Prenatal Air Pollution Exposure Research Articles

Prenatal Air Pollution Exposure and Blood Pressure during Childhood and Adolescence: findings from Project Viva

Prenatal Air Pollution Exposure and Blood Pressure during Childhood and Adolescence: findings from Project Viva

Prenatal ambient air pollutant mixture exposure and neurodevelopment in urban children in the Northeastern United States

BackgroundStudies of prenatal air pollution (AP) exposure on child neurodevelopment have mostly focused on a single pollutant. We leveraged daily exposure data and implemented novel data-driven statistical approaches to assess effects of prenatal exposure to a mixture of seven air pollutants on cognitive functioning in school-age children from an urban pregnancy cohort. MethodsAnalyses included 236 children born at ≥37 weeks gestation. Maternal prenatal daily exposure levels for nitrogen dioxide (NO2), ozone (O3), and constituents of fine particles [elemental carbon (EC), organic carbon (OC), nitrate (NO3−), sulfate (SO42−), ammonium (NH4+)] were estimated based on residential addresses using validated satellite-based hybrid models or global 3-D chemical-transport models. Children completed Wide Range Assessment of Memory and Learning (WRAML-2) and Conners’ Continuous Performance Test (CPT-II) at 6.5 ± 0.9 years of age. Time-weighted levels for mixture pollutants were estimated using Bayesian Kernel Machine Regression Distributed Lag Models (BKMR-DLMs), with which we also explored the interactions in the exposure-response functions among pollutants. Resulting time-weighted exposure levels were used in Weighted Quantile Sum (WQS) regressions to examine AP mixture effects on outcomes, adjusted for maternal age, education, child sex, and prenatal temperature. ResultsMothers were primarily ethnic minorities (81% Hispanic and/or black) reporting ≤12 years of education (68%). Prenatal AP mixture (per unit increase in WQS estimated AP index) was associated with decreased WRAML-2 general memory (GM; β = −0.64, 95%CI = −1.40, 0.00) and memory-related attention/concentration (AC; β = −1.03, 95%CI = −1.78, −0.27) indices, indicating poorer memory functioning, as well as increased CPT-II omission errors (OE; β = 1.55, 95%CI = 0.34, 2.77), indicating increased attention problems. When stratified by sex, association with AC index was significant among girls, while association with OE was significant among boys. Traffic-related pollutants (NO2, OC, EC) and SO42− were major contributors to these associations. There was no significant evidence of interactions among mixture components. ConclusionsPrenatal exposure to an AP mixture was associated with child neurocognitive outcomes in a sex- and domain-specific manner.

Prenatal exposure to air pollution is associated with structural changes in the neonatal brain

BackgroundPrenatal exposure to air pollution is associated with adverse neurologic consequences in childhood. However, the relationship between in utero exposure to air pollution and neonatal brain development is unclear. MethodsWe modelled maternal exposure to nitrogen dioxide (NO2) and particulate matter (PM2.5 and PM10) at postcode level between date of conception to date of birth and studied the effect of prenatal air pollution exposure on neonatal brain morphology in 469 (207 male) healthy neonates, with gestational age of ≥36 weeks. Infants underwent MR neuroimaging at 3 Tesla at 41.29 (36.71–45.14) weeks post-menstrual age (PMA) as part of the developing human connectome project (dHCP). Single pollutant linear regression and canonical correlation analysis (CCA) were performed to assess the relationship between air pollution and brain morphology, adjusting for confounders and correcting for false discovery rate. ResultsHigher exposure to PM10 and lower exposure to NO2 was strongly canonically correlated to a larger relative ventricular volume, and moderately associated with larger relative size of the cerebellum. Modest associations were detected with higher exposure to PM10 and lower exposure to NO2 and smaller relative cortical grey matter and amygdala and hippocampus, and larger relaive brainstem and extracerebral CSF volume. No associations were found with white matter or deep grey nuclei volume. ConclusionsOur findings show that prenatal exposure to air pollution is associated with altered brain morphometry in the neonatal period, albeit with opposing results for NO2 and PM10. This finding provides further evidence that reducing levels of maternal exposure to particulate matter during pregnancy should be a public health priority and highlights the importance of understanding the impacts of air pollution on this critical development window.

Cognitive Development and Prenatal Air Pollution Exposure in the CHAMACOS Cohort.

Because fine particulate matter [PM, with aerodynamic diameter ()] is a ubiquitous environmental exposure, small changes in cognition associated with exposure could have great societal costs. Prior studies have demonstrated a relationship between in utero exposure and cognitive development in urban populations, but it is not known whether these effects are similar in rural populations and whether they persist into late childhood. In this study, we tested for associations between prenatal exposure and both full-scale and subscale measures of IQ among a longitudinal cohort at age 10.5 y. This analysis used data from 568 children enrolled in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), a birth cohort study in California's agricultural Salinas Valley. Exposures were estimated at residential addresses during pregnancy using state of the art, modeled surfaces. IQ testing was performed by bilingual psychometricians in the dominant language of the child. A higher average over pregnancy was associated with full-scale IQ points [95% confidence interval (CI): , ], with decrements specifically in Working Memory IQ (WMIQ) and Processing Speed IQ (PSIQ) subscales [WMIQ (95% CI: , ) and PSIQ (95% CI: , 0.16)]. Flexible modeling over the course of pregnancy illustrated mid-to-late pregnancy (months 5-7) as particularly susceptible times, with sex differences in the timing of susceptible windows and in which subscales were most affected [Verbal Comprehension IQ (VCIQ) and WMIQ in males; and PSIQ in females]. We found that small increases in outdoor exposure in utero were associated with slightly lower IQ in late childhood, robust to many sensitivity analyses. In this cohort there was a larger effect of on childhood IQ than has previously been observed, perhaps due to differences in PM composition or because developmental disruption could alter the cognitive trajectory and thus appear more pronounced as children get older. https://doi.org/10.1289/EHP10812.

Prenatal exposure to ambient air pollution is associated with neurodevelopmental outcomes at 2 years of age

BackgroundHigher prenatal ambient air pollution exposure has been associated with impaired neurodevelopment in preschoolers and school-aged children. The purpose of this study was to explore the relationships between prenatal ambient air pollution exposure and neurodevelopment during infancy.MethodsThis study examined 161 Latino mother-infant pairs from the Southern California Mother’s Milk Study. Exposure assessments included prenatal nitrogen dioxide (NO2) and particulate matter smaller than 2.5 and 10 microns in diameter (PM2.5 and PM10, respectively). The pregnancy period was also examined as three windows, early, mid, and late, which describe the first, middle, and last three months of pregnancy. Infant neurodevelopmental outcomes at 2 years of age were measured using the Bayley-III Scales of Infant and Toddler Development. Multivariable linear models and distributed lag linear models (DLM) were used to examine relationships between prenatal exposures and neurodevelopmental scores, adjusting for socioeconomic status, breastfeeding frequency, time of delivery, pre-pregnancy body mass index, and infant birthweight and sex.ResultsHigher prenatal exposure to PM10 and PM2.5 was negatively associated with composite cognitive score (β = -2.01 [-3.89, -0.13] and β = -1.97 [-3.83, -0.10], respectively). In addition, higher average prenatal exposure to PM10 was negatively associated with composite motor (β = -2.35 [-3.95, -0.74]), scaled motor (β = -0.77 [-1.30, -0.24]), gross motor (β = -0.37 [-0.70, -0.04]), fine motor (β = -0.40 [-0.71, -0.09]), composite language (β = -1.87 [-3.52, -0.22]), scaled language (β = -0.61 [-1.18, -0.05]) and expressive communication scaled scores (β = -0.36 [-0.66, -0.05]). DLMs showed that higher prenatal air pollution exposure during mid and late pregnancy was inversely associated with motor, cognitive, and communication language scores.ConclusionsHigher exposure to air pollutants during pregnancy, particularly in the mid and late prenatal periods, was inversely associated with scaled and composite motor, cognitive, and language scores at 2 years. These results indicate that prenatal ambient air pollution may negatively impact neurodevelopment in early life.

Ambient prenatal air pollution exposure is associated with low cord blood IL‐17a in infants

Ambient prenatal air pollution exposure is associated with low cord blood IL‐17a in infants

In utero particulate matter exposure in association with newborn mitochondrial ND4L10550A>G heteroplasmy and its role in overweight during early childhood

BackgroundMitochondria play an important role in the energy metabolism and are susceptible to environmental pollution. Prenatal air pollution exposure has been linked with childhood obesity. Placental mtDNA mutations have been associated with prenatal particulate matter exposure and MT-ND4L10550A>G heteroplasmy has been associated with BMI in adults. Therefore, we hypothesized that in utero PM2.5 exposure is associated with cord blood MT-ND4L10550A>G heteroplasmy and early life growth. In addition, the role of cord blood MT-ND4L10550A>G heteroplasmy in overweight during early childhood is investigated.MethodsThis study included 386 mother-newborn pairs. Outdoor PM2.5 concentrations were determined at the maternal residential address. Cord blood MT-ND4L10550A>G heteroplasmy was determined using Droplet Digital PCR. Associations were explored using logistic regression models and distributed lag linear models. Mediation analysis was performed to quantify the effects of prenatal PM2.5 exposure on childhood overweight mediated by cord blood MT-ND4L10550A>G heteroplasmy.ResultsPrenatal PM2.5 exposure was positively associated with childhood overweight during the whole pregnancy (OR = 2.33; 95% CI: 1.20 to 4.51; p = 0.01), which was mainly driven by the second trimester. In addition, prenatal PM2.5 exposure was associated with cord blood MT-ND4L10550A>G heteroplasmy from gestational week 9 – 13. The largest effect was observed in week 10, where a 5 µg/m3 increment in PM2.5 was linked with cord blood MT-ND4L10550A>G heteroplasmy (OR = 0.93; 95% CI: 0.87 to 0.99). Cord blood MT-ND4L10550A>G heteroplasmy was also linked with childhood overweight (OR = 3.04; 95% CI: 1.15 to 7.50; p = 0.02). The effect of prenatal PM2.5 exposure on childhood overweight was mainly direct (total effect OR = 1.18; 95% CI: 0.99 to 1.36; natural direct effect OR = 1.20; 95% CI: 1.01 to 1.36)) and was not mediated by cord blood MT-ND4L10550A>G heteroplasmy.ConclusionsCord blood MT-ND4L10550A>G heteroplasmy was linked with childhood overweight. In addition, in utero exposure to PM2.5 during the first trimester of pregnancy was associated with cord blood MT-ND4L10550A>G heteroplasmy in newborns. Our analysis did not reveal any mediation of cord blood MT-ND4L10550A>G heteroplasmy in the association between PM2.5 exposure and childhood overweight.

Newborn ribosomal DNA content as a potential early marker of genomic instability and longevity in association with prenatal air pollution exposure

BACKGROUND AND AIM: Repetitive regions in the genome, including ribosomal DNA repeats, have essential functions in genome stability. Alterations in ribosomal DNA copy numbers (rDNAcn) associates with genome-wide methylation and gene-expression, and links with longevity, as proposed in the rDNA theory of aging. Prenatal air pollution exposures affect molecular markers of aging that may underly later life health effects. We studied the association between prenatal air pollution exposure and this novel potential aging marker (rDNAc) in newborns. METHODS: Cord blood rDNAcn (45S rDNA) was measured in 177 newborns from the ENVIRONAGE birth cohort using ddPCR. Maternal residential exposure to PM10, PM2.5, NO2, and BC during pregnancy was estimated using a high-resolution spatial-temporal interpolation method. Using multivariable-adjusted distributed lag models, newborn rDNAcn was associated with average weekly air pollution exposures. RESULTS: The mean cord blood rDNAcn was 245 (SD: 64). Higher prenatal exposure to PM10, PM2.5, and NO2 in early to mid-pregnancy (weeks 9-18) was associated with an increase in rDNAcn. Each SD increment in air pollutants was associated with an average increase of 22.5 (95%CI: 5.9 to 35.0) copy numbers. Higher exposure to PM10, PM2.5, NO2, and BC late in pregnancy (weeks 25-35) was strongly associated with a decrease in rDNAcn. Each SD increment in air pollutants was associated with an average decrease of –29.6 (95%CI: –49.9 to –9.4) copy numbers. CONCLUSIONS: We studied for the first time rDNAcn in newborns and show that prenatal air pollution exposure is associated with rDNA repeats at birth. These results add evidence to the impact of air pollution on genome stability and early aging mechanisms. Evaluating the rDNA concept of aging in relation to diseases may further show the link between prenatal air, molecular alterations, and health later in life. KEYWORDS: genome instability, aging, ribosomal DNA copy number, prenatal air pollution

Prenatal air pollution exposure and infant weight trajectories from 3rd trimester to 2 years of age

BACKGROUND AND AIM: Prenatal exposure to air pollution is increasingly viewed as harmful to fetal development and leads to childhood obesity. However, few studies have evaluated in utero growth measures and postnatal weight trajectories along a continuum in statistical models. This study aims to evaluate associations between prenatal air pollution and weight trajectories from the 3rd trimester through 2 years of life among infants in the Maternal and Development Risks from Environmental and Social Stressors (MADRES) pregnancy cohort, which comprises a low-income, primarily Hispanic population in Los Angeles, California. METHODS: Fetal weights during the 3rd trimester were abstracted from maternal ultrasound records. Infant weight measures were abstracted from medical records and measured by staff at study visits. Ambient particulate matter ≤2.5 μm and ≤10 μm in diameter (PM2.5 and PM10) concentrations were assigned using spatial interpolation from the regulatory air monitoring stations. Piecewise linear spline models were used to assess non-linear associations between prenatal air pollution exposure and infant weight trajectories. RESULTS: Weight increased most rapidly from 3 months prior to birth through 3 months of age, slowing thereafter. Pregnancy-averaged PM2.5 and PM10 were associated with a slower rate of growth from the 3rd trimester until age 2 years. A one IQR increase in PM2.5 (1.65 ug/m3) and PM10 (7.48 ug/m3) exposure were associated with a 0.28 kg and 0.38 kg lower weight at 2 years of age, respectively. In sex-stratified models, the effects of PM2.5 and PM10 were only significant in females. CONCLUSIONS: Our findings suggest that prenatal exposure to PM2.5 and PM10 could impact infant weight gain trajectories and thus, impact childhood obesity, with potentially more pronounced impacts among females. KEYWORDS: prenatal air pollution, growth trajectory

Exposure Errors due to Inaccurate Residential Addresses and their Impact on Epidemiological Associations: Evidence from a National Neonate Dataset

Background and aim: Studies assessing the associations between prenatal air pollution exposures and birth outcomes commonly use maternal addresses at the time of delivery as a proxy for residency throughout pregnancy. In large-scale studies, administrative addresses are widely used as a proxy for maternal residency throughout pregnancy under the assumption that they are up-to-date. However, if residential mobility is not reported, inaccurate addresses may introduce exposure estimation errors that might affect the study results. The aim of this study is to examine the use of the Israeli population registry addresses to assign exposure estimations and evaluates the impact of inaccurate addresses on estimates and association measures of prenatal exposures with congenital hypothyroidism. Methods: We used morbidity data from the national program for neonatal screening for 2009-2015 and address data from two sources. We selected neonates with geocoded addresses from both sources (N=685,491) and developed an address comparison algorithm. Next, we assigned neonates with exposures, evaluated exposure assessment differences, and used multivariable logistic regression models to assess the impact that these differences have on association measures. Results: We found that most of the exposure differences between neonates with addresses from both sources were around zero and had a leptokurtic distribution density, with most values being zero. Additionally, associations between exposure and congenital hypothyroidism were comparable, regardless of address source and when we limited the model to neonates with identical addresses. . Conclusions: For our study population and based on the exposure estimation models we used, we found that ignoring residential inaccuracies results in only a small bias of the associations towards the null. The results validate the use of administrative residential addresses for exposure assessment in studies of PM, NO2, and NOX exposures when more detailed residential data are not available. Keywords: Exposure errors, particulate matter, nitrogen oxides, congenital hypothyroidism.

DNA methylation as a potential mediator of the association between indoor air pollution and neurodevelopmental delay in a South African birth cohort

Background and Aim Prenatal exposure to indoor air pollution (IAP) has been linked to neurodevelopmental delay in toddlers. Changes in DNA methylation (DNAm) have been independently associated with both prenatal air pollution exposure and delayed neurodevelopment. Investigating DNAm as a mediator may help to elucidate the biological pathways driving the association between IAP and neurodevelopmental delay. In this study, we aim to identify differentially methylated CpG sites and gene regions that mediate this association. Methods We analyzed data from 142 mother-child pairs enrolled in the South African Drakenstein Child Health Study. DNAm from cord blood was measured using the Infinium MethylationEPIC and HumanMethylation450 arrays. Particulate matter with an aerodynamic diameter of 10m or less (PM10) was measured inside participants’ homes during the second trimester of pregnancy. Neurodevelopment was assessed at age 2 years using the Bayley Scales of Infant and Toddler Development III in four domains (cognitive function, general adaptive behavior, language, and motor function). We used three high-dimensional mediation analysis techniques (HIMA, DACT and gHMA) to identify potential mediators, complemented with causal mediation analysis to assess the robustness of our results. Results Differential methylation at 29 CpG sites and 4 gene regions (GOPC, RP11-74K11.1, DYRK1A, RNMT) was found to significantly mediate the association between prenatal PM10 exposure and cognitive neurodevelopment. Estimated proportion mediated (95%-confidence interval) ranged from 0.29 (0.01,0.86) for cg00694520 to 0.54 (0.11,1.56) for cg05023582. Conclusions DYRK1A and several of the genes our CpG sites mapped to, including CNKSR1, IPO13, IFNGR1, LONP2, and CDH1 are associated with biological pathways implicated in neurodevelopment and three of our identified CpG sites (cg23560546, cg22572779, cg15000966) have been previously associated with fetal brain development. These findings suggest that DNAm may mediate the association between prenatal PM10 exposure and cognitive neurodevelopment. Keywords: particulate matter, neurodevelopment, cord blood, epigenetics, newborn DNA methylation

In-utero exposure to air pollution and blood pressure in children from the Rhea birth cohort study, Greece

BACKGROUND AND AIM: High blood pressure (BP) in childhood has been linked with hypertension and impaired cardiovascular health within adulthood. Exposure to air pollution has been associated with elevated BP in children but only a few studies evaluated the persistence of these associations into early adolescence. We investigated the association between pregnancy exposure to air pollution and BP through childhood in the Rhea birth cohort in Greece. METHODS: Residential exposure to particulate matter <10 μm (PM10) and <2.5 μm (PM2.5) during pregnancy was estimated with temporally adjusted land-use regression models. We measured systolic (SBP) and diastolic (DBP) blood pressure at 4, 6, and 11 years. Hypertension was defined as DBP or SBP ≥95th sex-, age- and height-percentiles. Generalized estimating equation and multivariate regression models assessed the associations (per 5 µg/m³) with repeated and single time-point measures, respectively. We also tested effect modification by sex and maternal smoking. RESULTS: Median (IQR) levels of PM2.5 and PM10 during pregnancy were 14.4 (2.4) μg/m3 and 35.6 (2.3) μg/m3, respectively. PM10 was associated with higher SBP and DBP in boys but lower in girls (p-interaction= 0.025 and 0.036) at 4 years. We also observed higher risk for hypertension overall (1.62; 95% CI: 1.04, 2.53) and in boys (2.01; 95% CI: 1.07, 3.79), and in children born to non-smoking mothers during pregnancy (2.14; 95% CI: 1.25, 3.66). Higher PM2.5 was associated with lower SBP in boys at 6 (β= -3.75 mmHg; 95% CI: -7.14, -0.36) and 11 years (β= -4.49 mmHg; 95% CI: -9.09, 0.11; p-interaction= 0.068 and 0.072). Sex differences in BP trajectories were also observed. CONCLUSIONS: This study suggests that prenatal air pollution exposure may affect blood pressure during childhood. Further research is needed to understand sex differences and the role of co-exposure to maternal smoking. KEYWORDS: Blood pressure, childhood, air pollution, prenatal

Prenatal air pollution exposure and childhood obesity: Effect modification by maternal fruits and vegetables intake

Prenatal air pollution exposure and childhood obesity: Effect modification by maternal fruits and vegetables intake

Newborn Metabolomics linking prenatal air pollution exposure and autism spectrum disorder risk in children

Newborn Metabolomics linking prenatal air pollution exposure and autism spectrum disorder risk in children

Prenatal exposure to ambient air pollution is associated with early life immune perturbations

Exposure to ambient air pollution has been linked to asthma, allergic rhinitis, and other inflammatory disorders, but little is known about the underlying mechanisms. We studied the potential mechanisms leading from prenatal ambient air pollution exposure to asthma and allergy in childhood. Long-term exposure to nitrogen dioxide (NO2) as well as to particulate matter with a diameter of ≤2.5 and ≤10 μm (PM2.5 and PM10) were modeled at the residence level from conception to 6 years of age in 700 Danish children followed clinically for development of asthma and allergy. Nasal mucosal immune mediators were assessed at age 4 weeks and 6 years, inflammatory markers in blood at 6 months, and nasal epithelial DNA methylation and gene expression at age 6 years. Higher prenatal air pollution exposure with NO2, PM2.5, and PM10 was associated with an altered nasal mucosal immune profile at 4 weeks, conferring an increased odds ratio [95% confidence interval] of 2.68 [1.58, 4.62] for allergic sensitization and 2.63 [1.18, 5.81] for allergic rhinitis at age 6 years, and with an altered immune profile in blood at age 6 months conferring increased risk of asthma at age 6 years (1.80 [1.18, 2.76]). Prenatal exposure to ambient air pollution was not robustly associated with immune mediator, epithelial DNA methylation, or gene expression changes in nasal cells at age 6 years. Prenatal exposure to ambient air pollution was associated with early life immune perturbations conferring risk of allergic rhinitis and asthma. These findings suggest potential mechanisms of prenatal exposure to ambient air pollution on the developing immune system.

Exposure errors due to inaccurate residential addresses and their impact on epidemiological associations: Evidence from a national neonate dataset.

Studies assessing the associations between prenatal air pollution exposures and birth outcomes commonly use maternal addresses at the time of delivery as a proxy for residency throughout pregnancy. Yet, in large-scale epidemiology studies, maternal addresses commonly originate from an administrative source. This study aimed to examine the use of population registry addresses to assign exposure estimations and to evaluate the impact of inaccurate addresses on exposure estimates and association measures of prenatal exposures with congenital hypothyroidism. We used morbidity data for congenital hypothyroidism from the national program for neonatal screening for 2009-2015 and address data from two sources: population registry and hospital records. We selected neonates with geocoded addresses from both sources (N=685,491) and developed a comparison algorithm for these addresses. Next, we assigned neonates with exposures from ambient air pollution of PM and NO₂/NO_X, evaluated exposure assessment differences, and used multivariable logistic regression models to assess the impact that these differences have on association measures. We found that most of the exposure differences between neonates with addresses from both sources were around zero and had a leptokurtic distribution density, with most values being zero. Additionally, associations between exposure and congenital hypothyroidism were comparable, regardless of address source and when we limited the model to neonates with identical addresses. We found that ignoring residential inaccuracies results in only a small bias of the associations towards the null. These results strengthen the validity of addresses from population registries for exposure assessment, when detailed residential data during pregnancy are not available.

Prenatal Exposure to Ambient Air Pollution and Epigenetic Aging at Birth in Newborns.

In utero air pollution exposure has been associated with adverse birth outcomes, yet effects of air pollutants on regulatory mechanisms in fetal growth and critical windows of vulnerability during pregnancy are not well understood. There is evidence that epigenetic alterations may contribute to these effects. DNA methylation (DNAm) based age estimators have been developed and studied extensively with health outcomes in recent years. Growing literature suggests environmental factors, such as air pollution and smoking, can influence epigenetic aging. However, little is known about the effect of prenatal air pollution exposure on epigenetic aging. In this study, we leveraged existing data on prenatal air pollution exposure and cord blood DNAm from 332 mother-child pairs in the Early Autism Risk Longitudinal Investigation (EARLI) and Markers of Autism Risk in Babies-Learning Early Signs (MARBLES), two pregnancy cohorts enrolling women who had a previous child diagnosed with autism spectrum disorder, to assess the relationship of prenatal exposure to air pollution and epigenetic aging at birth. DNAm age was computed using existing epigenetic clock algorithms for cord blood tissue—Knight and Bohlin. Epigenetic age acceleration was defined as the residual of regressing chronological gestational age on DNAm age, accounting for cell type proportions. Multivariable linear regression models and distributed lag models (DLMs), adjusting for child sex, maternal race/ethnicity, study sites, year of birth, maternal education, were completed. In the single-pollutant analysis, we observed exposure to PM2.5, PM10, and O3 during preconception period and pregnancy period were associated with decelerated epigenetic aging at birth. For example, pregnancy average PM10 exposure (per 10 unit increase) was associated with epigenetic age deceleration at birth (weeks) for both Knight and Bohlin clocks (β = −0.62, 95% CI: −1.17, −0.06; β = −0.32, 95% CI: −0.63, −0.01, respectively). Weekly DLMs revealed that increasing PM2.5 during the first trimester and second trimester were associated with decelerated epigenetic aging and that increasing PM10 during the preconception period was associated with decelerated epigenetic aging, using the Bohlin clock estimate. Prenatal ambient air pollution exposure, particularly in early and mid-pregnancy, was associated with decelerated epigenetic aging at birth.

The role of cortisol in the association between prenatal air pollution and fetal growth: A prospective cohort study

Prenatal air pollutant exposure has been linked to impaired fetal growth. However, its special vulnerability windows and biological mechanisms remain unclear. A prospective birth cohort study including 7419 mother-newborn pairs was conducted from 2015 to 2020 to determine critical exposure windows and examine whether cortisol mediates the relationship between air pollutant exposure and fetal growth. Air pollutant data for PM2.5, PM10, SO2, and CO were obtained from the Hefei City Ecology and Environment Bureau. Data on fetal ultrasound measurements and birth size were collected. Maternal and cord blood samples were used for measuring cortisol. Prenatal air pollutant (PM2.5, PM10, SO2, and CO) exposure, particularly in the first trimester, was associated with reduced fetal size from later pregnancy to birth. An IQR increase in PM2.5 (β = 0.082, 95%CI: 0.029, 0.135), PM10 (β = 0.086, 95%CI: 0.036, 0.136), SO2 (β = 0.086, 95%CI: 0.028, 0.144), and CO (β = 0.063, 95%CI: 0.017, 0.109) exposure in the first trimester was associated with higher cord blood cortisol levels. Significant relationships were observed between air pollutant exposure in the first trimester and increased ratio of cord to maternal blood cortisol levels. Exposure to high levels of cord blood cortisol significantly reduced the Z scores of birth weight (β = −0.17, 95%CI: −0.23, −0.10), length (β = −0.09, 95%CI: −0.16, −0.03), and head circumference (β = −0.33, 95%CI: −0.42, −0.25). Mediation analysis showed that the association of air pollutant exposure in the first trimester with neonatal parameters mediated by cord blood cortisol was 20.62%. These results indicated that air pollutant exposure during pregnancy could reduce fetal growth by the increased fetal cortisol levels due to placental barrier impairment, with the critical window of exposure occurring in the first trimester.

Ambient air pollution during pregnancy and cardiometabolic biomarkers in cord blood

Background/Objectives:Prenatal air pollution exposure has been associated with adverse childhood cardiometabolic outcomes. It is unknown whether evidence of metabolic disruption associated with air pollution is identifiable at birth. We examined exposure to prenatal ambient air pollution and cord blood cardiometabolic biomarkers among 812 mother-infant pairs in the Healthy Start study.Methods:Using inverse-distance-weighted interpolation of ambient concentrations obtained from stationary monitors, we estimated daily particulate matter ≤2.5 micrometers (PM2.5) and ozone (O3) concentrations at participant residences. Daily estimates were averaged by trimester, full-pregnancy, and the 7 and 30 days prior to delivery. Associations of air pollution with the following cord blood biomarkers were estimated via multivariable linear regression: glucose, insulin, glucose/insulin ratio (GIR), leptin, high-density lipoprotein (HDL) cholesterol, non-HDL cholesterol, free fatty acids, and triglycerides.Results:In this Denver-based cohort, PM2.5 concentrations were lower than in many US urban areas, but O3 concentrations regularly exceeded federal air quality standards. Higher O3 concentrations during pregnancy were consistently associated with higher insulin and lower GIR in cord blood. For example, an interquartile range increase in full pregnancy O3 (6.3 parts per billion [ppb]) was associated with 0.13 log-µIU/ml (95% confidence interval [CI] = 0.04, 0.22) higher cord blood insulin, after adjusting for PM2.5 and other confounders. We found positive, but generally nonsignificant, associations between PM2.5 and leptin and isolated associations between pollutants during certain exposure periods and lipids.Conclusions:In this cohort with moderately high O3 exposure, prenatal concentrations of O3 were positively associated with cord blood insulin. Future studies should examine the implications for offspring long-term health.

Prenatal Exposure to Air Pollution and Immune Thrombocytopenia: A Nationwide Population-Based Cohort Study.

IntroductionImmune thrombocytopenia (ITP) is one of the most common hematologic disorders in children. However, its etiology is still unclear. Epidemiological studies have shown that air pollution is a plausible risk factor in stimulation of oxidative stress, induction of inflammation, and onset of autoimmune diseases. The objective of this article is to examine the effects of prenatal exposure to air pollution on the occurrence of immune thrombocytopenia (ITP) in children.Materials and MethodsThis is a nationwide, population-based, matched case-control study. Using data from Taiwan’s Maternal and Child Health Database (MCHD), we identified 427 children with ITP less than 6 years of age and age-matched controls without ITP between 2004 and 2016. Levels of prenatal exposure to air pollutants were obtained from 71 Environmental Protection Administration monitoring stations across Taiwan according to the maternal residence during pregnancy. Patients who had outpatient visits or admission with diagnosis of ITP and subsequently received first-line treatment of intravenous immunoglobulin or oral glucocorticoids were defined as incidence cases.ResultsPrenatal exposure to particulate matter <10 μm (PM10) in diameter and the pollutant standard index (PSI) increased the risk of childhood ITP. Conversely, carbon monoxide (CO) exposure during pregnancy was negatively associated with the development of ITP.ConclusionCertain prenatal air pollutant exposure may increase the incidence of ITP in children.