Is It Time to End Concerns over the Estrogenic Effects of Bisphenol A?

Medical Research Council Human Reproductive Sciences Unit, Centre for Reproductive Biology, The Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK.
Toxicological Sciences (Impact Factor: 3.85). 03/2010; 114(1):1-4. DOI: 10.1093/toxsci/kfp299
Source: PubMed
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    • "At present, there is a strong controversy regarding the adverse reproductive effects of xenoestrogen BPA in humans and animals. Recently, based on analysis of data obtained by Ryan et al.137 and others138139 that focused on the investigation of estrogenic effects of BPA; Sharpe concluded that BPA, at doses considerably higher than human exposure levels, does not reliably affect the parameters of development and function in male or female rats/mice that are estrogen sensitive.140 It has been further suggested that BPA could contribute to the additive effects of the mixture of estrogenic chemicals to which humans can be exposed,141 but the low estrogenic potency of BPA in vivo through oral exposure and the low levels of exposure in the general population suggest that its contribution to mixed estrogenic effects is minimal.140142 "
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    ABSTRACT: During the past few decades, scientific evidence has been accumulated concerning the possible adverse effects of the exposure to environmental chemicals on the well-being of wildlife and human populations. One large and growing group of such compounds of anthropogenic or natural origin is referred to as endocrine-disrupting chemicals (EDCs), due to their deleterious action on the endocrine system. This concern was first focused on the control of reproductive function particularly in males, but has later been expanded to include all possible endocrine functions. The present review describes the underlying physiology behind the cascade of developmental events that occur during sexual differentiation of males and the specific role of androgen in the masculinization process and proper organogenesis of the external male genitalia. The impact of the genetic background, environmental exposures and lifestyle factors in the etiology of hypospadias, cryptorchidism and testicular cancer are reviewed and the possible role of EDCs in the development of these reproductive disorders is discussed critically. Finally, the possible direct and programming effects of exposures in utero to widely use therapeutic compounds, environmental estrogens and other chemicals on the incidence of reproductive abnormalities and poor semen quality in humans are also highlighted.
    Asian Journal of Andrology 01/2014; 16(1):50-9. DOI:10.4103/1008-682X.122199 · 2.60 Impact Factor
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    • "Regarding EDs, aspects of hazard evaluation and applicability of the established risk assessment process have been questioned and are the subject of a strong debate within the scientific community (Ashby, 2003; Welshons et al., 2003; Phillips et al., 2008; Rhomberg and Goodman, 2012; Sharpe, 2010b; Vandenberg et al., 2009, 2012; vom Saal et al., 2010; Zoeller et al., 2012). The major points are related to the hypothesis that ED could (or not) (i) act with a non-threshold mechanism, (ii) give rise to a non-monotonic dose–response (NMDR) relationship, and (iii) at very low doses, particularly during critical windows of exposure. "
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    ABSTRACT: Some recent EU Regulations have focused on the potential risks posed by the presence of Endocrine Disrupters (ED) into the environment. However there are conflicting opinions on how to assess the risk from exposure to these molecules that can reversibly modulate hormonal activity, Endocrine Active Substances (EAS) rather than causing irreversible damage (ED).The present paper attempts to discuss that perturbation of normal endocrine homeostasis in itself may not be an adverse effect, since the endocrine system is naturally dynamic and responsive to various stimuli as part of its normal function and it is modulated according to the characteristic trend of the dose response curve.EDs should be evaluated using a weight-of-evidence (WoE) approach. If a chemical meets the criteria to be defined as an ED in experimental animals, the relevance of observed effects to the human then needs to be addressed.Hazard-based risk management is therefore not justified since does not meet the criteria for a sound scientifically-based assessment.
    Toxicology 08/2013; 314(1). DOI:10.1016/j.tox.2013.07.018 · 3.62 Impact Factor
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    • "Our comments below are a direct response to this particular review, but it should be noted that they also pertain more broadly to several earlier publications that have argued for the theory of low-dose nonmonotonicity of endocrine-mediated effects (e.g., vom Saal et al., 2007). These earlier arguments have drawn their own responses (e.g., Sharpe, 2010; Goodman et al., 2009). "
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    ABSTRACT: Vandenberg et al. (2012) claim that "most if not all [endocrine-disrupting chemicals (EDCs)] are likely to have low-dose effects" and "nonmonotonicity is a common occurrence after exposures to hormones and EDCs in cell culture and animals and across human populations." They present examples as anecdotes without attempting to review all available pertinent data, selectively citing studies without evaluating most of them or examining whether their putative examples are consistent and coherent with other relevant information. They assume that any statistically significant association indicates causation of an adverse effect, and their limited evaluation of specific studies is not done uniformly (i.e., studies with positive results are evaluated differently than those with null results). They also do not evaluate whether exposures in studies are truly "low-dose" and relevant to humans. They propose a number of different nonmonotonic dose-response curves, but do not consider reasons for why they should be expected to apply generally across species. Many of their examples would be - and indeed have been - questioned by many scientists. Overall, Vandenberg et al. put forth many asserted illustrations of their two conclusions without providing sufficient evidence to make the case for either and while overlooking evidence that suggests the contrary.
    Regulatory Toxicology and Pharmacology 06/2012; 64(1):130-3. DOI:10.1016/j.yrtph.2012.06.015 · 2.03 Impact Factor
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