Three epigenetic aging markers—AgeAccelPheno, AgeAccelGrim, and DunedinPACE—correlated significantly with total nicotine equivalents in urine, a precise measure of internal smoking dose among 1,969 current smokers from the Multiethnic Cohort Study. Over 13 years of follow-up, AgeAccelGrim and DunedinPACE each increased lung cancer risk by 40% and 31% per standard deviation increase, respectively, while longer DNA methylation-based telomeres reduced risk by 21%. These epigenetic clocks maintained predictive power even after adjusting for traditional pack-years and urinary nicotine levels. This represents a significant advance in personalized cancer risk assessment. While pack-years remain the clinical standard, they capture cumulative exposure poorly compared to biological aging signatures that reflect cellular damage in real-time. The findings suggest that epigenetic clocks could identify high-risk smokers who might benefit from intensified screening or cessation interventions, regardless of their reported smoking history. However, the technology requires specialized methylation arrays and computational expertise, limiting immediate clinical translation. The research confirms that biological age acceleration serves as a mechanistic bridge between smoking exposure and disease outcomes.