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One goal of the Philip Morris Behavioral Research Lab, described in a 1981 document, was to identify responses of the human brain that change in a predictable and reliable manner as a function of cigarette smoking.36 In research projects conducted by Philip Morris from 1982 to 1995 (e.g., Project 162037), electroencephalography (EEG), pattern reversal evoked potential (PREP), and chemo-sensory event-related potential (CSERP) were used to measure physiological, sensory, and cognitive changes related to nicotine and to cigarette additives.38 Increases in tobacco filler pH increased the impact (a tobacco industry term for smokers subjective awareness of the drug effects of nicotine) and decreased PREP P 1 latencies (an objective electrophysiological measure of brain activity).39 Philip Morriss research demonstrated a systematic relationship between increases in filler pH and increases in gas phase (presumably unprotonated) nicotine.37 Philip Morris researchers noted a significant positive correlation between impact scores and P 1 -N 2 amplitudes (another objective electrophysiological measure of brain activity), both of which were shown to increase with increased nicotine or menthol delivery

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