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Increased lung resistance after diesel particulate and ozone co-exposure not associated with enhanced lung inflammation in allergic mice

Exposure to diesel exhaust particulate matter (DEP) 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 tend to be simultaneously elevated, we investigated the possible synergistic effect of these agents on the exacerbation of allergic airways disease in mice. Male BALB/c mice were sensitized ip with ovalbumin (Ova) or vehicle only, then exposed once per week for 4 wk via nose-only inhalation (4 h) to the PM2.5 fraction of 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) and elastance (EL) in response to methacholine (MCh) aerosol challenge. DEP exposure did not enhance the Ova-induced increase in pulmonary cell infiltration, indicators of injury, or RL and EL. O3 exposure enhanced the Ova-induced increase in inflammatory cell infiltration and N-acetylglucosaminidase (NAG) in the lung, but had no effect on RL or EL. DEP co-exposure significantly attenuated the O3-induced increase in cell infiltration and indicators of injury; co-exposure had no effect on EL relative to air-exposed Ova-sensitized mice. However, only DEP-O3 co-exposure significantly increased the Ova-induced increase in RL. Thus, O3 and DEP co-exposure exacerbated airways hyperresponsiveness, a response that was not associated with parallel increases in pulmonary inflammation and one that may be mediated by a unique mechanism.