You are here:
Diesel Exhaust Exposure and Nasal Response to Attenuated Influenza in Normal and Allergic Volunteers
Citation:
Noah, T. L., K. Horvath, C. Robinette, H. Zhang, H. Zhou, D. DIAZ-SANCHEZ, AND I. JASPERS. Diesel Exhaust Exposure and Nasal Response to Attenuated Influenza in Normal and Allergic Volunteers . AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE. American Thoracic Society, New York, NY, 185(2):179-85, (2012).
Impact/Purpose:
Test whether acute exposure to diesel modifies inflammatory responses to influenza virus in normal and allergic humans
Description:
Rationale: Diesel exhaust enhances allergic inflammation, and pollutants are associated with heightened susceptibility to viral respiratory infections. The effects of combined diesel and virus exposure in humans are unknown. Objective: Test whether acute exposure to diesel modifies inflammatory responses to influenza virus in normal and allergic humans. Methods: We conducted a double-blind, randomized, placebo-controlled study of nasal responses to live attenuated influenza virus in normal volunteers and allergic rhinitics exposed to diesel (100 ug/m3) or clean air for 2 hr, followed by standard dose of virus and serial nasal lavages. Endpoints were inflammatory mediators (ELISA) and virus quantity (qRT-PCR). To test for exposure effect, we used multiple regression with exposure group (diesel vs. air) as the main explanatory variable and allergic status as an additional factor. Measurements and main results: Baseline levels of mediators did not differ among groups. For most post-virus nasal cytokine responses, there was no significant diesel effect, and no significant interaction with allergy. However, diesel was associated with significantly increased interferon-y responses (p=0.02), with no interaction with allergy in the regression model. Eotaxin-1 (p=0.01), eosinophil cationic protein (p<0.01), and influenza RNA sequences in nasal cells (p=0.03) were significantly increased with diesel exposure, linked to allergy. Conclusions: Short term exposure to diesel exhaust leads to increased eosinophil activation and increased virus quantity after virus inoculation in allergic rhinitics. This is consistent with previous literature suggesting a diesel "adjuvant" effect promoting allergic lnflarnmatlon, and our data further suggest this change may be associated with reduced virus clearance.
