Moreover, out of a number of inflammatory mediators, known to be involved in AE-IPF pathogenesis, that we examined in the peripheral blood, we detected the following in AE-IPF patients: 1) changes in IL-4 positively associated with an increase in long-term personal exposure to O3 but inversely with an increase in NO2, PM10 or PM2.5, 2) an indicative positive change in the levels of IL-13 and osteopontin with increased O3 and 3) an inverse association between changes in osteopontin and increased exposure in particles (PM10 or PM2.5). The gene discussed is IL4; the disease is idiopathic pulmonary fibrosis.