title: Meat intake, cooking-related mutagens and risk of colorectal adenoma in a sigmoidoscopy-based case-control study.
abstract: Reported habits of red meat consumption, particularly red meat that has been cooked to the degree termed 'well-done', is a positive risk factor for colorectal cancer. Under high, pyrolytic temperatures, heterocyclic amines (HCA) and benzo[a]pyrene (BP) molecules can form inside and on the surface of red meat, respectively. These compounds are precursors that are metabolically converted to compounds known to act as mutagens and carcinogens in animal models, yet their role in human colorectal carcinogenesis remains to be clarified. We investigated whether intake of these compounds is associated with risk of colorectal adenoma in the context of a polyp-screening study conducted in Southern California. Using a database of individual HCAs and BP in meats of various types and subjected to specified methods and degrees of cooking, we estimated nanogram consumption of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, 2-amino-3,4,8-trimethylimidazo[4,5-f] quinoxaline, 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline and benzo[a]pyrene (BP). We observed a 6% increased risk of large (>1 cm) adenoma per 10 ng/day consumption of BP [OR = 1.06 (95% CI, 1.00-1.12), P (trend) = 0.04]. A major source of BP is red meat exposed to a naked flame, as occurs during the barbecuing process. Consistent with this finding an incremental increase of 10 g of barbecued red meat per day was associated with a 29% increased risk of large adenoma [OR = 1.29 (95% CI, 1.02-1.63), P (trend) = 0.04]. Individuals in the top quintile of barbecued red meat intake were at increased risk of large adenoma [OR = 1.90 (95% CI, 1.04-3.45)], compared with never consuming barbecued red meat. The consumption of oven-broiled red meat was inversely related to adenoma risk compared with non-consumers [OR = 0.49 (95% CI, 0.28-0.85)]. We did not identify any association with consumption of individual HCAs and colorectal adenoma risk. These results support the hypothesis that BP contributes to colorectal carcinogenesis.
authors.affiliation: Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, EPS, 6120 Executive Boulevard, Rockville, MD 20852, USA. gunterm@mail.nih.gov
authors.forename: Marc J
authors.initials: MJ
authors.lastname: Gunter
authors.forename: Nicole M
authors.initials: NM
authors.lastname: Probst-Hensch
authors.forename: Victoria K
authors.initials: VK
authors.lastname: Cortessis
authors.forename: Martin
authors.initials: M
authors.lastname: Kulldorff
authors.forename: Robert W
authors.initials: RW
authors.lastname: Haile
authors.forename: Rashmi
authors.initials: R
authors.lastname: Sinha
mesh_terms: D000236:Adenoma / Q000139:chemically induced / Q000209:etiology*; D016022:Case-Control Studies; D015179:Colorectal Neoplasms / Q000139:chemically induced / Q000209:etiology*; D004032:Diet; D005260:Female; D006801:Humans; D008297:Male; D008460:Meat; D008875:Middle Aged; D009153:Mutagens / Q000633:toxicity*; D012812:Sigmoidoscopy
chemical_list: D009153:Mutagens