Chapter 11. Molecular Epidemiology of Food Pyrolysis Products in Relation to Colon, Breast, and Prostate Cancer

  1. Deutsche Forschungsgemeinschaft (DFG)
  1. Susan A. Nowell*,
  2. Rashmi Sinha1,
  3. Luke Ratnasinghe2,
  4. Nicholas P. Lang3 and
  5. Prof. Dr. Fred F. Kadlubar Director4

Published Online: 19 JUN 2007

DOI: 10.1002/9783527611492.ch11

Thermal Processing of Food: Potential Health Benefits and Risks

Thermal Processing of Food: Potential Health Benefits and Risks

How to Cite

Nowell, S. A., Sinha, R., Ratnasinghe, L., Lang, N. P. and Kadlubar, F. F. (2007) Molecular Epidemiology of Food Pyrolysis Products in Relation to Colon, Breast, and Prostate Cancer, in Thermal Processing of Food: Potential Health Benefits and Risks (ed Deutsche Forschungsgemeinschaft (DFG)), Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim, Germany. doi: 10.1002/9783527611492.ch11

Author Information

  1. 1

    National Cancer Institute, Rockville, MD 20852, USA

  2. 2

    National Center for Toxicological Research, Jefferson, AR 72079, USA

  3. 3

    Central Arkansas Veterans' Healthcare System, Little Rock, AR 72205, USA

  4. 4

    Division of Pharmacogenomics and Molecular Epidemiology, National Center for Toxicological Research, 3900 NCTR Road, Jefferson, AR 72079, USA

*Department of Environmental and Occupational Health, College of Public Health, University of Arkansas for Medical Sciences, 4301 W. Markham St., #820, Little Rock AR 72205, USA

Publication History

  1. Published Online: 19 JUN 2007
  2. Published Print: 23 FEB 2007

ISBN Information

Print ISBN: 9783527319091

Online ISBN: 9783527611492

SEARCH

Keywords:

  • thermal processing of food;
  • health benefits;
  • health risks;
  • molecular epidemiology of food pyrolysis products;
  • colon cancer;
  • breast cancer;
  • prostate cancer;
  • meat consumption;
  • particularly red meat;
  • exposure to PhIP (but not MeIQx) and BP more strongly associated with breast and prostate cancer

Summary

Certain food pyrolysis products are known mutagens that cause DNA damage, including both nucleotide alterations and chromosomal aberrations that are initiated by the formation of carcinogen-DNA adducts. However, adduct formation can be modified by host factors that affect the ultimate exposure of DNA to a food mutagen, such as variations in low-penetrance genes responsible for metabolic activation/detoxification (e.g., CYPs, NATs, SULTs, GSTs) of the putative mutagen or in genes responsible for cellular response to damage. The best characterized of these products are the heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs). Both PhIP- and benzo[a]pyrene-(BP)- DNA adducts have now been detected in human colon and breast, and PhIP in human prostate. Epidemiological studies have indicated that components of the Western-type diet, particularly high fat and meat consumption, are closely associated with the risk of colorectal cancer; prospective studies addressing meat consumption, particularly red meat, and colorectal cancer have shown a fairly consistent association. Over thirty case-control and cohort studies have examined the relationship between HCA exposure, genetic variation in metabolic enzymes, and colorectal cancer risk and many have shown a gene–diet interaction. In one study, metabolic phenotypes for CYP1A2 and NAT2, in combination with lifestyle variables showed that rapid phenotypes for these enzymes in conjunction with a preference for well-done meat conferred a substantial increased risk (OR = 6.45). Subsequent studies examining meat intake and metabolic genotypes and phenotypes in relation to both colorectal cancer and the occurrence of colorectal adenomas have not always provided consistent results, but this discrepancy could be due to differences in study design, and the fact that doneness of meat and the dietary content of individual HCAs and PAHs were not usually addressed. In two studies that provided study participants with photographs of meat cooked to varying degrees of doneness, there was a significant association between doneness and the occurrence of colorectal adenomas and of colon cancer risk. Moreover, this was correlated with the specific content of MeIQx, PhIP, and BP. High consumption of meat has also been associated with an increased risk of breast and prostate cancer. However, estimated exposure to PhIP (but not MeIQx) and BP was more strongly associated with breast and prostate cancer than intake of red meat alone. In a recent study, we have shown that the rapid SULT1A1 genotype and phenotype presumed to be responsible for activating N-OH-PhIP to form a DNA adduct in human prostate was associated with increased prostate cancer risk, particularly in African-Americans (OR=5.0 and 9.6, respectively).