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Background: Although human biomonitoring of environmental chemicals has been considered a gold standard, these methods can be costly, burdensome, and prone to unwanted sources of variability that may cause confounding. Silicone wristbands have recently emerged as innovative passive samplers for measuring personal exposures., Methods: In a pilot study from 2019 to 2021 involving 55 children aged 5-9 years in Seattle and Yakima, Washington, we utilized silicone wristbands to explore associations of sociodemographic variables and COVID-19-related restrictions, including school closures, with exposures to numerous chemicals including brominated and organophosphate ester (OPE) flame retardants, polychlorinated biphenyls, polycyclic aromatic hydrocarbons (PAHs), phthalates, and pesticides. We additionally conducted the first analysis testing silicone wristband chemicals as predictors of child wheeze, individually and in mixtures via logistic weighted quantile sum regression (WQS)., Results: Among 109 semi-volatile organic compounds measured, we detected 40 in >60% of wristbands worn by children continuously for an average of 5 days. Chemicals were generally positively correlated, especially within the same class. Male sex and increasing age were linked with higher exposures across several chemical classes; Hispanic/Latino ethnicity was linked with higher exposures to some phthalates and OPEs. COVID-19 restrictions were associated with lower wristband concentrations of brominated and triaryl OPE flame retardants. Each one-decile higher WQS exposure index was suggestively associated with 2.11-fold [95% CI: 0.93-4.80] higher odds of child wheeze. Risk of child wheeze was higher per 10-fold increase in the PAH chrysene (RR = 1.93[1.07-3.49]), the pesticide cis-permethrin (3.31[1.23-8.91]), and di-isononyl phthalate (DINP) (5.40[1.22-24.0]) CONCLUSIONS: Our identification of demographic factors including sex, age, and ethnicity associated with chemical exposures may aid efforts to mitigate exposure disparities. Lower exposures to flame retardants during pandemic restrictions corroborates prior evidence of higher levels of these chemicals in school versus home environments. Future research in larger cohorts is needed to validate these findings., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Brennan H Baker reports financial support was provided by National Institutes of Health. Heather M Stapleton reports financial support was provided by National Institutes of Health. Sheela Sathyanarayana reports financial support was provided by National Institutes of Health. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Ozone (O 3 ) exposure interrupts normal lung development in animal models. Epidemiologic evidence further suggests impairment with higher long-term O 3 exposure across early and middle childhood, although study findings to date are mixed and few have investigated vulnerable subgroups., Methods: Participants from the CANDLE study, a pregnancy cohort in Shelby County, TN, in the ECHO-PATHWAYS Consortium, were included if children were born at gestational age >32 weeks, completed a spirometry exam at age 8-9, and had a valid residential history from birth to age 8. We estimated lifetime average ambient O 3 exposure based on each child's residential history from birth to age 8, using a validated fine-resolution spatiotemporal model. Spirometry was performed at the age 8-9 year study visit to assess Forced Expiratory Volume in the first second (FEV 1 ) and Forced Vital Capacity (FVC) as primary outcomes; z-scores were calculated using sex-and-age-specific reference equations. Linear regression with robust variance estimators was used to examine associations between O 3 exposure and continuous lung function z-scores, adjusted for child, sociodemographic, and home environmental factors. Potential susceptible subgroups were explored using a product term in the regression model to assess effect modification by child sex, history of bronchiolitis in infancy, and allergic sensitization., Results: In our sample (n = 648), O 3 exposure averaged from birth to age 8 was modest (mean 26.6 [SD 1.1] ppb). No adverse associations between long-term postnatal O 3 exposure were observed with either FEV 1 (β = 0.12, 95% CI: -0.04, 0.29) or FVC (β = 0.03, 95% CI: -0.13, 0.19). No effect modification by child sex, history of bronchiolitis in infancy, or allergic sensitization was detected for associations with 8-year average O 3 ., Conclusions: In this sample with low O 3 concentrations, we did not observe adverse associations between O 3 exposures averaged from birth to age 8 and lung function in middle childhood., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Maternal exposure to air pollution has been associated with birth outcomes; however, few studies examined biologically critical exposure windows shorter than trimesters or potential effect modifiers., Objectives: To examine associations of prenatal fine particulate matter (PM 2.5 ), by trimester and in biologically critical windows, with birth outcomes and assess potential effect modifiers., Methods: This study used two pregnancy cohorts (CANDLE and TIDES; N = 2099) in the ECHO PATHWAYS Consortium. PM 2.5 was estimated at the maternal residence using a fine-scale spatiotemporal model, averaged over pregnancy, trimesters, and critical windows (0-2 weeks, 10-12 weeks, and last month of pregnancy). Outcomes were preterm birth (PTB, <37 completed weeks of gestation), small-for-gestational-age (SGA), and continuous birthweight. We fit multivariable adjusted linear regression models for birthweight and Poisson regression models (relative risk, RR) for PTB and SGA. Effect modification by socioeconomic factors (maternal education, household income, neighborhood deprivation) and infant sex were examined using interaction terms., Results: Overall, 9% of births were PTB, 10.4% were SGA, and mean term birthweight was 3268 g (SD = 558.6). There was no association of PM 2.5 concentration with PTB or SGA. Lower birthweight was associated with higher PM 2.5 averaged over pregnancy (β -114.2, 95%CI -183.2, -45.3), during second (β -52.9, 95%CI -94.7, -11.2) and third (β -45.5, 95%CI -85.9, -5.0) trimesters, and the month prior to delivery (β -30.5, 95%CI -57.6, -3.3). Associations of PM 2.5 with likelihood of SGA and lower birthweight were stronger among male infants (p-interaction ≤0.05) and in those with lower household income (p-interaction = 0.09)., Conclusions: Findings from this multi city U.S. birth cohort study support previous reports of inverse associations of birthweight with higher PM 2.5 exposure during pregnancy. Findings also suggest possible modification of this association by infant sex and household income., (Copyright © 2022. Published by Elsevier Inc.)

Background: Prenatal and early life air pollution exposure may impair healthy neurodevelopment, increasing risk of childhood behavioral disorders, but epidemiological evidence is inconsistent. Little is known about factors that determine susceptibility., Methods: Participants were mother-child dyads from the CANDLE study, an ECHO PATHWAYS Consortium birth cohort set in the mid-South United States, who completed a preschool visit. We estimated prenatal and childhood exposures to nitrogen dioxide (NO 2 ) and particulate matter less than 10 μm (PM 10 ) at participants' residences using a national annual average universal kriging model (land-use regression with spatial smoothing). Distance to nearest major roadway was used as a proxy for traffic-related pollution. Primary outcomes were children's internalizing and externalizing behavior problems. Regression models were adjusted for individual- and neighborhood-level socioeconomic measures, maternal IQ, and multiple other potential confounders. We tested for effect modification by select maternal and child characteristics., Results: The analytic sample (N = 975 of 1503 enrolled) was 64% African American and 53% had a household annual income below $35,000; child mean age was 4.3 years (SD: 0.4). Mean prenatal NO 2 and PM 10 exposures were 12.0 ppb (SD: 2.4) and 20.8 μg/m3 (SD: 2.0); postnatal exposures were lower. In fully adjusted models, 2 ppb higher prenatal NO 2 was positively associated with externalizing behavior (6%; 95% CI: 1, 11%). Associations with postnatal exposure were stronger (8% per 2 ppb NO 2 ; 95%CI: 0, 16%). Prenatal NO 2 exposure was also associated with an increased odds of clinically significant internalizing and externalizing behaviors. We found suggestive evidence that socioeconomic adversity and African American race increases susceptibility. PM 10 and road proximity were not associated with outcomes., Conclusions: Findings showed that air pollution exposure is positively associated with child behavior problems and that African American and low SES children may be more susceptible. Importantly, associations were observed at exposures below current air quality standards., Competing Interests: Declaration of competing interest The authors report no conflicts of interest relevant to this article., (Copyright © 2019. Published by Elsevier Inc.)

Objectives: Animal studies suggest that air pollution is neurotoxic to a developing fetus, but evidence in humans is limited. We tested the hypothesis that higher air pollution is associated with lower child IQ and that effects vary by maternal and child characteristics, including prenatal nutrition., Methods: We used prospective data collected from the Conditions Affecting Neurocognitive Development and Learning in Early Childhood study. Outdoor pollutant exposure during pregnancy was predicted at geocoded home addresses using a validated national universal kriging model that combines ground-based monitoring data with an extensive database of land-use covariates. Distance to nearest major roadway was also used as a proxy for traffic-related pollution. Our primary outcome was full-scale IQ measured at age 4-6. In regression models, we adjusted for multiple determinants of child neurodevelopment and assessed interactions between air pollutants and child sex, race, socioeconomic status, reported nutrition, and maternal plasma folate in second trimester., Results: In our analytic sample (N = 1005) full-scale IQ averaged 2.5 points (95% CI: 0.1, 4.8) lower per 5 μg/m 3 higher prenatal PM 10 , while no associations with nitrogen dioxide or road proximity were observed. Associations between PM 10 and IQ were modified by maternal plasma folate (p interaction  = 0.07). In the lowest folate quartile, IQ decreased 6.8 points (95% CI: 1.4, 12.3) per 5-unit increase in PM 10 ; no associations were observed in higher quartiles., Conclusions: Our findings strengthen evidence that air pollution impairs fetal neurodevelopment and suggest a potentially important role of maternal folate in modifying these effects., (Copyright © 2019 Elsevier Inc. All rights reserved.)