Exposure to PM2.5 during Pregnancy and Fetal Growth in Eastern Massachusetts, USA.
Ontology highlight
ABSTRACT: Background
Prior 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.Objectives
In 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.Methods
We 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.Results
Higher 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.Conclusions
Higher 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.
SUBMITTER: Leung M
PROVIDER: S-EPMC8734565 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:BackgroundLithium is an effective treatment in pregnancy and postpartum for the prevention of relapse in bipolar disorder, but there is a lack of knowledge about the potential adverse impact on fetal development.AimsTo investigate the impact of lithium exposure on early fetal growth.MethodsIn this retrospective observational cohort study, we included all singleton pregnancies of women using lithium and referred for advanced fetal ultrasound scanning between 1994 and 2018 to the University Medical Centers in Leiden and Rotterdam, the Netherlands (n=119). The Generation R study, a population-based cohort, served as a non-exposed control population from the same geographic region (n=8184). Fetal head circumference, abdominal circumference, femur length, and transcerebellar diameter were measured by ultrasound at 18-22 weeks of gestation.ResultsLithium use during pregnancy was associated with an average increase in head circumference of 1.77 mm (95% confidence interval: 0.53, 3.01), in abdominal circumference of 5.54 mm (95% confidence interval: 3.95, 7.12) and in femur length of 0.59 mm (95% confidence interval: 0.22, 0.96) at 18-22 weeks gestation. Furthermore, lithium use during pregnancy was associated with an average increase in birth weight of 142.43 grams (95% confidence interval: 58.01, 226.89), whereas it was associated with an average decrease of 1.41 weeks in gestational duration (95% confidence interval: -1.78, -1.05).ConclusionsLithium use during pregnancy was associated with increased fetal growth parameters at 18-22 weeks gestational age and increased birth weight. Further research is needed to evaluate both short- and long-term implications, as well as the mechanisms driving this difference in growth.
| S-EPMC7859661 | biostudies-literature
Project description:BACKGROUND:Exposure to particulate matter, particularly with aerodynamic diameter <?2.5?µm (PM2.5), may increase inflammation and oxidative stress in pregnant women and affect fetal growth. We examined trimester specific PM2.5 exposure levels and small for gestational age (SGA) using the statewide birth registry of Ohio from 2007 to 2010. METHODS:Exposure to PM2.5 in each trimester and for each gestational week was determined using data from 57 Environmental Protection Agency network monitoring stations across the state of Ohio. We restricted the data to 224,921 singleton live births, with a gestational age of 20-42 weeks, no genetic disorders or congenital abnormalities, and who had home addresses within a 10?km radius of any PM2.5 monitoring station. We estimated odds ratios of SGA using Generalized Linear Models (GLMs) and Distributed Lag Models (DLMs), and adjustment for maternal age, race, education, parity, body mass index, insurance type, tobacco use, prenatal care initiation, birth year, season of birth, and sex of the baby. RESULTS:Mean PM2.5 levels during the entire pregnancy were 13.03?µg/m3 with a standard deviation of 1.57?µg/m3. Covariates adjusted odds ratios and 95% confidence intervals of a 10?µg/m3 increase in PM2.5 levels with a 10?km buffer radius for SGA and trimesters modeled separately were 0.94 (0.88, 1.00) for the first trimester, 0.93 (0.86, 1.00) for the second trimester, 1.07 (1.00, 1.15) for the third trimester, and 0.92 (0.81, 1.06) for the entire pregnancy. When a 5?km buffer radius was used, adjusted odds ratios and 95% confidence intervals for SGA were 0.97 (0.89, 1.05) for the first trimester, 0.96 (0.88, 1.05) for the second trimester, 1.09 (1.02, 1.17) for the third trimester, and 0.99 (0.85, 1.14) for the overall pregnancy, indicating sensitivity to buffer choice. DLMs showed gestational weeks 30-35 to be a particular window of vulnerability. CONCLUSION:Increasing exposure to PM2.5 during the third trimester of pregnancy was associated with a small increase in risk of SGA in this population-based study. Selection of a buffer radius significantly impacted our results in the first trimester, but not in the third trimester.
| S-EPMC6382528 | biostudies-literature
Project description:Increasingly studies suggest prenatal exposure to air pollution may increase risk of childhood asthma. Few studies have investigated exposure during specific fetal pulmonary developmental windows. To assess associations between prenatal fine particulate matter exposure and asthma at age 4. This study included mother-child dyads from two pregnancy cohorts-CANDLE and TIDES-within the ECHO-PATHWAYS consortium (births in 2007-2013). Three child asthma outcomes were parent-reported: ever asthma, current asthma, and current wheeze. Fine particulate matter (PM2.5) exposures during the pseudoglandular (5-16 weeks gestation), canalicular (16-24 weeks gestation), saccular (24-36 weeks gestation), and alveolar (36+ weeks gestation) phases of fetal lung development were estimated using a national spatiotemporal model. We estimated associations with Poisson regression with robust standard errors, and adjusted for child, maternal, and neighborhood factors. Children (n=1469) were on average 4.3 (standard deviation 0.5) years old, 49% were male, and 11.7% had ever asthma; 46% of women identified as black and 53% had at least a college/technical school degree. A 2 μg/m3 higher PM2.5 exposure during the saccular phase was associated with 1.29 times higher risk of ever asthma (95% CI: 1.06-1.58). A similar association was observed with current asthma (RR 1.27, 95% CI: 1.04-1.54), but not current wheeze (RR 1.11, 95% CI: 0.92-1.33). Effect estimates for associations during other developmental windows had confidence intervals that included the null. Later phases of prenatal lung development may be particularly sensitive to the developmental toxicity of PM2.5.
| S-EPMC7943175 | biostudies-literature
Project description:Reduced fetal growth is associated with perinatal and later morbidity. Prenatal exposure to environmental pollutants is linked to reduced fetal growth at birth, but the impact of concomitant exposure to multiple pollutants is unclear. The purpose of this study was to examine interactions between early pregnancy exposure to cigarette smoke, traffic pollution, and select perfluoroalkyl substances (PFASs) on birth weight-for-gestational age (BW/GA).Among 1597 Project Viva mother-infant pairs, we assessed maternal cigarette smoking by questionnaire, traffic pollution at residential address by black carbon land use regression model, and plasma concentration of select PFASs in early pregnancy. We calculated sex-specific BW/GA z-scores, an index of fetal growth, from national reference data. We fit covariate-adjusted multi-pollutant linear regression models and examined interactions between exposures, using a likelihood-ratio test to identify a best-fit model.Two hundred six (13%) mothers smoked during pregnancy. Mean [standard deviation (SD)] for black carbon was 0.8 (0.3) ?g/m3, perfluorooctane sulfonate (PFOS) was 29.1 (16.5) ng/mL, and BW/GA z-score was 0.19 (0.96). In the best-fit model, BW/GA z-score was lower in infants of mothers exposed to greater black carbon [-?0.08 (95% CI: -0.15, -?0.01) per interquartile range (IQR)]. BW/GA z-score (95% CI) was also lower in infants of mothers who smoked [-?0.09 (-?0.23, 0.06)] or were exposed to greater PFOS [-?0.03 (-?0.07, 0.02) per IQR], although confidence intervals crossed the null. There were no interactions between exposures. In secondary analyses, instead of PFOS, we examined perfluorononanoate (PFNA) [mean (SD): 0.7 (0.4) ng/mL], a PFAS more closely linked to lower BW/GA in our cohort. The best-fit multi-pollutant model included positive two-way interactions between PFNA and both black carbon and smoking (p-interactions?=?0.03).Concurrent prenatal exposures to maternal smoking, black carbon, and PFOS are additively associated with lower fetal growth, whereas PFNA may attenuate associations of smoking and black carbon with lower fetal growth. It is important to examine interactions between multiple exposures in relation to health outcomes, as effects may not always be additive and may shed light on biological pathways.
| S-EPMC5819079 | biostudies-other
Project description:BackgroundAir pollution exposure during pregnancy might have trimester-specific effects on fetal growth.ObjectiveWe prospectively evaluated the associations of maternal air pollution exposure with fetal growth characteristics and adverse birth outcomes in 7,772 subjects in the Netherlands.MethodsParticulate matter with an aerodynamic diameter < 10 μm (PM10) and nitrogen dioxide (NO2) levels were estimated using dispersion modeling at the home address. Fetal head circumference, length, and weight were estimated in each trimester by ultrasound. Information on birth outcomes was obtained from medical records.ResultsIn cross-sectional analyses, NO2 levels were inversely associated with fetal femur length in the second and third trimester, and PM10 and NO2 levels both were associated with smaller fetal head circumference in the third trimester [-0.18 mm, 95% confidence interval (CI): -0.24, -0.12 mm; and -0.12 mm, 95% CI: -0.17, -0.06 mm per 1-μg/m3 increase in PM10 and NO2, respectively]. Average PM10 and NO2 levels during pregnancy were not associated with head circumference and length at birth or neonatally, but were inversely associated with birth weight (-3.6 g, 95% CI: -6.7, -0.4 g; and -3.4 g, 95% CI: -6.2, -0.6 g, respectively). Longitudinal analyses showed similar patterns for head circumference and weight, but no associations with length. The third and fourth quartiles of PM10 exposure were associated with preterm birth [odds ratio (OR) = 1.40, 95% CI: 1.03, 1.89; and OR = 1.32; 95% CI: 0.96, 1.79, relative to the first quartile]. The third quartile of PM10 exposure, but not the fourth, was associated with small size for gestational age at birth (SGA) (OR = 1.38; 95% CI: 1.00, 1.90). No consistent associations were observed for NO2 levels and adverse birth outcomes.ConclusionsResults suggest that maternal air pollution exposure is inversely associated with fetal growth during the second and third trimester and with weight at birth. PM10 exposure was positively associated with preterm birth and SGA.
| S-EPMC3261932 | biostudies-literature
Project description:Zika virus (ZIKV) can be transmitted sexually between humans. However, it is unknown whether ZIKV replicates in the vagina and impacts the unborn fetus. Here, we establish a mouse model of vaginal ZIKV infection and demonstrate that, unlike other routes, ZIKV replicates within the genital mucosa even in wild-type (WT) mice. Mice lacking RNA sensors or transcription factors IRF3 and IRF7 resulted in higher levels of local viral replication. Furthermore, mice lacking the type I interferon (IFN) receptor (IFNAR) became viremic and died of infection after a high-dose vaginal ZIKV challenge. Notably, vaginal infection of pregnant dams during early pregnancy led to fetal growth restriction and infection of the fetal brain in WT mice. This was exacerbated in mice deficient in IFN pathways, leading to abortion. Our study highlights the vaginal tract as a highly susceptible site of ZIKV replication and illustrates the dire disease consequences during pregnancy.
| S-EPMC5006689 | biostudies-literature
Project description:ImportancePodophyllotoxin is an antimitotic agent primarily used in the local treatment of anogenital warts. Data that enable the assessment of the fetal safety of podophyllotoxin use during pregnancy are lacking.ObjectiveTo investigate the association between local podophyllotoxin exposure during pregnancy and risk of adverse fetal outcomes.Design, setting, and participantsThis cohort study obtained individual-level pregnancy data from various nationwide registries in Denmark from the study period of January 1, 1997, through December 31, 2016, resulting in a cohort of 1 650 649 pregnancies. Pregnancies with multiple records on overlapping dates and pregnancy records with implausible or missing information on gestational age were excluded. Local podophyllotoxin-exposed pregnancies were compared with unexposed pregnancies and matched in a 1:10 ratio according to propensity scores on a wide set of baseline characteristics. Five distinct study cohorts were constructed, one for each outcome analysis. Sensitivity analyses included a comparison of podophyllotoxin-exposed pregnancies with pregnancies with podophyllotoxin use only before pregnancy onset. Data analyses were performed from April 27, 2019, to June 26, 2019.ExposuresFilled prescription for local podophyllotoxin.Main outcomes and measuresPrimary outcomes were major birth defects and spontaneous abortions. Secondary outcomes were preterm births, small-for-gestational-age (SGA) size, and stillbirths. Logistic regression was used to estimate the prevalence odds ratios (ORs) of major birth defects, preterm births, and SGA size, and Cox proportional hazards regression modeling was used to estimate hazard ratios (HRs) of spontaneous abortions and stillbirths.ResultsThis study included 9229 pregnancies (mean [SD] maternal age at pregnancy onset, 27.7 [5.2] years) for the analyses of major birth defects and 18 590 pregnancies (mean [SD] maternal age at pregnancy onset, 26.4 [6.0] years) for the analyses of spontaneous abortions. Among the podophyllotoxin-exposed pregnancies, 29 infants (3.5%) were diagnosed with major birth defects, compared with 286 (3.4%) among the unexposed pregnancies. A total of 141 podophyllotoxin-exposed pregnancies (8.3%) ended in spontaneous abortion, compared with 1626 (9.6%) among the unexposed pregnancies. No statistically significant associations were found between podophyllotoxin exposure during pregnancy and major birth defects (prevalence odds ratio [OR], 1.02 95% CI, 0.69-1.50), spontaneous abortions (HR, 0.87; 95% CI, 0.73-1.04), preterm births (prevalence OR, 1.08; 95% CI, 0.86-1.35), SGA size (prevalence OR, 1.01; 95% CI, 0.85-1.22), or stillbirths (HR, 0.58; 95% CI, 0.18-1.86). Sensitivity analyses of the primary outcomes achieved similar results.Conclusions and relevanceFindings from this study suggest that podophyllotoxin use during pregnancy may be safe, as it did not appear to be associated with an increased risk of adverse fetal outcomes. These findings may help guide clinicians, patients, and drug regulatory authorities when prescribing podophyllotoxin.
| S-EPMC6990942 | biostudies-literature
Project description:BackgroundPrenatal exposure to bisphenol A (BPA) and phthalates may affect fetal growth; however, previous findings are inconsistent and based on few studies.ObjectivesWe assessed whether prenatal exposure to BPA and phthalates was associated with fetal growth in a Spanish birth cohort of 488 mother-child pairs.MethodsWe measured BPA and eight phthalates [four di(2-ethylhexyl) phthalate metabolites (DEHPm), mono-benzyl phthalate (MBzP), and three low-molecular-weight phthalate metabolites (LMWPm)] in two spot-urine samples collected during the first and third trimester of pregnancy. We estimated growth curves for femur length (FL), head circumference (HC), abdominal circumference (AC), biparietal diameter (BPD), and estimated fetal weight (EFW) during pregnancy (weeks 12-20 and 20-34), and for birth weight, birth length, head circumference at birth, and placental weight.ResultsOverall, results did not support associations of exposure to BPA or DEHPm during pregnancy with fetal growth parameters. Prenatal MBzP exposure was positively associated with FL at 20-34 weeks, resulting in an increase of 3.70% of the average FL (95% CI: 0.75, 6.63%) per doubling of MBzP concentration. MBzP was positively associated with birth weight among boys (48 g; 95% CI: 6, 90) but not in girls (-27 g; 95% CI: -79, 25) (interaction p-value = 0.04). The LMWPm mono-n-butyl phthalate (MnBP) was negatively associated with HC at 12-20 pregnancy weeks [-4.88% of HC average (95% CI: -8.36, -1.36%)].ConclusionsThis study, one of the first to combine repeat exposure biomarker measurements and multiple growth measures during pregnancy, finds little evidence of associations of BPA or phthalate exposures with fetal growth. Phthalate metabolites MBzP and MnBP were associated with some fetal growth parameters, but these findings require replication.CitationCasas M, Valvi D, Ballesteros-Gomez A, Gascon M, Fernández MF, Garcia-Esteban R, Iñiguez C, Martínez D, Murcia M, Monfort N, Luque N, Rubio S, Ventura R, Sunyer J, Vrijheid M. 2016. Exposure to bisphenol A and phthalates during pregnancy and ultrasound measures of fetal growth in the INMA-Sabadell cohort. Environ Health Perspect 124:521-528; http://dx.doi.org/10.1289/ehp.1409190.
| S-EPMC4829997 | biostudies-literature
Project description:Maternal exposure to ambient air pollution has increasingly been linked to congenital heart defects (CHDs). The objective of this study was to evaluate whether high levels of maternal exposure to PM2.5 and PM10 are related to increased risk of CHDs in Wuhan, China. We conducted a cohort study with a total of 105,988 live-born infants, stillbirths, and fetal deaths. The study included mothers living in the urban district of Wuhan during pregnancy over the 2-year period from 10 June 2011 to 9 June 2013. For each study participant, we assigned 1-month and 1-week averages of PM10 and PM2.5 exposure based on measurements obtained from the nearest exposure monitor to the living residence of mothers during their early pregnancy period. Logistic regression analyses were conducted to calculate the adjusted odds ratios (aORs) and 95% confidence intervals (CI) for the association between exposure to these ambient air pollutants during early pregnancy and CHDs. We observed an increased risk of CHDs, particularly ventricular septal defect (VSD), with increasing PM2.5 exposure. Using 1-week averages, we also observed significant monotonically increasing associations between PM2.5 exposure during weeks 7-10 of pregnancy and risk of VSD, with aORs ranging from 1.11 to 1.17 (95% CI: 1.02-1.20, 1.03-1.22, 1.05-1.24, and 1.08-1.26 separately) per a 10??g/m(3) change in PM2.5 concentration. Our study contributes to the small body of knowledge regarding the association between in utero exposure to air pollution and CHDs, but confirmation of these associations will be needed in future studies.
| S-EPMC4913168 | biostudies-literature
Project description:1 in 5 women report cannabis use during pregnancy, with nausea cited as their primary motivation. Studies show that (-)-?9-tetrahydrocannabinol (?9-THC), the major psychoactive ingredient in cannabis, causes fetal growth restriction, though the mechanisms are not well understood. Given the critical role of the placenta to transfer oxygen and nutrients from mother, to the fetus, any compromise in the development of fetal-placental circulation significantly affects maternal-fetal exchange and thereby, fetal growth. The goal of this study was to examine, in rats, the impact of maternal ?9-THC exposure on fetal development, neonatal outcomes, and placental development. Dams received a daily intraperitoneal injection (i.p.) of vehicle control or ?9-THC (3?mg/kg) from embryonic (E)6.5 through 22. Dams were allowed to deliver normally to measure pregnancy and neonatal outcomes, with a subset sacrificed at E19.5 for placenta assessment via immunohistochemistry and qPCR. Gestational ?9-THC exposure resulted in pups born with symmetrical fetal growth restriction, with catch up growth by post-natal day (PND)21. During pregnancy there were no changes to maternal food intake, maternal weight gain, litter size, or gestational length. E19.5 placentas from ?9-THC-exposed pregnancies exhibited a phenotype characterized by increased labyrinth area, reduced Epcam expression (marker of labyrinth trophoblast progenitors), altered maternal blood space, decreased fetal capillary area and an increased recruitment of pericytes with greater collagen deposition, when compared to vehicle controls. Further, at E19.5 labyrinth trophoblast had reduced glucose transporter 1 (GLUT1) and glucocorticoid receptor (GR) expression in response to ?9-THC exposure. In conclusion, maternal exposure to ?9-THC effectively compromised fetal growth, which may be a result of the adversely affected labyrinth zone development. These findings implicate GLUT1 as a ?9-THC target and provide a potential mechanism for the fetal growth restriction observed in women who use cannabis during pregnancy.
| S-EPMC6969028 | biostudies-literature