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. 2022 Jun 27;13:3675. doi: 10.1038/s41467-022-31030-y

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — a Manhattan plot displaying the genome-wide association statistics as a function of chromosomal position. Genes were assigned to loci using FUMA⁷⁵. The $5 \times 10^{- 8}$ significance threshold is displayed as a dashed red line, and significant loci are highlighted with red stars. b Cryptic phenotype (CP) residuals are stratified by the Pi*MZ/Pi*MM genotypes and plotted as function of pack-year quantiles. Inset: CP residuals plotted against pack-year quantiles, now stratified by the Pi*ZZ/Pi*MM genotypes. In both panels, the points represent the mean value within each quantile, and the error bars represent the 95% confidence intervals (CIs) for the mean (obtained through bootstrapped re-sampling, N = 1000). The association statistics for the genotype x smoking interaction terms are included below the inset (estimated using linear regression and two-sided T-tests). c Smoking history (expressed as pack-years) is plotted against PGS quantiles (points/error bars indicate quantile means/95% CIs). d CP residuals, after adjusting for baseline covariates, genotype, and smoking history, are plotted against PGS quantiles and stratified by the Pi*MZ/Pi*MM genotypes. The inset displays the same information but now stratified by the Pi*ZZ/Pi*MM genotypes. Both panels depict the quantile means and their associated 95% CIs. The association statistics for the PGS effects (estimated using linear regression and two-sided T-tests) are included below the inset. e CP residuals within the upper and lower 50th percentiles of the PGS distribution are stratified by both genotype and smoking history (points/error bars represent subset means/95% CIs). f Kaplan–Meier curves for COPD onset after stratifying the target cohort according PGS quintiles. g Same as in f, except only subjects with the Pi*MZ/Pi*ZZ genotypes are included. The PGS effect size and association statistics (computed using a Cox Proportional-Hazards model, see the “Methods” section) are provided for the subjects depicted in f and g. The shaded regions represent the 95% CIs for the survival curves. The summary statistics reported in this figure were not adjusted for multiple testing.