Smoking is known as a powerful predictor of pathological coronary atherosclerosis. Thoracic aortic calcification (TAC), an alternative marker for pathological atherosclerosis, has also been shown to be associated unfavorable cardiovascular outcomes. We aimed to investigate the dose-response relationship between cigarette use and calcification burden in subjects free from clinical symptoms. Among 3109 patients enrolled in this analysis, we categorized study participants according to smoking exposure pattern as: non-smokers, ex-smokers and current smokers. Smoking dose (cigarette/day), duration (years) and pack-years were semi-quantified as smoking dose exposure variables. Thoracic aortic calcification burden (including TAC score, plaque volume and plaque density) were determined and related to smoking dose and pattern information. TAC burdens (including TAC score, plaque volume and density) were highest in current smoker compared to non-smoker group, with ex-smoker showing TAC burdens in-between (all ANOVA p<0.05). Linear regression models consistently demonstrated that TAC burdens as continuous variables were independently higher in a dose-dependent manner with smoking exposure, particularly in high-dose (> 10 cigarettes/day) and the long-duration (> 3 years) smokers, even after adjusting for baseline demographic differences (all p<0.05). By logistic regression, subjects who never smoke consistently demonstrated reduced risk of TAC existence (adjusted OR: 0.65 [95% CI: 0.48-0.86], P = 0.003) in contrary to those current smokers (adjusted OR: 1.47 [95% CI: 1.10-1.89], P = 0.009). A dose-response relationship between active cigarette use and TAC burden was observed, with those who never exposed to smoking or quitted demonstrating partial protective effects. Our data provided imaging-based evidence about the potential deleterious biological hazards of long-term and high-dose cigarette consumption.