Trimester specific PM2.5 exposure and fetal growth in Ohio, 2007-2010.
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ABSTRACT:
SUBMITTER: Percy Z
PROVIDER: S-EPMC6382528 | biostudies-literature | 2019 Apr
REPOSITORIES: biostudies-literature
Publications
Trimester specific PM<sub>2.5</sub> exposure and fetal growth in Ohio, 2007-2010.
Percy Zana Z DeFranco Emily E Xu Fan F Hall Eric S ES Haynes Erin N EN Jones David D Muglia Louis J LJ Chen Aimin A
Environmental research 20190115
<h4>Background</h4>Exposure to particulate matter, particularly with aerodynamic diameter < 2.5 µm (PM<sub>2.5</sub>), may increase inflammation and oxidative stress in pregnant women and affect fetal growth. We examined trimester specific PM<sub>2.5</sub> exposure levels and small for gestational age (SGA) using the statewide birth registry of Ohio from 2007 to 2010.<h4>Methods</h4>Exposure to PM<sub>2.5</sub> in each trimester and for each gestational week was determined using data from 57 Env ...[more]
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Project description:BackgroundPrior studies have examined the association between fine particulate matter [PM ≤2.5μm in aerodynamic diameter (PM2.5)] and fetal growth with either limited spatial or temporal resolution.ObjectivesIn this study, we examined the association between PM2.5 exposure during pregnancy and fetal growth measures (ultrasound parameters and birth weight) in a pregnancy cohort using spatiotemporally resolved PM2.5 in Eastern Massachusetts, USA.MethodsWe used ultrasound measures of biparietal diameter (BPD), head circumference, femur length, and abdominal circumference (AC), in addition to birth weight, from 9,446 pregnancies that were delivered at the Beth Israel Deaconess Medical Center from 2011-2016. We used linear mixed-effects models to examine the associations of PM2.5 in two exposure windows (the first 16 wk of pregnancy and the cumulative exposure up until the assessment of fetal growth) with anatomic scans (ultrasound measures at<24 wk), growth scans (ultrasound measures at≥24wk), and birth weight. All models were adjusted for sociodemographic characteristics, long-term trends, and temperature.ResultsHigher PM2.5 exposure in the first 16 wk was associated with smaller fetal growth measures, where associations were particularly strong for BPD, AC, and birth weight. For example, a 5-μg/m3 increase in PM2.5 was associated with a lower mean BPD z-score of -0.19 (95% CI: -0.31, -0.06) before 24 wk, a lower mean AC z-score of -0.15 (95% CI: -0.28, -0.01) after 24 wk, and a lower mean birth weight z-score of -0.11 (95% CI: -0.20, -0.01). Analyses examining the associations with cumulative PM2.5 exposure up until the assessment of fetal growth produced attenuated associations.ConclusionsHigher gestational exposure to PM2.5 was associated with smaller fetal growth measures at levels below the current national standards. https://doi.org/10.1289/EHP9824.
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Project description:Human chorionic gonadotropin (hCG) is a pregnancy-specific hormone that regulates placental development. hCG concentrations vary widely throughout gestation and differ based on fetal sex. Abnormal hCG concentrations are associated with adverse pregnancy outcomes including fetal growth restriction. We studied the association of hCG concentrations with fetal growth and birth weight. In addition, we investigated effect modification by gestational age of hCG measurement and fetal sex. Total serum hCG (median 14.4 weeks, 95 % range 10.1-26.2), estimated fetal weight (measured by ultrasound during 18-25th weeks and >25th weeks) and birth weight were measured in 7987 mother-child pairs from the Generation R cohort and used to establish fetal growth. Small for gestational age (SGA) was defined as a standardized birth weight lower than the 10th percentile of the study population. There was a non-linear association of hCG with birth weight (P = 0.009). However, only low hCG concentrations measured during the late first trimester (11th and 12th week) were associated with birth weight and SGA. Low hCG concentrations measured in the late first trimester were also associated with decreased fetal growth (P = 0.0002). This was the case for both male and female fetuses. In contrast, high hCG concentrations during the late first trimester were associated with increased fetal growth amongst female, but not male fetuses. Low hCG in the late first trimester is associated with lower birth weight due to a decrease in fetal growth. Fetal sex differences exist in the association of hCG concentrations with fetal growth.
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Project description:OBJECTIVE:To estimate the risk of adverse perinatal outcomes among women with isolated fetal growth restriction from 17 to 22 weeks of gestation. METHODS:This was a retrospective cohort study of all singleton, nonanomalous pregnancies undergoing ultrasonography to assess fetal anatomy between 17 and 22 weeks of gestation at a single center from 2010 to 2014. After excluding patients with fetal structural malformations, chromosomal abnormalities, or identified infectious etiologies, we compared perinatal outcomes between pregnancies with and without fetal growth restriction, defined as estimated fetal weight less than the 10th percentile for gestational age. Our primary outcome was small for gestational age (SGA) at birth, defined as birth weight less than the 10th percentile. Secondary outcomes included preterm delivery at less than 37 and less than 28 weeks of gestation, preeclampsia, abruption, stillbirth, neonatal death, neonatal intensive care unit admission, intraventricular hemorrhage, need for respiratory support, and necrotizing enterocolitis. RESULTS:Of 12,783 eligible patients, 355 (2.8%) had early second-trimester fetal growth restriction. Risk factors for growth restriction were African American race and tobacco use. Early second-trimester growth restriction was associated with a more than fivefold increase in risk of SGA at birth (36.9% compared with 9.1%, adjusted odds ratio [OR] 5.5, 95% CI 4.3-7.0), stillbirth (2.5% compared with 0.4%, OR 6.2, 95% CI 2.7-12.8), and neonatal death (1.4% compared with 0.3%, OR 5.2, 95% CI 1.6-13.5). Rates of indicated preterm birth at less than 37 weeks of gestation (7.3% compared with 3.3%, OR 2.3, 95% CI 1.5-3.5) and less than 28 weeks of gestation (2.5% compared with 0.2%, OR 10.8, 95% CI 4.5-23.4), neonatal need for respiratory support (16.9% compared with 7.8%, adjusted OR 1.6, 95% CI 1.1-2.2), and necrotizing enterocolitis (1.4% compared with 0.2%, OR 7.7, 95% CI 2.3-20.9) were also significantly higher for those with growth restriction. Rates of preeclampsia, abruption, and other neonatal outcomes were not significantly different. CONCLUSION:Although fetal growth restriction in the early second trimester occurred in less than 3% of our cohort and most of those with isolated growth restriction did not have adverse outcomes, it is a strong risk factor for SGA, stillbirth, neonatal death, and indicated preterm birth.
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Project description:BackgroundImpaired fetal growth is associated with increased risks of kidney diseases in later life. Because human development rates are highest during the first trimester, this trimester may be a particularly critical period for kidney outcomes. We have therefore examined the association of fetal first trimester growth with kidney outcomes in childhood.MethodsThis study was embedded in a prospective population-based cohort study among 1176 pregnant women and their children. We used fetal first trimester crown-length as the growth measure among mothers with a regular menstrual cycle and a known first day of the last menstrual period. At the childhood age of 6 (median 5.7-6.8) years, we measured combined kidney volume, microalbuminuria and estimated glomerular filtration rate (eGFR) based on serum creatinine and cystatin C concentrations.ResultsNo consistent associations of fetal first trimester crown-rump length with childhood combined kidney volume, eGFR and microalbuminuria were observed. Compared to children with a fetal first trimester crown-rump length in the highest quintile, those in the lowest quintile had a larger childhood combined kidney volume (difference 5.32 cm3, 95 % confidence interval 1.06 to 9.57), but no differences in kidney function.ConclusionOur results do not support the hypothesis that fetal first trimester growth restriction affects kidney size and function in childhood. Further studies are needed to focus on critical periods in early life for kidney function and disease in later life.
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Project description:Pregnancy-induced changes in plasma pharmacokinetics of many antiretrovirals (ARV) are well-established. Current knowledge about the extent of ARV exposure in lymphoid tissues of pregnant women and within the fetal compartment is limited due to their inaccessibility. Subtherapeutic ARV concentrations in HIV reservoirs like lymphoid tissues during pregnancy may constitute a barrier to adequate virological suppression and increase the risk of mother-to-child transmission (MTCT). The present study describes the pharmacokinetics of three ARVs (efavirenz, dolutegravir, and rilpivirine) in lymphoid tissues and fetal plasma during pregnancy using materno-fetal physiologically-based pharmacokinetic models (m-f-PBPK). Lymphatic and fetal compartments were integrated into our previously validated adult PBPK model. Physiological and drug disposition processes were described using ordinary differential equations. For each drug, virtual pregnant women (n = 50 per simulation) received the standard dose during the third trimester. Essential pharmacokinetic parameters, including Cmax, Cmin, and AUC (0-24), were computed from the concentration-time data at steady state for lymph and fetal plasma. Models were qualified by comparison of predictions with published clinical data, the acceptance threshold being an absolute average fold-error (AAFE) within 2.0. AAFE for all model predictions was within 1.08-1.99 for all three drugs. Maternal lymph concentration 24 h after dose exceeded the reported minimum effective concentration (MEC) for efavirenz (11,514 vs. 800 ng/ml) and rilpivirine (118.8 vs. 50 ng/ml), but was substantially lower for dolutegravir (16.96 vs. 300 ng/ml). In addition, predicted maternal lymph-to-plasma AUC ratios vary considerably (6.431-efavirenz, 0.016-dolutegravir, 1.717-rilpivirine). Furthermore, fetal plasma-to-maternal plasma AUC ratios were 0.59 for efavirenz, 0.78 for dolutegravir, and 0.57 for rilpivirine. Compared with rilpivirine (0 h), longer dose forgiveness was observed for dolutegravir in fetal plasma (42 h), and for efavirenz in maternal lymph (12 h). The predicted low lymphoid tissue penetration of dolutegravir appears to be significantly offset by its extended dose forgiveness and adequate fetal compartment exposure. Hence, it is unlikely to be a predictor of maternal virological failure or MTCT risks. Predictions from our m-f-PBPK models align with recommendations of no dose adjustment despite moderate changes in exposure during pregnancy for these drugs. This is an important new application of PBPK modeling to evaluate the adequacy of drug exposure in otherwise inaccessible compartments.
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Project description:BACKGROUND:Screening for prostate cancer using prostate-specific antigen (PSA) is common. Prostate cancer has been associated with higher total PSA (tPSA), lower free PSA (fPSA), lower percent free PSA (%fPSA), and higher complexed PSA (cPSA). METHODS:Total, free and complexed PSAs were performed on 3251 men ?40years in the 2007-2010 National Health and Nutrition Examination Survey. Distributions of the PSA tests were examined by age, race and ethnicity, and body mass index (BMI) groups. Percentages of men at PSA thresholds were examined. RESULTS:Total PSA geometric mean was 0.96?g/l among men aged ?40years and increased from 0.74?g/l for men 40-49years, to 1.82?g/l for men 80years and older. Non-Hispanic Whites had lower age-adjusted mean tPSA (1.03?g/l) and cPSA (0.56?g/l) than non-Hispanic Blacks (tPSA 1.25?g/l and cPSA 0.72?g/l). Obese men had lower age-adjusted mean total, free and complexed PSAs (0.94, 0.27, and 0.51?g/l, respectively) than men with normal BMI (tPSA 1.21, fPSA 0.32, and cPSA 0.68?g/l, respectively). CONCLUSION:Total, free and complexed PSAs increased with age; tPSA and cPSAs were highest in non-Hispanic Blacks; and total, free, and complexed PSAs were lowest in obese men.
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