<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>13</volume><submitter>Barrett ES</submitter><pubmed_abstract>Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous endocrine-disrupting combustion by-products that have been linked to preterm birth. One possible mechanism is through disruption of placental corticotropin releasing hormone (pCRH), a key hormone implicated in parturition. As an extension of recent research identifying pCRH as a potential target of endocrine disruption, we examined maternal PAH exposure in relation to pCRH in a large, diverse sample. Participants, drawn from the CANDLE cohort, part of the ECHO-PATHWAYS Consortium, completed study visits at 16-29 weeks (V1) and 22-39 weeks (V2) gestation (n=812). Seven urinary mono-hydroxylated PAH metabolites (OH-PAHs) were measured at V1 and serum pCRH at V1 and V2. Associations between individual log-transformed OH-PAHs (as well as t</pubmed_abstract><journal>Frontiers in endocrinology</journal><pagination>1011689</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9691680</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Prenatal polycyclic aromatic hydrocarbon (PAH) exposure in relation to placental corticotropin releasing hormone (pCRH) in the CANDLE pregnancy cohort.</pubmed_title><pmcid>PMC9691680</pmcid><pubmed_authors>Robinson M</pubmed_authors><pubmed_authors>Loftus C</pubmed_authors><pubmed_authors>Kauderer S</pubmed_authors><pubmed_authors>Hazlehurst MF</pubmed_authors><pubmed_authors>Kannan K</pubmed_authors><pubmed_authors>Smith AK</pubmed_authors><pubmed_authors>Sathyanarayana S</pubmed_authors><pubmed_authors>Barrett ES</pubmed_authors><pubmed_authors>Workman T</pubmed_authors><pubmed_authors>Smith R</pubmed_authors><pubmed_authors>Zhao Q</pubmed_authors><pubmed_authors>LeWinn KZ</pubmed_authors><pubmed_authors>Bush NR</pubmed_authors></additional><is_claimable>false</is_claimable><name>Prenatal polycyclic aromatic hydrocarbon (PAH) exposure in relation to placental corticotropin releasing hormone (pCRH) in the CANDLE pregnancy cohort.</name><description>Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous endocrine-disrupting combustion by-products that have been linked to preterm birth. One possible mechanism is through disruption of placental corticotropin releasing hormone (pCRH), a key hormone implicated in parturition. As an extension of recent research identifying pCRH as a potential target of endocrine disruption, we examined maternal PAH exposure in relation to pCRH in a large, diverse sample. Participants, drawn from the CANDLE cohort, part of the ECHO-PATHWAYS Consortium, completed study visits at 16-29 weeks (V1) and 22-39 weeks (V2) gestation (n=812). Seven urinary mono-hydroxylated PAH metabolites (OH-PAHs) were measured at V1 and serum pCRH at V1 and V2. Associations between individual log-transformed OH-PAHs (as well as t</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-21T21:21:40.629Z</modification><creation>2025-04-05T18:23:41.198Z</creation></dates><accession>S-EPMC9691680</accession><cross_references><pubmed>36440232</pubmed><doi>10.3389/fendo.2022.1011689</doi></cross_references></HashMap>