On the use of population attributable fraction to determine sample size for case-control studies of gene-environment interaction

Epidemiology

Volumn 14, Issue 2, 2003, Pages 161-167

  Yang, Quanhe ^a   Khoury, Muin J ^a   Friedman, J M ^b   Flanders, W Dana ^c  

^a NATIONAL CENTER ON BIRTH DEFECTS AND DEVELOPMENTAL DISABILITIES   (United States)

^b UNIVERSITY OF BRITISH COLUMBIA   (Canada)

^c EMORY UNIVERSITY   (United States)

Author keywords

Case control study; Gene environment interaction; Population attributable fraction; Sample size

Indexed keywords

ARTICLE; CALCULATION; CASE CONTROL STUDY; ENVIRONMENTAL EXPOSURE; ENVIRONMENTAL FACTOR; GENETIC SUSCEPTIBILITY; GENOTYPE; HEREDITY; POPULATION RESEARCH; PREVALENCE; PRIORITY JOURNAL; PUBLIC HEALTH; SAMPLE SIZE; ENVIRONMENT; GENETIC PREDISPOSITION; HUMAN; RISK; RISK FACTOR;

CASE-CONTROL STUDIES; ENVIRONMENT; GENETIC PREDISPOSITION TO DISEASE; GENOTYPE; HUMANS; ODDS RATIO; RISK FACTORS; SAMPLE SIZE;

EID: 0037946744     PISSN: 10443983     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001648-200303000-00009     Document Type: Article

References (27)

1. Yang Q, Khoury MJ. Evolving methods in genetic epidemiology. III. Gene-environment interaction in epidemiologic research. Epidemiol Rev 1997;19:33-43.
2. Marcus PM, Hayes RB, Vineis P, et al. Cigarette smoking, N-acetyltransferase 2 acetylation status, and bladder cancer risk: a case-series meta-analysis of a gene-environment interaction. Cancer Epidemiol Biomarkers Prev 2000;9:461-467.
3. Feng D, Tofler GH, Larson MG, et al. Factor VII gene polymorphism, factor VII levels, and prevalent cardiovascular disease: the Framingham Heart Study. Arterioscler Thromb Vasc Biol 2000;20:593-600.
4. Bellamy R. Evidence of gene-environment interaction in development of tuberculosis. Lancet 2000;355:588-589.
5. Psaty BM, Smith NL, Lemaitre RN, et al. Hormone replacement therapy, prothrombotic mutations, and the risk of incident non-fatal myocardial infarction in postmenopausai women. JAMA 2001;285:906-913.
6. Beaty TH, Maestri NE, Hetmanski JB, et al. Testing for interaction between maternal smoking and TGFA genotype among oral cleft cases born in Maryland 1992-1996. Cleft Palate Craniofac J 1997;34:447-454.
7. Hobbs CA, Sherman SL, Yi P, et al. Polymorphisms in genes involved in folate metabolism as maternal risk factors for Down syndrome. Am J Hum Genet 2000;67:623-630.
8. Rothman KJ, Greenland S, Walker AM. Concepts of interaction. Am J Epidemiol 1980;112:467-470.
9. Kleinbaum DG, Morgenstern H, Kupper LL. Epidemiologic Research: Principles and Quantitative Methods. Belmont, CA: Lifetime Learning Publications, 1982.
10. Greenland S, Robins JM. Conceptual problems in the definition and interpretation of attributable fractions. Am J Epidemiol 1988;128:1185-1197.
11. Rothman KJ, Greenland S. Modern Epidemiology. 2nd ed. Philadelphia: Lippincott-Raven, 1998.
12. Rothman KJ. Modern Epidemiology. 1st ed. Boston: Little Brown and Company, 1986.
13. Hwang SJ, Beaty TH, Liang KY, Coresh J, Khoury MJ. Minimum sample size estimation to detect gene-environment interaction in case-control designs. Am J Epidemiol 1994;140:1029-1037.
14. Foppa I, Spiegelman D. Power and sample size calculations for case-control studies of gene-environment interactions with a polytomous exposure variable. Am J Epidemiol 1997;146:596-604.
15. Garcia-Closas M, Lubin JH. Power and sample size calculations in case-control studies of gene-environment interactions: comments on different approaches. Am J Epidemiol 1999;149:689-692.
16. Gauderman WJ. Sample size requirements for matched case-control studies of gene-environment interaction. Stat Med 2002;21:35-50.
17. Browner WS, Newman TB. Sample size and power based on the population attributable fraction. Am J Public Health 1989;79:1289-1294.
18. Rockhill B, Newman B, Weinberg C. Use and misuse of population attributable fractions. Am J Public Health 1998;88:15-19.
19. Levin M. The occurrence of lung cancer in man. Acta Union International Contra Cancrum 1953;9:531-541.
20. Pearce N. Analytical implications of epidemiological concepts of interaction. Int J Epidemiol 1989;18:976-980.
21. Botto LD, Khoury MJ. Commentary: facing the challenge of gene-environment interaction: the two-by-four table and beyond. Am J Epidemiol 2001;153:1016-1020.
22. Yang Quanhe, Khoury MJ, Flanders WD. Sample size requirements in case-only designs to detect gene-environment interaction. Am J Epidemiol 1997;146:713-720.
23. Smith PG, Day NE. The design of case-control studies: the influence of confounding and interaction effects. Int J Epidemiol 1984;13:356-365.
24. Khoury MJ, Beaty TH, Cohen BH. Fundamentals of Genetic Epidemiology. Monographs in Epidemiology and Biostatistics. Version 22. New York: Oxford University Press, 1993.
25. Northridge ME. Public health methods-attributable risk as a link between causality and public health action. Am J Public Health 1995;85:1202-1204.
26. Walter SD. Attributable risk in practice. Am J Epidemiol 1998;148:411-413.
27. Bartsch H, Nair U, Risch A, Rojas M, Wikman H, Alexandrov K. Genetic polymorphism of CYP genes, alone or in combination, as a risk modifier of tobacco-related cancers. Cancer Epidemiol Biomarkers Prev 2000;9:3-28.