The pervasiveness of tobacco use in our society and the frequency of altered disposition and pharmacological effects of many common therapeutic and recreational drugs in smokers make it apparent that the smoking habit should be considered as one of the primary sources of drug interactions in man. Most of the experimental work in man, animals, and tissue on enzyme systems indicates that the dominant effect of smoking is enhanced disposition caused by induction of hepatic microsomal enzymes. The primary causal agents are probably the polynuclear aromatic hydrocarbons, which are potent and persistent in tissues. While several of the hepatic microsomal drug-metabolizing enzymes are stimulated in smokers, the selectivity of this enhancement in activity is unpredictable and the effects of tobacco smoke on other potential rate-limiting disposition processes are largely unexplored.
Key words tobacco - smoking effects on pharmacokinetics - polynuclear aromatic hydrocarbons - enzyme induction - marijuana
This work was supported in part by Grant 1079 from the Council for Tobacco Research and Grant 20852 from the National Institutes of General Medical Sciences, NIH.