Abstract
The contribution of maternal toxicity to the teratogenic effects of the herbicide cyanazine has been assessed to determine whether it may be a hazard to development. Eye defects such as anophthalmia and microphthalmia were observed in rat fetuses and pups. Maternal toxicity was determined from body weight data and clinical signs. Two approaches were used. First, the timing of maternal toxicity was correlated with the specific period of gestation during which the observed fetal defect was most likely to have occurred. Second, individual dams, as well as mean values for each group, were evaluated. The data at the individual level, i.e., in dams with affected litters, did not support conclusions based on the group means. Instead, it is suggested that the developmental effects were not a direct result of maternal toxicity of cyanazine. Data from a rabbit developmental toxicity study supported the findings from the Fischer 344 rat studies. The strategy employed may thus enable direct toxicity to the fetus to be distinguished from developmental toxicity arising as a secondary consequence of maternal toxicity.
Published Version
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