Abstract
Background: Mortality and cardiorespiratory diseases are well-documented effects of atmospheric pollutants. Because epigenetic mechanisms are identified as interaction factors between environmental exposures and gene expression, as well as pathogenic factors of impaired immune tolerance, it seems relevant to study autoimmune diseases in relation to air pollution. Methods: To study whether daily increases of particulate matter (PM10, PM2.5) and nitrogen dioxide (NO2) are associated with exacerbations of autoimmune diseases, a total of 23,898 residents of Rome (Italy) who were diagnosed in 2003-2014 with Hashimoto thyroiditis, systemic lupus erythematosus, rheumatoid arthritis, psoriasis, and multiple sclerosis were enrolled. Exacerbations were defined as subsequent hospitalizations for the initial disease or its complications, or a different autoimmune disease, and as dose increases or time reductions between drug prescriptions for autoimmune diseases. Data were analyzed for 2006-2014. Daily concentrations of PM10, PM2.5, and NO2 in Rome were available from a fixed monitoring network, during 2006-2014. A time-stratified case-crossover study was carried out. Results: All air pollutants were associated with more frequent changes than usual in treatment for all autoimmune diseases; the greatest increases in risk were observed for PM2.5 (10 μg/m3 increase) in thyroiditis (3.31% [2.21%, 4.2%]), lupus (3.55% [0.70%, 6.49%]), arthritis (4.93% [2.11%, 7.83%]), and psoriasis (4.04% [0.21%, 8.01%]). No associations were observed for hospitalizations for all studied diseases, whereas changes toward lower corticosteroids' dose in multiple sclerosis and less effective corticosteroids' forms in psoriasis were observed. Conclusions: PM2.5 and NO2 might exacerbate autoimmune diseases. As detected with treatment changes especially in younger patients.
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Faustini, A., Renzi, M., Kirchmayer, U., Balducci, M., Davoli, M., & Forastiere, F. (2018). Short-term exposure to air pollution might exacerbate autoimmune diseases. Environmental Epidemiology, 2(3). https://doi.org/10.1097/EE9.0000000000000025
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