News|Articles|October 20, 2026

Black children face higher odds of T2-high severe asthma

Fact checked by: Benjamin P. Saylor

Black race was the strongest predictor of T2-high inflammation in 451 children with severe asthma adjusted for social and environmental factors.

Among children with severe, treatment-refractory asthma, self-reported Black race was the strongest independent predictor of type 2 (T2)–high inflammation, outranking household income, urban residence, traffic exposure, and neighborhood social vulnerability, according to a cross-sectional study of 451 children published in the Journal of Allergy and Clinical Immunology: In Practice.¹

The University of Virginia (UVA) investigators say the findings support earlier biomarker testing in difficult-to-control asthma. W. Gerald Teague, MD, a pediatric pulmonologist at UVA Health Children's and the University of Virginia School of Medicine, said the results support "earlier intervention with therapies known to target type 2 inflammation" in all children with asthma, with particular attention to children of color.²

Study design and T2-high definitions in pediatric severe asthma

Investigators analyzed children referred to UVA for troublesome cough and wheeze between January 2011 and March 2025 who underwent clinically indicated bronchoscopy with bronchoalveolar lavage (BAL) after failing guideline-based therapy, including high-dose inhaled or oral corticosteroids.¹ T2-high status (n = 202) required blood eosinophils of at least 300 cells/μL or BAL eosinophils of at least 1%, plus specific IgE to at least 1 allergen; T2-low children (n = 249) had neither.¹ From a bioregistry of 935 children, 240 with discordant markers, 165 with nonasthma diagnoses, and 79 with missing data were excluded.¹ Social and environmental exposures were assigned by zip code using census, CDC, and EPA data.¹

Black race and T2-high asthma odds after social and environmental adjustment

Black children made up 38% of the T2-high group vs 9% of the T2-low group.¹ T2-high children were older (median, 6.3 vs 3.5 years), more often lived in low-income zip codes (37% vs 26%), and were more often hospitalized for wheeze (74% vs 49%).¹ Among 187 children with spirometry, median prebronchodilator FEV₁ was 86% vs 102% predicted.¹

In a model adjusted for age, sex, low income, urban residence, traffic proximity, and social vulnerability, Black race carried the largest odds ratio for T2-high inflammation (OR, 2.88; 95% CI, 1.79-4.64; P < .001).¹ In a second model adjusted for hospital admission, BAL neutrophils, BAL bacterial pathogens, and tracheomalacia, the OR was 3.84 (95% CI, 2.19-6.73; P < .001).¹ Neural network models largely reproduced these results, although age outranked race in the social and environmental analysis.¹

T2-high prevalence also rose with age. Among preschool-aged children, 63% of Black vs 29% of White children were T2-high; among those older than 5 years, the figures were 86% vs 50%.¹ Black children had more allergen sensitization in both urban and nonurban zip codes.¹

Racial disparities in pediatric asthma outcomes and T2-targeted care

US death data from 1999 to 2023 show higher asthma mortality among Black than White children,³ and non-Hispanic Black children continue to bear a disproportionate share of pediatric asthma hospitalizations.⁴ Prior studies have struggled to separate race from co-occurring exposures such as air pollution, housing, and income.¹

The authors recommend measuring blood eosinophils and allergen-specific IgE even in young children with difficult symptoms, and suggest T2-targeted biologics might be considered earlier in highly symptomatic Black children.¹ They also questioned routine high-dose corticosteroids for children with T2-low patterns, noting that 66% of preschoolers in the cohort were T2-low.¹

Limitations of race-based analysis in pediatric T2 asthma research

The published paper is more measured than the accompanying institutional statement, in which Teague said he hoped the work would dispel the idea that social and environmental factors are the main drivers of asthma severity.² The authors describe race as a sociopolitical construct distinct from genetic ancestry and urge cautious interpretation, since race was caregiver-reported and ancestry was not measured.¹

The study was cross-sectional and drawn from a single Virginia referral center, Hispanic children were underrepresented (4%), and exposures were estimated at the zip code level.¹ Secondhand smoke, access to specialty care, neighborhood violence, vitamin D levels, and adherence differences were not assessed.¹ About one-third of the bioregistry could not be classified as T2-high or T2-low, and the authors note that definitive conclusions about an individual child cannot be drawn.¹ They reported E-values of 5.2 and 7.1, arguing that an unmeasured confounder is unlikely to fully explain the association, and called for studies incorporating genetic ancestry and interaction terms.¹

References
1. Teague WG, Noth A, Lynch M, et al. Race adjusted for social and environmental disparities is the principal determinant of T2HIGH inflammation in children with severe asthma. J Allergy Clin Immunol Pract. Published online 2026. doi:10.1016/j.jaip.2026.07.042
2. Barney J. Black children at risk for severe form of asthma, research shows. UVA Health. October 15, 2026. Accessed October 19, 2026. https://www.uvahealth.com/news/black-children-at-risk-for-severe-form-of-asthma-research-shows
3. Hardee IJ, Monuteaux MC, Hoffmann RM, et al. Trends in asthma-related paediatric mortality. Thorax. 2026;81(7):702.
4. Binney S, Flanders WD, Sircar K, Idubor O. Trends in US pediatric asthma hospitalizations, by race and ethnicity, 2012–2020. Prev Chronic Dis. 2024;21:240049. doi:10.5888/pcd21.240049

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