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Effects of diesel exhaust on influenza-induced nasal inflammation
Citation:
NOAH, T., K. Horvath, C. Robinette, AND I. JASPERS. Effects of diesel exhaust on influenza-induced nasal inflammation. Presented at American Thoracic Society Annual Conference, San Diego, CA, May 05 - 20, 2009.
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Description:
Title: Effects of Diesel Exhaust on Influenza-Induced Nasal Inflammation T L Noah, MD1,2, K Horvath, BS3, C Robinette, RN2, 0 Diaz Sanchez, PhD4 and I Jaspers, PhD1,2. 1UNC Dept. of Pediatrics, United States; 2UNC Center for Environmental Medicine, Asthma and Lung Biology, United States; 3UNC Program in Toxicology, United States and 4US EPA, United States. Exposure to diesel exhaust (DE) may exacerbate allergic or asthmatic disease, but mechanisms are unclear. With milder exposures, a second stimulus such as viral infection may elicit DE effects on host defense. Hypothesis: DE suppresses live attenuated influenza virus (LAIV)-induced inflammatory and antiviral responses. Study design: Randomized, double blinded study of the effects of DE (100 ug/m3 x 2 hr, DE source idling truck) vs, air, on LAIV-induced nasal inflammation in healthy young adults. Protocol: Chamber exposure followed by LAIV inoculation (same day), serial followup nasal lavages post exposure day. Primary endpoints: change in IL-6 and IP-l0 measured by ELISA in nasal lavage fluids (NLF) compared to baseline. Other mediators measured as secondary endpoints. Results: 12 subjects have completed the protocol. LAIV induced increased IL-6 and IP-l0 lof2 1012412008 12:33 PM stract Pi, http://www.cail4abstracts.comlatslpreview.php?abs=~:) J 104.0 dtJit~" ,; ~"-4. declining back toward baseline by day 9. DE appeared to suppress LAIV-induced Il-6 most significantly on day 2, when DE-exposed subjects had a 1.2:tl0.4 fold increase, vs. 4.l:t1.5 for air. There was little effect of DE on IP-I0. LAIV-induced ECP increases appeared to be augmented in the DE exposed group by day 4 (7.7:1:3.3 fold Increase, YS. L4:!:O.5). Both Il-6 and ECPeffects were more marked among subjects with history of allergic rhinitis. Conclusions: DE may alter nasal inflammatory responses to respiratory virus. The net effect of these changes on viral replication and immunity are unclear, but merit further investigation. We speculate that exposure to DE may alter antiviral innate and acquired immunity, affecting risk for infection particularly among individuals with allergy. Funded in part by US EPA Cooperative Agreement CR83346301, but has not been subjected to review and does not necessarily reflect EPA policy.