ets exposure, lung cancer - Legacy Tobacco Documents Library

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Objectisrs . The causes of lung cancer among nonsmokers are not dearly understood . To funher evaluate the relation bctwecn passive smoke expxosure and lung canxr in nonsmok7ng women, w•c conductcd a population-based, case-control studr . Afer,'tods . Casc patients (n = 618), idcntined throueh the Missouri Cancer Repstry for thc period 1986 through 1991, included 432lifctime nonsmokers and 1So cx-smokers who had stopped at least 15 years before diaposis or who bad smoked for less than 1 pack-year . Control subjeeis (n = 1402) were selected from dri4'er's license and Medicare files . Restllu . No increased risk of lung cancer was associated with childhood passive smoke e .rposure . Adulthood analyses showed an increased lung cancer risk for lilctime noasznokers with exposure of more than 40 pack-years from all housebold roembers (odds rat)o (ORJ = 13 ; 95% confidence interval (CI) = 1 .0, 1-8) or fxom spouses only (OR = 1 .3 ; 95`'o CI s 1 .0, 1 .7) . When the tuneweighted product of pack-ycars and average bours ccposcd pcr day was considered, a 305'o excess risk was shown at the highest quamk of exposure among lifetirne nonsmokers . Cwtclunoru. Qurs and other recent studies suggest a small but consistent increased risk of lung caneer from passive snnoidng . Compr-ehensivc actions to limit smot^:ng in public places and worksitcs are weU-advised . (Am J Public Health . 1992 ;82• 1525--1530) Passive Smoking and Lung Cancer in Nonsmoking Women Ross C. E?row7uori, P1tD, Michael C R. Alavanja, DrPlf Edward T. Hoa-, BS, and Timo :hv S. Loy', hfD Introiurtion Although most lung cancer occurs in smokers, approximately 9c7c to 13% of lungcancer cases in US women develop in lifetime nonsmokers .'-S The causes of lung cancer in nonsmokers have not been wideiv studied, but probably comprise a diverx set of factors including eenctics, occupational factors, radon exposure, diet, and a history of nonrr,alignant lung discasc . In addition to these risk factors, the etioloac role of passive smoke exposure has received increastnQ scrutinv over the past decade . Numerous studies"0 have suggested an elevation in lung cancer risk for nonsmoking females who live with a smoker, with a summary excess risk of appro.tiunatcly 30`-c .=t•= However, several recent studiest= -' have shov .n no increased lung cancer risk due to spousal smoking . Limited evidence1-=6 also suggests that exposure to passive smoke in cht3dhood may inacase risk of lung cancer . For example, a recent case-control study from New York found that household exposure to tobacco smoke during childhood of 25 or more smoker-years' duration was associated with a doubling of lung cancer risk .'a Most previous studies of passive smoking and lung cancer, although suggestrve of a positive effect, have had several deficiencies . Thesee deficiencies includc sample sizes insufficient to singly demonstrate significant elevations in risk, limited data or, passive smoke exposure in both childhood and adulthood, and lack of histologic revicw of cases to venfy lung cancer diagnosis and to allow analyses by cell type . To more fuUy evaluate the rclationship betwecn lung cancer and passive smoke exposure in childhood and adulthood, we conducted a IarQe case-control study of lung cancer among nonsmoking womcn . Methods Case Group Case patients were identified through the Missouri Cancer Registry, which is maintained by the Missouri Department of Health . The Reaistry began collecting data on incident cancer cases from public and private hospitals in 19-72, and hospital reporting was mandated by law in 1984 . Registry rcporting procedures havc been discussed in more detail elsewhere .= To ensure complete reponing of lung cancer cases in women for the current study, we had Registry staff complete special case ascenainment visits to participating hospitals . The case series included White Missouri women, aged 30 to 84 years, who were diagnosed with primary lung cancer betwten January 1986 and June 1991 . Selection was limited to Whites because of small numbers of other racial/ethnic Ross C . Brownson is with the Division of C}uortic Diseasc Prevenhon and Health Pro motion, Missouri Deparanent of Health, Columbia, Mo. Michael C . R . ?.lavanja iswith the Epidemiology and Biostatistiec Progrant, National Cancer lrutitute, Roekvt7le, Md. Edward T . Hock is with Information Management Ser . vices, Rockvt7le, Md . Ttnwthy S . Loy is with the Pathology Deparunent, Universiry of Missouri School of Mcdicine, Columbia, Mo . Requests for reprints should be sent to Ross C. Brownson, PhD, Division of Chronic Disease Prevention and Health Promotion, Missouri Dcpartrnent of Health, 201 Business Loop 70 West, Columbia, MO 6520.3 . This paper was submitted to the Joumal February 19, 1992, and aecepted with revisions August 12, 199? . Novembtr 1993, Vol . $2, No. 1I Amcrxan Joumal of Public ltcalth 1525 http://legacy.library.ucsf.edu/tid/wyk81f00/pdf
groups . The case group included both li.fetime nonsmokers and ex-smokers who had stopped smoking at least 15 years before diagnosis or who had smoked for less than l pack-year . From the 3475 cases of lung cancer in women reported for the study period, 650 eligible patients were identified . Physicians denied interview perrnission for 24 (4%) of these padents and an additional 8 women (1 e/o) refused to be intervicwed . The final case group included 432 (70%) lifetime nonsmokers and 186 (30rro) ex-smokers . Of the 618 case intetvic.vs, 216 were conducted with patients thernsclves and 4-02 were conducted with surrogates because the patient was too IIl to be interviewed or had die .d . Of the surrogate interviews, 105 (26°lc) were condueted with the patient's spouse and 297 (74%) were conducted with another rclative (c .g„ odspring or sibling) . HLirOlCrgIC COrt f17rnG2rZOn of Cases Tissue slides were reviewed for histolopc verification for 468 (76CC) of the 618 cases . Slides for these cases were examined simultaneously by three pathologists (T .L, E .I ., and J .M .) using a multiheaded microscopc without knowledge of the refcrring pathologist's diagnosis . In surgical spedmens, consensus diagnoses were obtained v.ith the critcria outlined in the World Hcalth Or¢anization classification scheme .=9 Rfien orily cytologic material was available, consensus was obtained with standard cytologic critcria .30 Connrol Group A population-bascd sample of control subjects was ascertained by two mcthods . For women younger than 65 years, a sample of state driver's license files was provided by the Missouri Depanment of Revenue . For women aged 65 to 84 years, conurol subjecu were generated from the Health Care Finance Administration's rostcrof Medicare recipients .3t On the basis of age dismbution of lung cancer eases previously reponed to the Registry, the final control group was matched by aee group to case patients at an approximaLe 2 .2 to I ratio . All control subjects were interviewed direct}y . Of the 1862 potentially elig1le control subjects, 335 (18%) refused the initial screening interview and 125 (7%) of those screened and found eligpble rcfused the fttll interview . The fuial control group numbered 1402 . Quesrionnafre Design and Adminiriration Telephone interviews were con• ducted by trained interviewers . The first phase of the interview- consisted of a screening qucstionnaire to verify the age, race, and smoking status of case patients and control subjccu . For subjects who were screened and found cligiblc and who ag7ecd to the full interview, the study questionnaire consisted of sections on residential history, passive smoke expostire, personal health history, family health history, reproductivc history, occupational exposure, and dietary factors . Questions ragarding passive smoking focvsed on exposure in both cht7dhood (17 years and younger) and adulthood (18 years and older) . For each time period, respondents were questioned about the sourcee of exposure (e .g ., a parent or spouse) . Afrer an indMdual source was determined, a series of detailed questions were asked on the typc of tobacco used, duration of exposure, intensity of exposure, and avcraee number of hours per day exposed . These questions were partially modcled aftcr those dcvcloped by Wynder et al .3- In addition to quantitative estimates of exposure, respondents were asked to cuimate a perceived level of exposure during childhood and adulthood ("During most of your adult years, would you say that vour average exposure to smoke at home w•as liaht, modcrate, or heavy?") . Ana lyses Odds ratios (ORs) and 95% confidence intervals (Cls) were calculated .vith multip)c logistic regression .» The lincariry of trends in risk according to level of passive smoke exposure was evaluated with Mantel's one-tat7cd test .s' We initially examined numerous potential confounding factors . These included age, active smoking (for ex-smokers), history of previous lung diseases, dietary beta carotene, and dictary fat . Of these variables, only age, acm e smoking, and previous lung disease appeared to confound passive smoking findings ; therefore, the results presented are adjusted for these factors . Histologic r,vpe-specific analyses were conducted for cases for which consensus diagnoses were determined . Thesc analyses were undertaken bccause eariier studiess•tb-m have shown variations in risk by cell type, and biological mcchartisms have been proposed that might account for these variations .20•u Results Sociodcmographic and smoking-rclated charaeterisda of case panents and control subjects have been presented in dctail elsewhcre .M In brief, the average ages of case patients and control subjects were 71 .5 years and 69 .9 years, respcct'rvcly . The two groups were also comparable on level of education and income . Among ex-smokers, the median interval since cessation was 24 years, and average smoking intensity was 16.4 cigarettes per day . Tnere was little evidence of incTeased lung cancer risk associated w~ith passive smoke exposure in childhood (Table 1) . This lack of association was apparent for both the dichotomous variables (never vs evu exposed) and quantitative measures such as pack-years . The only suggestion of elevated risk was noted for less quantitative exposure variablcs (not shown in table) . Among lifetime nonsmokers, an increased risk of lung cancer was shown for those reporting moderate (OR = 1 .7 ; 95% CI = 1 .1, 2 .5) and heavy (OR = 2 .4 ; 95% C] = 1 .3, 4 .7) exposure to passive srrioke in childhood . Risk estimates for most childhood exposure variables were slightly higher (approximately 20% to 30%) when analyses included otrly direct interviews, although none achieved statistical significance . An clevate.d isk of lung cancer was identifiui for lifetime nonsmokers at the lughest quan0e of passive smoke exposure in adulthood (Table 2) . At an exposurc level of ntore than 40 pack-ycars, Iifetime nonsmokcrs showed a 30% increase in risk whether the source of exposure was all household members or spouses only . Similarly, when the product of pack-years and average number of hours exposed per day was considered, lung cancer risk for lifetime nonsmokers was elevated for the highest exposure quanile whether the source was all household members (OR - 1 .3 ; 95% CI = 1 .0, 1 .8) or spouses only (OR = 1 .3 ; 95PC CI = 1 .0, 1 .7) . Among lifetime nonsmokers, a positive increasing trend in risk was noted for packyears (P = .06) . Passive smoking-related risk estimates for adulthood exposures were slightly lower for all subjccts (i .e ., both ex-smokers and lifetime nonsmokers) than for lifetime nonsmokers alone, although the same general elevations in risk were notcd . When analyses were limitcd to direct intcrvinvs, no clear pattem of increase or decrease in risk estimates was apparent . Regarding less quantitative exposure variables, elevated risk was shown for all subjects (OR = 1 .7 ; 95% 0 = 1 .1, 2 .6) and for lifetime nonsmok- 15:b American loumal of Public Health November 1992 . Vol . 82, No . 11 http://legacy.library.ucsf.edu/tid/wyk81f00/pdf
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