<HashMap><database>biostudies-literature</database><scores><citationCount>0</citationCount><reanalysisCount>0</reanalysisCount><viewCount>66</viewCount><searchCount>0</searchCount></scores><additional><submitter>Everson TM</submitter><funding>the National Institutes of Health</funding><funding>NIEHS NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>NCI NIH HHS</funding><funding>United States Environmental Protection Agency</funding><funding>NIGMS NIH HHS</funding><pagination>263-271</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5226342</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>65</volume><pubmed_abstract>Cadmium (Cd) is a ubiquitous environmental contaminant implicated as a developmental toxicant, yet the underlying mechanisms that confer this toxicity are unknown. Mother-infant pairs from a Rhode Island birth cohort were investigated for the potential effects of maternal Cd exposure on fetal growth, and the possible role of the PCDHAC1 gene on this association. Mothers with higher toenail Cd concentrations were at increased odds of giving birth to an infant that was small for gestational age or with a decreased head circumference. These associations were strongest amongst those with low levels of DNA methylation in the promoter region of placental PCDHAC1. Further, we found placental PCDHAC1 expression to be inversely associated with maternal Cd, and PCDHAC1 expression positively associated with fetal growth. Our findings suggest that maternal Cd affects fetal growth even at very low concentrations, and some of these effects may be due to the differential expression of PCDHAC1.</pubmed_abstract><journal>Reproductive toxicology (Elmsford, N.Y.)</journal><pubmed_title>Maternal cadmium, placental PCDHAC1, and fetal development.</pubmed_title><pmcid>PMC5226342</pmcid><funding_grant_id>P30 CA023108</funding_grant_id><funding_grant_id>R01 ES022223</funding_grant_id><funding_grant_id>P42 ES007373</funding_grant_id><funding_grant_id>P20 GM104416</funding_grant_id><funding_grant_id>R01 MH094609</funding_grant_id><funding_grant_id>R25 CA134286</funding_grant_id><funding_grant_id>P01 ES022832</funding_grant_id><pubmed_authors>Marsit CJ</pubmed_authors><pubmed_authors>Armstrong DA</pubmed_authors><pubmed_authors>Karagas MR</pubmed_authors><pubmed_authors>Jackson BP</pubmed_authors><pubmed_authors>Green BB</pubmed_authors><pubmed_authors>Everson TM</pubmed_authors><view_count>66</view_count></additional><is_claimable>false</is_claimable><name>Maternal cadmium, placental PCDHAC1, and fetal development.</name><description>Cadmium (Cd) is a ubiquitous environmental contaminant implicated as a developmental toxicant, yet the underlying mechanisms that confer this toxicity are unknown. Mother-infant pairs from a Rhode Island birth cohort were investigated for the potential effects of maternal Cd exposure on fetal growth, and the possible role of the PCDHAC1 gene on this association. Mothers with higher toenail Cd concentrations were at increased odds of giving birth to an infant that was small for gestational age or with a decreased head circumference. These associations were strongest amongst those with low levels of DNA methylation in the promoter region of placental PCDHAC1. Further, we found placental PCDHAC1 expression to be inversely associated with maternal Cd, and PCDHAC1 expression positively associated with fetal growth. Our findings suggest that maternal Cd affects fetal growth even at very low concentrations, and some of these effects may be due to the differential expression of PCDHAC1.</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Oct</publication><modification>2024-11-13T12:59:55.226Z</modification><creation>2019-03-27T02:33:53Z</creation></dates><accession>S-EPMC5226342</accession><cross_references><pubmed>27544570</pubmed><doi>10.1016/j.reprotox.2016.08.011</doi></cross_references></HashMap>