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Tools for assessing multiple exposures across several domains (e.g., physical, chemical, and social) are of growing importance in social and environmental epidemiology because of their value in uncovering disparities and their impact on health outcomes. Here we describe work done within the Environmental influences on Child Health Outcomes (ECHO)-wide Cohort Study to build a combined exposure index. Our index considered both environmental hazards and social stressors simultaneously with national coverage for a 10-year period. Our goal was to build this index and demonstrate its utility for assessing differences in exposure for pregnancies enrolled in the ECHO-wide Cohort Study. Our unitless combined exposure index, which collapses census-tract level data into a single relative measure of exposure ranging from 0-1 (where higher values indicate higher exposure to hazards), includes indicators for major air pollutants and air toxics, features of the built environment, traffic exposures, and social determinants of health (e.g., lower educational attainment) drawn from existing data sources. We observed temporal and geographic variations in index values, with exposures being highest among participants living in the West and Northeast regions. Pregnant people who identified as Black or Hispanic (of any race) were at higher risk of living in a "high" exposure census tract (defined as an index value above 0.5) relative to those who identified as White or non-Hispanic. Index values were also higher for pregnant people with lower educational attainment. Several recommendations follow from our work, including that environmental and social stressor datasets with higher spatial and temporal resolutions are needed to ensure index-based tools fully capture the total environmental context.

Limited studies examine how prenatal environmental and social exposures jointly impact perinatal health. Here we investigated relationships between a neighborhood-level combined exposure (CE) index assessed during pregnancy and perinatal outcomes, including birthweight, gestational age, and preterm birth. Across all participants, higher CE index scores were associated with small decreases in birthweight and gestational age. We also observed effect modification by race; infants born to Black pregnant people had a greater risk of preterm birth for higher CE values compared to White infants. Overall, our results suggest that neighborhood social and environmental exposures have a small but measurable joint effect on neonatal indicators of health.

Summary: Background: Early‐life exposure to tobacco is associated with obesity, but the most susceptible developmental periods are unknown. Objective: To explore windows of susceptibility in a cohort of 568 mother–child pairs. Methods: We measured seven measures of tobacco exposure (five self‐reported and two biomarkers) spanning from pre‐conception to age 5 years. Mothers self‐reported active smoking (pre‐conception, 17 weeks, and delivery) and household smokers (5 and 18 months postnatally). Cotinine was measured in maternal urine (27 weeks) and child urine (5 years). Adiposity (fat mass percentage) was measured at birth and 5 years via air displacement plethysmography. Using a multiple informant approach, we tested whether adiposity (5 years) and changes in adiposity (from birth to 5 years) differed by the seven measures of tobacco exposure. Results: The associations may depend on timing. For example, only pre‐conception (β = 3.1%; 95% CI: 1.0–5.1) and late gestation (β = 4.0%; 95% CI: 0.4–7.6) exposures influenced adiposity accretion from birth to 5 years (p for interaction = 0.01). Early infancy exposure was also associated with 1.7% higher adiposity at 5 years (95% CI: 0.1–3.2). Mid‐pregnancy and early childhood exposures did not influence adiposity. Conclusions: Pre‐conception, late gestation, and early infancy exposures to tobacco may have the greatest impact on childhood adiposity. [ABSTRACT FROM AUTHOR]

Public school teachers represent one of the largest occupational groups in the United States and are vulnerable to job stress and burnout. School social and physical environments may be adversely impacting the health of teachers and other staff, though few studies have explored these relationships. We partnered with a suburban school district in Colorado to assess the association between school environmental quality, social climate, and staff member health. We modeled the number of self-reported frequent health symptoms (experienced at least once a week) using generalized linear models. School-level predictors of interest included: overall social climate scores (unitless), building operations report card (ORC) scores (unitless), and indoor air quality (IAQ) scores (unitless). In total, we had data from 134 staff members from 11 schools in the district. A majority (62%) of our participants were teachers, who reported a greater number of frequent (i.e., at least once a week) health symptoms (mean = 3.2 symptoms experienced at least once per week) compared to staff in other roles (mean = 2.3 symptoms per week). We found that a one standard-deviation (10.5) increase in the overall social climate score was associated with a 0.77-fold (95% CI: 0.60–0.99) change in the number of frequent health symptoms reported. However, this association was attenuated among teachers compared to other staff members. Our results suggested effect modification by social climate on the relationship between IAQ and health, albeit with some uncertainty. For participants with a school climate score below the mean, a one standard-deviation (10.5) increase in IAQ score was associated with a 0.49-fold (95% CI: 0.35–0.70) change in the number of frequently reported symptoms. Overall, our study suggests school climate may be associated with self-reported health symptoms, but that the benefits of improved school climates may not be as strong for teachers compared to other staff. Future work should assess perceived climate at the individual level to assess how staff roles impact how school environments are associated with health outcomes. [ABSTRACT FROM AUTHOR]

BACKGROUND: Although it is known that sperm aneuploidy contributes to early pregnancy losses and congenital abnormalities, the causes are unknown and environmental contaminants are suspected. OBJECTIVES: Our goal was to evaluate associations between lifetime exposure to organochlorines, specifically dichlorodiphenyldicholorethylene (p,p'-DDE) and polychlorinated biphenyls (PCBs), and sperm aneuploidy in men from the general population of the Faroe Islands, a population with a known history of organochlorine exposures. METHODS: Serum and semen samples from men (n = 90) 22-44 years old who participated in Faroe Islands health studies were analyzed for p,p'-DDE and PCBs 118, 138, 153, and 180 and adjusted for total lipids. Cord blood and age-14 serum were available for a subgroup (n = 40) and were also analyzed for p,p'-DDE and PCBs. Sperm fluorescence in situ hybridization (FISH) for chromosomes X, Y, and 18 was used to determine rates of XX18, XY18, YY18, and total disomy. Multivariable adjusted Poisson models were used to estimate the relationship between organochlorine exposure and sperm disomy outcomes. RESULTS: Adult p,p'-DDE and total PCB serum concentrations were both associated with significantly increased rates of XX18, XY18, and total disomy. Age-14 p,p'-DDE and PCB concentrations were both associated with significantly increased rates of XX, XY, and total disomy in adulthood. Associations between cord blood concentrations of p,p'-DDE and PCBs and sperm disomy in adulthood were not consistently significant. CONCLUSIONS: Organochlorine exposures measured at age 14 and in adulthood were associated with sperm disomy in this sample of high-exposure men, suggesting that the impacts of persistent pollutants on testicular maturation and function require further investigation. http://dx.doi.org/10.1289/ehp.1509779, Introduction Environmental endocrine-disrupting chemicals have been associated with impaired male reproductive function (Bergman et al. 2013; Woodruff et al. 2008) and may affect sperm development (Schiffer et al. 2014). Aneuploidy, [...]

As anthropogenic emissions continue to decline and emissions from landscape (wild, prescribed, and agricultural) fires increase across the coming century, the relative importance of landscape‐fire smoke on air quality and health in the United States (US) will increase. Landscape fires are a large source of fine particulate matter (PM2.5), which has known negative impacts on human health. The seasonal and spatial distribution, particle composition, and co‐emitted species in landscape‐fire emissions are different from anthropogenic sources of PM2.5. The implications of landscape‐fire emissions on the sub‐national temporal and spatial distribution of health events and the relative health importance of specific pollutants within smoke are not well understood. We use a health impact assessment with observation‐based smoke PM2.5 to determine the sub‐national distribution of mortality and the sub‐national and sub‐annual distribution of asthma morbidity attributable to US smoke PM2.5 from 2006 to 2018. We estimate disability‐adjusted life years (DALYs) for PM2.5 and 18 gas‐phase hazardous air pollutants (HAPs) in smoke. Although the majority of large landscape fires occur in the western US, we find the majority of mortality (74%) and asthma morbidity (on average 75% across 2006–2018) attributable to smoke PM2.5 occurs outside the West, due to higher population density in the East. Across the US, smoke‐attributable asthma morbidity predominantly occurs in spring and summer. The number of DALYs associated with smoke PM2.5 is approximately three orders of magnitude higher than DALYs associated with gas‐phase smoke HAPs. Our results indicate awareness and mitigation of landscape‐fire smoke exposure is important across the US. Plain Language Summary: The pollutants from landscape (wild, prescribed, and agricultural) fires are expected to have an increasing impact on air quality and health in the United States (US) across the current century. The implications of landscape‐fire smoke on the regional and seasonal distribution of health events and the relative health importance of specific pollutants within smoke are not well understood. In the present study, we assess the seasonal and regional distribution of the health impacts from US smoke exposure from 2006 to 2018. We also estimate the long‐term health impacts for both fine particles (PM2.5) and gas‐phase hazardous air pollutants (HAPs) in smoke. Although the majority of large landscape fires occur in the western US, we find the majority of deaths (74%) and asthma emergency department visits and hospital admissions (on average 75% across 2006–2018) attributable to smoke occur outside the West. Across the US, smoke‐attributable asthma emergency department visits predominantly occur in spring and summer. The long‐term health impacts associated with smoke PM2.5 are much higher than the estimated long‐term health impacts of gas‐phase smoke HAPs. Our results indicate awareness and mitigation of landscape‐fire smoke exposure is important across the US, not just in regions in proximity to large wildfires. Key Points: While the majority of large fires occur in the United States (US) West, a majority of smoke‐attributable US mortality and morbidity occur east of ∼100 degWA higher percent of mortality and morbidity is attributable to smoke in high fire‐impacted northwestern states, relative to other US statesDisability‐adjusted life years attributable to fine particles in smoke are much higher than that from gas‐phase hazardous air pollutants [ABSTRACT FROM AUTHOR]

Despite improvements in air quality over the past 50 years, ambient air pollution remains an important public health issue in the United States. In particular, emissions from coal‐fired power plants still have a substantial impact on both nearby and regional populations. Of particular concern is the potential for this impact to fall disproportionately on low‐income communities and communities of color. We conducted a quantitative health impact assessment to estimate the health benefits of the proposed decommissioning of two coal‐fired electricity generating stations in the Southern Front Range region of Colorado. We estimated changes in exposures to fine particulate matter and ozone using the Community Multiscale Air Quality model and predicted avoided health impacts and related economic values. We also quantitatively assessed the distribution of these benefits by population‐level socioeconomic status. Across the study area, decommissioning the power plants would result in 2 (95% CI: 1–3) avoided premature deaths each year due to reduced PM2.5 exposures and greater reductions in hospitalizations and other morbidities. Health benefits resulting from the modeled shutdowns were greatest in areas with lower educational attainment and other economic indicators. Our results suggest that decommissioning these power plants and replacing them with zero‐emissions sources could have broad public health benefits for residents of Colorado, with larger benefits for those that are socially disadvantaged. Our results also suggested that researchers and decision makers need to consider the unique demographics of their study areas to ensure that important opportunities to reduce health disparities associated with point‐source pollution. Key Points: Coal‐fired power plants in Colorado contribute to poor air quality, but two of the largest plants are slated to be decommissioned by 2035Retiring these plants now would result in ~40 fewer deaths and $274M in avoided impacts over the remaining 19‐year lifespan of the plantsReduced emissions would predominantly benefit low‐income communities which often bear the heaviest environmental burdens [ABSTRACT FROM AUTHOR]

Structural and numerical sperm chromosomal aberrations result from abnormal meiosis and are directly linked to infertility. Any live births that arise from aneuploid conceptuses can result in syndromes such as Kleinfelter, Turners, XYY and Edwards. Multi-probe fluorescence in situ hybridization (FISH) is commonly used to study sperm aneuploidy, however manual FISH scoring in sperm samples is labor-intensive and introduces errors. Automated scoring methods are continuously evolving. One challenging aspect for optimizing automated sperm FISH scoring has been the overlap in excitation and emission of the fluorescent probes used to enumerate the chromosomes of interest. Our objective was to demonstrate the feasibility of combining confocal microscopy and spectral imaging with high-throughput methods for accurately measuring sperm aneuploidy. Our approach used confocal microscopy to analyze numerical chromosomal abnormalities in human sperm using enhanced slide preparation and rigorous semi-automated scoring methods. FISH for chromosomes X, Y, and 18 was conducted to determine sex chromosome disomy in sperm nuclei. Application of online spectral linear unmixing was used for effective separation of four fluorochromes while decreasing data acquisition time. Semi-automated image processing, segmentation, classification, and scoring were performed on 10 slides using custom image processing and analysis software and results were compared with manual methods. No significant differences in disomy frequencies were seen between the semi automated and manual methods. Samples treated with pepsin were observed to have reduced background autofluorescence and more uniform distribution of cells. These results demonstrate that semi-automated methods using spectral imaging on a confocal platform are a feasible approach for analyzing numerical chromosomal aberrations in sperm, and are comparable to manual methods. © 2017 International Society for Advancement of Cytometry [ABSTRACT FROM AUTHOR]

In air quality management, reducing emissions from pollutant sources often forms the primary response to attaining air quality standards and guidelines. Despite the broad success of air quality management in the US, challenges remain. As examples: allocating emissions reductions among multiple sources is complex and can require many rounds of negotiation; health impacts associated with emissions, the ultimate driver for the standards, are not explicitly assessed; and long dispersion model run-times, which result from the increasing size and complexity of model inputs, limit the number of scenarios that can be evaluated, thus increasing the likelihood of missing an optimal strategy. A new modeling framework, called the “Framework for Rapid Emissions Scenario and Health impact ESTimation” (FRESH-EST), is presented to respond to these challenges. FRESH-EST estimates concentrations and health impacts of alternative emissions scenarios at the urban scale, providing efficient computations from emissions to health impacts at the Census block or other desired spatial scale. In addition, FRESH-EST can optimize emission reductions to meet specified environmental and health constraints, and a convenient user interface and graphical displays are provided to facilitate scenario evaluation. The new framework is demonstrated in an SO 2 non-attainment area in southeast Michigan with two optimization strategies: the first minimizes emission reductions needed to achieve a target concentration; the second minimizes concentrations while holding constant the cumulative emissions across local sources (e.g., an emissions floor). The optimized strategies match outcomes in the proposed SO 2 State Implementation Plan without the proposed stack parameter modifications or shutdowns. In addition, the lower health impacts estimated for these strategies suggest that FRESH-EST could be used to identify potentially more desirable pollution control alternatives in air quality management planning. [ABSTRACT FROM AUTHOR]

Health impact assessments (HIAs) inform policy and decision making by providing information regarding future health concerns, and quantitative HIAs now are being used for local and urban-scale projects. HIA results can be expressed using a variety of metrics that differ in meaningful ways, and guidance is lacking with respect to best practices for the development and use of HIA metrics. This study reviews HIA metrics pertaining to air quality management and presents evaluative criteria for their selection and use. These are illustrated in a case study where PM 2.5 concentrations are lowered from 10 to 8 μg/m 3 in an urban area of 1.8 million people. Health impact functions are used to estimate the number of premature deaths, unscheduled hospitalizations and other morbidity outcomes. The most common metric in recent quantitative HIAs has been the number of cases of adverse outcomes avoided. Other metrics include time-based measures, e.g., disability-adjusted life years (DALYs), monetized impacts, functional-unit based measures, e.g., benefits per ton of emissions reduced, and other economic indicators, e.g., cost-benefit ratios. These metrics are evaluated by considering their comprehensiveness, the spatial and temporal resolution of the analysis, how equity considerations are facilitated, and the analysis and presentation of uncertainty. In the case study, the greatest number of avoided cases occurs for low severity morbidity outcomes, e.g., asthma exacerbations (n = 28,000) and minor-restricted activity days (n = 37,000); while DALYs and monetized impacts are driven by the severity, duration and value assigned to a relatively low number of premature deaths (n = 190 to 230 per year). The selection of appropriate metrics depends on the problem context and boundaries, the severity of impacts, and community values regarding health. The number of avoided cases provides an estimate of the number of people affected, and monetized impacts facilitate additional economic analyses useful to policy analysis. DALYs are commonly used as an aggregate measure of health impacts and can be used to compare impacts across studies. Benefits per ton metrics may be appropriate when changes in emissions rates can be estimated. To address community concerns and HIA objectives, a combination of metrics is suggested. [ABSTRACT FROM AUTHOR]

Background: The role of environmental pesticide exposures, such as pyrethroids, and their relationship to sperm abnormalities are not well understood. This study investigated whether environmental exposure to pyrethroids was associated with altered frequency of sperm sex chromosome disomy in adult men.Methods: A sample of 75 subjects recruited through a Massachusetts infertility clinic provided urine and semen samples. Individual exposures were measured as urinary concentrations of three pyrethroid metabolites ((3-phenoxybenzoic acid (3PBA), cis- and trans- 3-(2,2-Dichlorovinyl)-1-methylcyclopropane-1,2-dicarboxylic acid (CDCCA and TDCCA)). Multiprobe fluorescence in situ hybridization for chromosomes X, Y, and 18 was used to determine XX, YY, XY, 1818, and total sex chromosome disomy in sperm nuclei. Poisson regression analysis was used to examine the association between aneuploidy rates and pyrethroid metabolites while adjusting for covariates.Results: Between 25-56% of the sample were above the limit of detection (LOD) for the pyrethroid metabolites. All sex chromosome disomies were increased by 7-30% when comparing men with CDCCA and TDCCA levels above the LOD to those below the LOD. For 3PBA, compared to those below the LOD, those above the LOD had YY18 disomy rates 1.28 times higher (95% CI: 1.15, 1.42) whereas a reduced rate was seen for XY18 and total disomy (IRR = 0.82; 95% CI: 0.77, 0.87; IRR = 0.93; 95% CI: 0.87-0.97), and no association was seen for XX18 and 1818.Conclusions: Our findings suggest that urinary concentrations of CDCCA and TDCCA above the LOD were associated with increased rates of aneuploidy. However the findings for 3BPA were not consistent. This is the first study to examine these relationships, and replication of our findings is needed before the association between pyrethroid metabolites and aneuploidy can be fully defined. [ABSTRACT FROM AUTHOR]

Background: Although it is known that sperm aneuploidy contributes to early pregnancy losses and congenital abnormalities, the causes are unknown and environmental contaminants are suspected. Objectives: Our goal was to evaluate associations between lifetime exposure to organochlorines, specifically dichlorodiphenyldicholorethylene (p,p´-DDE) and polychlorinated biphenyls (PCBs), and sperm aneuploidy in men from the general population of the Faroe Islands, a population with a known history of organochlorine exposures. Methods: Serum and semen samples from men (n = 90) 22–44 years old who participated in Faroe Islands health studies were analyzed for p,p´-DDE and PCBs 118, 138, 153, and 180 and adjusted for total lipids. Cord blood and age-14 serum were available for a subgroup (n = 40) and were also analyzed for p,p´-DDE and PCBs. Sperm fluorescence in situ hybridization (FISH) for chromosomes X, Y, and 18 was used to determine rates of XX18, XY18, YY18, and total disomy. Multivariable adjusted Poisson models were used to estimate the relationship between organochlorine exposure and sperm disomy outcomes. Results: Adult p,p´-DDE and total PCB serum concentrations were both associated with significantly increased rates of XX18, XY18, and total disomy. Age-14 p,p´-DDE and PCB concentrations were both associated with significantly increased rates of XX, XY, and total disomy in adulthood. Associations between cord blood concentrations of p,p´-DDE and PCBs and sperm disomy in adulthood were not consistently significant. Conclusions: Organochlorine exposures measured at age 14 and in adulthood were associated with sperm disomy in this sample of high-exposure men, suggesting that the impacts of persistent pollutants on testicular maturation and function require further investigation. Citation: Perry MJ, Young HA, Grandjean P, Halling J, Petersen MS, Martenies SE, Karimi P, Weihe P. 2016. Sperm aneuploidy in Faroese men with lifetime exposure to dichlorodiphenyldichloroethylene (p,p´-DDE) and polychlorinated biphenyl (PCB) pollutants. Environ Health Perspect 124:951–956; http://dx.doi.org/10.1289/ehp.1509779

Prenatal exposure to ambient air pollution has been associated with adverse offspring health outcomes. Childhood health effects of prenatal exposures may be mediated through changes to DNA methylation detectable at birth. Among 429 non-smoking women in a cohort study of mother-infant pairs in Colorado, USA, we estimated associations between prenatal exposure to ambient fine particulate matter (PM 2.5) and ozone (O 3), and epigenome-wide DNA methylation of umbilical cord blood cells at delivery (2010–2014). We calculated average PM 2.5 and O 3 in each trimester of pregnancy and the full pregnancy using inverse-distance-weighted interpolation. We fit linear regression models adjusted for potential confounders and cell proportions to estimate associations between air pollutants and methylation at each of 432,943 CpGs. Differentially methylated regions (DMRs) were identified using comb-p. Previously in this cohort, we reported positive associations between 3rd trimester O 3 exposure and infant adiposity at 5 months of age. Here, we quantified the potential for mediation of that association by changes in DNA methylation in cord blood. We identified several DMRs for each pollutant and period of pregnancy. The greatest number of significant DMRs were associated with third trimester PM 2.5 (21 DMRs). No single CpGs were associated with air pollutants at a false discovery rate <0.05. We found that up to 8% of the effect of 3rd trimester O 3 on 5-month adiposity may be mediated by locus-specific methylation changes, but mediation estimates were not statistically significant. Differentially methylated regions in cord blood were identified in association with maternal exposure to PM 2.5 and O 3. Genes annotated to the significant sites played roles in cardiometabolic disease, immune function and inflammation, and neurologic disorders. We found limited evidence of mediation by DNA methylation of associations between third trimester O 3 exposure and 5-month infant adiposity. • Air pollution during pregnancy was associated with DNA methylation in cord blood. • Associated genes were linked to cardiometabolic, immune, and neurologic diseases. • Limited support for mediation by methylation of associations with infant adiposity. [ABSTRACT FROM AUTHOR]

Air pollution exposure during pregnancy has been associated with adverse pregnancy and birth outcomes. Inflammation has been proposed as a potential link. We estimated associations between air pollution exposure during pregnancy and inflammatory biomarkers in maternal and cord blood. We evaluated whether maternal inflammation was associated with infant outcomes. Among 515 mother-infant dyads in the Healthy Start study (2009–2014), trimester-long, 7- and 30-day average concentrations of particulate matter ≤2.5 μm (PM 2.5) and ozone (O 3) during pregnancy were estimated, using inverse-distance-weighted interpolation. Inflammatory biomarkers were measured in maternal blood in mid-pregnancy (C-reactive protein [CRP], Interleukin [IL]-6, and tumor necrosis factor-α [TNFα]) and in cord blood at delivery (CRP, IL-6, IL-8, IL-10, monocyte chemoattractant protein-1 [MCP-1], and TNFα). We used linear regression to estimate associations between pollutants and inflammatory biomarkers and maternal inflammatory biomarkers and infant weight and body composition. There were positive associations between PM 2.5 during certain exposure periods and maternal IL-6 and TNFα. There were negative associations between recent O 3 and maternal CRP, IL-6, and TNFα and positive associations between trimester-long O 3 exposure and maternal inflammatory biomarkers, though some 95% confidence intervals included the null. Patterns were inconsistent for associations between PM 2.5 and O 3 and cord blood inflammatory biomarkers. No consistent associations between maternal inflammatory biomarkers and infant outcomes were identified. Air pollution exposure during pregnancy may impact maternal inflammation. Further investigations should examine the health consequences for women and infants of elevated inflammatory biomarkers associated with air pollution exposure during pregnancy. • Exposure to particulate matter ≤2.5 and ozone was estimated for 515 pregnant women. • Inflammatory biomarkers were measured in maternal and cord blood. • Early pregnancy air pollution associated with mid-pregnancy maternal inflammation. • Inconsistent associations between prenatal air pollution and cord blood inflammation. • Maternal inflammatory markers did not predict infant outcomes. [ABSTRACT FROM AUTHOR]

Prenatal exposures to ambient air pollution and traffic have been associated with adverse birth outcomes, and may also lead to an increased risk of obesity. Obesity risk may be reflected in changes in body composition in infancy. To estimate associations between prenatal ambient air pollution and traffic exposure, and infant weight and adiposity in a Colorado-based prospective cohort study. Participants were 1125 mother-infant pairs with term births. Birth weight was recorded from medical records and body composition measures (fat mass, fat-free mass, and adiposity [percent fat mass]) were evaluated via air displacement plethysmography at birth (n = 951) and at ~5 months (n = 574). Maternal residential address was used to calculate distance to nearest roadway, traffic density, and ambient concentrations of fine particulate matter (PM 2.5) and ozone (O 3) via inverse-distance weighted interpolation of stationary monitoring data, averaged by trimester and throughout pregnancy. Adjusted linear regression models estimated associations between exposures and infant weight and body composition. Participants were urban residents and diverse in race/ethnicity and socioeconomic status. Average ambient air pollutant concentrations were generally low; the median, interquartile range (IQR), and range of third trimester concentrations were 7.3 μg/m3 (IQR: 1.3, range: 3.3–12.7) for PM 2.5 and 46.3 ppb (IQR: 18.4, range: 21.7–63.2) for 8-h maximum O 3. Overall there were few associations between traffic and air pollution exposures and infant outcomes. Third trimester O 3 was associated with greater adiposity at follow-up (2.2% per IQR, 95% CI 0.1, 4.3), and with greater rates of change in fat mass (1.8 g/day, 95% CI 0.5, 3.2) and adiposity (2.1%/100 days, 95% CI 0.4, 3.7) from birth to follow-up. We found limited evidence of an association between prenatal traffic and ambient air pollution exposure and infant body composition. Suggestive associations between prenatal ozone exposure and early postnatal changes in body composition merit further investigation. • Exposure to traffic and air pollution was estimated for 1125 pregnant women. • Offspring body composition was assessed at birth and at ~5 months old. • We found limited evidence of associations with prenatal traffic and air pollution. • Third trimester 8-h maximum ozone was associated with greater 5-month adiposity. [ABSTRACT FROM AUTHOR]

Background/objectives: Prenatal exposure to ambient air pollution is associated with adverse cardiometabolic outcomes in childhood. We previously observed that prenatal black carbon (BC) was inversely associated with adiponectin, a hormone secreted by adipocytes, in early childhood. Changes to DNA methylation have been proposed as a potential mediator linking in utero exposures to lasting health impacts., Methods: Among 532 mother-child pairs enrolled in the Colorado-based Healthy Start study, we performed an epigenome-wide association study of the relationship between prenatal exposure to a component of air pollution, BC, and DNA methylation in cord blood. Average pregnancy ambient BC was estimated at the mother's residence using a spatiotemporal prediction model. DNA methylation was measured using the Illumina 450K array. We used multiple linear regression to estimate associations between prenatal ambient BC and 429,246 cysteine-phosphate-guanine sites (CpGs), adjusting for potential confounders. We identified differentially methylated regions (DMRs) using DMRff and ENmix-combp. In a subset of participants (n = 243), we investigated DNA methylation as a potential mediator of the association between prenatal ambient BC and lower adiponectin in childhood., Results: We identified 44 CpGs associated with average prenatal ambient BC after correcting for multiple testing. Several genes annotated to the top CpGs had reported functions in the immune system. There were 24 DMRs identified by both DMRff and ENmix-combp. One CpG (cg01123250), located on chromosome 2 and annotated to the UNC80 gene, was found to mediate approximately 20% of the effect of prenatal BC on childhood adiponectin, though the confidence interval was wide (95% CI: 3, 84)., Conclusions: Prenatal BC was associated with DNA methylation in cord blood at several sites and regions in the genome. DNA methylation may partially mediate associations between prenatal BC and childhood cardiometabolic outcomes., (Copyright © 2024 Elsevier GmbH. All rights reserved.)

Prenatal air pollution exposure has been associated with adverse childhood cardiometabolic outcomes. It is unknown whether evidence of metabolic disruption associated with air pollution is identifiable at birth. We examined exposure to prenatal ambient air pollution and cord blood cardiometabolic biomarkers among 812 mother-infant pairs in the Healthy Start study., Methods: Using inverse-distance-weighted interpolation of ambient concentrations obtained from stationary monitors, we estimated daily particulate matter ≤2.5 micrometers (PM 2.5 ) and ozone (O 3 ) concentrations at participant residences. Daily estimates were averaged by trimester, full-pregnancy, and the 7 and 30 days prior to delivery. Associations of air pollution with the following cord blood biomarkers were estimated via multivariable linear regression: glucose, insulin, glucose/insulin ratio (GIR), leptin, high-density lipoprotein (HDL) cholesterol, non-HDL cholesterol, free fatty acids, and triglycerides., Results: In this Denver-based cohort, PM 2.5 concentrations were lower than in many US urban areas, but O 3 concentrations regularly exceeded federal air quality standards. Higher O 3 concentrations during pregnancy were consistently associated with higher insulin and lower GIR in cord blood. For example, an interquartile range increase in full pregnancy O 3 (6.3 parts per billion [ppb]) was associated with 0.13 log-µIU/ml (95% confidence interval [CI] = 0.04, 0.22) higher cord blood insulin, after adjusting for PM 2.5 and other confounders. We found positive, but generally nonsignificant, associations between PM 2.5 and leptin and isolated associations between pollutants during certain exposure periods and lipids., Conclusions: In this cohort with moderately high O 3 exposure, prenatal concentrations of O 3 were positively associated with cord blood insulin. Future studies should examine the implications for offspring long-term health., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report. This work was supported in part by grants from the National Institute of Environmental Health Sciences (R00ES025817), the National Institute of Diabetes and Digestive and Kidney Diseases (R01DK076648), and the National Institutes of Health Office of the Director (UH3OD023248). The University of Colorado Cancer Center laboratory received support from the National Cancer Institute (UL1 TR001082). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. C.F., D.D., D.S.K.T., J.L.P., and A.P.S. contributed to the conception and design of this study. All authors contributed to the acquisition, analysis, and interpretation of data. C.F. and A.P.S. participated in drafting the article. D.D., L.D.B., D.S.K.T., J.L.P., J.L.A., S.M., S.E.M., and W.B.A. participated in revising the article critically for important intellectual content. All authors gave approval of the final article. Sponsorships or competing interests that may be relevant to content are disclosed at the end of the article., (Copyright © 2022 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)

Coexposure to air pollution and tobacco smoke may influence early-life growth, but few studies have investigated their joint effects. We examined the interaction between fetal exposure to maternal smoking and ozone (O 3 ) or fine particulate matter (PM 2.5 ) on birth weight, neonatal adiposity, and body mass index (BMI) trajectories through age 3 years., Methods: Participants were 526 mother-child pairs, born ≥37 weeks. Cotinine was measured at ~27 weeks gestation. Whole pregnancy and trimester-specific O 3 and PM 2.5 were estimated via. inverse-distance weighted interpolation from stationary monitors. Neonatal adiposity (fat mass percentage) was measured via. air displacement plethysmography. Child weight and length/height were abstracted from medical records. Interaction was assessed by introducing cotinine (<31.5 vs. ≥31.5 ng/mL [indicating active smoking]), O 3 /PM 2.5 (low [tertiles 1-2] vs. high [tertile 3]), and their product term in linear regression models for birth weight and neonatal adiposity and mixed-effects models for BMI trajectories., Results: The rate of BMI growth among offspring jointly exposed to maternal smoking and high PM 2.5 (between 8.1 and 12.7 μg/m 3 ) in the third trimester was more rapid than would be expected due to the individual exposures alone (0.8 kg/m 2 per square root year; 95% CI = 0.1, 1.5; P for interaction = 0.03). We did not detect interactions between maternal smoking and O 3 or PM 2.5 at any other time on birth weight, neonatal adiposity, or BMI trajectories., Conclusions: Although PM 2.5 was generally below the EPA annual air quality standards of 12.0 μg/m 3 , exposure during the third trimester may influence BMI trajectories when combined with maternal smoking., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2021 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)

Filters can reduce indoor concentrations of particulate matter (PM 2.5 ), but their benefits have not been well-characterized. This study investigates exposure, health, and cost impacts of high efficiency filters in homes and schools, focusing on the asthma-related outcomes. Reductions in indoor exposures to PM 2.5 from outdoor sources with enhanced filters (e.g., MERV 12) are estimated using probabilistic indoor air quality models, and avoided health impacts are quantified using health impact assessment. These methods are applied using data from Detroit, Michigan, an urban region with elevated asthma rates. Replacing inefficient filters with enhanced filters in schools would reduce the PM 2.5 -attributable asthma burden by 13% annually, with higher benefits for more efficient filters. Marginal costs average $63 per classroom or $32 per child with asthma per year. In homes, using efficient furnace filters or air cleaners yields 11 to 16% reductions in the asthma burden with an annualized marginal costs of $151-494 per household. Additional benefits include reductions in health risk for adults and lower exposures to other contaminants such as PM from indoor sources. On the basis of the included health outcomes, efficient filters in schools in particular is a potentially cost-efficient way to reduce the asthma-related health burden for children.

Background: The role of environmental pesticide exposures, such as pyrethroids, and their relationship to sperm abnormalities are not well understood. This study investigated whether environmental exposure to pyrethroids was associated with altered frequency of sperm sex chromosome disomy in adult men., Methods: A sample of 75 subjects recruited through a Massachusetts infertility clinic provided urine and semen samples. Individual exposures were measured as urinary concentrations of three pyrethroid metabolites ((3-phenoxybenzoic acid (3PBA), cis- and trans- 3-(2,2-Dichlorovinyl)-1-methylcyclopropane-1,2-dicarboxylic acid (CDCCA and TDCCA)). Multiprobe fluorescence in situ hybridization for chromosomes X, Y, and 18 was used to determine XX, YY, XY, 1818, and total sex chromosome disomy in sperm nuclei. Poisson regression analysis was used to examine the association between aneuploidy rates and pyrethroid metabolites while adjusting for covariates., Results: Between 25-56% of the sample were above the limit of detection (LOD) for the pyrethroid metabolites. All sex chromosome disomies were increased by 7-30% when comparing men with CDCCA and TDCCA levels above the LOD to those below the LOD. For 3PBA, compared to those below the LOD, those above the LOD had YY18 disomy rates 1.28 times higher (95% CI: 1.15, 1.42) whereas a reduced rate was seen for XY18 and total disomy (IRR = 0.82; 95% CI: 0.77, 0.87; IRR = 0.93; 95% CI: 0.87-0.97), and no association was seen for XX18 and 1818., Conclusions: Our findings suggest that urinary concentrations of CDCCA and TDCCA above the LOD were associated with increased rates of aneuploidy. However the findings for 3BPA were not consistent. This is the first study to examine these relationships, and replication of our findings is needed before the association between pyrethroid metabolites and aneuploidy can be fully defined.