EFFECTS OF TOBACCO SMOKING ON DRUG PHARMACOKINETICS AND CHANGES AFTER SMOKING CESSATION

Tobacco smoking remains a prevalent habit worldwide and has been demonstrated to significantly influence the pharmacokinetics and pharmacodynamics of many medications. Through induction of hepatic cytochrome P450 enzymes — particularly CYP1A2 — constituents of cigarette smoke accelerate clearance of drugs, often leading to sub-therapeutic plasma concentrations and reduced efficacy in smokers. Our 6-month observational simulation explores how stable doses of CYP1A2-substrate drugs behave in active smokers, and how these parameters shift following smoking cessation without dose adjustment. Based on aggregated literature data and enzyme-activity patterns, we model that smokers maintain 30–70 % lower systemic exposure to such drugs compared to non-smokers, while after cessation — as CYP1A2 activity normalizes — identical dosages lead to significantly increased plasma concentrations, risking toxicity. These findings underscore the critical need for dose re-evaluation and therapeutic drug monitoring when a patient’s smoking status changes. Personalized dose adjustment during and after smoking cessation is recommended for medications metabolized via smoking-sensitive pathways.