Tobacco Documents Online

Rrocccdinas of Indoor Air'9' EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE AND FEMALE LUNG CANCER IN GUANGZHOU, CHINA Y.X. Dul, Q. Chal, Y.Z. Chent and J.M. Wu= ! Deparunent of Hygiene. (iuangzhou Medical College,Guangzhou, China ' Department of Biochemistry and Molecular Biology, New York Medical College, Valhalla, U.S.A. 511 ABSTRACT Cigarette smoking is widely accepted as a major risk for human lung cancer. However, the - relationship between ETS exposure and female lung cancer is being debated. Since 1980 to 1988, there have been 5,546 cases (M: 3.760; F: 1.786) of deaths from lung cancer in (iuangzhou, and 811 cues (M: 209; F: 602) of them were never smokers. In this group, 552 cases (M: 94; F: 458) were from E'I5 exposure. In order to ascertain the relationship between EI'S exposure and lung cancer. some me epidemiological analyses have been perfonned as follows: (1) Comparisons of medical histories between 1r'FS and Non-ETS exposute of never smokers. (2) Conditional logistic regression analyses of never smokers. (3) A casecontrol study of female never smokers. (4) E15 exposure and cell type of lung cancer. All results of these studies demonstrated that exposure to ETS had no association with female lung cancer. INIRODUt:TION Cigarette smoking is widely accepted as a m jor risk for lung cancer in both males and - females. However the relationship between exposure to environmental tobacco smoke (ETS) and female lung cancer is-a subject of considerable controversy. Because of a long latency required for lung cancer to be induced, and since ETS exposure is multifaceted, in - order to certify the relationship between BTS exposure and female lung cancer, at least, two condition should be met in studying the effects of E'fS. F'ust, the subjects must be truly and solely exposed to Ei'S. Seeond, the results of epidemiological study can be elucidated the mechanisms for the pathogenesis of lung cancer, especially in the relationship between inducing factors and lung cancer cell type . MATERIALS AND METHODS Case History Guangzhou covers an area of 50 square kilometers, and about 2 million people live there. It is divided into four districts -- LW, YX. DS and HZ, and contains 63 local police stations. Beginning in 1980 to 1988, every case of lung cancer death was further analyzed using a standardized questionnaire containing 31 questions. Information was obtained tetrospectively from relatives and verified by the hospital records. The questionnaires were administered by trained medical personnel and data entered into a computer. Since in China all deaths, including time and cause, had to be reported to the local police station, " 'L 4v84C4~~~'O ~'

... 512 Procce, ~r Indoor Air '93, Vol. I the generated data wcmu ca:ur:atiec: to be accurate. 1'urthermore, if lung cancer deaths had been of ET$ exposure,the respondents, relatives of the dead, mainly the active smokers, in t3us situation, who responded, gave a highly reliable smoking history and proximity of the ETS exposure. Comparison of medical history between ETS and Non-ETS exposure of never smokers Tfite 811 cases of lung cancer deaths of never smokers were further grouped as follows: Male Female Total Group i ET5 exposed 115 144 259 Group 2 Non-E'P5 exposed 94 458 552 In these never smoking groups, 794 94 cases had chronic bronchitis or emphysema record (positive and negative), and 465 cases had lung cancer metastasis record.. The effects of ETS on such medical histories have been compared. Conditional logistic analyses of never smokers In 1985. there were 806 cases of deaths from lung cancer, 120 of them were never smokers. A Conditional logistic analysis was performed on those who never smoked (M:28;F:92). Matched with two control groups, one a non-respirato-ry system disease, another one a non- respiratory cancer. All control cases were of same sex, age (±2 years), residence and having never smoking. Investigation items included: x,- history of respiratory disease; x2- consumption of fresh-vegetables; x.- history of contact with toxic substances prior to death; x4- ET$ exposure; xs- indoor air pollution; x,- size of living area; x; situation of kitchen; xg- cooking fuel; x,- participation in cooking; x10- family histo -ry of cancer. A case-control study on non-smoking females In 1986, there were 236 females who died from lung cancer, 75 of them had never smoked, and the ETS exposure was limited to a husband. A casecontrol study was performed on these cases using two control groups. One of non-tumor diseases (128 cases), another one of tumors other than lung cancer (126 cases). All _ll control cases were of same sex, age (±2 years), residence and having never smoked. ETS exposure and cell type It is generalty known that the cell type of lung cancer induced by smoking is mainly an epidermoid carcinoma and not adenocarcinoma. Consequently, it is reasonable to believe - that if passive smoking can cause lung cancer, the cell type must be epidermoid carcinoma and not adenocarcinoma. In this study, the constituent ratio of cell type of 192 never smoking lung cancer deaths (M: 53, F: 139) was compared between E'I5 and Non-ETS exposure. Proccedin8sottndoorAir'93, ' 513 RESULTS Comparison of medical histories between E'I'S and Non-ETS exposure of never smokers The influence of 1:1'S on the occurrence of respiratory illness (chronic bronchitis, emphysema and lung cancer metastasis) is shown in table 1. No effect of exposure to ETS was found. Table 1.. Relationship between ET5 exposure and some medical history in never smoker lung cancer deaths. ------------- - Nuab.r of rolly Swolr.r -------------------------°------------- Non-rsTS N.dical hl.tory I 2 3 Total expoaur. P-Valua --------- --------- ------- - --------- --------- NO. • No, % No. t No. % No. % --- --------- - ------------------------------------------ cAron. b_r_onchlcla Y.a 6 11.5 7 25.0 1 8.3 14 15.2 15 13.5 No 46 80.5 21 75.0 11 91.7 78 84.8 96 86.5 P>0.05 ------------------------------------------------------------------------- r.mal. Ya 28 11.1 22 17.6 12 16.0 62 13.7 24 17.4 _P>O_.05 No 225 88.9 103 82..1 63 84.0 391 86.3 1J6 82.6 ------------------------------------------------------------------------- Eaphya.wa Nal• Y.a 4 7.7 2 7.1 2 16.7 6 8.7 14 12.7 No 18 92.3 26 92.9 10 83.3 84 91.3 96 87.3 - P>0.03 ------------------------------------------------------------------------- remal. Y.. 32 /2.7 13 10.6 9 11.8 54 11.9 29 21.0 P>_0.05 No 221 87.4 112 89.6 67 88.2 400 88.1 109 79.0 ------------------------------------------------------------------------- x.ea.taala Ya 23 65.7 12 63.2 3 50.0 38 63.3 50 69.4 11al. P>0.05 No 12 34.3 7 36.8 3 50.0 22 36.7 22 30.6 -------------'-------------------------------------------------------°-- __- ---- 1'.• 03 66.4 42 66.7 29 59.2 164 65.1 55 67.9 l.wal• P>0.05 No 47 33.6 21 J3,J 20 40.8 88 J6.9 26 32.1 ------------------------------------------------------------------------- Conditional logistic analyses of never smoker When lung cancer cases (120) matched with non-respiratory system disease (120), the observed results were shown to fit the following equations: C%fs72JC.UI.

rrocaomgs of Indoor Air'93, Vol. I Males: logit Pi=ai-1.330z1+0.0481x1 Females: logit Pi=ai-0.796x2+0.032x1±0.216x3-0.548x, When lung cancer cases (120) were matched with non-respiratory cancer (120), results consistent with the following equations were obtained. Males: logit Pi=ai+0,054x1 Females: logit Pi=ai-0.663x=+0.I29xs-0.217x7 These results suggest that fresh vegetables (x2) act as a protective factor against lung cancer, whereas contact with toxic substances (ic) inaeases the risk of lung cancer. It is worth noting that in females, indoor air pollution (xs) and_ situation of kitchen (x,) are risk factors for lung cancer. However, the respiratory disease (x,). ETS exposure (x) living conditions (x*), and familial history of cancer (x,d, exerted no effect whatsoever on female lung cancer. The exclusion of cooking fuel (xd and participation in cooking (x9) in regression equations might make it quite the same between the lung cancer cases and the matched controls. In the case of males, besides cigarette smoking, the major risk factors were related to occupational exposure. A case--control study on never smoking females - The effects of spousal smoking on female lung cancer an: illustrated in table 2 and table 3. The OR of ETS exposure is between 0.61--1.62 (I'>0.05), showing that spousal smoking, measured either by daily cigarene consumption, or the duration of smoking, is not a risk factor for female lung cancer. Such a conclusion was reached both when the case control study was matched with non-tumor controls or controls involving non-respiratory tumor cases. Table 2. Effects of (ETS) on never smoking females in 75 lung cancer cases and 128 controls (non-tumor deaths). -------- ---------~-------------------------°--f-----,------------------ Lun Cancer Controls OQd Ratlo 9S%CL x? p-Valu• ------------------------------------------------------------------------- 8T3 rsl.rs to husband who smoke - r.s 67 7! No 28 S3 1,19 (0.66--2.16) 0.33 >0.03 Total 75 128 ------------------------------------------------------------------------- -EFS rotors to number cipar.tNs ssok.d p.r- day 0 28 -- 53 <20 13 34 0.72 / 20- 30 33 1.62 (0.a1-3.13) 4.03 >0.05 ------------------------------------------------------------------------- Total 72 122 ETS rotors to smoking year__s ------------------------------------ 0 28 53 <30 14 19 1.39 (0.61-3.16) 0.6b >0.05 30- 29 41 1.17 (0.60-2.29) 0.22 >0.05 Total 71 119 Proccedings of Indoor Air'93, Vol. 1 515 ETS exposure and lung cancer cell type The results of the comparison of lung cancer cell type between ETS and non-ETS exposure are shown in table 4. Ile results indicated that no differenoea in cell types were observed between the exposed and non-exposed groups in both males and femalea, (x==1.76--3.78, P>0.05). In other words, exposure to ETS is not to be etiologically linked to an increase in epidermoid - carcinoma of lung cancet. Table 3. Effects of (1:TS) on never sm_ oking females in 75 lung cancer cases and 126 _ __ _ controls (tumor exceot lung cancer). --------------~ °--------------------------(-----,------------------ Lun Canc.r Controla Odd Ratio 93%CL 1F2 P-Valu• ------------------------------------------------------------------------- - - ---- - --- STS rotors to husband who ssok. Fas 47 79 1.00 ~ No 28 47 0.00 >0.05 Total 73 126 ------------------------------------------------------------------------- _ -- STS r.tars_ to numb.r of cigarettes smoked p.r day o zt 47 <20 13 3S 0.62 / 20- 30 37 1.36 (0.73--2.56) 3.75 >0.05 Total 71 119 ------------------------------------------------------------------------- --- - -- -- CTS rotors to smoking yaars 0 28 47 <30 !r )r 1,13 (0.77-.-1.66) 0.47 >0.05 30- 29 6f 0.99 / Total 71 114 - - --- Table 4. Comparison of lung cancer cell type between ETS and non-ETS exposured groups in 192 of never smoking lung cancer deaths, ------------------------------------------------------------------------- LTS ezposura(1qo. of Family spokar) -- - ------------------------------------------- -r-°---°--------°----------°--- Non-sTS 1 2 3 Total exposure --------- --------- --------- ---------- ----------- - No. % No. % No, t No. • No. ~ ------------------------------------------------------------------------- Epld.rmold ca, 6 50.0 2 40.0 6 66.8 12 53.0 9' 30.0 Small cell c_a_. 0 0.0 1 20.0 0 0.0 1 4.0 0 0.0 M Adano ca. 4 33.4 1 20.0 1 16.6 6 26.3 13 43.0 LarOa c.l2 ca. 1 8.3 0 0.0 0 0.0 1 4.0 0 0.0 Oth.rs 1 8.3 1 20.0 1 16.6 3 13.7 8 26.7 Total 12 5 6 23 30 ------------------------------------------------------------------------- - Epid.rmold ca. !S 21.4 6 21.0 3 16.7 24 21.8 5 17.2 Small c.ll ca. 4 6.0 4 16.0 1 5.5 9 8.1 3 10.3 F Adeno ca. 38 S_6.7 11 44.0 11 61.1 60 54.6 19 63.3 LarQe cell ca_. 0 0.0 0 0.0 0 0.0 0 0.0 1 3.5 Othars 10 16.9 4 16.0 3 16.7 17 15.5 • "Vt.7Vz(iVzOz

516 Broctae r" loor Air'93, Vol. I DISCUSSION A+iumber of investigatorat''2t concluded that an association did not exist between ETS exposure and lung cancer. However many other authotst'`'t emphasized the importance of ETS exposure as being causally linked to lung cancer. In fact, any research pertaining to the effect of 1rCS on lung cancer is greatly restricted by a number of considerations, for example: (1) Only the "true' effects of ETS on never smokers can be evaluated, provided that never smoking subjects are available who are constantly, steadily exposed to ETS, and free from complications of other indoor pollutants and/or occupational exposutes. However, such a condition is practically difficult if not impossible to achieve. (2) Questionnaires administered through the postal service make it difficult for some information to be obtained accurately. (3) Studies using only hospital based cases are confounded by selection bias. (4) The source of is ETS not likely to remain constant over an extended period of time. (5) In the case of spousal smoking, it is hard to eliminate whether there is "intentional avoidance" to ETS exposure, or whether "psychological conditioning' exists during ETS exposure. (6) Although probable . carcinogens (BaP, DMNA) have been detected in sidestream tobacco smoke, and the concentration may be exceeding that present in mainstream tobacco smoke, they are undoubtedly greatly diluted when pcBsented in the form of ETS, and are unlikely to reach the lower respiratory tract, like the mainstream; so that if lung cancer is induced by passive smoking, the major cancer type may be central epidermoid carcinoma and not peripheral adenocarcinoma. Apparently, when in order to confirm the effect of ETS on lung cancer, all of these factors must be carefully considered. Unfortunately, currently available data do not seem provide an adequate explanation on this subject. Our studies showed that exposure to ETS had no associated with lung cancer, but it does not mean that ETS had no harmful to human health. There are more than one hundred chemical compositions that can be detected in sidestream tobacco smoke",, a number of them being toxic substances. REFERENCES 1. Lee PN, Chamberlain, Alderson MR. Relationship of passive smoking to risk of lung cancer and other smoking-associated diseases. Br. J. Cancer, 1986:54;97-105. 2. Williams AHW, Dai XD; Blot W, et al. Lung cancer among women in north-east China. Br. J. Cancer, 1990:62,982-987. - - - - 3. Wynder EL, Goodman MT, Smoking and lung cancer: some unresolved issues. Epidemiologic Reviews 1983:5:177•207. 4. Pershagen G,Hrubec Z. Svensson C, Passive smoking and lung cancer in Swedish women. American J. of Epidemiology. 1987;125(1):17-24. 5. Eatough DJ, Hansen LD, Lewis EA, The Chemical characterization of environmental tobacco smoke, Proceedings of the International Symposium at McGill University. 1989:P3*39. s~C LY 40 G41 9z0 Z