Chronic obstructive pulmonary disease (COPD [MIM 606963]), which includes emphysema and chronic bronchitis, is a complex disease with genetic and environmental influences [9]. COPD is a major source of morbidity and mortality in the U.S. and worldwide [10]. Previous GWAS have identified three susceptibility loci for COPD, including HHIP (hedgehog interacting protein [MIM 606178]), FAM13A (family with sequence similarity 13, member A [MIM 613299]), and a multi-gene locus on chromosome 15q25 containing candidate genes CHRNA5 (cholinergic receptor, nicotinic, alpha 5 [MIM 118505]), CHRNA3 (MIM 118503), and IREB2 (iron-responsive element binding protein 2 [MIM 147582]) [11]–[13]. Cough and phlegm production is common among COPD patients, and sputum samples may provide a non-invasive window into pathobiologic processes in the lungs of COPD patients. Therefore, we integrated GWAS data with microarray gene expression profiles from induced sputum samples from well-characterized COPD subjects participating in the Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-points (ECLIPSE) Study [14]. We addressed two hypotheses: (1) eQTL analysis will improve understanding of previously known COPD susceptibility loci, such as chromosome 15q25; and (2) eQTL SNPs can be
