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Article ; Online: Evaluating endocrine disrupting chemicals: A perspective on the novel assessments in CLARITY-BPA.

Howdeshell, Kembra L / Beverly, Brandiese E J / Blain, Robyn B / Goldstone, Alexandra E / Hartman, Pamela A / Lemeris, Courtney R / Newbold, Retha R / Rooney, Andrew A / Bucher, John R

Birth defects research

2023 Volume 115, Issue 15, Page(s) 1345–1397

Abstract: Background: The Consortium Linking Academic and Regulatory Insights on Bisphenol A Toxicity (CLARITY-BPA) was a collaborative research effort to better link academic research with governmental guideline studies. This review explores the secondary goal ... ...

Abstract	Background: The Consortium Linking Academic and Regulatory Insights on Bisphenol A Toxicity (CLARITY-BPA) was a collaborative research effort to better link academic research with governmental guideline studies. This review explores the secondary goal of CLARITY-BPA: to identify endpoints or technologies from CLARITY-BPA and prior/concurrent literature from these laboratories that may enhance the capacity of rodent toxicity studies to detect endocrine disrupting chemicals (EDCs). Methods: A systematic literature search was conducted with search terms for BPA and the CLARITY-BPA participants. Relevant studies employed a laboratory rodent model and reported results on 1 of the 10 organs/organ systems evaluated in CLARITY-BPA (brain and behavior, cardiac, immune, mammary gland, ovary, penile function, prostate gland and urethra, testis and epididymis, thyroid hormone and metabolism, and uterus). Study design and findings were summarized, and a risk-of-bias assessment was conducted. Results: Several endpoints and methods were identified as potentially helpful to detect effects of EDCs. For example, molecular and quantitative morphological approaches were sensitive in detecting alterations in early postnatal development of the brain, ovary, and mammary glands. Hormone challenge studies mimicking human aging reported increased susceptibility of the prostate to disease following developmental BPA exposure. Statistical analyses for nonmonotonic dose responses, and computational approaches assessing multiple treatment-related outcomes concurrently in linked hormone-sensitive organ systems, reported effects at low BPA doses. Conclusions: This review provided an opportunity to evaluate the unique insights provided by nontraditional assessments in CLARITY-BPA to identify technologies and endpoints to enhance detection of EDCs in future studies.
MeSH term(s)	Male ; Female ; Humans ; Endocrine Disruptors/toxicity ; Organizations ; Benzhydryl Compounds/toxicity ; Phenols/toxicity
Chemical Substances	Endocrine Disruptors ; bisphenol A (MLT3645I99) ; Benzhydryl Compounds ; Phenols
Language	English
Publishing date	2023-08-30
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2104792-3
ISSN	2472-1727
ISSN (online)	2472-1727
DOI	10.1002/bdr2.2238
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Article ; Online: Developmental exposure to endocrine-disrupting chemicals programs for reproductive tract alterations and obesity later in life.

Newbold, Retha R

The American journal of clinical nutrition

2011 Volume 94, Issue 6 Suppl, Page(s) 1939S–1942S

Abstract: Many chemicals in the environment, especially those with estrogenic activity, are able to disrupt the programming of endocrine signaling pathways established during development; these chemicals are referred to as endocrine-disrupting chemicals. Altered ... ...

Abstract	Many chemicals in the environment, especially those with estrogenic activity, are able to disrupt the programming of endocrine signaling pathways established during development; these chemicals are referred to as endocrine-disrupting chemicals. Altered programming can result in numerous adverse consequences in estrogen-target tissues, some of which may not be apparent until later in life. For example, a wide variety of structural, functional, and cellular effects have been identified in reproductive tract tissues. In addition to well-documented reproductive changes, obesity and diabetes have joined the list of adverse effects that have been associated with developmental exposure to environmental estrogens and other endocrine-disrupting chemicals. Obesity is a significant public health problem reaching epidemic proportions worldwide. Experimental animal studies document an association of developmental exposure to environmental estrogens and obesity. For example, a murine model of perinatal exposure to diethylstilbestrol has proven useful in studying mechanisms involved in abnormal programming of differentiating estrogen-target tissues, including reproductive tract tissues and adipocytes. Other environmental estrogens, including the environmental contaminant bisphenol A, have also been linked to reproductive problems and obesity later in life. Epidemiology studies support similar findings in humans, as do studies of cells in culture. Together, these findings suggest new targets for abnormal programming by estrogenic chemicals and provide evidence supporting the scientific concept termed the developmental origins of adult disease. Furthermore, the association of environmental estrogens with obesity and diabetes expands the focus on these diseases from intervention or treatment to include prevention or avoidance of chemical modifiers, especially during critical windows of development.
MeSH term(s)	Adipocytes ; Animals ; Benzhydryl Compounds ; Diethylstilbestrol/toxicity ; Endocrine Disruptors/toxicity ; Environmental Exposure/adverse effects ; Environmental Pollutants/toxicity ; Epidemiologic Studies ; Estrogens/metabolism ; Estrogens, Non-Steroidal/toxicity ; Female ; Humans ; Models, Animal ; Obesity/epidemiology ; Obesity/etiology ; Phenols/toxicity ; Pregnancy ; Prenatal Exposure Delayed Effects ; Prevalence ; Public Health ; Reproduction/drug effects
Chemical Substances	Benzhydryl Compounds ; Endocrine Disruptors ; Environmental Pollutants ; Estrogens ; Estrogens, Non-Steroidal ; Phenols ; Diethylstilbestrol (731DCA35BT) ; bisphenol A (MLT3645I99)
Language	English
Publishing date	2011-11-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	280048-2
ISSN	1938-3207 ; 0002-9165
ISSN (online)	1938-3207
ISSN	0002-9165
DOI	10.3945/ajcn.110.001057
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Article: Impact of environmental endocrine disrupting chemicals on the development of obesity.

Newbold, Retha R

Hormones (Athens, Greece)

2010 Volume 9, Issue 3, Page(s) 206–217

Abstract: Environmental chemicals with hormone-like activity can disrupt programming of endocrine signaling pathways during development and result in adverse effects, some of which may not be apparent until much later in life. Recent reports link exposure to ... ...

Abstract	Environmental chemicals with hormone-like activity can disrupt programming of endocrine signaling pathways during development and result in adverse effects, some of which may not be apparent until much later in life. Recent reports link exposure to environmental endocrine disrupting chemicals during development with adverse health consequences, including obesity and diabetes. These particular diseases are quickly becoming significant public health problems and are fast reaching epidemic proportions worldwide. This review summarizes data from experimental animals and humans which support an association of endocrine disrupting chemicals, such as diethylstilbestrol, bisphenol A, phytoestrogens, phthalates, and organotins, with the development of obesity. Potential mechanisms are summarized and future research needs are discussed.
MeSH term(s)	Animals ; Endocrine Disruptors/adverse effects ; Environmental Pollutants/adverse effects ; Humans ; Obesity/chemically induced ; Obesity/physiopathology ; Risk Assessment ; Risk Factors ; Weight Gain/drug effects
Chemical Substances	Endocrine Disruptors ; Environmental Pollutants
Language	English
Publishing date	2010-08-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2075912-5
ISSN	1109-3099
ISSN	1109-3099
DOI	10.14310/horm.2002.1271
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Article ; Online: Prenatal exposure to diethylstilbestrol (DES).

Newbold, Retha R

Fertility and sterility

2008 Volume 89, Issue 2 Suppl, Page(s) e55–6

MeSH term(s)	Animals ; Diethylstilbestrol/adverse effects ; Estrogens, Non-Steroidal/adverse effects ; Female ; Genital Neoplasms, Female/chemically induced ; Humans ; Pregnancy ; Prenatal Exposure Delayed Effects/chemically induced
Chemical Substances	Estrogens, Non-Steroidal ; Diethylstilbestrol (731DCA35BT)
Language	English
Publishing date	2008-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	80133-1
ISSN	1556-5653 ; 0015-0282
ISSN (online)	1556-5653
ISSN	0015-0282
DOI	10.1016/j.fertnstert.2008.01.062
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Zs.A 73: Show issues

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Article: THE DIABETES EPIDEMIC: Environmental Chemical Exposure in Etiology and Treatment.

Sargis, Robert M / Howard, Sarah G / Newbold, Retha R / Heindel, Jerrold J

San Francisco medicine

2014 Volume 85, Issue 5, Page(s) 18–20

Language	English
Publishing date	2014-03-04
Publishing country	United States
Document type	Journal Article
ISSN	0361-705X
ISSN	0361-705X
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Article: Developmental exposure to endocrine-disrupting chemicals programs for reproductive tract alterations and obesity later in life

Newbold, Retha R

American journal of clinical nutrition. 2011 Dec., v. 94, no. 6

2011

Abstract	Many chemicals in the environment, especially those with estrogenic activity, are able to disrupt the programming of endocrine signaling pathways established during development; these chemicals are referred to as endocrine-disrupting chemicals. Altered programming can result in numerous adverse consequences in estrogen-target tissues, some of which may not be apparent until later in life. For example, a wide variety of structural, functional, and cellular effects have been identified in reproductive tract tissues. In addition to well-documented reproductive changes, obesity and diabetes have joined the list of adverse effects that have been associated with developmental exposure to environmental estrogens and other endocrine-disrupting chemicals. Obesity is a significant public health problem reaching epidemic proportions worldwide. Experimental animal studies document an association of developmental exposure to environmental estrogens and obesity. For example, a murine model of perinatal exposure to diethylstilbestrol has proven useful in studying mechanisms involved in abnormal programming of differentiating estrogen-target tissues, including reproductive tract tissues and adipocytes. Other environmental estrogens, including the environmental contaminant bisphenol A, have also been linked to reproductive problems and obesity later in life. Epidemiology studies support similar findings in humans, as do studies of cells in culture. Together, these findings suggest new targets for abnormal programming by estrogenic chemicals and provide evidence supporting the scientific concept termed the developmental origins of adult disease. Furthermore, the association of environmental estrogens with obesity and diabetes expands the focus on these diseases from intervention or treatment to include prevention or avoidance of chemical modifiers, especially during critical windows of development.
Keywords	adverse effects ; bisphenol A ; cell culture ; diabetes ; diethylstilbestrol ; endocrine-disrupting chemicals ; environmental exposure ; epidemiological studies ; estrogenic properties ; exposure models ; humans ; laboratory animals ; obesity ; pollution ; public health
Language	English
Dates of publication	2011-12
Size	p. 1939S-1942S.
Publishing place	American Society for Clinical Nutrition
Document type	Article
ZDB-ID	280048-2
ISSN	1938-3207 ; 0002-9165
ISSN (online)	1938-3207
ISSN	0002-9165
Database	NAL-Catalogue (AGRICOLA)

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Z 72/516: Show issues

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Article: Developmental exposure to endocrine-disrupting chemicals programs for reproductive tract alterations and obesity later in life

Newbold, Retha R

American journal of clinical nutrition. 2011 Dec., v. 94, no. 6_Suppl

2011

Abstract	Many chemicals in the environment, especially those with estrogenic activity, are able to disrupt the programming of endocrine signaling pathways established during development; these chemicals are referred to as endocrine-disrupting chemicals. Altered programming can result in numerous adverse consequences in estrogen-target tissues, some of which may not be apparent until later in life. For example, a wide variety of structural, functional, and cellular effects have been identified in reproductive tract tissues. In addition to well-documented reproductive changes, obesity and diabetes have joined the list of adverse effects that have been associated with developmental exposure to environmental estrogens and other endocrine-disrupting chemicals. Obesity is a significant public health problem reaching epidemic proportions worldwide. Experimental animal studies document an association of developmental exposure to environmental estrogens and obesity. For example, a murine model of perinatal exposure to diethylstilbestrol has proven useful in studying mechanisms involved in abnormal programming of differentiating estrogen-target tissues, including reproductive tract tissues and adipocytes. Other environmental estrogens, including the environmental contaminant bisphenol A, have also been linked to reproductive problems and obesity later in life. Epidemiology studies support similar findings in humans, as do studies of cells in culture. Together, these findings suggest new targets for abnormal programming by estrogenic chemicals and provide evidence supporting the scientific concept termed the developmental origins of adult disease. Furthermore, the association of environmental estrogens with obesity and diabetes expands the focus on these diseases from intervention or treatment to include prevention or avoidance of chemical modifiers, especially during critical windows of development.
Keywords	adult development ; adverse effects ; bisphenol A ; cell culture ; chemical risk assessment ; developmental stages ; diabetes ; diethylstilbestrol ; endocrine-disrupting chemicals ; environmental exposure ; epidemiological studies ; estrogenic properties ; exposure models ; health effects assessments ; humans ; laboratory animals ; maternal-fetal transfer ; obesity ; perinatal period ; pollution ; public health
Language	English
Dates of publication	2011-12
Size	p. 1939S-1942S.
Publishing place	American Society for Clinical Nutrition
Document type	Article
ZDB-ID	280048-2
ISSN	1938-3207 ; 0002-9165
ISSN (online)	1938-3207
ISSN	0002-9165
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Lou Guillette--in memorandum.

Heindel, Jerrold J / Newbold, Retha R / Williams, Carmen J / Iguchi, Taisen / Tyler, Charles R

Molecular reproduction and development

2015 Volume 82, Issue 10, Page(s) Fmi–v

MeSH term(s)	Ecology/history ; History, 20th Century ; History, 21st Century ; Marine Biology/history ; Obstetrics/history ; Science/history ; United States
Language	English
Publishing date	2015-10
Publishing country	United States
Document type	Historical Article ; Journal Article ; Portraits
ZDB-ID	20321-x
ISSN	1098-2795 ; 1040-452X
ISSN (online)	1098-2795
ISSN	1040-452X
DOI	10.1002/mrd.22587
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Zs.A 2759: Show issues

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Article: Lessons learned from perinatal exposure to diethylstilbestrol.

Newbold, Retha R

Toxicology and applied pharmacology

2004 Volume 199, Issue 2, Page(s) 142–150

Abstract: The synthetic estrogen diethylstilbestrol (DES) is well documented to be a perinatal carcinogen in both humans and experimental animals. Exposure to DES during critical periods of differentiation permanently alters the programming of estrogen target ... ...

Abstract	The synthetic estrogen diethylstilbestrol (DES) is well documented to be a perinatal carcinogen in both humans and experimental animals. Exposure to DES during critical periods of differentiation permanently alters the programming of estrogen target tissues resulting in benign and malignant abnormalities in the reproductive tract later in life. Using the perinatal DES-exposed rodent model, cellular and molecular mechanisms have been identified that play a role in these carcinogenic effects. Although DES is a potent estrogenic chemical, effects of low doses of the compound are being used to predict health risks of weaker environmental estrogens. Therefore, it is of particular interest that developmental exposure to very low doses of DES has been found to adversely affect fertility and to increase tumor incidence in murine reproductive tract tissues. These adverse effects are seen at environmentally relevant estrogen dose levels. New studies from our lab verify that DES effects are not unique; when numerous environmental chemicals with weak estrogenic activity are tested in the experimental neonatal mouse model, developmental exposure results in an increased incidence of benign and malignant tumors including uterine leiomyomas and adenocarcinomas that are similar to those shown following DES exposure. Finally, growing evidence in experimental animals suggests that some adverse effects can be passed on to subsequent generations, although the mechanisms involved in these trans-generational events remain unknown. Although the complete spectrum of risks to DES-exposed humans are uncertain at this time, the scientific community continues to learn more about cellular and molecular mechanisms by which perinatal carcinogenesis occurs. These advances in knowledge of both genetic and epigenetic mechanisms will be significant in ultimately predicting risks to other environmental estrogens and understanding more about the role of estrogens in normal and abnormal development.
MeSH term(s)	Adult ; Animals ; Animals, Newborn/physiology ; Carcinogens ; Diethylstilbestrol/adverse effects ; Diethylstilbestrol/history ; Diethylstilbestrol/toxicity ; Environmental Exposure ; Estradiol Congeners/adverse effects ; Female ; History, 20th Century ; Humans ; Neoplasms/chemically induced ; Neoplasms/epidemiology ; Pregnancy ; Prenatal Exposure Delayed Effects ; Risk Assessment
Chemical Substances	Carcinogens ; Estradiol Congeners ; Diethylstilbestrol (731DCA35BT)
Language	English
Publishing date	2004-09-01
Publishing country	United States
Document type	Historical Article ; Journal Article ; Review
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1016/j.taap.2003.11.033
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Article ; Online: The Conflict between Regulatory Agencies over the 20,000-Fold Lowering of the Tolerable Daily Intake (TDI) for Bisphenol A (BPA) by the European Food Safety Authority (EFSA).

Vom Saal, Frederick S / Antoniou, Michael / Belcher, Scott M / Bergman, Ake / Bhandari, Ramji K / Birnbaum, Linda S / Cohen, Aly / Collins, Terrence J / Demeneix, Barbara / Fine, Anne Marie / Flaws, Jodi A / Gayrard, Veronique / Goodson, William H / Gore, Andrea C / Heindel, Jerrold J / Hunt, Patricia A / Iguchi, Taisen / Kassotis, Christopher D / Kortenkamp, Andreas /

Environmental health perspectives

2024 Volume 132, Issue 4, Page(s) 45001

Abstract: Background: The European Food Safety Authority (EFSA) recommended lowering their estimated tolerable daily intake (TDI) for bisphenol A (BPA) 20,000-fold to : Objectives: We identify the flaws in the assumptions that the German BfR, as well as the ... ...

Abstract	Background: The European Food Safety Authority (EFSA) recommended lowering their estimated tolerable daily intake (TDI) for bisphenol A (BPA) 20,000-fold to Objectives: We identify the flaws in the assumptions that the German BfR, as well as the FDA, have used to justify maintaining the TDI for BPA at levels above what a vast amount of academic research shows to cause harm. We argue that regulatory agencies need to incorporate 21st century science into chemical hazard identifications using the CLARITY-BPA (Consortium Linking Academic and Regulatory Insights on BPA Toxicity) nonguideline academic studies in a collaborative government-academic program model. Discussion: We strongly endorse EFSA's revised TDI for BPA and support the European Commission's (EC) apparent acceptance of this updated BPA risk assessment. We discuss challenges to current chemical risk assessment assumptions about EDCs that need to be addressed by regulatory agencies to, in our opinion, become truly protective of public health. Addressing these challenges will hopefully result in BPA, and eventually other structurally similar bisphenols (called regrettable substitutions) for which there are known adverse effects, being eliminated from all food-related and many other uses in the EU and elsewhere. https://doi.org/10.1289/EHP13812.
MeSH term(s)	Humans ; Benzhydryl Compounds ; Food Safety ; No-Observed-Adverse-Effect Level ; Phenols ; Systematic Reviews as Topic
Chemical Substances	Benzhydryl Compounds ; bisphenol A (MLT3645I99) ; Phenols
Language	English
Publishing date	2024-04-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	195189-0
ISSN	1552-9924 ; 0091-6765 ; 1078-0475
ISSN (online)	1552-9924
ISSN	0091-6765 ; 1078-0475
DOI	10.1289/EHP13812
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