Cigarette exposure and aging pathways: interplay between IGF-1 suppression and TGF-β increase

Abstract

Chronic cigarette smoke exposure accelerates biological aging through sustained oxidative stress, DNA damage, and low-grade inflammation, thereby perturbing tissue homeostasis—notably by suppressing insulin-like growth factor-1 (IGF-1) signaling and activating transforming growth factor-β (TGF-β) pathways. Given the inconclusive evidence linking smoking or cotinine with circulating IGF-1 and TGF-β, we examined the association between blood cotinine and these biomarkers among healthy volunteers in Yogyakarta.  This research was a cross-sectional study involving 106 healthy males and females aged 18-65 years. The data on smoking habits were collected through interviews guided by a questionnaire. Hemogram and blood chemistry examinations were done using spectrophotometric methods, while the levels of cotinine, IGF-1, and TGF-β were measured using ELISA. An independent t-test was used to compare mean levels between smokers and non-smokers groups. Pearson correlation was used for bivariate analysis to determine the association between cotinine and IGF-1 and TGF-β levels. Compared with non-smokers, active smokers exhibited markedly higher blood cotinine (41.97 ± 20.54 vs. 9.70 ± 4.20 ng/mL; P < 0.001), lower IGF-1 (55.06 ± 27.39 vs. 78.84 ± 22.23 ng/mL; P < 0.001), and higher TGF-β1 (238.60 ± 89.02 vs. 167.48 ± 104.54 ng/mL; P = 0.001). Across participants, cotinine correlated negatively with IGF-1 (r = –0.608; P < 0.001) and positively with TGF-β1 (r = 0.281; P = 0.004).  In conclusion, cigarette smoking and cotinine levels were associated with IGF-1 suppression and TGF-β elevation in healthy volunteers in Yogyakarta.

Keywords: Aging, smoking, cotinine, IGF-1 level, TGF-β level