The Legacy of Redlining: Increasing Childhood Asthma Disparities Through Neighborhood Poverty.

RATIONALE: Identifying the root causes of racial disparities in childhood asthma is critical for health equity. OBJECTIVES: To determine if the 1930's racist policy of redlining led to present-day disparities in childhood asthma by increasing community-level poverty and decreasing neighborhood socioeconomic position (SEP). METHODS: We categorized census tracts at birth of participants from the Children's Respiratory and Environmental Workgroup birth cohort consortium into A, B, C, or D categories as defined by the Home Owners Loan Corporation (HOLC), with D being the highest perceived risk. Surrogates of present-day neighborhood-level SEP were determined for each tract including the percentage of low-income households, the CDC's social vulnerability index (SVI), and other tract-level variables. We performed causal mediation analysis, which, under the assumption of no unmeasured confounding, estimates the direct and mediated pathways by which redlining may cause asthma disparities through census tract-level mediators adjusting for individual-level covariates. MEASUREMENTS AND MAIN RESULTS: Of 4,849 children, the cumulative incidence of asthma through age 11 was 26.6% and 13.2% resided in census tracts with a HOLC grade of D. In mediation analyses, residing in grade D tracts (aOR = 1.03 [95%CI 1.01,1.05]) was significantly associated with childhood asthma, with 79% of this increased risk mediated by percentage of low-income households; results were similar for SVI and other tract-level variables. CONCLUSIONS: The historical structural racist policy of redlining led to present-day asthma disparities in part through decreased neighborhood SEP. Policies aimed at reversing the effects of structural racism should be considered to create more just, equitable, and healthy communities.

Rhinorrhea and watery eyes in infancy and risk of attention-deficit hyperactivity disorder in school-age children.

Increased parasympathetic nervous system (PNS) activity is associated with attention-deficit/hyperactivity disorder (ADHD) inattentive symptoms, but not hyperactive-impulsive symptoms, and may contribute to inattentive subtype etiology. Guided by prior work linking infant rhinorrhea and watery eyes without a cold (RWWC) to PNS dysregulation, we examined associations between infant RWWC and childhood ADHD symptoms in a longitudinal cohort of Black and Latinx children living in the context of economic disadvantage (N = 301 youth: 158 females, 143 males). Infant RWWC predicted higher inattentive (relative risk [RR] 2.16, p < .001) but not hyperactive-impulsive (RR 1.53, p = .065) ADHD symptoms (DuPaul scale), administered to caregivers at child age 8-14 years. Stratified analyses revealed that these associations were present in females but not males, who were three times more likely to have higher ADHD current total symptoms if they had infant RWWC than if they did not. Additionally, associations between RWWC and inattention symptoms were observed only in females. RWWC may thus serve as a novel risk marker of ADHD inattentive-type symptoms, especially for females.

Inverse associations of cord blood mitochondrial DNA copy number with childhood adiposity.

OBJECTIVE: The objective of this study was to examine associations between umbilical cord mitochondrial DNA copy number (mtDNAcn) and adiposity across childhood. METHODS: In a prospective birth cohort of Dominican and African American children from New York City, New York (1998-2006), mtDNAcn was measured in cord blood. Children (N = 336) were evaluated for their height, weight, and bioimpedance at age 5, 7, 9, and 11 years. We used linear mixed-effects models to assess associations of mtDNAcn tertiles in cord blood with child BMI, BMI z scores, fat mass index, and body fat percentage. Latent class growth models and interactions between mtDNAcn and child age or child age2 were used to assess associations between age and adiposity trajectories. RESULTS: BMI was, on average, 1.5 kg/m2 higher (95% CI: 0.58, 2.5) in individuals with mtDNAcn in the low- compared with the middle-mtDNAcn tertile. Results were similar for BMI z score, fat mass index, and body fat percentage. Moreover, children in the low-mtDNAcn group had increased odds of being in an "increasing" or "high-stable" adiposity class. CONCLUSIONS: Lower mtDNAcn at birth may predict greater childhood adiposity, highlighting the potential key role of perinatal mitochondrial function in adiposity during development.

Early-Life Exposure to Air Pollution and Childhood Asthma Cumulative Incidence in the ECHO CREW Consortium.

Importance: Exposure to outdoor air pollution contributes to childhood asthma development, but many studies lack the geographic, racial and ethnic, and socioeconomic diversity to evaluate susceptibility by individual-level and community-level contextual factors. Objective: To examine early life exposure to fine particulate matter (PM2.5) and nitrogen oxide (NO2) air pollution and asthma risk by early and middle childhood, and whether individual and community-level characteristics modify associations between air pollution exposure and asthma. Design, Setting, and Participants: This cohort study included children enrolled in cohorts participating in the Children's Respiratory and Environmental Workgroup consortium. The birth cohorts were located throughout the US, recruited between 1987 and 2007, and followed up through age 11 years. The survival analysis was adjusted for mother's education, parental asthma, smoking during pregnancy, child's race and ethnicity, sex, neighborhood characteristics, and cohort. Statistical analysis was performed from February 2022 to December 2023. Exposure: Early-life exposures to PM2.5 and NO2 according to participants' birth address. Main Outcomes and Measures: Caregiver report of physician-diagnosed asthma through early (age 4 years) and middle (age 11 years) childhood. Results: Among 5279 children included, 1659 (31.4%) were Black, 835 (15.8%) were Hispanic, 2555 (48.4%) where White, and 229 (4.3%) were other race or ethnicity; 2721 (51.5%) were male and 2596 (49.2%) were female; 1305 children (24.7%) had asthma by 11 years of age and 954 (18.1%) had asthma by 4 years of age. Mean values of pollutants over the first 3 years of life were associated with asthma incidence. A 1 IQR increase in NO2 (6.1 µg/m3) was associated with increased asthma incidence among children younger than 5 years (HR, 1.25 [95% CI, 1.03-1.52]) and children younger than 11 years (HR, 1.22 [95% CI, 1.04-1.44]). A 1 IQR increase in PM2.5 (3.4 µg/m3) was associated with increased asthma incidence among children younger than 5 years (HR, 1.31 [95% CI, 1.04-1.66]) and children younger than 11 years (OR, 1.23 [95% CI, 1.01-1.50]). Associations of PM2.5 or NO2 with asthma were increased when mothers had less than a high school diploma, among Black children, in communities with fewer child opportunities, and in census tracts with higher percentage Black population and population density; for example, there was a significantly higher association between PM2.5 and asthma incidence by younger than 5 years of age in Black children (HR, 1.60 [95% CI, 1.15-2.22]) compared with White children (HR, 1.17 [95% CI, 0.90-1.52]). Conclusions and Relevance: In this cohort study, early life air pollution was associated with increased asthma incidence by early and middle childhood, with higher risk among minoritized families living in urban communities characterized by fewer opportunities and resources and multiple environmental coexposures. Reducing asthma risk in the US requires air pollution regulation and reduction combined with greater environmental, educational, and health equity at the community level.

PM2.5 Is Insufficient to Explain Personal PAH Exposure.

To understand how chemical exposure can impact health, researchers need tools that capture the complexities of personal chemical exposure. In practice, fine particulate matter (PM2.5) air quality index (AQI) data from outdoor stationary monitors and Hazard Mapping System (HMS) smoke density data from satellites are often used as proxies for personal chemical exposure, but do not capture total chemical exposure. Silicone wristbands can quantify more individualized exposure data than stationary air monitors or smoke satellites. However, it is not understood how these proxy measurements compare to chemical data measured from wristbands. In this study, participants wore daily wristbands, carried a phone that recorded locations, and answered daily questionnaires for a 7-day period in multiple seasons. We gathered publicly available daily PM2.5 AQI data and HMS data. We analyzed wristbands for 94 organic chemicals, including 53 polycyclic aromatic hydrocarbons. Wristband chemical detections and concentrations, behavioral variables (e.g., time spent indoors), and environmental conditions (e.g., PM2.5 AQI) significantly differed between seasons. Machine learning models were fit to predict personal chemical exposure using PM2.5 AQI only, HMS only, and a multivariate feature set including PM2.5 AQI, HMS, and other environmental and behavioral information. On average, the multivariate models increased predictive accuracy by approximately 70% compared to either the AQI model or the HMS model for all chemicals modeled. This study provides evidence that PM2.5 AQI data alone or HMS data alone is insufficient to explain personal chemical exposures. Our results identify additional key predictors of personal chemical exposure.

Predicting personal PAH exposure using high dimensional questionnaire and wristband data.

BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) are a class of pervasive environmental pollutants with a variety of known health effects. While significant work has been completed to estimate personal exposure to PAHs, less has been done to identify sources of these exposures. Comprehensive characterization of reported sources of personal PAH exposure is a critical step to more easily identify individuals at risk of high levels of exposure and for developing targeted interventions based on source of exposure. OBJECTIVE: In this study, we leverage data from a New York (NY)-based birth cohort to identify personal characteristics or behaviors associated with personal PAH exposure and develop models for the prediction of PAH exposure. METHODS: We quantified 61 PAHs measured using silicone wristband samplers in association with 75 questionnaire variables from 177 pregnant individuals. We evaluated univariate associations between each compound and questionnaire variable, conducted regression tree analysis for each PAH compound and completed a principal component analysis of for each participant's entire PAH exposure profile to determine the predictors of PAH levels. RESULTS: Regression tree analyses of individual compounds and exposure mixture identified income, time spent outdoors, maternal age, country of birth, transportation type, and season as the variables most frequently predictive of exposure.

Trajectory analysis of rhinitis in a birth cohort from lower-income New York City neighborhoods.

BACKGROUND: Rhinitis is a prevalent, chronic nasal condition associated with asthma. However, its developmental trajectories remain poorly characterized. OBJECTIVE: We sought to describe the course of rhinitis from infancy to adolescence and the association between identified phenotypes, asthma-related symptoms, and physician-diagnosed asthma. METHODS: We collected rhinitis data from questionnaires repeated across 22 time points among 688 children from infancy to age 11 years and used latent class mixed modeling (LCMM) to identify phenotypes. Once children were between ages 5 and 12, a study physician determined asthma diagnosis. We collected information on the following asthma symptoms: any wheeze, exercise-induced wheeze, nighttime coughing, and emergency department visits. For each, we used LCMM to identify symptom phenotypes. Using logistic regression, we described the association between rhinitis phenotype and asthma diagnosis and each symptom overall and stratified by atopic predisposition and sex. RESULTS: LCMM identified 5 rhinitis trajectory groups: never/infrequent; transient; late onset, infrequent; late onset, frequent; and persistent. LCMM identified 2 trajectories for each symptom, classified as frequent and never/infrequent. Participants with persistent and late onset, frequent phenotypes were more likely to be diagnosed with asthma and to have the frequent phenotype for all symptoms (P < .01). We identified interaction between seroatopy and rhinitis phenotype for physician-diagnosed asthma (P = .04) and exercise-induced wheeze (P = .08). Severe seroatopy was more common among children with late onset, frequent and persistent rhinitis, with nearly 25% of these 2 groups exhibiting sensitivity to 4 or 5 of the 5 allergens tested. CONCLUSIONS: In this prospective, population-based birth cohort, persistent and late onset, frequent rhinitis phenotypes were associated with increased risk of asthma diagnosis and symptoms during adolescence.

Associations between mitochondrial biomarkers, urban residential exposures and childhood asthma outcomes over 6 months.

Determining biomarkers of responses to environmental exposures and evaluating whether they predict respiratory outcomes may help optimize environmental and medical approaches to childhood asthma. Relative mitochondrial (mt) DNA abundance and other potential mitochondrial indicators of oxidative stress may provide a sensitive metric of the child's shifting molecular responses to its changing environment. We leveraged two urban childhood cohorts (Environmental Control as Add-on Therapy in Childhood Asthma (ECATCh); Columbia Center for Children's Environmental Health (CCCEH)) to ascertain whether biomarkers in buccal mtDNA associate with airway inflammation and altered lung function over 6 months of time and capture biologic responses to multiple external stressors such as indoor allergens and fine particulate matter (PM2.5). Relative mtDNA content was amplified by qPCR and methylation of transfer RNA phenylalanine/rRNA 12S (TF/RNR1), cytochrome c oxidase (CO1), and carboxypeptidase O (CPO) was measured by pyrosequencing. Data on residential exposures and respiratory outcomes were harmonized between the two cohorts. Repeated measures and multiple regression models were utilized to assess relationships between mitochondrial biomarkers, respiratory outcomes, and residential exposures (PM2.5, allergens), adjusted for potential confounders and time-varying asthma. We found across the 6 month visits, a 0.64 fold higher level of TF/RNR1 methylation was detected among those with asthma in comparison to those without asthma ((parameter estimate (PE) 0.64, standard error 0.28, p = 0.03). In prospective analyses, CPO methylation was associated with subsequent reduced forced vital capacity (FVC; PE -0.03, standard error 0.01, p = 0.02). Bedroom dust mouse allergen, but not indoor PM2.5, was associated with higher methylation of TF/RNR1 (PE 0.015, standard error 0.006, p = 0.01). Select mtDNA measures in buccal cells may indicate children's responses to toxic environmental exposures and associate selectively with asthma and lung function.

Fungal diversity in homes and asthma morbidity among school-age children in New York City.

BACKGROUND: Asthma development has been inversely associated with exposure to fungal diversity. However, the influence of fungi on measures of asthma morbidity is not well understood. OBJECTIVES: This study aimed to test the hypothesis that fungal diversity is inversely associated with neighborhood asthma prevalence and identify specific fungal species associated with asthma morbidity. METHODS: Children aged 7-8 years (n = 347) living in higher (11-18%) and lower (3-9%) asthma prevalence neighborhoods were recruited within an asthma case-control study. Fungal communities were analyzed from floor dust using high-throughput DNA sequencing. A subset of asthmatic children (n = 140) was followed to age 10-11 to determine asthma persistence. RESULTS: Neighborhood asthma prevalence was inversely associated with fungal species richness (P = 0.010) and Shannon diversity (P = 0.059). Associations between neighborhood asthma prevalence and diversity indices were driven by differences in building type and presence of bedroom carpet. Among children with asthma at age 7-8 years, Shannon fungal diversity was inversely associated with frequent asthma symptoms at that age (OR 0.57, P = 0.025) and with asthma persistence to age 10-11 (OR 0.48, P = 0.043). Analyses of individual fungal species did not show significant associations with asthma outcomes when adjusted for false discovery rates. DISCUSSION: Lower fungal diversity was associated with asthma symptoms in this urban setting. Individual fungal species associated with asthma morbidity were not detected. Further research is warranted into building type, carpeting, and other environmental characteristics which influence fungal exposures in homes.

Development and psychometric validation of the Pandemic-Related Traumatic Stress Scale for children and adults.

To assess the public health impact of the COVID-19 pandemic on mental health, investigators from the National Institutes of Health Environmental influences on Child Health Outcomes (ECHO) research program developed the Pandemic-Related Traumatic Stress Scale (PTSS). Based on the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) acute stress disorder symptom criteria, the PTSS is designed for adolescent (13-21 years) and adult self-report and caregiver-report on 3-12-year-olds. To evaluate psychometric properties, we used PTSS data collected between April 2020 and August 2021 from non-pregnant adult caregivers (n = 11,483), pregnant/postpartum individuals (n = 1,656), adolescents (n = 1,795), and caregivers reporting on 3-12-year-olds (n = 2,896). We used Mokken scale analysis to examine unidimensionality and reliability, Pearson correlations to evaluate relationships with other relevant variables, and analyses of variance to identify regional, age, and sex differences. Mokken analysis resulted in a moderately strong, unidimensional scale that retained nine of the original 10 items. We detected small to moderate positive associations with depression, anxiety, and general stress, and negative associations with life satisfaction. Adult caregivers had the highest PTSS scores, followed by adolescents, pregnant/postpartum individuals, and children. Caregivers of younger children, females, and older youth had higher PTSS scores compared to caregivers of older children, males, and younger youth, respectively. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Synthetic Chemicals: What We Have Learned and Still Need to Learn About Their Associations with Childhood Allergy and Asthma.

PURPOSE OF REVIEW: Prenatal and childhood exposure to synthetic chemicals, such as phenols and phthalates, have been linked to asthma and allergy, but the extent of this association and the underlying mechanisms are not fully understood. Here we provide an up-to-date review of the evidence linking phenol and phthalate exposure with childhood asthma and allergy and of proposed mechanistic pathways. RECENT FINDINGS: Five experimental and 12 epidemiological studies that examined associations between exposures to synthetic chemicals to asthma and allergic diseases were included. An additional 14 studies provided mechanistic support for the importance of immune modification through epigenetic regulation, induction of pro-allergic T2 expression, and endocrine disruption. While recent studies have provided further experimental and epidemiological evidence for how these chemical exposures may induce childhood asthma and allergy, the recent literature remains limited. However, emerging mechanistic studies have identified chemical-induced alterations in DNA methylation of genes implicated in allergic inflammation and endocrine disruption as potential pathways. In addition, barriers to decrease exposure to synthetic chemicals at the individual level (facilitated through education) and areas for further action at the organizational and governmental levels are suggested. The latter includes transferring some of the onus from the individual to organizations and legislation to restrict marketing and access to products containing potentially harmful chemicals and provide alternative products. We also suggest future research that focuses on further elucidating pathways between exposure to disease development and identifying strategies to reduce exposure at the population level.

Socioeconomic Status at Birth and Breast Tissue Composition in Adolescence and Adulthood.

BACKGROUND: Socioeconomic status (SES) at birth is associated with breast cancer risk. Whether this association is driven by changes in breast tissue composition (BTC) prior to adulthood remains unclear. METHODS: We used multivariable linear regression models to examine whether SES at birth is associated with BTC in adolescence and adulthood using data from a New York City cohort of daughters (n = 165, 11-20 years) and mothers (n = 160, 29-55 years). We used maternal-reported data on daughters' household income and maternal education at birth, analyzed individually and in combination (SES index). Women also reported their own mothers' education at birth. We used optical spectroscopy to evaluate BTC measures that positively (water content, collagen content, optical index) and negatively (lipid content) correlate with mammographic breast density, a recognized breast cancer risk factor. RESULTS: Being in the highest versus lowest category of the SES index was associated with lower lipid content [ßadjusted (ßadj) = -0.80; 95% confidence interval (CI), -1.30 to -0.31] and higher collagen content (ßadj = 0.54; 95% CI, 0.09-0.99) in adolescence. In women with a body mass index (BMI) <30 kg/m2, higher maternal education at birth (≥ vs. < high school degree) was associated with lower lipid content (ßadj = -0.57; 95% CI, -0.97 to -0.17), higher water content (ßadj = 0.70; 95% CI, 0.26-1.14), and higher optical index (ßadj = 0.53; 95% CI, 0.10-0.95). CONCLUSIONS: This study supports that SES at birth is associated with BTC in adolescence and adulthood, although the latter association may depend on adult BMI. IMPACT: Further research is needed to identify the socially patterned early life factors influencing BTC.

Prenatal airborne polycyclic aromatic hydrocarbon exposure, altered regulation of peroxisome proliferator-activated receptor gamma (Ppar)γ, and links with mammary cancer.

Environmental exposure to polycyclic aromatic hydrocarbons (PAH) has been shown to be associated with chronic disease outcomes through multiple mechanisms including altered regulation of the transcription factor peroxisome proliferator-activated receptor gamma (Ppar) γ. Because PAH exposure and Pparγ each have been associated with mammary cancer, we asked whether PAH would induce altered regulation of Pparγ in mammary tissue, and whether this association may underlie the association between PAH and mammary cancer. Pregnant mice were exposed to aerosolized PAH at proportions that mimic equivalent human exposures in New York City air. We hypothesized that prenatal PAH exposure would alter Pparγ DNA methylation and gene expression and induce the epithelial to mesenchymal transition (EMT) in mammary tissue of offspring (F1) and grandoffspring (F2) mice. We also hypothesized that altered regulation of Pparγ in mammary tissue would associate with biomarkers of EMT, and examined associations with whole body weight. We found that prenatal PAH exposure lowered Pparγ mammary tissue methylation among grandoffspring mice at postnatal day (PND) 28. However, PAH exposure did not associate with altered Pparγ gene expression or consistently with biomarkers of EMT. Finally, lower Pparγ methylation, but not gene expression, was associated with higher body weight among offspring and grandoffspring mice at PND28 and PND60. Findings suggest additional evidence of multi-generational adverse epigenetic effects of prenatal PAH exposure among grandoffspring mice.

Impacts of the Certified Community Behavioral Health Clinic Demonstration on Emergency Department Visits and Hospitalizations.

OBJECTIVE: The Certified Community Behavioral Health Clinic (CCBHC) demonstration is designed to increase access to comprehensive ambulatory care and crisis services, which may reduce emergency department (ED) visits and hospitalizations. This study examined whether the demonstration had an impact on ED visits and hospitalizations in Missouri, Oklahoma, and Pennsylvania. METHODS: This difference-in-differences analysis used Medicaid claims data from 2015 to 2019 to examine service use during a 12-month baseline period and the first 24 months of the demonstration for beneficiaries who received care from CCBHCs and beneficiaries who received care from other behavioral health clinics in the same state, representing care as usual. Propensity score methods were used to develop treatment and comparison groups with similar characteristics. RESULTS: In Pennsylvania and Oklahoma, beneficiaries who received care from CCBHCs had a statistically significant reduction in the average number of behavioral health ED visits, relative to the comparison group (13% and 11% reductions, respectively); no impact on ED visits in Missouri was observed. The demonstration was associated with a statistically significant reduction in all-cause hospitalizations in Oklahoma, when the analysis used a 2-year rather than a 1-year baseline period, and also in Pennsylvania, when hospitalizations were truncated at the 98th percentile to exclude beneficiaries with outlier hospitalization rates. CONCLUSIONS: The CCBHC demonstration reduced behavioral health ED visits in two states, and the study also revealed some evidence of reductions in hospitalizations.

Incidence rates of childhood asthma with recurrent exacerbations in the US Environmental influences on Child Health Outcomes (ECHO) program.

BACKGROUND: Descriptive epidemiological data on incidence rates (IRs) of asthma with recurrent exacerbations (ARE) are sparse. OBJECTIVES: This study hypothesized that IRs for ARE would vary by time, geography, age, and race and ethnicity, irrespective of parental asthma history. METHODS: The investigators leveraged data from 17,246 children born after 1990 enrolled in 59 US with 1 Puerto Rican cohort in the Environmental Influences on Child Health Outcomes (ECHO) consortium to estimate IRs for ARE. RESULTS: The overall crude IR for ARE was 6.07 per 1000 person-years (95% CI: 5.63-6.51) and was highest for children aged 2-4 years, for Hispanic Black and non-Hispanic Black children, and for those with a parental history of asthma. ARE IRs were higher for 2- to 4-year-olds in each race and ethnicity category and for both sexes. Multivariable analysis confirmed higher adjusted ARE IRs (aIRRs) for children born 2000-2009 compared with those born 1990-1999 and 2010-2017, 2-4 versus 10-19 years old (aIRR = 15.36; 95% CI: 12.09-19.52), and for males versus females (aIRR = 1.34; 95% CI 1.16-1.55). Black children (non-Hispanic and Hispanic) had higher rates than non-Hispanic White children (aIRR = 2.51; 95% CI 2.10-2.99; and aIRR = 2.04; 95% CI: 1.22-3.39, respectively). Children born in the Midwest, Northeast and South had higher rates than those born in the West (P < .01 for each comparison). Children with a parental history of asthma had rates nearly 3 times higher than those without such history (aIRR = 2.90; 95% CI: 2.43-3.46). CONCLUSIONS: Factors associated with time, geography, age, race and ethnicity, sex, and parental history appear to influence the inception of ARE among children and adolescents.

Characteristics of peak exposure to black carbon pollution in school, commute and home environments among school children in an urban community.

Although real-time personal exposure monitoring devices have the ability to capture a wealth of data regarding fluctuations in pollutant levels, only a few studies have defined 'peaks' in black carbon (BC) exposure utilizing high-resolution data. Furthermore, studies to assess and characterize various features of peak exposure are very limited especially among children. A better understanding of characteristics of BC peak exposure would improve our understanding of health risks associated with BC. By capturing personal BC exposure at 5-min intervals using a real-time monitor during 24-hr monitoring periods among children in New York City (NYC), we defined 'peak characteristics' in 4 different ways across three major microenvironments (school vs. commute vs. home): 1) mean concentrations of BC across the 3 microenvironments, 2) 'peak duration' or time spent above the peak threshold (i.e., ≥1.5 µg/m3), 3) 'peak intensity' or the rate of exposure, defined as time spent above the threshold within each microenvironment divided by the total time spent in the microenvironment and 4) a novel metric of 'peak variability', defined as frequency of peaks (i.e., data points with +50% and -50% changes compared to the preceding and the subsequent data points), divided by the total time spent in the microenvironment. While peak duration was greatest at home, the intensity of peak exposure was greatest during commute hours, despite the short time spent in commute (p < 0.05). Peak variability was highest during commute, yet lowest in home environments (p < 0.05), particularly during non-sleeping hours. Children residing in a high-density urban setting spent on average, 5.4 hr per day above our peak threshold (≥1.5 µg/m3) in their everyday environments. Policies that limit children's exposure during high traffic periods and improved efforts to increase the number of vehicles using clean air technology could reduce the intensity of peaks and peak variability in children's BC exposure.

Performance of the Pediatric Asthma Risk Score across Diverse Populations.

BACKGROUND: Methods to determine whether a toddler is likely to develop asthma are of value to parents and clinical trialists testing primary prevention strategies. The Pediatric Asthma Risk Score (PARS) is a 14-point score of six factors designed to predict asthma in early life. PARS was developed and validated in relatively homogenous populations, so its generalizability is unknown. METHODS: We computed PARS using the six factors of self-declared race (parent-reported as "Black" or "not Black"), parental asthma, eczema, any wheezing, wheezing without a cold, and polysensitization in 5634 children from birth to 3 years of age. The primary outcome of our analysis was the ability of PARS to predict asthma development at 5 to 10 years of age using the area under the receiver operating curve in each cohort and across all cohorts with varying ethnicity, sex, cohort type, birth decades, missing PARS factors, and polysensitization definition. We also performed a meta-analysis across all the cohorts. Finally, we compared PARS predictive ability with the binary Asthma Predictive Index (API). RESULTS: Across 10 cohorts, the area under the receiver operating curve for PARS was 0.76. PARS performance did not differ by ethnicity, sex, cohort type, enrollment decade, missing PARS factors, or polysensitization definition (all P>0.05). The weights of each factor in the meta-analysis were similar to the original PARS weights. PARS and API equally identified children at high risk for developing asthma or not; API missed 31% of children at moderate asthma risk. CONCLUSIONS: PARS provided robust estimates of asthma risk in children from a wide range of ethnicities, backgrounds, and susceptibility. (Funded by the National Institute of Allergy and Infectious Diseases and others.)

The effects of the historical practice of residential redlining in the United States on recent temporal trends of air pollution near New York City schools.

BACKGROUND: In the 1930's the United States (US) sponsored Home Owners' Loan Corporation (HOLC) created maps that determined risk for mortgage lending based on the racial and ethnic composition of neighborhoods leading to disinvestment in "redlined" or highest risk neighborhoods. This historical practice has perpetuated racial and economic segregation, and health disparities, that persist today. Interventions near schools where children spend large portions of the day, could impact large groups of children but schools are an often-overlooked environment for exposure. Despite a declining trend of ambient pollution in New York City (NYC) between 1998 and 2012, little is known about differences in air quality improvement near schools by historical redlining neighborhood status. Our objective was to examine if recent temporal trends of air pollution near NYC public schools differed in historically redlined neighborhoods. METHODS: We examined annual average street-level concentrations of combustion-related air pollutants (black carbon (BC), particulate matter (PM2.5), nitrogen dioxide (NO2), and nitric oxide (NO)), within a 250-m radius around schools using NYC Community Air Survey land-use regression models (n = 1,462). Year of monitoring, historical redlining (binary), and summer ozone were included in multivariable linear regression using generalized estimating equation models. Average annual percent change (APC) in pollutant concentration was calculated. Models were further stratified by historical redlining and a multiplicative interaction term (year of monitoring × historical redlining) was used to assess effect modification. RESULTS: Overall, there was a decreasing trend of BC (APC = -4.40%), PM2.5 (-3.92%), NO2 (-2.76%), and NO (-6.20%) during the 10-year period. A smaller reduction of BC, PM2.5 and NO was observed in redlined neighborhoods (n = 722), compared to others (n = 740): BC (APC: -4.11% vs -4.69%; Pinteraction < 0.01), PM2.5 (-3.82% vs -4.11%; Pinteraction < 0.01), and NO (-5.73% vs -6.67%; Pinteraction < 0.01). Temporal trends of NO2 did not differ by historical redlining (Pinteraction = 0.60). CONCLUSIONS: Despite significant reductions in annual average pollution concentrations across NYC, schools in historically redlined neighborhoods, compared to others, experienced smaller decrease in pollution, highlighting a potential ongoing ramification of the discriminatory practice.

mRNA-1273 but not BNT162b2 induces antibodies against polyethylene glycol (PEG) contained in mRNA-based vaccine formulations.

Two messenger RNA (mRNA)-based vaccines are widely used globally to prevent coronavirus disease 2019 (COVID-19). Both vaccine formulations contain PEGylated lipids in their composition, in the form of polyethylene glycol [PEG] 2000 dimyristoyl glycerol for mRNA-1273, and 2 [(polyethylene glycol)-2000]-N,N-ditetradecylacetamide for BNT162b2. It is known that some PEGylated drugs and products for human use which contain PEG are capable of eliciting immune responses that lead to to detectable PEG-specific antibodies in serum. In this study, we determined if any of the components of mRNA-1273 or BNT162b2 formulations elicited PEG-specific antibody responses in serum by enzyme linked immunosorbent assay (ELISA). We detected an increase in the reactivity to mRNA vaccine formulations in mRNA-1273 but not BNT162b2 vaccinees' sera in a prime-boost dependent manner. Furthermore, we observed the same pattern of reactivity against irrelevant lipid nanoparticles from an influenza virus mRNA formulation and found that the reactivity of such antibodies correlated well with antibody levels against high and low molecular weight PEG. Using sera from participants selected based on the vaccine-associated side effects experienced after vaccination, including delayed onset, injection site or severe allergic reactions, we found no obvious association between PEG antibodies and adverse reactions. Overall, our data shows a differential induction of anti-PEG antibodies by mRNA-1273 and BNT162b2. The clinical relevance of PEG reactive antibodies induced by administration of the mRNA-1273 vaccine, and the potential interaction of these antibodies with other PEGylated drugs remains to be explored.