Outdoor air pollution is associated with rapid decline of lung function in α-1-antitrypsin deficiency

IntroductionOutdoor air pollutants are associated with respiratory morbidity and mortality, but little longitudinal work has been undertaken in this area in chronic obstructive pulmonary disease (COPD). Patients with α-1-antitrypsin deficiency (AATD) typically exhibit faster decline of lung function...

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Published inOccupational and environmental medicine (London, England) Vol. 67; no. 8; pp. 556 - 561
Main Authors Wood, Alice M, Harrison, Roy M, Semple, Sean, Ayres, Jon G, Stockley, Robert A
Format Journal Article
LanguageEnglish
Published London BMJ Publishing Group Ltd 01.08.2010
BMJ Publishing Group
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Summary:IntroductionOutdoor air pollutants are associated with respiratory morbidity and mortality, but little longitudinal work has been undertaken in this area in chronic obstructive pulmonary disease (COPD). Patients with α-1-antitrypsin deficiency (AATD) typically exhibit faster decline of lung function than subjects with usual COPD and thus represent a group in whom studies of factors influencing decline may be more easily clarified.MethodsDecline of FEV1 and KCO in subjects of the PiZZ genotype from the UK AATD registry were studied. Pollution levels (PM10, ozone, sulphur dioxide, nitrogen dioxide) during the exposure window were extracted from GIS maps, matching the measurement to each patient's home address. Clinical predictors of decline were sought using generalised estimating equations, and pollutants added to these subsequently. Single pollutant models were used due to multicollinearity.ResultsIn the FEV1 decline analysis, higher baseline FEV1 was associated with rapid decline of FEV1 (p<0.001). High PM10 exposure predicted more rapid decline of FEV1 (p=0.024). In a similar analysis for KCO decline, higher baseline KCO predicted rapid decline (p<0.001) as did higher exposure to ozone (p=0.018). High PM10 exposure also showed a trend towards this effect (p=0.056).ConclusionsExposure to ozone and PM10 predicts decline of lung function in AATD.
Bibliography:istex:AE3D813F87608B01F0E41D3E575F3A07944088EA
PMID:20519748
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ArticleID:oemed47589
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ISSN:1351-0711
1470-7926
DOI:10.1136/oem.2009.047589