Drug Interactions With Smoking

Lisa A. Kroon, Pharm.D


Am J Health Syst Pharm. 2007;64(18):1917-1921. 

In This Article

Mechanisms for Drug Interactions with Smoking

Polycyclic aromatic hydrocarbons (PAHs) -- products of incomplete combustion -- are some of the major lung carcinogens found in tobacco smoke.[4] PAHs are also potent inducers of the hepatic cytochrome P-450 (CYP) isoenzymes 1A1, 1A2, and, possibly, 2E1.[3] Other compounds such as acetone, pyridine, heavy metals, benzene, carbon monoxide, and nicotine may also interact with hepatic enzymes but their effects appear to be less significant. Many drugs are substrates for hepatic CYP1A2, and their metabolism can be induced in smokers, resulting in a clinically significant decrease in pharmacologic effects. Thus, smokers may require higher doses of drugs that are CYP1A2 substrates. Another metabolic pathway, glucuronide conjugation, can also be induced by PAHs.[3] It is important to recognize that these pharmacokinetic drug interactions are caused by the PAHs in tobacco smoke, not the nicotine. Nicotine-replacement therapy does not contribute to the pharmacokinetic drug interactions discussed in this article. However, pharmacodynamic drug interactions with tobacco smoke are largely due to nicotine. Because it activates the sympathetic nervous system, nicotine can counter the pharmacologic actions of certain drugs.[5]


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