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. 2012 Oct 15;7(10):e47705. doi: 10.1371/journal.pone.0047705

Table 3. Mediation analysis results using data from a lung cancer genome-wide association study.* .

Standard Approach Our Approach
Estimates 95% CIs Estimates 95% CIs
a1 0.2477 (0.1270, 0.3684) 0.2231 (0.1024, 0.3438)
a2 0.2395 (0.0741, 0.4049) 0.2092 (0.0438, 0.3746)
d 0.6482 (0.4148, 0.8816) 0.6397 (0.4063, 0.8731)
b1 0.1036 (−0.0667, 0.2739)
b2 1.0919 (0.8422, 1.3416)
c′ 0.2350 (0.1101, 0.3599)
IE1 ( PM1 ) 0.0257 (3.7%) (−0.0181, 0.0752) 0.1385 (18.3%) (0.0601, 0.2195)
IE2 ( PM2 ) 0.2615 (37.5%) (0.0283, 0.4059) 0.2284 (30.2%) (0.0398, 0.4624)
IE3 ( PM3 ) 0.1753 (25.1%) (0.0733, 0.2995) 0.1558 (20.6%) (0.0566, 0.3123)
IEt ( PMt ) 0.4625 (66.3%) (0.1890, 0.6481) 0.5227 (69.1%) (0.2722, 0.8476)
TE 0.6975 (0.3864, 0.9079) 0.7577 (0.4846, 1.0987)

CI: Confidence interval

*

Both daily smoking quantity and COPD were used as the mediators in the multiple-mediator model. The 95% CIs for the indirect effects were estimated based on 10,000 bootstraps. Includes the indirect effect through smoking (i.e., IE1 = a1b1), the indirect effect through COPD (i.e., IE2 = a2b2), the three-path indirect effect through smoking and COPD (i.e., IE3 = a1db2), the total indirect effect (i.e., IEt = IE1+IE2+IE3), the total effect (i.e., TE = IEt+c′), and the percentages of the SNP-lung cancer association explained by different paths (i.e., PM1 = IE1/TE, PM2 = IE2/TE, PM3 = IE3/TE, and PMt = IEt/TE).