from cooking oils affect carcinogenesis, and cause mutation and malformation (14-18), giving support to the notion that cooking fume exposure is indeed a significant risk factor for lung adenocarcinoma in females. With respect to the other major indoor air pollutant, smoke from burning coal, it should be noted that in Northeast China before mid 80s. most families used coal for heating and cookina. 'I:ang'. a traditional and most common form of brick bed and source of indoor heat in Shenyang. is heated in the winter b, burning coal practically fn almost every' family. Pre% 'iouslv it was reported that burning coal smoke was significantl% 2505655855

1258 ZHOU rr al: EXPOSURE TO INDOOR AIR POLLUTANTS AND LUNG ADENOCARCINOMA AMONG FEMALES associated with an increase in risk for lun_e cancer ( 1920). In this study. we did not detect a significant association for exposure to the smoke of burning coal between cases and controls. probably owing to the fact that the levei of exposure was comparable in cases and controls. - Exposure to ETS. Whether a statistically significant association exists between exposure to ETS and an increase in risk for lung cancer has been a topic of continuing debate ir. the scientific literature (20). Assessment of exposure requires information on the number of cigarette smoked, the habit of smokers, type of cigarettes smoked, the condition of ventilation in the immediate environment where the exposure occurs, etc.. all of which are subjected to recall bias, subject to misclassification, and a number of other uncertainties (20). Recall bias are known to exist in studies, can lead to mis- classification of cases and controls, and has been estimated to produce as much as 10% error in the calculation of risks associated with exposure (21). In this study, three types of exposure - workplace. spouses who smoke, and parents who smoke - were analyzed. The resuli.s consistently showed that t.cre no sienificant association between ET.S exposure and increase in risk in lune adenocarcinoma in females. Earlier. t+'c had performed a meta-analysis of exposure to ETS and risk of lung cancer in Chinese women (22), using a total of 767 cases and [193 controls pooled from data collected in Shanghai. Guangzhou, Shenyang, Harbin, and Xuanwei. in which the OR for ETS exposure was determined to he 0.91 (954r Cl. 0.75-].10) (22). Different results have been obtained in other studies (23 24). For example, a more recent meta- analysis reported that exposure to ETS increases the risk for luna cancer (25). Evidence of exposure to ETS has also been obtained based on analysis of blood and urine samples from non-smokers (26.27). Genetic factors and risk of lung adenocarcinoma. Genetic factors play an important role in the incidence of lung cancer (28). Risk of lung cancer increases 3-fold for women who had a family history of lung cancer in their first-degree relatives, especially mother or sisters. Such association is even stronger when the analysis performed was restricted to only lung adenocarcinoma. In contrast, no association can be demonstrated between family history of other cancers and risk of lung cancer in non-smokers, with ovarian carcinoma being one noted exception (29,30). In the present study, the risk of adenncarcinoma was increased 6.56-fold for patients with a family history of lung cancer among first-degree relatives. Higher number of live births also significantly increased the risk for lung adenocarcinoma, an effect which persisted in multivariate logistic analysis. Similar to the findines of Liao and coworkers in Shanehai (31), no statistically significant association was observed between reaularitv of menstruation and ase of first menstruation and risk of pulmonary adenocarcinoma. Diets in relation to risk of pulmonary adenocarcinoma. The relationship between dietary factors and the risk of maGenant tumor was first reported in the 60s (32). In 1981- Doll and Peto made Ihe seminal observation that 35'h of cancers are associated with unspecified factors in diets (33). The manner by which diet or specific nutritional ingredient act as chemopreventive agents is obviously complex, as indeed laree trials using B-carotene, which epidemioloeic studies have consistently shown to be protective for lung cancer, failed to demonstrate any beneficial effect (34.35). In our studies, the result showed that 6-carotene from the fruit and vegetables was protective for lung adenocarcinoma (OR=0.28). ~ In conclusion, results of this study suggest that it may be prudent to increase the intake of fruits and vegetables, to avoid exposure to ETS in private/public places, to decrease indoor air pollution from cooking fumes and coal burning smoke, to improve ventilation in the kitchen and air quality in general. Acknowledgments This research was supported by the National Eighth-Five Key Projects of China. Zhou Bao-sen, M.D., Ph.D. was a visiting scientist supported by a fellowship award from the Center for Indoor Air Research. References I. Du YX, Cha Q, Chen XW. er a7: An epidemiological study of risk factors for lung cancer in Guangzhou. China. Lung Cancer 14 (Supp) . 1): S9-S37. 1996. 2. Zhou BS- He AG, Wang TJ, er a7: The study on the risk and PAR of cigarette smoking to lung cancer. 1 China Med University 25: 28, 1996. 3. Yu SZ and Zhao N: Combined analysis of case-control studies of smoking and lung cancer in China. Lung Cancer 14 (Suppl. 1)'. S 161-S 170. 1996. 4. Wang TJ, Zhou BS and Shi JP: Lung cancer in non-smoking Chinese women a case-control study. Lung Cancer 14 (Suppl. 1): S93-S98- 1996. 5. Chinese Academy of Medical Sciences: Food composition tables. People's Health Publishing Co., Beijing- 1981. 6. Kabat, GC. Stellman SD and Wynder EL: Relation between exposure to environmental tobacco smoke and lung cancer in lifetime nonsmokers. Am I Epidemiol 142: 141-148. 1995. 7. Deaasa SS. Shaw GL and Blot w7: Changing pattern of lung cancer incidence by histological type. Cancer Epidemiol Biomarkers Prey 1: 29-34. 1991. 8. Charloux A. Quoix E. Wolkove N. er af: The increasing incidence of lung adenocarcinoma: reality or artefact? A review of the epidemiology of lung adenocarcinoma. Int J Epidemiol 26: 14-23, 1997. 9. Luo RX. Wu B. Yi YN. er a/: Indoor burning coal air pollution and lung cancer - a case-control study in Fuzhou- China. Lung Cancer 14 (Suppl. 1): S 113-S 119,1996. 10. Xu ZY. Blot Wl. Ziao HP- et al: Smoking air pollution and the high rates of lung cancer in Shenyang. China. I Natl Cancer lnsr 81: 1800-1809- 1989. 11 . Gao YT. Blot WJ. Zheng tx', er at: Luna cancer among Chinese women. Int J Cancer 40: 604-609, 1987. 12. Shen XB, Wang GX and Zhou BS: Relation of exposure to environmental tobacco smoke and pulrnonarv adenocarcinoma in non-smoking women: a case control study-in Nanjing. Oncol Rep 5: 1^_21-1223, 1998. 13. Ko YC, Lee CH- Chen MJ, er al: Risk factors for primary lung cancer among nonsmoking women in Taiwen. Int J Epidemiol 26' 24-31; 1997. 14. Yang CC. Jeng SN and Lee H: Characterization of the carcinogen 2-amino-3. 8-dimethylimidazo[4,5-Qquinoxatine in cooking aerosols under domestic conditions. Carcinogenesis 19: 359-363. 1998. 15. Chiang TA. Wu PF and Ko YC: Prevention of exposure to mutagenic fumes produced by hot cooking oil in Taiwanese kitchens. Environ Mol Mut 31: 92-96. 1998. 16. Chiang TA. Wu PF. Wang LF. er of: Mutagenicity and poly- cvclic aromatic hydrocarbon content of fumes from heated cooking oils produced in Taiwan. Mtnat Res 381: 157-161. 1997. 17. Qu YH. Xu GX. Zhou 1P. er aC Genotoxicity of heated cooking oil vapors. Mutat Res 298: 105-111. 1992, 2505655856