Purpose: Adverse health effects of developmental toxicants may induce abnormal functional programming that leads to lasting functional deficits. This notion is considered from epidemiological evidence using developmental methylmercury neurotoxicity as an example.
Most important findings: Accumulating evidence indicates that adverse effects may occur even at low-level methylmercury exposures from seafood and freshwater fish. Neurobehavioral outcomes are usually non-specific, and imprecise exposure assessment results in a bias toward the null. Essential nutrients may promote the development of certain brain functions, thereby causing confounding bias. The functional deficits caused by prenatal methylmercury exposure appear to be permanent, and their extent may depend on the joint effect of toxicants and nutrients.
Principal conclusions: The lasting functional changes caused by neurodevelopmental methylmercury toxicity fit into the pattern of functional programming, with effects opposite to those linked to beneficial stimuli.