Race and Ethnicity in Pulmonary Function Test Interpretation: An Official American Thoracic Society Statement.

Current American Thoracic Society (ATS) standards promote the use of race and ethnicity-specific reference equations for pulmonary function test (PFT) interpretation. There is rising concern that the use of race and ethnicity in PFT interpretation contributes to a false view of fixed differences between races and may mask the effects of differential exposures. This use of race and ethnicity may contribute to health disparities by norming differences in pulmonary function. In the United States and globally, race serves as a social construct that is based on appearance and reflects social values, structures, and practices. Classification of people into racial and ethnic groups differs geographically and temporally. These considerations challenge the notion that racial and ethnic categories have biological meaning and question the use of race in PFT interpretation. The ATS convened a diverse group of clinicians and investigators for a workshop in 2021 to evaluate the use of race and ethnicity in PFT interpretation. Review of evidence published since then that challenges current practice and continued discussion concluded with a recommendation to replace race and ethnicity-specific equations with race-neutral average reference equations, which must be accompanied with a broader re-evaluation of how PFTs are used to make clinical, employment, and insurance decisions. There was also a call to engage key stakeholders not represented in this workshop and a statement of caution regarding the uncertain effects and potential harms of this change. Other recommendations include continued research and education to understand the impact of the change, to improve the evidence for the use of PFTs in general, and to identify modifiable risk factors for reduced pulmonary function.

Neighborhood environmental vulnerability and pediatric asthma morbidity in US metropolitan areas.

BACKGROUND: Research suggests demographic, economic, residential, and health-related factors influence vulnerability to environmental exposures. Greater environmental vulnerability may exacerbate environmentally related health outcomes. We developed a neighborhood environmental vulnerability index (NEVI) to operationalize environmental vulnerability on a neighborhood level. OBJECTIVE: We explored the relationship between NEVI and pediatric asthma emergency department (ED) visits (2014-19) in 3 US metropolitan areas: Los Angeles County, Calif; Fulton County, Ga; and New York City, NY. METHODS: We performed separate linear regression analyses examining the association between overall NEVI score and domain-specific NEVI scores (demographic, economic, residential, health status) with pediatric asthma ED visits (per 10,000) across each area. RESULTS: Linear regression analyses suggest that higher overall and domain-specific NEVI scores were associated with higher annual pediatric asthma ED visits. Adjusted R2 values suggest that overall NEVI scores explained at least 40% of the variance in pediatric asthma ED visits. Overall NEVI scores explained more of the variance in pediatric asthma ED visits in Fulton County. NEVI scores for the demographic, economic, and health status domains explained more of the variance in pediatric asthma ED visits in each area compared to the NEVI score for the residential domain. CONCLUSION: Greater neighborhood environmental vulnerability was associated with greater pediatric asthma ED visits in each area. The relationship differed in effect size and variance explained across the areas. Future studies can use NEVI to identify populations in need of greater resources to mitigate the severity of environmentally related outcomes, such as pediatric asthma.

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.

The Creation of a Multidomain Neighborhood Environmental Vulnerability Index Across New York City.

Compared to previous studies commonly using a single summary score, we aimed to construct a multidomain neighborhood environmental vulnerability index (NEVI) to characterize the magnitude and variability of area-level factors with the potential to modify the association between environmental pollutants and health effects. Using the Toxicological Prioritization Index framework and data from the 2015-2019 U.S. Census American Community Survey and the 2020 CDC PLACES Project, we quantified census tract-level vulnerability overall and in 4 primary domains (demographic, economic, residential, and health status), 24 subdomains, and 54 distinct area-level features for New York City (NYC). Overall and domain-specific indices were calculated by summing standardized feature values within the subdomains and then aggregating and weighting based on the number of features within each subdomain within equally-weighted primary domains. In citywide comparisons, NEVI was correlated with multiple existing indices, including the Neighborhood Deprivation Index (r = 0.91) and Social Vulnerability Index (r = 0.87) but provided additional information on features contributing to vulnerability. Vulnerability varied spatially across NYC, and hierarchical cluster analysis using subdomain scores revealed six patterns of vulnerability across domains: 1) low in all, 2) primarily low except residential, 3) medium in all, 4) high demographic, economic, and residential 5) high economic, residential, and health status, and 6) high demographic, economic and health status. Created using methods that offer flexibility for theory-based construction, NEVI provided detailed vulnerability metrics across domains that can inform targeted research and public health interventions aimed at reducing the health impacts from environmental exposures across urban centers.

Urinary metabolites of polycyclic aromatic hydrocarbons and short-acting beta agonist or systemic corticosteroid asthma medication use within NHANES.

BACKGROUND: Within cross-sectional studies like the U.S. National Health and Nutritional Examination Survey (NHANES), researchers have observed positive associations between polycyclic aromatic hydrocarbon (PAH) exposure and asthma diagnosis. It is unclear whether similar relationships exist for measures of acute asthma outcomes, including short-term asthma medication use to alleviate symptoms. We examined the relationship between markers of recent PAH exposure and 30-day short-acting beta agonist (SABA) or systemic corticosteroid use, an indicator for recent asthma symptoms. MATERIALS AND METHODS: For 16,550 children and adults across multiple waves of NHANES (2005-2016), we fit quasi-Poisson multivariable regression models to describe the association between urinary 1-hydroxypyrene (a metabolite of PAH) and SABA or systemic corticosteroid use. We assessed for effect modification by age group and asthma controller medication use. All models were adjusted for urinary creatinine, age, female/male designation, race/ethnicity, poverty, insurance coverage, and serum cotinine. RESULTS: After controlling for confounding, an increase of one standard deviation of 1-hydroxypyrene was associated with greater prevalence of recent SABA or systemic corticosteroid use (PR: 1.06, 95% CI: 1.03-1.10). The results were similar among those with ever asthma diagnosis and across urine creatinine dilution methods. We did not observe effect modification by age group (p-interaction = 0.22) or asthma controller medication use (p-interaction = 0.73). CONCLUSION: Markers of recent PAH exposure was positively associated with SABA or systemic corticosteroid use, across various urine dilution adjustment methods. It is important to ensure appropriate temporality between exposures and outcomes in cross-sectional studies.

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.

Enhancing Recruitment and Retention of Minority Populations for Clinical Research in Pulmonary, Critical Care, and Sleep Medicine: An Official American Thoracic Society Research Statement.

Background: Well-designed clinical research needs to obtain information that is applicable to the general population. However, most current studies fail to include substantial cohorts of racial/ethnic minority populations. Such underrepresentation may lead to delayed diagnosis or misdiagnosis of disease, wide application of approved interventions without appropriate knowledge of their usefulness in certain populations, and development of recommendations that are not broadly applicable.Goals: To develop best practices for recruitment and retention of racial/ethnic minorities for clinical research in pulmonary, critical care, and sleep medicine.Methods: The American Thoracic Society convened a workshop in May of 2019. This included an international interprofessional group from academia, industry, the NIH, and the U.S. Food and Drug Administration, with expertise ranging from clinical and biomedical research to community-based participatory research methods and patient advocacy. Workshop participants addressed historical and current mistrust of scientific research, systemic bias, and social and structural barriers to minority participation in clinical research. A literature search of PubMed and Google Scholar was performed to support conclusions. The search was not a systematic review of the literature.Results: Barriers at the individual, interpersonal, institutional, and federal/policy levels were identified as limiting to minority participation in clinical research. Through the use of a multilevel framework, workshop participants proposed evidence-based solutions to the identified barriers.Conclusions: To date, minority participation in clinical research is not representative of the U.S. and global populations. This American Thoracic Society research statement identifies potential evidence-based solutions by applying a multilevel framework that is anchored in community engagement methods and patient advocacy.

The impact of environmental injustice and social determinants of health on the role of air pollution in asthma and allergic disease in the United States.

There is clear evidence that exposure to environmental air pollution is associated with immune dysregulation, asthma, and other allergic diseases. However, the burden of air pollution exposure is not equally distributed across the United States. Many social and environmental factors place communities of color and people who are in poverty at increased risk of exposure to pollution and morbidity from asthma and allergies. Here, we review the evidence that supports the relationship between air pollution and asthma, while considering the social determinants of health that contribute to disparities in exposures and outcomes.

Trajectories of adiposity indicators and association with asthma and lung function in urban minority children.

BACKGROUND: A relationship between adiposity and asthma has been described in some cohort studies, but little is known about trajectories of adiposity throughout early childhood among children at high risk for developing asthma in urban United States cities. Moreover, early life trajectories of adipokines that have metabolic and immunologic properties have not been comprehensively investigated. OBJECTIVE: Our objective was to characterize trajectories of adiposity in a longitudinal birth cohort of predominately Black and Latinx children (n = 418) using several different repeated measures including body mass index (BMI) z score, bioimpedance analysis, leptin, and adiponectin in the first 10 years of life. METHODS: In a longitudinal birth cohort of predominately Black and Latinx children, we used repeated annual measures of BMI, bioimpedance analysis (ie, percentage of body fat), leptin, and adiponectin to create trajectories across the first 10 years of life. Across those trajectories, we compared asthma diagnosis and multiple lung function outcomes, including spirometry, impulse oscillometry, and methacholine response. RESULTS: Three trajectories were observed for BMI z score, bioimpedance analysis, and leptin and 2 for adiponectin. There was no association between trajectories of BMI, percentage of body fat, leptin, or adipokine and asthma diagnosis or lung function (P > .05). CONCLUSIONS: Trajectories of adiposity were not associated with asthma or lung function in children at high risk for developing asthma. Risk factors related to geography as well as social and demographic factors unique to specific populations could explain the lack of association and should be considered in obesity and asthma studies.

Inducible expression quantitative trait locus analysis of the MUC5AC gene in asthma in urban populations of children.

BACKGROUND: Mucus plugging can worsen asthma control, lead to reduced lung function and fatal exacerbations. MUC5AC is the secretory mucin implicated in mucus plugging, and MUC5AC gene expression has been associated with development of airway obstruction and asthma exacerbations in urban children with asthma. However, the genetic determinants of MUC5AC expression are not established. OBJECTIVES: This study sought to assess single-nucleotide polymorphisms (SNPs) that influence MUC5AC expression and relate to pulmonary functions in childhood asthma. METHODS: This study used RNA-sequencing data from upper airway samples and performed cis-expression quantitative trait loci (eQTL) and allele-specific expression analyses in 2 cohorts of predominantly Black and Hispanic urban children, a high asthma-risk birth cohort, and an exacerbation-prone asthma cohort. Inducible MUC5AC eQTLs were further investigated during incipient asthma exacerbations. Significant eQTLs SNPs were tested for associations with lung function measurements and their functional consequences were investigated in DNA regulatory databases. RESULTS: Two independent groups of SNPs in the MUC5AC gene that were significantly associated with MUC5AC expression were identified. Moreover, these SNPs showed stronger eQTL associations with MUC5AC expression during asthma exacerbations, which is consistent with inducible expression. SNPs in 1 group also showed significant association with decreased pulmonary functions. These SNPs included multiple EGR1 transcription factor binding sites, suggesting a mechanism of effect. CONCLUSIONS: These findings demonstrate the applicability of organ-specific RNA-sequencing data to determine genetic factors contributing to a key disease pathway. Specifically, they suggest important genetic variations that may underlie propensity to mucus plugging in asthma and could be important in targeted asthma phenotyping and disease management strategies.

Development of nasal allergen challenge with cockroach in children with asthma.

BACKGROUND: Nasal allergen challenge (NAC) could be a means to assess indication and/or an outcome of allergen-specific therapies, particularly for perennial allergens. NACs are not commonly conducted in children with asthma, and cockroach NACs are not well established. This study's objective was to identify a range of German cockroach extract doses that induce nasal symptoms and to assess the safety of cockroach NAC in children with asthma. METHODS: Ten adults (18-37 years) followed by 25 children (8-14 years) with well-controlled, persistent asthma and cockroach sensitization underwent NAC with diluent followed by up to 8 escalating doses of cockroach extract (0.00381-11.9 µg/mL Bla g 1). NAC outcome was determined by Total Nasal Symptom Score (TNSS) and/or sneeze score. Cockroach allergen-induced T-cell activation and IL-5 production were measured in peripheral blood mononuclear cells. RESULTS: 67% (6/9) of adults and 68% (17/25) of children had a positive NAC at a median response dose of 0.120 µg/mL [IQR 0.0380-0.379 µg/mL] of Bla g 1. Additionally, three children responded to diluent alone and did not receive any cockroach extract. Overall, 32% (11/34) were positive with sneezes alone, 15% (5/34) with TNSS alone, and 21% (7/34) with both criteria. At baseline, NAC responders had higher cockroach-specific IgE (P = .03), lower cockroach-specific IgG/IgE ratios (children, P = .002), and increased cockroach-specific IL-5-producing T lymphocytes (P = .045). The NAC was well tolerated. CONCLUSION: We report the methodology of NAC development for children with persistent asthma and cockroach sensitization. This NAC could be considered a tool to confirm clinically relevant sensitization and to assess responses in therapeutic studies.

Multi-Level Socioenvironmental Contributors to Childhood Asthma in New York City: a Cluster Analysis.

Childhood asthma exacerbation remains the leading cause of pediatric emergency department visits and hospitalizations and disproportionately affects Latinx and Black children, compared to non-Latinx White children in NYC. Environmental exposures and socioeconomic factors may jointly contribute to childhood asthma exacerbations; however, they are often studied separately. To better investigate the multiple contributors to disparities in childhood asthma, we compiled data on various individual and neighborhood level socioeconomic and environmental factors, including education, race/ethnicity, income disparities, gentrification, housing characteristics, built environment, and structural racism, from the NYC Department of Health's KIDS 2017 survey and the US Census' American Community Survey. We applied cluster analysis and logistic regression to first identify the predominant patterns of social and environmental factors experienced by children in NYC and then estimate whether children experiencing specific patterns are more likely to experience asthma exacerbations. We found that housing and built environment characteristics, such as density and age of buildings, were the predominant features to differentiate the socio-environmental patterns observed in New York City. Children living in neighborhoods with greater proportions of rental housing, high-density buildings, and older buildings were more likely to experience asthma exacerbations than other children. These findings add to the literature about childhood asthma in urban environments, and can assist efforts to target actionable policies and practices that promote health equity related to childhood asthma.

Asthma among hospitalized patients with COVID-19 and related outcomes.

BACKGROUND: Several underlying conditions have been associated with severe acute respiratory syndrome coronavirus 2 illness, but it remains unclear whether underlying asthma is associated with worse coronavirus disease 2019 (COVID-19) outcomes. OBJECTIVE: Given the high prevalence of asthma in the New York City area, our objective was to determine whether underlying asthma was associated with poor outcomes among hospitalized patients with severe COVID-19 compared with patients without asthma. METHODS: Electronic heath records were reviewed for 1298 sequential patients 65 years or younger without chronic obstructive pulmonary disease who were admitted to our hospital system with a confirmed positive severe acute respiratory syndrome coronavirus 2 test result. RESULTS: The overall prevalence of asthma among all hospitalized patients with COVID-19 was 12.6%, yet a higher prevalence (23.6%) was observed in the subset of 55 patients younger than 21 years. There was no significant difference in hospital length of stay, need for intubation, length of intubation, tracheostomy tube placement, hospital readmission, or mortality between patients with and without asthma. Observations between patients with and without asthma were similar when stratified by obesity, other comorbid conditions (ie, hypertension, hyperlipidemia, and diabetes), use of controller asthma medication, and absolute eosinophil count. CONCLUSIONS: Among hospitalized patients 65 years or younger with severe COVID-19, asthma diagnosis was not associated with worse outcomes, regardless of age, obesity, or other high-risk comorbidities. Future population-based studies are needed to investigate the risk of developing COVID-19 among patients with asthma once universal testing becomes readily available.

Air pollution, urgent asthma medical visits and the modifying effect of neighborhood asthma prevalence.

BACKGROUND: Social and environmental stressors may modify associations between environmental pollutants and asthma symptoms. We examined if neighborhood asthma prevalence (higher: HAPN vs. lower: LAPN), a surrogate for underlying risk factors for asthma, modified the relationship between pollutants and urgent asthma visits. METHODS: Through zip code, home addresses were linked to New York City Community Air Survey's land use regression model for street-level, annual average nitrogen dioxide (NO2), particulate matter (PM2.5), elemental carbon (EC), summer average ozone (O3), winter average sulfur dioxide (SO2) concentrations. Poisson regression models were fit to estimate the association (prevalence ratio, PR) between pollutant exposures and seeking urgent asthma care. RESULTS: All pollutants, except O3 were higher in HAPN than LAPN (P < 0.01). Neighborhood asthma prevalence modified the relationship between pollutants and urgent asthma (P-interaction < 0.01, for NO2 and SO3). Associations between pollutants and urgent asthma were observed only in LAPN (NO2: PR = 1.38, P = 0.01; SO3: PR = 1.85, P = 0.04). No association was observed between pollutants and urgent asthma among children in HAPN (P > 0.05). CONCLUSIONS: Relationships between modeled street-level pollutants and urgent asthma were stronger in LAPN compared to HAPN. Social stressors that may be more prevalent in HAPN than LAPN, could play a greater role in asthma exacerbations in HAPN vs. pollutant exposure alone.

Assessment of exposure to air pollution in children: Determining whether wearing a personal monitor affects physical activity.

Personal air pollution monitoring in research studies should not interfere with usual patterns of behavior and bias results. In an urban pediatric cohort study we tested whether wearing an air monitor impacted activity time based on continuous watch-based accelerometry. The majority (71%) reported that activity while wearing the monitor mimicked normal activity. Correspondingly, variation in activity while wearing versus not wearing the monitor did not differ greatly from baseline variation in activity (P = 0.84).

Short-term exposure to PM2.5 and vanadium and changes in asthma gene DNA methylation and lung function decrements among urban children.

BACKGROUND: Both short and long-term exposure to traffic-related air pollutants have been associated with asthma and reduced lung function. We hypothesized that short-term indoor exposure to fine particulate matter <2.5 µm (PM2.5) and vanadium (V) would be associated with altered buccal cell DNA methylation of targeted asthma genes and decreased lung function among urban children in a nested subcohort of African American and Dominican children. METHODS: Six day integrated levels of air pollutants were measured from children's homes (age 9-14; n = 163), repeated 6 months later (n = 98). Buccal samples were collected repeatedly during visits. CpG promoter loci of asthma genes (i.e., interleukin 4 (IL4), interferon gamma (IFNγ), inducible nitric oxide synthase (NOS2A), arginase 2 (ARG2)) were pyrosequenced and lung function was assessed. RESULTS: Exposure to V, but not PM2.5, was associated with lower DNA methylation of IL4 and IFNγ. In exploratory analyses, V levels were associated with lower methylation of the proinflammatory NOS2A-CpG+5099 among asthmatic overweight or obese children but not nonasthmatics. Short-term exposure to PM2.5, but not V, appeared associated with lower lung function (i.e., reduced z-scores for forced expiratory volume in one second (FEV1, FEV1/ forced vital capacity [FEV1/FVC] and forced expiratory flow at 25-75% of FVC [FEF25-75]). CONCLUSIONS: Exposure to V was associated with altered DNA methylation of allergic and proinflammatory asthma genes implicated in air pollution related asthma. However, short-term exposure to PM2.5, but not V, appeared associated with decrements in lung function among urban children.

Reduced mouse allergen is associated with epigenetic changes in regulatory genes, but not mouse sensitization, in asthmatic children.

Chronic exposure to mouse allergen may contribute greatly to the inner-city asthma burden. We hypothesized that reducing mouse allergen exposure may modulate the immunopathology underlying symptomatic pediatric allergic asthma, and that this occurs through epigenetic regulation. To test this hypothesis, we studied a cohort of mouse sensitized, persistent asthmatic inner-city children undergoing mouse allergen-targeted integrated pest management (IPM) vs education in a randomized controlled intervention trial. We found that decreasing mouse allergen exposure, but not cockroach, was associated with reduced FOXP3 buccal DNA promoter methylation, but this was unrelated to mouse specific IgE production. This finding suggests that the environmental epigenetic regulation of an immunomodulatory gene may occur following changing allergen exposures in some highly exposed cohorts. Given the clinical and public health importance of inner-city pediatric asthma and the potential impact of environmental interventions, further studies will be needed to corroborate changes in epigenetic regulation following changing exposures over time, and determine their impact on asthma morbidity in susceptible children.

Physical activity, black carbon exposure and airway inflammation in an urban adolescent cohort.

OBJECTIVE: Regular physical activity can improve cardiopulmonary health; however, increased respiratory rates and tidal volumes during activity may increase the effective internal dose of air pollution exposure. Our objective was to investigate the impact of black carbon (BC) measured by personal sampler on the relationship between physical activity and fractional exhaled nitric oxide (FeNO), a marker of airway inflammation. We hypothesized that higher personal BC would attenuate the protective effect of physical activity on airway inflammation. METHODS: We performed a cross-sectional study nested in a birth cohort of African American and Dominican children living in the Bronx and Northern Manhattan, New York City. Children were recruited based on age (target 9-14 year olds) and presence (n=70) or absence (n=59) of current asthma. Children wore wrist mounted accelerometers for 6 days and were classified as 'active' if they had ≥60min of moderate-to-vigorous activity (MVA) each day and 'non-active' if they had <60min of MVA on any given day, based on CDC guidelines. Personal BC measured using a MicroAeth, was assessed during two 24-h periods, at the beginning and end of physical activity assessment. High BC was defined as the upper tertile of BC measured with personal sampler. FeNO measurements were sampled at the beginning and end of the of physical activity assessment. RESULTS: In multivariable linear regression models, 'active' children had 25% higher personal BC concentrations (p=0.02) and 20% lower FeNO (p=0.04) compared to 'non-active' children. Among children with high personal BC (n=33), there was no relationship between activity and FeNO (p=1.00). The significant protective relationship between activity and airway inflammation was largely driven by children with lower personal BC (n=96, p=0.04). CONCLUSIONS: Children that live in an urban environment and are physically active on a daily basis have higher personal exposure to BC. High BC offsets the protective relationship between physical activity and airway inflammation.