|Comments: ||While adverse neurological effects are unlikely at the estimated average exposure,
morphological changes in nerves cannot be excluded for individuals with a high dietary exposure to acrylamide. For a compound that is both genotoxic and carcinogenic, these MOEs indicate a health concern.
The Committee noted that mitigation after 2003 has been reported for food types with high acrylamide levels or single products that contain higher levels within their food type. Although this might significantly reduce the exposure for some individuals or population subgroups, the Committee noted that this will have little effect on the dietary exposure of the general population in all countries. In line with this, neither the estimated average acrylamide exposure for the general population (0.001 mg/kg bw per day) nor the exposure for consumers in the high percentile (0.004 mg/kg bw per day) had changed since the sixty-fourth meeting. The MOE calculated relative to the NOAEL of 0.2 mg/kg bw per day for the most sensitive non-carcinogenic end-point— namely, morphological changes in nerves, detected by electron microscopy, in rats—therefore remains unchanged. For the general population and consumers with high exposure, the MOE values are 200 and 50, respectively. Consistent with the conclusion made at the sixty-fourth meeting, the Committee noted that while adverse neurological effects are unlikely at the estimated average exposure, morphological changes in nerves cannot be excluded for individuals with a high dietary exposure to acrylamide. When average and high dietary exposures are compared with the BMDL10 of 0.31 mg/kg bw per day for the induction of mammary tumours in rats, the MOE values are 310 and 78, respectively. For Harderian gland tumours in mice, the BMDL10 is 0.18 mg/kg bw per day, and the MOE values are 180 and 45 for average and high exposures, respectively. The Committee considered that for a compound that is both genotoxic and carcinogenic, these MOEs indicate a human health concern. The Committee recognized that these MOE values were similar to those determined at the sixty-fourth meeting and that the extensive new data from cancer bioassays in rats and mice, PBPK modelling of internal dosimetry, a large number of epidemiological studies and updated dietary exposure assessments support the previous evaluation.|