Abstract Rationale Among atmospheric pollutants, particulate matter (PM) has the greatest impact on human health. In the ASTHMA-FENOP study (MCIN PID2020-114787RB-I00), personalised exposure to PM was determined using personal samplers, and the oxidative potential of this PM (PM-OP) was specifically measured for each participant. SEPAR grants 1383/23 and 1616/24 have made it possible to characterise systemic oxidative stress through five different markers, and to incorporate a control group (without asthma) to compare the results, with the hypothesis that higher airborne pollution is associated with greater oxidative stress and leads to greater airway and systemic inflammation. Methods Cross-sectional exploratory study in which 44 asthmatic patients and 37 age- and sex-matched controls were recruited and asked to wear a personal sampler for 24 hours (visit 1). At visit 3 (lag1, 25-48 hours after returning the sampler), the fraction of nitric oxide in exhaled air (FeNO) was determined as a marker of airway inflammation, serum IL-6 levels as a marker of systemic inflammation, and levels of protein carbonyl content, oxidized fraction of LDL lipoprotein (OxLDL), 8-hydroxydeoxyguanosine, superoxide anion production, and glutathione as markers of systemic oxidative stress. The values for each variable were dichotomized based on the median, and adjusted odds ratios (aORs) were calculated afther adjustding for sex, age, educational level, or body mass index among others using logistic regression. Results No evidence was found of an association between higher PM-OP and elevated levels of any of the oxidative stress markers. In contrast, we found an effect of higher PM-OP on higher systemic inflammation (IL-6). When compared asthmatic and controls we observed higher levels of OxLDL in asthmatics with a mean difference of 42,932.44 ng/mL (p 0.001). Finally, a statistically significant association independent of PM-OP or FeNO levels was found between OxLDL and IL-6: aOR= 7.90; 95%CI (1.40-44.68). This association was maintained when stratified in both asthmatics and controls. Conclusions Our findings support a role of PM-OP on systemic inflammation. In contrast, the oxidative stress generated by the inflammatory cells themselves seems to be more relevant than that generated by airborne PM-OP explaining the higher levels of OxLDL among asthmatics. Our association between OxLDL and IL-6, described in literature, would support the internal validity of our findings. Overall, our results support the idea that asthma is a molecularly heterogeneous disease mediated by the activation of inflammatory cells, for which airborne PM-OP, oxLDL, and IL-6 may have potential clinical implications. This abstract is funded by: This work was supported by the Spanish Society of Pneumology (SEPAR Nº 1383/23 and 1616/24) and the Spanish Ministry of Science and Innovation (Project PID2020-114787RBI00, funded by MCIN/AEI/10.13039/501100011033 and “ERDF A way of making Europe”)
Santibáñez et al. (Fri,) studied this question.