Prenatal opioid exposure has been associated with adverse child health outcomes. Changes to the epigenome provide a plausible mechanism through which effects may be elicited. We investigated whether prenatal opioid exposure was associated with locus-specific changes in umbilical cord blood DNA methylation (DNAm) and gestational epigenetic age. We leveraged data from the Environmental influences on Child Health Outcomes cohort. Prenatal opioid data was obtained from maternal self-report and/or medical record data. DNAm measures were generated from blood biospecimens collected at birth. Linear regression models tested associations between prenatal maternal opioid exposure and epigenetic outcomes in crude and fully adjusted models. We tested the association between prenatal opioid exposure and cord blood DNAm at 15 CpG sites in 385 (n = 25 exposed, n = 360 unexposed) individuals from three cohorts. We identified a single CpG site (cg14303187) that was nominally associated with prenatal opioid exposure (p = 0.02, β = −0.012; 95% CI, −0.023 to −0.0012). No significant associations between exposure and gestational epigenetic age were found (n = 716 individuals from eight cohorts; n = 29 exposed, n = 687 unexposed). We identified a nominally significant association between prenatal opioid exposure and DNAm at one CpG site. Future studies should continue investigating the effect of this exposure on the epigenome.

Prenatal opioid exposure has been associated with adverse child health outcomes. Changes to the epigenome provide a plausible mechanism through which effects may be elicited. We investigated whether prenatal opioid exposure was associated with locus-specific changes in umbilical cord blood DNA methylation (DNAm) and gestational epigenetic age. We leveraged data from the Environmental influences on Child Health Outcomes cohort. Prenatal opioid data was obtained from maternal self-report and/or medical record data. DNAm measures were generated from blood biospecimens collected at birth. Linear regression models tested associations between prenatal maternal opioid exposure and epigenetic outcomes in crude and fully adjusted models. We tested the association between prenatal opioid exposure and cord blood DNAm at 15 CpG sites in 385 (n = 25 exposed, n = 360 unexposed) individuals from three cohorts. We identified a single CpG site (cg14303187) that was nominally associated with prenatal opioid exposure (p = 0.02, β = −0.012; 95% CI, −0.023 to −0.0012). No significant associations between exposure and gestational epigenetic age were found (n = 716 individuals from eight cohorts; n = 29 exposed, n = 687 unexposed). We identified a nominally significant association between prenatal opioid exposure and DNAm at one CpG site. Future studies should continue investigating the effect of this exposure on the epigenome.

Prenatal opioid exposure has been associated with adverse child health outcomes. Changes to the epigenome provide a plausible mechanism through which effects may be elicited. We investigated whether prenatal opioid exposure was associated with locus-specific changes in umbilical cord blood DNA methylation (DNAm) and gestational epigenetic age. We leveraged data from the Environmental influences on Child Health Outcomes cohort. Prenatal opioid data was obtained from maternal self-report and/or medical record data. DNAm measures were generated from blood biospecimens collected at birth. Linear regression models tested associations between prenatal maternal opioid exposure and epigenetic outcomes in crude and fully adjusted models. We tested the association between prenatal opioid exposure and cord blood DNAm at 15 CpG sites in 385 (n = 25 exposed, n = 360 unexposed) individuals from three cohorts. We identified a single CpG site (cg14303187) that was nominally associated with prenatal opioid exposure (p = 0.02, β = −0.012; 95% CI, −0.023 to −0.0012). No significant associations between exposure and gestational epigenetic age were found (n = 716 individuals from eight cohorts; n = 29 exposed, n = 687 unexposed). We identified a nominally significant association between prenatal opioid exposure and DNAm at one CpG site. Future studies should continue investigating the effect of this exposure on the epigenome.

Prenatal opioid exposure has been associated with adverse child health outcomes. Changes to the epigenome provide a plausible mechanism through which effects may be elicited. We investigated whether prenatal opioid exposure was associated with locus-specific changes in umbilical cord blood DNA methylation (DNAm) and gestational epigenetic age. We leveraged data from the Environmental influences on Child Health Outcomes cohort. Prenatal opioid data was obtained from maternal self-report and/or medical record data. DNAm measures were generated from blood biospecimens collected at birth. Linear regression models tested associations between prenatal maternal opioid exposure and epigenetic outcomes in crude and fully adjusted models. We tested the association between prenatal opioid exposure and cord blood DNAm at 15 CpG sites in 385 (n = 25 exposed, n = 360 unexposed) individuals from three cohorts. We identified a single CpG site (cg14303187) that was nominally associated with prenatal opioid exposure (p = 0.02, β = −0.012; 95% CI, −0.023 to −0.0012). No significant associations between exposure and gestational epigenetic age were found (n = 716 individuals from eight cohorts; n = 29 exposed, n = 687 unexposed). We identified a nominally significant association between prenatal opioid exposure and DNAm at one CpG site. Future studies should continue investigating the effect of this exposure on the epigenome.

To describe tDRs in human milk EVs and their associations with maternal body mass index, age, dietary indices, breastfeeding frequency, season and time of milk collection in a Latina population. We sequenced small RNAs from EVs from 109 mature human milk samples collected at 1 month after delivery in the Southern California Mother’s Milk Study. We grouped tDRs using hierarchical clustering and clusters were compared across tDR characteristics. We analyzed associations of tDRs with intrinsic maternal variables (body mass index, age), maternal nutrition (caloric intake, Healthy Eating Index, Dietary Inflammatory Index), and variables related to feeding and milk collection (breastfeeding frequency, season and time of milk collection) using negative binomial models. We identified 338 tDRs expressed in 90% or more of milk EV samples, of which 113 were identified in all samples. tDR-1:26-Gly-CCC-1-M4 accounted for most reads (79%). Pathway analysis revealed a wide array of biological processes and disease mechanisms across the four tDR clusters. tDRs were associated with season of collection, time of collection, breastfeeding frequency, and the dietary inflammatory index. tDRs are abundant in milk EVs and may be sensitive to maternal diet, seasonality, time of day, and breastfeeding frequency. Human milk contains important nutrients and molecules that help to protect the infant from disease and ensure proper development. Small pieces of RNA that originate from transfer RNA molecules are enriched in human milk, particularly in compartments that exist outside of the cell and can be easily move from cell to cell. These small RNAs – referred to as tRNA-derived RNAs (or tDRs) – have gene silencing functions which may implicate them in health and development. Additionally, small RNAs like tDRs can survive digestion by the infant’s stomach when encapsulated in these extracellular compartments, meaning that they can be fully transferred from mom to baby. However, tDRs have not yet been characterized in human milk. In this study, we measured tDRs in mature milk samples from a cohort of mothers. We characterized these tDRs and tested their associations with several maternal characteristics, dietary variables, and variables related to milk collection and breastfeeding. We found that tDRs were readily identifiable and were associated with several tested variables, including maternal diet, seasonality, time of day, and breastfeeding frequency.

To describe tDRs in human milk EVs and their associations with maternal body mass index, age, dietary indices, breastfeeding frequency, season and time of milk collection in a Latina population. We sequenced small RNAs from EVs from 109 mature human milk samples collected at 1 month after delivery in the Southern California Mother’s Milk Study. We grouped tDRs using hierarchical clustering and clusters were compared across tDR characteristics. We analyzed associations of tDRs with intrinsic maternal variables (body mass index, age), maternal nutrition (caloric intake, Healthy Eating Index, Dietary Inflammatory Index), and variables related to feeding and milk collection (breastfeeding frequency, season and time of milk collection) using negative binomial models. We identified 338 tDRs expressed in 90% or more of milk EV samples, of which 113 were identified in all samples. tDR-1:26-Gly-CCC-1-M4 accounted for most reads (79%). Pathway analysis revealed a wide array of biological processes and disease mechanisms across the four tDR clusters. tDRs were associated with season of collection, time of collection, breastfeeding frequency, and the dietary inflammatory index. tDRs are abundant in milk EVs and may be sensitive to maternal diet, seasonality, time of day, and breastfeeding frequency. Human milk contains important nutrients and molecules that help to protect the infant from disease and ensure proper development. Small pieces of RNA that originate from transfer RNA molecules are enriched in human milk, particularly in compartments that exist outside of the cell and can be easily move from cell to cell. These small RNAs – referred to as tRNA-derived RNAs (or tDRs) – have gene silencing functions which may implicate them in health and development. Additionally, small RNAs like tDRs can survive digestion by the infant’s stomach when encapsulated in these extracellular compartments, meaning that they can be fully transferred from mom to baby. However, tDRs have not yet been characterized in human milk. In this study, we measured tDRs in mature milk samples from a cohort of mothers. We characterized these tDRs and tested their associations with several maternal characteristics, dietary variables, and variables related to milk collection and breastfeeding. We found that tDRs were readily identifiable and were associated with several tested variables, including maternal diet, seasonality, time of day, and breastfeeding frequency.