A131: Associations of Short–Term Pollution Exposures With Childhood Autoimmune Disease. Issue 11 (March 2014)

• Record Type: Journal Article
• Authors: Zeft, Andrew; Pope, C. Arden
• Is Part Of: Arthritis & rheumatology. Volume 66:Issue 11(2014)supplement
• Page Start: S172
• Page End: S172
• Publication Date: 2014-03
• Subjects: Arthritis -- Periodicals; Rheumatism -- Periodicals; 616.72
• DOI: 10.1002/art.38552
• Languages: English
• ISSNs: 2326-5191

Abstract

Abstract : Background/Purpose: Fine particulate matter (aerodynamic diameter less than or equal to a 2.5–mm cut point, PM2.5 ) is a measurable component of ambient urban pollution. Our preliminary data suggests that short‐term PM2.5 exposures are associated with the clinical presentation of Juvenile idiopathic Arthritis (JIA) in young children (1 ). In this EPA funded project, we are further testing the hypothesis that clinical autoimmune disease presentation and exacerbation is associated with exposures to short–term pollution, focusing on PM2.5. We are establishing associations between short–term PM2.5 exposure and the clinical onset of systemic onset Juvenile Idiopathic Arthritics (soJIA) and Kawasaki Disease (KD) and the clinical exacerbation of Henoch Schonlein Purpura (HSP). Methods: Cases are from existing physician operated SoJIA and KD datasets diagnosed in United States and Canadian metropolitan regions. Cases of HSP arise from a US national hospital database (Children's Hospital Association). The study utilizes a case–crossover study design to define associations of short‐term PM2.5 with the event dates of symptom onset of soJIA and KD (fever onset) and of hospitalization for HSP exacerbation from metropolitan regions, stratified by parameters of disease activity. Results: We have assembled PM2.5 exposure measurements from urban monitors and have carefully imputed PM2.5 to provide day–to–day temporal variability and resolution for reliable time series indexes of pollution exposures for each metropolitan area (Philadelphia, Boston, Toronto, Chicago, Atlanta, Cincinnati, San Diego, Salt Lake City, Denver, Cleveland). To date, case–crossover analysis results establishing risk of the event dates of clinical symptom onset and hospitalization exacerbation for the pediatric rheumatic diseases under study are preliminary. Conclusion: Well–constructed, environmental epidemiology studies examining the triggers of disease onset and exacerbation in pediatric rheumatic diseases are few and far between. Findings from this Environmental Protection Agency funded project will have a significant impact on the field of particulate induced environmental epidemiology research of autoimmune disease.