Similar to early life development, the preconception period (before fertilization) is a time of rapid cell growth, meiotic division, hormonal, and epigenetic changes. Exposures during this “sensitive” window can have lasting impacts on health. Because unfertilized male and female germ cells also respond to an environmental insult, and these effects can be transmitted to future generations, the Developmental Origins of Human Adult Diseases (DOHaD) hypothesis has been expanded to include preconceptional exposures.
There is a significant body of research showing that paternal and maternal preconception exposure to drugs, social instability, nutritional status, and smoking can have adverse effects on the offspring. For example, maternal smoking is associated with increased risk of congenital heart defects, and paternal smoking is associated with type 2 diabetes in the offspring. However, only a few studies have reported associations between preconception environmental chemical exposures to germ cells and later-life disease states.
Preconception program use animal models to investigate whether environmental chemical exposures during the preconception time period (pre-fertilization) to germ cells can be mechanistically linked to later-life traceable phenotypic outcomes in the first generation offspring.