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Warren G. Foster, Environmental Estrogens and Endocrine Disruption: Importance of Comparative Endocrinology, Endocrinology, Volume 149, Issue 9, 1 September 2008, Pages 4267–4268, https://doi.org/10.1210/en.2008-0736
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Recognition in the late 1980s that environmental contaminants possess hormone-like activity was a major advance (1) that has since captured the attention of scientists, industry, government regulators, policy specialists, and nongovernment organizations around the globe. Governments have responded with research programs designed to address the endocrine disruption hypothesis with the result that significant research resources have been directed toward this issue. Not surprisingly, the endocrine disruption literature continues to expand along with increasing calls from nongovernment organizations for government regulation and bans on the manufacture of suspect chemicals. However, the potential for adverse health effects in the human population, together with the socioeconomic implications and the cost to industry, make it vital that governments and industry undertake the necessary research to ensure that regulatory decisions are evidence based and delivered in a timely manner.
Adverse health effects in the human population thought to be linked to exposure to environmental contaminants with hormone-like activity include but are not limited to: increased prevalence of cryptorchidism and hypospadias (2); testicular (3), breast (4), and prostate cancer (5); endometriosis (6); polycystic ovarian syndrome (7); and declines in semen quality (8, 9). Of these health outcomes, the strength of the association is best for developmental abnormalities of the male reproductive tract, leading to the proposal of the testicular dysgenesis syndrome (10); however, this hypothesis needs to be tested. Nevertheless, there is an ever-expanding list of chemicals that have been found to bind with steroid receptors (estrogen and androgen) acting as either agonist or antagonist that activate the receptor and modify the expression of estrogen- and androgen-regulated genes in vitro and in vivo (11, 12). Tissue culture studies demonstrate that environmental contaminants can both increase the expression of steroidogenic enzymes such as steroid acute regulatory protein and aromatase (13, 14), as well as increase the expression of enzymes involved in the metabolism of gonadal steroids (15, 16). Furthermore, animal studies have demonstrated that exposure to chemicals with hormone-like activity change functional characteristics of steroid-dependent target tissues. Moreover, there is a growing body of evidence that shows that the developing organism is more sensitive to the potential adverse health effects resulting from exposure to endocrine toxicants (17). Of growing interest is the realization that hormone-like chemicals can program cells and thus affect endocrine function through epigenetic mechanisms (5, 18–21), effects that may persist across more than one generation. Finally, it is generally accepted that there are limitations in the translation of results from animal studies to humans. Overall, the weight of evidence for human health effects are thought to be weak to moderate (22), owing in part to inconsistencies in the epidemiological literature, lack of evidence documenting exposure, paucity of experimental data concerning mechanism of action, lack of suitable animal models for the outcome of interest such as testicular or prostate cancer, and limited evidence for the biological plausibility of the proposed hypothesis. Consequently, adverse health effects associated with exposure to hormonally active chemicals remain controversial and hotly debated.
