whole. As noted previously, the changes in function follow patterns similar to but not identical with physical growth. Functional development, like physical growth, is established to a large extent by genetic mechanisms. However, alterations in the patterns of functional development may be more readily modified by external (environmental) factors than the patterns of physical growth. In addition, there may well be external factors that modify growth but do not affect development and vice versa.
Understanding infant and child development in relation to the toxicity of pesticides requires an understanding of the constantly evolving interaction between a person's genetic endowment, developmental processes, and the environment. The infant or small child's phenotype (characteristics produced through interaction between genetic properties and environment) more closely resembles its genotype (genetic properties) than is true for the adult. At conception, each individual is genetically unique. From the time of conception, environmental factors may alter the genotype to produce a different phenotype. As the phenotype changes, it may alter the environment and be further altered by the environment. Specific enzyme systems may be enhanced, delayed, or altered permanently in their development by environmental factors. In addition, environmental exposures may impair, alter, or delay the development of some biochemical or physiological systems. Thus, not only will the programmed development of enzyme function alter the responses to xenobiotic compounds in immature, compared with mature, organisms, but environmental exposure to such substances before maturity may further modify response at a later time, or in some cases, throughout the life span. The specific stage in tissue or organ development when environmental factors can modify the cells to produce an effect apparent only in later life are termed critical periods of development. For example, giving insulin or glucosamine to newborn animals may permanently alter the mature animal's insulin levels and blood glucose values (Csaba and Dobozy, 1977; Csaba et al., 1979). Another example is the elevation of serum bilirubin in the human neonate, which produces altered brain function that becomes evident as the child matures. Similar elevations of serum bilirubin after infancy fail to produce these changes. Some of the damage to the central nervous system resulting from exposure to low levels of lead may not be apparent until the development of more mature functions in test animals (Csaba et al., 1979) or of such skills as reading and arithmetic in children. Similarly, neonatal exposure to diethylstilbestrol may produce effects later in life in the reproductive system (adenocarcinoma of the vagina and impaired function of the reproductive and immune systems) (Kalland, 1982).
As a general rule, compounds that interact with some genetic component