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TSO Wu, H .nd.rson, P1k ., and Yu smoking habits were observed for a history of hysterectomy (RR=1 .7 ; 95% C1=0 .9, 3 .2) and nullipariry (RR=1 .7 ; 95% CI=0 .8, 3 .7) among ADC cases and a history of miscarriage (RR=1 .5 ; 95% CI=0,5,4 .9) among SCC ases . Multiple logistic regression analysis was condutted to assess the possible confounding effects of personal smoking habits, childhood pneumonia, childhood coal burning, and S-arotene intake . The results were similar to those when each factor was adjusted for personal smoking habits alone . DISCUSSION This case-control study examined risk factors for the two main cell types of lung cancer in women-ADC and SCC . Although histologic typing was done by the individual pathologist at each participating hospital, studies comparing interobserver and intraobserver variability in classification of lung cell types reported a high concordance rate for cell types other than large cell carcinoma, which was excluded in this study (22, 23) . In this study population, about half of ADC and almost all of SCC can be attributed to personal smoking habits ; the amount smoked and the age at which smoking began were strong determinants of risk of disease . However, there are marked differences in the strength of association between smoking and cell type of lung cancer, as has been noted previously (24, 25) . The role of passive smoking in the etiology of ADC among nonsmokers is not clear . Our data are not consistent with the findings with regard to nonsmokers obtained by Hirayama (4) and Trichopoulos et al . (5) who reported a twofold to threefold increased risk due to passive smoking . However, the histology of the cases in these studies is not clear, and their data suggest that any effect of passive smoking is larger for SCC cases (5, 6) . Of our 29 nonsmoking ADC cases, 12 were bronchoalveolar cell carcinomas, and this cell type is specifically mentioned by Correa et al . (6) to have a weaker association with passive smoking . The effect of passive smoking by cell type of lung cancer needs to be investigated further in studies with much larger numbers of nonsmokers . Childhood lung disease may have a role in lung cancer etiology . Certain features of the lung of a child (e .g ., susceptibility to airway closure and high peripheral resistance) might make it more vulnerable to residual abnormalities from respiratory illness (26) . This notion is supported by observations that both smokers and nonsmokers with childhood respiratory diseases have impaired lung function capacity, that their rate of decline in ventilatory function capacity with age is more rapid than that in individuals without childhood respiratory problems, and that they have higher rates of clinical diagnosis of chronic obstructive pulmonary disease (27, 28) . Women with childhood respiratory problems may have incurred epithelial damage to the airway resulting in airway hyperreactivity and are more susceptible to other insults to the lung . We cannot rule out the possibility of a chance finding or of preferential recall of http://legacy.library.ucsf.edu/tid/wyk81f00/pdf childhood pneumonia by cases . However, our dat2 appear to be internally consistent, since we found a significantly higher frequency of lung scarring mentioned in the pathology reports among cases with previous childhood pneumonia (12/30=40%) compared to those without (39/189=21%) . The associ.ation of lung cancer risk with exposure to coal heating or cooking warrants further investigationAlthough coal was identified as the major heating or cooking fuel used during childhood and teenage years of a significantly higher proportion of cases, we did not have detailed information on the years of use . Excess risks of lung cancer have been reported for coke oven workers (29, 30) and British gas workers (31) who were heavilN exposed to products of coal carbonization . Studies of men suggest that their lung cancer risk is lowered by greater dietary S-carotene (12-14, 32, 33 anc vitamin A intake (15, 17, 32, 33), but the evidence for women is less clear (12, 13, 32, 33) . We observed a significantly increased risk for ADC with the lowest leve ; of 4-carotene consumption and a similar association foi SCC . These results are consistent with findings fot females in Singapore (12) and in Japan (13), but they art not supportive of data for females in Hawaii (32) anc England (33) . Our observation of no association with ar index of total preformed vitamin A (i .e ., dairy producu eggs, liver, and vitamin supplements) and no associatior with total vitamin A intake (preformed vitamin A an( S-carotene-data not shown due to domination b, preformed vitamin A) is consistent with findings fo, females in Hawaii (32) . Conflicting findings have beer reported for subgroups of preformed vitamin A foods anc supplements . A higher consumption of liver and vitamir supplements has been reported previously for femal• cases as compared to controls, but the opposite result have been observed for males (33, 34) . Our data shor no ase-control difference in the intake pattern o vitamin supplements and a higher consumption of live among cases . Our finding of an elevated lung cancer ris associated with low levels of intake of dairy products ha not been reported for females, although similar result have been observed for males (15-17) . Our results on th role of /4-arotene and preformed vitamin A were simila for ADC and SCC, despite suggestions thai vitamin A (c rg-carotene) is more strongly protective against SCC tha against ADC (17) . Initial reports of an inverse relationship between bloo retinol levels and subsequent risk of cancer at all sites (3` 36) have not been supported by recent studies (37, 38 This situation emphasizes the need to reexamine even tt consistently observed association of vitamin A (or ~ carotene) intake with male lung cancer . Possible sources of bias in our data must be considerr. ~ Both lung cancer cases and controls were derived fro~ ~ population-based samples . However, because this disea ~; is debilitating and rapidly fatal, 190 patients had died ( (4 were too ill to participate by the time of initial contac ~ We did not conduct proxy interviews because questiot ~ on childhood exposures and dietary history could not t assessed adeq uatel y . As ex pected , the grou p who was n ~ J Na, voL.'!1 . NO . 1. APRIL tll5 ' ' ~
,.' interviewed was murr likell to have metastatic disease at diagnosis but was similar in all demographic variables measured . In addititrtt, information abstracted from medical rti-cords showed similar smoking status for those intervicwed and those nt>t interviewed . If cases who were not interviewed bccause of poor survival differed from those who survived longer and were interviewed in terms of the other risk facturs under study, this could have biased our results . However, this appears unlikely since our data showed tha( histories of childhood pneumonia and exposure to coal fires were similar among cases regardless of stage of disease at diagnosis . There is also no evidence that cancer survival is associated with dietary vitamin A intake . The etiology of 5CC can be explained almost entirely bt cigarette smoking . Cigarette smoking, however, explains only about half of the ADC cases . On the basis of this study, childhood lung disease and exposure to coal fires in childhood explain at least another 22% of ADC cases . Passive smoking and vitamin A ma}• be involved, but more research is needed to clarify their roles in lung cancer etiolog} . REFERENCES (1) StU'ERaERG E Cancer sutisucs, 1982 . CA 1982, 32 :15-31, (?1 HEh'DERSOL' BE Descriptive cptdemology and geographic pathology . In : Burchenal JH . Oe+taen HF, eds . Cancer ach,evcrnenu- challense-s and prospecu (or the 1980 s 'Vol I . New York : Grune, 1981 :51-69 l) 1 U .S . Public Health Service . The health conscquences of smoking Cancer . Washington fK: L' .S, Govt Print Off, 1982 [DHEW publication No . (PHSM2-50179) (4) HtR.AYAMA T . Non•smoking wives of heavy smokers have a higher risk of lung cancer: A study from Japan Br Med J 1981 ; 282 :185-185 . (3) TatcHoroLLOs D, KALANDtD, A . SrARRoi L . MACMAHOn B Lung cancer and pauive smoking Int J Canca 1981 . 27 :1-4 (6) CORREA P, PtCrcLE LW, Fon-ntAM E, LrN Y. HAENSUL W . Passive smoking and lung oncer, Lancet 1983 ; 2 :595-597 . (7) Xt' ZY, X1AO HP, Li G . Air pollution and lung cancer in Liaonrng Province . Nail Cancer Inst MonogT . In press (8) BRESt-oM' L, HoACUN L . RASSa,sscn G . AIRAMS HK Occupa• tions and cigarette smoking as risk faaon in lung cancer . Am J Public Health 1954 ; 44 :171-181 . (9) WYNDER EL,BESta JW .Cancerofthelungamongnon•smokeraspecial reference to histologic patterns . Cancer 1967 ; ~ f.6:1161-1172. (1J) MErJCr HR, PI¢E MC, HENO[RSON BE, JtNG JS . Lung cancer risk 1 among beautioaru and other fernak workers : drieJ communsration . J Natl Cancer Irut 1977t 59 :1423-1425 . 1111 AutasACH 0, GAarrNVt L PAaas VR. Scu nrurr ol the lungirsaase over a 21 year period. Carscer 1979 ; 4l :656-642 . '(12) MACLENNAN R, DA COSTA J, DAY NE, LAMCH . Nc YK, SHAN . MucARATt+Aw K. Risk facton for lung cancer in Singapore Chine+e, a population with high female incidence rates . Int J Cancer 1977 ; 20 :854-864 (13/ HIRAYAIAA T. Diet and cancer . Nuv CGncer 1979 ; 1 :67-81 . (le, SHExEttx RB, LErPER M, Liu S, etal . Dietary vitamin A and risk http://legacy.library.ucsf.edu/tid/wyk81f00/pdf Lung Canc.r In Women 751 of cancer in the Western Electric study Lanttr 1981 . 2 1185-1190 (13) B1ELS:E E . Dteun vlumin A and human lung cancer Int J Cancer 1975, 15561-565 (16) METTLrr. G .GRAHAM S .SkANSON M VlumtnAandlungcancer JNCI 1979 . 62,14l5-14S8 (171 )t'ALL G . BIELKE E . GART JJ Dteury habtu and lung cancer risk Int J Cancer 1985, 51 :597-405 (181 MAC.,, TM Cancer Surveillance Program in Los Angeles Counn Nail Cancer Inst Monogr 1977 ; 47 :99-101 . (19) GRAHAM S . MErruN C Fiber and other consutuenu of vegeubles in cancer eptdemtololp In Newell GR . Ellrson NM, eds Nutrition and cancer euoloin and treatment . New York . Raven Press . 1981 ;1 g9-215 (20) ADAMS C. Nutriuvc value of American foods in common units L• .S Department of Agriculture Handbook No 456 Washtng~ ton . DC U .S Department of Agrtculture, 1975 (21) BRESLOM NE, DAV NE . Suusual methods in oncer rrsearch 1'ol I-The analvsn of case-rontrol studies IARC Set Publ 1980, 52 .5-558 (22) YEs!.ER R GER57 B, Al'ERLACH O . Application Of the World Health Organtnuon classifiatton of lung carcinoma to biopsy material Ann Thorac Surg 1965 . I :D3-49 . (2I! YESNER R . CARTER D Patholo=y of carcinoma o( the lung Cltn Chest Med 1982 . 5 :257-289 (24) DOLL R, HILL AB . KREYaERC L The significance of cell type in relauon to the aeuolog) of lung cancer, Br J Cancer 1957, 11 45-48 (25) WYNnER EL . CorEY L .S . MAancHl K Lung cancer in womenPresent and future trends, J Nail Cancer Inst 1973 . 551 :391-401 (26) KArrAn M Long-term sequelae of resptruory illness in infancy and childhood, Pediatr Cltn North Am 1979, 26 :525-555 . (27) BuRRows B . KNUtxor. RJ, LEaowrTz MD . The relationships of childhood respiratory illness to adult obstructive airway disease Am Rev Respir Du 1977 ; 115 :751-759, (28) SAMCT JM . TACCa IB . Srctga FE. The relauonship bccween resp,raiory itlneas in childhood and chronic airflow obsvuction in adulthood Am Rcv Respir Dts 1983 . 127 :548-525, (29) REDMOND CK, ClOCCO A, LLOYD JW, RusH HW, Long-term mortality study of steel workers, VI . Mortality from mals6nant neoplasms among coke oven workers J Occup Med 1972, 14 :621-629, (30) LLOVD JN' Long-term morulsty study of steelworkers V . Resptratory oncer in coke plant worken, J Occup Med 1971 ; 15 :55-68 (31) DoLt . R, FtsHER EJ, GAMwoN W, et al . Mortality of gvsworkers with special reference to dncen of the lung and bladder, chronic bronchitis, and pneumoconiosis Br J lnd Med 1965 ; 22 .1-12 . (32) HtNrx MVW . Kot.oNEL LN, HANRtN JH . Dseury viumin A, carotene, vitamin C and risk of lung cancer in Hawaii . Am J Epidemio) 1984 ; 119 .227-237 . (3)) GRECOR A, LEE PN . RoE FJ, W1LSON MJ . MELTON A. Compari• son of dseury histories in lung cancer tsses and controls with special reierence to vitamin A . Nuer Cancer 1980 ; 2 :95-97 . (3I) Ssarnt PG, Jrca H . Cancers among users of preparatiorts contain• ing vitamin A_ Cancer 1978 ; 42:806-811 . (i3) KAR . JD, SNrTH AH, SwrTZER BR, HAwES CC Serum vitamin A (rrtinol) and carscer irscidenae in Evaru County . C,eorgia . JNCI 1981 ; 66 :7-16. (36) WALD N, IDLE M, BoREHAM J . Low serum vitamin A and subsequent risk of arscer, Lanca 1980 ; 2:813-815 . (37) Wsutrr WC, PoLk BF, UNDeaM'ooD BA, et al . Relarion of serum vitamin A and E and nrotenoids to the risk of cancer . N Engl J Med 1964, 510 :450-454 . (JF) STAHEUN HB, BUESS E . ROSEL F, WIDIitR LK, BRAIAUtER B . Vitamin A, cardiovascular risk factors, and mortality . Lancet 1982, 1194-395 . JNCI . VOL 74 . NO 4, APRIL 1995
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