Respiratory Effects of Exposure to Diesel Traffic in Persons with Asthma

TLDR

Road‑traffic air pollution poses a serious health hazard, especially for people with preexisting respiratory disease, and our study demonstrates that ultrafine particles and elemental carbon are consistently linked to reduced lung function in asthma. The study aimed to assess the short‑term effects of diesel‑traffic exposure on lung function and inflammation in adults with mild or moderate asthma. Participants walked 2 hours along Oxford Street and, on a separate occasion, through Hyde Park, while researchers collected real‑time exposure data and performed physiological and immunologic measurements. Walking on Oxford Street caused significant, asymptomatic reductions in FEV1 (up to 6.1%) and FVC (up to 5.4%)—larger than in Hyde Park—and was linked to higher neutrophilic inflammation, airway acidification, and exposure to ultrafine particles and elemental carbon, with effects more pronounced in moderate asthma.

Abstract

Air pollution from road traffic is a serious health hazard, and people with preexisting respiratory disease may be at increased risk. We investigated the effects of short-term exposure to diesel traffic in people with asthma in an urban, roadside environment.We recruited 60 adults with either mild or moderate asthma to participate in a randomized, crossover study. Each participant walked for 2 hours along a London street (Oxford Street) and, on a separate occasion, through a nearby park (Hyde Park). We performed detailed real-time exposure, physiological, and immunologic measurements.Participants had significantly higher exposures to fine particles (<2.5 microm in aerodynamic diameter), ultrafine particles, elemental carbon, and nitrogen dioxide on Oxford Street than in Hyde Park. Walking for 2 hours on Oxford Street induced asymptomatic but consistent reductions in the forced expiratory volume in 1 second (FEV1) (up to 6.1%) and forced vital capacity (FVC) (up to 5.4%) that were significantly larger than the reductions in FEV1 and FVC after exposure in Hyde Park (P=0.04 and P=0.01, respectively, for the overall effect of exposure, and P<0.005 at some time points). The effects were greater in subjects with moderate asthma than in those with mild asthma. These changes were accompanied by increases in biomarkers of neutrophilic inflammation (sputum myeloperoxidase, 4.24 ng per milliliter after exposure in Hyde Park vs. 24.5 ng per milliliter after exposure on Oxford Street; P=0.05) and airway acidification (maximum decrease in pH, 0.04% after exposure in Hyde Park and 1.9% after exposure on Oxford Street; P=0.003). The changes were associated most consistently with exposures to ultrafine particles and elemental carbon.Our observations serve as a demonstration and explanation of the epidemiologic evidence that associates the degree of traffic exposure with lung function in asthma.