Carcinogenesis Advance Access originally published online on August 19, 2005
Carcinogenesis 2006 27(2):293-297; doi:10.1093/carcin/bgi212
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Carcinogenesis vol.27 no.2 © Oxford University Press 2005; all rights reserved.
Meat and meat-mutagen intake and risk of non-Hodgkin lymphoma: results from a NCI-SEER case–control study
Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Rockville, MD 20892, USA, 1 Karmanos Cancer Institute and Department of Family Medicine, Wayne State University, Detroit, MI 48201, USA, 2 Department of Ambulatory Care and Prevention Harvard Medical School and Harvard Pilgrim Health Care, 133 Brookline Avenue, Boston, MA 02215, USA, 3 University of Southern California, Los Angeles, CA 90089, USA, 4 Fred Hutchinson Cancer Research Center and the University of Washington, Seattle, WA 98109, USA and 5 Mayo Clinic College of Medicine, Rochester, MN 55904, USA
* To whom correspondence should be addressed. Tel: +1 301 4964378; Fax: +1 301 4966829; Email: crossa{at}mail.nih.gov
Non-Hodgkin Lymphoma (NHL) incidence has risen dramatically over past decades, but the reasons for most of this increase are not known. Meat cooked well-done using high-temperature cooking techniques produces heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) such as benzo[a]pyrene (B[a]P). This study was conducted as a population-based case–control study in Iowa, Detroit, Seattle and Los Angeles and was designed to determine whether meat, meat-cooking methods, HCAs or PAHs from meat were associated with NHL risk. This study consisted of 458 NHL cases, diagnosed between 1998 and 2000, and 383 controls. Participants completed a 117-item food frequency questionnaire (FFQ), with graphical aids to assess the meat-cooking method and doneness level, which was linked to a HCA and B[a]P database. Logistic regression, comparing the fourth to the first quartile, found no association between red meat or processed meat intake and risk for NHL [odds ratio (OR) and 95% confidence interval (CI): 1.10 (0.67–1.81) and 1.18 (0.74–1.89), respectively]. A marginally significant elevated risk for NHL was associated with broiled meat [OR and 95% CI: 1.32 (0.99–1.77); P trend = 0.09], comparing those who consumed broiled meat with those who did not. The degree to which meat was cooked was not associated with the risk for NHL, although one of the HCAs, DiMeIQx (2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline), was associated with an inverse risk. Fat intake was associated with a significantly elevated risk for NHL [OR and 95% CI: 1.60 (1.05–2.45); P trend = 0.12]; in contrast, animal protein was inversely associated with risk for NHL [OR and 95% CI: 0.39 (0.22–0.70); P trend = 0.004]. Overall, our study suggests that consumption of meat, whether or not it is well-done, does not increase the risk of NHL. Furthermore, neither HCAs nor B[a]P from meat increase the risk of NHL.
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