Search

Adequate thyroid hormone availability is required for normal brain development. Studies have found associations between prenatal exposure to air pollutants and thyroid hormones in pregnant women and newborns. We aimed to examine associations of trimester-specific residential exposure to common air pollutants with congenital hypothyroidism (CHT). All term infants born in Israel during 2009–2015 were eligible for inclusion. We used data on CHT from the national neonatal screening lab of Israel, and exposure data from spatiotemporal air pollution models. We used multivariable logistic regression models to estimate associations of exposures with CHT, adjusting for ethnicity, socioeconomic status, geographical area, conception season, conception year, gestational age, birth weight, and child sex. To assess residual confounding, we used postnatal exposures to the same pollutants as negative controls. The study population included 696,461 neonates. We found a positive association between third-trimester nitrogen oxide exposure and CHT (per interquartile-range change, odds ratio = 1.23, 95% confidence interval: 1.08, 1.41) and a similar association for nitrogen dioxide. There was no evidence of residual confounding or bias by correlation among exposure periods for these associations.

Background Exposure to air pollution is the main risk factor for morbidity and mortality in the world. Exposure to particulate matter with aerodynamic diameter ≤ 2.5 μm (PM2.5) is associated with cardiovascular and respiratory conditions, as well as with lung cancer, and there is evidence to suggest that it is also associated with type II diabetes (DM). The Mexico City Metropolitan Area (MCMA) is home to more than 20 million people, where PM2.5 levels exceed national and international standards every day. Likewise, DM represents a growing public health problem with prevalence around 12%. In this study, the objective was to evaluate the association between exposure to PM2.5 and DM in adults living in the MCMA. Methods Data from the 2006 or 2012 National Health and Nutrition Surveys (ENSANUT) were used to identify subjects with DM and year of diagnosis. We estimated PM2.5 exposure at a residence level, based on information from the air quality monitoring system (monitors), as well as satellite measurements (satellite). We analyzed the relationship through a cross-sectional approach and as a case - control study. Results For every 10 μg/m3 increase of PM2.5 we found an OR = 3.09 (95% CI 1.17–8.15) in the 2012 sample. These results were not conclusive for the 2006 data or for the case - control approach. Conclusions Our results add to the evidence linking PM2.5 exposure to DM in Mexican adults. Studies in low- and middle-income countries, where PM2.5 atmospheric concentrations exceed WHO standards, are required to strengthen the evidence.

Rationale: Ambient ultrafine particles (UFPs; with an aerodynamic diameter

BACKGROUND: Residual confounding is a major concern for causal inference in observational studies on air pollution–autism spectrum disorder (ASD) associations. This study is aimed at assessing confounding in these associations using negative control exposures. METHODS: This nested case–control study included all children diagnosed with ASD (detected through 31 December 2016) born during 2007-2012 in Israel and residing in the study area (N= 3,843), and matched controls of the same age (N= 38,430). We assigned individual house-level exposure estimates for each child. We estimated associations using logistic regression models, mutually adjusted for all relevant exposure periods (pre-pregnancy, pregnancy, and postnatal). We assessed residual confounding using post-outcome negative control exposure at age 28-36 months. RESULTS: In mutually adjusted models we observed positive associations with ASD for postnatal exposures to NOx (odds ratio [OR] per interquartile range, 95% confidence interval [CI]: 1.19, 1.02-1.38) and NO(2) (1.20, 1.00-1.43), and gestational exposure to PM(2.5-10) (1.08, 1.01-1.15). The result for the negative control period was 1.04, 0.99-1.10 for PM(2.5,) suggesting some residual confounding, but no associations for PM(2.5-10) (0.98, 0.81-1.18), NOx (1.02, 0.84-1.25) or NO(2) (0.98, 0.81-1.18), suggesting no residual confounding. CONCLUSIONS: Our results further support a hypothesized causal link with ASD that is specific to postnatal exposures to traffic-related pollution.

BACKGROUND: Emerging studies have investigated the adverse health effects of PM(2.5) using data from multiple cohorts, and results often are not generalizable across cohorts. We aimed to assess associations between prenatal PM(2.5) and childhood cognition in two U.S. cohorts while accounting for between-site heterogeneity. METHODS: Analyses included 348 mother-child dyads enrolled in the dual site (New York City and Boston) PRogramming of Intergenerational Stress Mechanisms (PRISM) cohort and in the First Thousand Days of Life (FTDL) study (Northern Virginia) participating in the Environmental influences on Child Health Outcomes (ECHO) national consortium. Residential prenatal PM(2.5) exposure was estimated using a validated satellite-based model and childhood cognition was measured using the NIH Toolbox Cognition Battery at three to eight years of age. We used a log-linear model applied to contingency tables formed by cross-classifying covariates by site to examine between-site heterogeneity using 3(rd) trimester PM(2.5) exposure, age-corrected cognition scores, and covariates potentially causing heterogeneities. Multivariable linear regression models informed by the combinability analysis were used to estimate the coefficients and 95% confidence intervals (CIs) for the association between 3(rd) trimester PM(2.5) exposure and age-corrected cognition scores (mean = 100, SD = 15). RESULTS: The log-linear model indicated that inter-study associations were similar between PRISM-NYC and FTDL, which were different from those in PRISM-Boston. Accordingly, we combined the data of PRISM-NYC and FTDL cohorts. We observed associations between 3(rd) trimester PM(2.5) and cognition scores, findings were varying by site, childsex, and test. For example, a 1 μg/m(3) increase of 3(rd) trimester PM(2.5) was associated with −4.35 (95% CI = −8.73, −0.25) mean early childhood cognition scores in females in PRISM-Boston. In the pooled NYC + FTDL site, the association between PM(2.5) and childhood cognition may be modified by maternal education and urbanicity. CONCLUSIONS: We found associations between prenatal PM(2.5) and impaired childhood cognition. Since multi-site analyses are increasingly conducted, our findings suggest the needed awareness of between-site heterogeneity.

Summary Background Pregnancy is associated with deteriorations in maternal bone strength and heightened susceptibility to bone fractures. We aimed to investigate whether ambient particulate matter (PM)2·5 concentrations were associated with bone strength during pregnancy. Methods In this longitudinal cohort study, we analysed longitudinal data from women participating in the Programming Research in Obesity, Growth, Environment and Social Stressors (PROGRESS) cohort in Mexico City, Mexico. Eligible women were aged 18 years or older, at less than 20 weeks' gestation at the time of recruitment, planning to stay in Mexico City for the next 3 years, without heart or kidney disease, did not use steroids or anti-epileptic drugs, were not daily consumers of alcohol, and had access to a telephone. Daily ambient PM2·5 concentrations were estimated from a spatio-temporal model that was based on the individual's address. Trabecular bone strength was measured using quantitative ultrasound from the radius of the middle finger and cortical bone strength from the proximal phalanx of the middle finger, during the second trimester, third trimester, and 1 and 6 months post partum. Bone strength T scores were modelled with PM2·5 concentrations using linear mixed models and distributed lag models. Findings Adjusting for multiple exposure windows, each 10 ug/m3 increase in PM2·5 exposure concentrations in the first trimester was associated with a 0·18 SD decrease (95% CI −0·35 to −0·01; p=0·033) in ultrasound speed-of-sound (SOS) T score of trabecular bone strength from the second trimester until 6 months post partum. Similarly, each 10 μg/m3 increase in third trimester PM2·5 exposure was associated with a 0·18 SD decrease (–0·36 to −0·01; p=0·044) in the SOS T score of trabecular bone strength from the third trimester until 6 months post partum. PM2·5 exposure in the first month post partum was associated with a 0·20 SD decline (–0·39 to −0·01; p=0·043) in cortical bone strength until 6 months post partum. Interpretation Ambient PM2·5 exposure during and after pregnancy was associated with diminished trabecular and cortical bone strength. Early pregnancy PM2·5 exposure was associated with a greater decline in bone strength later during pregnancy. Late pregnancy and early post-partum exposures adversely affected the post-partum bone strength recovery. Technological and policy solutions to reduce PM2·5 pollution could improve public health by reducing bone fracture risk. Funding US National Institute of Environmental Health Sciences.

Background: African ancestry is associated with a higher prevalence and greater severity of asthma than European ancestries, yet genetic studies of the most common locus associated with childhood-onset asthma, 17q12–21, in African Americans have been inconclusive. The aim of this study was to leverage both the phenotyping of the Children's Respiratory and Environmental Workgroup (CREW) birth cohort consortium, and the reduced linkage disequilibrium in African Americans, to fine map the 17q12–21 locus. Methods: We first did a genetic association study and meta-analysis using 17q12–21 tag single-nucleotide polymorphisms (SNPs) for childhood-onset asthma in 1613 European American and 870 African American children from the CREW consortium. Nine tag SNPs were selected based on linkage disequilibrium patterns at 17q12–21 and their association with asthma, considering the effect allele under an additive model (0, 1, or 2 effect alleles). Results were meta-analysed with publicly available summary data from the EVE consortium (on 4303 European American and 3034 African American individuals) for seven of the nine SNPs of interest. Subsequently, we tested for expression quantitative trait loci (eQTLs) among the SNPs associated with childhood-onset asthma and the expression of 17q12–21 genes in resting peripheral blood mononuclear cells (PBMCs) from 85 African American CREW children and in upper airway epithelial cells from 246 African American CREW children; and in lower airway epithelial cells from 44 European American and 72 African American adults from a case-control study of asthma genetic risk in Chicago (IL, USA). Findings: 17q12–21 SNPs were broadly associated with asthma in European Americans. Only two SNPs (rs2305480 in gasdermin-B [GSDMB] and rs8076131 in ORMDL sphingolipid biosynthesis regulator 3 [ORMDL3]) were associated with asthma in African Americans, at a Bonferroni-corrected threshold of p

Air pollution has been linked to obesity while higher ambient temperatures typically reduce metabolic demand in a compensatory manner. Both relationships may impact glucose metabolism, thus we examined the association between intermediate- and long-term exposure to fine particulate matter (PMWe assessed 3-month, 6-month, and 12-month average air pollution and ambient temperature at 1-kmWe analyzed 1,265 HbA1c measurements of 484 women. Per 1 µg/mIntermediate-term exposure to PM

BACKGROUND: Prenatal exposure to fine particulate matter with a diameter of ≤2.5 microns (PM(2.5)) has been linked to adverse neurodevelopmental outcomes in later childhood, while research on early infant behavior remains sparse. OBJECTIVES: We examined associations between prenatal PM(2.5) exposure and infant negative affectivity, a stable temperamental trait associated with longer-term behavioral and mental health outcomes. We also examined sex-specific effects. METHODS: Analyses included 559 mother-infant pairs enrolled in the PRogramming of Intergenerational Stress Mechanisms (PRISM) cohort. Daily PM(2.5) exposure based on geocoded residential address during pregnancy was estimated using a satellite-based spatiotemporal model. Domains of negative affectivity (Sadness, Distress to Limitations, Fear, Falling Reactivity) were assessed using the Infant Behavior Questionnaire-Revised (IBQ-R) when infants were 6 months old. Subscale scores were calculated as the mean of item-specific responses; the global Negative Affectivity (NA) score was derived by averaging the mean of the four subscale scores. Bayesian distributed lag interaction models (BDLIMs) were used to identify sensitive windows for prenatal PM(2.5) exposure on global NA and its subscales, and to examine effect modification by sex. RESULTS: Mothers were primarily racial/ethnic minorities (38% Black, 37% Hispanic), 40% had ≤12 years of education; most did not smoke during pregnancy (87%). In the overall sample, BDLIMs revealed that increased PM(2.5) at mid-pregnancy was associated with higher global NA, Sadness, and Fear scores, after adjusting for covariates (maternal age, education, race/ethnicity, sex). Among boys, increased PM(2.5) at early pregnancy was associated with decreased Fear scores, while exposure during late pregnancy was associated with increased Fear scores (cumulative effect estimate=0.57, 95% CI: 0.03–1.41). Among girls, increased PM(2.5) during mid-pregnancy was associated with higher Fear scores (cumulative effect estimate=0.82, 95% CI: 0.05–1.91). CONCLUSIONS: Prenatal PM(2.5) exposure was associated with negative affectivity at age 6 months, and the sensitive windows may vary by subdomains and infant sex.

Inhalation of ambient PM2.5, shown to be able to cross the placenta, has been linked to adverse obstetric and postnatal metabolic health outcomes. The placenta regulates fetal growth and influences postnatal development via fetal programming. Placental gene expression may be influenced by intrauterine exposures to PM2.5. Herein, we explore whether maternal PM2.5 exposure during pregnancy alters placental gene expression related to lipid and glucose metabolism in a U.S. birth cohort, the Rhode Island Child Health Study (RICHS). Average PM2.5 exposure level was estimated linking residential addresses and satellite data across the three trimesters using spatio-temporal models. Based on Gene Ontology annotations, we curated a list of 657 lipid and glucose metabolism genes. We conducted a two-staged analysis by leveraging placental RNA-Seq data from 148 subjects to identify top dysregulated metabolic genes associated with PM2.5 (Phase I) and then validated the results in placental samples from 415 participants of the cohort using RT-qPCR (Phase II). Associations between PM2.5 and placental gene expression were explored using multivariable linear regression models in the overall population and in sex-stratified analyses. The average level of PM2.5 exposure across pregnancy was 8.0μg/m

A growing body of literature reports associations between exposure to particulate matter with diameter ≤2.5 μm (PMTo assess the association between PMIn Israel, we used Maccabi Healthcare Services data to establish a population-based cohort of 381,265 singleton births reaching 24-42 weeks' gestation and birth weight of 500-5000 g (2004-2015). Daily PMIn fully adjusted models with a mother-level random intercept only, a 10-μg/mConsideration of mother-level variability in a region with high fertility rates provides new insights on the strength of associations between PM

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 PM2.5 exposure, 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.

Despite the unequal burden of environmental exposures borne by racially minoritized communities, these groups are often underrepresented in public health research. Here, we examined racial/ethnic disparities in exposure to metals among a multi-ethnic sample of pregnant women. Our objective was to examine what disparities, if any, exist in metal exposure among a sample of pregnant women. The sample included women enrolled in the PRogramming of Intergenerational Stress Mechanisms (PRISM) pregnancy cohort (N = 382). Urinary metal concentrations (arsenic [As], barium [Ba], cadmium [Cd], cesium [Cs], chromium [Cr], lead [Pb], antimony [Sb]) were measured during mid-pregnancy and information on individual- and neighborhood-level characteristics was ascertained during an in-person interview and from publicly available databases, respectively. Linear regression was used to examine individual and neighborhood characteristics in relation to metal concentrations. Black/Black-Hispanic women had Cd, Cr, Pb, and Sb levels that were 142.0%, 10.9%, 35.0%, and 32.1% higher than White, non-Hispanic women, respectively. Likewise, White-Hispanic women had corresponding levels that were 141.5%, 108.2%, 59.9%, and 38.3% higher. These same metals were also higher among women residing in areas with higher crime, higher diversity, lower educational attainment, lower household income, and higher poverty. Significant disparities in exposure to metals exist and may be driven by neighborhood-level factors. Exposure to metals for pregnant women can be especially harmful. Understanding exposure inequalities and identifying factors that increase risk can help inform targeted public health interventions.

Background Birthweight is a strong predictor of normal growth, healthy development, and survival. Several studies have found associations between temperature, fine particulate matter (PM2.5), and birth weight. However, the relevant timing of exposures varies between studies and is yet unclear. Therefore, we assessed the difference in term birthweight (TBW) associated with weekly exposure to temperature and PM2.5 throughout 37 weeks of gestation. Methods We included all singleton live term births in Massachusetts, U.S between 2004 and 2015 (n = 712,438). Weekly PM2.5 and temperature predictions were estimated on a 1 km grid from satellite-based models. We utilized a distributed lag nonlinear model (DLNM) to estimate the difference in TBW associated with weekly exposures from the last menstrual period to 37 weeks of gestation. Results We found a nonlinear association with prenatal temperature exposure. Larger effects were observed in warmer temperatures, where higher temperatures were negatively associated with TBW. Temperature effects were larger in the first and final weeks of gestation. We observed a negative difference in TBW associated with PM2.5 exposure. Overall, a 1 µg/m3 increase in prenatal exposure was associated with 3.9 g lower TBW (95% CI −5.0 g; −2.9 g). PM2.5 effects were larger in the final weeks of gestation. Conclusion We found heat and PM2.5 exposure to be related to lower TBW. Our findings suggest that women are more susceptible to both exposures towards the end of pregnancy. Susceptibility to heat was higher in the initial weeks of pregnancy as well. These critical windows of susceptibility can be communicated to pregnant women during routine prenatal visits to increase awareness and target interventions to reduce exposures.

The effects of particulate matter (PM) air pollution on adipose tissue have mainly been studied in animal models. The aim of this study was to examine the potential associations between PM exposure and 25 cellular markers in human omental (OM) and subcutaneous (SC) adipose tissue. The PM exposure assessments for both PM

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

Background Recent studies have reported that air pollution exposure may have neurotoxic properties. Objective To examine longitudinal associations between prenatal particles less than 2.5 μm in diameter (PM2.5) exposure and neurodevelopment during the first two years of children's life. Methods Analysis was conducted in PROGRESS, a longitudinal birth cohort between 2007 and 2013 in Mexico City. We used satellite data to predict daily PM2.5 concentrations at high spatial resolution. Multivariate mixed-effect regression models were adjusted to examine cognitive, language and motor scores in children up to 24 months of age (n = 740) and each trimester-specific and whole pregnancy exposure to PM2.5. Results: Models adjusted by child sex, gestational age, birth weight, smoking and mother's IQ, showed that each increase of 1 μg/m3 of PM2.5 was associated with a decreased language function of −0.38 points (95% CI: −0.77, −0.01). PM2.5 exposure at third trimester of pregnancy contributed most to the observed association. Conclusion Our findings suggest that language development up to 24 months of age may be particularly sensitive to PM2.5 exposure during pregnancy.

Hormones play critical roles in facilitating pregnancy progression and the onset of parturition. Several classes of environmental contaminants, including fine particulate matter (PM

PURPOSE: Increasingly epidemiological evidence supports that environmental factors are associated with breast cancer (BC) outcomes after a BC diagnosis. Although evidence suggests that air pollution exposure is associated with higher mortality in women with BC, studies investigating potential mechanisms have been lacking. METHODS: We evaluated women with BC (N=151) attended at the National Cancer Institute–Mexico from 2012–2015. We calculated one-year average exposures to particulate matter

BACKGROUND: A growing body of evidence links maternal exposure to particulate matter < 2.5 μM in diameter (PM(2.5)) and deviations in fetal growth. Several studies suggest that the placenta plays a critical role in conveying the effects of maternal PM(2.5) exposure to the developing fetus. These include observed associations between air pollutants and candidate placental features, such as mitochondrial DNA content, DNA methylation and telomere length. However, gaps remain in delineating the pathways linking the placenta to air pollution-related health effects, including a comprehensive profiling of placental processes impacted by maternal PM(2.5) exposure. In this study, we examined alterations in a placental transcriptome-wide network in relation to maternal PM(2.5) exposure prior to and during pregnancy and infant birthweight. METHODS: We evaluated PM(2.5) exposure and placental RNA-sequencing data among study participants enrolled in the Rhode Island Child Health Study (RICHS). Daily residential PM(2.5) levels were estimated using a hybrid model incorporating land-use regression and satellite remote sensing data. Distributed lag models were implemented to assess the impact on infant birthweight due to PM(2.5) weekly averages ranging from 12 weeks prior to gestation until birth. Correlations were assessed between PM(2.5) levels averaged across the identified window of susceptibility and a placental transcriptome-wide gene coexpression network previously generated using the WGCNA R package. RESULTS: We identified a sensitive window spanning 12 weeks prior to and 13 weeks into gestation during which maternal PM(2.5) exposure is significantly associated with reduced infant birthweight. Two placental coexpression modules enriched for genes involved in amino acid transport and cellular respiration were correlated with infant birthweight as well as maternal PM(2.5) exposure levels averaged across the identified growth restriction window. CONCLUSION: Our findings suggest that maternal PM(2.5) exposure may alter placental programming of fetal growth, with potential implications for downstream health effects, including susceptibility to cardiometabolic health outcomes and viral infections.

Background Both elemental metals and particulate air pollution have been reported to influence adult blood pressure (BP). The aim of this study is to examine which elemental components of particle mass with diameter ≤2.5 μm (PM 2.5 ) are responsible for previously reported associations between PM 2.5 and neonatal BP. Methods and Results We studied 1131 mother‐infant pairs in Project Viva, a Boston‐area prebirth cohort. We measured systolic BP (SBP) and diastolic BP (DBP) at a mean age of 30 hours. We calculated average exposures during the 2 to 7 days before birth for the PM 2.5 components—aluminum, arsenic, bromine, sulfur, copper, iron, zinc, nickel, vanadium, titanium, magnesium, potassium, silicon, sodium, chlorine, calcium, and lead—measured at the Harvard supersite. Adjusting for covariates and PM 2.5 , we applied regression models to examine associations between PM 2.5 components and median SBP and DBP, and used variable selection methods to select which components were more strongly associated with each BP outcome. We found consistent results with higher nickel associated with significantly higher SBP and DBP, and higher zinc associated with lower SBP and DBP. For an interquartile range increase in the log Z score (1.4) of nickel, we found a 1.78 mm Hg (95% CI, 0.72–2.84) increase in SBP and a 1.30 (95% CI, 0.54–2.06) increase in DBP. Increased zinc (interquartile range log Z score 1.2) was associated with decreased SBP (−1.29 mm Hg; 95% CI, −2.09 to −0.50) and DBP (−0.85 mm Hg; 95% CI: −1.42 to −0.29). Conclusions Our findings suggest that prenatal exposures to particulate matter components, and particularly nickel, may increase newborn BP.

Background: Studies have reported associations between maternal exposure to atmospheric pollution and lower birth weight. However, the evidence is not consistent and uncertainties remain. We used advanced statistical approaches to robustly estimate the association of atmospheric pollutant exposure during specific pregnancy time windows with term birth weight (TBW) in a nationwide study. Methods: Among 13,334 women from the French Longitudinal Study of Children (ELFE) cohort, exposures to PM2.5, PM10 (particles &lt, 2.5 µm and &lt, 10 µm) and NO2 (nitrogen dioxide) were estimated using a fine spatio-temporal exposure model. We used inverse probability scores and doubly robust methods in generalized additive models accounting for spatial autocorrelation to study the association of such exposures with TBW. Results: First trimester exposures were associated with an increased TBW. Second trimester exposures were associated with a decreased TBW by 17.1 g (95% CI, −26.8, −7.3) and by 18.0 g (−26.6, −9.4) for each 5 µg/m3 increase in PM2.5 and PM10, respectively, and by 15.9 g (−27.6, −4.2) for each 10 µg/m3 increase in NO2. Third trimester exposures (truncated at 37 gestational weeks) were associated with a decreased TBW by 48.1 g (−58.1, −38.0) for PM2.5, 38.1 g (−46.7, −29.6) for PM10 and 14.7 g (−25.3, −4.0) for NO2. Effects of pollutants on TBW were larger in rural areas. Conclusions: Our results support an adverse effect of air pollutant exposure on TBW. We highlighted a larger effect of air pollutants on TBW among women living in rural areas compared to women living in urban areas.

Exposure to PM2.5 has been associated with the prevalence of obesity. In the Greater Mexico City Area (GMCA), both are ranked among the highest in the world. Our aim was to analyze this association in children, adolescents, and adults in the GMCA. We used data from the 2006 and 2012 Mexican National Surveys of Health and Nutrition (ENSANUT). Participants’ past-year exposure to ambient PM2.5 was assessed using land use terms and satellite-derived aerosol optical depth estimates; weight and height were measured. We used survey-adjusted logistic regression models to estimate the odds ratios (ORs) of obesity (vs. normal-overweight) for every 10 µg/m3 increase in annual PM2.5 exposure for children, adolescents, and adults. Using a meta-analysis approach, we estimated the overall odds of obesity. We analyzed data representing 19.3 million and 20.9 million GMCA individuals from ENSANUT 2006 and 2012, respectively. The overall pooled estimate between PM2.5 exposure and obesity was OR = 1.96 (95% CI: 1.21, 3.18). For adolescents, a 10 µg/m3 increase in PM2.5 was associated with an OR of 3.53 (95% CI: 1.45, 8.58) and 3.79 (95% CI: 1.40, 10.24) in 2006 and 2012, respectively. More studies such as this are recommended in Latin American cities with similar air pollution and obesity conditions.

Previous findings concerning the risk for preeclampsia following exposure to particulate matter are inconclusive.We used data from all singleton pregnancies of women insured by the "Clalit health services" (CHS) maintenance organization in southern Israel that resulted in delivery or perinatal mortality at Soroka Medical Center (SMC). Daily PMA total of 133,197 pregnancies ended at SMC during the study period, of which 68,126 (51.1%) were Jewish and 65,071 (48.9%) were Bedouin. For pregnancies of Jewish women, exposure to PMExposure to PM

Background Intrauterine Fetal Death (IUFD) is a rare and tragic pregnancy complication. The main causes for IUFD are largely unknown. Particulate Matter (PM)2.5 exposure has been suggested as an IUFD risk factor. Objectives To study the association between maternal PM2.5 levels and IUFD risk, to address ethnicity as a possible effect modifier, and to identify a prenatal period during which PM2.5 is most harmful regarding IUFD risk. Methods This is a retrospective cohort study, which included pregnant women at the Soroka University Medical Center between the years 2003–2017. Estimated PM2.5 levels were calculated per residence, using a hybrid model incorporating daily satellite remote sensing data at a 1 km spatial resolution. Multiple gestations, fetuses with congenital malformations or chromosomal abnormalities were excluded. Mean PM2.5 level was calculated per trimester, the entire pregnancy and the last gestational week. Analyses were also performed separately for the two ethnic groups in the study: Jews and Bedouin-Arabs. Multivariable analysis were applied to study the association between PM2.5 exposure at the different periods and IUFD risk. Results The study included 87,887 pregnancies, 444 (0.5%) ended with IUFD. Mean PM2.5 levels ranged between 18.18 and 22.32 μm. First trimester and entire pregnancy PM2.5 levels were significantly associated with increased IUFD risk among Jewish women only. In a multivariable model, for every 10 μg/m3 unit increase in PM2.5 the risk for IUFD increases by 2.98 (95%CI 1.50–5.90) and by 3.61 (95%CI 1.32–9.85) during first trimester and the entire pregnancy, respectively, while adjusting for maternal age, smoking, socioeconomic score and season. Conclusions In this retrospective cohort an association was found between PM2.5 levels and IUFD among Jewish women only. These results strengthen the importance of addressing this effect modifier when studying air pollution effects on human health.

Background Numerous studies have confirmed the association of ambient temperature and air pollution with a higher risk of morbidities, yet few have addressed their effect on the ocular system. The purpose of this study was to assess the association between temperature, air pollution, and emergency room visits for conjunctivitis. Methods In this case-crossover study, the records of all emergency room visits to Soroka University Medical Center (SUMC) from 2009 to 2014 were reviewed for patients with conjunctivitis. Daily exposure to fine and coarse particulate matter and temperature were determined by a hybrid model involving satellite sensors. Mean relative humidity was obtained from the Ministry of Environmental Protection meteorological monitoring station located in Beer-Sheva. Results Six hundred one patients were diagnosed with conjunctivitis in the SUMC emergency room. We discovered a positive association between temperature increments and incidence of conjunctivitis. The strongest effect was found during summer and autumn, with an immediate (lag0) incidence increase of 8.1% for each 1 °C increase in temperature (OR = 1.088, 95%CI: 1.046–1.132) between 24 and 28 °C in the summer and 7.2% for each 1 °C increase in temperature (OR = 1.072, 95%CI: 1.036–1.108) between 13 and 23 °C in the autumn. There was no statistically significant association between fine and coarse particulate matter and conjunctivitis incidence. Conclusion Temperature increases during summer and autumn are significantly associated with an increased risk of conjunctivitis. Conjunctivitis is not associated with non-anthropogenic air pollution. These findings may help community clinics and hospital emergency rooms better predict conjunctivitis cases and will hopefully lead to improved prevention efforts that will lower the financial burden on both the individual and the public.

PMWe aimed to study associations of fine particulate matter PMWe conducted nasal epigenome-wide association analyses within 503 children from Project Viva (mean age 12.9 y), and examined various exposure durations (1-day, 1-week, 1-month, 3-months and 1-year) prior to nasal sampling. We used residential addresses to estimate average daily PMIn adjusted analyses, we found 362 CpGs associated with 1-year PMWe observed wide-spread DNAm variability associated with average past year PM

Background: Preterm birth is a major determinant of adverse health consequences, and early term births are also associated with increased risk of various outcomes. In light of climate change, the effect of ambient temperature on earlier delivery is an important factor to consider. Several studies have focused on associations of ambient air temperature (Ta) on preterm birth, but few have examined associations with early term births. Aims: To investigate the association of prenatal exposure to Ta with preterm birth (

Background Sedentary behavior is a worldwide public health concern. There is consistent and growing evidence linking sedentary behavior to mortality and morbidity. Early monitoring and assessment of environmental factors associated with sedentary behaviors at a young age are important initial steps for understanding children's sedentary time and identifying pertinent interventions. Objective This study examines the association between daily temperature (maximum, mean, minimum, and diurnal variation) and all-day sedentary time among 4-6 year old children in Mexico City (n = 559) from the year 2013 to 2015. Methods We developed a spatiotemporally resolved hybrid satellite-based land use regression temperature model and calculated percent daily sedentary time from aggregating 10-second epoch vertical counts captured by accelerometers that participants wore for one week. We modeled generalized additive models (GAMs), one for each temperature type as a covariate (maximum, mean, minimum, and diurnal variation). All GAMs included percent all-day sedentary time as the outcome and participant-level random intercepts to account for repeated measures of sedentary time. Our models were adjusted for demographic factors and environmental exposures. Results Daily maximum temperature, mean temperature, and diurnal variation have significant negative linear relationships with all-day sedentary time (p

International audience; Background: Heat stress during pregnancy may limit fetal growth, with ramifications throughout the life course. However, critical exposure windows are unknown, and effects of meteorological variability have not been investigated.Objectives: We aimed to identify sensitive windows for the associations of mean and variability of temperature and humidity with term birthweight.Methods: We analyzed data from two French mother–child cohorts, EDEN and PELAGIE (n = 4771), recruited in 2002–2006. Temperature exposure was assessed using a satellite-based model with daily 1-km2 resolution, and relative humidity exposure data were obtained from Météo France monitors. Distributed lag models were constructed using weekly means and standard deviation (SD, to quantify variability) from the first 37 gestational weeks. Analyses were then stratified by sex. Results for each exposure were adjusted for the other exposures, gestational age at birth, season and year of conception, cohort and recruitment center, and individual confounders.Results: There was no evidence of association between term birthweight and mean temperature. We identified a critical window in weeks 6–20 for temperature variability (cumulative change in term birthweight of −54.2 g [95% CI: −102, −6] for a 1 °C increase in SD of temperature for each week in that window). Upon stratification by sex of the infant, the relationship remained for boys (weeks 1–21, cumulative change: −125 g [95% CI: −228, −21]). For mean humidity, there was a critical window in weeks 26–37, with a cumulative change of −28 g (95% CI: −49, −7) associated with a 5% increase in humidity for each week. The critical window was longer and had a stronger association in boys (weeks 29–37; −37 g, 95% CI: −63, −11) than girls (week 14; −1.8 g, 95% CI: −3.6, −0.1).Discussion: Weekly temperature variability and mean humidity during critical exposure windows were associated with decreased term birthweight, especially in boys.

BackgroundLower respiratory tract infections (LRTI) in early life, including pneumonia, bronchitis and bronchiolitis, can lead to decreased lung function, persistent lung damage and increased susceptibility to various respiratory diseases such as asthma. In-utero exposure to particulate matter (PM) during pregnancy may disrupt biological mechanisms that regulate fetal growth, maturation and development. We aimed to estimate the association between intrauterine exposure to PM of size 2.5) and incidence of LRTIs during the first year of life.MethodsA retrospective population-based cohort study in a population of mothers and infants born in Soroka University Medical Center (SUMC) in the years 2004–2012. All infants 2spatial resolution. Data from monitoring stations was used for imputation of main exposure and other pollutants. Levels of environmental exposures were assigned to subjects based on their residential addresses and averaged for each trimester. Analysis was conducted by a multivariable generalized estimating equation (GEE) Poisson regression. Data was analyzed separately for the two main ethnic groups in the region, Jewish and Arab-Bedouin.ResultsThe study cohort included 57,331 deliveries that met the inclusion criteria. Overall, 1871 hospitalizations of infants 2.5(> 24 μg/m3) in the first and second trimesters was found to be adversely associated with LRTIs in the Arab-Bedouin population (1st trimester, RR = 1.31, CI 95% 1.08–1.60; 2nd trimester: RR = 1.34, CI 95% 1.09–1.66).ConclusionIntrauterine exposure to high levels of PM2.5is associated with a higher risk of hospitalizations due to lower respiratory tract infections in Arab-Bedouin infants.

BACKGROUND: Childhood exposure to air pollution has been linked with maladaptive cognitive development; however, less is known about the association between prenatal fine particulate matter (PM(2.5)) exposure and childhood behavior. OBJECTIVES: Our aim was to assess the association between prenatal PM(2.5) exposure and behavioral development in 4–6 year old children residing in Mexico City. METHODS: We used data from 539 mother-child pairs enrolled in a prospective birth cohort in Mexico City. We estimated daily PM(2.5) using a 1km(2) 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/m(3) increases in PM(2.5). All models were mutually adjusted for PM(2.5) 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 PM(2.5) and sex. RESULTS: Higher first trimester PM(2.5) 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 PM(2.5) 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 1(st) trimester PM(2.5) 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). CONCLUSIONS: Exposure to PM(2.5) 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.

Numerous studies have found higher cardiovascular (CVD) risk associated with particulate matter smaller than 2.5 μm in diameter (PM2.5) ([1][1]). Most studies have used classical regression methods, which are limited in their ability to establish causality. Alternatively, causal inference analyses

Accumulating evidence suggests that air pollution increases pregnancy loss; however, most previous studies have focused on case identification from medical records, which may underrepresent early pregnancy losses. Our objective was to investigate the association between acute and chronic exposure to ambient air pollution and time to pregnancy loss among women undergoing assisted reproductive technologies (ART) who are closely followed throughout early pregnancy. We included 275 women (345 human chorionic gonadotropin (hCG)-confirmed pregnancies) undergoing ART at a New England academic fertility center. We estimated daily nitrogen dioxide (NO(2)), ozone (O(3)), fine particulate matter

Neighborhood demographic polarization, or the extent to which a privileged population group outnumbers a deprived group, can affect health by influencing social dynamics. While using birth records from 2001 to 2013 in Massachusetts (n = 629,675), we estimated the effect of two demographic indices, racial residential polarization (RRP) and economic residential polarization (ERP), on birth weight outcomes, which are established predictors of the newborn&rsquo, s future morbidity and mortality risk. Higher RRP and ERP was each associated with higher continuous birth weight and lower odds for low birth weight and small for gestational age, with evidence for effect modification by maternal race. On average, per interquartile range increase in RRP, the birth weight was 10.0 g (95% confidence interval: 8.0, 12.0) higher among babies born to white mothers versus 6.9 g (95% CI: 4.8, 9.0) higher among those born to black mothers. For ERP, it was 18.6 g (95% CI: 15.7, 21.5) higher among those that were born to white mothers versus 1.8 g (95% CI: &minus, 4.2, 7.8) higher among those born to black mothers. Racial and economic polarization towards more privileged groups was associated with healthier birth weight outcomes, with greater estimated effects in babies that were born to white mothers than those born to black mothers.

Background The ambient exposure does not always reflect the internal levels of pollution absorbed in the body. While human biomonitoring (HBM) could provide a valid estimate of exposure extent, it is usually an expensive and a heavily manpowered enterprise. Using samples collected during blood donations for HMB may provide a more efficient platform for a routine biomonitoring. Methods The current study is aimed to explore the feasibility of using the national blood banking system for the purposes of HBM, to compare between residents of a suspected polluted area in northern Israel (Haifa Bay) to the rest of the country. Specifically, we will assemble a geographically representative sample of blood donors residing in the study area and of the general population, to test for four industry and traffic-related metals: lead (Pb), cadmium (Cd), arsenic (As) and chromium (Cr). Samples of whole blood from donors will be tested in the Laboratory of Public Health Services managed by the Ministry of Health. The information on donors’ biomarkers levels will be further linked with the air pollution and meteorological data assessed at the location of the blood collection sites (short-term exposure) and donors’ permanent address (long-term exposure), as recorded by the monitoring stations spread throughout Israel and the satellite-based exposure models. The association between biomarkers and ambient environmental exposures will be assessed. The samples’ collection is planned for 2 years of 2020–2021. Discussion The information collected in this study could lead to environmental regulations within Haifa Bay area aimed to prevent exposure to high levels of hazardous chemicals.

Background: The increase in ambient temperatures (Ta) and emissions of greenhouse gases over the last century has focused attention on the effects of ambient temperatures on health outcomes. We aimed to investigate the association between Ta and the clinical measures of term low birth weight (tLBW) and small for gestational age (SGA) in singleton term infants using a decade of regional hospital data in southern Israel.Methods: We linked all births in Soroka University Medical Center in the southern district of Israel insured by Clalit Health Services with pregnancy Ta estimated by our novel hybrid spatio-temporally resolved prediction model. Logistic regression generalized additive models and general linear models were used, with either tLBW or SGA as the dependent variable, modeling entire pregnancy and trimester-specific Ta adjusting for seasonality, time trend, particulate matter, maternal age, gravidity, parity, ethnicity, sex, poverty index and population density.Results: The study population included 56,141 singleton term newborns, with 1716 (3.1%) cases of tLBW and 8634 (15.4%) cases of SGA. The average and the median Ta across the entire pregnancy were 19.9 (SD: 1.77, range: 14.6–24.9) degrees centigrade. The lowest Ta quartile (Ta = =21.3) was not significantly associated with tLBW (odds ratio = 1.17, 95%CI 0.99–1.38), in comparison to the two intermediate quartiles. When analyzing SGA as the dependent variable, the lowest Ta quartile was associated with significantly higher risk of SGA (odds ratio = 1.18, 95%CI 1.09–1.29) while the highest quartile was associated with significantly lower risk of SGA (odds ratio = 0.91, 95%CI 0.84–0.99) in comparison to the two intermediate quartiles.Conclusions: Our findings suggest that lower pregnancy Ta may increase the risk of tLBW and SGA, and higher pregnancy Ta may decrease the risk of SGA in singleton term infants in southern Israel.

BACKGROUND: Several studies have shown that exposure to particulate matter (PM) may lead to increased systemic blood pressure, but the underlying biological mechanisms remain unknown. Emerging evidence shows that extracellular vesicle-enriched miRNAs (evmiRNAs) are associated with PM exposure and cardiovascular risk. In this study, we investigated the role of evmiRNAs in the association between PM and blood pressure, as well as their epigenetic regulation by DNA methylation. METHODS: Participants (n=22, men) were randomly selected from the Veterans Affairs Normative Aging Study (NAS). Long-term (1-year and 6-month average) PM(2.5) exposure was estimated at 1×1-km resolution using spatio-temporal prediction models and BC was estimated using validated time varying land use regression models. We analyzed 31 evmiRNAs detected in ≥90% of all individuals and for statistical analysis, we used mixed effects models with random intercept adjusted for age, body mass index, smoking, C-reactive protein, platelets, and white blood cells. RESULTS: We found that per each 2-standard deviations increase in 6-month PM(2.5) ambient levels, there was an increase in 0.19 mm Hg (95% Confidence Interval [95%CI]: 0.11, 0.28 mmHg; p

BACKGROUND: Prenatal particulate air pollution exposure may alter lung growth and development in utero in a time-sensitive and sex-specific manner, resulting in reduced lung function in childhood. Such relationships have not been examined for nitrate (NO(3)(−)). METHODS: We implemented Bayesian distributed lag interaction models (BDLIMs) to identify sensitive prenatal windows for the influence of NO(3)(−) on lung function at age 7 years, assessing effect modification by fetal sex. Analyses included 191 mother-child dyads. Daily ambient NO(3)(−) exposure over pregnancy was estimated using a hybrid chemical transport (Geos-Chem)/land-use regression model. Spirometry was performed at mean (SD) age of 6.99 (0.89) years, with forced expiratory volume in one second (FEV(1)) and forced vital capacity (FVC) z-scores accounting for child age, sex, height and race/ethnicity. RESULTS: Most mothers were Hispanic (65%) or Black (22%), had ≤ high school education (67%), and never smoked (71%); 17% children had asthma. BDILMs adjusted for maternal age and education and child’s asthma identified an early sensitive window of 6-12 weeks gestation, during which increased NO(3)(−) was significantly associated with reduced FEV(1) z-scores specifically among boys. BDLIM analyses demonstrated similar sex-specific patterns for FVC. CONCLUSION: Early gestational NO(3)(−) exposure is associated with reduced child lung function, especially in boys.

BACKGROUND: The impact of prenatal ambient air pollution on child asthma may be modified by maternal stress, child sex and exposure dose and timing. OBJECTIVE: We prospectively examined associations between co-exposure to prenatal particulate matter with an aerodynamic diameter of less than 2.5 microns (PM(2.5)) and maternal stress on childhood asthma (n=736). METHODS: Daily PM(2.5) exposure during pregnancy was estimated using a validated satellite-based spatio-temporally resolved prediction model. Prenatal maternal negative life events (NLEs) were dichotomized around the median (high: NLE≥3; low: NLE

Our aim is to estimate associations between acute increases in particulate matter with diameter of 2.5 µm or less (PM2.5) concentrations and risk of infant bronchiolitis and otitis media among Massachusetts births born 2001 through 2008.Our case-crossover study included 20,017 infant bronchiolitis and 42,336 otitis media clinical encounter visits. PM2.5 was modeled using satellite, remote sensing, meteorological and land use data. We applied conditional logistic regression to estimate odds ratios (ORs) and confidence intervals (CIs) per 10-µg/m3 increase in PM2.5. We assessed effect modification to determine the most susceptible subgroups. Infant bronchiolitis risk was elevated for PM2.5 exposure 1 day (OR = 1.07, 95% CI = 1.03-1.11) and 4 days (OR = 1.04, 95% CI = 0.99-1.08) prior to clinical encounter, but not 7 days. Non-significant associations with otitis media varied depending on lag. Preterm infants were at substantially increased risk of bronchiolitis 1 day prior to clinical encounter (OR = 1.17, 95% CI = 1.08-1.28) and otitis media 4 and 7 days prior to clinical encounter (OR = 1.09, 95% CI = 1.02-1.16 and OR = 1.08, 95% CI = 1.02-1.15, respectively). In conclusion, preterm infants are most susceptible to infant bronchiolitis and otitis media associated with acute PM2.5 exposures.

Recent studies have linked urban environmental factors and body mass index (BMI); however, such factors are often examined in isolation, ignoring correlations across exposures.Using data on Nurses' Health Study participants living in the Northeastern United States in 2006, we estimated associations between neighborhood walkability (a composite of population density, street connectivity, and business access), greenness (from satellite imagery), and ambient air pollution (from satellite-based spatiotemporally resolved PM2.5 predictions and weighted monthly average concentrations of NO2 from up to five nearest monitors) and self-reported BMI using generalized additive models, allowing for deviations from linearity using penalized splines.Among 23,435 women aged 60-87 years, we observed nonlinear associations between walkability and BMI and between PM2.5 and BMI in single-exposure models adjusted for age, race, and individual- and area-level socioeconomic status. When modeling all exposures simultaneously, only the association between walkability and BMI remained nonlinear and nonmonotonic. Increasing walkability was associated with increasing BMI at lower levels of walkability (walkability index1.8), while increasing walkability was linked to lower BMI in areas of higher walkability (walkability index1.8). A 10 percentile increase in walkability, right above 1.8 was associated with a 0.84% decrease in log BMI. The relationship between walkability and BMI existed only among younger participants (71 years old).Neighborhood walkability was nonlinearly linked to lower BMI independent of air pollution and greenness. Our findings highlight the importance of accounting for nonlinear confounding by interrelated urban environmental factors when investigating associations between the environment and BMI.

Background: Numerous studies show associations between exposure to Particulate Matter and Cardiovascular disease (CVD). Current cardiovascular equations incorporate the major risk factors for CVD. The patients' environment, however, is not incorporated in these equations. Methods: In a retrospective analysis, we assessed the contribution of neighborhood greenness and particulate matter (coarse-PM and PM0.2. The c-statistics slightly improved from 77.30%–77.40% for the prediction of MI (p=0.004) and from 75.60%–75.76% for the prediction of stroke (p=0.027). Calibration was fair in all models. The associations were partially mediated through the patients' comorbidities. Conclusion: The negligible improvement in the prediction performance, despite significant associations with PM and NDVI, may be due to partial mediation of these associations through the conventional cardiovascular risk factors, suggesting the importance in assessing the environmental effects on more basic physiological pathways when addressing the contribution to the cardiovascular risk. Keywords: Air pollution, Neighborhood greenness, Cardiovascular risk, Stroke, Myocardial infarction

Background: Long-term PM2.5 exposure and aging have been implicated in multiple shared diseases; studying their relationship is a promising strategy to further understand the adverse impact of PM2.5 on human health. Objective: We assessed the relationship of major PM2.5 component species (ammonium, elemental carbon, organic carbon, nitrate, and sulfate) with Horvath and Hannum DNA methylation (DNAm) age, two DNA methylation-based predictors of chronological age. Methods: This analysis included 552 participants from the Normative Aging Study with multiple visits between 2000 and 2011 (n = 940 visits). We estimated 1-year PM2.5 species levels at participants' addresses using the GEOS-chem transport model. Blood DNAm-age was calculated using CpG sites on the Illumina HumanMethylation450 BeadChip. We fit linear mixed-effects models, controlling for PM2.5 mass and lifestyle/environmental factors as fixed effects, with the adaptive LASSO penalty to identify PM2.5 species associated with DNAm-age. Results: Sulfate and ammonium were selected by the LASSO in the Horvath DNAm-age models. In a fully-adjusted multiple-species model, interquartile range increases in both 1-year sulfate (95%CI: 0.28, 0.74, P

Background: The autonomic nervous system plays a key role in maintaining homeostasis and responding to external stimuli. In adults, exposure to fine particulate matter (PM2.5) has been associated with reduced heart rate variability (HRV), an indicator of cardiac autonomic control. Objectives: Our goal was to investigate the associations of exposure to fine particulate matter (PM2.5) with HRV as an indicator of cardiac autonomic control during early development. Methods: We studied 237 maternal–infant pairs in a Boston-based birth cohort. We estimated daily residential PM2.5 using satellite data in combination with land-use regression predictors. In infants at 6 months of age, we measured parasympathetic nervous system (PNS) activity using continuous electrocardiogram monitoring during the Repeated Still-Face Paradigm, an experimental protocol designed to elicit autonomic reactivity in response to maternal interaction and disengagement. We used multivariable linear regression to examine average PM2.5 exposure across pregnancy in relation to PNS withdrawal and activation, indexed by changes in respiration-corrected respiratory sinus arrhythmia (RSAc)—an established metric of HRV that reflects cardiac vagal tone. We examined interactions with infant sex using cross-product terms. Results: In adjusted models we found that a 1-unit increase in PM2.5 (in micrograms per cubic meter) was associated with a 3.53% decrease in baseline RSAc (95% CI: −6.96, 0.02). In models examining RSAc change between episodes, higher PM2.5 was generally associated with reduced PNS withdrawal during stress and reduced PNS activation during recovery; however, these associations were not statistically significant. We did not observe a significant interaction between PM2.5 and sex. Discussion: Prenatal exposure to PM2.5 may disrupt cardiac vagal tone during infancy. Future research is needed to replicate these preliminary findings. https://doi.org/10.1289/EHP4434

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.

Background Maternal exposure to fine particulate air pollution (PM2.5) during pregnancy is associated with lower newborn birthweight, which is a risk factor for chronic disease. Existing studies typically report the average association related with PM2.5 increase, which does not offer information about potentially varying associations at different points of the birthweight distribution. Methods We retrieved all birth records in Massachusetts between 2001 and 2013 then restricted our analysis to full-term live singletons (n = 775,768). Using the birthdate, gestational age, and residential address reported at time of birth, we estimated the average maternal PM2.5 exposure during pregnancy of each birth. PM2.5 predictions came from a model that incorporates satellite, land use, and meteorologic data. We applied quantile regression to quantify the association between PM2.5 and birthweight at each decile of birthweight, adjusted for individual and neighborhood covariates. We considered effect modification by indicators of individual and neighborhood socioeconomic status (SES). Results PM2.5 was negatively associated with birthweight. An interquartile range increase in PM2.5 was associated with a 16 g [95% confidence interval (CI) = 13, 19] lower birthweight on average, 19 g (95% CI = 15, 23) lower birthweight at the lowest decile of birthweight, and 14 g (95% CI = 9, 19) lower birthweight at the highest decile. In general, the magnitudes of negative associations were larger at lower deciles. We did not find evidence of effect modification by individual or neighborhood SES. Conclusions In full-term live births, PM2.5 and birthweight were negatively associated with more severe associations at lower quantiles of birthweight.

BACKGROUND. An increasing number of studies have linked air pollution to decreased fertility. Whether this is due to an effect on ovarian reserve is unknown. METHOD. Our study included 632 women attending the Massachusetts General Hospital Fertility Center (2004–2015) who had a measured antral follicle count. Validated spatiotemporal models estimated daily particulate matter

A few studies suggest that air pollution may decrease fertility, but prospective studies and examinations of windows of susceptibility remain unclear.We aimed to examine the association between time-varying exposure to nitrogen dioxide ([Formula: see text]), ozone ([Formula: see text]), fine particulate matter [Formula: see text] ([Formula: see text]), and black carbon (BC) onWe included 345 women (522 IVF cycles) for the [Formula: see text], [Formula: see text], and [Formula: see text] analyses and 339 women (512 IVF cycles) for the BC analysis enrolled in a prospective cohort at a Boston fertility center (2004–2015). We used validated spatiotemporal models to estimate daily residential exposure to [Formula: see text], [Formula: see text], [Formula: see text], and BC. Multivariable discrete time Cox proportional hazards models with four periods [ovarian stimulation (OS), oocyte retrieval to embryo transfer (ET), ET to implantation, implantation to live birth] estimated odds ratios (OR) and 95% confidence intervals (CI) of failing at IVF. Time-dependent interactions were used to identify vulnerable periods.An interquartile range (IQR) increase in [Formula: see text], [Formula: see text], and BC throughout the IVF cycle was associated with an elevated odds of failing at IVF prior to live birth ([Formula: see text], 95% CI: 0.95, 1.23 for [Formula: see text]; [Formula: see text], 95% CI: 0.88, 1.28 for [Formula: see text]; and [Formula: see text], 95% CI: 0.96, 1.41 for BC). This relationship significantly varied across the IVF cycle such that the association with higher exposure to air pollution during OS was strongest for early IVF failures. An IQR increase in [Formula: see text], [Formula: see text], and BC exposure during OS was associated with 1.42 (95% CI: 1.20, 1.69), 1.26 (95% CI: 0.96, 1.67), and 1.23 (95% CI: 0.96, 1.59) times the odds of failing prior to oocyte retrieval, and 1.32 (95% CI: 1.13, 1.54), 1.27 (95% CI: 0.98, 1.65), and 1.32 (95% CI: 1.10, 1.59) times the odds of failing prior to ET.Increased exposure to traffic-related pollutants was associated with higher odds of early IVF failure. https://doi.org/10.1289/EHP4601.

Traffic-related air pollution has been linked to higher risks of infertility and miscarriage. We evaluated whether folate intake modified the relationship between air pollution and livebirth among women using assisted reproductive technology (ART). Our study included 304 women (513 cycles) presenting to a fertility center in Boston, Massachusetts (2005–2015). Diet and supplements were assessed by food frequency questionnaire. Spatiotemporal models estimated residence-based daily nitrogen dioxide (NO2), ozone, fine particulate, and black carbon concentrations in the 3 months before ART. We used generalized linear mixed models with interaction terms to evaluate whether the associations between air pollutants and livebirth were modified by folate intake, adjusting for age, body mass index, race, smoking, education, infertility diagnosis, and ART cycle year. Supplemental folate intake significantly modified the association of NO2 exposure and livebirth (P = 0.01). Among women with supplemental folate intakes of