Respiratory Effects of Exposure to Diesel Traffic in Persons with Asthma
James McCreanor, M.R.C.P., Paul Cullinan, M.D., Mark J. Nieuwenhuijsen, Ph.D., James Stewart-Evans, M.Sc., Eleni Malliarou, M.Sc., Lars Jarup, Ph.D., Robert Harrington, M.S., Magnus Svartengren, M.D., In-Kyu Han, M.P.H., Pamela Ohman-Strickland, Ph.D., Kian Fan Chung, M.D., and Junfeng Zhang, Ph.D.
Background Air pollution from road traffic is a serious healthhazard, and people with preexisting respiratory disease maybe at increased risk. We investigated the effects of short-termexposure to diesel traffic in people with asthma in an urban,roadside environment.
Methods We recruited 60 adults with either mild or moderateasthma to participate in a randomized, crossover study. Eachparticipant walked for 2 hours along a London street (OxfordStreet) and, on a separate occasion, through a nearby park (HydePark). We performed detailed real-time exposure, physiological,and immunologic measurements.
Results Participants had significantly higher exposures to fineparticles (<2.5 µm in aerodynamic diameter), ultrafineparticles, elemental carbon, and nitrogen dioxide on OxfordStreet than in Hyde Park. Walking for 2 hours on Oxford Streetinduced asymptomatic but consistent reductions in the forcedexpiratory volume in 1 second (FEV1) (up to 6.1%) and forcedvital capacity (FVC) (up to 5.4%) that were significantly largerthan the reductions in FEV1 and FVC after exposure in Hyde Park(P=0.04 and P=0.01, respectively, for the overall effect ofexposure, and P<0.005 at some time points). The effects weregreater in subjects with moderate asthma than in those withmild asthma. These changes were accompanied by increases inbiomarkers of neutrophilic inflammation (sputum myeloperoxidase,4.24 ng per milliliter after exposure in Hyde Park vs. 24.5ng per milliliter after exposure on Oxford Street; P=0.05) andairway acidification (maximum decrease in pH, 0.04% after exposurein Hyde Park and 1.9% after exposure on Oxford Street; P=0.003).The changes were associated most consistently with exposuresto ultrafine particles and elemental carbon.
Conclusions Our observations serve as a demonstration and explanationof the epidemiologic evidence that associates the degree oftraffic exposure with lung function in asthma.
Source Information
From the National Heart and Lung Institute, Imperial College, and Royal Brompton Hospital (J.M., P.C., K.F.C.) and the Department of Epidemiology and Public Health, Imperial College (J.S.-E., E.M., L.J.) — all in London; the Center for Research in Environmental Epidemiology, Barcelona (M.J.N.); the University of Medicine and Dentistry of New Jersey School of Public Health, Piscataway (R.H., I.-K.H., P.O.-S., J.Z.); and the Department of Public Health Sciences, Karolinska Institutet, Stockholm (M.S.).
Address reprint requests to Dr. Cullinan at the Department of Occupational and Environmental Medicine, National Heart and Lung Institute, 1b Manresa Rd., London SW3 6LR, United Kingdom, or at p.cullinan{at}imperial.ac.uk.
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