The number of loci identified as influencing risk to COPD to date is modest, despite the relatively large sample size of this study; these loci explain < 5% of the liability-scale variance. To explore whether additional true association signals of weaker effect – beyond the ability to detect in our current analysis – might be present, we examined the characteristics of the top results (P < 0•01) in a meta-analysis of three white cohorts (ECLIPSE, NETT/NAS, and GenKOLS) within the COPDGene non-Hispanic whites. We found the direction of effect in the first three cohorts was consistent with the direction of effect in COPDGene more often than expected by chance alone (P = 0•03). This result suggests additional signals of significance may be found in larger GWAS, and are consistent with a recent analysis of COPDGene data18. As with most GWAS studies, the effect sizes of these identified loci are relatively small; however one subject may carry multiple risk loci. Within the COPDGene non-Hispanic whites, each additional copy of a risk allele within a composite risk score resulted in an increase
