EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals

A. C. Gore, V. A. Chappell, S. E. Fenton, Jodi A Flaws, A. Nadal, G. S. Prins, J. Toppari, R. T. Zoeller

Research output: Contribution to journalReview article

Abstract

The Endocrine Society's first Scientific Statement in 2009 provided a wake-up call to the scientific community abouthow environmental endocrine-disrupting chemicals (EDCs) affect health and disease. Five years later, a substantially larger body of literature has solidified our understanding of plausible mechanisms underlying EDC actions and how exposures in animals and humans-especially during development-may lay the foundations for disease later in life. At this point in history, we have much stronger knowledge about how EDCs alter gene-environment interactions via physiological, cellular, molecular, andepigeneticchanges, therebyproducingeffects inexposedindividuals as well as theirdescendants. Causal links between exposure and manifestation of disease are substantiated by experimental animal models and are consistent with correlative epidemiological data in humans. There are several caveats because differences in how experimental animal work is conducted can lead to difficulties in drawing broad conclusions, and we must continue to be cautious about inferring causality in humans. In this second Scientific Statement, we reviewed the literature on a subset of topics for which the translational evidence is strongest: 1) obesity and diabetes; 2) female reproduction; 3) male reproduction; 4) hormone-sensitive cancers in females; 5) prostate; 6) thyroid; and 7) neurodevelopment and neuroendocrine systems. Our inclusion criteria for studies were those conducted predominantly in the past 5 years deemed to be of high quality based on appropriate negative and positive control groups or populations, adequate sample size and experimental design, and mammalian animal studies with exposure levels in arange that was relevant to humans. We also focused on studies using the developmental origins of health and disease model. No report was excluded based on a positive or negative effect of the EDC exposure. The bulk of the results across the board strengthen the evidence for endocrine health-related actions of EDCs. Based on this much more complete understanding of the endocrine principles by which EDCs act, including nonmonotonic dose-responses, low-dose effects, and developmental vulnerability, these findings canbemuchbetter translated tohumanhealth. Armedwith this information, researchers, physicians, andother healthcare providers can guide regulators and policymakers as they make responsible decisions.

Original languageEnglish (US)
Pages (from-to)1-150
Number of pages150
JournalEndocrine reviews
Volume36
Issue number6
DOIs
StatePublished - Jan 1 2015

Fingerprint

Endocrine Disruptors
Reproduction
Health
Pharmacologic Actions
Gene-Environment Interaction
Neurosecretory Systems
Causality
Health Personnel
Sample Size
Prostate
Thyroid Gland
Research Design
Animal Models
Obesity
History
Research Personnel
Hormones
Physicians
Control Groups
Population

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Gore, A. C., Chappell, V. A., Fenton, S. E., Flaws, J. A., Nadal, A., Prins, G. S., ... Zoeller, R. T. (2015). EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals. Endocrine reviews, 36(6), 1-150. https://doi.org/10.1210/er.2015-1010

EDC-2 : The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals. / Gore, A. C.; Chappell, V. A.; Fenton, S. E.; Flaws, Jodi A; Nadal, A.; Prins, G. S.; Toppari, J.; Zoeller, R. T.

In: Endocrine reviews, Vol. 36, No. 6, 01.01.2015, p. 1-150.

Research output: Contribution to journalReview article

Gore, AC, Chappell, VA, Fenton, SE, Flaws, JA, Nadal, A, Prins, GS, Toppari, J & Zoeller, RT 2015, 'EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals', Endocrine reviews, vol. 36, no. 6, pp. 1-150. https://doi.org/10.1210/er.2015-1010
Gore, A. C. ; Chappell, V. A. ; Fenton, S. E. ; Flaws, Jodi A ; Nadal, A. ; Prins, G. S. ; Toppari, J. ; Zoeller, R. T. / EDC-2 : The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals. In: Endocrine reviews. 2015 ; Vol. 36, No. 6. pp. 1-150.
@article{a993b9f29a8b466d89aeb1f03c9f1173,
title = "EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals",
abstract = "The Endocrine Society's first Scientific Statement in 2009 provided a wake-up call to the scientific community abouthow environmental endocrine-disrupting chemicals (EDCs) affect health and disease. Five years later, a substantially larger body of literature has solidified our understanding of plausible mechanisms underlying EDC actions and how exposures in animals and humans-especially during development-may lay the foundations for disease later in life. At this point in history, we have much stronger knowledge about how EDCs alter gene-environment interactions via physiological, cellular, molecular, andepigeneticchanges, therebyproducingeffects inexposedindividuals as well as theirdescendants. Causal links between exposure and manifestation of disease are substantiated by experimental animal models and are consistent with correlative epidemiological data in humans. There are several caveats because differences in how experimental animal work is conducted can lead to difficulties in drawing broad conclusions, and we must continue to be cautious about inferring causality in humans. In this second Scientific Statement, we reviewed the literature on a subset of topics for which the translational evidence is strongest: 1) obesity and diabetes; 2) female reproduction; 3) male reproduction; 4) hormone-sensitive cancers in females; 5) prostate; 6) thyroid; and 7) neurodevelopment and neuroendocrine systems. Our inclusion criteria for studies were those conducted predominantly in the past 5 years deemed to be of high quality based on appropriate negative and positive control groups or populations, adequate sample size and experimental design, and mammalian animal studies with exposure levels in arange that was relevant to humans. We also focused on studies using the developmental origins of health and disease model. No report was excluded based on a positive or negative effect of the EDC exposure. The bulk of the results across the board strengthen the evidence for endocrine health-related actions of EDCs. Based on this much more complete understanding of the endocrine principles by which EDCs act, including nonmonotonic dose-responses, low-dose effects, and developmental vulnerability, these findings canbemuchbetter translated tohumanhealth. Armedwith this information, researchers, physicians, andother healthcare providers can guide regulators and policymakers as they make responsible decisions.",
author = "Gore, {A. C.} and Chappell, {V. A.} and Fenton, {S. E.} and Flaws, {Jodi A} and A. Nadal and Prins, {G. S.} and J. Toppari and Zoeller, {R. T.}",
year = "2015",
month = "1",
day = "1",
doi = "10.1210/er.2015-1010",
language = "English (US)",
volume = "36",
pages = "1--150",
journal = "Endocrine Reviews",
issn = "0163-769X",
publisher = "The Endocrine Society",
number = "6",

}

TY - JOUR

T1 - EDC-2

T2 - The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals

AU - Gore, A. C.

AU - Chappell, V. A.

AU - Fenton, S. E.

AU - Flaws, Jodi A

AU - Nadal, A.

AU - Prins, G. S.

AU - Toppari, J.

AU - Zoeller, R. T.

PY - 2015/1/1

Y1 - 2015/1/1

N2 - The Endocrine Society's first Scientific Statement in 2009 provided a wake-up call to the scientific community abouthow environmental endocrine-disrupting chemicals (EDCs) affect health and disease. Five years later, a substantially larger body of literature has solidified our understanding of plausible mechanisms underlying EDC actions and how exposures in animals and humans-especially during development-may lay the foundations for disease later in life. At this point in history, we have much stronger knowledge about how EDCs alter gene-environment interactions via physiological, cellular, molecular, andepigeneticchanges, therebyproducingeffects inexposedindividuals as well as theirdescendants. Causal links between exposure and manifestation of disease are substantiated by experimental animal models and are consistent with correlative epidemiological data in humans. There are several caveats because differences in how experimental animal work is conducted can lead to difficulties in drawing broad conclusions, and we must continue to be cautious about inferring causality in humans. In this second Scientific Statement, we reviewed the literature on a subset of topics for which the translational evidence is strongest: 1) obesity and diabetes; 2) female reproduction; 3) male reproduction; 4) hormone-sensitive cancers in females; 5) prostate; 6) thyroid; and 7) neurodevelopment and neuroendocrine systems. Our inclusion criteria for studies were those conducted predominantly in the past 5 years deemed to be of high quality based on appropriate negative and positive control groups or populations, adequate sample size and experimental design, and mammalian animal studies with exposure levels in arange that was relevant to humans. We also focused on studies using the developmental origins of health and disease model. No report was excluded based on a positive or negative effect of the EDC exposure. The bulk of the results across the board strengthen the evidence for endocrine health-related actions of EDCs. Based on this much more complete understanding of the endocrine principles by which EDCs act, including nonmonotonic dose-responses, low-dose effects, and developmental vulnerability, these findings canbemuchbetter translated tohumanhealth. Armedwith this information, researchers, physicians, andother healthcare providers can guide regulators and policymakers as they make responsible decisions.

AB - The Endocrine Society's first Scientific Statement in 2009 provided a wake-up call to the scientific community abouthow environmental endocrine-disrupting chemicals (EDCs) affect health and disease. Five years later, a substantially larger body of literature has solidified our understanding of plausible mechanisms underlying EDC actions and how exposures in animals and humans-especially during development-may lay the foundations for disease later in life. At this point in history, we have much stronger knowledge about how EDCs alter gene-environment interactions via physiological, cellular, molecular, andepigeneticchanges, therebyproducingeffects inexposedindividuals as well as theirdescendants. Causal links between exposure and manifestation of disease are substantiated by experimental animal models and are consistent with correlative epidemiological data in humans. There are several caveats because differences in how experimental animal work is conducted can lead to difficulties in drawing broad conclusions, and we must continue to be cautious about inferring causality in humans. In this second Scientific Statement, we reviewed the literature on a subset of topics for which the translational evidence is strongest: 1) obesity and diabetes; 2) female reproduction; 3) male reproduction; 4) hormone-sensitive cancers in females; 5) prostate; 6) thyroid; and 7) neurodevelopment and neuroendocrine systems. Our inclusion criteria for studies were those conducted predominantly in the past 5 years deemed to be of high quality based on appropriate negative and positive control groups or populations, adequate sample size and experimental design, and mammalian animal studies with exposure levels in arange that was relevant to humans. We also focused on studies using the developmental origins of health and disease model. No report was excluded based on a positive or negative effect of the EDC exposure. The bulk of the results across the board strengthen the evidence for endocrine health-related actions of EDCs. Based on this much more complete understanding of the endocrine principles by which EDCs act, including nonmonotonic dose-responses, low-dose effects, and developmental vulnerability, these findings canbemuchbetter translated tohumanhealth. Armedwith this information, researchers, physicians, andother healthcare providers can guide regulators and policymakers as they make responsible decisions.

UR - http://www.scopus.com/inward/record.url?scp=84983150574&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84983150574&partnerID=8YFLogxK

U2 - 10.1210/er.2015-1010

DO - 10.1210/er.2015-1010

M3 - Review article

C2 - 26544531

AN - SCOPUS:84983150574

VL - 36

SP - 1

EP - 150

JO - Endocrine Reviews

JF - Endocrine Reviews

SN - 0163-769X

IS - 6

ER -