Biomarkers of inflammation associated with radon exposure in the School Inner-City Asthma Study (SICAS)

Abstract

Background

Radon is an omnipresent radioactive gas recently reported to be associated with increased asthma morbidity.

Objectives

We aimed to identify biomarkers associated with radon exposure and hypothesized elevated radon exposure to be associated with increased inflammatory biomarker levels in an exploratory analysis.

Methods

In 137 schoolchildren with asthma in the School Inner-City Asthma Study, we assessed estimated radon exposure (1-month averaged radon) by a spatiotemporal model and 46 inflammatory biomarker outcomes, adjusting for copollutants (particulate matter with diameter ≤2.5 μm, NO₂, O₃) and performed mixed-effect regression analysis. Causal mediation analysis was used to determine the association between radon exposure and absolute eosinophil count.

Results

In a total of 137 observations, we found a positive association with radon exposure and IL-5, a T_H2-cell cytokine known to recruit eosinophils to asthmatic airways. Higher radon was significantly associated with a greater increase in IL-5 compared to low radon exposure (observations = 137; 1-month moving radon average [% change = 13.4%; 95% CI: 0.4%-28.0%; P = .044]). Mediation analysis revealed an indirect effect of IL-5 (β = 0.006; 95% CI:0.001-0.012; P = .024) on the association between radon exposure and absolute eosinophil count. This suggests the effect of radon on eosinophil count is mediated through IL-5.

Conclusions

Radon is a potential novel, modifiable risk factor for asthma recently reported to be associated with asthma morbidity. This work identifies important biological disease pathways via biomarkers that may be central to the exposure-outcome relationship.