Article

A Prospective Study on Dietary Acrylamide Intake and the Risk for Breast, Endometrial, and Ovarian Cancers

Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA.
Cancer Epidemiology Biomarkers & Prevention (Impact Factor: 4.32). 10/2010; 19(10):2503-15. DOI: 10.1158/1055-9965.EPI-10-0391
Source: PubMed

ABSTRACT Acrylamide is a probable human carcinogen formed during cooking of many common foods. Epidemiologic studies on acrylamide and breast cancer risk have been null; however, positive associations with ovarian and endometrial cancers have been reported. We studied acrylamide intake and risk for breast, endometrial, and ovarian cancers in a prospective cohort study.
We assessed acrylamide intake among 88,672 women in the Nurses' Health Study using food frequency questionnaires administered every 4 years. Between 1980 and 2006, we identified 6,301 cases of invasive breast cancer, 484 cases of invasive endometrial adenocarcinoma, and 416 cases of epithelial ovarian cancer. We used Cox proportional hazards models to study the association between acrylamide and cancer risk.
We found no association between acrylamide intake and breast cancer overall or according to estrogen and progesterone receptor status. We found an increased risk for endometrial cancer among high acrylamide consumers (adjusted relative risk for highest versus lowest quintile = 1.41; 95% CI, 1.01-1.97; P for trend = 0.03). We observed a nonsignificant suggestion of increased risk for ovarian cancer overall (relative risk, 1.25; 95% CI, 0.88-1.77; P trend = 0.12), with a significantly increased risk for serous tumors (relative risk, 1.58; 95% CI, 0.99-2.52; P trend = 0.04). Associations did not differ by smoking status.
We observed no association between acrylamide and breast cancer. Risk for endometrial cancer and possibly ovarian cancer was greater among high acrylamide consumers.
This is the second prospective study to report positive associations with endometrial and ovarian cancers. These associations should be further evaluated to inform public health policy.

Download full-text

Full-text

Available from: Kathryn M Wilson, Aug 13, 2015
0 Followers
 · 
179 Views
  • Source
    • "The overall sample size of this meta-analysis was relatively large, and all the cohorts provided separate RRs among all women as well as neversmoking women. Although each study attempted to adjust NOTE: Weights are from random effects analysis Overall (I-squared = 0.0%, p = 0.547) Larsson et al, 2009 Wilson et al, 2010 ID Obon-Santacana, 2014 Hogervorst et al, 2007 "
    [Show abstract] [Hide abstract]
    ABSTRACT: Purpose Acrylamide has been associated with carcinogenicity in experimental animals, but potential health risks of dietary acrylamide intake and endometrial cancer in human are inconclusive. Thus, a meta-analysis of prospective cohort studies was conducted to provide a quantitative assessment of the association between dietary acrylamide intake and endometrial cancer risk. Methods PubMed database was used to identify prospective cohort studies on dietary acrylamide intake and endometrial cancer risk published up to June 2014. Since smoking is an important source of acrylamide and is inversely associated with endometrial cancer risk, the association was examined in women who never smoked as well. Multivariable relative risks (RR) adjusting for potential confounders were combined using random effects models. Results Four large prospective cohort studies were identified, which included 453,355 female participants and 2,019 endometrial cancer cases. There was no association between dietary acrylamide intake and endometrial cancer risk overall [pooled RR for high vs. low intake = 1.10; 95 % confidence interval (CI) 0.91–1.34]. High acrylamide intake, however, was significantly associated with increased risk of endometrial cancer among women who never smoked (pooled RR for high vs. low intake = 1.39; 95 % CI 1.09–1.77). In dose–response analyses, pooled RRs for an increase of 10 µg/day were 1.04 (95 % CI 0.97–1.11) among all women and 1.11 (95 % CI 1.04–1.19) among never-smoking women. Conclusions Endometrial cancer risk was not associated with dietary acrylamide intake overall. Among women who never smoked, however, there was a significantly increased endometrial cancer risk in women who consumed high dietary acrylamide.
    Archives of Gynecology and Obstetrics 12/2014; 291(6). DOI:10.1007/s00404-014-3595-8 · 1.28 Impact Factor
  • Source
    • "Under such circumstances, there was no evidence of an overall association between AA intake and breast cancer (Burley et al., 2010; Wilson et al., 2010) although a weak association might exist with premenopausal breast cancer (Burley et al., 2010). Endometrial cancer also exhibited bidirectional trends, namely an increased risk among high AA consumers (Hogervorst et al., 2007; Wilson et al., 2010) and no association when the comparison was between high and low consumers (Larsson et al., 2009). Other types of cancer, e.g. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Acrylamide (AA) is known to induce tumors in various organs/tissues in rats and mice. Epidemiological studies of oral exposure have generated controversial results but mortality studies of people who work with AA have indicated increased rates of pancreatic cancer. In the present study, for dose selection for chronic toxicity/carcinogenicity studies, 13-week toxicity of AA was evaluated in Syrian hamsters, which are sensitive to induction of pancreatic ductal carcinogenesis, at concentrations required to provide doses of 0 (control), 20, 30 and 50 mg kg(-1) body weight in drinking water. Treatment with AA caused abnormal gait advancing to hind limb paralysis in all males and females at 50 mg kg(-1) . Body weights in 30 and 50 mg kg(-1) males and 50 mg kg(-1) females were lower than in the controls. At termination of the study, red blood cells (RBC) and hemoglobin (Hb) were decreased or showed a tendency for a decrease at 20 and 30 mg kg(-1) in females. Microscopically, axonal/myelin degeneration of sciatic nerves was observed in all AA-treated groups with dose dependence. No obvious changes were found in pancreatic ducts/ductules in any groups of animal. These results indicated the maximum tolerated dose for long-term studies of AA to be 20 mg kg(-1) or less in both male and female Syrian hamsters. Copyright © 2012 John Wiley & Sons, Ltd.
    Journal of Applied Toxicology 01/2014; 34(1). DOI:10.1002/jat.2831 · 3.17 Impact Factor
  • Source
    • "While some studies have found significant associations between oral exposure to AA and cancer, others failed to prove such a relationship. For instance, a recent study by Wilson et al. [12] found no association between acrylamide and breast cancer. However, with high acrylamide consumption a greater risk for endometrial and possibly ovarian cancer was observed. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Acrylamide (AA) is a probable human carcinogen generated in carbohydrate-rich foodstuffs upon heating. Glycidamide (GA), formed via epoxidation, presumably mediated by cytochrome P450 2E1, is considered to be the active metabolite that plays a central role in the genotoxicity of AA. The aim of this work was to evaluate the cytogenetic damage induced by AA and GA in cultured human lymphocytes by use of the sister chromatid exchange (SCE) assay. Furthermore, this report addresses the role of individual genetic polymorphisms in key genes involved in detoxification and DNA-repair pathways (BER, NER, HRR and NHEJ) on the induction of SCE by GA. While AA induced the number of SCE/metaphase only slightly, especially for the highest concentration tested (2000μM), GA markedly induced SCEs in a concentration-dependent manner up to concentrations of 750μM, leading to an increase in SCEs of up to about ten-fold compared with controls. By combining DNA damage in GA-treated lymphocytes and data on polymorphisms, associations between the induction of SCEs with GSTP1 (Ile105Val) and GSTA2 (Glu210Ala) genotypes are suggested.
    Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 01/2013; 752(1-2). DOI:10.1016/j.mrgentox.2012.12.013 · 4.44 Impact Factor
Show more