In utero and childhood DDT, DDE, PBDE and PCBs exposure and sex hormones in adolescent boys: The CHAMACOS study
Dichlorodiphenyltrichloroethane (DDT), polybrominated diphenyl ether (PBDE) flame retardants, and polychlorinated biphenyls (PCBs) are believed to be endocrine-disrupting chemicals (EDCs) in humans and animals. The purpose of this study is to examine the relationship of in utero and childhood exposu...
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description | Dichlorodiphenyltrichloroethane (DDT), polybrominated diphenyl ether (PBDE) flame retardants, and polychlorinated biphenyls (PCBs) are believed to be endocrine-disrupting chemicals (EDCs) in humans and animals. The purpose of this study is to examine the relationship of in utero and childhood exposure to these purported EDCs and reproductive hormones in adolescent boys who participated in CHAMACOS, an ongoing birth cohort in California's Salinas Valley. We measured o,p′- and p,p′-DDT, p,p′-DDE, PBDEs and PCBs in serum collected from mothers during pregnancy or at delivery and from their sons at 9 years. We measured concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and total testosterone (T) from 234 of their sons at 12 years. In adjusted models, we found that a 10-fold increase in maternal prenatal serum concentrations of BDE-153 was associated with a 22.2% increase (95% CI: 1.0, 47.9) in FSH, a 96.6% increase (95% CI: 35.7, 184.7) in LH, and a 92.4% increase (95% CI: 20.9, 206.2) increase in T. Similarly, BDE-100 concentrations were associated with increases in boys’ LH levels. A 10-fold increase in total prenatal ΣPCBs was associated with a 64.5% increase (95% CI: 8.6, 149.0) in FSH, primarily driven by non- dioxin-like congeners. Boys' hormone levels were only marginally associated with prenatal DDT or DDE in primary models, but when boys' Tanner stage at age 12 was added to models, prenatal maternal DDT levels were associated with decreases in LH (adjusted percent change per 10-fold increase=−18.5%, 95% CI: −29.8, −5.4) and T (percent change=−18.2%, 95% CI: −30.2, −4.2) and DDE with LH (percent change=−18.3%, 95% CI: −32.9, −0.6). Exposures measured in the children's serum at 9 years also showed associations between BDE-153 and ΣPCBs. However, there is evidence that these associations appear to be mediated by child BMI. This study suggests associations on male hormones of 12year old boys related to exposure to certain EDC exposure prenatally. The implications on future reproductive function in puberty and adulthood should be determined. |
doi_str_mv | 10.1016/j.ijheh.2016.11.001 |
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The purpose of this study is to examine the relationship of in utero and childhood exposure to these purported EDCs and reproductive hormones in adolescent boys who participated in CHAMACOS, an ongoing birth cohort in California's Salinas Valley. We measured o,p′- and p,p′-DDT, p,p′-DDE, PBDEs and PCBs in serum collected from mothers during pregnancy or at delivery and from their sons at 9 years. We measured concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and total testosterone (T) from 234 of their sons at 12 years. In adjusted models, we found that a 10-fold increase in maternal prenatal serum concentrations of BDE-153 was associated with a 22.2% increase (95% CI: 1.0, 47.9) in FSH, a 96.6% increase (95% CI: 35.7, 184.7) in LH, and a 92.4% increase (95% CI: 20.9, 206.2) increase in T. Similarly, BDE-100 concentrations were associated with increases in boys’ LH levels. A 10-fold increase in total prenatal ΣPCBs was associated with a 64.5% increase (95% CI: 8.6, 149.0) in FSH, primarily driven by non- dioxin-like congeners. Boys' hormone levels were only marginally associated with prenatal DDT or DDE in primary models, but when boys' Tanner stage at age 12 was added to models, prenatal maternal DDT levels were associated with decreases in LH (adjusted percent change per 10-fold increase=−18.5%, 95% CI: −29.8, −5.4) and T (percent change=−18.2%, 95% CI: −30.2, −4.2) and DDE with LH (percent change=−18.3%, 95% CI: −32.9, −0.6). Exposures measured in the children's serum at 9 years also showed associations between BDE-153 and ΣPCBs. However, there is evidence that these associations appear to be mediated by child BMI. This study suggests associations on male hormones of 12year old boys related to exposure to certain EDC exposure prenatally. The implications on future reproductive function in puberty and adulthood should be determined.</description><identifier>ISSN: 1438-4639</identifier><identifier>EISSN: 1618-131X</identifier><identifier>DOI: 10.1016/j.ijheh.2016.11.001</identifier><identifier>PMID: 27876543</identifier><language>eng</language><publisher>Germany: Elsevier GmbH</publisher><subject>Adolescence ; Adolescent ; Adult ; Child ; DDE ; DDT ; DDT - blood ; Dichlorodiphenyl Dichloroethylene - blood ; Endocrine disruptors ; Endocrine Disruptors - blood ; Environmental Monitoring ; Environmental Pollutants - blood ; Female ; Flame Retardants - analysis ; Follicle stimulating hormone ; Follicle Stimulating Hormone - blood ; Halogenated Diphenyl Ethers - blood ; Humans ; In utero ; Luteinizing hormone ; Luteinizing Hormone - blood ; Male ; Maternal Exposure ; Middle Aged ; PCBs ; Polychlorinated Biphenyls - blood ; Pregnancy ; Prenatal ; Prenatal Exposure Delayed Effects ; Puberty ; Testosterone ; Testosterone - blood ; Young Adult</subject><ispartof>International journal of hygiene and environmental health, 2017-04, Vol.220 (2), p.364-372</ispartof><rights>2016 Elsevier GmbH</rights><rights>Copyright © 2016 Elsevier GmbH. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-28d1e9edf14d2159dba80c01968d4319ccd4fabbcf6a312728102a8c4c68cd8d3</citedby><cites>FETCH-LOGICAL-c525t-28d1e9edf14d2159dba80c01968d4319ccd4fabbcf6a312728102a8c4c68cd8d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ijheh.2016.11.001$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,777,781,882,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27876543$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Eskenazi, Brenda</creatorcontrib><creatorcontrib>Rauch, Stephen A.</creatorcontrib><creatorcontrib>Tenerelli, Rachel</creatorcontrib><creatorcontrib>Huen, Karen</creatorcontrib><creatorcontrib>Holland, Nina T.</creatorcontrib><creatorcontrib>Lustig, Robert H.</creatorcontrib><creatorcontrib>Kogut, Katherine</creatorcontrib><creatorcontrib>Bradman, Asa</creatorcontrib><creatorcontrib>Sjödin, Andreas</creatorcontrib><creatorcontrib>Harley, Kim G.</creatorcontrib><title>In utero and childhood DDT, DDE, PBDE and PCBs exposure and sex hormones in adolescent boys: The CHAMACOS study</title><title>International journal of hygiene and environmental health</title><addtitle>Int J Hyg Environ Health</addtitle><description>Dichlorodiphenyltrichloroethane (DDT), polybrominated diphenyl ether (PBDE) flame retardants, and polychlorinated biphenyls (PCBs) are believed to be endocrine-disrupting chemicals (EDCs) in humans and animals. The purpose of this study is to examine the relationship of in utero and childhood exposure to these purported EDCs and reproductive hormones in adolescent boys who participated in CHAMACOS, an ongoing birth cohort in California's Salinas Valley. We measured o,p′- and p,p′-DDT, p,p′-DDE, PBDEs and PCBs in serum collected from mothers during pregnancy or at delivery and from their sons at 9 years. We measured concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and total testosterone (T) from 234 of their sons at 12 years. In adjusted models, we found that a 10-fold increase in maternal prenatal serum concentrations of BDE-153 was associated with a 22.2% increase (95% CI: 1.0, 47.9) in FSH, a 96.6% increase (95% CI: 35.7, 184.7) in LH, and a 92.4% increase (95% CI: 20.9, 206.2) increase in T. Similarly, BDE-100 concentrations were associated with increases in boys’ LH levels. A 10-fold increase in total prenatal ΣPCBs was associated with a 64.5% increase (95% CI: 8.6, 149.0) in FSH, primarily driven by non- dioxin-like congeners. Boys' hormone levels were only marginally associated with prenatal DDT or DDE in primary models, but when boys' Tanner stage at age 12 was added to models, prenatal maternal DDT levels were associated with decreases in LH (adjusted percent change per 10-fold increase=−18.5%, 95% CI: −29.8, −5.4) and T (percent change=−18.2%, 95% CI: −30.2, −4.2) and DDE with LH (percent change=−18.3%, 95% CI: −32.9, −0.6). Exposures measured in the children's serum at 9 years also showed associations between BDE-153 and ΣPCBs. However, there is evidence that these associations appear to be mediated by child BMI. This study suggests associations on male hormones of 12year old boys related to exposure to certain EDC exposure prenatally. The implications on future reproductive function in puberty and adulthood should be determined.</description><subject>Adolescence</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Child</subject><subject>DDE</subject><subject>DDT</subject><subject>DDT - blood</subject><subject>Dichlorodiphenyl Dichloroethylene - blood</subject><subject>Endocrine disruptors</subject><subject>Endocrine Disruptors - blood</subject><subject>Environmental Monitoring</subject><subject>Environmental Pollutants - blood</subject><subject>Female</subject><subject>Flame Retardants - analysis</subject><subject>Follicle stimulating hormone</subject><subject>Follicle Stimulating Hormone - blood</subject><subject>Halogenated Diphenyl Ethers - blood</subject><subject>Humans</subject><subject>In utero</subject><subject>Luteinizing hormone</subject><subject>Luteinizing Hormone - blood</subject><subject>Male</subject><subject>Maternal Exposure</subject><subject>Middle Aged</subject><subject>PCBs</subject><subject>Polychlorinated Biphenyls - blood</subject><subject>Pregnancy</subject><subject>Prenatal</subject><subject>Prenatal Exposure Delayed Effects</subject><subject>Puberty</subject><subject>Testosterone</subject><subject>Testosterone - blood</subject><subject>Young Adult</subject><issn>1438-4639</issn><issn>1618-131X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kVFv0zAQxyMEYmPwCZCQH3lYgs9OUgeJSV1a2KShTaJIvFmOfSGu0rjYybR-e9x2TPDCi-3z_e9_Z_-S5C3QDCiUH9aZXXfYZSwGGUBGKTxLTqEEkQKHH8_jOecizUtenSSvQlhTyoCK6mVywmZiVhY5P03c9UCmEb0jajBEd7Y3nXOGLBar87gsz8nd5WJ5SN7Vl4Hgw9aFyePhJuAD6ZzfuAEDsQNRxvUYNA4jadwufCSrDkl9Nf86r2-_kTBOZvc6edGqPuCbx_0s-f55uaqv0pvbL9f1_CbVBSvGlAkDWKFpITcMiso0SlBNoSqFyTlUWpu8VU2j21JxYDMmgDIldK5LoY0w_Cy5OPpup2aDZj-TV73certRfiedsvLfzGA7-dPdy4ILRvksGrx_NPDu14RhlBsbn9b3akA3BQki5xVwWrIo5Uep9i4Ej-1TG6Byj0qu5QGV3KOSADKiilXv_p7wqeYPmyj4dBRg_Kd7i14GbXHQaKxHPUrj7H8b_AZvH6Vt</recordid><startdate>20170401</startdate><enddate>20170401</enddate><creator>Eskenazi, Brenda</creator><creator>Rauch, Stephen A.</creator><creator>Tenerelli, Rachel</creator><creator>Huen, Karen</creator><creator>Holland, Nina T.</creator><creator>Lustig, Robert H.</creator><creator>Kogut, Katherine</creator><creator>Bradman, Asa</creator><creator>Sjödin, Andreas</creator><creator>Harley, Kim G.</creator><general>Elsevier GmbH</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170401</creationdate><title>In utero and childhood DDT, DDE, PBDE and PCBs exposure and sex hormones in adolescent boys: The CHAMACOS study</title><author>Eskenazi, Brenda ; Rauch, Stephen A. ; Tenerelli, Rachel ; Huen, Karen ; Holland, Nina T. ; Lustig, Robert H. ; Kogut, Katherine ; Bradman, Asa ; Sjödin, Andreas ; Harley, Kim G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c525t-28d1e9edf14d2159dba80c01968d4319ccd4fabbcf6a312728102a8c4c68cd8d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adolescence</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Child</topic><topic>DDE</topic><topic>DDT</topic><topic>DDT - blood</topic><topic>Dichlorodiphenyl Dichloroethylene - blood</topic><topic>Endocrine disruptors</topic><topic>Endocrine Disruptors - blood</topic><topic>Environmental Monitoring</topic><topic>Environmental Pollutants - blood</topic><topic>Female</topic><topic>Flame Retardants - analysis</topic><topic>Follicle stimulating hormone</topic><topic>Follicle Stimulating Hormone - blood</topic><topic>Halogenated Diphenyl Ethers - blood</topic><topic>Humans</topic><topic>In utero</topic><topic>Luteinizing hormone</topic><topic>Luteinizing Hormone - blood</topic><topic>Male</topic><topic>Maternal Exposure</topic><topic>Middle Aged</topic><topic>PCBs</topic><topic>Polychlorinated Biphenyls - blood</topic><topic>Pregnancy</topic><topic>Prenatal</topic><topic>Prenatal Exposure Delayed Effects</topic><topic>Puberty</topic><topic>Testosterone</topic><topic>Testosterone - blood</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Eskenazi, Brenda</creatorcontrib><creatorcontrib>Rauch, Stephen A.</creatorcontrib><creatorcontrib>Tenerelli, Rachel</creatorcontrib><creatorcontrib>Huen, Karen</creatorcontrib><creatorcontrib>Holland, Nina T.</creatorcontrib><creatorcontrib>Lustig, Robert H.</creatorcontrib><creatorcontrib>Kogut, Katherine</creatorcontrib><creatorcontrib>Bradman, Asa</creatorcontrib><creatorcontrib>Sjödin, Andreas</creatorcontrib><creatorcontrib>Harley, Kim G.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of hygiene and environmental health</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Eskenazi, Brenda</au><au>Rauch, Stephen A.</au><au>Tenerelli, Rachel</au><au>Huen, Karen</au><au>Holland, Nina T.</au><au>Lustig, Robert H.</au><au>Kogut, Katherine</au><au>Bradman, Asa</au><au>Sjödin, Andreas</au><au>Harley, Kim G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>In utero and childhood DDT, DDE, PBDE and PCBs exposure and sex hormones in adolescent boys: The CHAMACOS study</atitle><jtitle>International journal of hygiene and environmental health</jtitle><addtitle>Int J Hyg Environ Health</addtitle><date>2017-04-01</date><risdate>2017</risdate><volume>220</volume><issue>2</issue><spage>364</spage><epage>372</epage><pages>364-372</pages><issn>1438-4639</issn><eissn>1618-131X</eissn><abstract>Dichlorodiphenyltrichloroethane (DDT), polybrominated diphenyl ether (PBDE) flame retardants, and polychlorinated biphenyls (PCBs) are believed to be endocrine-disrupting chemicals (EDCs) in humans and animals. The purpose of this study is to examine the relationship of in utero and childhood exposure to these purported EDCs and reproductive hormones in adolescent boys who participated in CHAMACOS, an ongoing birth cohort in California's Salinas Valley. We measured o,p′- and p,p′-DDT, p,p′-DDE, PBDEs and PCBs in serum collected from mothers during pregnancy or at delivery and from their sons at 9 years. We measured concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and total testosterone (T) from 234 of their sons at 12 years. In adjusted models, we found that a 10-fold increase in maternal prenatal serum concentrations of BDE-153 was associated with a 22.2% increase (95% CI: 1.0, 47.9) in FSH, a 96.6% increase (95% CI: 35.7, 184.7) in LH, and a 92.4% increase (95% CI: 20.9, 206.2) increase in T. Similarly, BDE-100 concentrations were associated with increases in boys’ LH levels. A 10-fold increase in total prenatal ΣPCBs was associated with a 64.5% increase (95% CI: 8.6, 149.0) in FSH, primarily driven by non- dioxin-like congeners. Boys' hormone levels were only marginally associated with prenatal DDT or DDE in primary models, but when boys' Tanner stage at age 12 was added to models, prenatal maternal DDT levels were associated with decreases in LH (adjusted percent change per 10-fold increase=−18.5%, 95% CI: −29.8, −5.4) and T (percent change=−18.2%, 95% CI: −30.2, −4.2) and DDE with LH (percent change=−18.3%, 95% CI: −32.9, −0.6). Exposures measured in the children's serum at 9 years also showed associations between BDE-153 and ΣPCBs. However, there is evidence that these associations appear to be mediated by child BMI. This study suggests associations on male hormones of 12year old boys related to exposure to certain EDC exposure prenatally. The implications on future reproductive function in puberty and adulthood should be determined.</abstract><cop>Germany</cop><pub>Elsevier GmbH</pub><pmid>27876543</pmid><doi>10.1016/j.ijheh.2016.11.001</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adolescence Adolescent Adult Child DDE DDT DDT - blood Dichlorodiphenyl Dichloroethylene - blood Endocrine disruptors Endocrine Disruptors - blood Environmental Monitoring Environmental Pollutants - blood Female Flame Retardants - analysis Follicle stimulating hormone Follicle Stimulating Hormone - blood Halogenated Diphenyl Ethers - blood Humans In utero Luteinizing hormone Luteinizing Hormone - blood Male Maternal Exposure Middle Aged PCBs Polychlorinated Biphenyls - blood Pregnancy Prenatal Prenatal Exposure Delayed Effects Puberty Testosterone Testosterone - blood Young Adult |
title | In utero and childhood DDT, DDE, PBDE and PCBs exposure and sex hormones in adolescent boys: The CHAMACOS study |
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