Association of early-life dust allergens and endotoxin with childhood asthma and lung function: An analysis of the CHILD study

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Rationale: Childhood asthma is characterized by altered lung function and airway inflammation, thought to result from complex gene-environment interactions, especially with allergens. Previous studies show inconsistent associations between allergen exposure and asthma. Objectives: We aimed to examine the longitudinal relationship between indoor allergen exposure during infancy with subsequent asthma and spirometry, and potential effect modification by genetic factors. Methods: Data from a subcohort of the CHILD study with analyzed dust samples (including Can f1 (dog), Fel d1 (cat), and endotoxin) and physician diagnosed asthma or spirometry were used to examine relationships between dust analytes at 3 months and asthma and, separately, FEV1 at 5 years, including potential effect modification by genetic factors using polygenic scores (PGSs). Results: Among 1050 children with dust samples (mean age 3.94 months), 6.6% developed asthma by age 5 years. In an adjusted multivariable model, higher Can f1 significantly decreased the risk of asthma (OR 0.52, 95% CI 0.25, 0.98). Compared to children exposed to low Can f1, those exposed to high Can f1 had significantly higher FEV1 z-scores (β=0.23, 95% CI 0.06, 0.40) regardless of asthma status. There was a significant gene-environment interaction between Can f1 and PGSs on FEV1 (β=-0.14, 95%CI -0.32, 0.03). Conclusions: In a general population birth cohort, early-life exposure to high levels of Can f1 was associated with improved lung function and was protective against asthma at age 5. There were significant gene-environment interactions in the relationship between Can f1 and PGSs on lung function.

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