Table 2 Key characteristics of the BPA-neurobehavior context, and their implications for interpreting the available human evidence

Ubiquity

Exquisite sensitivity of the developing brain

The whole population may be at risk, with a special consideration for the developing fetus

Low-dose effects cannot always be predicted from high doses

Non-traditional endpoints such as behavior and molecular brain changes are more realistic

Subtle subclinical effects at a population level are expected, rather than obvious clinical effects at the individual level

Multiple modes of action

Windows of particular susceptibility

BPA exposure at different points in gestation may be linked to slightly different neurobehavioral endpoints

Challenging human exposure characterization

Indirect behavior assessment with questionnaires completed by parents or teachers

The expected bias arising from limitations when evaluating both BPA exposure and behavioral outcomes across studies is a tendency to underestimate potential effects

Exposure to complex chemical mixtures

Organizational vs. activational effects in the brain

Human BPA exposure always coexist and probably interacts with many other chemicals. Prenatal exposures may “organize” brain areas, leading to long-lasting effects in the offspring