Background The associations between exposure to air pollution and asthma control are not well known. The objective of this study was to assess the association between long-term exposure to NO2, O3 and PM10 and asthma control in the follow-up of the Epidemiological study on the Genetics and Environment of Asthma (EGEA2) (2003–2007).
Methods Modelled outdoor NO2, O3 and PM10 estimates were linked to each residential address using the 4 km grid air pollutant surface developed by the French Institute of Environment in 2004. Asthma control was assessed in 481 subjects with current asthma using a multidimensional approach following the 2006–2009 Global Initiative for Asthma guidelines. Multinomial and ordinal logistic regressions were conducted adjusted for sex, age, body mass index, education, smoking and use of inhaled corticosteroids. The association between air pollution and the three domains of asthma control (symptoms, exacerbations and lung function) was assessed. ORs are reported per IQR.
Results Median concentrations (in micrograms per cubic metre) were 32 (IQR 25–38) for NO2 (n=465), 46 (41–52) for O3 and 21 (18–21) for PM10 (n=481). In total, 44%, 29% and 27% had controlled, partly controlled and uncontrolled asthma, respectively. The ordinal ORs for O3 and PM10 with asthma control were 1.69 (95% CI 1.22 to 2.34) and 1.35 (95% CI 1.13 to 1.64), respectively. When including both pollutants in the same model, both associations persisted. Associations were not modified by sex, smoking status, use of inhaled corticosteroids, atopy, season of examination or body mass index. Both pollutants were associated with each of the three main domains of control.
Conclusions The results suggest that long-term exposure to PM10 and O3 is associated with uncontrolled asthma in adults, defined by symptoms, exacerbations and lung function.
- Air pollution
- asthma control
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EGEA cooperative group. Coordination: F Kauffmann; F Demenais (genetics); I Pin (clinical aspects). Respiratory epidemiology: Inserm U 700, Paris M Korobaeff (EGEA1), F Neukirch (EGEA1); Inserm U 707, Paris: I Annesi-Maesano; Inserm CESP/U 1018, Villejuif: F Kauffmann, N Le Moual, R Nadif, MP Oryszczyn; Inserm U 823, Grenoble: V Siroux Genetics: Inserm U 393, Paris: J Feingold; Inserm U 946, Paris: E Bouzigon, F Demenais, MH Dizier; CNG, Evry: I Gut, M Lathrop. Clinical centers: Grenoble: I Pin, C Pison; Lyon: D Ecochard (EGEA1), F Gormand, Y Pacheco; Marseille: D Charpin (EGEA1), D Vervloet; Montpellier: J Bousquet; Paris Cochin: A Lockhart (EGEA1), R Matran (now in Lille); Paris Necker: E Paty, P Scheinmann; Paris-Trousseau: A Grimfeld, J Just. Data and quality management: Inserm ex-U155 (EGEA1): J Hochez; Inserm CESP/U 1018, Villejuif: N Le Moual, Inserm ex-U780: C Ravault; Inserm ex-U794: N Chateigner; Grenoble: J Ferran.
Funding The EGEA study was supported in part by grants from Merck Sharp & Dohme (MSD); Hospital Program of Clinical Research (PHRC)-Paris; National Research Agency—health environment, health work program; National Research Agency (ANR)—Biological collections for health program; French Agency of Health, Safety, Environment and Work (AFSSET), Agence de l'Environnement et de la Maitrise de l'Energie (ADEME), the National Scientific Committee of the Medico-technology support at home (AGIR à dom) and the Isere Committee against Respiratory Diseases (COMARES).
Competing interest None to declare.
Patient consent Obtained.
Ethics approval This study was conducted with the approval of the Cochin Royal Hospital, Paris, for the first survey (EGEA1); Necker Enfants Malades Hospital, Paris, for the second survey (EGEA2).
Provenance and peer review Not commissioned; externally peer reviewed.
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