Studies On Central Nervous System Effects Of Nicotine

The documents include summaries of several research reports that examine the effects of nicotine on the central nervous system (CNS). All but one are internal BAT reports. The exception is a 1971 report from the labs of the Imperial Tobacco Group, Limited, in the United Kingdom.

G. Lawrence Willey and D. Neville Kellett of the Huntingdon Research Centre of the Imperial Tobacco Group reported their preliminary work with nicotine administration to squirrel monkeys in early 1971 {1218.01}. Experiments in this series of studies were to include

measurements at the brain surface of acetylcholine, the naturally occurring neurotransmitter that nicotine mimics; effects of nicotine on the electroencephalogram; electrical stimulation studies of the brain; and behavioral effects. In their report the authors explicitly acknowledge that their experiments with monkeys sought to model the human experience.

Actions of nicotine at peripheral sites in the body have been extensively investigated, but much less is known about its central effects. The aim of the studies to be reported here is to determine whether, in doses comparable to those taken into the blood by smokers, nicotine affects physiological processes and behavioural functions of the central nervous system of the primate. {1218.01, p. 1}

Later in the report, the authors again explicitly acknowledge that the experiment was based on the conceptualization of nicotine as a drug.

We also intend to compare changes produced by nicotine with those elicited by other drugs which are known to affect central nervous system function e.g. caffeine, amphetamine, chlorpromazine [an antipsychotic drug], meprobamate [a sedative]. {1218.01, p. 4}

Two electroencephalograph (EEG) studies of smoking were reported in late 1974 {1205.15; 1221.01}. The first, by R. F. Brotzge and Dr. J. E. Kennedy of B&W, describes an increase in alpha brain wave activity of adults after they smoked a cigarette {1121.01}. The report speculates that the effect "may reflect both psychological and physiological responses." (In this context, as mentioned, the term "physiological" appears to mean "pharmacological.") Evidently, this study was undertaken at B&W to facilitate product development.

The development of new products and the modification of existing ones requires that we have some knowledge of the smoker toward whom these efforts are directed. The work described in this report is focused on the acute, or immediate physiological response of smokers. {1221.01, p. 1}

By saying that product design can be guided by pharmacological studies such as this, the authors reveal an intention to affect the structure or function of the body. As with other material in this chapter, it contributes to a determination that the FDA has jurisdiction over tobacco products.

The second EEG study was conducted by A. K. Comer and R. E. Thornton at BAT's Southampton laboratory {1205.15}. The study found that smoking increased the activity being measured in some subjects but decreased it in others. In their discussion the authors note that nicotine "has been assumed to be the main pharmacologically active component

in smoke." They speculate that the disparate results may be explained by the hypothesis "that smoking may assist some people to optimise the level of activity in the brain."

These three reports illustrate the fact that, twenty years ago, Imperial, B&W, and BAT each thought that it was useful to examine the effects of nicotine on the central nervous system.