Air Pollution Exposure During Pregnancy and Fetal Markers of Metabolic function: The MIREC Study.
Ontology highlight
ABSTRACT:
SUBMITTER: Lavigne E
PROVIDER: S-EPMC4851989 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Importance:Air pollutants interact with estrogen nuclear receptors, but their effect on thyroid signaling is less clear. Thyroid function is of particular importance for pregnant women because of the thyroid's role in fetal brain development. Objective:To determine the short-term association of exposure to air pollution in the first trimester with thyroid function throughout pregnancy. Design, Setting, and Participants:In this cohort study, 9931 pregnant women from 4 European cohorts (the Amsterdam Born Children and Their Development Study, the Generation R Study, Infancia y Medio Ambiente, and Rhea) and 1 US cohort (Project Viva) with data on air pollution exposure and thyroid function during pregnancy were included. The recruitment period for the Amsterdam Born Children and Their Development Study was January 2003 to March 2004; for Generation R, April 2002 to January 2006; for Infancia y Medio Ambiente, November 2003 to January 2008; for Rhea, February 2007 to February 2008; and for Project Viva, April 1999 to November 2002. Statistical analyses were conducted from January 2018 to April 2019. Main Outcomes and Measures:Residential air pollution concentrations (ie, nitrogen oxide and particulate matter [PM]) during the first trimester of pregnancy were estimated using land-use regression and satellite-derived aerosol optical depth models. Free thyroxine, thyrotropin, and thyroid peroxidase antibody levels were measured across gestation. Hypothyroxinemia was defined as free thyroxine below the fifth percentile of the cohort distribution with normal thyrotropin levels, following the American Thyroid Association guidelines. Results:Among 9931 participants, the mean (SD) age was 31.2 (4.8) years, 4853 (48.9%) had more than secondary educational levels, 5616 (56.6%) were nulliparous, 404 (4.2%) had hypothyroxinemia, and 506 (6.7%) tested positive for thyroid peroxidase antibodies. Concentrations of nitrogen dioxide and PM with an aerodynamic diameter of 2.5 ?m or less (PM2.5) were lower and had less variation in women in the US cohort than those in European cohorts. No associations of nitrogen oxide with thyroid function were found. Higher exposures to PM2.5 were associated with higher odds of hypothyroxinemia in pregnant women (odds ratio per 5-?g/m3 change, 1.21; 95% CI, 1.00-1.47). Although exposure to PM with an aerodynamic diameter of 10 ?m or less was not significantly associated with hypothyroxinemia, the coefficient was similar to that for the association of PM2.5 with hypothyroxinemia (odds ratio per 10-?g/m3 change, 1.18; 95% CI, 0.93-1.48). Absorbances of PM2.5 and PM with aerodynamic diameter from 2.5 to 10 ?g and were not associated with hypothyroxinemia. There was substantial heterogeneity among cohorts with respect to thyroid peroxidase antibodies (P for heterogeneity, <.001), showing associations of nitrogen oxide and PM with thyroid autoimmunity only in the women in the Generation R Study. Conclusions and Relevance:The findings of this study suggest that first-trimester exposures to PM2.5 were associated with mild thyroid dysfunction throughout pregnancy. The association of PM2.5 exposure with thyroid function during pregnancy is of global health importance because air pollution exposure is widespread and hypothyroxinemia may adversely influence the brain development of offspring.
| S-EPMC6806433 | biostudies-literature
Project description:Fetal heart rate (FHR) monitoring is essential for fetal management during pregnancy and delivery but results in many false-positive diagnoses. Air pollution affects the uterine environment; thus, air pollution may change FHR reactivity. This study assessed the association between exposure to air pollution during pregnancy and FHR monitoring abnormalities using 2005-2010 data from the Japan Perinatal Registry Network database. Participants were 23,782 singleton pregnant women with FHR monitoring, without acidemia or fetal asphyxia. We assessed exposure to air pollutants, including particulate matter (PM), ozone, nitrogen dioxide (NO2), and sulfur dioxide (SO2). In a multi-trimester model, first-trimester PM exposure was associated with false positives in FHR monitoring (odds ratio [OR] per interquartile range (10.7 ?g/m3) increase?=?1.20; 95% CI: 1.05-1.37), but not second-trimester exposure (OR?=?1.05; 95% CI: 0.91-1.21) and third-trimester exposure (OR?=?1.06; 95% CI: 0.96-1.17). The association with first-trimester PM exposure persisted after adjustment for exposure to ozone, NO2, and SO2; however, ozone, NO2, and SO2 exposure was not associated with false positives in FHR monitoring. First-trimester PM exposure may alter fetal cardiac response and lead to false positives in FHR monitoring.
| S-EPMC5622039 | biostudies-literature
Project description:Maternal exposure to ambient air pollution has been associated with adverse birth outcomes such as preterm delivery. However, only one study to date has linked air pollution to blood pressure changes during pregnancy, a period of dramatic cardiovascular function changes.We examined whether maternal exposures to criteria air pollutants, including particles of less than 10 ?m (PM(10)) or 2.5 ?m diameter (PM(2.5)), carbon monoxide (CO), nitrogen dioxide (NO(2)), sulfur dioxide (SO(2)), and ozone (O(3)), in each trimester of pregnancy are associated with magnitude of rise of blood pressure between the first 20 weeks of gestation and late pregnancy in a prospectively followed cohort of 1684 pregnant women in Allegheny County, PA.Air pollution measures for maternal ZIP code areas were derived using Kriging interpolation. Using logistic regression analysis, we evaluated the associations between air pollution exposures and blood pressure changes between the first 20 weeks of gestation and late pregnancy.First trimester PM(10) and ozone exposures were associated with blood pressure changes between the first 20 weeks of gestation and late pregnancy, most strongly in non-smokers. Per interquartile increases in first trimester PM(10) and O(3) concentrations were associated with mean increases in systolic blood pressure of 1.88 mm Hg (95% CI=0.84 to 2.93) and 1.84 (95% CI=1.05 to 4.63), respectively, and in diastolic blood pressure of 0.63 mm Hg (95% CI=-0.50 to 1.76) and 1.13 (95% CI=-0.46 to 2.71) in non-smokers.Our novel finding suggests that first trimester PM(10) and O(3) air pollution exposures increase blood pressure in the later stages of pregnancy. These changes may play a role in mediating the relationships between air pollution and adverse birth outcomes.
| S-EPMC3656658 | biostudies-literature
Project description:BackgroundExposure to air pollution has been associated with higher C-reactive protein (CRP) levels, suggesting an inflammatory response. Not much is known about this association in pregnancy.ObjectivesWe investigated the associations of air pollution exposure during pregnancy with maternal and fetal CRP levels in a population-based cohort study in the Netherlands.MethodsParticulate matter (PM) with an aerodynamic diameter ? 10 ?m (PM10) and nitrogen dioxide (NO2) levels were estimated at the home address using dispersion modeling for different averaging periods preceding the blood sampling (1 week, 2 weeks, 4 weeks, and total pregnancy). High-sensitivity CRP levels were measured in maternal blood samples in early pregnancy (n = 5,067) and in fetal cord blood samples at birth (n = 4,450).ResultsCompared with the lowest quartile, higher PM10 exposure levels for the prior 1 and 2 weeks were associated with elevated maternal CRP levels (> 8 mg/L) in the first trimester [fourth PM10 quartile for the prior week: odds ratio (OR), 1.32; 95% confidence interval (CI): 1.08, 1.61; third PM10 quartile for the prior 2 weeks: OR, 1.28; 95% CI: 1.06, 1.56]; however, no clear dose-response relationships were observed. PM10 and NO2 exposure levels for 1, 2, and 4 weeks preceding delivery were not consistently associated with fetal CRP levels at delivery. Higher long-term PM10 and NO2 exposure levels (total pregnancy) were associated with elevated fetal CRP levels (> 1 mg/L) at delivery (fourth quartile PM10: OR, 2.18; 95% CI: 1.08, 4.38; fourth quartile NO2: OR, 3.42; 95% CI: 1.36, 8.58; p-values for trend < 0.05).ConclusionsOur results suggest that exposure to air pollution during pregnancy may lead to maternal and fetal inflammatory responses.
| S-EPMC3346784 | biostudies-literature
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:In this study, we modeled early life air pollution exposure using C57BL/6J male mice on a controlled chow diet, exposed to real-world inhaled concentrated PM2.5 (~10x ambient level/ ~60-120g/m3) or filtered air (FA) over 14 weeks. We investigated PM2.5 effects on phenotype, transcriptome and chromatin accessibility, compared the effects with a prototypical high-fat diet (HFD) stimulus, and examined the effects of cessation of exposure on reversibility of phenotype/genotype.
2020-11-05 | GSE145840 | GEO
Project description:PURPOSE:Maternal asthma increases adverse neonatal respiratory outcomes, and pollution may further increase risk. Air quality in relation to neonatal respiratory health has not been studied. METHODS:Transient tachypnea of the newborn (TTN), asphyxia, and respiratory distress syndrome (RDS) were identified using medical records among 223,375 singletons from the Consortium on Safe Labor (2002-2008). Community Multiscale Air Quality models estimated pollutant exposures. Multipollutant Poisson regression models calculated adjusted relative risks of outcomes for interquartile range increases in average exposure. Maternal asthma and preterm delivery were evaluated as effect modifiers. RESULTS:TTN risk increased after particulate matter (PM) less than or equal to 10-micron exposure during preconception and trimester one (9-10%), and whole-pregnancy exposure to PM less than or equal to 2.5 microns (PM2.5; 17%) and carbon monoxide (CO; 10%). Asphyxia risk increased after exposure to PM2.5 in trimester one (48%) and whole pregnancy (84%), CO in trimester two and whole pregnancy (28-32%), and consistently for ozone (34%-73%). RDS risk was associated with increased concentrations of nitrogen oxides (33%-42%) and ozone (9%-21%) during all pregnancy windows. Inverse associations were observed with several pollutants, particularly sulfur dioxide. No interaction with maternal asthma was observed. Restriction to term births yielded similar results. CONCLUSIONS:Several pollutants appear to increase neonatal respiratory outcome risks.
| S-EPMC6232679 | biostudies-literature
Project description:BackgroundPrenatal exposure to outdoor air pollution has been shown to have health effects in many studies; low birth weight, preterm delivery, small for gestational age, and stillbirth are the most often cited. However, exposure of pregnant women is difficult to quantify, especially with regard to their mobility, which is rarely taken into account in epidemiological studies. This study aimed to assess the impact of mobility of pregnant women living in Paris, France, on their exposure estimates to nitrogen dioxide (NO2).MethodsA total of 486 pregnant women were recruited in 5 maternity hospitals in Paris between January and April 2016. A questionnaire was used to collect mothers' characteristics (demography, education, etc.) and to assess their daily mobility during pregnancy (time spent at work, commuting time and mode used to move from residential to occupational places). Daily NO2 concentrations were estimated based on the combination of annual average concentrations modeled at the census block scale and daily concentrations measured from fixed monitoring stations. Different models were used to compare the exposure of pregnant women in residential and occupational places, also taking into account travel time and travel mode. The socioeconomic profile of the census blocks was characterized using a multi-component index.ResultsDuring the first trimester of pregnancy, women living in the least deprived census blocks were exposed to higher concentrations of NO2 than those living in the most deprived ones. Occupational mobility had a small impact on exposure levels (average increase after taking account of mobility: + 0.52 μg/m3) which was not related to the socioeconomic profile of the women. The commuting mode made a greater difference (+ 1.46 μg/m3 on average), in particular among women living in the most deprived census blocks.ConclusionsOur study illustrates that air pollution exposure can be underestimated when ignoring occupational mobility and commuting mode of pregnant women. This effect might be differential according to the neighborhood deprivation profile.
| S-EPMC6194718 | biostudies-literature
Project description:BackgroundPerinatal exposure to air pollution and immune system dysregulation are two factors consistently associated with autism spectrum disorders (ASD) and other neurodevelopmental outcomes. However, little is known about how air pollution may influence maternal immune function during pregnancy.ObjectivesTo assess the relationship between mid-gestational circulating levels of maternal cytokines/chemokines and previous month air pollution exposure across neurodevelopmental groups, and to assess whether cytokines/chemokines mediate the relationship between air pollution exposures and risk of ASD and/or intellectual disability (ID) in the Early Markers for Autism (EMA) study.MethodsEMA is a population-based, nested case-control study which linked archived maternal serum samples collected during weeks 15-19 of gestation for routine prenatal screening, birth records, and Department of Developmental Services (DDS) records. Children receiving DDS services for ASD without intellectual disability (ASD without ID; n = 199), ASD with ID (ASD with ID; n = 180), ID without ASD (ID; n = 164), and children from the general population (GP; n = 414) with no DDS services were included in this analysis. Serum samples were quantified for 22 cytokines/chemokines using Luminex multiplex analysis technology. Air pollution exposure for the month prior to maternal serum collection was assigned based on the Environmental Protection Agency's Air Quality System data using the maternal residential address reported during the prenatal screening visit.ResultsPrevious month air pollution exposure and mid-gestational maternal cytokine and chemokine levels were significantly correlated, though weak in magnitude (ranging from - 0.16 to 0.13). Ten pairs of mid-pregnancy immune markers and previous month air pollutants were significantly associated within one of the child neurodevelopmental groups, adjusted for covariates (p < 0.001). Mid-pregnancy air pollution was not associated with any neurodevelopmental outcome. IL-6 remained associated with ASD with ID even after adjusting for air pollution exposure.ConclusionThis study suggests that maternal immune activation is associated with risk for neurodevelopmental disorders. Furthermore, that prenatal air pollution exposure is associated with small, but perhaps biologically relevant, effects on maternal immune system function during pregnancy. Additional studies are needed to better evaluate how prenatal exposure to air pollution affects the trajectory of maternal immune activation during pregnancy, if windows of heightened susceptibility can be identified, and how these factors influence neurodevelopment of the offspring.
| S-EPMC7745402 | biostudies-literature
Project description:BackgroundAir pollution nowadays has seriously threatened the health of the Chinese population, especially in the vulnerable groups of fetuses, infants and toddlers. In particular, the effects of air pollution on children's neurobehavioral development have attracted widespread attention. Moreover, the early detection of a sensitive period is very important for the precise intervention of the disease. However, such studies focusing on hyperactive behaviors and susceptible window identification are currently lacking in China.ObjectivesThe study aims to explore the correlation between air pollution exposure and hyperactive behaviors during the early life stage and attempt to identify whether a susceptible exposure window exists that is crucial for further precise intervention.MethodsBased on the Longhua Child Cohort Study, we collected the basic information and hyperactivity index of 26,052 children using a questionnaire conducted from 2015 to 2017, and the Conners' Parent Rating Scale-revised (CPRS-48) was used to assess hyperactive behaviors. Moreover, the data of air pollution concentration (PM10, PM2.5, NO2, CO, O3 and SO2) were collected from the monitoring station between 2011 to 2017, and a land-use random forest model was used to evaluate the exposure level of each subject. Furthermore, Distributed lag non-linear models (DLNMs) were applied for statistic analysis.ResultsThe risk of child hyperactivity was found to be positively associated with early life exposure to PM10, PM2.5 and NO2. In particular, for an increase of per 10 µg/m3 in PM10, PM2.5 and NO2 exposure concentration during early life, the risk of child hyperactivity increased significantly during the seventh month of pregnancy to the fourth month after birth, with the strongest association in the ninth month of pregnancy (PM10: OR = 1.043, 95% CI: 1.016-1.071; PM2.5: OR = 1.062, 95% CI: 1.024-1.102; NO2: OR = 1.043, 95% CI: 1.016-1.071). However, no significant associations among early life exposure to CO, O3 and SO2 and child hyperactive behaviors were observed.ConclusionsEarly life exposure to PM10, PM2.5 and NO2 is associated with an increased risk of child ADHD-like behaviors at the age around 3 years, and the late-prenatal and early postnatal periods might be the susceptible exposure windows.
| S-EPMC9518584 | biostudies-literature