Abstract Body (Do not enter title and authors here): Background: Ambient fine particulate matter (PM_2.5) air pollution is associated with inflammatory conditions in the lungs, heart, and circulation. Inflammation may be causal in poor health outcomes, especially for people with existing disease. This study evaluated the association PM_2.5 levels with concentrations of 115 plasma inflammatory proteins.
Methods: Patients with heart failure (HF) with preserved ejection fraction (HFpEF, n=44) and HF-free controls (n=35) from the Intermountain INSPIRE registry (NCT02450006) were tested for 115 targeted proteins (EMD Millipore and ELISA). HFpEF cases and controls were stratified by ambient PM_2.5 levels for low (PM_2.5 ≤7 µg/m³) and higher exposure (PM_2.5 >20 µg/m³). PM_2.5 levels on the day of sample collection were evaluated, as well as 3-day and 7-day PM_2.5 moving averages (mAvg) of the concurrent day plus 2 or 6 immediately previous days. Samples drawn on days with PM_2.5 = 7.1-20.0 µg/m³ were excluded.
Results: Patients with HFpEF averaged 74.6±11.7 years of age (2.8 years since HF diagnosis) and 65.9% were female (controls: 72.0±8.7 years, 62.9% female). In HFpEF cases (Table), PM_2.5 >20 µg/m³ on the sample collection day was associated with higher IL-18 (p<0.001 vs. ≤7 µg/m³) and C-C motif chemokine ligand 27 [CCL27, also known as cutaneous T cell-attracting chemokine (CTACK)] (p<0.001 vs. ≤7 µg/m³), with a trend for TNF-α (p=0.012). The 3-day PM_2.5 mAvg was significant for IL-18 and CCL27, while CCL27 remained significant for the 7-day mAvg (Table). In controls, none of the 115 biomarkers differed based on PM_2.5 levels. Age did not differ in cases or controls by PM_2.5 category.
Conclusions: In a pilot study evaluating the inflammatory response to air pollution, CCL27 and IL-18 were higher in patients with HFpEF during short-term PM_2.5 elevations. Inflammatory biomarkers were not different based on PM_2.5 levels in people free of HF. Short-term PM_2.5 elevations may induce inflammation and these findings suggest that people with HFpEF struggle to restore homeostasis.