Table 2.
Effect estimates for the association between genetic predisposition to having chronic or aggressive periodontitisa and the risk of lung cancer by histologic subtype and smoker status
| Lung cancer | Overall |
Smokers |
Nonsmokers |
|||
|---|---|---|---|---|---|---|
| (Ncontrols = 13 780) |
(ncontrols = 9084)b |
(ncontrols = 4415) |
||||
| Ncases | βc (P) | ncases | β (P) | ncases | β (P) | |
| Overall | 18 082 | 0.004 (.83) | 15 984 | 0.002 (.93) | 1800 | −0.021 (.65) |
| Adenocarcinoma | 6730 | 0.025 (.31) | 5639 | 0.029 (.32) | 975 | 0.012 (.84) |
| Squamous cell | 4429 | −0.010 (.74) | 4209 | −0.019 (.54) | 158 | −0.040 (.77) |
| Small cell | 1853 | −0.035 (.40) | 1761 | −0.023 (.59) | 64 | −0.383 (.06) |
aThe inverse-variance weighted Mendelian randomization analysis included 8 SNPs (rs729876, rs1537415, rs2738058, rs12461706, rs16870060, rs2521634, rs3826782, and rs7762544). SNP = single nucleotide polymorphism.
bControls were shared across lung cancer histologic subtypes.
cBetas indicate the effect estimate for the association between a 1-unit increase in genetic predisposition to having chronic or aggressive periodontitis and the natural log risk for each lung cancer outcome. All statistical tests were 2-sided.