Abstract

Introduction: Exposure to ultrafine particles (UFP, particles with aerodynamic diameter less than 100nm) is associated with reduced pulmonary function and increased airway inflammation in asthmatics. A recent study showed that UFP number concentrations downwind of the Los Angeles International Airport (LAX) are elevated 4- to 5- fold, putting a large fraction of the population at risk. Methods: We conducted a randomized crossover study of 21 non-smoking adults with mild to moderate asthma in Nov-Dec 2014 and May-Jul 2015. Participants conducted scripted, mild walking activity for 2 hours, resting every 15 minutes, on 2 occasions, in public parks inside (exposure) and outside (control) of the LAX high UFP impact zone. Spirometry (FVC, FEV1), multiple flow exhaled nitric oxide (FeNO, at 30, 50, 100 and 300 ml/s), and blood draws for inflammatory cytokines (hsIL-6, sTNFrII, vWF, fibrinogen) were performed pre- and post- exposure. Personal UFP particle numbers (PN) and lung deposited surface area (LDSA) and stationary UFP PN, black carbon (BC), particle-bound PAHs (PB-PAH), ozone (O3), and particulate matter (PM2.5) mass were measured. Results: A high contrast of ~ 30,000 #/cm3 was achieved with mean (std) PN concentrations at the exposure and control site of 46,062 (38,932) and 17,160 (22,590) #/cm3, and LDSA of 58.6 (35.2) and 27.7 (26.2) cm2, respectively. Median particle size was 28.8nm (std 14.6) at the LAX site. The increase in hsIL-6, a pro-inflammatory cytokine, and reduction in FEV1 were larger under LAX exposure conditions. Preliminary FeNO results from the first phase (N=9) show a greater increase in distal alveolar NO concentration, CANO, in the exposure scenario compared to the control. Analyses using linear mixed effects models are underway to estimate the magnitude of the effect of UFP exposure and dose on these outcomes. Conclusions: Preliminary data suggest a relationship between airport-related UFP exposures and adverse lung effects in asthmatics.

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