Dataset Information

Trends in Risk of Pregnancy Loss Among US Women, 1990-2011.

ABSTRACT: BACKGROUND:Pregnancy loss can have physical and psychological consequences for women and their families. Though a previous study described an increase in the risk of self-reported pregnancy loss from 1970 to 2000, more recent examinations from population-based data of US women are lacking. METHODS:We used data from the 1995, 2002, 2006-2010, 2011-2015 National Survey of Family Growth on self-reported pregnancy loss (miscarriage, stillbirth, ectopic pregnancy) among US women (15-44 years) who reported at least one pregnancy conceived during 1990-2011 that did not result in induced termination (n = 20 012 women; n = 42 526 pregnancies). Trends in the risk of self-reported pregnancy loss and early pregnancy loss (<12 weeks) were estimated, separately, by year of pregnancy conception (limited to 1990-2011 to ensure a sufficient sample of pregnancies for each year and maternal age group) using log-Binomial and Poisson models, adjusted for maternal- and pregnancy-related factors. RESULTS:Among all self-reported pregnancies, excluding induced terminations, the risk of pregnancy loss was 19.7% and early pregnancy loss was 13.5% during 1990-2011. Risk of pregnancy loss increased by a relative 2% (rate ratio [RR] 1.02, 95% confidence interval [CI] 1.01, 1.02) per year in unadjusted models and 1% per year (RR 1.01, 95% CI 1.00, 1.02) during 1990-2011, after adjustment for maternal characteristics and pregnancy-related factors. In general, trends were similar for early pregnancy loss. CONCLUSION:From 1990 to 2011, risk of self-reported pregnancy loss increased among US women. Further work is needed to better understand the drivers of this increase in reported pregnancy loss in the US.

SUBMITTER: Rossen LM

PROVIDER: S-EPMC5771868 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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Trends in Risk of Pregnancy Loss Among US Women, 1990-2011.

Rossen Lauren M LM Ahrens Katherine A KA Branum Amy M AM

Paediatric and perinatal epidemiology 20171020 1

<h4>Background</h4>Pregnancy loss can have physical and psychological consequences for women and their families. Though a previous study described an increase in the risk of self-reported pregnancy loss from 1970 to 2000, more recent examinations from population-based data of US women are lacking.<h4>Methods</h4>We used data from the 1995, 2002, 2006-2010, 2011-2015 National Survey of Family Growth on self-reported pregnancy loss (miscarriage, stillbirth, ectopic pregnancy) among US women (15-44 ...[more]

PMID: 29053188

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Project description:Accumulating evidence suggests that air pollution increases pregnancy loss; however, most previous studies have focused on case identification from medical records, which may underrepresent early pregnancy losses. Our objective was to investigate the association between acute and chronic exposure to ambient air pollution and time to pregnancy loss among women undergoing assisted reproductive technologies (ART) who are closely followed throughout early pregnancy. We included 275 women (345 human chorionic gonadotropin (hCG)-confirmed pregnancies) undergoing ART at a New England academic fertility center. We estimated daily nitrogen dioxide (NO2), ozone (O3), fine particulate matter <2.5 μm (PM2.5), and black carbon (BC) exposures using validated spatiotemporal models estimated from first positive hCG test until day of failure or live birth. Air pollution exposures were averaged over the past week and the whole pregnancy. Multivariable Cox proportional hazards models were used to estimate the hazards ratio (HR) for pregnancy loss for an interquartile range (IQR) increase in pollutant exposure. We tested for violation of proportional hazards by considering an interaction between time (in days) since positive hCG (<30 days vs. ≥30 days) and air pollution. The incidence of pregnancy loss was 29 per 100 confirmed pregnancies (n = 99). Among pregnancies not resulting in live birth, the median (IQR) time to loss was 21 (11, 30) days following positive hCG. Average past week exposures to NO2, O3, PM2.5, and BC were not associated with time to pregnancy loss. Exposure throughout pregnancy to NO2 was not associated with pregnancy loss; however, there was a statistically significant interaction with time (p-for-interaction<0.001). Specifically, an IQR increase in exposure to NO2 was positively associated with pregnancy loss after 30 days (HR = 1.34, 95% CI: 1.13, 1.58), but not in the first 30 days after positive hCG (HR = 0.83, 95% CI: 0.57, 1.20). Overall pregnancy exposure to O3, PM2.5, and BC were not associated with pregnancy loss regardless of timing. Models evaluating joint effects of all pollutants yielded similar findings. In conclusion, acute and chronic exposure to NO2, O3, PM2.5, and BC were not associated with risk of pregnancy loss; however, higher exposure to NO2 throughout pregnancy was associated with increased risk of loss 30 days after positive hCG. In this cohort, later pregnancy losses appeared more susceptible to the detrimental effects of air pollution exposure.

Project description:Pregnancy loss is the most common complication of human pregnancy. Recurrent early pregnancy loss (REPL) has multiple etiologies, including endometrial dysregulation leading to “suboptimal” implantation. Although the implantation process is tightly regulated in Eutherian (placental) mammals, the molecular factors contributing to dysregulated endometrial gene expression patterns in women with REPL are largely unknown. We hypothesized that genes that gained novel expression in the endometria of mammals that evolved in the Eutherian stemlineage, coincident with the evolution of pregnancy, are likely essential for establishment and maintenance of normal pregnancy and are, therefore, good candidates for genes whose expression may be dysregulated in disorders such as REPL. To test this hypothesis, we took an evolutionary forward genomics approach to characterize gene expression profiles of midsecretory endometria from women with REPL associated with abnormal endometria based either on histology or molecular expression of cyclin E. We identified 58 genes that were differentially expressed (P<0.001) between women with out-of-phase histological dating vs normal histology, and 81 genes that were differentially expressed (P<0.001) between women with abnormally elevated cyclin E levels vs normal cyclin E. Remarkably, genes that were recruited into endometrial expression during the evolution of pregnancy in Eutherian mammals were significantly enriched for dysregulated genes (P=0.002 for histology, P=0.021 for cyclin E), as well as for immune and signaling pathways with essential roles in endometrial biology. Thus, our novel evolutionary-based forward genomics approach identified genes whose dysregulation during the mid-secretory phase likely contributes to the molecular etiologies of recurrent early pregnancy loss. Total RNA obtained from mid luteal phase endometrium (two replicates per biopsy) from women with recurrent early pregnancy loss (REPL). Endometrial gene expression levels were compared 1) between women with out-of-phase (n=10) and normal histological dating (n=22), 2) between women with abnormally elevated (n=9) and normal (n=23) cyclin E levels. For 5 additional women with abnormally high cyclin E levels, biopsy samples were collected before and after progesterone treatment to investigate the gene expression profiles in response to progesterone.

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Trends in Risk of Pregnancy Loss Among US Women, 1990-2011.

Publications

Trends in Risk of Pregnancy Loss Among US Women, 1990-2011.

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