Background and aim: Systemic inflammation is one potential mechanism underlying negative impact of air pollution on lung function. We examined the interplay between air pollution exposure and inflammation-related proteins on infant lung function.

Methods: In the EMIL birth cohort from Stockholm (n=82), dynamic spirometry, along with plasma levels of 92 systemic inflammation-related proteins (Olink Proseek Multiplex Inflammation panel) were measured in infants aged six months. Time-weighted average exposure to particles with an aerodynamic diameter of <10 µm (PM₁₀), <2.5 µm (PM_2.5), and nitrogen dioxide (NO₂) at residential addresses from birth and onwards was estimated via validated dispersion models. To characterize the abnormality of inflammation-related protein profile, for each protein in each infant, we calculated the relative deviance of the protein level from age- and sex-specific median in terms of its age- and sex-specific interquartile range (IQR), followed by computing the absolute value of the smallest relative deviance, ?minimum absolute deviance?. Using linear regression models, interaction of air pollution and the abnormal inflammatory profile on lung function was estimated on the additive scale.

Results: For 0.1 increment in minimum absolute deviance, one IQR increase in PM₁₀ was associated with 85.9 ml (95% CI: -122.9, -48.9) additional decrease in FEV_0.5, and 72.3 ml (95% CI: -121.5, -23.2) additional decrease in FVC. Similar results were obtained with PM_2.5, while less apparent for NO₂.

Conclusions: Early life air pollution exposure and abnormal inflammation-related protein profiles may interact synergistically towards lower lung function in infants.