Tobacco smoke interacts with medications through pharmacokinetic and pharmacodynamic mechanisms. Pharmacokinetic interactions affect the absorption, distribution, metabolism, or elimination of other drugs, potentially causing an altered response.

Polycyclic aromatic hydrocarbons in tobacco are responsible for induction of cytochrome P450 enzymes CYP1A1, CYP1A2, and possibly CYP2E1 and CYP3A .

The majority of drug interactions with tobacco smoke are pharmacokinetic, resulting from the induction of drug-metabolizing enzymes by compounds in tobacco smoke. All of these drugs are metabolized via CYP1A2. Induction of CYP1A2 by PAHs in tobacco smoke will increase metabolism, resulting in potentially clinically significant decreased pharmacologic effects of the following drugs. Following smoking cessation, a patient titrated on these medications might experience enhanced pharmacologic effects or toxicity.

This slide lists many of the clinically-significant drug interactions with smoking. Please refer to the “Drug Interactions with Smoking” handout found under the Additional Resources tab.