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:. 1-•or Air '93, VoIl~ Procccdinas of Indoor Air'93, Vol. I St t Prok •r , Table 6. Relation between Indoor CO. CO personal exposure and COHb levels. Pupila from homes using coal as fuel Pupils from homes using gas as fuel Indoor CO (mg/m) 9.11 4.38 CO exposure (mg/m) 7.90 , 4.14 pupils' COHb ( % ) 1.11 0.50 Pulmonary functions Although the indoor air popution in winter was serious, the pu pils_ pulmonary functions did not seem to be affected by the pollution. ACKNOWLEDGEMENT The authors want to express our thanks to Lars Molhave, ph.D ., Associate professor, Aarhus University, for checking and revising this manuscript. REFERENCES 1. Chinese Academy of Preventive Medicine, Measurement methods of atmospheric pollution, Chinese Chemical Industrial publication Company. The first edition, Beijing 1984. 2. X.Y. Guo. G.H. Jians, A sampling investigation of the daily consumption of time of the people in Wuhan City, Environment and Health, Vol.2. No.3, 1985.(Chinese Joumal). 3. Yao Zhiqi, Environmental Hygiene (the second edition), Chinese people Health publishing House, 1987, Beijing. zTTCisCzo% EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE AND FEMALE LUNG CANCER IN GUANGZNOU, CHINA Y.X. Du', Q. Cha', Y.Z. Chen' and J.M. Wu' ' Department of Hygiene, Guangzhou Medical College,Guangzhou, China = Department of Biochemistry and Molecular Diology, New York Medical College, Valhalla, U.S.A. ABSTRACT Cigarette smoking is widely accepted as a ntqjor 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 Guangthou, and 811 cases (M: 209; F: 602) of them were never smokers. In this group, 552 cases (M: 94; F:. 458) were from ETS exposure. In order to ascertain the relationship between ETS exposure and lung cancer, some epidemiological analyses have been performed as follows: (1) Comparisons of medical histories between ETS and Non-ETS exposure of never smokers. (2) Conditional logistic regression analyses of never smokers. (3) A casecontrol study of female never smokers. (4) ETS exposure and cell type of lung cancer. All results of these studies demonstrated that exposure to ETS had no association with female lung cancer. INTRODUCTION Cigarette smoking is widely accepted as a major 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 ETS exposure and female lung cancer, at least, two condition should be met in studying the effects of ETS. First, the subjects must be truly and solely exposed to ETS. Second, 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 METf1ODS Case Hi.story Guangzhou covers an anea of 50 square kilometers, and about 2 million people live thcre. 4 is divided into four districtt -- LW, YX, DS and HZ, and contains 63 local police atations. Beginning in 1980 to 1988, every case of lung cancer death was further analyzed Using a standardized questionnaire containing 31 questions. Information was obtained retrnspec6vely 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 dcaths, including time and cause, had to be reported to the local police station,

512 ~ Proceedings or Ind t Yl, yol. I Proceedinas of Indoor Air'93, Vol. I 513 the generated data h•uc co:>v;oerr.c; to be accurate. F wihermore, if lung cancer deaths had been of Ei"5 exposure,the respondents, relatives of the dead, mainly the active smokers, in this situation, who responded, gave a highly reliable smoking history and proximity of the Ei'S exposure. RESUL75 Comparison of medical histories between ET3 and Non-ETS exposure of never smokers Comparison of medical history between ETS and Non-E`IS exposure of never smokers The 811 cases of lung cancer deaths of never smokers were further grouped as follows: Male Female Total Group 1 ET5 exposed 115 144 259 Group 2 Non-ETS exposed 94 458 552 In these never smoking groups, 794 cases had chronic bronchitis or emphysema record (positive and negative),>rnd 465 cases had lung cancer metastasis record. The effects of ETS on such medical histories have been compared. Conditional logistie 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-respiratory system disea.4e. another one a non- respiratory cancer. All control cases were of same sex, age (±2 years), residence and having never smoking. Investigation items included: xl- history of respiratory disease; x1- consumption of fresh vegetables; x,- history of contact with toxic substances prior to death; x; ETS exposure; xs- indoor air pollution: x,- size of living area; xY situation of kitchen; x,- cooking fuel; x,- participadon in cooking; x,o family history 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 EI'S 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 control cases were of same sex, age (t2 years), residence and having never smoked. ET5 exposure and cell type It is generally 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 ETS and Non-EfS exposure. UUTSC%oz The influence of ETS 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 ETS exposure and some medical history in never smoker lung cancer deathi. ----------------------- Nunrb.r of Paw11y 6wok.r ---------------------------------------- Non-6lJ ' M.Clcal hlstory 1 2 3 loeal .rposur• P-Yalu• No. % No, % Mo. % Mo,--~- - -Nc~---~- - ------->------------------------- Chron. bronchltl !a 4 11.3 7 13.0 1 s.J 14 15.1 15 13.5 Na1o P>0._03 Mo 16 ta.S 21 73.0 11 a1.7 7a 84.8 96 06.3 ------------------------------------------------------------------------- Ls !1 11.1 22 17.6 12 16.0 6! 1i,7 ?1 17.4 f.walo P>0.05 No tJ3 11.! 103 82.4 13 14.0 3!1 s6..) 111 a].6 -------------------------------------------- Rwphyl.wa l.a 4 7.7 1 7..1 2 16.7 s 8.7 1I 12.7 Mal. P>0.05 No If 02.3 16 92.9 10 aJ.) 04 !1.) tt 87.3 ------------------------------------------------------------------------- ra 32 12.7 13 10.6 ! 11.8 SI 11.! 1s 21.0 r.aalo P>0.03 Mo 221 07.1 112 89.6 97 18.2 100 J1.1 10f 79.0 - ------------------------------------------------------- a.tasta.ls ' 1 a 23 65.7 12 6J.? 3 50.0 Ss 93.3 30 99.4 Nalo P>0.05 Mo 1] 31.) 7 31.8 ) $0.0 22 34.7 22 30.6 ra 93 66,1 Il 66.1 29 59.2 161 65.1 SS 67.9 t.wale P>0.03 No 47 J).6 21 33.3 20 10.s 11 ~l,f 16 J2.1 ------------------------------------------------------------------------- Conditlon.l logistic analyses of never smoker When lung cancer cases (120) matched with non-respintaryry system dise.se (120), the obscrved rzsults were shown to fit the following equations: ~

~ Proceedings of Indoor Air'93, Vol. I 1'+nctrdinat or Indoor Air '93, Vol. 1 515 514 Males: logit Pi=ai-1.330x1+0.0A81x, Females: logit Pi=ai-0.796xx+0.032xt+0.216xs-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+0.054x, Females: logit Pi=ai•0.663xz+0.129xs•0.217x, These results suggest that fresh vegetables (x,) act as a protective factor against lung cancer, whereas contact with toxic substances (x) increases the risk of lung cancer.7t 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 (x4) living conditions (xr), and familial history of cancer (x,d, exerted no effect whatsoever on female lung cancer. '(he exclusion of cooking fuel (xd and participation in cooking (x,) 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 amoking females The effects of spousal smoking on female lung cancer are illustrated in table 2 and table 3. - The OR of ET'S exposure is between 0.61--1.62 (P>0.05),, showing that spousal smoking, measured either by daily cigarette 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 (E'tS) on never smoking females in 75 lung cancer cases and 128 controls (non-tumor deaths). ------------- ----------------------------------------------------------- Lunp Canc.r Controls odd Ratio (MCL) xl !-Yalu• ------------------------------------------------------------------------- iTN r.f.rs to husband who ssoka 7.a 67 7! Ro 11 SJ 1,1! (0,66--J,16) 0.33 Total 73 111 ------------------------------------------------------------------------- NT1 r.f.rs to nu.b.r ci0ar.tt.s saak.d p.r day 0 11 S1 / <J0 13 JI 0.72 20- 30 )s 1.4? (0,a3-J.is) 4.03 >0.0s Total 71 177 ------------------------------------------------------------------------- 6TJ r.f.rs to swokinp y.ars 0 ]1 sJ <J0 16 1! 1.)! (0.61-).16) 0.13 >0.05 30- 1! 47 1,17 (0.60-I.1!) 0.22 >0.0s rotal 71 ll! ------------------------------------------------------------------------- ETS exposure and lung cancer cell type The results of the comparison of lung cancer cell type between E•TS and non-ETS exposure are shown in table 4, The results indicated that no differences in cell types were observed between the exposed and non-exposed groups in both males and females, W-1.76-.-3.78, P>0.05). In other words, exposure to ETS is not to be_ e_tiologically linked to an increase in epidcrmoid carcinoma of lung cancer . Table 3. Effects of (E'TS) on never smoking females in 75 lung cancer cases and 126 controls (tumor exceot lunq cancer). - --------'--------------------------- . -- Lunq-Canc.r Controls Odd Ratio (lS%CL) 72 ---p-Valu• - ------------ --- If3 r.f.rs to husband who snok. 7.s 47 71 1.00 / No )1 47 0.00 >0.0s Total 73 126 _ I -----------° afJ r.f.rs to nu.b.r of ciyar.tt.s swok.d p.r day 0 7a 61 <10 1J Js 0.6? / 20- 30 37 1.39 (0.7J--7.s6) 3.75 >0.05 Total 71 11! ------------------------- aTS r.f.rs to snoklnp y.ars 0 11 47 <J0 14 11 1.13 (0.77--1.66) 0.47 >0.05 30- I! 6! 0.!! / Total 71 116 - ---------------------------------------------- ----------- Table 4. Comparison of lung cancer cell type between ETS and non-E_TS exposured groups in 192 of never smoking lung cancer deaths. ------------------------------------------------------------------------- ars arposur.(No. of Pamily ;.okar) ----------------°--------------°----- °-- Non-6rs 1 1 3 !'otal •xposur• --------- --------- --------- ---------- ----------- No. % No. • Mo. % No. 1 Mo. % - ---------------------- Npld.rwrotd ca, 6 50,0 ] 40.0 4 66.0 12 $3.0 ! 30.0 Small csll ca. 0 0.0 1 20.0 0 0.0 1 4.0 0 0.0 N kd.no ca.. 4 JJ.6 1 20.0 1 16.1 6 26.3 13 6J.0 Larpo c.1l ca. 1 e.) 0 0.0 0 0.0 1 4.0 0 0.0 Oth.rs 1 0.3 1 20.0 1 16.6 3 13.7 1 26.7 Total 12 3 6 23 30 ----------------------- ------------ spldsrsoid ca. 1s 22.4 6 24.0 J 16.7 24 21.1 5 11.2 Small call ca.. 4 6.0 4 16,0 1 5,3 9 1.1 1 10.3 1 Ad.no ca. Ja 56,7 il 44.0 11 61.1 60 34.6 1! 65.5 Larpo c.ll 04. 0 0.0 0 0.0 0 0.0 0 0.0 1 3.5 >0.05

516 Proceedinas of Indoor Air'93, Vol. I DISCUSSfON A number of invesHgatorsll.2l concluded that an association did not exist between ETS exposure and lung cancer. However many other authorst'-'I emphasized the importance of ETS exposure as being causally linked to lung cancer. In fact, any research pertaining to the effect of ETS on lung cancer is greatly restrieted 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 indoot' pollutants and/or occupational exposures. 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 ho•pital based cases are confounded by selection biaa. (4) The source of is ETS not likely to remain constant over an extended period of tirne. (5) In the case of spousal smoking, it is hard to eliminate whether there is "intentional avoidance" to E15 exposure, or whether "psychological conditioning" exists during ETS exposure. (6) Although probable carcinogens (D_ aP, 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 presented 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, curr>sntly available data do not seem provide an adequate explanation on this subject. pur 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. Titere are more *than one hundred chemical compositions that can be detected in sidestream tobacco smokelst, 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 ai. Lung cancer among women in north-east China. Br. J. Cancer, 1990;62,982-987. 3. Wyndcr 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. Ealough DJ, 1lansen LD, Lewis EA,'fhe Chemical characterization of environmenul tobacco smoke, Proceedings of the International Symposium at McGill University. 1989:P3-39. sITMEZQ-V ,Pcoceedinas of Indoor Air'93, Vol. I 517 EFFECTS OF RESTRICTIVE SivtOKING POLICIES ON INDOOR AIR QUALITY AND SICK BUILDING SYNDROME: A STUDY OF 27 AIR- CONDITIONED OFFICES Alan Hedge', William A. Erickson', and Gail Rubin' 'Depanmcat of Design and Environmental Analysis, ComeQ University, Ithaca, USA 'Biomctrics Unit. Cornell University, Ithaca, USA ABSTRACT A field experiment Investigated the effects of five nPstrictive or prohibitive smoking polici( indoor air quality and sick building syndromc complaints in 27 a'v-cotditioned office build Indoor air quality was measured in each building. No differences among policies were fou, numbers of smokers, average number of cigarettes smoked daily. No differences among I were found for carbon monoxide, carbon dioxide, respirable pa'ticulates, relative humidil, temperature or illumination levels. There were differences among policies in ultra-violet p mass and formaldehyde. There were differences in nicotine among the spatially restricted t policies. ETS pollutant levels were highest where smoking was nstricyed to ronrm with la filtntion. A questionnaire survey of workers measured sick building syndrarne symptoms. Symplorvu were marginally less prevalent for the restrictive smoking policies than the smo prohibited policy. Evidence that ETS is a cause of sick building syndrome complaints was found. INTRODUCTION Environmental tobacco smoke (ET$) is a source of many Indoor air pollutants.Various spatiall) rauiclive or prohibitive smoking policies can be implemenlod to lessen the impact of ETS polluuants on indoor air quality. Studies have shown that some restrictive smoking policies have" liule impact on indoor air quality (f,2) These studies, however, have not examined the effects of Onoking policies on the sick building syndrome (Sf3S). Other work suggests that passive exposure b EfS increases SBS symploms in nonsmokers (3..4,5). although smoking activity and_ Sf3S tonplaints are not associated (5,6). To investigate the effect of five smoking policies (prohibition t"d vvious forms of spatial restriction) on indoor air quality and on the SBS a field experiment Mu conducted. MEI7IODS Smoking policies and office budldinp Fi ve smoking policies were invettigated: smoking prohibited (SP); smoking restricted to rooms with kxal elcctiostatic and sorbt:nl air filtration units (RF); smok_ing restricted to areas with no local air aeNmenl (RNT); smoking restricyed to roomy ventilated by a separate exhaust ventilation system (RSV): smoking restricted to enclosod offices and open plan cubicle workstations (RWS). Twenty arvt'n ur-conditionod buildings with different smoking policies were studied. The buildings had ri'lier variable air volume (VAV) or constant air volume (CAV) ventilation systems. Scvcntccn e'6Nizatioru (insuranoe, finance, sales and marketing, etc.) occupied these offices. Fifteen of lhece_ " privaue companies occupying 25 of the 27 officn, I was a federal agency, and I a 'n-Kipallty. N