There is increasing evidence both from epidemiology studies and animal models that specific endocrine-disrupting compounds may influence the development or progression of prostate cancer. In large part, these effects appear to be linked to interference with estrogen signaling, either through interacting with ERs or by influencing steroid metabolism and altering estrogen levels within the body.
In humans, epidemiologic evidence links specific pesticides, PCBs and inorganic arsenic exposures to elevated prostate cancer risk. Studies in animal models also show augmentation of prostate carcinogenesis with several other environmental estrogenic compounds including cadmium, UV filters and BPA.
Importantly, there appears to be heightened sensitivity of the prostate to these endocrine disruptors during the critical developmental windows including in utero and neonatal time points as well as during puberty. Thus infants and children may be considered a highly susceptible population for ED exposures and increased risk of prostate cancers with aging.
Prostate cancer is the most common solid cancer in males and is the second leading cause of cancer deaths in American men Jemal et al. While rates today are markedly higher than rates observed three decades ago, the most recent statistics show that prostate cancer incidence rates have now stabilized which is thought to reflect changes in utilization of prostate-specific antigen PSA testing.
Despite extensive research, the basis for these high rates of abnormal prostatic growth is not well understood. It is recognized, however, that steroids play a role in the initiation and progression of prostate cancer which is the basis for hormonal treatment strategies. Furthermore, it is believed that early prostatic developmental events which are regulated by steroids may be linked to the predisposition of this structure to high rates of disease in adult men Henderson et al. It is noteworthy that relative to adult estrogenic responses, the prostate gland is particularly sensitive to estrogen exposures during the critical developmental period Prins et al.
