Prenatal Air Pollution Exposure Research Articles

Windows of susceptibility and joint effects of prenatal and postnatal ambient air pollution and temperature exposure on asthma and wheeze in Mexican children

IntroductionPrenatal and early-life exposure to air pollution and extreme temperatures are associated with childhood asthma and wheeze. However, potential windows of susceptibility and their sex-specific and interactive effects have not been fully elucidated. We aimed to identify critical windows of susceptibility and evaluate sex-specific effects in these associations, and evaluate exposure interactions. MethodsWe analyzed data from 468 mother–child pairs enrolled in the PROGRESS birth cohort in Mexico City. Daily residential levels of PM2.5, NO2, and temperature were generated from our validated spatiotemporally resolved models from conception to age 4 years. Childhood asthma and wheeze outcomes were collected at 4–6 and 7–8 years. Distributed lag nonlinear models (DLNMs) were used to identify susceptible windows for prenatal weekly-specific and postnatal monthly-specific associations of air pollution and temperature with respiratory outcomes adjusting for covariates. To evaluate sex-specific effects, DLNMs were stratified. Joint effects were assessed using relative excess risk due to interaction and attributable proportion. ResultsMid-gestation was a critical window for both PM2.5 (weeks 20–28, cumulative OR: 1.18 [95% CI: 1.01, 1.37]; weeks 19–26, cumulative OR: 1.18 [95% CI: 1.02, 1.36]) and NO2 (weeks 18–25, cumulative OR: 1.16 [95% CI: 1.02, 1.31]) exposure, associated with higher odds of wheeze. Postnatal exposure to PM2.5 and NO2 during the first year of life was also linked to higher odds of wheeze. The warmer and colder temperatures showed mixed effects on respiratory outcomes. We observed a synergistic interaction between high PM2.5 and high temperature exposure during the first year of life, associated with higher odds of current wheeze. The associations of prenatal air pollution and temperature exposure with respiratory outcomes were more pronounced in males. ConclusionsEarly-life air pollution exposure contributes to the development of childhood asthma and wheeze, while exposure to temperature showed mixed associations with respiratory outcomes.

Effect of environmental air pollutants on placental function and pregnancy outcomes: a molecular insight.

Air pollution has become a major health concern, particularly for vulnerable populations such as the elderly, children, and pregnant women. Studies have reported a strong association between prenatal exposure to air pollutants and adverse pregnancy outcomes, including lower birth weight, reduced fetal growth, and an increased frequency of preterm births. This review summarizes the harmful effects of air pollutants, such as particulate matter, on pregnancy and outlines the mechanistic details associated with these adverse outcomes. Particulate pollutant matter may be able to cross the placenta barrier, and alterations in placental functions are central to the detrimental effects of these pollutants. In addition to associations with preeclampsia and gestational hypertension, air pollutants also induce oxidative stress, inflammation, and epigenetic alteration in the placenta. These pollutants can also affect placental homeostasis and endocrine function, contributing to pregnancy complications and possible transgenerational effects. Prenatal air pollution exposure has been linked to reduced cognitive and motor function in infants and newborns, increasing the predisposition to autism spectrum disorders and other neuropsychiatric disorders. This review also summarizes the use of various animal models to study the harmful effects of air pollution on pregnancy and postnatal outcomes. These findings provide valuable insight into the molecular events associated with the process and can aid in risk mitigation and adopting safety measures. Implementing effective environmental protocols and taking appropriate steps may reduce the global disease burden, particularly for developing nations with poor regulatory compliance and large populations of pregnant women.

Prenatal air pollution exposure and risk of autism: findings from ECHO cohorts

Prenatal air pollution exposure and risk of autism: findings from ECHO cohorts

Mediating effects of placental DNA methylation in the association between prenatal air pollution exposure and child lung function

Mediating effects of placental DNA methylation in the association between prenatal air pollution exposure and child lung function

Prenatal and Early Life Exposure to Ambient Air Pollutants Is Associated with the Fecal Metabolome in the First Two Years of Life.

Prenatal and early life air pollution exposure has been linked with several adverse health outcomes. However, the mechanisms underlying these relationships are not yet fully understood. Therefore, this study utilizes fecal metabolomics to determine if pre- and postnatal exposure to ambient air pollutants (i.e., PM10, PM2.5, and NO2) is associated with the fecal metabolome in the first 2 years of life in a Latino cohort from Southern California. The aims of this analysis were to estimate associations between (1) prenatal air pollution exposure with fecal metabolic features at 1-month of age, (2) prior month postnatal air pollution exposure with fecal metabolites from 1-month to 2 years of age, and (3) how postnatal air pollution exposure impacts the change over time of fecal metabolites in the first 2 years of life. Prenatal exposure to air pollutants was associated with several Level-1 metabolites, including those involved in vitamin B6 and tyrosine metabolism. Prior month air pollution exposure in the postnatal period was associated with Level-1 metabolites involved in histidine metabolism. Lastly, we found that pre- and postnatal ambient air pollution exposure was associated with changes in metabolic features involved in metabolic pathways including amino acid metabolism, histidine metabolism, and fatty acid metabolism.

Association between prenatal air pollutant exposure and autism spectrum disorders in young children: A matched case-control study in Canada

The direction and magnitude of association between maternal exposure to ambient air pollutants across gestational windows and offspring risk of autism spectrum disorders (ASD) remains unclear. We sought to evaluate the time-varying effects of prenatal air pollutant exposure on ASD. We conducted a matched case-control study of singleton term children born in Ontario, Canada from 1-Apr-2012 to 31-Dec-2016. Provincial birth registry data were linked with applied behavioural analysis services and ambient air pollutant datasets to ascertain prenatal exposure to nitrogen dioxide (NO2), ground-level ozone (O3), fine particulate matter (PM2.5), and ASD diagnoses. Covariate balance between cases and controls was established using coarsened exact matching. Conditional logistic regression was used to assess the association between prenatal air pollutant exposure and ASD. Distributed lag non-linear models (DLNM) were used to examine the effects of single-pollutant exposure by prenatal week. Sensitivity analyses were conducted to assess the impact of exposure period on the observed findings. The final sample included 1589 ASD cases and 7563 controls. Compared to controls, cases were more likely to be born to mothers living in urban areas, delivered by Caesarean section, and assigned male sex at birth. NO2 was a consistent and significant contributor to ASD risk after accounting for co-exposure to O3, PM2.5 and covariates. The odds ratio per interquartile range increase was 2.1 (95%CI 1.8–2.3) pre-conception, 2.2 (2.0–2.5) for the 1st trimester, 2.2 (1.9–2.5) for the 2nd trimester, and 2.1 (1.9–2.4) for the 3rd trimester. In contrast, findings for O3 and PM2.5 with ASD were inconsistent. Findings from DLNM and sensitivity analyses were similar. Exposure to NO2 before and during pregnancy was significantly associated with ASD in offspring. The relationship between prenatal O3 and PM2.5 exposure and ASD remains unclear. Further investigation into the combined effects of multi-pollutant exposure on child neurodevelopment is warranted.

Association between trimester-specific prenatal air pollution exposure and placental weight of twins

IntroductionThis study investigates the association between maternal exposure to particulate matter (PM10) and nitric dioxide (NO2) during the first, second and third trimester and placental weight and birth weight/placental weight (BW/PW) ratio in twins at birth. MethodsCross-sectional data of 3340 twins from the East Flanders Prospective Twin Survey was used. Air pollutant exposure was estimated via spatial temporal interpolation. Univariable and multivariable mixed model analyses with a random intercept to account for the relatedness of newborns were conducted for twins with separate placentas. Twin pairs with one placental mass were studied with linear and logistic regression. ResultsIn the third trimester, for each 10 μm/m3 increase in PM10 or NO2 placental weight decreased −19.7 g (95%-C.I. −35.1; −4.3) and −17.7 g (95%-C.I. −30.4; −0.5) respectively, in moderate to late preterm twins with separate placentas. Consequently, BW/PW ratio increased with higher air pollution exposure. PM10 exposure in the last week of pregnancy was associated with a higher odds ratio (OR) of 1.20 (95%-C.I. 1.00; 1.44) for a “small for gestational age placenta” (placental weight <10th percentile). Conversely, first trimester air pollutant exposure was associated with lower ORs of 0.55 (95%-C.I. 0.35; 0.88) and 0.60 (95%-C.I. 0.42; 0.84). DiscussionThe association of PM10 and NO2 on placental weight is trimester-specific, differs for twins with one versus two placentas and is most pronounced in moderate to late preterm twins. Longitudinal studies are needed to better understand the relationship between air pollutant exposure and placental weight evolution across different trimesters.

Air pollution exposure during pregnancy and lung function in childhood: The LUIS study.

The adverse effects of high air pollution levels on childhood lung function are well-known. Limited evidence exists on the effects of moderate exposure levels during early life on childhood lung function. We investigated the association of exposure to moderate air pollution during pregnancy, infancy, and preschool time with lung function at school age in a Swiss population-based study. Fine-scale spatiotemporal model estimates of particulate matter with a diameter <2.5 µm (PM2.5) and nitrogen dioxide (NO2) were linked with residential address histories. We compared air pollution exposures within different time windows (whole pregnancy, first, second, and third trimester of pregnancy, first year of life, preschool age) with forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) measured cross-sectionally using linear regression models adjusted for potential confounders. We included 2182 children, ages 6-17 years. Prenatal air pollution exposure was associated with reduced lung function at school age. In children aged 12 years, per 10 µg·m-3 increase in PM2.5 during pregnancy, FEV1 was 55 mL lower (95% CI -84 to -25 mL) and FVC 62 mL lower (95% CI -96 to -28 mL). Associations were age-dependent since they were stronger in younger and weaker in older children. PM2.5 exposure after birth was not associated with reduced lung function. There was no association between NO2 exposure and lung function. In utero lung development is most sensitive to air pollution exposure, since even modest PM2.5 exposure during the prenatal time was associated with reduced lung function, most prominent in younger children.

Placental DNA methylation signatures of prenatal air pollution exposure and potential effects on birth outcomes: an analysis of three prospective cohorts.

Pregnancy air pollution exposure (PAPE) has been linked to a wide range of adverse birth and childhood outcomes, but there is a paucity of data on its influence on the placental epigenome, which can regulate the programming of physiological functions and affect child development. This study aimed to investigate the association between prenatal air pollutant exposure concentrations and changes in placental DNA methylation patterns, and to explore the potential windows of susceptibility and sex-specific alterations. This multi-site study used three prospective population-based mother-child cohorts: EDEN, PELAGIE, and SEPAGES, originating from four French geographical regions (Nancy, Poitiers, Brittany, and Grenoble). Pregnant women were included between 2003 and 2006 for EDEN and PELAGIE, and between 2014 and 2017 for SEPAGES. The main eligibility criteria were: being older than 18 years, having a singleton pregnancy, and living and planning to deliver in one of the maternity clinics in one of the study areas. A total of 1539 mother-child pairs were analysed, measuring placental DNA methylation using Illumina BeadChips. We used validated spatiotemporally resolved models to estimate PM2·5, PM10, and NO2 exposure over each trimester of pregnancy at the maternal residential address. We conducted a pooled adjusted epigenome-wide association study to identify differentially methylated 5'-C-phosphate-G-3' (CpG) sites and regions (assessed using the Infinium HumanMethylationEPIC BeadChip array, n=871), including sex-specific and sex-linked alterations, and independently validated our results (assessed using the Infinium HumanMethylation450 BeadChip array, n=668). We identified four CpGs and 28 regions associated with PAPE in the total population, 469 CpGs and 87 regions in male infants, and 150 CpGs and 66 regions in female infants. We validated 35% of the CpGs available. More than 30% of the identified CpGs were related to one (or more) birth outcome and most significant alterations were enriched for neural development, immunity, and metabolism related genes. The 28 regions identified for both sexes overlapped with imprinted genes (four genes), and were associated with neurodevelopment (nine genes), immune system (seven genes), and metabolism (five genes). Most associations were observed for the third trimester for female infants (134 of 150 CpGs), and throughout pregnancy (281 of 469 CpGs) and the first trimester (237 of 469 CpGs) for male infants. These findings highlight the molecular pathways through which PAPE might affect child health in a widespread and sex-specific manner, identifying the genes involved in the major physiological functions of a developing child. Further studies are needed to elucidate whether these epigenetic changes persist and affect health later in life. French Agency for National Research, Fondation pour la Recherche Médicale, Fondation de France, and the Plan Cancer.

Persistent DNA Methylation Changes across the First Year of Life and Prenatal Exposure in a Canadian Prospective Birth Study.

Evidence suggests that prenatal air pollution exposure alters DNA methylation (DNAm), which could go on to affect long-term health. It remains unclear whether DNAm alterations present at birth persist through early life. Identifying persistent DNAm changes would provide greater insight into the molecular mechanisms contributing to the association of prenatal air pollution exposure with atopic diseases. This study investigated DNAm differences associated with prenatal nitrogen dioxide () exposure (a surrogate measure of traffic-related air pollution) at birth and 1 y of age and examined their role in atopic disease. We focused on regions showing persistent DNAm differences from birth to 1 y of age and regions uniquely associated with postnatal exposure. Microarrays measured DNAm at birth and at 1 y of age for an atopy-enriched subset of Canadian Health Infant Longitudinal Development (CHILD) study participants. Individual and regional DNAm differences associated with prenatal () were identified, and their persistence at age 1 y were investigated using linear mixed effects models (). Postnatal-specific DNAm differences () were isolated, and their association with in the first year of life was examined. Causal mediation investigated whether DNAm differences mediated associations between and age 1 y atopy or wheeze. Analyses were repeated using biological sex-stratified data. At birth (), 18 regions of DNAm were associated with , with several annotated to HOX genes. Some of these regions were specifically identified in males (), but not females (). The effect of prenatal across CpGs within altered regions persisted at 1 y of age. No significant mediation effects were identified. Sex-stratified analyses identified postnatal-specific DNAm alterations. Regional cord blood DNAm differences associated with prenatal persisted through at least the first year of life in CHILD participants. Some differences may represent sex-specific alterations, but replication in larger cohorts is needed. The early postnatal period remained a sensitive window to DNAm perturbations. https://doi.org/10.1289/EHP13034.

Prenatal air pollution exposure is associated with inflammatory, cardiovascular, and metabolic biomarkers in mothers and newborns

BackgroundPrenatal air pollution exposure has been associated with individual inflammatory, cardiovascular, and metabolic biomarkers in mothers and neonates. However, studies of air pollution and a comprehensive panel of biomarkers across maternal and cord blood samples remain limited. Few studies used data-driven methods to identify biomarker groupings that converge biomarkers from multiple biological pathways. This study aims to investigate the impacts of prenatal air pollution on groups of biomarkers in maternal and cord blood samples. MethodsIn the Maternal And Developmental Risks from Environmental and Social Stressors (MADRES) cohort, 87 biomarkers were quantified from 45 trimester 1 maternal blood and 55 cord blood samples. Pregnancy and trimester 1-averaged concentrations of particulate matter ≤2.5 μm and ≤10 μm in diameter (PM2.5 and PM10), nitrogen dioxide (NO2), and ozone (O3) were estimated, using inverse distance squared weighted spatial interpolation from regulatory air monitoring stations. Traffic-related NOx was assessed using California Line Source Dispersion Model: freeway/highway roads, non-freeway major roads, non-freeway minor roads, and their sum as total NOx. Elastic Net (EN) regression within the rexposome R package was used to group biomarkers and assess their associations with air pollution. ResultsIn maternal samples, trimester 1-averaged PM10 was associated with elevated inflammation biomarkers and lowered cardiovascular biomarkers. NO2 exhibited positive associations with cardiovascular and inflammation markers. O3 was inversely associated with inflammation, metabolic, and cardiovascular biomarkers. In cord blood, pregnancy-averaged PM2.5 was associated with higher cardiovascular biomarkers and lower metabolic biomarkers. PM10 was associated with lower inflammation and higher cardiovascular biomarkers. Total and major road NOx was associated with lower cardiovascular biomarkers. ConclusionPrenatal air pollution exposure was associated with changes in biomarkers related to inflammation, cardiovascular, metabolic, cancer, and neurological function in both mothers and neonates. This study shed light on mechanisms by which air pollution can influence biological function during pregnancy.

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

Background & aimsPrenatal exposure to air pollution is robustly associated with fetal growth restriction but the extent to which it is associated with postnatal growth and the risk of childhood obesity remains unknown. We examined the association of prenatal exposure to air pollution with offspring obesity related measures and evaluated the possible protective effect of maternal fruits and vegetables intake (FV). MethodsWe included 633 mother-child pairs from the Rhea pregnancy cohort in Crete, Greece. Fine particles (PM2.5 and PM10) exposure levels during pregnancy were estimated using land-use regression models. We measured weight, height and waist circumference at 4 and 6 years of age, and body composition analysis was performed at 6 years using bioimpedance. Maternal diet was evaluated by means of a semi-quantitative food frequency questionnaire in mid-pregnancy. Adjusted associations were obtained via multivariable regression analyses and multiplicative interaction was used to evaluate the potential modifying role of FV intake. ResultsExposure to PMs in utero was not associated with measures of adiposity at 4 or 6 years of age. Associations at 4 years did not differ according to maternal consumption of FV. However, at 6 years, among children whose mothers reported consuming less than 5 servings of FV per day, one SD increase in PM10 during pregnancy was associated with increased BMI (beta 0.41 kg/m2, 95% CI: −0.06, 0.88, p-interaction = 0.037) and increased waist circumference (beta 0.83 cm, 95% CI: −0.38, 2.05, p-interaction = 0.043) and one SD increase in PM2.5 was associated with increased fat mass (beta 0.5 kg, 95% CI: 0.0, 0.99, p-interaction = 0.039) and increased percentage of body fat (beta 1.06%, 95% CI: −0.06, 2.17, p-interaction = 0.035). Similarly, higher prenatal PM2.5 and PM10 exposure was associated with increased risk for obesity and abdominal obesity at 6 years only in the low FV group. ConclusionsExposure to fine particulate matter during pregnancy was not associated with obesity-related measures at 4 and 6 years. However, only among offspring of mothers who consumed inadequate FV, we observed higher obesity-related measures at 6 years. Our results indicate that mothers' diet during pregnancy may play a role in the relationship between air-pollution and childhood obesity.

Prenatal Exposure to Air Pollution and Respiratory Distress in Term Newborns: Results from the MIREC Prospective Pregnancy Cohort.

Respiratory distress is the leading cause of neonatal morbidity and mortality worldwide, and prenatal exposure to air pollution is associated with adverse long-term respiratory outcomes; however, the impact of prenatal air pollution exposure on neonatal respiratory distress has not been well studied. We examined associations between prenatal exposures to fine particular matter () and nitrogen dioxide () with respiratory distress and related neonatal outcomes. We used data from the Maternal-Infant Research on Environmental Chemicals (MIREC) Study, a prospective pregnancy cohort () recruited in the first trimester from 10 Canadian cities. Prenatal exposures to () and () were estimated using land-use regression and satellite-derived models coupled with ground-level monitoring and linked to participants based on residential location at birth. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) for associations between air pollution and physician-diagnosed respiratory distress in term neonates in hierarchical logistic regression models adjusting for detailed maternal and infant covariates. Approximately of newborns experienced respiratory distress. Neonates received clinical interventions including oxygen therapy (6%), assisted ventilation (2%), and systemic antibiotics (3%). Two percent received multiple interventions and 4% were admitted to the neonatal intensive care unit (NICU). Median and concentrations during pregnancy were and , respectively. Prenatal exposures to air pollution were not associated with physician-diagnosed respiratory distress, oxygen therapy, or NICU admissions. However, exposures were strongly associated with assisted ventilation (OR per increase in ; 95% CI: 1.02, 1.35), multiple clinical interventions (OR per increase in ; 95% CI: 1.07, 1.26), and systemic antibiotics, (OR per increase in ; 95% CI: 1.04, 1.21). These associations were consistent across exposure periods-that is, during prepregnancy, individual trimesters, and total pregnancy-and robust to model specification. exposure was associated with administration of systemic antibiotics (OR per 1-ppb increase in ; 95% CI: 1.00, 1.06). Prenatal exposures to increased the risk of severe respiratory distress among term newborns. These findings support the development and prioritization of public health and prenatal care strategies to increase awareness and minimize prenatal exposures to air pollution. https://doi.org/10.1289/EHP12880.

Association of prenatal exposure to PM2.5 and NO2 with gestational diabetes in Western New York

BackgroundAlthough many studies have examined the association between prenatal air pollution exposure and gestational diabetes (GDM), the relevant exposure windows remain inconclusive. We aim to examine the association between preconception and trimester-specific exposure to PM2.5 and NO2 and GDM risk and explore modifying effects of maternal age, pre-pregnancy body mass index (BMI), smoking, exercise during pregnancy, race and ethnicity, and neighborhood disadvantage. MethodsAnalyses included 192,508 birth records of singletons born to women without pre-existing diabetes in Western New York, 2004–2016. Daily PM2.5 and NO2 at 1-km2 grids were estimated from ensemble-based models. We assigned each birth with exposures averaged in preconception and each trimester based on residential zip-codes. We used logistic regression to examine the associations and distributed lag models (DLMs) to explore the sensitive windows by month. Relative excess risk due to interaction (RERI) and multiplicative interaction terms were calculated. ResultsGDM was associated with PM2.5 averaged in the first two trimesters (per 2.5 μg/m3: OR = 1.08, 95% CI: 1.01, 1.14) or from preconception to the second trimester (per 2.5 μg/m3: OR = 1.10, 95% CI: 1.03, 1.18). NO2 exposure during each averaging period was associated with GDM risk (per 10 ppb, preconception: OR = 1.10, 95% CI: 1.06, 1.14; first trimester: OR = 1.12, 95% CI: 1.08, 1.16; second trimester: OR = 1.10, 95% CI: 1.06, 1.14). In DLMs, sensitive windows were identified in the 5th and 6th gestational months for PM2.5 and one month before and three months after conception for NO2. Evidence of interaction was identified for pre-pregnancy BMI with PM2.5 (P-for-interaction = 0.023; RERI = 0.21, 95% CI: 0.10, 0.33) and with NO2 (P-for-interaction = 0.164; RERI = 0.16, 95% CI: 0.04, 0.27). ConclusionPM2.5 and NO2 exposure may increase GDM risk, and sensitive windows may be the late second trimester for PM2.5 and periconception for NO2. Women with higher pre-pregnancy BMI may be more susceptible to exposure effects.

Early exposure to air pollution and cognitive development later in life: Evidence from China

This paper studies the relationship between prenatal exposure to air pollution and youth cognitive skill development in China. This study combines the city-level air pollution data compiled by the World Bank with the Chinese Household Income Project. A one-milligram decrease in prenatal exposure to total suspended particulates is associated with an increase of 6.16 standard deviations in literature scores and 3.95 standard deviations in math scores for children aged between 6 and 19. A one-milligram decrease in both prenatal and postnatal air pollution exposure is associated with an increase of 6.41 standard deviations in literature scores and 4.21 standard deviations in math scores. Prenatal air pollution exposure has a persistent detrimental effect on children's health, which in turn negatively affects their academic performance. These findings provide additional evidence supporting the “fetal origins” hypothesis, which predicts early shocks in utero affect the outcomes later in life.

Prenatal air pollution, fetal β-cell dysfunction and neurodevelopmental delay

BackgroundEmerging evidence has reported significant associations of prenatal air pollution exposure with neurodevelopmental delay in offspring. Sensitive exposure windows and the modifiable factor remain elusive. ObjectiveWe aim to identify sensitive windows of air pollution during pregnancy on neurodevelopmental delay, and examine whether cord blood C-peptide mediates the relationship. MethodsThis study included 7438 mother-newborn pairs in Hefei, China, from 2015 to 2021. Weekly exposure to particulate matter of aerodynamic diameter <2.5 µm, 10 µm (PM2.5, PM10), nitrogen dioxide (NO2) and carbon monoxide (CO) was estimated at regulatory air monitoring stations in Hefei. Denver Developmental Screening Test-II and the Gesell Developmental Schedules were applied to assess the neurodevelopmental delay in children 6–36 mon of age. Distributed lag nonlinear models examined sensitive time windows of prenatal air pollutants exposure. Mediation analysis estimated the mediating role of cord blood C-peptide. ResultsThe sensitive PM2.5, PM10, NO2, and CO exposure windows associated with neurodevelopmental delay were throughout pregnancy. Weekly air pollutants exposure was related to higher neurodevelopmental delay risks [cumulative odds ratio (OR): 1.40(1.29,1.53) in PM2.5 (per 10 μg/m3), 1.40(1.28,1.53) in PM10 (per 10 μg/m3), 1.41(1.30,1.52) in CO (per 0.1 mg/m3), and 1.49(1.29,1.72) in NO2 (per 5 μg/m3)]. Mediation analysis indicated 18.3 % contributions of cord C-peptide to the relationship [average mediation effect: 0.04(0.01.0.06); average direct effect: 0.15(0.07.0.25)]. Conclusions: Exposure to air pollution throughout pregnancy is linked to neurodevelopmental delay mediated by poorer fetal β-cell function. Screening and treatment of abnormal glucose metabolism in infants could benefit the prevention of air pollution-associated neurodevelopment delay.

The effect of ambient air pollution on birth outcomes in Norway

BackgroundAmbient air pollution can be harmful to the fetus even in countries with relatively low levels of pollution. Most of the established literature estimates the association between air pollution and health rather than causality. In this paper, I examine the causal effects of ambient air pollution on birth outcomes in Norway.MethodsWith the large sample size and geographic division of sub-postal codes in Norway, I can control for a rich set of spatio-temporal fixed effects to overcome most of the endogeneity problems caused by the choice of residential area and date of delivery. After controlling for a rich set of spatio-temporal fixed effects, my paper uses the variance in ambient air pollutant concentrations over narrow time intervals and in a small geographic area of Norway to determine how prenatal air pollution exposure affects birth outcomes. My data contain extensive information about parents as well as meteorological conditions that can be used to control for potential confounding factors.ResultsI find that prenatal exposure to ambient nitric oxide in the last trimester causes significant birth weight and birth length loss under the same sub-postcode fixed effects and calendar month fixed effects, whereas other ambient air pollutants such as nitrogen dioxide and sulfur dioxide appear to be at safe levels for the fetus in Norway. In addition, the marginal adverse effect of ambient nitric oxide is larger for newborns with disadvantaged parents. Both average concentrations of nitric oxide and occasional high concentration events can adversely affect birth outcomes.ConclusionsPrenatal exposure to NO pollution has an adverse effect on birth outcomes. This suggests that government and researchers should pay more attention to examining NO pollution and that health care providers need to advise pregnant women about the risks of air pollution during pregnancy.

Weekly prenatal PM2.5 and NO2 exposures in preterm, early term, and full term infants: Decrements in birth weight and critical windows of susceptibility

BackgroundPrevious studies have observed associations between birth weight and prenatal air pollution exposure, but there is not consensus on timing of critical windows of susceptibility. ObjectiveWe estimated the difference in birth weight among preterm, early term and full term births associated with weekly exposure to PM2.5 and NO2 throughout gestation. MethodsWe included all singleton live births in the Lower Peninsula of Michigan (United States) between 2007 and 2012 occurring at or after 32 weeks gestational age (n = 497,897). Weekly ambient PM2.5 and NO2 concentrations were estimated at maternal residences using 1-km gridded data from ensemble-based models. We utilized a distributed lag nonlinear model to estimate the difference in birth weight associated with weekly exposures from the last menstrual period (week 0) through 31 weeks gestation for preterm births; through 36 weeks gestation for early term births; and through 38 weeks gestation for full term births. ResultsIn single-pollutant models, a 5 μg/m3 increase in PM2.5 exposure was associated with a reduction in birth weight among preterm births (−37.1 g [95% confidence interval [CI]: 60.8 g, −13.5 g]); early term births (−13.5 g [95% CI: 26.2 g, −0.67 g]); and full term births (−8.23 g [95% CI: 15.8 g, −0.68 g])]. In single-pollutant models, a 10 ppb increase in NO2 exposure was associated with a −11.7 g (95% CI: 14.46 g, −8.92 g) decrement in birth weight among full term births only. In models co-adjusted for PM2.5 and NO2, PM2.5 exposure was associated with reduced birth weight among preterm births (−36.9 g [95% CI: 61.9 g, −11.8 g]) and NO2 exposure was associated with reduced birth weight among full term births (−11.8 g [95% CI: 14.7 g, −8.94 g]). The largest decrements in birth weight were associated with PM2.5 exposure between approximately 10 and 26 weeks of pregnancy; for NO2 exposure, the largest decrements in birth weight in full term births were associated with exposure between weeks 6–18. ConclusionWe observed the largest and most persistent adverse associations between PM2.5 exposure and birth weight in preterm infants, and between NO2 exposure and birth weight in full term infants. Exposure during the first half of pregnancy had a greater impact on birthweight.

Associations between prenatal air pollution exposure and placental DNA methylation: a French multi-cohort study

Associations between prenatal air pollution exposure and placental DNA methylation: a French multi-cohort study

Prenatal air pollution exposure and mitochondrial DNA copy number at birth, a systematic review and meta-analysis

Prenatal air pollution exposure and mitochondrial DNA copy number at birth, a systematic review and meta-analysis