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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.

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]

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

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.)

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.