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. 2021 Nov 23;11:22773. doi: 10.1038/s41598-021-01965-1

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© The Author(s) 2021

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Visualization of the results of primary and ordinal sensitivity analyses—Smoking. Gene expression results for six smoke-specific DEGs (upper panel) and six common DEGs (lower panel), as determined by primary and PY sensitivity analyses, are shown. Concordant statistically significant differential expression results for target genes in primary and PY sensitivity analyses indicates that smoking dose (i.e., intensity and duration of smoking) is significantly associated with gene dysregulation in smokers. In the PY sensitivity model, smokers were divided in two categories, including Light smokers [Smokers 1: PY < 7], and Heavy smokers [Smokers 2: PY ≥ 7] in comparison to Controls [No smoking history: PY = 0] (see, also legend for Fig. 2).