Bisphenol A is widely used in food contact materials and other products and is 
detected in human urine and blood. Bisphenol A may affect reproductive and 
neurological development; however, opinion of the European Food Safety Authority 
(EFSA) on bisphenol A (EFSA J, 13, 2015 and 3978) concluded that none of the 
available studies were robust enough to provide a point of departure for setting 
a tolerable daily intake for bisphenol A. In the present study, pregnant Wistar 
rats (n = 17-21) were gavaged from gestation day 7 to pup day 22 with bisphenol 
A doses of 0, 25 μg, 250 μg, 5 mg or 50 mg/kg bw/day. In the offspring, growth, 
sexual maturation, weights and histopathology of reproductive organs, oestrus 
cyclicity and sperm counts were assessed. Neurobehavioural development was 
investigated using a behavioural testing battery including tests for motor 
activity, sweet preference, anxiety and spatial learning. Decreased sperm count 
was found at the lowest bisphenol A dose, that is 25 μg/kg/day, but not at the 
higher doses. Reproductive organ weight and histology were not affected and no 
behavioural effects were seen in male offspring. In the female offspring, 
exposure to 25 μg/kg bw/day bisphenol A dose resulted in increased body weight 
late in life and altered spatial learning in a Morris water maze, indicating 
masculinization of the brain. Decreased intake of sweetened water was seen in 
females from the highest bisphenol A dose group, also a possible sign of 
masculinization. The other investigated endpoints were not significantly 
affected. In conclusion, the present study using a robust experimental study 
design, has shown that developmental exposure to 25 μg/kg bw/day bisphenol A can 
cause adverse effects on fertility (decreased sperm count), neurodevelopment 
(masculinization of spatial learning in females) and lead to increased female 
body weight late in life. These results suggest that the new EFSA temporary 
tolerable daily intake of 4 μg/kg bw/day is not sufficiently protective with 
regard to endocrine disrupting effects of bisphenol A in humans.