Prenatal Fine Particulate Matter Research Articles

The joint effects of prenatal exposure to PM2.5 constituents and reduced fetal growth on children's accelerated growth in the first 3 years: a birth cohort study.

Prenatal fine particulate matter (PM2.5) constituents exposure and reduced fetal growth may be risk factors for accelerated growth in early childhood, an important indicator for lifelong health. The study investigated whether the joint effects are present between PM2.5 constituents and reduced fetal growth. The study was embedded in a birth cohort in China, including 5424 mother-child pairs. Prenatal PM2.5 and its constituents' [organic carbon (OC), elementary carbon (EC), ammonium (NH4+), nitrate (NO3-), and sulfate (SO42-)] concentrations were estimated based on maternal residential addresses. Fetal growth was evaluated by fetal growth trajectory in utero and preterm birth (PTB), low birth weight (LBW), and small for gestational age (SGA). Children's accelerated growth was defined as body mass index (BMI) Z-score change of >0.67 between birth and 3 years. Generalized logistic regression was used to analyze the effects of prenatal PM2.5 constituents exposure and fetal growth on children's accelerated growth. Joint effect was tested on multiplicative scale and additive scale with the relative excess risk due to interaction (RERI). Children with lower fetal growth trajectory, PTB, LBW, and SGA had increased odds of children's accelerated growth, with odds ratios (ORs) ranging from 1.704 to 11.605. Compared with lower exposure (≤median), higher exposure (>median) of PM2.5, OC, and SO42- were significantly associated with increased odds of children's accelerated growth, varying in ORs from 1.163 to 1.478. Prenatal exposure to OC had joint effects with lower fetal growth on children's accelerated growth. We observed that the interaction was statistically significant on an additive scale in OC and lower fetal growth trajectory (RERI: 0.497, 95% CI: 0.033,0.962). Fine particulate matter (PM2.5) is a huge threat to human health worldwide, causing 6.7 million death globally in 2019. According to the theory of DOHaD, prenatal PM2.5 exposure could influence early childhood growth, which is important for lifelong health. We found that prenatal exposure to PM2.5, OC, and SO42- was associated with higher risk of accelerated childhood growth in the first 3 years. More importantly, reduced fetal growth moderated these associations. Our findings highlight the need for policies and interventions on PM2.5 constituents to improve lifelong health, especially for those vulnerable populations with reduced fetal growth.

Individual and joint effects of prenatal PM2.5 and maternal stress on child temperament

Prenatal fine particulate matter (PM2.5) and maternal psychological functioning have been associated with child cognitive outcomes, though their independent and joint impacts on earlier behavioral outcomes remains less studied. We used data from 382 mother-child pairs from a prospective birth cohort in Mexico City. Temperament was measured at 24 months using the Carey Toddler Temperament Scale (TTS). Exploratory factor analysis (EFA) was used to update the factor structure of the TTS. During pregnancy, mothers completed the Crisis in Family Systems-Revised, Edinburgh Depression Scale, pregnancy-specific anxiety scale, and the Perceived Stress Scale. Pregnancy PM2.5 was assessed using estimates from a satellite-based exposure model. We assessed the association between prenatal maternal stress and PM2.5 on temperament, in both independent and joint models. Quantile g-computation was used to estimate the joint associations. Models were adjusted for maternal age, SES, education, child sex, and child age. In EFA, we identified three temperament factors related to effortful control, extraversion, and negative affect. Our main results showed that higher levels of PM2.5 and several of the maternal psychological functioning measures were related to both effortful control and negative affect in the child, both individually and as a mixture. For instance, a one quartile increase in the prenatal mixture was associated with higher negative affect scores in the child (0.34, 95% CI: 0.16, 0.53). We observed modification of these associations by maternal SES, with associations seen only among lower SES participants for both effortful control (−0.45, 95% CI: -0.70, −0.20) and negative affect outcomes (0.60, 95% CI: 0.35, 0.85). Prenatal PM2.5 and maternal psychological functioning measures were associated with toddler temperament outcomes, providing evidence for impacts of chemical and non-chemical stressors on early child health.

Gestational age modifies the association between exposure to fine particles and fetal death: findings from a nationwide epidemiological study in the contiguous United States

BackgroundsThe vulnerability of fetuses differs at different developmental stages, in response to environmental stressors such as fine particulate matter (PM2.5), a ubiquitous air pollutant. Whether gestational age (GA) modifies the association between prenatal fine particulate matter (PM2.5) exposure and fetal death remains unclear.MethodsWe selected approximately 47.8 million eligible United States (US) livebirth and fetal death (defined as a termination at a GA of 20–43 weeks) records from 1989 to 2004. For each record, we took the level of prenatal exposure to PM2.5 as the average concentration in the mother’s residential county during the entire gestational period, or a specific trimester (i.e., GA-specific exposure), according to well-established estimates of monthly levels across the contiguous US. First, we evaluated the associations between PM2.5 exposure and fetal death at a specific GA (i.e., GA-specific outcome) using five different logit models (unadjusted, covariate-adjusted, propensity-score, double robust, and diagnostic-score models). Double robust model was selected as the main model due to its advantages in causal inference. Then, we conducted meta-analyses to pool the estimated GA-specific associations, and explored how the pooled estimates varied with GA.ResultsAccording to the meta-analysis, all models suggested gestational PM2.5 exposure was associated with fetal death. However, there was slight heterogeneity in the estimated effects, as different models revealed a range of 3.6–10.7% increase in the odds of fetal death per 5-µg/m3 increment of PM2.5. Each 5-µg/m3 increase in PM2.5 exposure during the entire gestation period significantly increased the odds of fetal death, by 8.1% (95% confidence interval [CI]: 5.1–11.2%). In terms of GA-specific outcomes, the odds of fetal death at a GA of 20–27, 28–36, or ≥ 37 weeks increased by 11.0% (5.9–16.4%), 5.2% (0.4–10.1%), and 8.3% (2.5–14.5%), respectively. In terms of GA-specific exposure, the odds of fetal death increased by 6.0% (3.9–8.2%), 4.1% (3.9–8.2%), and 4.3% (0.5–8.2%) with 5-µg/m3 increases in PM2.5 exposure during the first, second, and third trimester, respectively. The association had the largest effect size (odds ratio = 1.098, 95% CI: 1.061–1.137) between PM2.5 exposure during early gestation (i.e., first trimester) and early fetal death (i.e., 20–27 weeks).ConclusionsPrenatal exposure to PM2.5 was significantly associated with an increased risk of fetal death. The association was varied by gestational-age-specific exposures or outcomes, suggesting gestation age as a potential modifier on the effect of PM2.5. The fetus was most vulnerable during the early stage of development to death associated with PM2.5 exposure.

Trimester-specific ambient PM2.5 exposures and risk of intellectual disability in Utah

Prenatal fine particulate matter (PM2.5) exposure is an understudied risk factor for neurodevelopmental outcomes, including intellectual disability (ID). Associations among prenatal exposures and neurodevelopmental outcomes may vary depending on the timing of exposure. Limited numbers of studies examining PM2.5 and neurodevelopmental outcomes have considered exposures occurring during the preconception period. To address these gaps, we conducted a case-control study of children born in Utah between 2002 and 2008 (n = 1032). Cases were identified using methods developed by the Centers for Disease Control and Prevention's Autism and Developmental Disabilities Monitoring Network and matched with controls on birth year, sex, and birth county. We estimated the daily average PM2.5 concentration during a period spanning 12 weeks before the estimated conception date, as well as during each of the three trimesters at the maternal residential address listed on the child's birth certificate. In a multivariable model, the third (OR: 2.119, CI: 1.123–3.998, p = .021) and fourth (OR: 2.631, CI: 1.750–3.956, p < .001) quartiles for preconception average PM2.5 demonstrated significantly increased risk of ID relative to the first quartile. Second quartile preconception exposure was also associated with increased risk, though it did not reach significance (OR: 1.385, CI: 0.979–1.959, p = .07). The fourth quartile of first trimester average PM2.5 was positive and significant (OR: 2.278, CI: 1.522–3.411, p < .001); the third quartile was positive, but not significant (OR: 1.159, CI: 0.870–1.544, p = .312). Quartiles of second and third trimester were not associated with higher risk of ID. These findings from Utah, which were robust to a variety of sensitivity analyses, provide initial evidence that preconception and prenatal PM2.5 exposure may be associated with ID. Future studies are needed across other geographic locations and populations.

Prenatal fine particulate matter exposure associated with placental small extracellular vesicle derived microRNA and child neurodevelopmental delays

Background and aimsPrenatal fine particulate matter (PM2.5) exposure has been linked to adverse neurodevelopment. However, epidemiological evidence remains inconclusive and little information about the effects of various PM2.5 components on child neurodevelopment is currently known. The underlying mechanism was also not elucidated. The study aimed to evaluate the effects of PM2.5 and components exposure on child neurodevelopmental delays and the role of placental small extracellular vesicles (sEVs)-derived miRNAs in the associations. MethodsWe included 267 mother-child pairs in this analysis. Prenatal PM2.5 and components (i.e. elements, water-soluble ions, and PAHs) exposure during three trimesters were monitored through personal PM2.5 sampling. Child neurodevelopment at 2, 6, and 12 months old were evaluated by Ages and Stages Questionnaire (ASQ). We isolated sEVs from placental tissue to analyze the change of sEVs-derived miRNAs in response to PM2.5. Associations between the PM2.5-associated miRNAs and child neurodevelopment were evaluated using multivariate linear regression models. ResultsThe PM2.5 exposure levels in the three trimesters range from 2.51 to 185.21 μg/m3. Prenatal PM2.5 and the components of Pb, Al, V and Ti exposure in the second and third trimester were related to decreased ASQ scores communication, problem-solving and personal-social domains in children aged 2 or 6 months. RNA sequencing identified fifteen differentially expressed miRNAs. The miR-101-3p and miR-520d-5p were negatively associated with PM2.5 and Pb component. miR-320a-3p expression was positively associated with PM2.5 and V component. Meanwhile, the miR-320a-3p was associated with decreased ASQ scores, as reflected by ASQ-T (β: -2.154, 95 % CI: −4.313, −0.516) and problem-solving domain (β: -0.605, 95 % CI: −1.111, −0.099) in children aged 6 months. ConclusionPrenatal exposure to PM2.5 and its Pb, Al, V & Ti component were associated with infant neurodevelopmental delays. The placenta sEVs derived miRNAs, especially miR-320a-3p, might contribute to an increased risk of neurodevelopmental delays.

Association of prenatal exposure to ambient air pollution with adverse birth outcomes and effect modification by socioeconomic factors

BackgroundMaternal exposure to air pollution has been associated with birth outcomes; however, few studies examined biologically critical exposure windows shorter than trimesters or potential effect modifiers. ObjectivesTo examine associations of prenatal fine particulate matter (PM2.5), by trimester and in biologically critical windows, with birth outcomes and assess potential effect modifiers. MethodsThis study used two pregnancy cohorts (CANDLE and TIDES; N = 2099) in the ECHO PATHWAYS Consortium. PM2.5 was estimated at the maternal residence using a fine-scale spatiotemporal model, averaged over pregnancy, trimesters, and critical windows (0–2 weeks, 10–12 weeks, and last month of pregnancy). Outcomes were preterm birth (PTB, <37 completed weeks of gestation), small-for-gestational-age (SGA), and continuous birthweight. We fit multivariable adjusted linear regression models for birthweight and Poisson regression models (relative risk, RR) for PTB and SGA. Effect modification by socioeconomic factors (maternal education, household income, neighborhood deprivation) and infant sex were examined using interaction terms. ResultsOverall, 9% of births were PTB, 10.4% were SGA, and mean term birthweight was 3268 g (SD = 558.6). There was no association of PM2.5 concentration with PTB or SGA. Lower birthweight was associated with higher PM2.5 averaged over pregnancy (β −114.2, 95%CI -183.2, −45.3), during second (β −52.9, 95%CI -94.7, −11.2) and third (β −45.5, 95%CI -85.9, −5.0) trimesters, and the month prior to delivery (β −30.5, 95%CI -57.6, −3.3). Associations of PM2.5 with likelihood of SGA and lower birthweight were stronger among male infants (p-interaction ≤0.05) and in those with lower household income (p-interaction = 0.09). ConclusionsFindings from this multi city U.S. birth cohort study support previous reports of inverse associations of birthweight with higher PM2.5 exposure during pregnancy. Findings also suggest possible modification of this association by infant sex and household income.

Prenatal Fine Particulate Matter, Maternal Micronutrient Antioxidant Intake, and Early Childhood Repeated Wheeze: Effect Modification by Race/Ethnicity and Sex.

Fine particulate matter (PM2.5) potentiates in utero oxidative stress influencing fetal development while antioxidants have potential protective effects. We examined associations among prenatal PM2.5, maternal antioxidant intake, and childhood wheeze in an urban pregnancy cohort (n = 530). Daily PM2.5 exposure over gestation was estimated using a satellite-based spatiotemporally resolved model. Mothers completed the modified Block98 food frequency questionnaire. Average energy-adjusted percentile intake of β-carotene, vitamins (A, C, E), and trace minerals (zinc, magnesium, selenium) constituted an antioxidant index (AI). Maternal-reported child wheeze was ascertained up to 4.1 ± 2.8 years. Bayesian distributed lag interaction models (BDLIMs) were used to examine time-varying associations between prenatal PM2.5 and repeated wheeze (≥2 episodes) and effect modification by AI, race/ethnicity, and child sex. Covariates included maternal age, education, asthma, and temperature. Women were 39% Black and 33% Hispanic, 36% with ≤high school education; 21% of children had repeated wheeze. Higher AI was associated with decreased wheeze in Blacks (OR = 0.37 (0.19–0.73), per IQR increase). BDLIMs identified a sensitive window for PM2.5 effects on wheeze among boys born to Black mothers with low AI (at 33–40 weeks gestation; OR = 1.74 (1.19–2.54), per µg/m3 increase in PM2.5). Relationships among prenatal PM2.5, antioxidant intake, and child wheeze were modified by race/ethnicity and sex.

Preconceptional and the first trimester exposure to PM2.5 and offspring neurodevelopment at 24 months of age: Examining mediation by maternal thyroid hormones in a birth cohort study

Prenatal fine particulate matter (PM2.5) exposure has been associated with impaired offspring neurodevelopment; however, the association of PM2.5 exposure during preconception with offspring’s neurodevelopment and factors responsible for this association are still unclear. This study estimated the associations of PM2.5 exposure during preconception and the first trimester with offspring neurodevelopment and evaluated whether maternal thyroid hormones mediate these associations. We recruited 1329 mother-child pairs between 2013 and 2015 in Wuhan, China. PM2.5 exposure levels of each woman during the 3 months preconception and the first trimester were estimated using land-use regression models. Offspring neurodevelopment characterized by mental developmental index (MDI) and psychomotor developmental index (PDI) were measured at 24 months of age. Maternal serum levels of free thyroxine (FT3), free triiodothyronine (FT4), and thyroid-stimulating hormone (TSH) during early pregnancy were measured of a subset of the 1329 women (551 women). Generalized estimation equation and general linear regression models were used to estimate the associations between maternal PM2.5 exposure, thyroid hormones, and offspring neurodevelopment. After adjusting for potential confounders, we found that either among all participants or the subset, PM2.5 exposure during preconception and the first trimester was negatively associated with offspring PDI. Double increment in the first trimester PM2.5 exposure was significantly associated with 3.43 and 6.48 points decrease in offspring MDI. In the subset, each doubling of PM2.5 exposure during preconception and the first trimester was significantly associated with 7.93 and 8.02 points decrease in maternal FT4 level, respectively. Increased maternal FT4, in turn, was associated with increased PDI (β = 16.69, 95% CI: 5.39, 27.99). About 7.7% (95% CI: 2.0%–19.4%) and 8.6% (95% CI: 3.0%, 22.1%) of the effect of PM2.5 exposure during preconception on offspring PDI was mediated through maternal FT4 and the FT4/FT3 ratio, respectively.

Maternal exposure to PM2.5 during pregnancy and asthma risk in early childhood: consideration of phases of fetal lung development.

Increasingly studies suggest prenatal exposure to air pollution may increase risk of childhood asthma. Few studies have investigated exposure during specific fetal pulmonary developmental windows. To assess associations between prenatal fine particulate matter exposure and asthma at age 4. This study included mother-child dyads from two pregnancy cohorts-CANDLE and TIDES-within the ECHO-PATHWAYS consortium (births in 2007-2013). Three child asthma outcomes were parent-reported: ever asthma, current asthma, and current wheeze. Fine particulate matter (PM2.5) exposures during the pseudoglandular (5-16 weeks gestation), canalicular (16-24 weeks gestation), saccular (24-36 weeks gestation), and alveolar (36+ weeks gestation) phases of fetal lung development were estimated using a national spatiotemporal model. We estimated associations with Poisson regression with robust standard errors, and adjusted for child, maternal, and neighborhood factors. Children (n=1469) were on average 4.3 (standard deviation 0.5) years old, 49% were male, and 11.7% had ever asthma; 46% of women identified as black and 53% had at least a college/technical school degree. A 2 μg/m3 higher PM2.5 exposure during the saccular phase was associated with 1.29 times higher risk of ever asthma (95% CI: 1.06-1.58). A similar association was observed with current asthma (RR 1.27, 95% CI: 1.04-1.54), but not current wheeze (RR 1.11, 95% CI: 0.92-1.33). Effect estimates for associations during other developmental windows had confidence intervals that included the null. Later phases of prenatal lung development may be particularly sensitive to the developmental toxicity of PM2.5.

Prenatal fine particulate matter exposure, placental DNA methylation changes, and fetal growth

This study was designed to examine the impact of prenatal fine particulate matter (PM2.5) exposure on fetal growth and the underlying placental epigenetic mechanism in a cohort of Chinese women. Within the prospective Shanghai Mother-Child Pairs cohort (Shanghai MCPC), 329 women carrying singleton pregnancy with a due date in 2018 were recruited between 2017 and 2018. Maternal PM2.5 exposure levels were estimated using gestational exposure prediction model combining satellite-driven ambient concentrations and personal air sampling. Fetal growth characteristics were evaluated by prenatal ultrasound examinations and anthropometric measurements at birth. In a discovery phase, whole-genome DNA methylation analysis was performed using the Infinium 850 K array. In a validation phase, placental DNA methylation was measured using bisulfite pyrosequencing for five candidate genes that showed the most significant alterations and function relevance in our methylation array screen, including BID (BH3 interacting domain death agonist), FOXN3 (Forkhead box N3), FOXP1 (Forkhead box P1), IGF2 (Insulin-like growth factor 2) and HSD11B2 (Hydroxysteroid 11-beta dehydrogenase 2). Multivariate linear regression models were applied to examine the associations among PM2.5 exposure, fetal growth characteristics and DNA methylation on placental candidate genes. Sobel tests were used to evaluate the mediating role of DNA methylation in multivariable models. After excluding women who withdrew or failed to provide placenta, a total of 287 pregnant women with an average age of 30 entered the final analysis. Increased PM2.5 exposure was significantly associated with reduced biparietal diameter (BPD) (β: −0.136 mm, 95% CI: −0.228 to −0.043), head circumference (HC) (β: −0.462 mm, 95% CI: −0.782 to −0.142), femur length (FL) (β: −0.113 mm, 95% CI: −0.185 to −0.041) and abdominal circumference (AC) (β: −0.371 mm, 95% CI: −0.672 to −0.071) in the second trimester and birth length (β: −0.013 cm, 95% CI: −0.025 to −0.001). Prenatal PM2.5 exposure could lead to aberrant changes in DNA methylation profile of placenta genome, which were mainly enriched in reproductive development, energy metabolism and immune response. DNA methylation of IGF2 and BID showed significant associations with PM2.5 exposures during all exposure windows. In addition, BID methylation was negatively correlated with HC (β: −1.396 mm, 95% CI: −2.582 to −0.209) and BPD (β: −0.330 mm, 95% CI: −0.635 to −0.026) in the second trimester. Further mediation analysis indicated that BID methylation mediated about 30% of the effects of PM2.5 exposure on HC. These findings collectively suggested that prenatal PM2.5 exposure may cause adverse effects on fetal growth by modifying placental DNA methylation.

Prenatal Fine Particulate Matter Exposure and Childhood Anxiety Symptoms

Background: Air pollution has been linked to neurotoxic effects; however, there is limited research on mental health, particularly in younger populations in which symptoms often first arise. We studied the association between prenatal fine particulate matter (PM2.5) exposure and symptoms of anxiety in a cohort of 8-9 year olds in Mexico City.Methods: Participants included 173 mother-child pairs from the Programming Research in Obesity, Growth, Environment and Social Stressors longitudinal birth cohort in Mexico City. Daily PM2.5 predictions were estimated using a 1km satellite-based exposure model and averaged over trimesters and the entire pregnancy. Symptoms of anxiety were assessed using the Revised Children’s Manifest Anxiety Scale (RCMAS-2) (Spanish Version) administered by psychologists during the face-to-face interview at the 8-9 year study visit. Linear regression models were used to estimate the change in continuous anxiety symptoms with each 5-µg/m3 increase in PM2.5, for each trimester and the entire pregnancy. Models were adjusted for maternal education, maternal SES, maternal depression, maternal age, child’s age at study visit, and season of conception. We additionally assessed sex-specific effects by including an interaction term between PM2.5 and sex.Results: Higher levels of PM2.5 exposure averaged over the entire pregnancy was associated with increases in childhood anxiety symptoms at age 8-9, in males only (β for males = 2.06, 95% CI: 0.20, 3.91; β for females = -0.45, 95% CI: -2.38, 1.48; p-int: 0.02). This sex-specific effect was primarily seen for exposures during the 1st trimester (β for males= 1.13, 95% CI: -0.06, 2.32, p-int: 0.06).Conclusions: PM2.5 exposure in early pregnancy may be a critical window for elevated symptoms of anxiety in the mid/late childhood period. Future analyses will use distributed lag models to further define time and sex-specific effects, as well as adjust for other urban stress correlates such as environmental noise.

Prenatal PM2.5 exposure and behavioral development in children from Mexico City

BackgroundChildhood exposure to air pollution has been linked with maladaptive cognitive development; however, less is known about the association between prenatal fine particulate matter (PM2.5) exposure and childhood behavior. ObjectivesOur aim was to assess the association between prenatal PM2.5 exposure and behavioral development in 4-6 year old children residing in Mexico City. MethodsWe used data from 539 mother-child pairs enrolled in a prospective birth cohort in Mexico City. We estimated daily PM2.5 exposure using a 1 km2 satellite-based exposure model and averaged over each trimester of pregnancy. We assessed childhood behavior at 4-6 years of age using the parent-completed Behavioral Assessment Scale for Children (BASC-2) composite scores and subscales. We used linear regression models to estimate change in BASC-2 T-scores with trimester specific 5-μg/m3 increases in PM2.5. All models were mutually adjusted for PM2.5 exposures during the other trimesters, maternal factors including age, education, socioeconomic status, depression, and IQ, child’s age at study visit, and season. We additionally assessed sex-specific effects by including an interaction term between PM2.5 and sex. ResultsHigher first trimester PM2.5 exposure was associated with reduced Adaptive Skills scores (β: -1.45, 95% CI: -2.60, -0.30). Lower scores on the Adaptive Skills composite score and subscales indicate poorer functioning. For PM2.5 exposure during the first trimester, decrements were consistent across adaptive subscale scores including Adaptability (β: -1.51, 95% CI: -2.72, -0.30), Social Skills (β: -1.63, 95% CI: -2.90, -0.36), and Functional Communication (β: -1.21, 95% CI: -2.21, -0.21). The association between 1st trimester PM2.5 and depression was stronger in males than females (β for males: 1.52, 95% CI: -0.41, 3.45; β for females: -0.13, 95% CI: -1.99, 1.72; p-int: 0.07). ConclusionsExposure to PM2.5 during early pregnancy may be associated with impaired behavioral development in children, particularly for measures of adaptive skills. These results suggest that air pollution impacts behavioral domains as well as cognition, and that the timing of exposure may be critical.

Prenatal Fine Particulate Matter (PM2.5) Exposure and Pregnancy Outcomes-Analysis of Term Pregnancies in Poland.

Air pollution is currently one of the greatest threats to global health. Polish cities are among the most heavily polluted in Europe. Due to air pollution 43,100 people die prematurely in Poland every year. However, these data do not take into account the health consequences of air pollution for unborn children. Thus, the aim of this study was to evaluate the effects of the fine particulate matter air pollution (less than 2.5 μm in diameter) on pregnancy outcomes. An analysis of pregnant women and their children was made using a questionnaire survey from a nationwide study conducted in 2017. Questionnaires from 1095 pregnant women and data from their medical records were collected. An analysis of air pollution in Poland was conducted using the air quality database maintained by the Chief Inspectorate for Environmental Protection in Poland. A higher concentration of PM2.5 was associated with a decrease in birth weight and a higher risk of low birthweight (i.e., <2500 g). We also observed lower APGAR scores. Thus, all possible efforts to reduce air pollution are critically needed.

Associations of exposure to fine particulate matter during pregnancy with maternal blood glucose levels and gestational diabetes mellitus: Potential effect modification by ABO blood group.

Previous studies have examined the relationships between prenatal fine particulate matter (PM2.5) exposure and gestational diabetes mellitus (GDM), but the results were inconsistent. Furthermore, the possible effect modification by ABO blood group has not been explored. To assess the associations of PM2.5 exposures during pregnancy with maternal glucose levels as well as GDM, and further to evaluate the potential effect modification by ABO blood group. Between January 2013 and January 2015, 4783 pregnant women were enrolled in our study based on a birth cohort in Wuhan. Daily PM2.5 exposure levels for each woman during pregnancy were estimated using a spatial-temporal land-use regression model. Linear regressions with general estimating equations (GEE) were performed to assess the associations between trimester-specific PM2.5 exposures and maternal glucose levels. Modified Poisson regressions with GEE analyses were used to evaluate the impacts of PM2.5 exposures during each trimester on the risk of GDM. The associations of PM2.5 exposure during the whole study period with glucose levels and GDM were estimated using multiple linear regression model and modified Poisson regression model, respectively. We conducted a stratified analysis to explore the potential effect modification by ABO blood group. Among all the 4783 participants, 394 (8.24%) had GDM. Exposure to PM2.5 was found to be positively associated with elevated fasting glucose level during the whole study period [0.382mg/dL, 95% confidence interval (CI): 0.179-0.586, per 10μg/m3 increase in PM2.5], the first trimester (0.154mg/dL ,95% CI: 0.017-0.291) and the second trimester (0.541mg/dL, 95% CI: 0.390-0.692). No statistically significant results were observed between PM2.5 and 1-h and 2-h glucose levels during any study period. Increased risks of GDM for each 10μg/m3 increase in PM2.5 levels were observed during the whole study period [relative risk (RR): 1.120, 95% CI: 1.021-1.228] and the first trimester (RR: 1.074, 95% CI: 1.012-1.141), but not the second trimester (RR: 1.035, 95% CI: 0.969-1.106). Stratified analysis indicated that the associations of PM2.5 exposures with GDM were more pronounced among pregnant women with blood group A, but no significant effect modifications were observed. Our study enriched epidemiological evidence linking PM2.5 exposures during pregnancy to elevated maternal glucose levels and increased risk of GDM. More importantly, we first highlighted that the impact of PM2.5 on GDM might be greater among pregnant women with blood group A.

Effects of Maternal Homelessness, Supplemental Nutrition Programs, and Prenatal PM2.5 on Birthweight.

Few studies examined the impact of maternal socioeconomic status and of its combined effects with environmental exposures on birthweight. Our goal was to examine the impact of maternal homelessness (mothers ever homeless or who lived in shelters during pregnancy) and participation in the Special Supplemental Nutrition Program for Women, Infants and Children (WIC) during pregnancy in conjunction with air pollution exposure on birthweight in the Boston-based Children’s HealthWatch cohort from 2007 through 2015 (n = 3366). Birthweight was obtained from electronic health records. Information on maternal homelessness and WIC participation during pregnancy were provided via a questionnaire. Prenatal fine particulate matter (PM2.5) exposures, estimated at the subject’s residential address, were calculated for each trimester. We fit linear regression models adjusting for maternal and child characteristics, seasonality, and block-group-level median household income and examined the interactions between PM2.5 and each covariate. Prenatal maternal homelessness was associated with reduced birthweight (−55.7 g, 95% CI: −97.8 g, −13.7 g), while participating in WIC was marginally associated with increased birthweight (36.1 g, 95% CI: −7.3 g, 79.4 g). Only average PM2.5 during the second trimester was marginally associated with reduced birthweight (−8.5 g, 95% CI: −19.3, 2.3) for a 1 µg/m3 increase in PM2.5. The association of PM2.5 during the second trimester with reduced birthweight was stronger among non-Hispanic Black mothers and trended toward significance among immigrants and single mothers. Our study emphasizes the independent and synergistic effects of social and environmental stressors on birthweight, particularly the potentially protective effect of participating in WIC for vulnerable populations.

Associations between PM2.5 and mid-pregnancy inflammation measured using a novel proteomics chip

OPS 20: Chemicals, biomarkers, omics, Room 110, Floor 1, August 27, 2019, 4:30 PM - 5:30 PM Background/Aim: Prenatal fine particulate matter (PM2.5) exposure is linked with adverse pregnancy outcomes and developmental problems in children; PM2.5-induced changes to maternal immune activity may underlie these relationships. We examined maternal prenatal PM2.5 exposure in relation to inflammatory signals using a targeted proteomics approach. Methods: Analyses include 373 pregnant women enrolled in a prospective study in the northeastern United States between 2011 and 2015. We estimated daily residential PM2.5 exposure using high-resolution satellite data combined with ground monitoring measures and spatiotemporal predictors. We analyzed 92 inflammatory proteins in mid-pregnancy serum using a novel multiplex proximity extension assay. To explore the influence of exposure timing, we examined PM2.5 averaged across the previous 3 months, 1 month, or week of blood draw. We regressed PM2.5 on each inflammatory marker in separate models adjusting for week of gestation, maternal age, and season. For associations with a Bonferroni-adjusted p-value <0.05, we next used multivariable logistic regression to examine continuous PM2.5 exposure in relation to high (highest 20%) versus low (lowest 80%) inflammatory marker levels. Results: Mothers were primarily minorities (60% black or Hispanic). After Bonferroni correction, monocyte-chemotactic protein-3 (MCP-3), interleukin-8 (IL-8), and oncostatin M (OSM) were (p<0.001) positively associated with PM2.5 for one or more exposure interval. The odds of having high MCP-3 levels increased per unit (µg/m3) increase in PM2.5 when averaged across the previous 3 months (OR=1.48, 95% CI=1.22, 1.80), 1 month (OR=1.30, 95%CI=1.12, 1.51), or week (OR=1.18, 95% CI=1.06, 1.31). Parallel findings were true for OSM (1 month: OR=1.24, 95% CI=1.08, 1.44; 1 week: OR=1.22, 95% CI=1.10, 1.35) and IL-8 (1 month: OR=1.27, 95% CI=1.10, 1.46; 1 week: OR=1.23, 95% CI=1.11, 1.37) for more recent exposure only. Conclusions: These data link increased prenatal PM2.5 with markers of enhanced inflammation. Future analysis in this longitudinal cohort will examine whether identified markers (MCP3, OSM and IL8) mediate associations between PM2.5 and maternal-child health outcomes.

Maternal Lifetime Stress and Prenatal Psychological Functioning and Decreased Placental Mitochondrial DNA Copy Number in the PRISM Study.

Psychosocial stress contributes to placental oxidative stress. Mitochondria are vulnerable to oxidative stress, which can lead to changes in mitochondrial DNA copy number (mtDNAcn). We examined associations of maternal lifetime stress, current negative life events, and depressive and posttraumatic-stress-disorder symptom scores with placental mtDNAcn in a racially/ethnically diverse sample (n = 147) from the Programming of Intergenerational Stress Mechanisms (PRISM) study (Massachusetts, March 2011 to August 2012). In linear regression analyses adjusted for maternal age, race/ethnicity, education, prenatal fine particulate matter exposure, prenatal smoking exposure, and the sex of the child, all measures of stress were associated with decreased placental mtDNAcn (all P values < 0.05). Weighted-quantile-sum (WQS) regression showed that higher lifetime stress and depressive symptoms accounted for most of the effect on mtDNAcn (WQS weights: 0.25 and 0.39, respectively). However, among white individuals, increased lifetime stress and posttraumatic stress disorder symptoms explained the majority of the effect (WQS weights: 0.20 and 0.62, respectively) while among nonwhite individuals, lifetime stress and depressive symptoms accounted for most of the effect (WQS weights: 0.27 and 0.55, respectively). These analyses are first to link increased maternal psychosocial stress with reduced placental mtDNAcn and add to literature documenting racial/ethnic differences in the psychological sequelae of chronic stress that may contribute to maternal-fetal health.

Prenatal exposure to fine particles and polycyclic aromatic hydrocarbons and birth outcomes: a two-pollutant approach

BackgroundPrevious epidemiologic studies have considered the effects of individual air pollutants on birth outcomes, whereas a multiple-pollutant approach is more relevant to public health policy.ObjectivesThe present study compared the observed effect sizes of prenatal fine particulate matter (PM2.5) and polycyclic aromatic hydrocarbons (PAH) (a component of PM2.5) exposures on birth outcome deficits, assessed by the single vs. two-pollutant approaches.MethodsThe study sample included 455 term infants born in Krakow to non-smoking mothers, among whom personal exposures to PM2.5 and PAH were monitored in the second trimester of pregnancy. The exposure effect estimates (unstandardized and standardized regression coefficients) on birth outcomes were determined using multivariable linear regression models, accounting for relevant covariates.ResultsIn the single-pollutant approach, each pollutant was inversely associated with all birth outcomes. The effect size of prenatal PAH exposure on birth weight and length was twice that of PM2.5, in terms of standardized coefficients. In the two-pollutant approach, the negative effect of PM2.5 on birth weight and length, adjusted for PAH exposure, lost its significance. The standardized effect of PAH on birth weight was 10-fold stronger (β = −0.20, p = 0.004) than that estimated for PM2.5 (β = −0.02, p = 0.757).ConclusionThe results provide evidence that PAH had a greater impact on several measures of fetal development, especially birth weight, than PM2.5. Though in the single-pollutant models PM2.5 had a significant impact on birth outcomes, this effect appears to be mediated by PAH.

Ambient PM2.5 exposure in pregnancy, maternal prenatal antioxidant intakes, and infant autonomic response

Introduction: Factors disrupting fetal oxidant balance impact autonomic nervous system (ANS) development. We examined links among prenatal fine particulate matter (PM2.5), maternal antioxidant inta...