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Traffic-related air pollution correlates with adult-onset asthma among never-smokers
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  1. N Künzli1,2,3,4,
  2. P-O Bridevaux5,
  3. L-J S Liu6,7,
  4. R Garcia-Esteban1,3,4,
  5. C Schindler6,
  6. M W Gerbase5,
  7. J Sunyer1,3,4,8,
  8. D Keidel6,
  9. T Rochat5
  1. 1Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain
  2. 2Catalan Institution for Research and Advanced Studies (ICREA), Spain
  3. 3Municipal Institute of Medical Research (IMIM), Barcelona, Spain
  4. 4CIBER en Epidemiología y Salud Pública (CIBERESP), Spain
  5. 5University Hospitals of Geneva, Geneva, Switzerland
  6. 6Institute of Social and Preventive Medicine, University of Basel, Switzerland
  7. 7University of Washington, Seattle, Washington, USA
  8. 8Universitat Pompeu Fabra (UPF), Barcelona, Spain
  1. Dr N Künzli, Center for Research in Environmental Epidemiology (CREAL), C Doctor Aiguader 88, 08003 Barcelona, Spain; kuenzli{at}creal.cat

Abstract

Background: Traffic-related pollution is associated with the onset of asthma in children. Its effect on adult-onset asthma is poorly investigated. The SAPALDIA cohort study was used to investigate associations between the 11-year change (1991–2002) in home outdoor traffic-related particulate matter up to 10 μm in diameter (TPM10) and the incidence of asthma.

Methods: Never-smokers without asthma at baseline aged 18–60 years in 1991 were eligible for inclusion in the study. Subjects reporting doctor-diagnosed asthma at follow-up were considered incident cases. TPM10 at baseline and follow-up was predicted and interpolated to subjects’ place of residence by dispersion models using emission and meteorological data. Cox proportional hazard models for time to asthma onset were adjusted (age, gender, baseline atopy, body mass index, bronchial reactivity, maternal allergies).

Results: Of 2725 never-smokers, 41 reported asthma onset in 2002. Home outdoor TPM10 concentrations improved during the interval (mean −0.6; range −9 to +7.2; IQR 0.6 μg/m3). The incidence of asthma was associated with a change in TPM10. The hazard ratio (1.30; 95% CI 1.05 to 1.61) per 1 μg/m3 change in TPM10 (IQR) was not sensitive to further adjustments (education, workplace exposure, passive smoking, parental asthma or allergies, random area effects, lung function or co-pollutants such as regional, secondary, total PM10 or proximity to busy roads).

Conclusion: The data suggest a role for traffic-related pollution in adult-onset asthma. Space, time and source-specific individual assignment of exposure to traffic-related pollution is a key strength of SAPALDIA. It may explain why findings were statistically significant despite the limited number of new cases. As traffic-related pollution prevails, the finding may be of substantial public health relevance.

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Footnotes

  • Competing interests: None.

  • Funding: Swiss National Science Foundation (grants no 4026-28099, 3347CO-108796, 3247BO-104283, 3247BO-104288, 3247BO-104284, 32-65896.01, 32-59302.99, 32-52720.97, 32-4253.94); Federal Office for Forest, Environment and Landscape; Federal Office of Public Health; Federal Office of Roads and Transport; canton’s government of Aargau, Basel-Stadt, Basel-Land, Geneva, Luzern, Ticino, Zurich; Swiss Lung League; canton’s Lung League of Basel Stadt/Basel Landschaft, Geneva, Ticino and Zurich; Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain; Catalan Institution for Research and Advanced Studies (ICREA), Barcelona, Spain. None of the funding sources had a role in the study design, data collection, analysis and interpretation of the data.

  • ▸ Additional details are published online only at http://thorax.bmj.com/content/vol64/issue8

  • Ethics approval: Ethical approval was obtained from the Swiss Academy of Medical Sciences and the regional ethics committees and written informed consent was obtained from all participants.

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