Another mechanism by which reproductive development of the male fetus might be adversely affected is by altered exposure to maternal/placental estrogens during pregnancy (5). There is evidence that the risk of cryptorchidism and testicular germ cell cancer are both increased in twin and first pregnancies in which estrogen levels are higher and administration of the potent estrogen diethylstibestrol (DES) to pregnant women also increased risk of these disorders in the offspring (4,5,8). The relationship between circulating estrogen levels in the pregnant mother and levels in target organs in the fetus is unclear, but maternal factors that could alter estrogen bioavailability could (in theory) increase fetal estrogen exposure. Therefore, dietary factors in the mother may be influential, because obesity and associated insulin resistance are well established to lower levels of SHBG, which, in turn, will affect the levels of free estrogen and androgen and influence the androgen-estrogen balance. More recently, another environmental mechanism has emerged through which maternal/fetal estrogen levels during pregnancy could be altered, at least in theory. Two classes of environmental chemicals (112,113) to which there is universally high human exposure are both potent suppressors of estrogen sulfotransferase (SULT1E1). The latter is the main pathway by which estrogens are inactivated as a prelude to their excretion (114), so inhibition of this enzyme is likely to increase estrogen levels. The compounds in question are poly-halogenated hydrocarbons (PAHs), found in combustion/exhaust/tobacco smoke, and PCBs, which are now banned but are still widely present in the environment because of their persistence and lipophilicity (112,113). The risk, if any, to humans and to the reproductive development of the fetus from exposure to such compounds remains unknown, but these examples serve as useful reminders to us that there may be other (and perhaps more important) presently unknown pathways by which environmental/lifestyle factors may affect the fetus, or even the adult male, by perturbation of endogenous hormone action.
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