We invited investigators from 22 studies with genome-wide association data and COPD case-control or general population samples with spirometry to participate in a genome-wide association meta-analysis. Additionally, we included four cohorts with Illumina HumanExome v1.2 and custom genotyping based primarily on prior top results from a previously published COPD GWAS13, using results with P < 1×10−4 using plink ‘–clump’ on the COPDGene non-Hispanic whites to perform linkage disequilibrium pruning (r2 < 0.8), preferentially retaining both an imputed and genotyped top SNP at each locus. An additional group of variants was a candidate panel, based on results from a previous candidate gene analysis54, as well as variants identified in association with lung function (supplementing the existing content on the array, which included variants from previous genome-wide association studies), including the lead SNP and a 200kb region around that SNP pruned for variants with P < 0.01 and r2 < 0.8, and additional top-ranked SNPs for COPDGene-specific analyses for lung function, bronchodilator responsiveness, exacerbations, and SNPs from candidate genes.
