Dietary acrylamide and the risk of pancreatic cancer in the International Pancreatic Cancer Case–Control Consortium (PanC4)

Abstract

Background. Occupational exposure to acrylamide was associated with excess mortality from pancreatic cancer, though in the absence of dose-risk relationship. Few epidemiological studies have examined the association between acrylamide from diet and pancreatic cancer risk.Patients and methods. We considered this issue in a combined set of 1975 cases of pancreatic cancer and 4239 controls enrolled in six studies of the Pancreatic Cancer Case-Control Consortium (PanC4). We calculated pooled odds ratios (ORs) and their 95% confidence intervals (CI) by estimating study-specific ORs through multivariate unconditional logistic regression models and pooling the obtained estimates using random-effects models.Results. Compared with the lowest level of estimated dietary acrylamide intake, the pooled ORs were 0.97 (95% CI, 0.79-1.19) for the second, 0.91 (95% CI, 0.71-1.16) for the third, and 0.92 (95% CI, 0.66-1.28) for the fourth (highest) quartile of intake. For an increase of 10 µg/day of acrylamide intake, the pooled OR was 0.96 (95% CI, 0.87-1.06), with heterogeneity between estimates (I 2 = 67%). Results were similar across various subgroups, and were confirmed when using a one-stage modelling approach.Conclusions. This PanC4 pooled-analysis found no association between dietary acrylamide and pancreatic cancer.

Dietary Acrylamide and the Risks of Developing Cancer: Facts to Ponder

“…Since the discovery of AA in foods, numerous studies have set to explore the carcinogenic potential in humans. Although AA was shown to be carcinogenic in both male and female rodent models, numerous studies reported no statistically significant association between dietary AA intake and various cancers in humans, e.g., pancreatic, prostate, breast, ovarian, and endometrial cancer ( 23 – 30 ). Obon-Santacana et al ( 26 ) analyzed the AA and GA hemoglobin adduct levels in quintiles based on control distributions and showed no effect on overall endometrial cancer risk (HR HbAA;Q5vsQ1 : 0.84, 95% CI: 0.49–1.48; HR HbGA;Q5vsQ1 : 0.94, 95% CI: 0.54–1.63).…”

Silymarin Ameliorates Acrylamide-Induced Hyperlipidemic Cardiomyopathy in Male Rats

“…In the Maillard reaction, the NH 2 of asparagine and the carbonyl group of glucose react together to produce acrylamide [6]. Previous studies have shown that AA is absorbed in a very rapid and e ective manner through the gastrointestinal system [7,8]. AA can undergo cellular biotransformation by a cytochrome P450 enzyme (CYP2El) into a more potent epoxide derivative (glycidamide) that has more reactivity toward DNA and proteins than the AA itself [9].…”

The cancer threshold of toxicological concern (TTC) in relation to foodstuffs and pharmaceuticals: A potentially useful concept compromised by a dubious derivation

“…More recent epidemiological reports have detected no association with dietary AA and cancer. [34][35][36] Whether or not dietary AA constitutes an unambiguous carcinogenic risk is currently uncertain; however, AA is considered to be a rare example of genotoxic rodent carcinogen that has been subjected to an extremely comprehensive epidemiological evaluation and found to show no overall association with an increased cancer risk. The average dietary exposure of AA is approximately 0.5 mg/kg/day, 200 times the EFSA cancer TTC of 0.0025 mg/kg/day, which does seem to raise concerns over the human relevance of the latter value based entirely on extrapolation of rodent carcinogenic potency data.…”