Protective effects of dog allergen and endotoxin for lung function and asthma.

Abstract

Childhood asthma is characterized by altered lung function and airway inflammation that is thought to result from complex gene-environment interactions, especially with allergens. However, previous studies have shown inconsistent associations between allergen exposure and asthma. We aimed to examine the longitudinal relationship between indoor allergen exposure during infancy with subsequent asthma and spirometry and the potential effect modification by genetic factors. Data from a subcohort of the CHILD (Canadian Healthy Infant Longitudinal Development) study with analyzed dust samples (including Canis familiaris 1 [dog], Felinus domesticus 1 [cat], and endotoxin) and physician-diagnosed asthma or spirometry data were used to examine the relationships between allergen levels in dust analytes at age 3 months and asthma and, separately, spirometry data at age 5 years, including potential effect modification by genetic factors obtained by using lung function polygenic scores (PGSs). Of 1050 children with dust samples, 6.6% developed asthma by age 5 years. In an adjusted multivariable model, higher Can f 1 level significantly decreased the risk of asthma (odds ratio = 0.52 [95% CI = 0.25-0.98]). Independently, children exposed to high levels of Can f 1 had significantly higher FEV₁z scores (β = 0.23 [95% CI = 0.06-0.40]), regardless of asthma status. In the gene-environment analyses, there were significant effects of gene-environment interactions in the relationship between Can f 1 and PGS on lung function, independent of asthma status. In a general population birth cohort, early-life exposure to high levels of Can f 1 was associated with improved lung function and protection against asthma at age 5 years. Furthermore, exposure to high levels of Can f 1 may modulate lung function in individuals with low PGSs.