Effect of Earlier Age of Tobacco Exposure on Accelerated Biological Aging in Adulthood.

Abstract

To investigate how early-life tobacco exposures implicate accelerated biological aging in adulthood and the potential mechanism. This study used questionnaires to determine when the participants smoked and whether their mothers smoked when pregnant. Early-life tobacco exposures included in utero tobacco exposure and age of smoking initiation. For evaluating biological aging, we used the following 8 outcome measures: telomere length, frailty index, homeostatic dysregulation score, Klemera-Doubal method biological age, age-related hospitalization rate, premature death, and life expectancy. Mediation analysis was used to identify the role of inflammation factors. During a median follow-up of 14.6 years, 8 outcome measures in participants were analyzed for age of smoking initiation (N=320,453). Compared with never smoking, smoking initiation at age 5 to 12 years (β=3.043; 95% CI, 2.683 to 3.403 and β=-0.011; 95% CI, -0.016 to -0.006), 13 to 17 years (β=1.343; 95% CI, 1.226 to 1.460 and β=-0.007; 95% CI, -0.009 to -0.005), and 18 years and above (β=0.949; 95% CI, 0.823 to 1.075 and β=-0.004; 95% CI, -0.006 to -0.003) were significantly associated with increased Klemera-Doubal method bioage and shorter telomere length, as well as with other aging-related outcome measures. Markers of inflammation significantly mediated up to 0.00% to 43.58% of the studied associations above. In utero tobacco exposure and earlier age of smoking initiation were significantly associated with accelerated biological aging. These associations were in part mediated through inflammation markers.