Diesel exhaust exposure enhances the ozone induced airway inflammation in healthy humans

¹ Dept of Respiratory Medicine and Allergy, University Hospital, Umeå, Sweden

^* To whom correspondence should be addressed. E-mail: jenny.bosson{at}gmail.com.

	Abstract

Exposure to particulate matter (PM) and ozone (O₃) cause adverse airway reactions. Individual pollutant effects are often addressed separately, despite co-existing in ambient air. The present investigation was performed to study the effects of sequential exposures to diesel exhaust (DE) and O₃ on airway inflammation in human subjects.

Healthy subjects underwent bronchoscopy with bronchoalveolar lavage (BAL) and bronchial wash (BW) sampling on two occasions; once following a DE exposure (PM₁₀ 300 µg·m^-3) with a subsequent exposure to O₃ (0.2 ppm) five hours later. The other bronchoscopy was performed after a filtered air exposure followed by an O₃ exposure, using an identical protocol. Bronchoscopy was performed 24 hours after the start of the initial exposure.

Significant increases in neutrophil and macrophage numbers were found in (BW) after DE followed by O₃ exposure, vs. air followed by O₃ exposure (p<0.01 and p<0.05, respectively). DE pre-exposure also raised eosinophil protein X (EPX) levels in BAL as compared with air (p<0.05).

The study indicates additive effects of DE on the O₃-induced airway inflammation. Together with similar results from a recent study with sequential diesel exhaust and ozone exposures, the present data stress a need to consider the interaction and cumulative effects of different air pollutants.