No abstract

Mycotoxins, such as ochratoxin A (OTA), can occur from fungal growth on foods. OTA is considered a possible risk factor for adverse renal effects in humans based on renal tumors in male rats. For risk mitigation. Health Canada proposed maximum limits (MLs) for OTA based largely on a comparative risk assessment conducted by Health Canada (Kuiper-Goodman et al., 2010), in which analytical data of OTA in foods were used to determine the possible impact adopting MLs may have on OTA risks. The EU MLs were used for comparison and resultant risk was determined based on age–sex strata groups. These data were reevaluated here to determine comparative risk on a lifetime basis instead of age strata. Also, as there is scientific disagreement over the mechanism of OTA-induced renal tumors, mechanistic data were revisited. On a lifetime basis, risks associated with dietary exposure were found to be negligible, even without MLs, with dietary exposures to OTA three to four orders of magnitude below the pivotal animal LOAEL and the TD05. Our review of the mechanistic data supported a threshold-based mechanism as the most plausible. In particular, OTA was negative in genotoxicity assays with the highest specificity and levels of DNA adducts were very low and not typical of genotoxic carcinogens. In conclusion, OTA exposures from Canadian foods do not present a significant cancer risk.

No abstract

The discovery of trace levels of semicarbazide (SEM) in bottled foods (especially baby foods) led to a consideration of the safety of this hydrazine compound by regulatory agencies worldwide. Azodicarbonamide, which is used in the jar-sealing technology known as Press On-Twist Off (or Push-Twist/PT) closures for the formation of a hermetic, plastisol seal, partially degrades with the heat of processing to form trace amounts of SEM. This review has evaluated the potential toxicological risks of resulting exposure to SEM and also the benefit of the PT technology (with azodicarbonamide) in the context of possible microbial contamination. It also considers the potential impact on infant nutrition if parents come to the conclusion that commercial baby foods are unsafe. SEM shows limited genotoxicity in vitro that is largely prevented by the presence of mammalian metabolic enzymes. Negative results were found in vivo in DNA alkaline elution, unscheduled DNA synthesis and micronucleus assays. This pattern is in contrast to the genotoxic hydrazines that also have been shown to cause tumours. Carcinogenicity studies of SEM are of limited quality, show a questionable weak effect in mice at high doses, which are not relevant to human exposure at trace levels, and show no effect in the rat. The IARC has assigned SEM as Group 3, 'Not classifiable as to its carcinogenicity to humans'. Based on estimates of exposure to infants consuming baby foods (with the assumption of SEM levels at the 95th percentile of 20 ng g(-1) in all of the consumed 'ready-to-eat' foods) compared with a no observed adverse effect level (NOAEL) in developmental toxicity studies, the margin of safety is more than 21 000. Since the risk of an adverse effect is negligible, it is clear that any theoretical risk is outweighed by the benefits of continuing use of the PT closure (with azodicarbonamide blowing agent) to ensure both the microbial integrity and availability of commercial baby foods as a valuable source of infant nutrition.