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

Abstract

Outdoor 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 alpha-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. Decline of FEV(1) and KCO in subjects of the PiZZ genotype from the UK AATD registry were studied. Pollution levels (PM(10), 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. In the FEV(1) decline analysis, higher baseline FEV(1) was associated with rapid decline of FEV(1) (p<0.001). High PM(10) exposure predicted more rapid decline of FEV(1) (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 PM(10) exposure also showed a trend towards this effect (p=0.056). Exposure to ozone and PM(10) predicts decline of lung function in AATD.