Bisphenol-A and the Great Divide: A Review of Controversies in the Field of Endocrine Disruption

被引:1078
作者
Vandenberg, Laura N. [1 ]
Maffini, Maricel V. [1 ]
Sonnenschein, Carlos [1 ]
Rubin, Beverly S. [1 ]
Soto, Ana M. [1 ]
机构
[1] Tufts Univ, Sch Med, Dept Anat & Cellular Biol, Boston, MA 02111 USA
关键词
MEMBRANE ESTROGEN-RECEPTOR; MAMMARY-GLAND DEVELOPMENT; PROSTATE-CANCER-CELLS; IN-UTERO EXPOSURE; PERINATAL EXPOSURE; GENE-EXPRESSION; FETAL EXPOSURE; ANDROGEN RECEPTOR; PRENATAL EXPOSURE; UDP-GLUCURONOSYLTRANSFERASE;
D O I
10.1210/er.2008-0021
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
In 1991, a group of 21 scientists gathered at the Wingspread Conference Center to discuss evidence of developmental alterations observed in wildlife populations after chemical exposures. There, the term "endocrine disruptor" was agreed upon to describe a class of chemicals including those that act as agonists and antagonists of the estrogen receptors (ERs), androgen receptor, thyroid hormone receptor, and others. This definition has since evolved, and the field has grown to encompass hundreds of chemicals. Despite significant advances in the study of endocrine disruptors, several controversies have sprung up and continue, including the debate over the existence of nonmonotonic dose response curves, the mechanisms of low-dose effects, and the importance of considering critical periods of exposure in experimental design. One chemical found ubiquitously in our environment, bisphenol-A (BPA), has received a tremendous amount of attention from research scientists, government panels, and the popular press. In this review, we have covered the above-mentioned controversies plus six additional issues that have divided scientists in the field of BPA research, namely: 1) mechanisms of BPA action; 2) levels of human exposure; 3) routes of human exposure; 4) pharmacokinetic models of BPA metabolism; 5) effects of BPA on exposed animals; and 6) links between BPA and cancer. Understanding these topics is essential for educating the public and medical professionals about potential risks associated with developmental exposure to BPA and other endocrine disruptors, the design of rigorously researched programs using both epidemiological and animal studies, and ultimately the development of a sound public health policy. (Endocrine Reviews 30: 75-95, 2009)
引用
收藏
页码:75 / 95
页数:21
相关论文
共 194 条
[81]   Thyroid hormone action is disrupted by bisphenol A as an antagonist [J].
Moriyama, K ;
Tagami, T ;
Akamizu, T ;
Usui, T ;
Saijo, M ;
Kanamoto, N ;
Hataya, Y ;
Shimatsu, A ;
Kuzuya, H ;
Nakao, K .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2002, 87 (11) :5185-5190
[82]   THE DEVELOPMENTAL TOXICITY OF BISPHENOL-A IN RATS AND MICE [J].
MORRISEY, RE ;
GEORGE, JD ;
PRICE, CJ ;
TYL, RW ;
MARR, MC ;
KIMMEL, CA .
FUNDAMENTAL AND APPLIED TOXICOLOGY, 1987, 8 (04) :571-582
[83]   Perinatal exposure to bisphenol-A alters peripubertal mammary gland development in mice [J].
Muñoz-de-Toro, M ;
Markey, CM ;
Wadia, PR ;
Luque, EH ;
Rubin, BS ;
Sonnenschein, C ;
Soto, AM .
ENDOCRINOLOGY, 2005, 146 (09) :4138-4147
[84]   Induction of mammary gland ductal hyperplasias and carcinoma in situ following fetal bisphenol A exposure [J].
Murray, Tessa J. ;
Maffini, Maricel V. ;
Ucci, Angelo A. ;
Sonnenschein, Carlos ;
Soto, Ana M. .
REPRODUCTIVE TOXICOLOGY, 2007, 23 (03) :383-390
[85]   Why Public Health Agencies Cannot Depend on Good Laboratory Practices as a Criterion for Selecting Data: The Case of Bisphenol A [J].
Myers, John Peterson ;
vom Saal, Frederick S. ;
Akingbemi, Benson T. ;
Arizono, Koji ;
Belcher, Scoff ;
Colborn, Theo ;
Chahoud, Ibrahim ;
Crain, D. Andrew ;
Farabollini, Francesca ;
Guilleffe, Louis J., Jr. ;
Hassold, Terry ;
Ho, Shuk-mei ;
Hunt, Patricia A. ;
Iguchi, Taisen ;
Jobling, Susan ;
Kanno, Jun ;
Laufer, Hans ;
Marcus, Michele ;
McLachlan, John A. ;
Nadal, Angel ;
Oehlmann, Joerg ;
Olea, Nicolas ;
Palanza, Paola ;
Parmigiani, Stefano ;
Rubin, Beverly S. ;
Schoenfelder, Gilbert ;
Sonnenschein, Carlos ;
Soto, Ana M. ;
Taisness, Chris E. ;
Taylor, Julia A. ;
Vandenberg, Laura N. ;
Vandenbergh, John G. ;
Vogel, Sarah ;
Watson, Cheryl S. ;
Welshons, Wade V. ;
Zoeller, R. Thomas .
ENVIRONMENTAL HEALTH PERSPECTIVES, 2009, 117 (03) :309-315
[86]   Fecal bacterial enzyme activities in infants increase with age and adoption of adult-type diet [J].
Mykkanen, H ;
Tikka, J ;
Pitkanen, T ;
Hanninen, O .
JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION, 1997, 25 (03) :312-316
[87]   Gene expression profile induced by 17α-ethynyl estradiol, bisphenol A, and genistein in the developing female reproductive system of the rat [J].
Naciff, JM ;
Jump, ML ;
Torontalli, SM ;
Carr, GJ ;
Tiesman, JP ;
Overmann, GJ ;
Daston, GP .
TOXICOLOGICAL SCIENCES, 2002, 68 (01) :184-199
[88]   Disentangling the molecular mechanisms of action of endogenous and environmental estrogens [J].
Nadal, A ;
Alonso-Magdalena, P ;
Ripoll, C ;
Fuentes, E .
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 2005, 449 (04) :335-343
[89]   Developmental effects of estrogenic chemicals are predicted by an in vitro assay incorporating modification of cell uptake by serum [J].
Nagel, SC ;
vom Saal, FS ;
Welshons, WV .
JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY, 1999, 69 (1-6) :343-357
[90]   HORMONES AND MAMMARY CARCINOGENESIS IN MICE, RATS, AND HUMANS - A UNIFYING HYPOTHESIS [J].
NANDI, S ;
GUZMAN, RC ;
YANG, J .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (09) :3650-3657