Life-Long Implications of Developmental Exposure to Environmental Stressors: New Perspectives
The Developmental Origins of Health and Disease (DOHaD) paradigm is one of the most rapidly expanding areas of biomedical research. Environmental stressors that can impact on DOHaD encompass a variety of environmental and occupational hazards as well as deficiency and oversupply of nutrients and ene...
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creator | Grandjean, Philippe Barouki, Robert Bellinger, David C Casteleyn, Ludwine Chadwick, Lisa H Cordier, Sylvaine Etzel, Ruth A Gray, Kimberly A Ha, Eun-Hee Junien, Claudine Karagas, Margaret Kawamoto, Toshihiro Paige Lawrence, B Perera, Frederica P Prins, Gail S Puga, Alvaro Rosenfeld, Cheryl S Sherr, David H Sly, Peter D Suk, William Sun, Qi Toppari, Jorma van den Hazel, Peter Walker, Cheryl L Heindel, Jerrold J |
description | The Developmental Origins of Health and Disease (DOHaD) paradigm is one of the most rapidly expanding areas of biomedical research. Environmental stressors that can impact on DOHaD encompass a variety of environmental and occupational hazards as well as deficiency and oversupply of nutrients and energy. They can disrupt early developmental processes and lead to increased susceptibility to disease/dysfunctions later in life. Presentations at the fourth Conference on Prenatal Programming and Toxicity in Boston, in October 2014, provided important insights and led to new recommendations for research and public health action. The conference highlighted vulnerable exposure windows that can occur as early as the preconception period and epigenetics as a major mechanism than can lead to disadvantageous “reprogramming” of the genome, thereby potentially resulting in transgenerational effects. Stem cells can also be targets of environmental stressors, thus paving another way for effects that may last a lifetime. Current testing paradigms do not allow proper characterization of risk factors and their interactions. Thus, relevant exposure levels and combinations for testing must be identified from human exposure situations and outcome assessments. Testing of potential underpinning mechanisms and biomarker development require laboratory animal models and in vitro approaches. Only few large-scale birth cohorts exist, and collaboration between birth cohorts on a global scale should be facilitated. DOHaD-based research has a crucial role in establishing factors leading to detrimental outcomes and developing early preventative/remediation strategies to combat these risks. |
doi_str_mv | 10.1210/EN.2015-1350 |
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Environmental stressors that can impact on DOHaD encompass a variety of environmental and occupational hazards as well as deficiency and oversupply of nutrients and energy. They can disrupt early developmental processes and lead to increased susceptibility to disease/dysfunctions later in life. Presentations at the fourth Conference on Prenatal Programming and Toxicity in Boston, in October 2014, provided important insights and led to new recommendations for research and public health action. The conference highlighted vulnerable exposure windows that can occur as early as the preconception period and epigenetics as a major mechanism than can lead to disadvantageous “reprogramming” of the genome, thereby potentially resulting in transgenerational effects. Stem cells can also be targets of environmental stressors, thus paving another way for effects that may last a lifetime. Current testing paradigms do not allow proper characterization of risk factors and their interactions. Thus, relevant exposure levels and combinations for testing must be identified from human exposure situations and outcome assessments. Testing of potential underpinning mechanisms and biomarker development require laboratory animal models and in vitro approaches. Only few large-scale birth cohorts exist, and collaboration between birth cohorts on a global scale should be facilitated. DOHaD-based research has a crucial role in establishing factors leading to detrimental outcomes and developing early preventative/remediation strategies to combat these risks.</description><identifier>ISSN: 0013-7227</identifier><identifier>ISSN: 1945-7170</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/EN.2015-1350</identifier><identifier>PMID: 26241067</identifier><language>eng</language><publisher>Washington, DC: Endocrine Society</publisher><subject>Animal models ; Biocompatibility ; Biomarkers ; Boston ; Consensus Statement ; Embryology - methods ; Endocrinology ; Environmental Exposure ; Environmental stress ; Epigenesis, Genetic ; Epigenetics ; Epigenomics ; Exposure ; Female ; Health hazards ; Humans ; Laboratory animals ; Life Sciences ; Male ; Maternal Exposure ; Medical research ; Nutrients ; Obesity - etiology ; Occupational exposure ; Occupational hazards ; Placenta - metabolism ; Pregnancy ; Prenatal experience ; Prenatal Exposure Delayed Effects ; Public health ; Risk Factors ; Stem cells ; Stem Cells - cytology ; Stress, Psychological ; Telomere - ultrastructure ; Toxic hazards ; Toxicity</subject><ispartof>Endocrinology (Philadelphia), 2015-10, Vol.156 (10), p.3408-3415</ispartof><rights>Copyright © 2015 by the Endocrine Society</rights><rights>Copyright © 2016 by the Endocrine Society 2016</rights><rights>Copyright © 2016 by the Endocrine Society</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>Copyright © 2015 by the Endocrine Society 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c631t-9d3f92d6f3f3a29156140b7f147d8019a595471aa47d308738ef073ebf29c1993</citedby><cites>FETCH-LOGICAL-c631t-9d3f92d6f3f3a29156140b7f147d8019a595471aa47d308738ef073ebf29c1993</cites><orcidid>0000-0001-9471-399X ; 0000-0002-2349-2277</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26241067$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://univ-rennes.hal.science/hal-01187409$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Grandjean, Philippe</creatorcontrib><creatorcontrib>Barouki, Robert</creatorcontrib><creatorcontrib>Bellinger, David C</creatorcontrib><creatorcontrib>Casteleyn, Ludwine</creatorcontrib><creatorcontrib>Chadwick, Lisa H</creatorcontrib><creatorcontrib>Cordier, Sylvaine</creatorcontrib><creatorcontrib>Etzel, Ruth A</creatorcontrib><creatorcontrib>Gray, Kimberly A</creatorcontrib><creatorcontrib>Ha, Eun-Hee</creatorcontrib><creatorcontrib>Junien, Claudine</creatorcontrib><creatorcontrib>Karagas, Margaret</creatorcontrib><creatorcontrib>Kawamoto, Toshihiro</creatorcontrib><creatorcontrib>Paige Lawrence, B</creatorcontrib><creatorcontrib>Perera, Frederica P</creatorcontrib><creatorcontrib>Prins, Gail S</creatorcontrib><creatorcontrib>Puga, Alvaro</creatorcontrib><creatorcontrib>Rosenfeld, Cheryl S</creatorcontrib><creatorcontrib>Sherr, David H</creatorcontrib><creatorcontrib>Sly, Peter D</creatorcontrib><creatorcontrib>Suk, William</creatorcontrib><creatorcontrib>Sun, Qi</creatorcontrib><creatorcontrib>Toppari, Jorma</creatorcontrib><creatorcontrib>van den Hazel, Peter</creatorcontrib><creatorcontrib>Walker, Cheryl L</creatorcontrib><creatorcontrib>Heindel, Jerrold J</creatorcontrib><title>Life-Long Implications of Developmental Exposure to Environmental Stressors: New Perspectives</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>The Developmental Origins of Health and Disease (DOHaD) paradigm is one of the most rapidly expanding areas of biomedical research. Environmental stressors that can impact on DOHaD encompass a variety of environmental and occupational hazards as well as deficiency and oversupply of nutrients and energy. They can disrupt early developmental processes and lead to increased susceptibility to disease/dysfunctions later in life. Presentations at the fourth Conference on Prenatal Programming and Toxicity in Boston, in October 2014, provided important insights and led to new recommendations for research and public health action. The conference highlighted vulnerable exposure windows that can occur as early as the preconception period and epigenetics as a major mechanism than can lead to disadvantageous “reprogramming” of the genome, thereby potentially resulting in transgenerational effects. Stem cells can also be targets of environmental stressors, thus paving another way for effects that may last a lifetime. Current testing paradigms do not allow proper characterization of risk factors and their interactions. Thus, relevant exposure levels and combinations for testing must be identified from human exposure situations and outcome assessments. Testing of potential underpinning mechanisms and biomarker development require laboratory animal models and in vitro approaches. Only few large-scale birth cohorts exist, and collaboration between birth cohorts on a global scale should be facilitated. DOHaD-based research has a crucial role in establishing factors leading to detrimental outcomes and developing early preventative/remediation strategies to combat these risks.</description><subject>Animal models</subject><subject>Biocompatibility</subject><subject>Biomarkers</subject><subject>Boston</subject><subject>Consensus Statement</subject><subject>Embryology - methods</subject><subject>Endocrinology</subject><subject>Environmental Exposure</subject><subject>Environmental stress</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetics</subject><subject>Epigenomics</subject><subject>Exposure</subject><subject>Female</subject><subject>Health hazards</subject><subject>Humans</subject><subject>Laboratory animals</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Maternal Exposure</subject><subject>Medical research</subject><subject>Nutrients</subject><subject>Obesity - etiology</subject><subject>Occupational exposure</subject><subject>Occupational hazards</subject><subject>Placenta - metabolism</subject><subject>Pregnancy</subject><subject>Prenatal experience</subject><subject>Prenatal Exposure Delayed Effects</subject><subject>Public health</subject><subject>Risk Factors</subject><subject>Stem cells</subject><subject>Stem Cells - cytology</subject><subject>Stress, Psychological</subject><subject>Telomere - ultrastructure</subject><subject>Toxic hazards</subject><subject>Toxicity</subject><issn>0013-7227</issn><issn>1945-7170</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kdFr1TAUh4Mo7jp981kKPohgZ06SNo0PwpjVDcpVUB8l5LYnW0dvUpO26n9vS-_mFHwKJ-fLl3P4EfIU6AkwoK_L7QmjkKXAM3qPbECJLJUg6X2yoRR4KhmTR-RRjNdzKYTgD8kRy5kAmssN-Va1FtPKu8vkYt93bW2G1ruYeJu8wwk73-_RDaZLyp-9j2PAZPBJ6aY2eHfofB4CxuhDfJNs8UfyCUPssR7aCeNj8sCaLuKTw3lMvr4vv5ydp9XHDxdnp1Va5xyGVDXcKtbklltumIIsB0F30oKQTUFBmUxlQoIxc81pIXmBlkqOO8tUDUrxY_J29fbjbo9NPQ8WTKf70O5N-KW9afXfHdde6Us_aZEVRcHYLHi5Cq7-eXZ-WunljgIUUlA1wcw-P3wW_PcR46Cv_RjcvJ_mwGnOVS4W46uVqoOPMaC91QLVS3AanV6C00twM_7s7ga38E1SM_BiBfzY_0-VHlR8JdE1vg6tw34J6M-UN6_K7Z0BfgMyWLAK</recordid><startdate>20151001</startdate><enddate>20151001</enddate><creator>Grandjean, Philippe</creator><creator>Barouki, Robert</creator><creator>Bellinger, David C</creator><creator>Casteleyn, Ludwine</creator><creator>Chadwick, Lisa H</creator><creator>Cordier, Sylvaine</creator><creator>Etzel, Ruth A</creator><creator>Gray, Kimberly A</creator><creator>Ha, Eun-Hee</creator><creator>Junien, Claudine</creator><creator>Karagas, Margaret</creator><creator>Kawamoto, Toshihiro</creator><creator>Paige Lawrence, B</creator><creator>Perera, Frederica P</creator><creator>Prins, Gail S</creator><creator>Puga, Alvaro</creator><creator>Rosenfeld, Cheryl S</creator><creator>Sherr, David H</creator><creator>Sly, Peter D</creator><creator>Suk, William</creator><creator>Sun, Qi</creator><creator>Toppari, Jorma</creator><creator>van den Hazel, Peter</creator><creator>Walker, Cheryl L</creator><creator>Heindel, Jerrold J</creator><general>Endocrine Society</general><general>Oxford University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9471-399X</orcidid><orcidid>https://orcid.org/0000-0002-2349-2277</orcidid></search><sort><creationdate>20151001</creationdate><title>Life-Long Implications of Developmental Exposure to Environmental Stressors: New Perspectives</title><author>Grandjean, Philippe ; Barouki, Robert ; Bellinger, David C ; Casteleyn, Ludwine ; Chadwick, Lisa H ; Cordier, Sylvaine ; Etzel, Ruth A ; Gray, Kimberly A ; Ha, Eun-Hee ; Junien, Claudine ; Karagas, Margaret ; Kawamoto, Toshihiro ; Paige Lawrence, B ; Perera, Frederica P ; Prins, Gail S ; Puga, Alvaro ; Rosenfeld, Cheryl S ; Sherr, David H ; Sly, Peter D ; Suk, William ; Sun, Qi ; Toppari, Jorma ; van den Hazel, Peter ; Walker, Cheryl L ; Heindel, Jerrold J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c631t-9d3f92d6f3f3a29156140b7f147d8019a595471aa47d308738ef073ebf29c1993</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animal models</topic><topic>Biocompatibility</topic><topic>Biomarkers</topic><topic>Boston</topic><topic>Consensus Statement</topic><topic>Embryology - 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Environmental stressors that can impact on DOHaD encompass a variety of environmental and occupational hazards as well as deficiency and oversupply of nutrients and energy. They can disrupt early developmental processes and lead to increased susceptibility to disease/dysfunctions later in life. Presentations at the fourth Conference on Prenatal Programming and Toxicity in Boston, in October 2014, provided important insights and led to new recommendations for research and public health action. The conference highlighted vulnerable exposure windows that can occur as early as the preconception period and epigenetics as a major mechanism than can lead to disadvantageous “reprogramming” of the genome, thereby potentially resulting in transgenerational effects. Stem cells can also be targets of environmental stressors, thus paving another way for effects that may last a lifetime. Current testing paradigms do not allow proper characterization of risk factors and their interactions. 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source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection; Journals@Ovid Complete |
subjects | Animal models Biocompatibility Biomarkers Boston Consensus Statement Embryology - methods Endocrinology Environmental Exposure Environmental stress Epigenesis, Genetic Epigenetics Epigenomics Exposure Female Health hazards Humans Laboratory animals Life Sciences Male Maternal Exposure Medical research Nutrients Obesity - etiology Occupational exposure Occupational hazards Placenta - metabolism Pregnancy Prenatal experience Prenatal Exposure Delayed Effects Public health Risk Factors Stem cells Stem Cells - cytology Stress, Psychological Telomere - ultrastructure Toxic hazards Toxicity |
title | Life-Long Implications of Developmental Exposure to Environmental Stressors: New Perspectives |
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