Environmental Factors

How do environmental influences affect fetal development?
If a pregnant woman takes a drug (exogenous), or is infected with a virus to which she mounts an immune response (endogenous), those events have the potential to affect cell receptors and cell signaling. Most drugs work by stimulating cell surface receptors and changing signaling in cells. This may happen, not only in the mother, but also in the developing fetus. Immune reactions and antibodies, which are generated by a mother in response to a virus or other foreign protein, target the infectious agent or foreign protein to get rid of it. However, antibodies produced in this way may later cross-react with fetal receptors to stimulate or block them, causing interruptions to critical pathways in development. Functioning after birth depends upon the groundwork set during fetal development. This groundwork is created by stimulation of cell surface receptors and signaling responses in fetal cells. If enough of the critical pathways for normal development are interrupted or over or under stimulated during fetal life, the groundwork for functioning in many tissues may become abnormal. A child that is born with altered physiology is further vulnerable to the environment, because normal mechanisms and physiologic responses have already been altered. Certain genetic variances in the DNA of the child could further increase the likelihood that altered physiological mechanisms may occur, by creating increased susceptibility to environmental influences.

The Beta2 Adrenergic Receptor is an example of a cell surface receptor, which has polymorphisms of its genes (genetic variances) and provides a model for genetic vulnerability that may be acted on by environmental factors.

Epigenetic influences are also emerging as contributors to neurodevelopmental disorders. Epigenetic factors change gene expression over time without affecting the genes themselves. It is believed that certain environmental factors can have an affect on epigenetic influences, which in turn alter gene expression during fetal development.