Prenatal Particulate Matter Research Articles

Prenatal particulate matter exposure is linked with neurobehavioural development in early life

BackgroundEarly life exposure to ambient particulate matter (PM) may negatively affect neurobehavioral development in children, influencing their cognitive, emotional, and social functioning. Here, we report a study on prenatal PM2.5 exposure and neurobehavioral development focusing on different time points in the first years of life. MethodsThis study was part of the ENVIRONAGE birth cohort that follows mother-child pairs longitudinally. First, the Neonatal Behavioral Assessment Scale (NBAS) was employed on 88 newborns aged one to two months to assess their autonomic/physiological regulation, motor organisation, state organisation/regulation, and attention/social interaction. Second, our study included 393 children between the ages of four and six years, for which the Strengths and Difficulties Questionnaire (SDQ) was used to assess the children's emotional problems, hyperactivity, conduct problems, peer relationship, and prosocial behaviour. Prenatal PM2.5 exposure was determined using a high-resolution spatial-temporal method based on the maternal address. Multiple linear and multinomial logistic regression models were used to analyse the relationship between prenatal PM2.5 exposure and neurobehavioral development in newborns and children, respectively. ResultsA 5 μg/m³ increase in first-trimester PM2.5 concentration was associated with lower NBAS range of state cluster scores (−6.11%; 95%CI: −12.00 to −0.23%; p = 0.04) in one-to-two-month-old newborns. No other behavioural clusters nor the reflexes cluster were found to be associated with prenatal PM2.5 exposure. Furthermore, a 5 μg/m³ increment in first-trimester PM2.5 levels was linked with higher odds of a child experiencing peer problems (Odds Ratio (OR) = 3.89; 95%CI: 1.39 to 10.87; p = 0.01) at ages four to six. Additionally, a 5 μg/m³ increase in second-trimester PM2.5 concentration was linked to abnormal prosocial behaviour (OR = 0.49; 95%CI: 0.25 to 0.98; p = 0.04) at four to six years old. No associations were found between in utero PM2.5 exposure and hyperactivity or conduct problems. ConclusionsOur findings suggest that prenatal exposure to PM may impact neurobehavioural development in newborns and preschool children. We identified sensitive time windows during early-to-mid pregnancy, possibly impacting stage changes in newborns and peer problems and prosocial behaviour in children.

Prenatal particulate matter exposure is linked with neurobehavioral development in early life

Abstract Background Particulate matter (PM) is a major environmental health concern and there is growing evidence that early exposure to PM can have adverse effects on neurobehavioral development in children, including attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). In this study, we hypothesized that prenatal PM2.5 exposure is linked with changes in neurobehavioral development in early life. Methods This study was part of the prospective ENVIRONAGE birth cohort and included 85 mother-newborn pairs. The Neonatal Behavioral Assessment Scale (NBAS) was administered to 1-2-month-olds to evaluate newborn's behavior. In addition, 392 children aged 4-6 years of the ENVIRONAGE cohort were included. The Strengths and Difficulties Questionnaire (SDQ) was used to assess the child's behavior. PM2.5 concentrations were determined by a high-resolution spatial-temporal method based on the maternal residential address. Multiple linear and multinomial logistic regression models were used to link prenatal PM2.5 exposure and neurobehavioral development in newborns and children, respectively. Results A 5 µg/m3 increase in PM2.5 concentration in early pregnancy was linked with lower scores for the NBAS range of state cluster (-0.22; 95% CI: -0.42 to -0.02; p = 0.03) in newborns aged 1-2 months old, as well as with higher odds of a child having peer problems (OR 3.90; 95% CI: 1.39 to 10.88; p = 0.01), higher total difficulties scores (OR 1.67; 95% CI: 1.01 to 2.78; p = 0.047), and abnormal prosocial behavior (OR 0.49; 95% CI: 0.25 to 0.98; p = 0.04) at age 4-6 years. Conclusions This study provides indications that prenatal PM2.5 exposure influences neurobehavioral development, both in newborns and in early childhood. This evidence suggests that reducing exposure to PM2.5 during pregnancy may be an important public health strategy for promoting optimal neurodevelopment in early life. Key messages • In utero PM2.5 exposure is related to changes in neurobehavior in newborns. • Prenatal PM2.5 exposure is linked with higher chances of abnormal behavior in children aged 4-6 years old.

In Utero Exposure to Air Pollutants and Mitochondrial Heteroplasmy in Neonates.

Mitochondria are sensitive to oxidative stress, which can be caused by traffic-related air pollution. Placental mitochondrial DNA (mtDNA) mutations have been previously linked with air pollution. However, the relationship between prenatal air pollution and cord-blood mtDNA mutations has been poorly understood. Therefore, we hypothesized that prenatal particulate matter (PM2.5) and NO2 exposures are associated with cord-blood mtDNA heteroplasmy. As part of the ENVIRONAGE cohort, 200 mother-newborn pairs were recruited. Cord-blood mitochondrial single-nucleotide polymorphisms were identified by whole mitochondrial genome sequencing, and heteroplasmy levels were evaluated based on the variant allele frequency (VAF). Outdoor PM2.5 and NO2 concentrations were determined by a high-resolution spatial-temporal interpolation method based on the maternal residential address. Distributed lag linear models were used to determine sensitive time windows for the association between NO2 exposure and cord-blood mtDNA heteroplasmy. A 5 μg/m3 increment in NO2 was linked with MT-D-Loop16311T>C heteroplasmy from gestational weeks 17-25. MT-CYTB14766C>T was negatively associated with NO2 exposure in mid pregnancy, from weeks 14-17, and positively associated in late pregnancy, from weeks 31-36. No significant associations were observed with prenatal PM2.5 exposure. This is the first study to show that prenatal NO2 exposure is associated with cord-blood mitochondrial mutations and suggests two critical windows of exposure in mid-to-late pregnancy.

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.

Effects of maternal exposure to particulate matter during pregnancy on the birth weight of offspring: A negative control exposures study

The impact of prenatal particulate matter (PM) on birth weight in full-term children remains unclear. Our study aimed to explore the causal effect of maternal PM exposure during pregnancy on birth weight of full-term offspring. Subjects, from the birth cohort in Jinan City, were born at full term, singleton, and with normal birth weight. The daily exposure concentration for each mother during pregnancy and the mirror period was assessed by the inverse distance weighted method. The generalized linear models and negative control exposures method were used to evaluate causality between them through evaluating known and unknown confounding. Finally, 4114 subjects were included in this study. In the entire pregnancy, for a 10 μg/m3 PM increase, the reduction of the birth weight was 17.36 g (95%CI: −30.96 g, −3.77 g) for PM10 and 28.92 g (95%CI: −56.96 g, −0.89 g) for PM2.5 after adjusting known confounding, and it was 26.93 g (95%CI: −44.82 g, −9.03 g) for PM10 and 34.41 g (95%CI: −68.28 g, −0.54 g) for PM2.5 after assessing unknown confounding. Additionally, in the first and third trimester, they were 24.13 g (95%CI: −36.41 g, −11.84 g) and 11.60 g (95%CI: −22.75 g, −0.35 g) for PM10, and 30.53 g (95%CI: −55.15 g, −5.91 g) and 29.47 g (95%CI: −54.98 g, −3.96 g) for PM2.5, respectively. Consequently, there was a causal effect of maternal exposure to PM during pregnancy on birth weight loss of full-term offspring. The first and third trimester may be the critical windows.

Maternal urban particulate matter exposure and signaling pathways in fetal brains and neurobehavioral development in offspring

It is well understood that exposure to particulate matter (PM) can have adverse effects on the nervous system. When pregnant women are exposed to PM, their fetuses are also affected through the placenta. However, the mechanisms by which fetal brain development is regulated between mother and fetus remain unclear. C57BL/6J pregnant mice were exposed to PM at embryonic day (E) 2.5, 5.5, 8.5, 11.5, 14.5, and 17.5 via nasal drip at three doses (3, 6, 12 mg/kg of body weight) or PBS control. Neurobehavioral changes in the offspring were examined at 5–6-week-old by open field test (OFT) and elevated plus maze (EPM). The maternal and fetal brain and placenta were collected at E18.5, and molecular signal changes were explored using transcriptome analysis. We found that both male and female low-dose pups and male middle-dose pups traveled a significantly longer distance than controls in EPM tests. Both male and female low-dose pups showed a higher frequency of entering the center area and female low-dose pups exhibited a higher percentage of distance moved in the center area than controls in OFT tests. Gene expression in the maternal brain, fetal brain, and placenta at E18.5 was altered. Differentially expressed genes were enriched in the neuroactive ligand-receptor interaction pathway in all three tissue types. Pathway analysis revealed that the PI3K-Akt and PKC signaling was dysregulated in the fetal brain in the high-dose group compared with the control group. The pathways play a role in neuronal survival and apoptosis. Furthermore, there is a dose-dependent increase in Caspase-6, neuronal apoptosis and neurodegeneration biomarker, levels in E18.5 fetal brain (P = 0.06). In conclusion, our study demonstrated that prenatal PM exposure enhanced exploration and locomotor activity in adolescent offspring and altered molecular events in maternal brain, fetal brain, and placenta. The connections of these changes warrant further investigations.

Prenatal particulate matter exposure and mitochondrial mutational load at the maternal-fetal interface: Effect modification by genetic ancestry

Prenatal ambient particulate matter (PM2.5) exposure impacts infant development and alters placental mitochondrial DNA abundance. We investigated whether the timing of PM2.5 exposure predicts placental mitochondrial mutational load using NextGen sequencing in 283 multi-ethnic mother-infant dyads. We observed increased PM2.5exposure, particularly during mid- to late-pregnancy and among genes coding for NADH dehydrogenase and subunits of ATP synthase, was associated with a greater amount of nonsynonymous mutations. The strongest associations were observed for participants of African ancestry. Further work is needed to tease out the role of mitochondrial genetics and its impact on offspring development and emerging disease disparities.

Prenatal Particulate Matter Exposure Is Associated with Saliva DNA Methylation at Age 15: Applying Cumulative DNA Methylation Scores as an Exposure Biomarker.

Exposure in utero to particulate matter (PM2.5 and PM10) is associated with maladaptive health outcomes. Although exposure to prenatal PM2.5 and PM10 has cord blood DNA methylation signatures at birth, signature persistence into childhood and saliva cross-tissue applicability has not been tested. In the Fragile Families and Child Wellbeing Study, a United States 20-city birth cohort, average residential PM2.5 and PM10 during the three months prior to birth was estimated using air quality monitors with inverse distance weighting. Saliva DNA methylation at ages 9 (n = 749) and 15 (n = 793) was measured using the Illumina HumanMethylation 450 k BeadArray. Cumulative DNA methylation scores for particulate matter were estimated by weighting participant DNA methylation at each site by independent meta-analysis effect estimates and standardizing the sums. Using a mixed-effects regression analysis, we tested the associations between cumulative DNA methylation scores at ages 9 and 15 and PM exposure during pregnancy, adjusted for child sex, age, race/ethnicity, maternal income-to-needs ratio, nonmartial birth status, and saliva cell-type proportions. Our study sample was 50.5% male, 56.3% non-Hispanic Black, and 19.8% Hispanic, with a median income-to-needs ratio of 1.4. Mean exposure levels for PM2.5 were 27.9 μg/m3/day (standard deviation: 7.0; 23.7% of observations exceeded safety standards) and for PM10 were 15.0 μg/m3/day (standard deviation: 3.1). An interquartile range increase in PM2.5 exposure (10.73 μg/m3/day) was associated with a −0.0287 standard deviation lower cumulative DNA methylation score for PM2.5 (95% CI: −0.0732, 0.0158, p = 0.20) across all participants. An interquartile range increase in PM10 exposure (3.20 μg/m3/day) was associated with a −0.1472 standard deviation lower cumulative DNA methylation score for PM10 (95% CI: −0.3038, 0.0095, p = 0.06) across all participants. The PM10 findings were driven by the age 15 subset where an interquartile range increase in PM10 exposure was associated with a −0.024 standard deviation lower cumulative DNA methylation score for PM10 (95% CI: −0.043, −0.005, p = 0.012). Findings were robust to adjustment for PM exposure at ages 1 and 3. In utero PM10-associated DNA methylation differences were identified at age 15 in saliva. Benchmarking the timing and cell-type generalizability is critical for epigenetic exposure biomarker assessment.

Prenatal PM2.5 affects atopic dermatitis depending on maternal anxiety and gender: COCOA study.

BackgroundThe prevalence of atopic dermatitis (AD) is increasing worldwide. Prenatal particulate matter with an aerodynamic diameter <2.5 μm (PM2.5) and maternal anxiety during pregnancy has been suggested as a potential causes of AD. This study investigated the effects of prenatal PM2.5 and maternal anxiety on AD and identified the critical period of PM2.5 exposure for AD in infants.MethodsThis study included 802 children from the COCOA birth cohort study with follow‐up data at 1 year of age. PM2.5 was estimated by land‐use regression models and prenatal anxiety was measured with a questionnaire. AD was diagnosed by doctor at 1 year of age. Logistic regression analysis and Bayesian distributed lag interaction models were applied.ResultsHigher PM2.5 during the first trimester of pregnancy, higher prenatal maternal anxiety, and male gender were associated with AD at 1 year of age (adjusted odds ratio [aOR] and 95% confidence interval [CI]: 1.86 [1.08–3.19], 1.58 [1.01–2.47], and 1.54 [1.01–2.36], respectively). Higher PM2.5 during the first trimester and higher maternal anxiety during pregnancy showed an additive effect on the risk of AD (aOR: 3.13; 95% CI: 1.56–6.28). Among boys exposed to higher maternal anxiety during pregnancy, gestational weeks 5–8 were the critical period of PM2.5 exposure for the development of AD.ConclusionsHigher PM2.5 exposure during gestational weeks 5–8 increased the probability of AD in infancy, especially in boys with higher maternal anxiety. Avoiding PM2.5 exposure and maternal anxiety from the first trimester may prevent infant AD.

Mid-pregnancy PM2.5 exposure affects sex-specific growth trajectories via ARRDC3 methylation

Prenatal particulate matter <2.5 μm (PM2.5) is associated with adverse birth growth. However, the longitudinal growth impacts have been little studied, and no mechanistic relationships have been described. We investigated the association between prenatal PM2.5 exposure and growth trajectories, and the possible role of epigenetics. We enrolled 1313 neonates with PM2.5 data measured by ordinary kriging from the COhort for Childhood Origin of Asthma and allergic diseases, followed up at 1, 3, and 5 years to evaluate growth. Differential DNA methylation and pyrosequencing of cord blood leukocytes was evaluated according to the prenatal PM2.5 levels and birth weight (BW). PM2.5 exposure during the second trimester (T2) caused the lowest BW in both sexes, further adjusted for indoor PM2.5 levels [female, aOR 1.39 (95% CI 1.05–1.83); male, aOR 1.36 (95% CI 1.04–1.79)]. Bayesian distributed lag models with indoor PM2.5 adjustments revealed a sensitive window for BW effects at 10–26 weeks gestation, but only in females. Latent class mixture models indicated that a persistently low weight-for-height percentile trajectory was more prevalent in the highest PM2.5 exposure quartile at T2 in females, compared to a persistently high trajectory (36.5% vs. 20.3%, P = 0.022). Also, in the females only, the high PM2.5 and low BW neonates showed significantly greater ARRDC3 methylation changes. ARRDC3 methylation was also higher only in females with low weight at 5 years of age. Higher fetal PM2.5 exposure during T2 may cause a decreased growth trajectory, especially in females, mediated by ARRDC3 hyper-methylation-associated energy metabolism.

Prenatal Particulate Matter (PM) Exposure and Natriuretic Peptides in Newborns from Mexico City.

(1) Background: The aim of this study was to assess associations between particulate matter (PM) exposure and natriuretic peptide concentrations in cord blood from newborns. (2) Methods: we conducted a cross-sectional study in Mexico City with 101 pregnant women from CIMIGEN Hospital. Atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) were measured in plasma from cord blood in 51 newborns by ELISA. We estimated PM exposure (PM2.5 and PM10) at first, second and third trimester of pregnancy. (3) Results: The median and interquartile range for ANP, BNP and CNP plasma concentrations were 66.71 (46.92–80.23), 98.23 (73.64–112.30) and 1129.11 (944.10–1452.02) pg/mL, respectively. PM2.5 and PM10 levels for the whole pregnancy period were 22.2 µg/m3 and 41.63 µg/m3, respectively. Employing multivariable linear regression models adjusted for maternal age, newborn sex, smoking before pregnancy, maternal occupation and newborns’ length and height, we observed a 2.47 pg/mL (95%CI: −4.67, −0.27) decrease in BNP associated with PM2.5 exposure during second trimester. Adjusted for the same set of confounders, third trimester PM10 exposure was inversely associated with ANP concentrations (beta estimate: −0.90; 95% CI: −1.80, −0.03). Neither PM10 nor PM2.5 were associated with CNP at any trimester of pregnancy. (4) Conclusions: Prenatal exposure to particulate matter was associated with ANP and BNP decrease in newborns.

Effects of exposure to urban particulate matter SRM 1648a during pregnancy on the neurobehavioral development of offspring mice

The development of the nervous system is crucial to a child's health. However, the nervous system is also susceptible to a variety of factors during development. To date, epidemiological studies have reported controversial results on the relationship between prenatal exposure to particulate matter (PM) and neurobehavioral development. Thus, we investigated the effect of PM exposure during pregnancy on the neurobehavioral development of offsprings. Adult C57BL/6 mice were exposed to PM from gestation day (GD) 0.5–21 by the intratracheal instillation. The daily exposure doses were 250 µg/kg.b.w and 2500 µg/kg.b.w respectively. The offspring mice began behavioral tests at the 5th week. We assessed neurobehavioral development, and the gene expression level changes in the mouse hippocampus using RNA-seq. In the open field test, the movement distance in the central area was significantly decreased in the high-dose group. Serum free triiodothyronine (FT3) levels were significantly increased in male offspring mice with prenatal high-dose PM exposure. The RNA-seq results suggested that the Prkca, Med12l, Ep300, and Slc16a10 in the thyroid hormone signaling pathway were significantly decreased in offspring mice in the high-dose group.Our data showed that prenatal PM exposure caused the offspring mice’s anxiety-like behaviors and increased serum FT3 levels. The changes in thyroid hormone pathway-related genes might be the causes of the above series of changes.

The association of prenatal exposure to particulate matter with infant growth: A birth cohort study in Beijing, China.

Limited studies examined the associations of prenatal exposure to particulate matter (PM) and children's growth with inconsistent results, and no study focused on PM1. We matched a birth cohort (10,547 children) with daily PM1 and PM2.5 concentrations by maternal home addresses. Air pollution concentrations were predicted by satellite remote sensing data, meteorological factors, and land use information. The weight and length of children in the birth cohort were measured at approximately one year old. We calculated the Z-score of weight for length (WFL) and body mass index (BMI) and then defined overweight and obesity (OWOB) based on WHO Standards. Generalized linear regression and modified Poisson regression were used to identify the association of prenatal exposure to PM1 or PM2.5 with anthropometric measurements and risk of OWOB. We also determined the mediation effect of preterm birth on the associations. Results showed that a 10μg/m3 increase in prenatal exposure to PM1 and PM2.5 was significantly associated with a 0.105 [95% confidence interval (CI): 0.067, 0.144] and 0.063 (95% CI: 0.029, 0.097) increase in WFL Z-score for one-year-old children. Similar associations were found for BMI Z-score. A 10μg/m3 increase in prenatal PM1 and PM2.5 exposure was significantly associated with 1.012 (95%CI: 1.003, 1.021) and 1.010 (95%CI: 1.002, 1.018) times higher risk of OWOB. . Preterm birth mediated 7.5% [direct effect (DE)=0.106, P<0.001; indirect effect (IE)=0.009, P<0.001)] and 9.9% (DE=0.064, P<0.001; IE=0.007, P<0.001) of the association between prenatal PM1 and PM2.5 exposure and WFL Z-score of the children. The association of prenatal PM1 and PM2.5 exposure with BMI Z-score of children was also mediated by preterm birth by 6.6% (DE=0.111, P<0.001; IE=0.008, P<0.001) and 9.1% (DE=0.064, P<0.001; IE=0.006, P<0.001). These results remained robust in the sensitivity analyses. In conclusion, prenatal exposure to PM1 and PM2.5 increased WFL, BMI Z-scores and higher risk of OWOB for one-year-old children. The associations were partially mediated by preterm birth. These findings call for the urgent action on air pollution regulation to protect early-life health among children.

Length of chronic exposure to particulate matter and adverse birth outcomes: A population-based cohort study

Background/Aim: Previous studies have shown associations between particulate matter (PM) air pollution and adverse birth outcomes. However, most studies focused on relatively short periods of prenatal exposure to PM and in a low to moderate polluted areas. We examined the possible impact of exposure to particulate matter with diameter ≤10 μm (PM10) and ≤2.5 μm (PM2.5) for a number of years before delivery on the occurrence of adverse birth outcomes: term low birth weight (TLBW), preterm delivery (PTB), and small for gestational age (SGA) in a region exposed to long-range dust transport. Methods: This study was based on a cohort of births (N=90,505) that occurred in Israel during 2013-2015. We calculated prenatal PM averages during 1, 5, and 10 years prior to delivery. Logistic regression models with mother-level as a random intercept were used to determine the association between exposure and adverse birth outcomes, adjusting for a priori known covariates. Results: In fully adjusted models, a 10-μg/m3 increase in PM2.5 during 1-, 5- and 10-years prior to delivery was associated with a monotonically increasing risk of TLBW [odds ratio (OR)=1.51 95% confidence interval (CI): (1.14-1.99), 1.54 (1.12-2.14) and 1.70 (1.21-2.41), respectively] and SGA [1.25 (1.03-1.49), 1.43 (1.16-1.77) and 1.45 (1.16-1.80), respectively]. ORs increased with the length of exposure period also for PM10. For example, ORs for TLBW in association with a 20-μg/m3 increase in PM10 over 1-, 5-, and 10-years prior to delivery were 1.25 (1.00-1.58), 1.32 (1.01-1.72) and 1.46 (1.11-1.90), respectively. PTB was not associated with neither PM2.5 nor PM10. For example, the OR for PTB in association with a 10-μg/m3 increase in PM2.5 over 10-years prior to delivery was 1.19 (0.91-1.52).Conclusions The magnitude of the estimated associations between maternal exposure to both PM2.5 and PM10 exposure and birth outcomes increased with the length of the exposure period.

Prenatal exposure to particulate matter and ADHD in children: a prospective cohort study

Background/Aim Environmental factors may play a role in the development of attention-deficit/hyperactivity disorder (ADHD) and some studies have shown that ambient air pollution is associated with the ADHD. This study was designed to investigate the impact of prenatal particulate matter (PM10) exposure on ADHD among children over 60 months of age in Korea by using MOCEH birth cohort study’s data.Methods This study is a part of the Mothers and Children's Environmental Health (MOCEH) study, a Korean multi-center prospective birth cohort study initiated in 2006. After the delivery, children were followed up at 60, 72, 84 and 96 months of age. The average exposure level of particulate matter (PM10) were estimated using the inverse distance weighting (IDW) method from the prenatal period. ADHD behaviour were assessed using the K-ARS, K-CBCL/1.5-5 and 6-18 at each follow-up period. Generalized Linear Models (GLM) were used to explore the association between PM10 and ADHD.Results The mean PM10 concentrations during total pregnancy was 54.1μg/m3 with a range from 24.2 to 85.7μg/m3. In the GLM model, exposure to PM10 at first trimester and during pregnancy showed significant positive association with 72 months K-ARS score (β=0.06, 95% CI: 0.01,0.11 for first trimester, β=0.10, 95% CI: 0.01,0.19 for total pregnancy exposure). Furthermore, exposure to PM10 at first trimester and during total pregnancy showed significant association with 60, 72, and 84 months K-CBCL score, especially with total problems, attention problems and aggressive behaviour (β=0.26, 95% CI: 0.07,0.44 between first trimester and total problem score at 60 months, β=0.10, 95% CI: 0.05,0.15 between first trimester and attention problems at 72 months).Conclusions In conclusions, our results have demonstrated that the prenatal PM10 concentration was significantly associated with ADHD behaviour in Korean children. Further studies regarding other air pollutants’ effects to the neurodevelopment in children are recommended.

Prenatal PM2.5 exposure and vitamin D–associated early persistent atopic dermatitis via placental methylation

BackgroundThe effects of prenatal particulate matter with an aerodynamic diameter ranging from 0.1 μm to 2.5 μm (PM2.5) and vitamin D on atopic dermatitis (AD) phenotypes have not been evaluated. DNA methylation and cord blood (CB) vitamin D could represent a plausible link between prenatal PM2.5 exposure and AD in an offspring. ObjectiveTo determine the critical windows of prenatal PM2.5 exposure on the AD phenotypes, if vitamin D modulated these effects, and if placental DNA methylation mediated these effects on AD in offspring. MethodsMother–child pairs were enrolled from the birth cohort of the Cohort for Childhood Origin of Asthma and allergic diseases (COCOA) study. PM2.5 was estimated by land-use regression models, and CB vitamin D was measured by chemiluminescence immunoassay. AD was identified by the parental report of a physician’s diagnosis. We defined the following 4 AD phenotypes according to onset age (by the age of 2 years) and persistence (by the age of 3 years): early-onset transient and persistent, late onset, and never. Logistic regression analysis and Bayesian distributed lag interaction model were used. DNA methylation microarray was analyzed using an Infinium Human Methylation EPIC BeadChip (Illumina, San Diego, California) in placenta. ResultsPM2.5 exposure during the first trimester of pregnancy, especially during 6 to 7 weeks of gestation, was associated with early-onset persistent AD. This effect increased in children with low CB vitamin D, especially in those with PM2.5 exposure during 3 to 7 weeks of gestation. AHRR (cg16371648), DPP10 (cg19211931), and HLADRB1 (cg10632894) were hypomethylated in children with AD with high PM2.5 and low CB vitamin D. ConclusionHigher PM2.5 during the first trimester of pregnancy and low CB vitamin D affected early-onset persistent AD, and the most sensitive window was 6 to 7 weeks of gestation. Placental DNA methylation mediated this effect.

What are the Long-Term Effects of Prenatal Air Pollution Exposure? Evidence from the BHPS

The detrimental impacts of air pollution on human health are significant. Pollution increases mortality in the elderly and reduces worker productivity. While a consensus is beginning to emerge on the contemporaneous effects of air pollution, the long-term effects are still largely unknown. By combining restricted data from a comprehensive national survey with historical pollution data, I plausibly isolate the impact of prenatal particulate matter exposure on adult outcomes. I find that those with higher levels of prenatal exposure during the second trimester of gestation are more likely to be disabled, earn lower wages, and have worse health.

Associations of α- and γ-tocopherol during early life with lung function in childhood

Tocopherol isoforms may regulate child lung growth and spirometric measures. Our aim was to determine the extent to which plasma α-tocopherol (α-T) or γ-tocopherol (γ-T) isoform levels in early childhood or in utero are associated with childhood lung function. We included 622 participants in the Project Viva cohort who had lung function at a mid-childhood visit (age 6-10 years). Maternal and child tocopherol isoform levels were measured by HPLC at the second trimester and 3 years of age, respectively. Multivariable linear regression models (adjusted for mid-childhood body mass index z scores, maternal education, smoking in pregnancy, and prenatal particulate matter with diameter of <2.5 micrometers (PM2.5) particulate exposure) stratified by tertiles of child γ-T level were used to assess the association of α-T levels with FEV1 and forced vital capacity (FVC) percent predicted. Similarly, models stratified by child α-T tertile evaluated associations of γ-T levels with lung function. We performed similar analyses with maternal second trimester tocopherol isoform levels. The median maternal second trimester α-T level was 63 μM (interquartile range= 47-82). The median early-childhood level was 25 μM (interquartile range= 20-33 μM). In the lowest tertile of early-childhood γ-T, children with a higher α-T level (per 10 μM) had a higher mid-childhood FEV1 percent predicted (β= 3.09; 95% CI= 0.58-5.59 and a higher FVC percent predicted (β= 2.77; 95% CI= 0.47-5.06). This protective association of α-T was lost at higher γ-T levels. We did not see any consistent associations of second trimester levels of either α-T or γ-T with mid-childhood FEV1 or FVC. When γ-T levels were in the lowest tertile, a higher early-childhood α-T level was associated with better lung function at mid-childhood. Second trimester maternal plasma α-T concentration was 3-fold higher than in the adult nonpregnant female population.

Prenatal particulate matter exposure with skin barrier dysfunction affects offspring's atopic dermatitis: COCOA study

Prenatal particulate matter exposure with skin barrier dysfunction affects offspring's atopic dermatitis: COCOA study

Identifying critical windows of prenatal particulate matter (PM2.5) exposure and early childhood blood pressure

BackgroundExposure to air pollution is associated with increased blood pressure (BP) in adults and children. Some evidence suggests that air pollution exposure during the prenatal period may contribute to adverse cardiorenal health later in life. Here we apply a distributed lag model (DLM) approach to identify critical windows that may underlie the association between prenatal particulate matter ≤ 2.5 μm in diameter (PM2.5) exposure and children's BP at ages 4–6 years. MethodsParticipants included 537 mother-child dyads enrolled in the Programming Research in Obesity, GRowth Environment, and Social Stress (PROGRESS) longitudinal birth cohort study based in Mexico City. Prenatal daily PM2.5 exposure was estimated using a validated satellite-based spatio-temporal model and BP was measured using the automated Spacelabs system with a sized cuff. We used distributed lag models (DLMs) to examine associations between daily PM2.5 exposure and systolic and diastolic BP (SBP and DBP), adjusting for child's age, sex and BMI, as well as maternal education, preeclampsia and indoor smoking report during the second and third trimester, seasonality and average postnatal year 1 PM2.5 exposure. ResultsWe found that PM2.5 exposure between weeks 11–32 of gestation (days 80–226) was significantly associated with children's increased SBP. Similarly, PM2.5 exposure between weeks 9–25 of gestation (days 63–176) was significantly associated with increased DBP. To place this into context, a constant 10 μg/m3 increase in PM2.5 sustained throughout this critical window would predict a cumulative increase of 2.6 mmHg (CI: 0.5, 4.6) in SBP and 0.88 mmHg (CI: 0.1, 1.6) in DBP at ages 4–6 years. In a stratified analysis by sex, this association persisted in boys but not in girls. ConclusionsSecond and third trimester PM2.5 exposure may increase children's BP in early life. Further work investigating PM2.5 exposure with BP trajectories later in childhood will be important to understanding cardiorenal trajectories that may predict adult disease. Our results underscore the importance of reducing air pollution exposure among susceptible populations, including pregnant women.