**1. Introduction**

Bisphenol A (BPA, CAS #80-05-7) is widely used in manufacturing polycarbonate plastics, epoxy resins, and thermal paper including food containers, baby bottles, dental sealant, and store receipts. BPA can produce the estrogenic activity through binding with estrogen receptor [1] and can also exert the actions through androgen receptor, peroxisome proliferator-activated receptor γ, and others [2]. Thus, BPA is classified as an endocrine disruptor (ED) because of the estrogenic potency.

Traditional toxicology considers that the effect would consistently increase with the amount of treatment. The dose levels of BPA below low observed adverse effects level (LOAEL) at 50 mg/kg/day [3] are regard as safe. However, recent studies describe the nonmonotonic dose response relationship of BPA. Perinatal exposure to lower dose of BPA than LOAEL has been reported the harmful effects on endocrine system including reproductive

system [4–7], immune system [8–10], pituitary gland [11–20], and metabolic system [21–24]. Because, the fetus and neonates are extremely sensitive to perturbation by hormone like chemicals, early life exposure to low dose BPA probably is able to affect the epigenetic mechanism. The epigenetic changes caused by BPA may explain the increased risk of developing adult onset diseases.

The mixed exposure to several low-level EDs should be tested because humans are exposed to various EDs simultaneously. Mixture can produce significant adverse effects, even when each chemical is present at low doses that individually do not induce observable effects in reproductive system [4, 25] neuroendocrine system [26], and endocrine system [27, 28].

Therefore, this chapter describes the harmful effects on adulthood caused by exposure to lowdose BPA during early life stage.
