The effect of long-term personal air pollution exposure on the inflammatory mediators in Idiopathic Pulmonary Fibrosis

Abstract

<b>Background:</b> Air pollution affects idiopathic pulmonary fibrosis (IPF) patients and is a risk factor for IPF-Acute-Exacerbation (IPF-AE). Pathogenetic mechanisms could implicate pathways of tissue regeneration and repair following injury. <b>Aim and objectives:</b> To examine the association of long-term air pollution exposure with inflammatory mediators involved in lung repair, in IPF and AE-IPF. <b>Methods:</b> Consecutive IPF patients referred to our Department from October 2013 to June 2019 were included. Diagnoses were based on international guidelines. Long-term personal air pollution exposures were assigned to each patient retrospectively, for O3, NO2, PM2.5, PM10 based on geo-coded residential addresses. Inflammatory mediators (IL-1a, IL-1b, IL-4, IL-5, IL-6, IL-8, IL-10, IL-13, active TGF-β, TNFa, CCL2, CCL3, CCL-18, MMP-1, MMP-7, MMP-9, osteopontin) were measured in the peripheral blood by ELISA. Linear regression models were used adjusting for confounders. <b>Results:</b> 118 IPF patients (mean age 72±8.3 years) were included. In AE-IPF, a 10μg/m3 increase in O3 was significantly positively associated with 40.4% change of IL-4 (p=0.011) and marginally with 40% &amp;amp; 62.2% changes of IL-13 (p=0.052) and osteopontin (p=0.097). PM2.5, PM10 and NO2 were inversely associated with 50.6, 50.8 &amp;amp; 21.7% changes of IL-4 (p=0.003, p=0.003, p=0.022, respectively) and 73.2, 74.6 &amp;amp; 32.4% changes of osteopontin (p=0.024, p=0.022, p=0.097, respectively). In stable IPF patients, PM2.5 and PM10 were positively associated with an increase in the 76% changes of IL-13 (p=0.059, p=0.058, respectively). <b>Conclusion:</b> Our findings support an association of IL-4, IL-13 and osteopontin with IPF-AE related to air pollution long-term exposure. Discrepancies in the impact of different pollutants need further investigation.