Lung Cancer Risk in White and Black Americans.docx

1、Lung Cancer Risk in White and Black AmericansLung Cancer Risk in White and Black AmericansSTEVEN D. STELLMAN, PHD, MPH, YU CHEN, MPH, JOSHUA E. MUSCAT, MPH,MIRJANA V. DJORDJEVIC PHD, JOHN P. RICHIE, JR., PHD, PHILIP LAZARUS, PHD,SETH THOMPSON, PHD, NASSER ALTORKI, MD, MARIANNE BERWICK, PHD,MARC L. C

2、ITRON, MD, SUSAN HARLAP, MD, TAJINDER B. KAUR, MD,ALFRED I. NEUGUT, MD, PHD, SARA OLSON, PHD, JOHN M. TRAVALINE, MD,PHILIP WITORSCH, MD, AND ZUO-FENG ZHANG, MD, PHDPURPOSE: To test whether differences in smoking-related lung cancer risks in blacks and whites can ex-plain why lung cancer incidence is

3、 greater in black males than in white males but about equal in black and white females, given that a greater proportion of blacks are smokers, but smoke far fewer cigarettes per day than do whites.METHODS: A hospital-based case-control study was conducted between 1984 and 1998 that included intervie

4、ws with 1,710 white male and 1,321 white female cases of histologically confirmed lung cancer, 254 black male and 163 black female cases, and 8,151 controls. Relative risks were estimated via odds ra-tios using logistic regression, adjusted for age, education, and body mass index.RESULTS. We confirm

5、ed prior reports that smoking prevalence is higher but overall dosage is lower among blacks. Overall ORs were similar for blacks and whites, except among the heaviest smoking males (21 cigarettes per day or 37.5 packyears), in whom ORs for blacks were considerably greater than for whites. Long-term

6、benefits of cessation were similar for white and black ex-smokers. Smokers of menthol flavored cigarettes were at no greater risk for lung cancer than were smokers of unflavored brands.CONCLUSIONS. Lung cancer risks were similar for whites and blacks with similar smoking habits, ex-cept possibly for

7、 blacks who were very heavy smokers; this sub-group is unusual in the general population of African American smokers. Explanations of racial disparities in lung cancer risk may need to account for modifying factors including type of cigarette (yield, mentholation), diet, occupation, and host factors

8、 such as ability to metabolize mainstream smoke carcinogens.Ann Epidemiol 2003;13:294302 (C) 2003 Elsevier Science Inc. All rights reserved.KEY WORDS: Lung Cancer, Cigarettes, Smoking, Risk, Racial Differences, Dosage, Menthol.Lung cancer rates in the US show substantial unexplained racial variabili

9、ty. SEER incidence rates have been reported higher for blacks than whites in every year since 1973, with rate differentials between 34% and 67%. (1, 2). The preva-lence of cigarette smoking has been considerably higher in black than in white males since 1950. It was slightly higher in black than in

10、white females from 1962 until 1992, after which the rates have been nearly equal (36). The seemingFrom the American Health Foundation, One Dana Road, Valhalla, NY10595 (S.D.S.); Department of Epidemiology, Mailman School of PublicHealth, Columbia University, 630 West 168th Street, PH-18, New York,NY

11、 10032 (S.D.S., Y.C., A.I.N.); Division of Epidemiology, AmericanHealth Foundation, One Dana Road, Valhalla, NY 10595 (J.E.M.); To-bacco Control Research Branch, Division of Cancer Control and Popula-tion Sciences, National Cancer Institute, 6130 Executive Boulevard, EPN4039, Rockville, MD 20852 (M.

12、V.D.); Division of Nutritional Carcinogen-esis, American Health Foundation, One Dana Road, Valhalla, NY 10595(J.P.R.); Divisions of Cancer Control and Mol. Oncology, H. Lee MoffittCancer Center, MRC-2E, 12902 Magnolia Drive, Tampa, FL 33612 (P.L.);Bristol-Meyers Squibb, 5 Research Parkway, Wallingfo

13、rd, CT 06492 (S.T.);Division of Thoracic Surgery, New York Presbyterian Hospital, 525 East68th Street, New York, NY 10021 (N.A.); Department of Epidemiology &Biostatistics, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue,New York, NY 10021 (M.B., S.O.); ProHealth, Inc., 2800 Marcus Avenue,L

14、ake Success, NY 11042 (M.L.C.); Dept. of Obstetrics and Gynecology anKaplan Cancer Center, NYU Medical CenterRoom NBV-9E-2, 550 FirsAvenue, New York, NY 10016 (S.H.); Dept. of Obstetrics and GynecologyTemple University Hospital, 3401 N. Broad Street, Philadelphia, PA 1914(T.B.K.); Pulmonary Division

15、, Temple University School of Medicine3400 N. Broad Street, Philadelphia, PA 19140 (J.M.T.); Division of Clinical Pharmacology, Departments of Medicine and Pharmacology, Georgetown University Medical Center, 3900 Reservoir Road NW, WashingtonDC 20007 (P.W.); Department of Epidemiology, UCLA School o

16、f PubliHealth, 71-225 CHS, Box 951772, 10833 Le Conte Avenue, Los AngelesCA 90095-1772.(Z-F.Z.).Address correspondences to: Steven D. Stellman, Ph.D. M.P.H., Deptof Epidemiology, Mailman School of Public Health, 630 West 168tStreetPH-18, New York, NY 10032, USA. Tel.: 212-305-4911. E-mailsds91columb

17、ia.eduReceived May 9, 2001; revised May 9, 2002; accepted May 22, 2002.consistency between smoking and lung cancer rates isweakened, however, by substantial differences in the num-ber of cigarettes smoked per day (CPD). In 1991, 29.2% ofadult blacks currently smoked cigarettes compared with25.5% of

18、whites, but blacks smoked on average 15.0 CPDwhile whites smoked 21.0 CPD. (7). Comparable differ-ences have been reported in many other studies (5, 810).Few analytic studies have addressed this anomaly. Schwartzand Swanson (11) concluded that racial differences in inci-dence could be “entirely expl

19、ained” by smoking habits,based on an epidemiological study of over 5500 cases diag-nosed in Detroit area hospitals in 1984 to 1987. Neverthe-less, their conclusion did not apply to persons under 55 years ofage, and was based on large numbers of proxy interviews,which might have affected the precisio

20、n of reported ORs.Although smoking is the overwhelming cause of lungcancer, other host and environmental factors may also mod-ify risk. Modifying factors that have been studied includediet (12, 13), genetic polymorphisms in metabolizing genes(1418) as well as more general familial factors (19, 20),m

21、etabolism differences (21, 22), occupation (23), and non-biological factors such as social class (24) and education(25). The hypothesis that the strong preference for men-thol flavored cigarettes among black smokers may alsopartly explain risk differences has led to conflicting resultsamong investig

22、ators, with no association reported by ourgroup (26), and a positive association reported for men butnot women by Sidney et al. (27).To better delineate smoking-related risks for lung cancerbetween racial groups, it is important to make direct assess-ments of risk in relation to smoking habits as an

23、 essentialbackdrop for interpreting the impact of other risk factors,including those observed in metabolic and molecular stud-ies. To address these issues we examined smoking habitsand lung cancer risk in black and white Americans.METHODSBetween 1984 and 1998 the American Health Foundationperformed

24、a hospital-based case-control study in the threemajor New York City cancer centers plus other hospitals inNew York, Philadelphia, Washington DC, and other UScities (see Acknowledgments). Only incident cases were se-lected, defined as persons diagnosed with lung cancer forthe first time during the 12

25、 months preceding interview(most within 2 months). All cases were confirmed by histo-pathology. Adenocarcinomas were more common in women(46% of cases) than in men (37%), but differed little byrace. Controls were selected from the daily admission ros-ters and frequency matched to cases on the basis

26、of sex, age(5 y), hospital, and year of interview. Eligible control di-agnoses excluded tobacco-related diseases such as coronaryheart disease, stroke, peripheral vascular disease, chronicobstructive pulmonary disease, gastric ulcer, cirrhosis of theliver, and cancers of the mouth, larynx, esophagus

27、, bladder,kidney, pancreas, or liver (28). Control patients for studiesof other tobacco-related cancers besides lung were being in-terviewed at the same time as cases, so that a large controlpool of patients with non-tobacco-related diseases wasavailable. Approximately half of male controls had beni

28、gnor malignant diseases including benign prostatic hypertro-phy (9%), prostate cancer (8%), colon-rectum cancer(11%); bone and joint diseases (5%); kidney stones, ne-phritis, and other kidney diseases (8%); abscesses (2%);sprains, strains, and fractures including hip, and a wide vari-ety of other no

29、n-malignant conditions requiring hospital-ization. Forty percent of female controls had cancers whichincluded breast (15%), colon-rectum (7%), ovary (4%),connective tissue (2%), and melanoma (2%); other femalecontrols were hospitalized for osteoarthritis (5%), fracturesincluding hip (5%), genital pr

30、olapse (2%), abscesses (2%)and a wide variety of other non-malignant conditions. Af-ter providing written informed consent using a form ap-proved by the Institutional Review Board of each hospital,every subject was interviewed by an AHF-trained inter-viewer using a structured questionnaire that elic

31、ited infor-mation on demographic variables, smoking history, andother possible risk factors. Approximately 85% of eligiblepatients who were approached agreed to be interviewed.The 15-year accrual interval was chosen because it in-cluded large numbers of black and white patients who wererecruited wit

32、h a uniform protocol and interviewed undersimilar circumstances. The present analysis overlaps andextends earlier reports (26, 29) that included patients inter-viewed between 1977 and 1991. This is a significant exten-sion, since it makes use of data obtained via face to faceinterviews with 11,599 patients (4192 interviewed after1991), of whom 3448 were cases and 8151 were controls. Itincludes 417 black cases, 254 of whom