A lifetime oncogenicity study in Fischer 344 rats was conducted to accurately characterize the carcinogenic potency of acrylamide. Acrylamide was administered in drinking water throughout the 106-week study at concentrations required to provide a dose of 0, 0.1, 0.5, or 2.0 mg/kg/day to males or 0, 1.0, or 3.0 mg/kg/day to females. Complete necropsy and gross pathology examinations were performed on all study animals. Histopathology examinations were conducted on selected tissues of all high-dose and control animals. Selected tissues from intermediate and low-dose groups were subjected to histopathological examinations as required to clarify high- and controldose group observations. There was no visual observation of neurotoxicity in any study animal but sciatic nerve degeneration was observed in the male and female high-dose groups. Increased mortality related to acrylamide was observed in the high- dose male group from Month 17 to the end of the study and in the high-dose females during Month 24. Mesotheliomas of the testicular tunic were significantly increased in the high-dose male group. The combined incidence of mammary gland adenocarcinomas and fibroadenomas was significantly increased in both acrylamide-dosed female groups. Males and females in the high-dose groups as well as females of the low-dose group had significantly (
p
<0.001) increased thyroid follicular cell adenomas and adenocarcinomas. A variety of other tumor types observed with increased incidence in a previous acrylamide onco genicity study (i.e., combined CNS glial neoplasms, papillomas of the oral cavity, adenomas of the clitoral gland, and uterine adenocarcinomas) were not observed to be present at increased incidence in this study. This study confirms previously described acrylamide induction of benign tumors of the thyroid and mammary glands as well as mesotheliomas of the testis. By using a larger number of animals with an unbalanced study design, this study showed that acrylamide did not induce glial tumors and demonstrated that the no-observable-effect level for scrotal mesotheliomas is 0.5 mg/kg. It also demonstrated that the in creased incidence of mammary tumors was again within historical control ranges.
The purpose of this study was to determine if chronic, low-level exposure of mice prone to mammary tumors to 435 MHz radiofrequency (RF) radiation promotes an earlier onset, a faster growth rate or a greater total incidence of mammary tumors than in sham-exposed controls. Two hundred female C3H/HeJ mice were exposed for 21 months (22 h/day, 7 days/week) to a horizontally polarized 435 MHz pulse-wave (1.0 micros pulse width, 1.0 kHz pulse rate) RF radiation environment with an incident power density of 1.0 mW/cm2 (SAR = 0.32 W/kg). An additional 200 mice were sham-exposed. Animals that died spontaneously, became moribund or were euthanized after 21 months of exposure were completely necropsied; tissues were subjected to histopathological examinations. Concerning mammary carcinomas, there were no significant differences between the two groups with respect to latency to tumor onset, tumor growth rate and overall tumor incidence. Histopathological examination revealed no significant differences in numbers of malignant, metastatic or benign neoplasms between groups. Survival probability was estimated by the Kaplan-Meier method; no significant difference between groups was noted (Cox's test). Under the conditions of this long-term study, low-level exposure of mice prone to mammary tumors to 435 MHz RF radiation did not affect the incidence of mammary tumors, tumor growth rate, latency to tumor onset or animal longevity when compared to sham-exposed controls.
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