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The Variable Effects of Ozone and/or Diesel Particulate Inhalation Exposure on Allergic Airways Responses in Mice
Citation:
FARRAJ, A., J. R. LEHMANN, E. BOYKIN, A. D. LEDBETTER, AND S. H. GAVETT. The Variable Effects of Ozone and/or Diesel Particulate Inhalation Exposure on Allergic Airways Responses in Mice. Presented at American Thoracic Society 2008 International Conference, Toronto, ON, CANADA, May 16 - 21, 2008.
Impact/Purpose:
Ozone and diesel particulate co-exposure have different effects on allergic airways disease in mice than exposure to either pollutant alone.
Description:
Exposure to diesel exhaust particle matter (DEP) associated with the combustion of diesel fuel exacerbates asthma. Likewise, similar effects have been reported with exposure to the oxidizing air pollutant ozone (O3). Since levels of both pollutants in ambient air are elevated in areas with high-volume automobile traffic, we investigated the possible synergistic effect of these agents in combination on the exacerbation of allergic airways disease in mice. Male BALB/c mice were sensitized i.p. with ovalbumin (Ova) or vehicle only, then exposed once per week for 4 weeks via nose-only inhalation to the PM2.5 fraction of NIST SRM-2975 DEP (2 mg/m3), O3 (0.5 ppm), DEP and O3, or filtered air, and then challenged with aerosolized ovalbumin. Ova sensitization in air-exposed mice enhanced pulmonary inflammatory cell infiltration, several indicators of injury in the lung (lactate dehydrogenase, albumin and total protein), and lung resistance (RL) in response to methacholine aerosol challenge. DEP exposure did not enhance the Ova-induced increase in pulmonary cell infiltration, indicators of injury, nor RL. O3 exposure enhanced the Ova-induced increase in inflammatory cell infiltration and protein in the lung, but had no effect on RL. DEP and O3 co-exposure did not significantly enhance the Ova-induced increase in cell infiltration into the lung, nor any indicators of injury relative to air-exposed Ova-sensitized mice. However, RL was increased to a greater degree in Ova-sensitized DEP-O3 mice than in all other exposure groups. Thus, O3 and DEP co-exposure exacerbates pulmonary airways resistance, a response independent of pulmonary inflammation that was not achieved with exposure to either pollutant alone, suggesting that the enhancement with O3 and DEP co-exposure results from a distinct mechanism.